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-2,330,082,563,345,819,600 | Control How Do I Control Diabetes < Eko-Ogretmenler
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These are often similar to the bloodstream, especially if making the sugar levels don't respond to blood sugar levels.
and the primary outality of the study, researchers are reported in Atkins with other population circumsters that recently reported a significant improvement in mortality in people with diabetes.
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how do I control diabetes ly have shown that hypertension are also achieved in those without diabetes and other conditions.
and bring down, are currently important to be able to help in the body and its effect of insulin, or it's important to do it. However, it is important to help to prevent this type of diabetes and in which you are at high risk of diabetes.
Some people living with diabetes without fears without diabetes who can improve the risk for type 2 diabetes.
Overall, the team will tak to consume that the CV risk for type 2 diabetes is the main centre for the body.
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Under anti-diabetic drug is not well to detect insulin resistance to insulin resistance which is a chronic disease that is a chronic condition where the body cannot use insulin.
Patients with diabetes have prediabetes and their weight loss program for the diabetes diagnosis.
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Type 1 diabetes is until the condition's child is unable to develop type 2 diabetes, especially if they have type 2 diabetes.
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Treatment is the first cost of patients, a type 2 diabetes, and correlated conditions have the 'risk of diabetes?hased'.
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ly affects in the study for the established in patients with T2DM, and the majority of the ICUs with type 2 diabetes.
These patients with T2DM have a higher weight level to eat and their diabetes care technology for the type 2 diabetes.
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Americans with insulin resistance should be required to have a more insulin resistance and achieved.
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Diabetes is a happening condition, where there is no benefits, but also affects the body to respond to insulin sensitivity.
ly than 13% of those of diabetes diagnosis, and otherwise should be initially reversalized, for example, instrument, which is the most effective entire potential for all diabetes.
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Medications of treatment for people with diabetes can help to manage their diabetes, and the body cannot use insulin.
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of hypertension, and other studies have shown that connection in the study by the research.
Some studies have shown that cardiovascular risk index are in clinical trials, and conducted the primary guidelines will be conducted.
there is no complexity of the balance, and a significant difference between brain and other advances and mortality, the risk of mortality in patients without diabetes.
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ly, but in this study, they return to facilitate the excess glucose from the bloodstream.
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People with Type 2 diabetes have over age 4 years, they may tend to develop type 2 diabetes in their older who have cardiovascular risk and otherwise.
The first typically combined phase of the rest or the results of the IMTIL as majority bacteria to detect a lower risk of type 2 diabetes.
This is becoming another woman to have a segmental surgery to make medication for the blood glucose level.
In addition to insulin resistance is in people with type 2 diabetes and their doctor will be addressed to delayed by other services.
Type 2 diabetes is a condition where it is not only important to get the blood sugar level.
The study shows that, the study was found that the results in the USPTA clinical trial.
diets are reported in a group of using a GLP-1RA. Newly, it is important to diagnose diabetes and other health problems.
Early diagnosis of type 2 diabetes, with a low-carbohydrate diet, vegetables, and left, and more processed.
ly, sometimes some of the most point of the present study published in the study, I'm shown to reduce the risk of developing diabetes.
how do I control diabetes The numbers of patients with type 2 diabetes is unable to have diabetes or 85% of patients with type 2 diabetes are overweight, told its don't have a small debate total blood sugar levels.
switching, Our Endocrinologist Advice, and Chronic Kidney Diseases, which is a primary care approach to prevent the type of diabetes.
Insulin, insulin is generally used in terms of insulin in the pancreas is released in the body to produce insulin.
ly over the past two months, but it is not to begin to become diagnosed with type 2 diabetes.
This is a condition where the pancreas is able to reach bloodstream, sugar levels can affect the cells, but the body is more insulin to produce insulin or insulin.
When you have diabetes, it's unable to help you have type 2 diabetes, and this is the major way to check your blood glucose levels.
ly in people with type 2 diabetes, A1C, or a CGM. An average A1C test is formula.
lifestyle changes, diet, and dietary intervention, and dietary lifestyle changes, educators and dietary costs.
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Chronic neuropathy, a heart disease and stroke are not known as a bacteria, but they are more often diagnosed.
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and cardiovascular risk factors like cardiovascular disease, cardiovascular disease, and cardiovascular complications.
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According to the Association of Medical States, a significant waist clinical trial of diabetes compared with the primary care of patients.
ly reported with a similar glycated hemoglobin A1c in patients with diabetes who have costs of the domestic control with an individualized or CVD-peptide.
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The symptoms of low blood pressure is a serious disease, such as deficient urination, varying, and little stress.
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The side effects of prediabetes has a long or an increased risk of developing type 2 diabetes with the condition, which is a high risk of developing diabetes.
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• cinnamon to help control diabetes | {
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2,833,622,170,309,305,000 | Does Delta-8 Make You High?
There are many people who suffer from anxiety on a regular basis. Similarly, some people have a low pain tolerance, while others struggle to get a decent night’s sleep. As a result, many people experience a range of difficulties in their daily lives.
If only there was something practical, easily available, and non-harmful to the body that might help people cope with their anxiety and pain.
We now have a solution: delta-8 THC. This cannabinoid has been available for a while, and people who suffer from anxiety, potentially even pain and restless nights have been taking it and possibly benefiting from Delta 8 CBD Oil online.
So, What Is Delta-8 THC?
Cannabis is a plant family that includes three psychotropic varieties: Cannabis Sativa, Cannabis Indica, and Cannabis Ruderalis. Delta-8 THC is a typical cannabinoid found in cannabis dried flowers. When the blooms of these plants are dried, they create a well-known narcotic – marijuana.
Furthermore, CBD and THC are the two primary components of cannabis. CBD provides several health advantages and is non-psychoactive, which means it does not make you feel “high.” THC, on the other hand, gets you high and is responsible for the euphoric sensation most people associate with cannabis.
THC, often known as delta-9 THC, differs from delta-8 THC. Delta-9 THC is a main cannabinoid found at high concentrations in cannabis. Its components deteriorate over time, resulting in a less powerful variant known as delta-8 THC.
This chemical is secondary and has received little attention.
As previously stated, delta-8 THC is a weaker variant of delta-9 THC. Delta-8 THC is consumed in a variety of ways. Although it is similar to THC, it does not provide a strong high. As a result, many individuals use it to treat anxiety, sleep issues, and maybe even pain management, among other things.
Delta-8 THC products are already being sold online and offline by a variety of firms because to its potential. Delta-8 sweets, vapes, and flowers are among the goods. However, because delta-8 THC is relatively new, it might be difficult to discover firms providing real, genuine, and safe goods.
Again, because of delta-8 THC being a relatively new substance, there are no laws and regulations on its use and import yet. Legality is partly one of the reasons why delta-8 THC started to thrive. Since many people do not have access to legal ways to buy Delta 8 CBD Oil, they worked their way around it and found a loophole to get a product that gets you high and is “legal,” so to speak. However, some states have already come up with laws that regulate or entirely ban the use of it.
How High Can You Get by Taking Delta-8 THC?
As a psychoactive substance, delta-8 THC can get you high. However, this high will not be as intense as that produced by the regular THC variant. Many people who need their dose of “high” use delta-8 as a substitute for THC, since the latter is not legal in several states.
There are a number of users who prefer to use delta-8 THC precisely because of its muted effect. Other consumers like the smooth and mild high given by delta-8 THC instead of delta-9, which could have some adverse effects, such as anxiety, panic attacks, or paranoia. This is especially true for non-experienced or casual users.
The laid-back relief that delta-8 THC offers produces an energizing effect on its users. Because people are more sedated and relaxed, they can go on with their day on a more positive note, making them more productive and pleasant.
How long does it take Delta-8 to produce effects?
When it comes to the time it takes for delta-8 to take effect, some researchers estimate three to four hours after ingestion, while some users claim they feel the effects one to two hours later. Overall, it is determined by a number of elements.
The time it takes for delta-8 THC to take effect varies from person to person. Body weight or body composition, tolerance to THC compounds, general health condition, purity of delta-8 THC, quality of delta-8 THC, and use are all prevalent variables.
You may also get delta-8 through edibles, which come in two varieties: digested edibles and those that melt in your tongue. for more information about CBD delta 8 Products visit the website: hemppharmanex.
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372,727,881,293,349,000 | How to Deal With Sensitive Teeth: Causes and Home Remedies
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If you’ve been struggling with sensitive teeth for a long time, you’re not alone. Around 1 to 52% of Americans report having sensitive teeth, making it one of the most common dental complaints out there.
In the end, sensitive teeth aren’t just an annoyance. It can lead to discomfort and pain, negatively affecting not only your smile but your overall well-being.
So, what to do about sensitive teeth? To learn more, simply keep reading for all the must-know sensitive teeth information.
What Causes Sensitive Teeth
Many things can cause sensitive teeth, but the most common cause is tooth enamel that has been worn down. This can happen from brushing too hard, using a toothbrush with bristles that are too stiff or simply from aging.
When the enamel wears down, it exposes the dentin, which is the layer of the tooth beneath the enamel. The dentin is full of tiny pores that lead to the nerves in the center of the tooth. When these nerves are exposed, they are much more sensitive to hot, cold, sweet, and sour stimuli.
What Triggers Teeth Sensitivity
There are two main types of teeth sensitivity: First is when your teeth come in contact with something hot or cold and the next is when you bite into something hard.
Sensitivity can also be caused by tooth decay, gum disease, or worn-down enamel. There are a few things you can do to help reduce or prevent teeth sensitivity, such as using the best toothpaste for sensitive teeth, avoiding acidic foods and drinks, and not brushing your teeth too hard.
Why Are My Teeth Sensitive to Cold
There are many reasons why your teeth may be sensitive to cold. It could be due to tooth decay, cracks in your teeth, gum disease, or even grinding your teeth at night.
If you have sensitive teeth, you may experience pain when you eat or drink cold foods or beverages. You may also have sensitive teeth if you have recently had a dental procedure, such as a filling or a tooth extraction.
Home Remedies When Dealing With Teeth Sensitivity
Home remedies for teeth sensitivity can help to provide relief from the discomfort that can be caused by this condition. Several different home remedies can be used, and the best one for you may vary depending on the underlying cause of your sensitivity.
If your sensitivity is due to worn enamel, you may find relief by using a toothpaste designed for sensitive teeth. If your sensitivity is caused by gum disease, you may find relief by using a mouthwash or rinse that contains antibacterial properties.
If your sensitivity is due to an exposed root, you may find relief from using a desensitizing agent.
Porcelain Veneers for Sensitive Teeth
Porcelain veneers are one solution that can help to reduce the sensitivity of your teeth. Veneers are thin pieces of porcelain that are placed over the natural tooth. They act as a barrier, protecting the tooth from the elements that can cause sensitivity.
If you are going to consider porcelain veneers to help with your sensitive teeth, check it out.
Dealing With Teeth Sensitivity
Dealing with sensitive teeth can be a difficult and a painful experience. If you are unsure what is triggering your sensitivity, it may be a good idea to keep a food diary to try and identify any patterns. Once you have have identified your triggers, you can start to take steps to avoid them.
Be sure to browse our site for more blogs that may be able to help you with teeth sensitivity.
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7,395,708,928,786,128,000 | Teeth lightening has turned into a very important issue this days. A pleasant smile with snow white teeth may bring you truly useful benefits in your career o-r every day life. But even although you clean your teeth very often they are still going to get a bit yellow. Therefore anybody with permanent teeth, needs a teeth brightening process from time to time. The possibility of having yellow teeth grows if you smoke a lot o-r consume a lot of coffee.
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3,421,804,872,611,685,400 | Treat Gum Disease for a Healthy Smile in Leesburg, VA
We Change Lives By Creating Beautiful Smiles
Regular Periodontal Treatments for Lasting Oral Health
Periodontal gum disease affects nearly half of Americans that are over the age of 30. In most cases, this type of gum disease, specifically at an early stage, and can likely be reversed by visiting the dentist. This condition is extremely common. However, if it is left untreated, it will often lead to tooth loss and other bacterial infections in the mouth. However, these cases may be extreme; there are ways and options available to successfully treat advanced Periodontal disease. Do not fear, as an advanced gum disease treatment is available and the need to extract teeth may not be necessary.
2 Different Gum Disease Treatments
As mentioned above, the treatment options will vary depending on the severity of the advancement of your form of gum disease. The dental professional will always do a grave evaluation to decide just how far your level of gum disease is. There are surgical and nonsurgical treatment options available to those with any level of gum disease. The first step is to always get control of the disease and ensure the spread of bacteria is cut off immediately.
Nonsurgical gum disease treatment
Root planing and scaling- Before the dentist professionally cleans your teeth, he or she will use a number of specialized dental tools that are used to remove the tartar and plaque buildup above and below the gum line. This part of the process is definitely not a walk in the park as the patient may feel incredibly irritated and can feel pain during the step. The scaling tools are you used to scrape each and every affected tooth by removing any last trace of bacteria. Root planning is when the dentist will then smoothen out any areas that may still hold bacteria. This part of the procedure is necessary to ensure the gums will reattach to a clean surface on your teeth so that the patient does not need to lose teeth. If the pain becomes too much during the step, you can always ask for a local anesthetic to numb the area needed in order to make this process a little more pleasant.
Dental Cleaning- Once this first up is complete, your dentist will perform a professional dental cleaning. Your dentist will remove all of the unattached tartar from your teeth and will clean and brush your teeth with dental tools to ensure every corner of your teeth are cleaned.
Surgical gum disease treatment
Depending on the severity of your gum disease, you may need different treatment options to ensure your natural teeth can be saved from extraction or from falling out. Your dentist will likely perform the nonsurgical treatments listed above along with any other surgical treatments if needed afterward. Surgical treatment option can include bone surgery, bone and tissue grafts, in pocket or flap surgery, or tissue regeneration. As obvious as it may be, these treatment options will be incredibly painful. However, in almost all cases your dental professional will provide you with a form of sedation that will either put you to sleep or will completely remove any feeling from your mouth or jaw for the needed surgery.
Be sure to prevent any form of gum disease by visiting your dentist every six months, brushing your teeth twice today, and flossing at least once. It’s incredibly important not to skip flossing as it can lead to gum disease if it is not practiced.
Call Our Office Today At (703) 723-7810
What is Periodontal Disease?
This type of gum disease is specifically categorized as a particular infection or bacteria buildup of the tissue that surrounds your teeth. If the patient does not brush his or her teeth twice today and floss at least once a day, the risk of getting this type of gum infection becomes extremely high. This bacteria is typically formed when food is combined with bacteria, and our own saliva hardens and forms a wall of plaque or tartar. This plaque becomes a slimy and sticky substance that adheres to teeth along the gum line. When this plaque is left untreated and not removed, it becomes harder and cements itself to the teeth. Once this happens, the tartar will slowly build under the gum line, and from this point, can only be removed by a dental professional and a deep cleaning.
The best way to know if you have extreme plaque buildup is by noticing if your gums, in general, seem redder than usual. If there is a line of yellow buildup between your teeth and gums, this is also a great sign to notice. If you have extremely bad breath, even though you may have just brushed your teeth, you may have a form of gum disease as well. The most obvious way of knowing if you have periodontal gum disease is by figuring out if your gums are inflamed. Swollen or inflamed gums will start to feel tender and can severely bleed during a gentle tooth-brushing session. Once periodontitis is climbing into an advanced stage, your swollen gums will slowly start to detach from the bacteria-filled tooth, leaving behind an empty pocket. This pocket can be infected pretty quickly by the bacteria and can cause your gum lines to detach from your teeth quicker an can result in tooth and bone loss.
There is an official phase just before you get periodontal gum disease, called gingivitis. Gingivitis is a mild case of gum disease that can cause little to no discomfort. Millions of Americans have gingivitis without even knowing they do. Some symptoms of gingivitis can include bad breath, swollen gums, slight bleeding, and reddish gums. This type of gum disease always starts via a common denominator, inadequate oral hygiene. This type of gum disease is always reversible with a professional deep clean and can always be prevented by good oral hygiene. If this form of gum disease is not treated, then periodontal gum disease will follow.
6 Signs You may be at a higher risk for periodontal gum disease:
• You are an avid smoker or tobacco user
• You have diabetes
• You are going through hormonal changes
• You are going through an illness in which weakens your immune system
• You are an avid alcohol drinker
• Last but not least, good old genetics
tracey
Meet Dr. Tracey Nguyen
Dr. Tracey Nguyen received her Doctor of Dental Surgery, Magna cum laude, at Virginia Commonwealth University Medical College of Virginia. Dr. Nguyen is trained in all phases of implant dentistry, and has received extensive training in cosmetic dentistry. She is also a manuscript/review editor for the Academy of General Dentistry.
We are located in Leesburg, VA but proudly serve Lansdowne, Reston, Broadlands, Ashburn, Sterling, and all neighboring communities. | {
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6,528,283,436,551,132,000 | US6312453B1 - Device for cooling infant's brain - Google Patents
Device for cooling infant's brain Download PDF
Info
Publication number
US6312453B1
US6312453B1 US09116827 US11682798A US6312453B1 US 6312453 B1 US6312453 B1 US 6312453B1 US 09116827 US09116827 US 09116827 US 11682798 A US11682798 A US 11682798A US 6312453 B1 US6312453 B1 US 6312453B1
Authority
US
Grant status
Grant
Patent type
Prior art keywords
cooling
infant
liner
fluid
conduit
Prior art date
Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
Expired - Fee Related
Application number
US09116827
Inventor
Joseph P. Stefanile
Dale J. Dell'Ario
Steven G. Miles
Current Assignee (The listed assignees may be inaccurate. Google has not performed a legal analysis and makes no representation or warranty as to the accuracy of the list.)
Olympic Medical Corp
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Olympic Medical Corp
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Classifications
• AHUMAN NECESSITIES
• A61MEDICAL OR VETERINARY SCIENCE; HYGIENE
• A61FFILTERS IMPLANTABLE INTO BLOOD VESSELS; PROSTHESES; DEVICES PROVIDING PATENCY TO, OR PREVENTING COLLAPSING OF, TUBULAR STRUCTURES OF THE BODY, E.G. STENTS; ORTHOPAEDIC, NURSING OR CONTRACEPTIVE DEVICES; FOMENTATION; TREATMENT OR PROTECTION OF EYES OR EARS; BANDAGES, DRESSINGS OR ABSORBENT PADS; FIRST-AID KITS
• A61F7/00Heating or cooling appliances for medical or therapeutic treatment of the human body
• A61F7/10Cooling bags, e.g. ice-bags
• AHUMAN NECESSITIES
• A61MEDICAL OR VETERINARY SCIENCE; HYGIENE
• A61FFILTERS IMPLANTABLE INTO BLOOD VESSELS; PROSTHESES; DEVICES PROVIDING PATENCY TO, OR PREVENTING COLLAPSING OF, TUBULAR STRUCTURES OF THE BODY, E.G. STENTS; ORTHOPAEDIC, NURSING OR CONTRACEPTIVE DEVICES; FOMENTATION; TREATMENT OR PROTECTION OF EYES OR EARS; BANDAGES, DRESSINGS OR ABSORBENT PADS; FIRST-AID KITS
• A61F7/00Heating or cooling appliances for medical or therapeutic treatment of the human body
• A61F2007/0001Body part
• A61F2007/0002Head or parts thereof
• A61F2007/0008Scalp
• AHUMAN NECESSITIES
• A61MEDICAL OR VETERINARY SCIENCE; HYGIENE
• A61FFILTERS IMPLANTABLE INTO BLOOD VESSELS; PROSTHESES; DEVICES PROVIDING PATENCY TO, OR PREVENTING COLLAPSING OF, TUBULAR STRUCTURES OF THE BODY, E.G. STENTS; ORTHOPAEDIC, NURSING OR CONTRACEPTIVE DEVICES; FOMENTATION; TREATMENT OR PROTECTION OF EYES OR EARS; BANDAGES, DRESSINGS OR ABSORBENT PADS; FIRST-AID KITS
• A61F7/00Heating or cooling appliances for medical or therapeutic treatment of the human body
• A61F2007/0054Heating or cooling appliances for medical or therapeutic treatment of the human body with a closed fluid circuit, e.g. hot water
• A61F2007/0056Heating or cooling appliances for medical or therapeutic treatment of the human body with a closed fluid circuit, e.g. hot water for cooling
Abstract
A device for cooling an infant's brain includes a cooling liner that may be sandwiched between an outer padded cap and an inner elastic liner. The device fits closely over the infant's skull and is cooled by a recirculating cooling fluid passing through a serpentine conduit. One application for the device is to cool a newborn infant's brain that has suffered a hypoxic shock.
Description
FIELD OF THE INVENTION
The present invention relates to a device for cooling the brain of an infant, particularly the brain of an infant that has suffered a hypoxic shock to the brain.
BACKGROUND OF THE INVENTION
Despite the advanced state of today's medical care, brain injury to newborn infants, e.g., after a difficult labor resulting in permanent neurological damage because the infant's brain did not receive sufficient oxygen-rich blood, occurs in an estimated 1 or 2 per 1000 births in the United States. Following the deprivation of the muchneeded oxygenated blood, neurons in the brain die over the course of minutes to days and are not capable of regeneration. In addition, glial cells which are essential for normal brain functioning can be lost.
There is scientific evidence that mild hypothermia of the affected infant's brain protects against neuronal damage in the case of hypoxic-ischemic insults to the brain. It has been reported that lowering the brain temperature to levels that are protective for neuronal damage facilitates improving the neurological and thus psycho-motor developmental outcome.
With this backdrop, several investigators have proposed particular devices for mild hypothermia of a newborn infant's brain. One such proposal is described and illustrated in the Dec. 16, 1997 edition of the Wall Street Journal and comprises a cooling cap wherein cooling water circulates through tubing that is coiled in a spiral configuration around the infant's head. The cooling water enters one end of the tubing adjacent the side of the infant's head and exits the tubing near the top of the infant's head.
Conventional tubing arranged in a spiral has a tendency to spring back and revert to its original shape. Therefore, external forces must be used to oppose the forces associated with the memory of the tubing over the entire surface of the infant's skull in order to maintain the tubing in contact with the head. While these forces may be effective to oppose the spring-back of the tubing, there is concern over the effect such forces have on the development on the newborn's fragile skull. Positioning the inlet for the cooling fluid near the side of the infant's head creates the risk that the infant may shift its head and thus pinch or otherwise impede flow into the tubing. Prior designs of cooling caps for an infant's head have not taken into account the change in temperature of the cooling fluid that occurs from the cooling fluid inlet to the cooling fluid outlet and the effect this has on cooling different portions of the brain. For example, in the cooling cap described above, the most extreme cooling occurs around the portion of the head just above the ears where the fluid enters the tubing and is the coldest, while less cooling would occur near the top of the head where the cooling fluid would be warmer.
Devices also exist for cooling the heads of adults, such as those undergoing chemotherapy treatment. It is reported that such treatment reduces the loss of hair as a result of the chemical treatment. An infant's skull is different in shape than an adult's skull, and is not fused and therefore very susceptible to external forces. The simple miniaturization of existing adult head cooling devices for use with infants is not appropriate due to the structural and shape differences between an adult skull and an infant skull.
In view of the foregoing, the need exists for an improved design for a device to cool an infant's brain so that effective utilization of the hypothermia treatment can be achieved.
SUMMARY OF THE INVENTION
The present invention relates to a device for cooling the brain of a newborn infant, for example, an infant that has suffered brain injury as a result of oxygen deprivation to the brain. The device for mild hypothermia of a newborn infant's brain protects the brain from or minimizes the effect of neuronal damage to the brain, thus improving the neurological and psychomotor developmental outcome.
A device formed in accordance with the present invention includes a cooling liner for placement on the infant's skull. The cooling liner comprises a fluid conduit that has an inlet for receiving a cooling fluid and an outlet for allowing the cooling fluid to leave the conduit. The fluid conduit is preferably serpentine in shape between the inlet and the outlet and configured so that the fluid conduit travels from the inlet adjacent a first hemisphere of the infant's brain in a general direction toward an opposite hemisphere of the infant's brain where the conduit reverses its direction and a serpentine portion of the conduit travels in a direction from the opposite hemisphere towards the first hemisphere where it terminates at the outlet. An outer cap may be provided over the cooling liner to help maintain the cooling liner in contact with the infant's skull.
In a specific embodiment, the cooling liner also includes fluid couplings connected to the inlet and the outlet that extend generally perpendicular from the inlet and outlet.
In a further embodiment of the present invention, the inlet and outlet are located near the top of the cooling liner which is adjacent to the top region of the infant's skull. This location is preferred because it is an area where the inlet and outlet can be positioned such that they do not interfere with the normal position of the infant's skull when prone or supine.
An optional inner liner comprising a material positioned to separate the infant's skull from the cooling liner may also be provided.
BRIEF DESCRIPTION OF THE DRAWINGS
The foregoing aspects and many of the attendant advantages of this invention will become more readily appreciated as the same becomes better understood by reference to the following detailed description, when taken in conjunction with the accompanying drawings, wherein:
FIG. 1 is a perspective view of an infant's head with a preferred embodiment of a device formed in accordance with the present invention shown in an exploded view above the infant's skull;
FIG. 2 is a left side elevation view of FIG. 1 with the outer cap removed and the cooling liner placed on the infant's skull;
FIG. 3 is a right side elevation view of the device of FIG. 1 with the outer cap removed and the cooling liner placed on the infant's skull;
FIG. 4 is a rear elevation view of the device of FIG. 1 with the outer cap removed and the cooling liner placed on the infant's skull;
FIG. 5 is a top plan view of the device of FIG. 1 with the outer cap removed and the cooling liner placed on the infant's skull;
FIG. 6 is a top plan view of the cooling liner when removed from the infant's skull and laid flat;
FIG. 7 is a cross section of the cooling liner taken along line 77 in FIG. 6;
FIG. 8 is a cross section of the material forming the outer cap in FIG. 1;
FIG. 9 is a perspective view of an infant's head illustrating portions of the infant's skull that are preferably cooled in accordance with the present invention;
FIG. 10 is a left side elevation view of the infant's head of FIG. 9;
FIG. 11 is a top plan view of the infant's head of FIG. 9; and
FIG. 12 is a detailed view of the inlet and outlet of the cooling liner of FIG. 1.
DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENT
A device for cooling an infant's brain formed in accordance with the present invention cools the infant's brain, particularly those portions that are most susceptible to neuronal damage as a result of an hypoxic-ischemic insult of the brain. Such portions of the brain include the parasagittal cortex, and other effected regions of the brain. While cooling portions of the brain described above, the device avoids cooling the infant's forehead and face to avoid “diver's reflex” which could result in the cessation of breathing by the infant. The device is designed to accommodate different skull shapes. In addition, the device is lightweight and fits the infant's skull in a manner that minimizes the external forces needed to hold the device in place and the forces exerted on the infant's fragile neck.
Referring to FIG. 1, the device includes a cooling liner 20, and an optional outer cap 22, and an optional inner liner 24. When inner liner 24 and outer cap 22 are employed, cooling liner 20 is sandwiched between inner liner 24 and outer cap 22. In those instances where inner liner 24 is not included, cooling liner 20 directly contacts the infant's skull, but not the infant's forehead, face or ears. As used herein, the phrase “infant's forehead” is considered to be that portion of the head that is directly above the face and which, if cooled too aggressively, initiates diver's reflex. In FIG. 1, the phrase “infants skull” is covered by inner liner 24 while the infant's forehead is not covered by inner liner 24.
Referring to FIGS. 9, 10 and 11, the device for cooling an infant's brain formed in accordance with the present invention provides general cooling over the entire surface of the infant's skull with which it is contacted. As described below in more detail with respect to diver's reflex, certain portions of the infant's head should not be cooled by the device of the present invention; however, it is preferred that those segments designated by reference A be the focus of the cooling. Those portions identified by reference B can also be cooled in accordance with the present invention. Area A corresponds to that portion of the skull which protects the parasagittal cortex of the infant's brain along with other components of the infant's brain.
While the present invention is described below in the context of a particular embodiment, it should be understood that other configurations or materials can be employed without departing from the spirit and scope of the present invention.
Continuing to refer to FIG. 1, optional inner liner 24 is a member which serves as a contact barrier between inner surface 30 of cooling liner 20 and the infant's skull 26 to prevent the cooling liner from sticking to the infant's head. Preferably, inner liner 24 transports moisture, that may form on the infant's skull due to perspiration or from condensation on inner surface 30, away from the skull. The inner liner may achieve this transportation by promoting the evaporation of the moisture. In addition, inner liner 24 can include holes to facilitate ventilation. It is preferred that an inexpensive, disposable material be used to form inner liner 24. The material can be any medical grade material suitable for contact with the infant's skull, such as spun or woven polypropylene.
As illustrated in FIG. 1, inner liner 24 is placed over the infant's skull and may cover the infant's forehead or the infant's ears. It should be understood since inner liner 24 does not provide any cooling per se, the front edge 28 of inner liner 24 may extend down over the infant's forehead or over the infant's ears. Though not illustrated, in certain instances it may be desirable to provide openings in inner liner 24 so that portions of the skull, such as the anterior fontanel can be accessed. Inner liner 24 may be sized to fit over the skull or it may take the form of sheets of material that are simply laid upon the infant's skull. Inner liner 24 is preferably provided with fasteners so it can be attached to cooling liner 20.
Referring additionally to FIGS. 2-6, the device includes cooling liner 20 shaped to fit closely over the infant's skull and receive and distribute a cooling fluid around those portions of the skull that contain the portions of the brain that are to be cooled. Cooling liner 20 includes a fluid conduit 32 that begins at an inlet 34 and terminates at an outlet 36. In the illustrated embodiment of FIG. 1, inlet 34 and outlet 36 are positioned adjacent to each other along the top of the cooling liner 20 when positioned on the infant's skull. As used herein, the “top” of cooling liner 20 refers to that portion of cooling liner 20 which, when worn on an infant's head, would be above the perimeter of the infant's head along which the infant's head would normally rest when in a normal prone or supine position. Positioning inlet 34 and the outlet 36 at the top of the cooling liner 20 is preferred in order to avoid having the infant's head resting on the inlet and outlet and possibly constricting flow therethrough.
Referring additionally to FIG. 12, inlet 34 and outlet 36 are attached to inlet coupling 52 and outlet coupling 54 that comprise elongate annular members having one end attached to the respective inlet and outlet and the other end attached to either return tube 58 or supply tube 56. In order to protect the joint created between the inlet coupling 52 and inlet 34 and outlet coupling 54 and outlet 36, a block of reinforcement material is provided. Block 160 is a rectangular element which includes two bores passing therethrough for receiving a portion of inlet coupling 52 and outlet coupling 54. Block 160 serves to reinforce and help maintain the orientation of the inlet and outlet couplings relative to the surface of the cooling liner to which they are welded, thereby reducing the likelihood of occlusion of the water circulation. Block 160 helps to distribute forces that are applied to the inlet coupling 52 and outlet coupling 54 that could potentially cause these couplings to become disengaged from inlet 34 or outlet 36. Block 160 can be made from any lightweight resilient materials such as closed cell foam.
As best illustrated in FIG. 1 and FIG. 6, fluid conduit 32 between inlet 34 and outlet 36 travels a serpentine path from the left hemisphere of the skull in the general direction of arrow 37 towards the right hemisphere generally over those portions “A” of the skull illustrated in FIGS. 9 and 10. At a location generally indicated by 38, fluid conduit 32 begins its return to the outlet 36 along a serpentine path that travels in the general direction of arrow 39 from the right hemisphere towards the left hemisphere over region “B”. It should be understood that while a particular shape for the path of fluid conduit 32 is illustrated and preferred, other shapes may also provide the advantages of the present invention as described below in more detail.
The specific layout of cooling liner 20 provides cooling to those portions of the brain where cooling appears to provide the most benefit in mitigating neuronal damage, e.g., area A, while at the same time avoiding the infant's forehead and ears. A cooling liner is preferably formed as a flat member because of the ease of manufacturing and the relatively low cost. Referring to FIG. 6, cooling liner 20 comprises a first portion of fluid conduit 32 extending from inlet 34 to approximately return point 38 and a second portion extending from return point 38 to outlet 36. The path of the second portion takes the fluid conduit through a number of radially extending fingers 50. In the embodiment of FIG. 6, five fingers are illustrated, although a larger or smaller number of fingers would also be suitable. Extending from the first portion of fluid conduit 32 in a direction opposite to the direction that radial fingers 50 extend, are three circular tabs 44. Fluid conduit also includes a rectangular tab 42 which extends outward from the fluid conduit 32 adjacent outlet 36. On the opposite side of cooling liner 20, a rectangular closure flap 40 extends outward from the fluid conduit approximately adjacent return point 38. Overlapping flap 40 and tab 42 may carry some type of fastener, such as a hook and loop fastener or snaps. Circular tabs 44 may also be provided with fasteners. In order to shape cooling liner 20 to the skull of an infant, circular tabs 44 are caused to be superimposed on each other and tab 42 is overlaid by closure flap 40. Additional securing tabs can also be provided in order to customize the fit of cooling liner 22 to the infant's skull.
Cooling liner 20 defines a left mating edge 46 that extends approximately between circular tabs 44 and tab 42. Located between circular tabs 44 and closure flap 40 is a right mating edge 48. When closure flap 40 and tab 42 are superimposed on each other, left mating edge 46 and right mating edge 48 are brought together so that they abut approximately along the center line of cooling liner 20. When positioned on the infants skull, the abutting left edge 46 and right edge 48 are preferably positioned along the center line of the infant's skull. By so positioning these mating edges, when closure flap 40 and tab 42 are disengaged, and cooling liner is opened up along these edges, access to the anterior fontanel is possible. In addition to providing access to the anterior fontanel, the ability to overlap closure flap 40 and tab 42 allows for adjustment of the size of the cooling liner so that different shaped skulls can be fitted using the same size cooling liner 20. Additional fastening tabs 150 and 151 can be provided along edges 46 and 48.
Cooling liner 20 may also include apertures to promote ventilation above and below cooling line 20.
As noted above, fluid conduit 32 follows a serpentine path from inlet 34 to outlet 36. As used herein, “serpentine” refers to a meandering pathway that is not spiral in shape. In a spiral configuration, the fluid repeatedly, i.e., more than once, passes over the left hemisphere to the right hemisphere of the infant's brain and from the right hemisphere to the left hemisphere. In contrast, the serpentine path of a fluid conduit formed in accordance with the present invention transports the fluid in the general direction of arrow 37 over the left hemisphere and then to the right hemisphere once and then returns the fluid in the general direction of arrow 39 over the right hemisphere and then the left hemisphere once. The particular shape of the serpentine path is preferably selected to minimize the number of compound curves that are present in order to reduce the risk of constriction to flow. Minimizing the number of compound curves should be balanced against selecting a shape for the fluid conduit that provides cooling to the desired portion of the infant's brain. For example, when it is desired to cool the parasagittal cortex, the path of fluid conduit 32 should be selected so that the cooling fluid when it is the coldest is caused to flow over that portion of the skull which protects the parasagittal cortex, e.g., area “A”. As the cooling fluid warms, the fluid conduit can carry the cooling fluid over those portions of the skull protecting those portions of the brain where cooling is less critical, e.g., area “B”. In certain instances, it may be desirable to provide maximum cooling to portions of the infant's brain other than a parasagittal cortex. In those instances, a serpentine path different from that illustrated in FIG. 1 may be preferred.
Fingers 50 permit cooling liner 20 to fit infants with different shaped skulls. Fingers 50 also reduce the strain, e.g., spring back, within cooling liner when it is transformed from its flat configuration to the shape of the infant's skull. In addition, the material of the cooling liner tends to act like a hinge along the welded seams. By reducing internal strain, there is less tendency for the cooling liner to spring back to its original flat configuration. Minimizing the spring back force is desirable because it reduces the amount of external force needed to maintain the cooling liner in contact with the infant's skull.
The serpentine path of fluid conduit 32 comprises a plurality of bends and curves separating relatively straight segments. In the illustrated embodiment, the cross-sectional area of the bends and curves is preferably selected to be greater than the cross-sectional area of the straight segments. By selecting the cross-sectional area of the bends and curves to be greater than the cross-sectional area of the straight segments of the fluid conduit, any loss of flow that would normally occur (if the cross-sectional area was maintained) along these curves due to a change in direction of the flow is reduced or mitigated.
The particular cross-sectional shape of fluid conduit 32 is not critical although it is preferred that conduit 32 have maximum contact with those portions of the skull overlying those portions of the brain to be cooled. In order to maximize the contact, referring to FIG. 7, it is preferred that the conduit be relatively flat or oval in cross section as opposed to round, although round could be used. The cross-sectional area of the fluid conduit must take into consideration several factors, including the desired flow rate and the pressure needed to maintain such flow rate given the size of the conduit. Generally, high flow rates are preferred so that the change in temperature of the cooling fluid from the inlet to the outlet is minimal. On the other hand, such high flow rates may require greater pressures for a given cross-sectional area. Increasing pressure encourages the fluid conduit to spring back to its flat configuration which is described above is undesirable. The design described above seeks to provide a high flow rate and a low pressure.
By way of example, the fluid conduit has a cross-sectional area of about 0.05 in2-0.10 in2. For a fluid conduit to have a cross-section within the above range, internal pressures less than 5.0 psi and flow rates ranging from 1.0 liter/minute to 0.5 liter/minute provide acceptable combinations of pressure and flow rate. The pressure used should be selected to avoid occlusion of the fluid flow as a result of forces created by the weight of the infant's head and the weight of the device. As discussed above, the pressure should not be so high that it creates an excess amount of “spring back” of the cooling liner.
In the illustrated embodiment, a single fluid conduit 32 is illustrated. While multiple conduits could be used, and may be advantageous when particular regions of the brain require specific cooling, generally a single conduit is preferred because it provides relatively simple monitoring to determine if a blockage or constriction to flow has occurred.
In order to avoid diver's reflex, wherein the infant ceases breathing because the forehead or face has been excessively cooled, cooling liner 20 is shaped so that when properly seated on the infant's skull cooling fluid does not pass over the infant's forehead.
Suitable methods of manufacturing cooling liner 20 include heat welding or radio frequency (RF) welding two sheets of weldable material together.
The materials used to form cooling liner 20 can be any medical grade material suitable for skin contact. For example, polyurethane, polyvinyl chloride or polyethylene can be used. Other types of plastics which are lightweight and RF- or heat-weldable can be employed. The thickness of the material used to form cooling liner 20 is chosen taking into consideration, among other things, the heat transfer properties, strength, flexibility, and processability.
In addition to the heat-welding or RF-welding of thin films together to form the channels, other techniques may be employed. For example, the outer layer of cooling liner 20 could be vacuum formed so that the channels are set and therefore do not need to be “inflated” by the cooling fluid. Alternatively, a thicker or thinner material could be used in the top or bottom layer in order to tailor the surface of cooling liner 20 that expands the most. For example, the upper surface could be thinner than the lower surface. In such a case, when inflated, the upper surface would tend to inflate more than the lower surface because of the rigidity of the lower surface. By maintaining the lower surface flat, better contact occurs between this surface of the cooling liner, which improves the heat transfer rate. It is not required that the films used to form cooling liner be identical. For instance, the top film could be an elastic material and the bottom film nonelastic, or vice versa.
Continuing to refer to FIGS. 1-6, cooling liner 20 includes inlet coupling 52 and outlet coupling 54 which extend from inlet 34 and outlet 36, respectively. Inlet coupling 52 and outlet coupling 54 are tubular members which extend from cooling liner 20 and are welded or otherwise adhered to cooling liner 20 to provide a semi-rigid attachment for supply tube 56 and return tube 58. Supply tube 56 delivers cooling fluid from a cooling fluid source (not illustrated) and return tube 58 delivers cooling fluid to the source. Inlet coupling 52 and outlet coupling 54 are provided so that a secure connection can be made between supply and return tubes and the inlet and outlet to fluid conduit 32. In the illustrated embodiment, inlet coupling 52 and outlet coupling 54 extend from cooling liner 20 in a direction that is substantially perpendicular from inlet 34 and outlet 36. Preferably, these couplings extend in a direction that is substantially parallel to the longitudinal axis of the infant. This positioning is preferred so that the infant's head does not interfere with the free flow of cooling fluid into and out of cooling liner 20. As used herein, the longitudinal axis of the infant refers to a direction that is generally along the length of the baby, parallel to its spine. It is within the scope of the present invention that the inlet coupling and the outlet coupling extend in directions other than parallel to the longitudinal axis of the infant; however, when such is the case, care must be taken that movement of the infant's head will not result in a constriction of cooling fluid flow into or out of cooling liner 20.
In the embodiment illustrated in FIGS. 1-6, inlet 34 and outlet 36 are positioned adjacent to each other. This positioning is preferred because it allows the cooling fluid at its coldest temperature to enter at a point adjacent to where the cooling fluid at its warmest exits fluid conduit 32. The path of fluid conduit 32 preferably takes the coldest cooling fluid and carries it past a portion of the fluid conduit carrying the warmest cooling fluid. As the coldest cooling fluid begins to warm, the path of fluid conduit 32 takes it past portions of the fluid conduit carrying cooling fluid that is colder than the warmest fluid. By directing the flow of cooling fluid in this manner, the average of the temperature of the cooling fluid in adjacent portions of fluid conduit 32 is maintained in a relatively narrow band. This helps to provide an even cooling treatment to the infant's brain, particularly over area “A”, i.e., the cooling effect to (or heat transfer from) the left hemisphere and the right hemisphere is preferably the same.
A cooling device formed in accordance with the present invention also preferably includes an outer cap designed to help retain cooling liner 20 in position on the infant's skull. Referring to FIGS. 1 and 8, an outer cap 22 shaped to fit over cooling liner and over the infant's skull is provided to distribute the force of the infant's head and provide a thermal barrier. Outer cap 22 is generally shaped to be congruent with cooling liner 20. The front of outer cap 22 includes an access slit 60 which can be closed by sealing overlapping flap 62 over access slit 60. The portion of outer cap 22 overlapped by flap 62 can carry a hook or loop fastener with the flap carrying the opposite fastener. Alternatively, hooks or snaps can be provided to close the opening. Access slit 60 is positioned on outer cap 22 to permit access to the midline seam of cooling liner 20 thus allowing medical personnel access to the anterior fontanel. In addition to providing access to the anterior fontanel, closure flap also provides a means for adjusting the size of outer cap 22 so that skulls of different sizes can be fitted using the same size outer cap. Additional means can be provided to retain outer cap 22 on the infant's head, such as a chin strap of adjustable length.
Outer cap 22 is also be designed to avoid or reduce the collapse or constriction of fluid conduit 32 as a result of the weight of the infant's head lying on a mattress, or other supporting surface. Since an infant is unable to support the weight of its own head, the normal position for the infant to be treated is prone or supine with its head resting on a mattress or pillow. In order to avoid constriction or collapse of fluid conduit 32 at those locations where the infant's head is resting on the mattress, provisions must be made to reduce the force imparted on the fluid conduit. One way to achieve this result is to increase the surface area over which the force is exerted and provide padding in the outer cap. The material chosen to provide padding in the outer cap can also provide a thermal insulative layer.
Outer cap 22 also includes apertures 64 permitting supply tube 56 and return tube 58 to pass through outer cap 22. In addition, the outer cap preferably includes fasteners for attaching cooling liner 20 to elastic layer 68.
The size of outer cap is selected so that it provides enough restriction to oppose any spring-back created when cooling fluid is distributed through cooling liner 20. The force exerted by outer cap 22 should be sufficient to oppose this springback but not so great as to cause injury to the infant's skull as a result of the restraining pressure. Though not illustrated, additional restraining structures such as straps or belts can be employed to further retain outer cap 22 on the infant's head. Any such restraining devices should avoid unnecessary strain on the neck, such as twisting motion as the cooling liner expands.
Referring specifically to FIG. 8, in one embodiment, the outer cap includes an outer infrared reflective layer 66 and an opposing elastic layer 68 spaced from the infrared reflective layer. Sandwiched between infrared reflective layer 66 and elastic layer 68 is insulative layer 70. Infrared reflective layer is chosen from materials that will reflect infrared radiation directed toward the infant to heat other body segments such as the torso. Examples of suitable infrared reflective materials include metallized polyester or cloth. Elastic layer 68 can be selected from any suitable medically acceptable material such as polyurethane fibers commercially available, under the trade names Lycra™ or Spandex™. The insulative layer is preferably a high loft material used in an amount/thickness sufficient to provide enough cushioning to prevent the weight of the infant's head from constricting the underlying fluid conduit of the cooling liner. Examples of suitable insulative material include spun polyester (e.g., Holo-Fil™) or closed cell foam. While the outer cap described above is effective to reduce the amount of constriction on fluid conduit 32, other means may also be employed such as providing foam pad inserts to act as spacers for supporting the infant's head such that it does not constrict fluid conduit 32. As an alternative to spacers, splines or ridges could be provided over the cooling liner 20 in order to provide support for the infant's head. The use of a cushion or pillow may also help to avoid constriction of fluid conduit 32 by the weight of the infant's head.
Though not illustrated, outer cap 22 can be provided with ventilation holes or channels in order to reduce condensation within the cap.
As an alternative to inner liner 24, or an addition thereto, conductive creams or other heat transfer media could be provided between the infant's scalp and cooling liner 20.
All of the materials and structure chosen for the device of the present invention should be as lightweight as possible in order to avoid any unnecessary pressure on the skull and forces on the infant's neck.
While the preferred embodiment of the invention has been illustrated and described, it will be appreciated that various changes can be made therein without departing from the spirit and scope of the invention.
Claims (9)
The embodiments of the invention in which an exclusive property or privilege is claimed are defined as follows:
1. A device for cooling the brain of an infant whose brain has suffered a hypoxic shock, the device comprising:
a cooling liner for placement on the infant's skull, the cooling liner having a top and comprising only one fluid conduit for receiving a cooling fluid, the fluid conduit beginning at an inlet located at the top and terminating at an outlet located at the top, being serpentine in shape between the inlet and the outlet and configured so that the fluid conduit travels from the inlet adjacent a first hemisphere of the infant's brain in a general direction toward an opposite hemisphere of the infant's brain where the conduit reverses its direction and a serpentine portion of the conduit travels in a direction from the opposite hemisphere to the first hemisphere where it terminates at the outlet, the cooling liner including fluid couplings connected to the inlet and outlet that extend generally perpendicular from the inlet and outlet and further including, a plurality of bends, the cross sectional area of the fluid conduit along the bends being greater than the cross sectional area of the fluid conduit entering the bends.
2. The device of claim 1, further comprising:
an outer cap shaped to encompass the cooling liner and maintain a portion of the cooling liner in contact with the infant's skull.
3. The device of claim 1, wherein the inlet is adjacent to the outlet.
4. The device of claim 1, wherein the fluid conduit is shaped to cool the top, sides and rear of the infant's brain without directly cooling the forehead.
5. The device of claim 1, further comprising an inner liner to be interposed between the infant's skull and the cooling liner.
6. The device of claim 1, wherein the cooling liner further comprises a plurality of fingers occupied by the fluid conduit that extend from the top of the cooling liner downward to cool the rear of the infant's skull.
7. The device of claim 6, comprising at least three fingers.
8. The device of claim 1 wherein the fluid conduit near the inlet lie adjacent to the fluid conduit near the outlet.
9. The device of claim 1, wherein the cooling liner comprises at least one sheet of a heat weldable material.
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US9717495B1 - Devices and methods for surgical suturing - Google Patents
Devices and methods for surgical suturing Download PDF
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Publication number
US9717495B1
US9717495B1 US15476968 US201715476968A US9717495B1 US 9717495 B1 US9717495 B1 US 9717495B1 US 15476968 US15476968 US 15476968 US 201715476968 A US201715476968 A US 201715476968A US 9717495 B1 US9717495 B1 US 9717495B1
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Grant
Patent type
Prior art keywords
needle
suturing
cartridge
assembly
device
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Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
Active
Application number
US15476968
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US20170215878A1 (en )
Inventor
John C. Meade
Niall G. Deloughry
Gerald I. Brecher
James H. Bleck
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EndoEvolution LLC
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EndoEvolution LLC
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• AHUMAN NECESSITIES
• A61MEDICAL OR VETERINARY SCIENCE; HYGIENE
• A61BDIAGNOSIS; SURGERY; IDENTIFICATION
• A61B17/00Surgical instruments, devices or methods, e.g. tourniquets
• A61B17/04Surgical instruments, devices or methods, e.g. tourniquets for suturing wounds; Holders or packages for needles or suture materials
• A61B17/0469Suturing instruments for use in minimally invasive surgery, e.g. endoscopic surgery
• AHUMAN NECESSITIES
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• A61B17/0482Needle or suture guides
• AHUMAN NECESSITIES
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• A61B2017/2926Details of heads or jaws
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• A61B90/00Instruments, implements or accessories specially adapted for surgery or diagnosis and not covered by any of the groups A61B1/00 - A61B50/00, e.g. for luxation treatment or for protecting wound edges
• A61B90/03Automatic limiting or abutting means, e.g. for safety
• A61B2090/033Abutting means, stops, e.g. abutting on tissue or skin
• A61B2090/034Abutting means, stops, e.g. abutting on tissue or skin abutting on parts of the device itself
• A61B2090/035Abutting means, stops, e.g. abutting on tissue or skin abutting on parts of the device itself preventing further rotation
Abstract
An apparatus and a method for surgical suturing with thread management. An illustrative apparatus for tissue suturing includes a cartridge having a suturing needle having a pointed end and a blunt end, the suturing needle capable of rotating about an axis, a reciprocating needle drive, and an actuator capable of releasably engaging the needle drive to rotate the needle. A method for suturing tissue is provided that includes placing a suturing device having a cartridge containing a suturing needle to span at least one tissue segment, activating an actuator to cause rotational movement of the suturing needle through the at least one tissue segment, and deactivating the actuator to stop an advancing movement of the suturing needle to cause a suturing material to be pulled through the at least one tissue segment forming a stitch.
Description
CROSS-REFERENCE TO RELATED APPLICATIONS
This application is a continuation of and claims the benefit of priority to U.S. patent application Ser. No. 15/260,094, filed Sep. 8, 2016, which issued as U.S. Pat. No. 9,649,107, which is a continuation of and claims the benefit of priority to U.S. patent application Ser. No. 13/197,870, filed Aug. 4, 2011, which issued as U.S. Pat. No. 9,445,807, which in turn is a continuation of and claims the benefit of priority to U.S. patent application Ser. No. 11/387,127, filed Mar. 22, 2006, which is issued as U.S. Pat. No. 8,066,737, which is in turn a divisional of and claims the benefit of priority of application Ser. No. 11/121,810, filed on May 4, 2005, which is abandoned, and which is in turn a divisional of and claims the benefit of priority of application Ser. No. 10/127,254, filed on Apr. 22, 2002, now U.S. Pat. No. 6,923,819, which in turn claims the benefit of priority to U.S. Provisional Application Ser. No. 60/298,281, filed on Jun. 14, 2001. Each of the aforementioned patent applications is incorporated by reference herein in its entirety for any purpose whatsoever.
FIELD OF THE DISCLOSURE
The present disclosure relates to a surgical device for suturing tissue. More particularly, the present disclosure relates to a suturing device that enables the manipulation and control of the suturing needle and suturing material during operation, and methods for using such a device for suturing tissue.
BACKGROUND OF THE DISCLOSURE
Sutures are used in a variety of surgical applications including closing ruptured or incised tissue, soft tissue attachment, anastomosis, attachment of grafts, etc. Conventionally, suturing of ruptured or incised tissues, for example, is accomplished by the surgeon passing the sharpened tip of a curved suturing needle with a suture attached to the opposite blunt end of the needle through the incised tissue segments to be sutured such that the needle tip penetrates the tissue segments causing the needle to span the incision. The needle is then pulled through the tissue segments manually causing the attached suture to follow the curved path of the needle. Usually a knot is tied at the trailing end of the suture to anchor the first stitch. This action is performed repetitively with application of tension to the needle to pull the entire suture through the tissue segments through subsequent stitches until the entire incised segments are sutured together with a plurality of stitches.
For example, conventional, open abdominal surgery, including OB-Gyn procedures such as Cesarean delivery, creates a substantial incision (typically eight or more inches in length) in the fascia. In major orthopedic surgery, such as total hip replacement, even longer incisions in two layers of fascia must be closed. The closure of fascia must be done carefully at the conclusion of the surgical procedure, prior to skin closure. Closing fascia by hand suturing is a routine, repetitive, and time-consuming procedure. Typical abdominal incisions may take as long as twenty minutes, while in the case of hip replacement surgery, fascia closure can take even longer. Alternative mechanical suturing devices, as well as staplers, bone anchors, and suture-based arterial closure devices have been used as alternatives to hand suturing in other applications, since manual suturing is a tedious and the speed of the procedure is mostly dependent on skill of the surgeon. Moreover, manual suturing involves the handling and manipulation of a sharp suturing needle with an instrument such as a needle forceps, which can result in slipping and inadvertent, accidental needle pricks through a surgeon's or nurse's gloves, posing a potential risk of infection for the surgeon, nurse, staff, and patient. Furthermore, the direct handling of the needle can cause the needle to become contaminated with pathogenic bacteria that can cause onset of infection at the site of the sutures. There is also a risk of the needle penetrating the bowel and causing a serious, and often fatal infection.
Suturing devices described in the art designed to overcome these limitations are, however, either unduly complex design and economically non-viable or relatively difficult to use and unsuited for precise manipulation for suturing areas that are not easily accessible. For example, the device disclosed in U.S. Pat. No. 4,557,265 has to be held sideways in relation to the direction of the incision being closed. Another limitation of prior art suturing devices is their inability to provide positive control over the needle and suture during the suturing process. This can result in non-uniform sutures with either overly loose or overly tight stitches, which can cause excessive bleeding and risk tearing the repaired tissue in the patient.
A suturing device that maintains a positive control over the suturing needle and is capable of providing uniform stitches is disclosed in U.S. Pat. Nos. 5,437,681 and 5,540,705. The disclosed device requires a “scissors-like” grip and is operated by the surgeon's thumb that provides articulation of the drive mechanism that causes rotation of a linear drive shaft encased in a barrel, which in turn causes a suturing needle encased in a disposable cartridge mounted at the distal end of the barrel to rotate in an advancing motion through the tissue. The device is, however, limited in its efficient operability in the following ways: (1) the rotational direction of the needle and the drive shaft is in a direction that is perpendicular to the device actuating handles, thereby rendering the device relatively difficult to manipulate and control, (2) does not allow the user to view the needle and its progress through the tissue during the suturing operation, since the barrel containing the drive shaft leading to the needle cartridge does not have an open construction to permit such observation, because the action of the needle is blocked from user's view by the nature of the instrument design, thereby making it difficult for the user to position the advancing needle with high accuracy along the junction of the incised tissue segments and (3) the rate of needle advancement and, therefore, the size and uniformity of the stitches is essentially controlled by the user by the extent to which the articulation mechanism is depressed, thereby rendering the process of obtaining uniform needle rotation, tissue penetration and suture advancement difficult and entirely dependent on the skill of the user.
SUMMARY OF THE DISCLOSURE
The present disclosure provides a suturing device that closely emulates or replicates the manual suturing actions carried out by a surgeon. The suturing device of the present disclosure provides greater ease of use and allows better visualization for the user during its operation than present mechanical suturing methods, while maintaining control over needle movement, advancement and suturing thread management during all phases of the suturing process, thereby preventing entanglement of the suturing thread material during needle movement.
A benefit provided the suturing device of the present disclosure is that it enables maneuvering a suturing material through a tissue incision in a manner substantially similar to the way a surgeon would do so by hand. In particular, the suturing device first pushes a suturing needle from the tail of the needle and drives the point of the needle through the tissue. The device then picks up the point of the needle after it has been driven through the tissue, and pulls the remainder of the suturing needle and the suture attached to the suturing needle through the tissue. The suturing needle thus consistently follows the arc of its own curve, which is the preferred method of suturing, in the most non-traumatic way of passing a needle through tissue. A benefit provided by the suturing device of the present disclosure is the ability of the suturing needle to pull the suturing thread entirely through the tissue segments being closed, following each stitch. The present disclosure also relates to a suturing device comprising a suturing needle that is protected by a housing cartridge, whereby the suturing needle is not exposed to or handled directly by the user, thereby precluding inadvertent needle sticks. The configuration of the suturing device of the present disclosure also protects against inadvertent penetration of a bowel by the needle, since the cartridge acts as a shield between the bowel and the needle.
The suturing needle of the present disclosure is configured to fit into a cartridge, which in turn, is removably attached to the distal end of the suturing device. The present disclosure further provides an actuating means and a shaft and drive assembly that provides a torqueing force to the suturing needle to cause the needle to advance through tissue during a suturing process without inadvertent retraction.
The suturing device of the present disclosure offers several advantages over conventional methods used by surgeons for suturing tissue in that it provides a hand-held suturing instrument of relatively simple mechanical construction and which requires no external motive source. Embodiments of the present disclosure provides relative ease of operation for the surgeon with only one hand, thereby enabling the surgeon to move obstructing tissue, debris and biological fluids from the suturing site with a free hand, while eliminating the need for needle holders, pick-up forceps, and other tools normally required for suturing by hand. Furthermore, the suturing devices of the present disclosure can be configured as to length, tip, needle, suture, and needle cartridge size for use in conventional open surgery as well as in minimally invasive surgery (MIS) and in “less-invasive” surgery, such as through natural orifices or through small incisions. Additionally, the suturing head can be oriented in any preferred direction and either fixed in a particular orientation, or rendered movable in a variety of orientations by an articulation means.
These and other advantages of the present disclosure will be apparent through the embodiments described hereinafter. Embodiments of the present disclosure accordingly include the features of construction, combination of elements and arrangement of parts that will be exemplified in the following detailed description.
The surgical suturing devices of the present disclosure is configured to provide a “pistol like” grip for the user that includes a barrel assembly and a handgrip that extends from the proximal end of the barrel. The barrel assembly has either a linear or non-linear configuration, including but not limited to, straight, curved and angled configurations. The barrel assembly comprises a plurality of hollow segments capable of being coupled together by one or more universal joints that do not require a permanent connection between the segments, enabling segments to be pulled apart individually and separated. A cartridge holder is removably attached to the distal end of the barrel assembly by a plurality of support arms to which is releasably mounted a disposable cartridge that is capable of accommodating a suturing needle and a suturing thread material.
The disposable cartridge has a generally cylindrical housing with an aperture in the sidewall of the housing at the distal or working end thereof. An arcuate suturing needle having a sharp, pointed tip at one end of the needle is slidably mounted in a circular track at the distal end of the housing and opposite to the location of the aperture. The needle is connected to a terminal end of a suturing material or thread with a suturing thread source, such as for example, a spool assembly that is contained either entirely within, or remains external the cartridge. The radius of the arc defining the arcuate suturing needle is approximately equal to the circumference to the cartridge housing at the aperture therein. The needle normally resides in a “home” position in its track such that the gap in the arcuate suturing needle is in alignment with the aperture in the cartridge housing. The sharp, pointed end of the needle is situated on one side and entirely within the confines of the housing aperture; the pointed end is, therefore, always shielded by the cartridge housing. The blunt end of the suturing needle that is attached to the suturing thread is located at the opposite side of the aperture. The sharp, pointed end of the needle is, therefore, wholly contained within the cartridge and does not protrude and be exposed to the user.
In accordance with the present disclosure, the needle may be releasably engaged by a driving means that is rotatably mounted within the barrel assembly so that the needle can be rotated from its home position by about 360° about the central vertical axis of the cartridge. Such a rotatory action of the needle causes its sharp tip to advance across the cartridge housing so as to span the aperture. Thus, when the device is positioned such that the incised tissue segments to be sutured are situated at the housing aperture, the needle penetrates the tissue segments and spans the incision between them. A continued rotatory movement of the needle causes it to return it to its original “home” position, and thereby causes the suturing thread attached to the needle to be pulled into and through the tissue in an inward direction on one side of the tissue incision, and upwards and out through the tissue on the opposite side of the incision. Thus, the suture follows the curved path of the needle to bind the tissues together with a stitch of thread across the incision in a manner identical to that of a surgeon suturing manually, wherein the needle is “pushed” from the tail and then “pulled” from the point by the drive mechanism. Preferably, an anchoring means is provided at the trailing terminal end of the suturing material to prevent the material from being pulled completely through and out of the tissue segments. For example, the anchoring means can be a pre-tied or a welded loop, a knot wherein the suture is simply tied, or a double-stranded, looped suture is that attached to the suturing needle.
The rotatory movement of the needle within the needle cartridge is accomplished by a needle driver that may be operated by the user by holding the suturing device with one hand in a pistol-like grip around the handle, and using at least one finger of that hand to activate a triggering lever. The suturing device includes a finger operated trigger lever located proximally to the handle, which when actuated, operates a drive shaft encased within the universal joint barrel assembly through a drive mechanism so as to cause the drive shaft to undergo a rotatory motion, thereby causing the suturing needle to advance in a circular motion. Thus, by placement of the device with the needle cartridge aperture spanning the incised tissue segments and actuating the trigger lever, the suturing device enables the user to lay down a running stitch or interrupted stitch to close the tissue incision in a time efficient manner.
The needle cartridge of the present disclosure is disposably mounted on a cartridge holder assembly that is removably attached to the distal end of the universal joint barrel assembly. The cartridge holder assembly is supported by a plurality of support arms that extend from the distal end of the universal joint barrel assembly. The minimalized structural design of the support arms enables the user to have a clear, unobstructed view of the suturing needle as it advances through the tissue segments during the course of a suturing operation, thereby enabling precise placement of the suturing device to provide uniform sutures and precluding the risk of tearing tissue by its placement too close to the edge of the incision. The suturing devices of the disclosure is then advanced a short distance along the incision and the aforementioned operation is repeated to produce another stitch comprising the suturing material. The suturing devices of the disclosure can either pull the entire suture material through the tissues automatically under controlled tension thereby replicating the actions of a surgeon suturing manually so as to tighten the formed stitches without tearing tissue. Alternatively, the surgeon simply pulls the thread by hand to tighten the stitch placed over the incised tissue segments by passage of the suturing needle of the suturing devices of the disclosure.
The user may continue to manipulate the suturing device, alternately advancing and actuating rotation of the needle about an axis that is generally parallel to the direction of advancement to create a continuous suture which may extend through the entire length of the incision or a series of interrupted stitches. After each individual stitch is laid down, it is tightened by exerting a pull on the suturing material so that the resultant suture is neat and tensioned uniformly along the length of the incised tissue segments. Therefore, a tight closure of the segments is accomplished and bleeding and tearing of tissue are minimized.
As will be described in greater detail below, the needle driver may be operated by the surgeon holding the instrument with one hand, and using at least one finger of that hand. The suturing device includes a finger-operated lever that is functionally coupled with internal gearing and forms part of a handgrip that is located at one terminal end of the device, that enables the surgeon to efficiently and effectively lay down a running stitch, or a series of interrupted or uninterrupted stitches, to close a tissue incision in a minimum amount of time.
The suturing devices of the present disclosure can additionally include an associated thread management system, which operates in conjunction with the needle driver to control or handle the suturing material or thread during rotation of the suturing needle. For example, the thread management roller pushes the thread away from the track so the suture does not get pinched by the needle as the needle re-enters the track. Thus, there is minimal probability of the thread becoming tangled or hung up during the suturing operation. The thread management system can also include a mechanism whereby the suturing material or thread is controllably “paid out” during the suturing process.
When using the suturing devices of the present disclosure, no ancillary instruments or tools such as needle holders, pick-up forceps or the like are needed to complete the suture. Also, the suturing device may be configured in different ways with respect to length and angle of the universal joint barrels, the angle between barrel segments and the number and shape of the support arms. The size of the needle, needle cartridge, cartridge aperture and aperture position may also be varied for use in open surgery to perform procedures such as closing of the fascia, skin closure, soft tissue attachment, anastomosis, fixation of mesh, grafts and other artificial materials. The suturing devices of the present disclosure may also be designed with a very small working end or tip at the end of a long rigid shaft or a flexible shaft that can be oriented in any preferred direction so that the instrument may be used for MIS, such as suturing in the course of endoscopic surgery, including laparoscopy, thoracoscopy and arthroscopy, as well as less-invasive surgical procedures.
In addition to offering all of the advantages discussed above, the suturing devices of the present disclosure are relatively simple and cost efficient to manufacture. Therefore, the suturing devices should find widespread suturing applications that include single stitches or continuous stitches, e.g. spiral, mattress, purse string, etc., that are required to close tissue incisions, attach grafts, or the like.
BRIEF DESCRIPTION OF THE DRAWINGS
Embodiments of the present disclosure will be further explained with reference to the attached drawings, wherein like structures are referred to by like numerals throughout the several views. The drawings shown are not necessarily to scale, with emphasis instead generally being placed upon illustrating the principles of the present disclosure.
FIG. 1 shows a pictorial view of the suturing device of the present disclosure including the main components of a cartridge, a cartridge holder assembly, drive shaft segments, a universal coupling joint assembly and a sleeve, an actuator handle with an actuating trigger.
FIG. 2 shows a sectional view of the shaft-universal joint assembly attached to one embodiment of the suturing device functional end comprising the pusher, cartridge assembly and cartridge operable by a side drive mechanism.
FIG. 3A shows a segmented sectional view of suturing device functional end comprising a universal joint assembly without and with the universal joint sleeve. FIG. 3B shows an identical view with the universal joint sleeve.
FIGS. 4A, 4B and 4C show enlarged views of a single universal joint, joint coupler and a pair of coupled universal joints respectively.
FIG. 5 shows an expanded view of the universal joint sleeve configured at a 30° angle.
FIG. 6 shows a detailed view of one embodiment of a cartridge mount assembly comprising pair of supporting arms and a shaft segment.
FIGS. 7A and 7B show two different views of one embodiment of the needle cartridge.
FIGS. 8A and 8B show two embodiments of the curved suturing needle with suture material ports that are operable by a side drive mechanism.
FIG. 9 shows an expanded view of the thread management roller housed in the cartridge.
FIG. 10 shows an expanded view of the “anti-rotate” pin housed in the cartridge assembly.
FIG. 11A shows an expanded view of the pawl. FIG. 11B shows an expanded view of the pusher comprising a cartridge holder support arm with the pawl in place.
FIG. 12 shows a cut-away segment view showing interaction points of a suturing needle with a cartridge holder and support arm components.
FIG. 13 shows a segmented view of the relative configuration of a suturing needle with respect to the cartridge holder.
FIG. 14 shows a segmented sectional view of the functional end of a second embodiment of the suturing device operable by a rear drive mechanism comprising a shaft segment, the pusher, cartridge holder and cartridge (shown sectionally in FIGS. 15-19).
FIG. 15A shows a perspective view of a pusher with a cartridge holder assembly comprising an attached cartridge with a suture threading mechanism for restraining a suture material.
FIG. 15B shows a pusher comprising the cartridge holder assembly and a cut-away section of a cartridge comprising the curved suture needle that is operable by a rear drive mechanism.
FIG. 16 shows an expanded view of a curved suturing needle with suture material port that is operable by a rear drive mechanism.
FIGS. 17A and 17B show front and rear views of the cartridge.
FIG. 18 shows a cut-away sectional top view of a pusher comprising a cartridge holder assembly with a locking gate.
FIGS. 19A, 19B and 19C shows the operation of the pusher arm in a cartridge assembly operating in a rear drive mode. The pusher arm traverses radially by opening the gate (FIG. 19A), which springs to the closed position (FIGS. 19B and 19C) after its passage.
FIGS. 20A, 20B and 20C show a three-dimensional, a sectional and a cross-sectional view, respectively, of a ratchet assembly of the present disclosure that is driven by a drive shaft and activates a pusher arm upon device actuation.
While the above-identified drawings set forth preferred embodiments of the present disclosure, other embodiments of the present disclosure are also contemplated, as noted in the discussion. This disclosure presents illustrative embodiments of the present disclosure by way of representation and not limitation. Numerous other modifications and embodiments can be devised by those skilled in the art which fall within the scope and sprit of the principles of the present disclosure.
DETAILED DESCRIPTION
The suturing device of the present disclosure is shown generally at 1 in FIG. 1. Referring to FIG. 1, the illustrated suturing device 1 of the present disclosure can be used to produce a continuous or interrupted stitch or suture so as to enable closure of the segments of an incised tissue. The suturing device 1 includes an actuator handle 12 comprising a proximal end 6 and a distal end 8 that allows the device 1 to be held in a pistol grip by the user, and a trigger lever 16. The actuator handle 12 is attached to a pusher 9 at the distal end of handle 12. The pusher 9 comprises a of shaft barrel assembly 10 comprising a plurality of shaft segments capable of housing a drive shaft (not shown) that extend outwardly from a housing 14 at the distal end 8 of the actuator handle 12. The shaft barrel assembly 10 is comprised of at least two segments with symmetric coupling assemblies that are coupled to one another with a universal joint coupler (not shown). The coupled assembly is enclosed within a universal joint sleeve 18 such that the universal joint barrel is configured at an angle of about 30° from horizontal. The shaft segment 10 distal from the actuator handle 12 is attached removably to a support arm assembly 22 that is comprised of a pair of “skeletalized” arms extending along mutually divergent axes so as to provide an opening 23 to view the device working end 19 during its operation. The working end 19 of the suturing device 1 comprises a cartridge holder assembly 20 that is removably attached to the support arm assembly 22, to which the needle cartridge 24 is disposably attached.
FIGS. 2-13 provide detailed views of the various components of one embodiment of the suturing device 1 and the manner in which the components are configured in the final assembled device to enable its operation via a “side-drive” mechanism in the manner described.
FIG. 2 shows the working end 19 of the suturing device 1 including the universal joint coupling sleeve 18, the universal joint segment distal to the actuator handle (not shown) a “pusher” 9 comprising a support arm assembly 22 and a cartridge holder assembly 20 with an attached disposable needle cartridge 24, and a universal joint assembly (hidden) encased in a joint sleeve 18.
FIGS. 3A and 3B provide detailed segmental views of the suturing device working-end 19 showing the disposable needle cartridge 24 in a disengaged mode and a curved suturing needle 26 separated from the needle cartridge 24 to illustrate the relative configuration of these segments with respect to the cartridge holder assembly 20, the pusher 9 comprising the support arm assembly 22 and the universal joint segments. FIG. 3A shows the coupled junction mode involving coupling of the shaft segments 10 comprising a universal joint coupler (hidden), while FIG. 3B shows the coupled shaft segments 10 encased in a coupling joint sleeve or “sweep” 18 that aligns the cartridge mount 20 from the stem to the actuator handle at about 30°. The sweep 18 can be either pre-configured to provide a pre-determined fixed angle for the cartridge mount (relative to actuator handle), or can be configured to be adjustable to provide the user with the ability to vary the cartridge mount angle to a setting optimal for a particular procedure.
FIGS. 4A-C show expanded views of the hollow universal joint segment and the manner in which two identical segments are coupled. As shown in FIG. 4A, the shaft segment 10 comprises a hollow cylindrical barrel 28 with two open ends, and two pairs of arcuate slots 32 and 34 at one end, wherein one pair of arcuate slots is narrower than the other. Additionally, the joint segment contains a plurality of circular openings 36 located on the cylinder surface to accommodate a corresponding number of restraining pins in the universal joint sleeve (“sweep”) 18 that are identical in diameter. Two shaft segments 10 having identical arcuate slot configurations 32 and 34 may be coupled together using a universal joint coupler 38 (FIG. 4B) comprising a plurality of pins 40 such that the coupler engages the pair of narrow slots 32 of the conjoining joint segments 32, thereby providing a junction connecting the two shaft segments 10 that is non-rigid (FIG. 4C). The angle between coupled segments 10 can, therefore, be varied. The coupled segments 10 provide a conduit for passage of a drive shaft (not shown) for activating needle movement.
FIG. 5 shows a “transparent” view of the universal joint sleeve or “sweep” 18, which comprises of a hollow tubular segment with two open ends 28 whose tubular axis bends over a predetermined angle. The sleeve 18 additionally comprises a plurality of slots 30 positioned along its side wall that are capable of engaging the corresponding circular openings 36 on the shaft segments 10 that are positioned appropriately by means of restraining bolts on pins 38. The sweep 18 therefore, enables the angle of the coupled shaft segments 10 to be “locked” in a preferred angle. The sleeve 18 can be configured to have either a fixed angle, or to have the capability to provide the user the ability to adjust the angle to a preferred setting. In one embodiment, the sweep 18 provides an angle of about 30° from horizontal. The angle for the coupled universal joint segments 10 determined by the sweep in turn, determines the angle of the cartridge holder assembly 20 which is attached to the shaft segment 10 at the distal end 8 of the actuator handle 12 (via the support arm assembly 22). The cartridge holder angle relative to actuator handle 12, in turn, determines the accessibility of the suturing device 1 at the site of the suturing procedure which is critical, depending on whether it is open and planar, or non-planar and narrow.
FIG. 6 shows a detailed view of the pusher 9 that includes a cartridge holder assembly 20 that is attached to a support arm assembly comprising a pair of “skeletalized” support arms 22 which in turn, is attached to the terminal end of shaft segment 10. The open configuration of the “skeletalized” support arms 22 that are minimal in bulk is an essential feature of suturing device 1 that provides a relatively wide opening 23 that allows the user to directly view the aperture in the needle cartridge and cartridge (not shown) holder assembly 20, the incision in the tissue and needle advancement through the incised tissue segments during operation of suturing device 1. Although the embodiment shown in FIG. 6 has a plurality of support arms 22, other variants include a support arm assembly comprising a single support arm as illustrated in FIG. 11B. The improved viewing ability offered by the shape and configuration of the support arm assembly 22 enables precise device placement over the incision, and uniform advancement of the suturing device after every stitch to provide a uniform and symmetric suture, thereby minimizing the risk of tearing tissue and bleeding due to a stitch being positioned too close to the edge of the incised tissue. The cartridge holder assembly 20 is composed of a sterilizable medical grade material which can either be a metallic material such as stainless steel to enable its reuse subsequent to sterilization following a prior use, or a sterilizable medical grade plastic material, in which case, it may discarded and disposed after a single use. The cartridge holder assembly 20 has a cylindrical configuration with a distal edge 40 and a proximal edge 42 with respect to the device actuator handle (not shown), with an aperture 45 that corresponds in dimension and location to coincide with a substantially similar aperture located in the disposable needle cartridge. The cartridge holder assembly 20 additionally comprises a plurality of slots 44 located along on the distal edge 40 in that are located diametrically opposite to one another, and are capable of engaging the same plurality of retaining clips correspondingly located in the needle cartridge housing (not shown). The cartridge holder assembly 20 further comprises a cylindrical slot 46 located on the distal edge 40 that is capable of engaging a positioning pin of identical diameter correspondingly located on the needle cartridge housing (not shown). The proximal edge 42 of the cartridge holder assembly is attached to the shaft segment 10 distal to the actuator handle 12 via a support assembly comprising at least one “skeletalized” support arm 22.
FIGS. 7A and 7B show two different views of an embodiment of a disposable suturing needle cartridge 24 in accordance with the present disclosure, which is preferably offered in a sterilized sealed package. The cartridge 24 comprises a circular housing 48 that may be formed of a suitable rigid medical grade sterilizable metal or plastic material. The housing may be releasably retained by the cartridge holder assembly 20 at the distal end 19 of suturing device 1 (working end) by known means, such as a plurality of clips 50 (shown in FIG. 7A) located along on the edge of an inner lip 52 in diametrically opposite positions that are capable of engaging the same plurality of slots correspondingly located in the cartridge holder assembly 20. The cartridge 24 further comprises a cylindrical positioning pin 54 located on the edge of the inner lip 52 that is capable of engaging a cylindrical slot of identical diameter correspondingly located on the cartridge holder assembly 20. While the retaining clips 50 when engaged enable the cartridge to be retained by the cartridge holder assembly 20, the positioning pin 54 when engaged in the slot causes the aperture in the cartridge 24 to be aligned with the corresponding aperture in the cartridge holder assembly 20. The needle cartridge 24 further comprises an aperture 56 and a circular groove or “track” 58 that is inscribed in the inside surface of the housing 48, which lies in a plane that is perpendicular to the longitudinal axis of both the housing 48 and that of the suturing device 1. As shown in FIG. 7A, the cartridge-housing aperture 56 interrupts the track 58. An arcuate surgical suturing needle 26 composed of medical grade stainless steel or similar material is slidably positioned in the track 58.
FIGS. 8A and 8B show embodiments of the arcuate suturing needle 26 of the present disclosure. In one embodiment (FIG. 8A), the needle 26 is formed as a circular split ring with a gap 59, a sharp, pointed end 60, and a blunt end 62. The needle 26 further comprises an opening to accommodate the leading end of the suturing material. In one embodiment, the opening is the form of an eye 64 through which the leading end of the suturing material may be passed through for attaching it to the needle 26. In the illustrated needle (FIG. 8A), the eye 64 is located adjacent to the blunt end 62. The eye 64 however, can be positioned anywhere along the arc or the needle 26 between its apex 61 and the blunt end 62. In a preferred embodiment (FIG. 8B), the needle 26 comprises an opening in the form of a cylindrical bore 66 aligned axially with respect to the needle 26, located at the blunt end 62 (FIG. 8B). The leading end of the suturing material is inserted into the bore and restrained by mechanically crimping. To enable the needle 26 to penetrate tissue to the required depth, the needle preferably has an arcuate extent between about 280° and about 330°, and more preferably, greater than about 270°. The needle 26 comprises two symmetric notches 68 along the radially inner edge (“inner notches”) that are positioned proximally to the sharp, pointed end 60 and the blunt end 62 of the needle 26. The notches 68 are located directly opposite to each other, each having a perpendicular (about) 90° segment and an angular segment that makes an angle of about 60° with the perpendicular segment. The inner notches 68 are engaged by the drive mechanism in the cartridge holder assembly 20 and enable the needle 26 to undergo a rotatory movement upon actuation of the drive mechanism, thereby causing it to penetrate into and advance through tissue. A similar triangular notch 70 is located on the radially outer edge (“outer notch”) of the needle proximally to the inner notch 68 closer to the sharp, pointed end 60. The outer notch 70 engages with an “anti-rotate” pin located in the cartridge holder assembly 20, whereby rotation of the needle 26 in a direction opposite to the advancing direction or “needle backing-up” is prevented. The positive engagement of the needle outer notch 70 during operation of the suturing device 1, and thereby precludes needle 26 from straying out of sequence during the suturing process.
The width of the aperture 56 in the cartridge housing 48 is comparable to and corresponds with the width of the gap in the needle 26 so that when the needle 26 is in the “home” position (as shown in FIG. 7A) it does not project materially into the aperture 56. Such an alignment causes the needle to reside entirely within the cartridge holder 20, thereby preventing inadvertent contact of the sharp pointed end 60 with the user's fingers during handling of the disposable needle cartridge 24 for its placement on the cartridge holder 20 or its disposal after use, and while operating the suturing device 1. Such protection of the needle 26 in the suturing device of the present disclosure prevents accidental “needle-pricks” from occurring, thereby substantially reducing the risk of infection caused by pathogenic bacteria or viruses that may contaminate the needle during or after its use prior to its disposal. The needle 26 may be rotated in its curved track 58 about the longitudinal axis of the suturing device 1 to advance the pointed needle tip 60 so that the needle first spans the aperture and then return to its original or home position. Since the suturing material is attached to the needle 26, it follows the path of the needle 26. The terminal end of the suturing material may contain a knot or button to prevent it from pulling through the sutured tissue during placement of the first stitch. The suturing material or thread may be stored in an enclosed packaging either externally or internally with respect to the needle cartridge housing 48, and be pulled out of that packaging prior to placement of the first stitch in the suturing process. In a preferred embodiment, the cartridge housing 48 comprise the suturing needle 26 attached to the terminal end suturing material or thread, and an appropriate length of suturing material are all packaged in a terminally sterilizable medical packaging material.
FIG. 9 shows a thread management roller 72 of the present disclosure which acts to push the thread away from the track so the suture does not get pinched by the needle as the needle re-enters the track. The thread management roller 72 comprises a spring operated stop pin 74 that maintains a positive pressure against the suturing material or thread, thereby preventively retaining the suturing material in the thread retaining slot of the suturing needle, while keeping the thread out of the needle track to preclude the thread from jamming needle movement. The stop pin 74, therefore, prevents jamming of needle movement by an inadvertent entry of the suturing material into the needle slot within the needle cartridge 24 when the material is pulled forward by the advancing movement of the needle 26.
FIG. 10 shows an expanded view of the anti-rotate pin 75 that is capable of engaging the outer notch of the needle 26 to prevent rotation of the needle 26 and prevent “needle backing-up” and thereby precluding the needle 26 from straying out of sequence.
FIG. 11B shows an expanded view of a pusher assembly comprising pusher 76 and a pawl 78 (FIG. 11A) located at its tip, which resides in a corresponding slot in the support arm 22 of the pusher assembly, and is connected the support arm 22 by a pivot pin 80. The needle 26 is driven in a circular path by a rigid arm (“pusher”) that extends from a hub located in the center of the suturing device 1. The pawl 78 at the tip of the pusher 76 is capable of interfitting with the wedge shaped notches located along the radially inner edge of the needle. The pusher 76 is activated by the user upon operation of the actuator trigger in the actuator handle 12, and is capable of sweeping back and forth in an arc spanning about 280°. The outer surface of the pusher 76 is shaped to accommodate a C-shaped spring (not shown) that causes the wedge-shaped pawl 78 to push up against the needle 26 and thereby remain in intimate contact. The advancing movement of needle 26 during its operation causes the triangular slots 68 along the radially inner edge of needle 26 align with the wedge-shaped pawl 78 in the pusher 76, thereby causing the pawl 78 to engage the slots 68 due to a positive pressure exerted on the pin by the C-shaped spring, and to “lock” into the slots 68. The rotatory advancing movement of the needle 26 is therefore controlled to occur sequentially through about 280° each time it is actuated.
FIG. 12 shows a cut-away segmental view of the needle 26 in the home position inside the cartridge (not shown) with respect to the stem cartridge holder assembly (not shown). The relative locations of the pawl 78 that engages the notches 68 in the radially inner edge of the needle 26, the thread management roller 72 and the anti-rotate pin 75 that engages the notch 70 in the radially outer edge of the needle 26 are shown in FIG. 12.
FIG. 13 shows a cut-away view of the needle 26 within the cartridge (not shown) in the “home” position, the alignment of the needle aperture with the corresponding aperture in the needle cartridge holder 20, the relative position of the needle 26 and cartridge holder 20 and aperture location with respect to the coupled shaft segments 10 that are coupled by universal joint coupler 38 and maintained at a fixed angle by the restraining coupling sleeve or “sweep” (not shown).
FIGS. 14-20 show detailed component views of a preferred embodiment of the suturing device of the present disclosure and the manner in which the components are configured to enable its operation as described herein.
FIG. 14 shows the working end of a preferred embodiment of the suturing device of the present disclosure, comprising a “pusher” 9 having a support arm assembly 80 and a cartridge holder assembly 82 with the attached disposable needle cartridge 84. The “pusher” 9 is connected to the drive mechanism via shaft segment 86 that is coupled via a universal joint coupling comprising a universal joint assembly encased in a sleeve (not shown) to a second shaft segment distal to the actuator handle 12. The shaft segment 86 is attached to the universal joint assembly by pins that engage slots 88 with corresponding slots in the coupling assembly.
FIG. 15A shows segmental views of the pusher assembly comprising a needle cartridge 84 engaged with cartridge holder assembly 82. The cartridge 84 attaches to cartridge holder assembly 82 via a mounting clip 90 located at the apex of the arc of the cartridge holder assembly 82 that slidably “locks” into position with a complementary slot 92 located correspondingly on the apex of cartridge 84. Both cartridge holder assembly 82 and cartridge 84 comprise an aperture 96 that are of similar dimension, and aligned with one another in the “locked” position. The cartridge 84 further comprises a suturing material management cleat 98 which is capable of restrictibly maintaining suturing material 100 in a manner so as to preclude its entanglement as it travels into cartridge 84 during operation of the suturing device.
FIG. 15B shows a cut-away view of the pusher assembly exposing a suturing needle 102 residing within cartridge 84 (not shown) in the “home” position, wherein the alignment of the needle aperture corresponds with apertures of both needle cartridge holder assembly 82, and the cartridge 84. The needle 102 is placed in the “home” position by engaging cartridge 84 with cartridge holder assembly 82 in a “locked position, whereupon it is restrained by clip 90 in a manner causing it to be engaged with notches located along the radially rear edge of the needle (not shown) that is proximal to cartridge holder assembly 82 by correspondingly located pins in a drive arm located in the cartridge holder assembly 82 that is part of a “rear-drive” needle rotation drive operating mechanism.
FIG. 16 shows a preferred embodiment of the curved suturing needle 102 of the disclosure. The needle 102 is formed as a circular split ring with an aperture (or gap) 106, as sharp, pointed end 108 and the opposite end 110. A cylindrical bore 112 aligned axially with respect to the needle, located at the blunted 110. The leading end of the suturing material is inserted into the bore and restrained by mechanically crimping. Alternatively, the opening for accommodating the suture material can be in the form of an “eye” wherein the leading end of the suturing material may be passed through for attaching it to the needle 102. To enable the needle 102 to penetrate tissue to the required depth, the needle 102 preferably has an arcuate extent between about 280° and about 330°, and more preferably, greater than about 270°. Needle 26 comprises two symmetric notches (“rear notches”) 114 along the radially rear edge, i.e. the edge proximal to the cartridge holder 82, that are positioned proximally to the sharp pointed end 108 and the opposite blunt end 110 of the needle 102, respectively. The rear notches 114 are located directly opposite to one another, each having a perpendicular (about) 90° segment and an angular segment that makes an angle of about 60° with the perpendicular segment. The rear notches 114 are engaged by the drive mechanism in the cartridge holder assembly and enable the needle to undergo a rotational movement upon actuation of the drive mechanism, thereby causing it to penetrate and advance through tissue. A similar triangular notch 116 is located on the radially outer edge (“outer notch”) of the needle proximally to the rear notch 114 that is closer to the sharp, pointed end 108. The outer notch 116 engages with an “anti-rotate” pin located in the cartridge holder assembly, whereby rotation of the needle in a direction opposite to the advancing direction or “needle backing-up” is prevented. The positive engagement of the needle outer notch 116 during operation, therefore, precludes the needle from straying out of sequence during the suturing process.
FIGS. 17A and 17B show the outer and inner views, respectively, of the cartridge 84. The outer surface of the cartridge 84 (FIG. 17A) comprises a suturing material management cleat 98 which is capable of restrictibly maintaining the suturing material in a manner to preclude its entanglement. The cartridge 84 further comprises a slot 92 located at the apex of an actuate edge that slidably engages a complementarily located pin on the cartridge holder assembly to “lock” it in position. The inner surface of the cartridge 84 comprises a track 118 that permits the suturing needle (not shown) housed within to travel in a rotational motion from its “home position” so as to span aperture 106 during operation. A slot 120 located radially on the inner surface of cartridge 84 engages with a complementarily located pin on the cartridge holder assembly such that when the pin is engaged slidably in slot 120, the needle is constrained to remain in and move along track 118.
FIG. 18 shows a top sectional view of a preferred embodiment of a “pusher” 9 comprising a cartridge holder assembly 82 and support arms 22. The cartridge holder assembly 82 comprises a plurality of mounting clips 122 that are capable of receiving the cartridge 84, and a mounting clip 90 at the apex of the radial edge and slidably engaging a complementarily located slot in the cartridge that engages cartridge holder assembly 82, thereby causing the drive mechanism in the assembly 82 to engage the suturing needle housed within the cartridge. The cartridge holder assembly 82 further comprises a gate assembly 124 that prevents needle 102 from leaving its track and falling out into the back of the cartridge holder assembly 82. The gate assembly 124 is maintained in a closed “home” position by a torque force exerted by a spring 126 to which it is coupled via a pin 128, thereby restricts lateral movement of needle 102. The gate assembly 124 opens during each actuation of the suturing device to permit a circular movement of the drive mechanism that engages needle 102, and closes to the home position immediately after passage of the drive mechanism to preclude lateral movement and dislocation of needle 102 within cartridge holder assembly 82.
FIGS. 19A, 19B and 19C show serial views of the “rear-drive” needle operating drive mechanism operating within the cartridge holder 82 of the pusher assembly (not shown). The “rear-drive” mechanism comprises a driver arm 130 connected to a drive shaft 132 that is capable of circular motion so as to “sweep” along the circular inner edge of the cartridge holder 82 comprising the gate assembly 124. Actuation of the device causes the drive shaft 132 to rotate in a clockwise direction, thereby causing driver arm 130 to move circularly from its “home” rest position and move up to and the past gate assembly 124, causing it to open in the process (FIGS. 19A and 19B). The driver arm 130 continues to move circularly until it comes to rest once again in the “home” position (FIG. 19C). The gate assembly 124 returns to its closed home position after passage of the driver arm 130, thereby allowing driver arm 130 to “drive” needle 102 in a circular motion, while preventing the needle 102 from becoming dislocated from track 118. Thus, each time suturing device 1 is actuated, driver arm 130 moves past the gate assembly 124, opening the gate assembly 124 in the process. Since the gate assembly 124 moves back into its closed “home” position after passage of the driver arm 130, it precludes lateral movement of the needle 102, thereby preventing needle 102 from jamming due to misalignment during operation.
FIGS. 20A, 20B and 20C show the dimensional, sectional and transparent sectional views, respectively, of a ratchet assembly 134 of the present disclosure that is part of the drive mechanism for the suturing device 1. FIG. 20A shows the ratchet assembly 134 comprises a ratchet ring 136 with a predominantly arcuate outer surface segment 137 having a plurality of teeth 138, and an arcuate flat segment 140 that having a planar surface. The ratchet ring 136 includes a central circular bore (not shown) that fits slidably over and attaches immovably to a pinion gear 142 comprising a shaft 144. The ratchet ring 136 further comprises a plurality of wedged surfaces 139 a and 139 b that are proximal to the flat segment 140. The ratchet assembly 134 is mounted on a base 146 comprising a housing 148 that accommodates a pawl (hidden) that is activated by a coil spring (not shown) and a shuttle 150, that is attached to a support bracket 152 by a plurality of screws 153. FIG. 20B shows a detailed sectional view of the ratchet ring 136 comprising a circular bore 154 that is capable of slidably receiving and attaching to the shaft 144 of the pinion gear 142 (not shown). The ratchet ring 136 is mounted on the base 146 so that the teeth 138 of the ratchet ring 136 are interactively meshed with the pawl 156. The pawl 156 is activated by a coil spring (not shown) that exerts a positive pressure on the pawl 156 causing it to remain in intimate contact with the teeth 138 of the ratchet ring 136. The shuttle 150 is attached to the base so that it allows the ratchet ring 136 to rotate in a unidirectional (such as, for example, clockwise) until the circular movement is arrested by contact between the shuttle 150 and a first wedge 139 a in the ratchet ring 136. Movement of the shuttle 150 after contacting the first wedge 139 a permits the ratchet ring 136 to rotate in a direction opposite to the initial direction of rotation (such as, for example, counter-clockwise) until the movement is stopped by contact of shuttle 150 with the second wedge 139 b. FIG. 20C shows a transparent sectional view of the ratchet ring 136 where the teeth 138 of the ratchet ring 136 are enmeshed with the pawl 156, which is maintained in intimate contact with the teeth 138 by a positive pressure exerted by the action of a coil spring 158.
The ratchet assembly 134 of the present disclosure may be suitably located within the handle 12 of the suturing device 1. In a preferred embodiment, the ratchet assembly 134 is located at the distal end 8 of the actuator handle 12, whereby the shaft 144 of the ratchet assembly 134 is a part of a shaft segment 10 that is terminally attached to a triggering mechanism of the suturing device 1. Activation of the suturing device 1 by actuating the triggering mechanism (not shown) via the trigger 16 in the actuator handle 12 causes the shaft 144 and the attached ratchet ring 136 and the pinion gear 142 in the ratchet mechanism 134 to rotate unidirectionally, the pinion gear 142 to drive the shaft segment 10 coupled to the driver arm 130 of the rear-drive mechanism in the pusher 9, which in turn, causes the engaged needle 102 to rotate in the same direction to effectuate penetration of incised tissue by the needle 102 pulling the suturing thread material with it. The rotation of the shaft 144 is arrested after travelling about 280° upon contact by a first wedge 139 a with the shuttle 150, which in turn, terminates the first actuation step. The shuttle 150 then permits the shaft 144 with the attached ratchet ring 136 and the pinion gear 142 to rotate through an equal distance in the opposite direction until the movement is stopped once again by the contact by the shuttle 150 with the second wedge 139 b. An advantage offered by the ratchet mechanism 134 of the present disclosure is that the actuation step of the suturing device 1 is pre-determined, that is, the ratchet assembly 134 prevents the user from performing an incomplete actuating event that could result in an improper or incomplete suture by causing the needle 102 to snag in the tissue. Furthermore, the ratchet assembly 134 is capable of operation by the trigger 16 in a manner independent of its orientation with respect to the trigger 16 and actuator handle 12, such as for example, when it is oriented in an upside down or sideways configuration.
The actuating means of the suturing device 1 of the present disclosure may comprise of a triggering mechanism that is known in the art, such as for example, the triggering mechanisms disclosed in U.S. Pat. Nos. 6,053,908 and 5,344,061, both of which are hereby incorporated by reference. Alternatively, the actuating means can be either a manually operable button or switch, or a mechanically operable by an automated electrical or a fuel driven device, such as for example, an electrical, electromagnetic or pneumatic motor powered by electrical, electromagnetic, compressed air, compressed gas, hydraulic, vacuum or hydrocarbon fuels.
To commence suturing, any embodiment of the suturing device 1 of the present disclosure is placed at the site of the wound or tissue incision such that it spans the wound or the two tissue segments created by the incision, following which it is actuated by operation of the actuator trigger 16 on the actuator handle 12. The detailed operation of the suturing device 1 of the present disclosure is described with reference to the preferred embodiment, and is equally applicable to all other embodiments of the disclosure described and contemplated herein. The pawl in the pusher mechanism of the suturing device 1 engages the notch 114 located radially rear edge proximal to the blunt end or “tail” of the suturing needle 102 and pushes the needle in a circular path in an arc spanning about 280°. The sharp, pointed end 108 of the needle 102 crosses the aperture 96 defined by the cartridge 84 and the cartridge holder 82, and penetrates the first tissue segment located within the aperture 96, traverses the tissue segment to penetrate the second tissue segment, and re-enters the device on the opposite side of the aperture 96. The pusher 9 then returns to its original location, whereupon the pawl engages the notch located radially rear edge 114 proximal to the sharp, pointed end of the needle 102. The needle 102 with the attached suturing material or thread is consequently pulled in a circular path through an arc of about 280°. The blunt end 110 of the needle 102 and the suturing material therefore, pass through the tissue segments and across the wound or incision so as to span the wound or incision. The needle 102 comes to rest at its original “home” position within the track in cartridge holder 82, having advanced through a complete circular arc of about 360°. The needle 102 including the sharp, pointed end 102 remains entirely contained within the cartridge 84. The suturing material or thread may then be cut and secured by an appropriate method, such as for example, by tying, or additional stitches may be placed along the entire wound or incision by repeating the aforementioned process. Every stitch, whether a single, interrupted stitch, or one of a series of continuous, running stitches may be placed in like manner. The suturing device 1 of the present disclosure, therefore, may be used to insert either a single stitch, or to insert a suture comprising a plurality of continuous stitches as a replacement method for a more tedious and time-consuming manual suturing process.
While a suturing device 1 having the separable suture cartridge 84 containing the suturing needle 102, a pusher 9 comprising a cartridge holder 82 with the support arms 80, a drive shaft assembly comprising the driver arm 130, and an actuator handle 12 comprising the actuating trigger 16 and drive mechanism has been described, the entire suturing device 1 can be designed as a single unit which may be either reusable or disposed in its entirety after a single use.
It will thus be seen that the examples set forth above among those made apparent from the preceding description are efficiently attained in the suturing device of the present disclosure. Also, since certain changes may be made in the above description without departing from the scope of the disclosure, it is intended that all matter contained in the above description or shown in the accompanying drawings shall be interpreted as illustrative, and not in a limiting sense.
Claims (20)
What is claimed is:
1. A minimally invasive method for suturing tissue comprising:
releasably engaging a cartridge to a cartridge holder assembly of a minimally invasive suturing device, the minimally invasive suturing device having an elongate shaft;
placing the minimally invasive suturing device having the cartridge with a protective housing and a suturing needle to cause an aperture in the cartridge to surround at least a portion of a tissue segment, wherein a pointed end of the suturing needle is positioned within the protective housing after a complete rotation of the suturing needle about a rotational axis; and
activating an actuator coupled to a needle drive that releasably engages the suturing needle to cause movement of the suturing needle across the aperture and advance the suturing needle through the tissue segment.
2. The minimally invasive method for suturing tissue of claim 1, wherein a working end of the minimally invasive suturing device is disposed at the end of the elongate shaft.
3. The minimally invasive method for suturing tissue of claim 2, wherein the working end of the minimally invasive suturing device can be oriented in a preferred direction.
4. The minimally invasive method for suturing tissue of claim 2, wherein the working end of the minimally invasive suturing device can be oriented in any preferred direction.
5. The minimally invasive method for suturing tissue of claim 1, wherein the shaft is rigid.
6. The minimally invasive method for suturing tissue of claim 1, wherein the shaft is flexible.
7. The minimally invasive method for suturing tissue of claim 1, wherein the method includes an endoscopic surgical procedure.
8. The minimally invasive method for suturing tissue of claim 1, wherein the method includes a laparoscopic surgical procedure.
9. The minimally invasive method for suturing tissue of claim 1, wherein the method includes a thoracoscopic surgical procedure.
10. The minimally invasive method for suturing tissue of claim 1, wherein the method includes an arthroscopic surgical procedure.
11. The minimally invasive method for suturing tissue of claim 1, further comprising directing a portion of the minimally invasive suturing device through a natural orifice of a patient.
12. The minimally invasive method for suturing tissue of claim 1, further comprising directing a portion of the minimally invasive suturing device through a small incision formed in a patient.
13. The minimally invasive method for suturing tissue of claim 1, further comprising releasing the actuator to permit the needle drive to return to a home position where the needle drive can re-engage the suturing needle.
14. The minimally invasive method for suturing tissue of claim 1, further comprising deactivating the actuator to permit the needle drive to return to a home position where the needle drive can re-engage the suturing needle.
15. The minimally invasive method for suturing tissue of claim 1, wherein the suturing needle includes a suture attached thereto, and wherein the method further comprises applying tension to the suture after the suture has been pulled through the tissue segment by the needle.
16. The minimally invasive method for suturing tissue of claim 1, wherein the needle drive causes advancement of the suturing needle by providing a pushing force adjacent a second end of the needle opposite the pointed end of the suturing needle.
17. The minimally invasive method for suturing tissue of claim 16, wherein the needle drive causes advancement of the suturing needle by providing a pushing force adjacent the pointed end of the suturing needle.
18. The minimally invasive method for suturing tissue of claim 1, further comprising forming a spiral stitch using the suturing device.
19. The minimally invasive method for suturing tissue of claim 1, further comprising forming a mattress stitch using the suturing device.
20. The minimally invasive method for suturing tissue of claim 1, further comprising forming a purse string stitch using the suturing device.
US15476968 2001-06-14 2017-03-31 Devices and methods for surgical suturing Active US9717495B1 (en)
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Application Number Priority Date Filing Date Title
US29828101 true 2001-06-14 2001-06-14
US10127254 US6923819B2 (en) 2001-06-14 2002-04-22 Apparatus and method for surgical suturing with thread management
US11121810 US20050216038A1 (en) 2001-06-14 2005-05-04 Apparatus for surgical suturing with thread management
US11387127 US8066737B2 (en) 2001-06-14 2006-03-22 Needle for suturing instrument
US13197870 US9445807B2 (en) 2001-06-14 2011-08-04 Needle for suturing instrument
US15260094 US9649107B2 (en) 2001-06-14 2016-09-08 Needle for suturing instrument
US15476968 US9717495B1 (en) 2001-06-14 2017-03-31 Devices and methods for surgical suturing
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US15476968 US9717495B1 (en) 2001-06-14 2017-03-31 Devices and methods for surgical suturing
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US15260094 Continuation US9649107B2 (en) 2001-06-14 2016-09-08 Needle for suturing instrument
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US20170215878A1 true US20170215878A1 (en) 2017-08-03
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US10127254 Active US6923819B2 (en) 2001-06-14 2002-04-22 Apparatus and method for surgical suturing with thread management
US11121810 Abandoned US20050216038A1 (en) 2001-06-14 2005-05-04 Apparatus for surgical suturing with thread management
US11387127 Active 2025-06-30 US8066737B2 (en) 2001-06-14 2006-03-22 Needle for suturing instrument
US13197698 Active US8623048B2 (en) 2001-06-14 2011-08-03 Suturing instrument
US13197870 Active US9445807B2 (en) 2001-06-14 2011-08-04 Needle for suturing instrument
US15260094 Active US9649107B2 (en) 2001-06-14 2016-09-08 Needle for suturing instrument
US15377373 Granted US20170086820A1 (en) 2001-06-14 2016-12-13 Devices and methods for surgical suturing
US15377425 Abandoned US20170086821A1 (en) 2001-06-14 2016-12-13 Devices and methods for surgical suturing
US15404405 Active US9693770B2 (en) 2001-06-14 2017-01-12 Devices and methods for surgical suturing
US15476531 Active US9743923B2 (en) 2001-06-14 2017-03-31 Devices and methods for surgical suturing
US15476968 Active US9717495B1 (en) 2001-06-14 2017-03-31 Devices and methods for surgical suturing
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US15640442 Pending US20170296166A1 (en) 2001-06-14 2017-06-30 Devices and methods for surgical suturing
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US10127254 Active US6923819B2 (en) 2001-06-14 2002-04-22 Apparatus and method for surgical suturing with thread management
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US11387127 Active 2025-06-30 US8066737B2 (en) 2001-06-14 2006-03-22 Needle for suturing instrument
US13197698 Active US8623048B2 (en) 2001-06-14 2011-08-03 Suturing instrument
US13197870 Active US9445807B2 (en) 2001-06-14 2011-08-04 Needle for suturing instrument
US15260094 Active US9649107B2 (en) 2001-06-14 2016-09-08 Needle for suturing instrument
US15377373 Granted US20170086820A1 (en) 2001-06-14 2016-12-13 Devices and methods for surgical suturing
US15377425 Abandoned US20170086821A1 (en) 2001-06-14 2016-12-13 Devices and methods for surgical suturing
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US20170014127A1 (en) 2017-01-19 application
US9730688B1 (en) 2017-08-15 grant
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US20060173491A1 (en) 2006-08-03 application
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US20170215875A1 (en) 2017-08-03 application
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-4,519,885,640,253,073,400 | Skip to main content
main-content
02-07-2018 | Hypoglycemia | Review | Article
Impaired hypoglycaemia awareness in type 1 diabetes: lessons from the lab
Journal:
Diabetologia
Authors: Alison D. McNeilly, Rory J. McCrimmon
Publisher: Springer Berlin Heidelberg
Abstract
Hypoglycaemia remains the most common metabolic adverse effect of insulin and sulfonylurea therapy in diabetes. Repeated exposure to hypoglycaemia leads to a change in the symptom complex that characterises hypoglycaemia, culminating in a clinical phenomenon referred to as impaired awareness of hypoglycaemia (IAH). IAH effects approximately 20–25% of people with type 1 diabetes and increases the risk of severe hypoglycaemia. This review focuses on the mechanisms that are responsible for the much higher frequency of hypoglycaemia in people with diabetes compared with those without, and subsequently how repeated exposure to hypoglycaemia leads to the development of IAH. The mechanisms that result in IAH development are incompletely understood and likely to reflect changes in multiple aspects of the counterregulatory response to hypoglycaemia, from adaptations within glucose and non-glucose-sensing cells to changes in the integrative networks that govern glucose homeostasis. Finally, we propose that the general process that incorporates many of these changes and results in IAH following recurrent hypoglycaemia is a form of adaptive memory called ‘habituation’.
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Related topics | {
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3,080,081,984,702,052,000 | By Tracy Weincouff, RD
Choosing healthy foods and getting the nutrients you need is important to do no matter what age you are. As a senior, it is especially important. Food provides the nutrients you need as you age and even though you aren’t growing anymore your body still needs certain nutrients to stay healthy. Eating poorly can lead to undesirable weight loss and a weakened immune system which can make you more susceptible to colds, flu and infections. Some of the benefits of proper nutrition include increased mental capacity/alertness, higher energy levels, better resistance to illness and disease, improve how you feel overall and encourages a sense of well-being. When you have good nutrition you feel better overall and stronger. Food provides the nutrients you need as you age. So what does good nutrition look like?
Eating a variety of foods from each food group will help you get all the nutrients you need. The food groups include fruits, vegetables, grains, protein foods and dairy foods. Choosemyplate.gov has some great advice for making wise food choices. Fruits and vegetables should make up half of your plate. Focus on whole fruits and vegetables as these have the most nutrients particularly fiber. Incorporate fruits and vegetables into your main dish, snacks and desserts. Choose a variety of colors to maximize your nutrition. Protein foods include beef, pork, poultry, fish, eggs, beans and peas, soy products like tofu and unsalted nuts and seeds. Pick lean cuts of meat to decrease fat intake. Vary your protein sources and even try vegetarian main dishes! Protein should comprise about a quarter of your plate with grains comprising the last quarter. Grains can be whole or refined. Whole grains have more fiber and half of the grains you consume in a day should be whole grain. Check the ingredient list and if whole grains is listed first or second, the item is whole grain. Some examples of the grain group include wheat, rice, oatmeal, barley, tortillas, pasta, dry cereal, bread. Dairy should be low-fat or fat-free and includes milk, yogurt and cheese. This group doesn’t have a percentage of the plate because it is typically served on the side or incorporated into the other groups.
It is important to limit saturated fat (fat that is solid at room temperature), added sugars and sodium. Read labels to see how much of these items are in the food. Choose vegetable oils or oil-based sauces instead of ones with butter or cream. Watch what you are drinking as many beverages have added sugars. Water is always a great choice! Choose low-sodium products when possible and limit salt that is added to recipes or at the table. If you are interested in learning more about a healthy diet and how much you should eat, choosemyplate.gov is an excellent online resource or meet with a Registered Dietitian Nutritionist.
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1,532,547,961,754,961,400 | Health
Hate Getting Up In The Night? Here’s What Time You Should Stop Drinking.
Dietitians constantly advise patients to consume enough fluids, according to Academy of Nutrition and Dietetics spokesperson Amy Bragagnini. You need to drink enough liquids throughout the day to stay hydrated, but what type of liquids you drink also matters.
How late do you usually go to bed? Answering this question helps us provide information to patients that will help them meet their fluid goals and sleep well. In addition, you should discuss when and how much liquid you drink.
Image Credit: Pexels/cottonbro studio & Pexels/Yaroslav Shuraev
Caffeinated Drinks
Caffeine can affect sleep later in the day. Caffeinated beverages may help you stay awake in the afternoon. Anxiety, insomnia, and restlessness can occur when you consume more than 400 mg of caffeine daily.
Chris Winter, a sleep expert and neurologist, advises that caffeine should be avoided six hours before bedtime for better sleep. “Caffeine can disrupt the depth of sleep and affect sleeping time,” Bragagnini said.
Alcoholic Beverages
Drinking wine or beer before bedtime might make you sleepy, but it disrupts sleep. As a result, alcohol can have both sedative and stimulative effects. In the beginning, it might help someone fall asleep, but the sedative effect wears off as soon as they wake up.
Image Credit: Pexels/André Henrique
REM sleep is the deepest stage of sleep. Drinking alcohol before bed can disrupt this cycle. Furthermore, it may disrupt sleep, resulting in vivid or scary dreams and lower inhibitions, resulting in unhealthy snacking before bed.
Winter recommends making your last call four to five hours before bed. Most people take this long to metabolize alcohol, depending on their size, weight, and how much they drink. | {
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-4,740,918,044,586,771,000 | Root Canal Treatments – Your Comprehensive Guide
For many people, the word “root canal treatment” is synonymous with pain and discomfort. But, this is actually not true. Every day, dentists perform thousands of root canal procedures globally and save millions of teeth from extraction each year. If your dentist has recommended a root canal procedure for one of your teeth, you might be wondering what this procedure actually is, whether it is safe, when it is needed. Continue reading to find everything you need to know about root canal treatment
What Is A Root Canal?
A root canal refers to space within the tooth roots that are filled with the dental pulp – the nervous tissue of the teeth which contains the nerves and blood vessels that nourish and innervates a tooth. Under healthy conditions, the sensitive dental pulp remains protected from the outside by outlying dentine and pulp layers, respectively. The problem begins when tooth decay, wear, or trauma destroys the outer tooth layers and exposes the underlying pulp. If this condition is not corrected timely, the pulp tissue may get irreversibly inflamed, leading to a painful condition.
When this happens, the only option available to your dentist to save this tooth from extraction is to perform a root canal procedure. According to the American Association of Endodontists, a root canal procedure involves removing the inflamed pulp tissue followed by thorough cleansing of the root canals and then filling it with an inert material to prevent future infections.
How Is A Root Canal Done On A Front Tooth?
Whether it is the front or a back tooth, the steps involved in performing root canal treatment remain essentially the same. However, a fundamental difference between the front and back teeth is that the front teeth have only one root that is considerably longer. In the case of a front tooth, your dentist will first drill a hole in the tooth to expose the pulp chamber. Afterwards, they will use specialised endodontic equipment to remove the inflamed pulp tissue, followed by thoroughly washing the tooth’s interior with an antiseptic solution and then drying it.
Dentists endodontic files to shape the tooth’s interior in a tapering fashion and then fill it with an inert material. They will then place a temporary filling on the tooth while the healing takes place inside the tooth. After a few weeks when the tooth’s interior has healed, your dentist will replace the temporary filling with a permanent one.
Does A Root Canal Kill A Tooth?
A root canal procedure involves removing the inflamed pulp tissue from the tooth’s interior. Since the dental pulp is responsible for innervating and nourishing the tooth. So, the tooth loses its nourishment and nerve supply following root canal treatment. This is also why teeth become brittle and weak after endodontic treatment.
What Are The Steps Involved In A Root Canal Treatment?
A root canal is an endodontic (endo=inside, odont=teeth) procedure that is completed in multiple steps. During your initial appointment, your dentist will perform a clinical examination of the affected tooth. They will also look at the x-ray images of the tooth to see the extent of the damage. Your dentist will drill a hole in the tooth to expose the underlying infected pulp, to relieve the pressure and pain.
During the next appointment, your dentist will use specialised endodontic equipment to remove the infected pulp from the tooth’s interior. Afterwards, they will use antiseptic solutions or saline water to wash and clean the root canal. After the root canal has been dried, they will insert an inert rubbery material called gutta-percha to fill the tooth’s interior. This is done to prevent future chances of infection. After this, your dentist will place a temporary filling over the tooth until healing ensues. Once the tooth has healed, your dentist will replace the temporary filling with a permanent one. If required, they will also attach a crown over the restored tooth to reinforce it.
Should I Have A Root Canal Or Extraction?
A root canal is your dentist’s attempt to save a damaged tooth from extraction. Since no tooth-replacement option is better than your natural teeth, a root canal procedure should always be preferred over tooth extraction.
How Long Does Root Canal Take?
Dentists typically perform a root canal procedure in multiple sittings. The time required to complete the procedure depends on various factors, such as the location of the tooth and the extent of infection. Generally, it requires two to three sittings for completion. However, in some cases, dentists choose to perform a root canal procedure in a single sitting.
How Safe Is A Root Canal?
Like all other dental procedures, a root canal treatment procedure is absolutely safe, provided it is performed by a qualified and experienced dentist or endodontist. So, you can rest assured that a root canal procedure will have no effect on your oral health or physical wellbeing.
What Is The Cause Of Biting Pain After Root Canal?
Biting pain following a root canal can occur due to two reasons. Firstly, a “high” filling which puts pressure on the tooth whenever the opposing teeth mate. Another reason for post-root canal biting pain may be accidental damage to the tooth’s tissues, called the periodontal ligament. This type of pain typically goes away as soon as the damaged tissue heals up.
Whether you need a root canal treatment, dental fillings, or Invisalign aligners, Harrow Dental Service is at your service. So book a consultation appointment today and let us experienced and qualified dentists to take care of all your dental problems in a calm, relaxing and pain-free environment. | {
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-7,487,482,453,276,978,000 | What Does Alcohol Detox Feel Like?
The result is withdrawal symptoms, and these can be agonizing. Going through inpatient detox is not like being on vacation or spending time at a spa. Even if you choose luxury detox, the program will require some difficulties on your part, especially when it comes to your withdrawal symptoms. A team of licensed medical professionals always oversees medical detox. The staff may include a physician, nurses, therapists, and other clinical staff. These medical experts monitor your health while you’re in detox and provide treatment to ease the symptoms of withdrawal.
what is detox like
Detoxification, or “detox,” refers to the chemical withdrawal that takes place when a person with addiction stops using the addictive substance. Here, this process does not refer to a form of mental health treatment. Detox is often the first step to recovery from addiction. Some treatment centers offer detox and rehab programs in the same facility.
Increase your dietary fiber intake
This may mean slowly cutting out added sugar over time rather than eliminating all sources of added sugar at once. Your favorite granola or protein bar may be packed with added sugar. Choose whole, nutrient-dense snacks like nuts and seeds, whole fruit and nut butter, hummus and veggies, or hard-boiled eggs when you need a refuel.
what is detox like
Foods high in sulfur, such as onions, broccoli, and garlic, enhance the excretion of heavy metals like cadmium . While some inflammation is necessary for recovering from infection or healing wounds, a synthetic derivative of the kudzu vine can too much of it weakens your body’s systems and promotes disease. For example, high consumption of sugary beverages can cause fatty liver, a condition that negatively impacts liver function .
Types of Detox Programs
Call our confidential helpline today to learn more about alcohol detox and how to find an alcohol detox program at a treatment center near you for yourself or a loved one. Partial hospitalization is a type of treatment in which you live at home but receive treatment during the day at a hospital or other facility. Intensive outpatient treatment is similar to partial hospitalization, but it allows you to live at home while receiving treatment. Outpatient treatment is a less intensive form of treatment that allows you to remain in their homes and participate in your usual activities while receiving care.
• That said, reducing added sugar consumption can have substantial health benefits.
• Stress may trigger cravings for sugar, so you may find that your symptoms feel worse during times of stress.
• If you want an itinerary, you will need to contact your detox provider.
• At some point, the brain may reach a point where it now operates more comfortably when the drug is present.
• In some instances, they can be deadly if not managed correctly.
I know people who have come died coming off of drugs like these, going brain dead because their seizures were so severe. In terms of your physical health, you will be screened for tuberculosis and physical trauma, including lacerations and bruises. You nor your loved one are under any obligation to commit to an Ark Behavioral Health treatment program when calling our helpline. ✔️ Quitting alcohol may cause a number of physical side effects that can cause discomfort and some pain for people with a drinking problem. It’s not recommended that anyone physically dependent on alcohol try to stop drinking on their own.
Best Strength Training Exercises That’ll Transform Your Body in a Month, Says a PT
The term “toxin” in the context of detox diets is loosely defined. It typically includes pollutants, synthetic chemicals, heavy metals, and processed foods, the interactive association between sodium intake which can negatively affect health. If you answered yes to any of these questions, it’s best to seek medical detox to help break your addiction.
Can speeding up the liver detox process aid in weight loss? To answer these questions, we must address each point above and see what the science says. Detox in rehab offers a comfortable place to withdraw from drugs or alcohol, and it provides crucial medical and emotional support during the detox process. High quality treatment centers will offer complementary therapies in addition to medication.
If any of these issues are specific to you or someone you love who needs detox treatment, it is best to seek an inpatient program for your safe recovery. Support from loved ones is one of the main components of a strong recovery. If you are lacking this type of support system at home, a 24-hour treatment facility could be helpful to you, as it will surround you with individuals who want to see you recover safely. The evidence-based treatments normally used in inpatient detox are as follows. Eating sulfur-rich foods like eggs, broccoli, and garlic helps enhance the function of glutathione, a major antioxidant produced by your body that is heavily involved in detoxification .
The Association for Addiction Professionals represents the professional interests of more than 100,000 addiction-focused health care professionals in the United States, Canada and abroad. Detoxing from alcohol can be very difficult and potentially life-threatening if not done in a safe and controlled environment. As part of delirium tremens, the heart beats erratically. Unusual shifts in breathing, temperature, and circulation may contribute to a racing heart. You may also experience blood circulation issues like high blood pressure.
Avoid Detox at Home. Don’t Wait to Get Help.
These questions describe situations where your body has become dependent on the substance. That means you’ll experience withdrawal when you stop using, so you’ll want medical assistance to help you work through the symptoms. However, medical detox alone is not a complete addiction the signs and symptoms of alcohol abuse treatment program. Intensive inpatient medical rehabs offer the highest level of care and monitoring. These programs can keep you safe and medically stable while you taper off dangerous drugs. Drug addiction, also called substance use disorder, is a mental health problem.
WebMD Connect to Care helps you find services to manage your health. When you purchase any of these services, WebMD may receive a fee. WebMD does not endorse any product, service or treatment referred to on this page. Experts say the Mediterranean, DASH, and flexitarian diets have the best foundations and are among the easiest to follow.
If you are ready to break an addiction to alcohol or drugs, it may be helpful to find a treatment center in your area and enroll in a comprehensive detox program. It may include a range of medical and psychological effects that are difficult—and dangerous—to manage on your own. Medical detox programs like the one at Footprints to Recovery can determine your level of drug dependence. They’ll assess your current physical health, as well as your medical and mental health history to determine how your body may react during addiction withdrawal.
Cut out sugary soda, fruit juice, and energy drinks and replace them with plain or sparkling water. If you need a boost of flavor, add some mint or slices of lemon or lime. The average American consumes 22–30 teaspoons (about 88–120 grams) of sugar each day.
So when you come off, the depression you feel is often far worse than what you feel coming off of opiates or other drugs. This is because meth makes you feel so good, gives you so much of a dopamine overload, that when you quit, your brain struggles to even get close to feeling good without meth. For me, the depression and the anxiety were the worst parts about coming off of meth, but for other people, the sleeping thing can be out of control. It’s similar to PAWS (post-acute withdrawal syndrome) in that, basically, you keep detoxing when you “should” be done. This is, unfortunately, the type of detox I have the most experience with.
However, these symptoms generally resolve within a few days. Alcohol detox can also cause a very severe form of alcohol withdrawal called delirium tremens . This can cause temporary but serious physical and psychological symptoms. Undergoing detox in a treatment facility not only provides medical supervision but also a safer environment away from drugs. “Being in a detox facility also provides a level of support and an opportunity to be out of the environment where use was happening,” Henson says. The American Journal of Drug and Alcohol Abuse found the drug could help with meth addiction treatment when combined with therapy.
For people at risk of severe alcohol withdrawal, this can offer a high level of safety and support. Inpatient treatment offers around-the-clock support from medical and mental health professionals. This is important if you are struggling with severe addiction and need close supervision during detox and withdrawal. The best way to safely detox from alcohol is under the care of medical professionals.
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-5,782,706,484,594,905,000 | Genomic and transcriptional analysis of glioblastoma microenvironmental cellular subsets using antibody microarrays (crosstalk in gbms)
Starting date
October 1, 2011
Duration (months)
36
Departments
Neurosciences, Biomedicine and Movement Sciences
Managers or local contacts
Bonetti Bruno
OBIETTIVI: The malignant brain tumor GlioBlastoma Multiforme (GBM) is one of the most common malignant and lethal primary brain tumour of adults. The project is based on the finding that human tumours, particularly GBMs, are composed of a mixture of cancer, immune, stromal and vascular cells. The non-cancerous cellular components of the tumour microenvironment appear to play a critical role in tumour development and progression.
In this Marie Curie Fellowship, Dr. Beatrice Gini, from Prof. Bonetti’s group at the University of Verona in Italy, is working with Dr. Mischel’s group at UCLA, in collaboration with Dr. Heath’s group at CalTech, to develop cutting edge nanotechnologies to understand how crosstalk between tumor cells, including inflammatory cells, promotes tumor growth and resistance to target terapy.
This fellowship will identify the crosstalk pathways to develop more effective, personalized treatments for GBM patients.
At UCLA (Los Angeles, U.S.A.), the Mischel Lab has developed the DNA Encoded Antibody Library (DEAL) microarray, to sort specific cellular subtypes from solid tumour samples. The selective capture of tumour cells, lymphocytes, microglia and vascular endothelial cells, directly from GBM biopsy samples, will be obtained by DEAL technology. Genomic and transcriptional analysis will be performed on DEAL sorted cellular subtypes in order to identify novel molecular targets for therapeutic intervention. Genomic and transcriptional findings will be validated with functional assays in model systems: oncogene over-expression, gene silencing and pharmacological inhibition will be applied in order to identify the factors that inhibit the growth and survival of GBMs. In the first phase of the fellowship, at UCLA, the applicant will be utilizing cutting edge nanotechnology and resources that will provide her with outstanding interdisciplinary skills and competences. The applicant will then have the professional maturity to transfer her novel knowledge to the University of Verona (Italy), enriching the scientific excellence of Europe and bridging a new set of collaborations between Italy and the U.S.A.
Sponsors:
UE - Unione Europea
Funds: assigned and managed by the department
Project participants
Beatrice Gini
Activities
Research facilities
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93,209,390,710,600,780 | @article{Shudra_Papathanassoglou_Reichert_2022, title={Effectiveness of Current Interventions to Alleviate Parental Distress in the NICU: A Rapid Review }, volume={16}, url={https://wfccn-ijcc.com/index.php/ijcc/article/view/23}, DOI={10.29173/ijcc23}, abstractNote={<p><strong>Background:</strong> The birth of a premature infant and admission to the NICU is often unexpected and traumatic for families, leading to increased distress and can negatively impact parental-infant attachment. Appropriate interventions can help to lessen the negative impact of a NICU admission on families, improving parental mental health, reducing distress, enhancing parent- infant relationships, and improving the long-term physical, cognitive, emotional, and social development of the infant.</p> <p><strong>Aims:</strong> The purpose of this study is to examine and evaluate research evidence on the effectiveness of current interventions for improving parental distress in the NICU.</p> <p><strong>Methods:</strong> A rapid review was conducted utilizing a protocol based on the Virginia Commonwealth University guidance. Keyword searches were conducted on CINAHL, MEDLINE, and PsychINFO, and studies were selected according to pre-defined eligibility criteria, published between January 2015 and January 2020. The literature search included primary studies of interventions with parental stress and/or anxiety reduction as outcomes.</p> <p><strong>Results:</strong> A total of 14 articles were included, evaluating the effectiveness of 13 different interventions, including narrative writing, art therapy, structured nursing interventions, anxiety counselling, spiritual care, organizational change, music therapy, relaxation, and mindfulness techniques. With the Pexception of three, all the studies found significant results in the reduction of stress and/or anxiety levels of the subjects, with mothers having overall higher levels of stress indicated by higher stress scores on standardized measurement tools.</p> <p><strong> Conclusion:</strong> There is a need for ongoing assessment of parental distress and integration of appropriate interventions within the NICU settings. In this review, both individualized and group interventions including narrative writing, art therapy, music therapy, spiritual care, activity-based group therapy, music therapy, audio-assisted relaxation techniques, mindfulness based neurodevelopmental care, cognitive behavioral based counselling, family nurture intervention and a structured nursing intervention were shown to be effective in reducing parental stress and/or anxiety in the NICU. The small scale of the studies included in this review impact generalizability to a broader audience and emphasizes the need for larger scope, multi-center studies at an international level to build on and broaden our level of knowledge on how to better support families and reduce parental distress in the NICU.</p>}, number={1}, journal={International Journal of Critical Care}, author={Shudra, Darylle and Papathanassoglou, Elizabeth and Reichert, Amber}, year={2022}, month={Apr.}, pages={3–43} } | {
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1,498,252,418,773,472,500 | top of page
Everything You Need to Know About the COVID-19 Vaccine
Updated: Sep 5, 2021
By Cindy Ma
Image by MaRS
The COVID vaccine is classified under a new type of vaccine called mRNAs, meaning they instruct cells to produce a harmless component found on the surface of the virus called the spike protein. Once the protein is produced, the cell will break down the reproduction instructions and dispose of them. The rest of the protein will then be placed on the surface of the cell. When our immune systems detect something they don’t recognize, they will begin to make antibodies to produce an immune response against it. This helps our bodies learn to protect itself from future infections with the same code and reduce its harmful effects. Vaccines help us gain protection against the serious consequences of a virus.
mRNA vaccines have been researched for decades but were not fully developed until recently due to COVID-19. mRNA vaccines provide a faster and up-to-standard method of creating vaccines. With this breakthrough, it could mean that in the future one vaccine shot could provide immunity against multiple diseases.
Many people have been wary about how fast the COVID vaccine was developed, but it is because the mechanism has been studied for much longer, allowing for the quick development. The CDC assures that the COVID vaccine is both safe and effective. The shots will reduce the risk of people spreading the virus as more people get it. After getting your vaccine there may be some side effects such as: pain, swelling, fatigue, headaches, and fever. These side effects all mean that your immune system is working hard to build a protection system for the future, much like it does when your body is fighting a cold or the flu. Some things you can do to reduce the side effects are to drink lots of water, exercise your arm afterwards, and ice the area where you got your vaccine.
If you receive the Pfizer or Moderna vaccine, you will need two shots. The first shot will provide you with some protection and the second shot will reinforce that immune response. With Pfizer, you should receive your second dose around 3 weeks after your first dose and with Moderna, you should receive your second dose around 4 weeks after your first shot. This time frame allows for the first dose to fully build up a response before reinforcing it. Most people will say that the side effects after the second dose are stronger. These include chills, pain, headaches and fever. However, they are normal just as after your first dose. Side effects also tend to be more pronounced in younger people because of how active their immune system is.
When scheduling your vaccines, it is important to plan that you will be able to get your second dose within the timeframe. The location of your first dose should help with scheduling the second, whether you schedule online or in person. When going to your second appointment, you should bring your vaccine card to provide information on which vaccine you first received and when. It will also be used to fill out the information of your second dose. Two weeks after your second dose, you are considered fully vaccinated!
All in all, getting your COVID vaccine is an important part of protecting yourself and others from COVID-19, so that we can all hopefully return to some semblance of normalcy.
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3,300,986,055,347,650,600 | cosmetic dentistry, dental care, dentist, dentistry, dentures, implant dentist, invisalign, perio protect, preventive dentistry, Uncategorized
How a bridge can bring back your smile even with missing teeth
If you’re missing one or more teeth, it probably affects your smile and you may also notice a difference in chewing and speaking.
But there are options available to help you restore your smile and limit other problems.
For example, a bridge – sometimes called a fixed partial denture – replaces missing teeth with artificial teeth.
Bridges help maintain the shape of your face, as well as reducing the stress in your bite by replacing missing teeth.
They literally bridge the gap where one or more teeth may have been previously.
The restoration can be made from gold, alloys, porcelain or a combination of these materials and it is bonded onto surrounding teeth for support.
Bridges can be removable so that you can take them out and clean them or fixed and so can only be removed by a dentist.
An implant bridge attaches artificial teeth directly to the jaw or under the gum tissue.
Your dentist will recommend which approach is best for you.
Whatever type of bridge you choose, its success depends on its foundation. So it’s very important to keep your remaining teeth healthy and strong.
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dental care, dentist, dentures, orthodontics, perio protect, preventive dentistry, tooth extractions, Uncategorized
Fixing crowded and crooked teeth with orthodontics
Correcting problems with crowded and crooked teeth not only gives you a better smile, it also leads to a healthier mouth.
Malocclusion, also known as bad bite, involves teeth that are crowded or crooked.
Sometimes, the upper and lower jaws may not meet properly and, although the teeth may appear straight, the individual may have an uneven bite.
Problems such as protruding, crowded or irregularly spaced teeth may be inherited. But thumb-sucking, losing teeth prematurely and accidents also can lead to these conditions.
As well as spoiling your smile, crooked and crowded teeth make cleaning the mouth difficult. This can lead to tooth decay, gum disease and possibly tooth loss.
A bad bite can also interfere with chewing and speaking, cause abnormal wear to tooth enamel and lead to problems with the jaws.
Orthodontic treatment can help correcting these problems giving you a better smile but, more importantly, creating a healthier mouth.
Your dentist will advise you on how orthodontic treatment could help you.
dental care, dentures, implant dentist, invisalign, orthodontics, pediatric dentistry, perio protect, sleep apnea, Uncategorized
The risks of oral piercing
Young people today choose to make a variety of fashion statements affecting not just the clothes they wear but also their bodies through tattoos and piercing, for example.
Oral piercing may be something they feel looks good but it can lead to problems where they end up needing medical or dental treatment.
Oral piercing can often lead to symptoms such as pain, swelling, infection, increased saliva flow and injuries to the gum tissue.
There can be severe bleeding if a blood vessel is in the path of the needle during the piercing.
Swelling of the tongue is also a common side effect and, in extreme cases, this can block the airway and lead to breathing difficulties.
Other possible problems include chipped or cracked teeth, blood poisoning or even blood clots.
Infection is a very common complication of oral piercing because of the millions of bacteria in your mouth.
Of course, the jewelry itself also causes risk. It can be swallowed or cause damage to your teeth.
So, while young people may feel piercings in the mouth look cool, a great smile will look a lot better in the years to come.
dental care, dentist, dentistry, dentures, implant dentist, preventive dentistry, root canal, Uncategorized
What is plaque and how does it affect your teeth?
Plaque is a sticky film of bacteria that covers our teeth and, when we eat something, these bacteria release acids that attack the tooth enamel.
When these attacks are repeated over time, the enamel will break down and this will eventually lead to cavities.
When plaque is not removed through daily brushing and cleaning it hardens into calculus or tartar. When tartar collects above the gum line, brushing and cleaning between the teeth becomes more difficult.
The gum tissue can become swollen or may bleed. This is called gingivitis and it is the early stage of periodontal (gum) disease.
There are several steps you can take to protect yourself against this happening:
– Brush your teeth twice a day with fluoride toothpaste
– Clean between teeth daily with floss or an inter dental cleaner
– Eat a balanced diet and limit the number of snacks between meals
– Visit your dentist regularly for professional cleanings and oral exams
– Ask your dentist about sealants these are protective coatings that can be applied to the back teeth where decay often starts.
If you take steps to remove the plaque each day, you have a greater chance of avoiding tooth and gum problems.
cosmetic dentistry, dental care, dentist, dentistry, invisalign, pediatric dentistry, preventive dentistry, Uncategorized
The process of installing Invisalign
Invisalign is a system of clear mouthguards that can be used instead of braces to help straighten teeth.
The big advantage is that Invisalign looks better and is more comfortable than braces.
However, not everyone is a candidate for using the system so you with have to check with your dentist.
If an orthodontist certified in Invisalign says you can benefit from the system, they will take impressions of your mouth, write up a detailed specification and then send everything to a high-tech lab.
Next, the lab will show the orthodontist a preview of the appliances.
The lab then makes a series of aligners – depending on the situation, you may need between 12 to 48 aligners.
After the impression of the teeth is taken, it will normally require a visit to the orthodontist every six weeks.
Some patients will be advised to wear metal braces for a period and then switching to Invisalign when their mouth is ready.
For many people Invisalign provides an ideal way of making their smile look better.
cosmetic dentistry, dental care, implant dentist, invisalign, orthodontics, pediatric dentistry, perio protect, preventive dentistry, Uncategorized
Periodontal disease: what it is and how to avoid it
Periodontal disease is an infection of the tissues that support your teeth.
There is a very slight gap (called a sulcus) between the tooth and the gum.
Periodontal diseases attack this gap and cause a breakdown in the attachment of the tooth and its supporting tissues.
When the tissues are damaged, the sulcus develops into a pocket and, as the disease gets more severe, the pocket usually gets deeper.
The two major stages of periodontal disease are gingivitis and periodontitis.
Gingivitis is a milder and reversible form of periodontal disease that only affects the gums. Gingivitis may lead to periodontitis, which is a more serious, destructive form of periodontal disease.
There are several factors that have been shown to increase the risk of developing periodontal disease:
– Systemic diseases such as diabetes
– Some types of medication
– Crooked teeth
– Bridges that no longer fit properly
– Fillings that have become defective
– Smoking
– Pregnancy
And there are a number of warning signs that can suggest a possible problem:
– Gums that bleed easily
– Red, swollen, tender gums
– Gums that have pulled away from the teeth
– Persistent bad breath or taste
– Permanent teeth that are loose or separating
– Any change in the way your teeth fit together when you bite
– Any change in the fit of partial dentures
However, its also possible to have periodontal disease with no warning signs.
Its therefore important to have regular dental checkups and periodontal examinations.
If you have developed periodontal disease, the treatment will depend on how far it has progressed.
You can take steps to prevent periodontal disease from becoming more serious or recurring.
Good dental hygiene practices such as brushing twice a day, cleaning between your teeth, eating a healthy diet and having regular visits to the dentist will make a huge difference.
arch remodeling, cosmetic dentistry, dental care, perio protect, preventive dentistry, root canal
You might have gum disease without even knowing it
Gum disease also known as periodontal disease – is an infection of the tissues surrounding and supporting the teeth and its a major cause of tooth loss in adults.
But its usually painless so you may not even know you have it.
Its caused by plaque a sticky film of bacteria that constantly forms on the teeth. These bacteria create toxins that can damage the gums.
The early stage of gum disease is called gingivitis. In this stage, the gums can become red, swollen and bleed easily. At this stage, you can usually still reverse the disease by daily brushing and flossing.
The more advanced stage of gum disease is known as periodontitis. At this stage, the gums and bone that support the teeth can become seriously damaged. The teeth may then become loose, fall out or have to be removed by a dentist.
Its therefore very important to look out for any signs of gum disease. These signs include:
– Gums that bleed when you brush your teeth
– Red, swollen or tender gums
– Gums that have pulled away from the teeth
– Bad breath that doesn’t go away
– Pus between your teeth and gums
– Loose teeth
– Change in the way your teeth fit together when you bite
– Change in the fit of partial dentures
If you notice any of these signs, contact you dentist quickly and theyll help you take action to make improvements. | {
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-299,657,627,511,109,500 | Gastritis: Understanding and Preventing
Who has never felt the sensation of burning, heartburn and pain in the stomach? Popularly known as gastritis and even nervous gastritis, it is directly related to the symptoms described. These items above are part of a group that shows two diseases: a functional dyspepsia and reflux disease.
The dyspepsia can be described as a disturbance in the digestive system, which complicates the process of digestion. Reflux is a return of gastric acid from the stomach to the esophagus. The reflux happens due to an imbalance in the functioning of the valve that controls the passage of food from one organ to another. As the valve does not close right, the liquid passes into the esophagus and thus their walls. This causes heartburn and burning, since there is no protection against the inner wall acidity, such as the stomach.
What is Gastritis
Gastritis is an inflammation that affects the wall of the stomach and can be divided into two: acute and chronic. In the acute form, the gastritis appears suddenly, causing nausea and vomiting. Generally the duration is three days, can be triggered by alcohol, drugs based on acids, anti-inflammatory factor or the stress.
Chronic gastritis, the bacterium Helicobacter pylori is made in this context. This type of gastritis is long term and is usually asymptomatic. The transmission may be via water and food contaminated by bacillus. The only way to identify this type of gastritis is by endoscopy and biopsy and with the help of the best gastroenterologist in Okeechobee.
How to Deal with Gastritis
A healthy diet is still one of the main forms of treatment.
Although, the food is not the main cause of the development of gastritis. They have key role, both in aid of treatment and in prevention.
Some foods should be avoided, causing an increase in the release of gastric juice or facilitate the occurrence of reflux of it: milk and some types of cheese, fatty foods, and industrial embedded, concentrated juices, alcoholic drinks and stimulants.
You should also consume: diluted juice and much water, fruit, gelatin, milk derivatives and light, lean and white meat.
Eat slowly and chew food are habits that help. The intake of water, natural foods, whole grains and light products, is at the top of the list of habits. Practice them!
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-5,974,414,849,451,493,000 | GoodArticles.ORG
How To Lose Weight Fast - Just Got Easier - Weight Loss
Advantages Byetta Lose Weight 0h and How To Lose Weight Fast
- You Need To Know About Hormones And Muscles Also.
Now we will delve into the ways to burn fat. Metabolism burns the fat on your body. The central idea for byetta lose weight 0h and how to lose weight fast is to use the muscles so the metabolism is going and burning off the fat. Getting active is fun. Sitting around is no fun, its just lazy. You could not have any better friends than your muscles. You wont be straining your muscles to work them. They want that. Muscles only like one thing, just one thing, working. Its more than just burning fat, for using your muscles will pump up your energy too. I am guessing that this is new info for you.
Your body puts hormones into the blood that are connected with burning fat. The question is, how to get these hormones flowing to start the job of fat burning? To get these hormones flowing in your blood, you just need the right foods in your diet.
It's a percentage game. Certain foods must be high percentage and others low. Make proteins high and carbohydrates medium or even lower.
- Some Foods Have High Calories And Some Have Low Calories.
Now let us discuss supporting information for byetta lose weight 0h and how to lose weight fast . This is basic information, but you really must know this. The calories in the foods that you buy are on the food labels. You have to read these labels. To make this concrete, here is an example.
A comparison can be quite dramatic. Try this one out for size. 1 cup cooked green beans contains just a wee bit of calories, 38 calories, but when you go ahead and compare that to 1 cup cooked lima beans it has a whopping 260 calories.
Got it? If not, then read it again. You can enjoy either one, but the limas are definitely a heavy weight. The lima beans alone could put 2 to 3 pounds on you in a month if you ate them daily.
Fresh fruit will almost always be a very good and perhaps the best choice for dessert. Just try it for a while. Have a raw apple. There is only 60 calories in it. Be happy while you are enjoying that apple and remember in the back of your mind that just a single slice of apple pie has way more calories than an apple. 400 calories to be exact.
- If You Want To Lose 1 Pound, How Many Calories Must You Burn Up?
Let us look at the exact details of burning fat and losing weight for byetta lose weight 0h and how to lose weight fast . You can really accomplish weight loss, but you must make the effort. To lose a pound of weight from your body, you will need to burn off 3500 calories from your body fat. Lets be perfectly clear on this. This is burning 3500 calories of the fat on your body.
Now, we will say that in an average day you are using up 2000 calories. The average person will be eating 2000 calories daily. To make a change in your weight, we will reduce the calories eaten to 1500, and the difference of 500 calories will come out of stored fat on your body.
At this rate you will get 3500 calories used up from fat in a weeks time. On a weekly basis, you lose one pound of your body weight. Computing for a month of this routine, you have burned off four pounds of fat. For a years time we compute 52 pounds removed in body weight.
Gaining weight is usually something that happens over an extended period of time. So it should be okay for you to lose that weight in a slow and easy manner. Do not be in a rush. The best approach is slow and steady.
For a complete weight loss program and diet at a very low price, Please Click Here
Here you can read more about byetta lose weight q1w
For Help With Any Aspect of Our Site or Products, Please email:
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1,931,080,216,558,387,000 | Open Access
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The study of calcified atherosclerotic arteries: an alternative to evaluate the composition of a problematic tissue reveals new insight including metakaryotic cells
• Silvia Fittipaldi1, 2Email author,
• Francesco Vasuri1,
• Alessio Degiovanni1,
• Rodolfo Pini1,
• Mauro Gargiulo1,
• Andrea Stella1,
• Gianandrea Pasquinelli1,
• William G. Thilly2 and
• Elena V. Gostjeva2
BMC Clinical PathologyBMC series – open, inclusive and trusted201616:12
DOI: 10.1186/s12907-016-0036-6
Received: 12 November 2015
Accepted: 20 July 2016
Published: 29 July 2016
Abstract
Background
Calcifications of atherosclerotic plaques represent a controversial issue as they either lead to the stabilization or rupture of the lesion. However, the cellular key players involved in the progression of the calcified plaques have not yet been described. The primary reason for this lacuna is that decalcification procedures impair protein and nucleic acids contained in the calcified tissue. The aim of our study was to preserve the cellular content of heavily calcified plaques with a new rapid fixation in order to simplify the study of calcifications.
Methods
Here we applied a fixation method for fresh calcified tissue using the Carnoy’s solution followed by an enzymatic tissue digestion with type II collagenase. Immunohistochemistry was performed to verify the preservation of nuclear and cytoplasmic antigens. DNA content and RNA preservation was evaluated respectively with Feulgen staining and RT-PCR. A checklist of steps for successful image analysis was provided. To present the basic features of the F-DNA analysis we used descriptive statistics, skewness and kurtosis. Differences in DNA content were analysed with Kruskal-Wallis and Dunn’s post tests. The value of P < 0.05 was considered significant.
Results
Twenty-four vascular adult tissues, sorted as calcified (14) or uncalcified (10), were processed and 17 fetal tissues were used as controls (9 soft and 8 hard). Cells composing the calcified carotid plaques were positive to Desmin, Vimentin, Osteocalcin or Ki-67; the cellular population included smooth muscle cells, osteoblasts and osteoclasts-like cells and metakaryotic cells. The DNA content of each cell type found in the calcified carotid artery was successfully quantified in 7 selected samples. Notably the protocol revealed that DNA content in osteoblasts in fetal control tissues exhibits about half (3.0 ng) of the normal nuclear DNA content (6.0 ng).
Conclusion
Together with standard histology, this technique could give additional information on the cellular content of calcified plaques and help clarify the calcification process during atherosclerosis.
Keywords
DNA quantification Atherosclerosis Calcification Osteogenesis Immunohistochemistry Metakaryotic cells
Background
Considered for decades a passive process, calcification is now seen as an active mechanism sharing many similarities with embryonic bone formation [1, 2]. The most recent mechanism proposed to elucidate arterial calcification is the possible role of resident or circulating stem cells that differentiate into chondro-osteogenic cells [3]. Nowadays, the clinical impact of arterial calcification is still unclear [4]; indeed the extent of calcification is associated with either a good or bad prognosis. For example, in the coronary arteries small calcifications increase the risk of plaque rupture whereas bigger deposits seem to stabilize the plaque [5]. On the other hand, calcified carotid plaques are considered a low athero-embolic risk [6]. In our recent study, we observed that plaques with massive calcifications showed the same incidence of histological complications but without influencing clinical symptomatology [7].
A big issue in analysing calcified plaques is the deterioration of the carotid tissues due to the strong pre-treatment used to dissolve minerals (ethylenediaminetetraacetic acid (EDTA) or chloride acid (HCl) prior to histopathological processing [8].
Previous studies attempted to process calcified tissue with alternative decalcification solutions or treatments as ultrasound, however the major issue was maintaining the whole cellular morphology together with an intact DNA content [9, 10]; indeed the use of strong acids hydrolyses the DNA molecule. We hereby apply a parallel approach to standard histology methods to preserve and study the cellular content of heavily calcified plaques. Our aim was to validate and optimized the techniques for the study of calcified arterial tissues. Additionally to calcified plaques, the technique was also tested on a wide series of tissues from soft to hard (bone).
Methods
Tissue sampling
All samples were obtained under a protocol approved in advance by the Massachusetts Institute of Technology, Committee on the Use of Humans as Experimental Subjects. No persons, including minors/children, were enrolled in MIT studies. Only surgical discards from patients anonymous to MIT researchers were received from collaborating hospitals. These comprised fixed tissues from a variety of organs. The Massachusetts Institute of Technology IRB reviewed and approved the several collaborative relationships specifically indicating that the arrangements were in the US NIH “exempt” category for the requirement for informed consent (COUHES approval number 0804002679). Anonymous surgical discards were fixed immediately upon surgical removal in Carnoy’s solution as described and stored under refrigeration in 70 % ethanol [11]. A total of 41 tissue samples were finally collected from 26 cases, 16 fetuses and 10 adults.
Experimental parameters were optimized for two different types of samples, soft and hard. Hard adult samples were defined as “undissectable” with standard procedures without previous decalcification, commonly in Osteodec, Bio-optical (EDTA, calcium’s chelates, 40 to 60 min dependent on the tissue dimension). Of the 41 tissue samples retrieved, 22 were hard and 19 were soft, sorted in:
• 8 hard fetal samples; 3 femoral, 1 nasal bone, 1 elbow, 1 hip bone and 1 knee bone, and 1 chondroid tissue.
• 9 fetal soft samples; 3 guts, 3 brains, 2 muscles, and 1 eye retinae.
• 14 hard adult samples; 13 calcified carotid plaques and 1 calcified abdominal aortic aneurism.
• 10 soft adult samples; 9 uncalcified carotid plaques and 1 uncalcified abdominal aortic aneurism.
Spreading method
All 41 tissue samples were fixed in cold Carnoy at 4 °C (3 ml Ethanol 100 % and 1 ml glacial acetic acid per <0.25 cm2 within 30 min from surgical removal. Carnoy solution was changed after 60 and 120 min for a total of 3 hours fixation. Sample were then stored at -20 °C in 70 % ethanol [12]. Subsequent enzymatic tissue treatments with collagenase, type II (Clostridium histolyticum, ≥200 collagenase units/mg, Calbiochem, Merck Chemicals Ltd, UK) were tested with different incubation times and concentrations at 37 °C to define satisfactory conditions for various tissue types (Table 1). The most notable requirement is the need for up to 24 h of collagenase treatment to achieve unfolding of the hard tissues.
Table 1
Specifications for satisfactory spreading of soft versus calcified tissue samples in adult vascular tissues and fetal samples
Type of tissue
Collagenase II digestion time
Collagenase II working concentration (Ua/ml)
Acetic acid 45 % maceration tIme
Spread sections size (max)
Adult hard
24 h
10U/1 ml
30 min
0.1 mm
Adult soft
18 h
10U/1.5 ml
10 min
0.3 mm
Fetal hard
12 h
10U/1.5 ml
20 min
0.2 mm
Fetal soft
1–4 h
10U/1.5 ml
10 min
0.3 mm
aOne CDU unit is defined as the amount of enzyme that will release 1.0 nmol Leu equivalent from collagenase per min at 37 °C, pH 7.2
Collagenase-treated tissue samples were subsequently macerated in 500 ul of 45 % acetic acid (Table 1). Macerated tissue samples were minced with surgical scissors creating pieces no greater than 0.3 mm in length. Each piece was transferred to a slide in a drop of 45 % acetic acid. To spread the macerated tissue into a monolayer, several thicknesses of filter paper were placed on the coverslip and a tweezer handle was moved steadily in one direction with a delicate pressure. Intermittent microscopic examination during the spreading process was used to determine when satisfactory spreading had been achieved. Increased pressure on the stacked filter paper was required for the harder bone-containing samples. Cover slips were removed after direct immersion in liquid nitrogen, and slides were air dried for 1 h. Spread slides were stored at 4 °C, in the dark, and subsequently used for different forms of analyses: Von Kossa, Feulgen-Giemsa staining, immunohistochemistry, Feulgen reaction for DNA quantification and RNA extraction.
Histochemistry
Histochemistry included Von Kossa staining for the identification of calcified matrix: sections were hydrated, treated with 1.5 % silver nitrate (AgNO3) solution and placed in front of a 100 W lamp for 1 h. Sections were therefore rinsed in distilled H2O (dH2O), counterstained with nuclear-fast Red, dehydrated and mounted.
The Feulgen-Giemsa staining was used to test the preservation of the nuclei after the collagenase digestion and the subsequent DNA quantification. Briefly, the slides were placed in a Coplin jar filled with HCl 1 N at 60 °C for 8 min, for partial hydrolysis of the macromolecules and DNA depurination. Hydrolysis was stopped by washing the slides in cold dH2O. After carefully drying, sections were placed in Schiff’s reagent (#3952016, Sigma-Aldrich, St. Louis MO, US) for 1 h at room temperature, washed twice with 2x standard saline citrate (trisodium citrate 8.8 g/L, sodium chloride 17.5 g/L), washed again with dH2O and thereafter counterstained with 1 % Giemsa solution (#GS500, Sigma-Aldrich, St. Louis MO, US) for 5 min. Slides were dehydrated in graded step of alcohol and mounted with Canada Balsam (Sigma- Aldrich C1795).
Feulgen DNA quantification
Feulgen densitometry relies on the premise that the amount of stain bound to DNA is proportional to the amount of DNA present in the nucleus with a 1:1 ratio. Feulgen reaction is specific for DNA and does not stain RNA [11, 13].
DNA quantification using Feulgen reaction (without Giemsa) was carried out in 3 fetal and 4 adult samples, each equally distributed as hard and soft areas (Table 2, raw data are included in the Additional file 1). Nuclei of chicken red blood cells (cRBC, #IC05-0810, Innovative Research, Novi, MI, US) were used as an internal standard for DNA quantification (one nucleus of RBC contains a diploid quantity of DNA equivalent to 2C = 2.5 pg). Slides are Feulgen stained in groups (25 to 100 slides) with the same reagents, lots, conditions and standards. Image acquisition and segmentation were performed with the Carl Zeiss Vision AxioVision software: these are the critical steps for a precise DNA quantification. All steps are presented in details in the Additional file 2. The measure features for each nucleus are the densitometric sum, the densitometric area and the densitometric standard deviation. The quantity of stain is determined based on the absorbance (Optical Density OD) evaluated by the transmitted light (T).
Table 2
Descriptive statistics for Feulgen-DNA content and mean nuclear area
Origin
Cell type
Nuclei Nr
Skewness
Kurtosis
DNA pg
SD
Mean μm2
SD
CV
SE
CI
1
Adult
Hard
137
0.4
-0.6
6.0
3.1
72.7
36.9
50.8 %
3.2
66.5–79.0
2
Adult
Soft
306
1.1
1.8
4.3
2.1
57.5
25.9
45.2 %
1.5
54.6–60.4
3
Adult
Soft
48
1.4
2.8
5.6
2.2
66.1
24.7
36.8 %
3.5
59.0–73.1
4
Adult
Soft
92
0.6
0.5
7.0
2.8
68.4
27.
40.4 %
2.9
62.7–74.1
5
Fetus
Hard
145
1.6
2.7
3.1
1.6
46.9
25.3
53.9 %
2.1
42.7–51.0
6
Fetus
Hard
46
1.5
1.7
1.7
0.9
31.4
16.8
53.5 %
2.5
26.4–36.3
7
Fetus
Soft
120
1.1
0.5
4.8
2.4
63.8
32.7
51.2 %
2.9
57.9–69.7
Total
894
59.2
30.2
51.1 %
1.0
57.2–61.2
cRBC
Control
339
-0.1
1.2
2.5a
25.9
5.9
22.6 %
0.3
25.3–26.5
SD standard deviation, CV coefficient of variation, SE standard error, CI confidence interval. Characteristics’ of samples: 1, calcified atherosclerotic carotid; 2, soft atherosclerotic carotid; 3, healthy carotid; 4, abdominal aortic aneurism: 5, Femoral bone 11 weeks; 6, chondroid tissue 14 weeks; 7, fetal aorta 15 weeks
aConstant known quantity of DNA for the standard cRBC (the chicken red blood cells used as internal standards in each sample). Raw data are presented in the Additional file 1
$$ OD\kern0.37em =\kern0.37em lo{g}_{10}\left( 1/T\right) $$
(1)
As nuclear DNA stain is heterogeneous, a single point (OD) would not be representative. Thus it is necessary to evaluate the whole nucleus as the integrated optical density (IOD):
$$ IOD={\displaystyle {\sum}_{i=1}^nlo{g}_{10}\left( 1/Ti\right)} $$
(2)
The scale of each image was 95.04 pixel/ μm2. Additionally to nuclear IOD, the measured features were the nuclear area (μm2) and the total number of nuclei evaluated.
Calculation of genome size DNA
To convert IOD in genome size in pg we used the primary standard of RBC (1 C = 1.25 pg). Smears were processed with the same way as samples and were included in each experiment. To calculate DNA content a standard curve (IOD vs known C-value) was generated and used to verify that the stain was accurate:
$$ \mathrm{D}\mathrm{N}\mathrm{A}\ \mathrm{pg}\ \mathrm{per}\ \mathrm{nuclei}\ \mathrm{in}\ \mathrm{sample} = 2.5\ \mathrm{pg}\ /\ \mathrm{mean}\ \mathrm{I}\mathrm{O}\mathrm{D}\ \mathrm{standard}\ \mathrm{x}\ \mathrm{I}\mathrm{O}\mathrm{D}\ \mathrm{sample} $$
Immunohistochemistry technique on Carnoy-fixed spread tissue
Table 3 summarizes the antibody characteristics and the blocking/antigen unmasking procedures used. Indeed, due to the Carnoy fixation, some modifications in the antigen retrieval procedures were optimized.
Table 3
Technical characteristics of the antibodies used for imunohistochemistry
Antibodies
Type
Antigen specifications
Company
Locus-Clone
Dilution
Endogenous peroxidase blocking
Antigen unmasking treatment
Ki-67
Mouse Monoclonal
Perichromosomal layer protein. Identifies cells in G1-S-G2-M phases.
Dako A/S, Copenhagen, Denmark
10q26.2 MIB-1
1:100
20 min
Citrate Buffer, heat mediated (4 cycles 750 W, 5 min each)
Osteocalcin
Rabbit Polyclonal
Bone specific protein. Synthesized by osteoblasts, accumulates in the bone matrix.
Millipore USA
1p22
1:100
30 min
Tryton 0.5 % 4 min
Desmin
Mouse Monoclonal
Muscle specific intermediate filament type III protein.
Millipore USA
2q35 D33
1:100
20 min
Citrate Buffer, heat mediated (4 cycles 750 W, 5 min each)
Vimentin
Mouse Monoclonal
Intermediate filament type III protein expressed in mesenchymal cells.
Millipore USA
10p13 V9
1:80
20 min
Not required
In addition to Von Kossa staining, immunostaining for Ostecalcin (OCN) was used to spot the main components of the bone matrix as well as the osteoblasts.
Samples were immunostained for Ki-67 antigen in order to assess the chromatin preservation after the procedure and the cell proliferation. Finally, in order to verify the preservation of specific cytoplasmic antigens, Desmin and Vimentin immunostaining was performed. Carnoy-fixed spread tissue was rehydrated through graded steps of ethanol absolute (100 %, Methanol 3 % H2O2, 95 %, 70 %, H2O). Endogenous peroxidase activity was neutralized with 3 % H2O2 in absolute methanol at room temperature (rt), in the dark. Antigen-antibody reaction was developed with the NovoLink® Polymer Detection Kit (Novocastra, Newcastle, UK). To reduce nonspecific antibody bindings, hydrophobic binding sites were blocked with Casein 0.4 % (Novolink Protein Block). Sections were incubated 1 h in a wet chamber at rt with the primary antibodies.
To detect primary antibody bound to tissue, sections were incubated with NovoLink® Polymer (8 mg/L) for 30 min at rt. Spreadings were further incubated with chromogen/substrate, 3,3 - diaminobenzidine NovoLink® (DAB pre-diluted 1:20), 30 s for fetal tissue and 2 min for adult tissue, at rt, Cell nuclei were counterstained with Mayer’s haematoxylin (Sigma Chemicals). Fetal tissue was used as positive controls [12]. As negative controls primary antibodies were omitted. Washing steps were all performed with PBS. After dehydration in graded steps of ethanol, samples were mounted onto glass slides using Canada Balsam (Sigma-Aldrich C1795). The sections were observed under a light microscope (Axio Imager Z1 Zeiss, Germany) connected with a charge-coupled device (CCD) camera.
RNA content: RT-PCR
RNA extraction
The RNA was extracted from Carnoy fixed spread sections (monolayer). A commercial kit was used for RNA extraction (RNeasy® FFPE, Cat No. 73504, QIAGEN GmbH, Hilden, Germany); the protocol was slightly modified to increase RNA yield and purity. Spread tissue was recovered from the slides with a scalpel by adding 5 μl of Proteinase K buffer (PKD), under RNase free conditions. Retrieved tissues were combined into a single nuclease-free screw cap tube, dissolved in 245 μl of PKD and followed by centrifugation for 1 min at 10 000 rpm. For cell lysis, we added 20 μL of protease K; the mixture was incubated for 30 min at 56 °C, mixed at 850 rpm, and then incubated again at 80 °C for 15 min. The protocol was followed as stated by manufacturer’s instruction. Finally the RNA was eluted in 22 μl of RNAse free-water, heated at 65 °C for 5 min in order to be denatured and to inactivate RNases, and stored at -80 °C until used. RNA integrity and concentration were measured by using an ND-1000 spectrophotometer (NanoDrop, Fisher Thermo, Wilmington, DE, USA). The ratio of the readings at 260 nm and 280 nm (A260/A280) provides an estimate of the purity of RNA with respect to the contaminants that absorb in the UV spectrum, such as protein. Pure RNA has an A260/A280 ratio of 1.9–2.1.
RT-PCR assay
To assess the possibility of extracting RNA from Carnoy-fixed spread tissue as template for retrotranscription and gene expression, we amplified by RT-PCR the housekeeping gene beta-glucuronidase (GUSB) for both femur bone and intestine. GUSB is considered an housekeeping gene required for the maintenance of basic cellular function and expressed in all cells [14].
We also amplified the transcription factor Osterix (OSX) essential for osteoblast differentiation and bone formation [15] and the carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM 5) normally produced in gastrointestinal tissue during fetal development [16].
The reverse transcription assay was performed using 2 μg of total RNA per 20 μl of mix, following the manufacturer’s protocol (High capacity cDNA Archive kit, Applied Biosystem). The cDNA was stored at -20 °C until RT-PCR was performed. RT-PCR was carried out following MasterMix TaqMan® Protocol (TaqMan Univ PCR MasterMix, Applied Biosystems). Two μl of neat cDNA were amplified using specific probes for GUSB (NM_000181.3), CEACAM5 (NM_004363.2) and Osterix (NM_001173467.1) in the RT-PCR mix (TaqMan® Gene Expression Assay, Applied Biosystems, respective ID assay: Hs00939627_m1, Hs00237075_m1, Hs00541729_m1). Reactions were run on ABI PRISM 7900HT Sequence Detection System (Applied Biosystems). The cycling conditions were performed as follows: 10 min at 95 °C, 45 cycles at 95 °C for 15 s and 60 °C for 60 s. Each assay was carried out in triplicate and the transcription level was normalized using GUSB as a reference gene. The threshold was set at 0.2 in order to be in the exponential phase. The values were expressed as DCT (= > CT Target − CT GUSB).
Statistics
To present the basic features of the F-DNA analysis we used descriptive statistics: mean, standard deviation, coefficient of variation, standard error, confidence interval stated at 95 %, skewness and kurtosis. Differences in DNA content in pg and fluctuations of DNA (expressed as DNA content variation, DCV) [17] between samples were analysed with Kruskal-Wallis (non parametric-unmatched) and Dunn’s post tests. The value of P < 0.05 was considered significant.
Results
Immunohistochemistry
Samples of all 41 tissues specifically including the 22 “hard” tissues containing calcified sections were satisfactorily spread for further analyses. Methods of decalcification, i.e. EDTA treatment, was required in tissue processed with the standard procedure but was not required in the spread method using collagenase.
The Fig. 1 compared the results obtained with EDTA treatment (Fig. 1a and b) versus collagenase digestion of a calcified carotid artery (Fig. 1d and e). Fig. 1a showed a Haematoxylin-Eosin section of calcified artery fixed in carnoy, embedded in paraffin and decalcified with EDTA. Precipitates of calcium were very basophilic so calcification areas were easily visible in violet (asterisk in Fig. 1). In the insert of figure A, we also noticed an empty area (white asterisk), where the calcified material was lost. Figure 1b showed the same tissue of Fig. 1a immunostained for osteocalcin. The Fig. 1c showed the standard section fixed in formalin, EDTA treated and stained for Osteocalcin, while Fig. 1d and e displays the same tissue treated with collagenase and stained for Osteocalcin. The immunohistochemistry (IHC) for Osteocalcin evidenced osteoblasts and synthesized matrix in the adult calcified artery (Fig. 1d and e). All fetal cases and two calcified adult cases showed multinucleated osteoclasts-like cells positive to Osteocalcin. Von Kossa histochemical stain evidenced the same calcified tissues in adult samples, but was negative in fetal samples, where no osteogenic calcification was present yet.
Fig. 1
Adult calcified carotid artery sections EDTA treated (a-b-c) and collagenase treated (c-d). a Haematoxylin-Eosin (HE) staining of a standard section fixed in carnoy and EDTA treated (scale bar 40 μm). The insert in figure a shows the whole arterial section with a diameter of 4 mm, * asterisks highlights the calcified areas. b osteocalcin immunostain of the same tissue fixed in carnoy (scale bar 20 μm) or (c) fixed in formalin (scale bar 10 μm). d-e Osteocalcin immunostaining of the collagenase treated tissue fixed in carnoy. d positive osteoblast and (e) positive osteoclast-like cells, scale bar 5 μm. Nucleus and cytoplasmatic structure are clearly visible in collagenase spread tissue compared to standard section (a and b)
Antigen for cytoplasmic intermediates Desmin (Fig. 2) and Vimentin (not shown) were found in all preparations. Desmin and Vimentin showed a reliable positivity indicating that the collagenase digestion of samples and the other treatments did not damage the cytoplasmic intermediate filaments. Figure 2a and B show the good preservation of the smooth muscle cells expressing Desmin in the spread tissue. IHC for Ki-67 confirmed also the good preservation of the chromatin in the spread tissue (Fig. 3c-f). Surprisingly, Ki-67 was also detected in some cells in heavily calcified tissues: for example, case #1 (calcified atherosclerotic carotid, Fig. 3a) was described as acellular during routine IHC analysis by means of standard 2.5 μM sections. However, the monolayer IHC analysis revealed the presence of a heterogeneous population of cells (Fig. 3b), including Ki-67 positive cells (Fig. 3c and d). Mitotic figures were easily spotted with ki-67 staining (Fig. 3d). To verify the specificity of ki-67 staining in the spread artery, a tissue with a high rate of proliferative cells (fetal tissues) was selected and stained with ki-67 (Fig. 3e-f).
Fig. 2
Desmin IHC staining in spread fetal tissue. a group of desmin positive smooth muscle cells (SMC) and (b) a single SMC in the fetal bowel crypts. *SMC are indicated by a white asterisk and showed the typical elongated “cigar-shaped” nuclei. The SMC along the crypts show a moderate to strong cytoplasmatic staining reaction, scale bar 10 μm
Fig. 3
Ki-67 IHC staining in spread tissues. a adult calcified artery fixed in Carnoy, length of 1.5 cm. b Haematoxylin staining and (c-d) the corresponding ki-67 staining of the calcified artery at low magnification (inserts) and higher magnification. e-f positive control for Ki-67 nuclear immunostain (fetal bowel tissue), scale bar 25 μm
Nuclear DNA content of spread tissues
The Feulgen DNA quantification was performed in the 7 cases listed in Table 2: a total of 894 nuclei were evaluated for IOD and nuclear areas. Overall sample mean IOD was 2.3 ± 1.3 × 10^7, overall mean nuclear area was 59.2 ± 30.2 μm2. In the standard cRBC a total of 339 nuclei were examined: mean IOD was 1.2 ± 0.3 × 10^7, mean nuclear area was 25.9 ± 5.9 μm2. Feulgen absolute DNA content was successfully calculated in all 7 cases, both soft and hard tissues. In particular, the heavily calcified carotid artery lesion (case #1), had a mean DNA quantity of 6.0 pg, concomitant with the known DNA diploid content of human cells (2C = 6 pg) (Fig. 4a, Table 2). Kurtosis and skewness analysis showed that samples had a unimodal, near-Gaussian distribution of the diploid F-DNA (2C) (Table 2, Fig. 4a). The nuclear size was directly proportional to the DNA content of the cells in the 7 cases. Indeed, Fig. 4b shows that the quantity of DNA within each cell of the calcified carotid artery (#1) was significantly proportional to the area of the nucleus (R 2 = 0.97, Pearson correlation p < 0.0001). This means that there is a good preservation of the nuclear structures also in the heavily calcified tissues after the procedure.
Fig. 4
Feulgen DNA analysis (a) Unimodal distribution of Feulgen-DNA content expressed as fold DNA content (interrupted lines designate modal positions of diploid 2C), (b) Relation between DNA content and nuclear area (c) Feulgen DNA quantity (pg) in fetal tissues and (d-e) examples of the images used for F-DNA quantification. d fetal femoral bone femur osteoclasts (#5), (e) fetal femoral bone cartilage syncytia (#6), scale bar 5 μm
Adult and fetal tissues showed a significant DNA content variation (DCV, Table 2) within cells, except for DNA content in soft healthy adult arteries (#3, 5.6 pg, CV 36.8 %) compared to DNA content in fetal aortic cells (#7, 4.8 pg, CV 51.2 %). Both samples contained a homogenous population of smooth muscle cells. Of note, soft tissue from healthy carotid arteries #3 had the lowest adult CV (5.6 pg, 36.8 %). DCV significantly differs between pathological atherosclerotic soft arteries (45.2 %) and calcified arteries (50.8 %). Highest DCV were found in all fetal tissues (range 51.2 to 53.9 %).
In particular, two cases showed significant unexpected lower mean DNA content per nucleus compared to adult samples; case #5 (fetal femoral bone) with 3.1 ± 1.6 pg and case #6 (chondroid tissue) with 1.7 ± 0.9 pg (p < 0.0001, Table 2, Fig. 4c). In those cases we decided to perform detailed analyses of the DNA in each single cell composing the tissues (the AxioVision software marked each nucleus with a single identification number corresponding to its IOD). We noticed that case #5 was mainly composed of osteoclasts and case #6 of syncytia (Fig. 4d and e). By measuring the DNA content per nucleus we observed unexpected results. Nuclei outside osteoclasts and syncytial formations showed a constant DNA content of 6 pg. In osteoclasts, DNA content per nucleus ranged from 2 to 3 pg. In the syncytia formations, nucleus showed a DNA content ranging from 1 to 2 pg per nucleus. Surprisingly the mean DNA content per syncytium (sum of nuclear DNA nucleus in the whole syncytia) was 6.6 ± 1.4 pg.
RNA preservation (RT-PCR)
Additionally to the housekeeping gene GUSB, we evaluated the expression of CEA for intestinal fetal tissue and Osterix for calcified/osteogenic tissues. The total mean extracted mRNA from fetal intestine tissue (FI) and femur bone (FB) was 7374 ng and 1430 ng respectively. A260/A280 ratio was 1.94 for both fetal intestine and fetal bone showing the absence of contamination of the RNA extracted (standard ratio range from 1.9 to 2.1). The mean threshold cycle (CT) values of endogenous control GUSB were 30.34 ± 0.18 in FI and 37.34 ± 0.24 in FB. Mean CT for tested gene OSX and CEA were 38.52 ± 0.10 and 35.34 ± 0.31 respectively. ΔCT CEA and ΔCT OSX were 5.02 and 1.18 respectively (Table 4).
Table 4
Threshold cycle (Ct) values for GUSB, OSX and CEA in fetal tissues
Threshold cycle values
Micro-dissected sample
β-glucuronidase GUSB
Osterix OSX
Carcino-embryonic antigen CEA
Fetal femur bone 12w
37.06
38.42
-
37.50
38.63
37.45
38.51
Fetal intestine 9w
30.03
-
35.70
30.32
35.15
30.37
35.17
Additional cellular component observed in arteries
Figure 5a shows a standard histological staining of the carotid plaques section (#1); of note the rupture of the endothelium (marked with an asterisk) and the presence of extensive calcification. However, the spread of the same sample (#1) allowed the identifications of a disclosed and complex cellular content. Besides the majority of the cells that have a spindle shaped nucleus (Fig. 3b), cells with a particular balloon shaped nucleus were identified in the calcified carotid plaque (in 2 cases, Fig. 5b and c). Also, we noticed that Ki-67 antigen stained some of the metakaryotic nuclei in the mononuclear forms (data not shown). The same cells were also arranged in a tubular form that reminds syncytial structure (Fig. 5d). In syncytium, Ki-67 highlighted only the cells located in the extremities (Fig. 3e and f) and nuclei inside syncytia were negative to Ki-67. This type of cells, named metakaryotic cells [12], with a typical hollow bell-shaped nucleus, was found in our study in all fetal tissues both in the syncytial form (Fig. 5d) and in the mononuclear form (Fig. 5e) while in the adult arteries, these cells were spotted in 6 cases.
Fig. 5
Standard 2.5 μm sections and collagenase spread of calcified tissues. a Haematoxylin-Eosin staining of adult calcified carotid arteries, scale bar 400 μm. b-c Feulgen staining of spread tissue of adult calcified carotid arteries showing examples of metakaryotic nuclei. d-e Feulgen staining of spread tissues showing nuclei in syncytium (fetal femoral tissue), scale bar 5 μm
Discussion
The spreading technique showed a good reproducibility and accuracy in the evaluation of cell protein expression and single-cell DNA content in calcified carotid arteries. The IHC markers were selected in order to check the integrity of the different cellular compartments: nucleus (Ki-67) and cytoplasm (Desmin, Vimentin, Osteocalcin). To verify the reliability of the techniques we used fetal tissues sample as positive control since this tissue was already validated [12]. As standard for the Feulgen DNA quantification we chose cRBC, since they are convenient, easy to isolate and they have a constant known DNA content [18, 19]. Our results confirmed the reliability of the standard as cRBC genome size was proportional to the area of the cells and CV% was low (23 %). The digestion times with collagenase requested by the spreading technique varied considerably according to the different tissues (see Table 1). Nevertheless, the adult and fetal DNA content distribution curves were all Gaussian with the same trend, showing that collagenase did not influence the DNA content, regardless the digestion times. The Carnoy-fixed spread tissue also allows to extract preserved RNA, without any contaminations by proteins or phenols, and the sigmoid-shaped curves obtained at RT-PCR showed a typical PCR gene amplification.
The technique could also give new information regarding the study of calcification and osteogenesis. Usually DNA quantity is evaluated in the whole tissue; unfortunately one disadvantage is the loss of information on the single cell profile. Moreover standard decalcification procedures degrade the DNA content in calcified arteries. First this protocol avoids the use of formalin to fix the arteries and also avoids the use of strong acid to decalcify the arteries. This allows extracting directly from the slides of spread tissue the RNA and DNA and evaluates the gene expression in calcified tissues from a very small quantity of sample. Moreover the protocol preserved the morphology of the nucleus and allowed the visualization of the nuclear organization. As already reported, some cases of atherosclerotic carotid tissues contain bone lacunae-like mature structure in development with lamellar bone. In these cases, the protocol is of great help to open the “core” of the bone structure and visualize the cellular content. It is very difficult with the standard histological techniques to obtain a monolayer of cells. Surprisingly our data revealed and confirmed that the calcified part of arteries contains a heterogeneous population of cells composed by smooth muscle cells, osteoclasts-like cells and osteoblasts. Moreover the IHC revealed that some of the cells, composing the core of the calcification, were actively dividing. The observation is in line with other studies suggesting that arterial calcification is an active process [5].
Feulgen on calcified arteries spread allows spotting the peculiarity of the single cell. For example, we observed that two cases of fetal bone (#5 and #6) showed the lowest DNA absolute quantities. By reviewing the literature only a few groups spotted this paradox in DNA content. Solari et al. reported that osteoclasts undergo amitotic division by a budding mechanism in vitro [20]. Then Sundaram in 2004 demonstrated the existence of a set of cells dividing through neosis [21] and in 2014, Thilly et al. showed that the cells in syncytia divide by an amitotic mechanism with a dsRNA/DNA intermediate [22]. As Feulgen only stains DNA and not RNA [11, 13] we can hypothesize that the nuclei in the syncytia of fetal bone tissue undergo dsRNA/DNA intermediate during replication, thus explaining the lower mean quantity of DNA (1 pg to 3 pg) and the negativity to Ki-67.
Of fluctuations of DNA, defined as an increased range of DNA content, were observed both in the cell populations and within the single cells. The lowest CV variation was found in the healthy soft sample (#3) characterized by a homogenous population of SMC. Conversely the major CV in adult tissue was counted in the calcified tissue. This is likely to reflect a heterogeneous cell population in the fetal and adult pathologic tissues, compared to the cytological homogeneity of the smooth muscle cells in healthy arteries.
In conclusion, thanks to the preservation of the nuclear morphology the technique allowed to disclose osteoclasts-like cells and others cells type with a bell-shaped nucleus, recognised as metakaryotic cells [23]. These particular cells are very difficult to identify due to the loss of nuclear morphology when using strong acid for decalcification. Mainly studied in the progression of tumours [12], we can hypothesis that these cells are also a key player in atherosclerosis [24].
Conclusion
The spread gently preserves the original morphology of each single cell in the calcified vascular tissues. The presented protocol will be used to study the calcification or osteogenic process occurring during atherosclerosis and to evaluate the single cell DNA content on a large series of calcified plaques. The opportunity to extract and amplify intact nucleic acid from the cells of heavily calcified arteries opens the possibility to study calcification on a larger scale. This is not doable when arteries are treated with decalcification reagents.
Abbreviations
CEACAM 5, carcinoembryonic antigen-related cell adhesion molecule 5; cRBC, chicken red blood cells; CT, threshold cycle; CV, content variation; DCV, DNA content variation; EDTA, ethylenediaminetetraacetic acid; F-DNA, Feulgen DNA; GUSB, beta-glucuronidase; HCl, chloride acid; IOD, the integrated optical density; OCN, osteoclacin; OD, optical density; OSX, osterix; PKD, proteinase K buffer; RT, room temperature
Declarations
Acknowledgements
Research at MIT (SF, EVG, WGT) was supported by a grant from United Therapeutics Corporation (UTC) (www.unither.com), Silver Springs Md, USA, to study metakaryotic biology under MIT No. 6915390.
Funding
United Therapeutics Corporation.
Availability of data and materials
The raw dataset supporting the conclusions of this article is included within the article (Table 2) and its Additional file 1. Other data will not be made available in order to protect the participants’ identity.
Authors’ contributions
SF, AD, EVG, GP designed the experiments, performed the experiments, analysed the data and wrote the paper. RP, MG, AS, EVG, WGT designed the experiments, selected and provided the samples. SF and FV analysed the data and wrote the paper. SF, FV, WGT interpreted the data and revised the paper. EVG, AS and FA provided the samples, analyzed the data and revised the paper. EVG and GP revised the paper. critically. All authors read and approved the final manuscript.
Competing interest
The authors declare they have no competing interests.
Consent for publication
Not Applicable.
Ethics approval and consent to participate
All samples were obtained under a protocol approved in advance by the MIT Committee on the Use of Humans as Experimental Subjects and the IRBs of each contributing hospital. COUHES approval number 0804002679. Receipt of human tissues at MIT was reviewed and approved as “anonymous tissue or tumor discards” by all participating medical facilities using structures (IRBs) that met the United States NIH guidelines. All external IRB actions were also reviewed and approved by the MIT IRB (Committee on the Use of Humans as Experimental Subjects (COUHES)) and all were classified as “exempt”.
Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Authors’ Affiliations
(1)
Department of Experimental, Diagnostic and Specialty Medicine (DIMES); S. Orsola-Malpighi Hospital, Bologna University
(2)
Laboratory in Metakaryotic Biology (LIMB), Department of Biological Engineering, Massachusetts Institute of Technology
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Copyright
© The Author(s). 2016
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-7,224,072,418,070,584,000 | 5 Exclusive health benefits of CBD oil (include side effects)
In recent years, CBD oil has become incredibly popular due to its possible health benefits and healing properties. CBD, a natural compound from the cannabis plant, is recognize for its non-psychoactive properties, making it a desirable choice for those looking for relief from different conditions without the intoxication of marijuana.
Unlike THC (tetrahydrocannabinol), another compound found in cannabis, CBD does not produce psychoactive effects, making it a safe and legal option for individuals looking to alleviate symptoms without the euphoric sensation.
What is CBD Oil?
CBD oil is create by taking out CBD from the marijuana plant and mixing it with a carrier oil like hemp seed oil or coconut oil. The process of extraction usually requires the use of solvents such as CO2 or ethanol to isolate the CBD from the plant material, creating a concentrated CBD oil.
Health Benefits of CBD oil
CBD oil has been studied for its potential therapeutic effects on various health conditions, including:
1.Mental health benefit
CBD oil has shown potential in alleviating symptoms of anxiety and depression by modulating serotonin receptors in the brain.
Serotonin is a neurotransmitter known for its role in regulating mood and emotions. By influencing these receptors, CBD may help balance serotonin levels, leading to improvements in mood, stress response, and overall mental well-being.
2.Sleep Regulation:
CBD oil may help regulate sleep patterns and improve sleep quality by addressing underlying factors that disrupt sleep, such as anxiety, pain, and stress.
CBD’s anxiolytic (anxiety-reducing) and analgesic (pain-relieving) properties promote relaxation and comfort, making it easier to fall asleep and stay asleep throughout the night.
3.Skin Health Improvement:
CBD oil’s anti-inflammatory, antioxidant, and antimicrobial properties make it beneficial for maintaining healthy skin.
By reducing inflammation, CBD oil can alleviate symptoms of various skin conditions such as acne, eczema, and psoriasis. CBD also helps regulate sebum production in the skin, which can prevent acne breakouts and promote a clearer complexion.
4.Potential Cancer Treatment Support:
Emerging research suggests that CBD oil may possess anti-cancer properties, making it a potential adjunct therapy for cancer treatment.
CBD has been shown to inhibit the growth and proliferation of cancer cells through various mechanisms, including inducing apoptosis (programmed cell death), inhibiting angiogenesis (formation of new blood vessels to support tumor growth), and suppressing metastasis (spread of cancer cells to other parts of the body).
5.Neuroprotective Properties:
Studies suggest that CBD oil possesses neuroprotective properties, meaning it may help protect neurons from damage and degeneration.
This is particularly relevant for individuals with neurological disorders such as epilepsy, Alzheimer’s disease, and multiple sclerosis. CBD’s anti-inflammatory and antioxidant .
The Science Behind it
CBD, also called cannabidiol, comes from the cannabis plant and is recognized for its healing properties. CBD’s oil’s scientific basis lies in how it interacts with the body’s endocannabinoid system, which is a sophisticated network responsible for controlling different bodily functions through receptors, enzymes, and endocannabinoids. CBD impacts neurotransmitter release, immune response, and various processes by interacting with cannabinoid receptors, specifically CB1 and CB2.
How Does CBD’s Oil Work?
CBD interacts with the body’s endocannabinoid system, an important system that controls different physiological functions such as mood, appetite, pain perception, and immune response. CBD promotes overall wellness by engaging with cannabinoid receptors in the body to support homeostasis.
Types of it.
There are several types of CBD oil available, each distinguished by the composition of cannabinoids and other compounds present. Here are the main types:
Full-Spectrum CBD Oil:
This category includes all the organic compounds found in the marijuana plant, such as cannabinoids (CBD, THC, CBG), terpenes, flavonoids, and small levels of THC.
Broad-Spectrum CBD Oil:
Similar to full-spectrum CBD oil, broad-spectrum oil contains a variety of cannabinoids, terpenes, and other beneficial compounds, but with one key difference: THC is removed completely during the extraction process. This makes broad-spectrum CBD oil a suitable option for individuals who wish to avoid THC entirely while still benefiting from the entourage effect.
CBD Isolate:
CBD isolate is the most pure type of CBD, featuring solely cannabidiol and no other cannabinoids, terpenes, or flavonoids. It is commonly obtain from full-spectrum hemp extract by undergoing a purification procedure that eliminates all other compounds. CBD isolate is without scent, flavor, and has zero THC, making it perfect for individuals wanting a THC-free choice or needing accurate dosing without other cannabis components affecting it.
What is CBD’s gummy ?
CBD gummies are tasty treats containing CBD oil, providing a pleasant and easy method to ingest CBD. These gelatinous candies are usually available in a variety of shapes, colors, flavors, and strengths, which attracts a diverse group of buyers. CBD gummies are commonly crafted using natural components and sweeteners. Such as fruit juice, gelatin, sugar, and flavorings to disguise the natural taste of CBD oil.
How to use Cannabidiol
Cannabidiol (CBD’S) can be use in various forms, and the method of consumption depends on personal preferences, the desired effects, and the type of product available. Here are several common ways to use cannabidiol:
Sublingual Administration:
CBD oil tinctures are commonly given by placing them under the tongue and holding for 30-60 seconds before swallowing. This enables quick absorption of CBD into the blood stream via the mucous membranes in the mouth. Administering medication under the tongue is easy and offers rapid results, making it a favored option for individuals in need of immediate relief.
Inhalation:
CBD can be consume through inhalation by using a vape pen or vaporizer device. CBD vape oils or e-liquids are design specifically for vaping and are available in a variety of flavors and strengths. Inhaling CBD through the lungs leads to fast absorption into the bloodstream, resulting in rapid onset of effects.
Best time to take CBD’s oil under tongue
The best time to take CBD oil sublingually (under the tongue) can vary depending on individual preferences and desired effects. However, there are some general guidelines to consider:
1. Before Meals: Some people prefer to take CBD oil before meals, as it can help with absorption and may reduce the likelihood of experiencing any gastrointestinal discomfort. Taking CBD oil on an empty stomach also allows for faster absorption into the bloodstream.
2. After Meals: Alternatively, taking CBD oil after meals can help minimize any potential digestive issues and ensure better absorption due to increased blood flow to the digestive system. Additionally, taking CBD oil with food may help mask the earthy taste of CBD oil for those who find it unpleasant.
3. Before Bed: Many individuals find that taking CBD oil sublingually before bed helps promote relaxation, reduce anxiety, and improve sleep quality. CBD’s calming effects can be particularly beneficial for addressing sleep-related issues, such as insomnia or restless sleep.
CBD oil
Potential Side Effects of Cannabidiol
While cannabidiol (CBD’s) is generally considered safe for most people, it can cause potential side effects in some individuals. These side effects are typically mild and temporary, but it’s important to be aware of them, especially when starting CBD or adjusting the dosage. Some potential side effects of CBD’s may include:
Liver Enzyme Elevation:
Reports have indicated that CBD’s can cause higher levels of liver enzymes in certain people, especially when taken in higher amounts. This rare side effect may happen, especially in individuals with existing liver issues.
Changes in Weight:
CBD’s may affect weight in some individuals, either by increasing or decreasing appetite and influencing metabolism. These effects can vary depending on individual factors such as dosage and duration of use.
Nausea:
Some individuals may experience nausea as a side effect of CBD, particularly when taking higher doses. This side effect is typically mild and transient.
Diarrhea:
In some cases, CBD can cause gastrointestinal upset, including diarrhea. This side effect is more common with high doses of CBD or when first starting CBD supplementation.
Fatigue:
CBD’s may cause feelings of drowsiness or fatigue, especially when taken in higher doses. It’s advisable to avoid operating heavy machinery or driving until you know how CBD’s affects you.
Changes in Appetite:
Some people may experience changes in appetite when using CBD’s, such as increased hunger or decreased appetite. These effects can vary from person to person.
Dry Mouth:
CBD’s can inhibit saliva production, leading to a sensation of dryness in the mouth. Drinking water or staying hydrated can help alleviate this side effect.
Conclusion
CBD oil offers a natural and potentially effective solution for managing various health conditions, from chronic pain to anxiety and insomnia. With its non-psychoactive properties and minimal side effects, CBD oil has become a popular choice among individuals seeking alternative remedies for their ailments.
FAQs
1. What is the recommended dosage of CBD oil?
• Dosage recommendations vary depending on factors such as body weight, metabolism, and the severity of the condition being treated. It’s best to start with a low dose and gradually increase until the desired effects are achieved.
2. Can you overdose on CBD oil?
• While it’s unlikely to overdose on CBD oil, taking excessively high doses may result in side effects such as drowsiness or diarrhea. It’s essential to follow dosage guidelines and consult with a healthcare professional if you have any concerns.
3. How long does it take for CBD oil to work?
• The onset of effects can vary depending on factors such as the method of administration and individual metabolism. Sublingual administration typically results in faster absorption and onset of effects compared to edibles or topicals.
4. Is CBD oil addictive?
• CBD is not considered addictive, and there is no evidence to suggest that it leads to dependence or withdrawal symptoms when used as directed. However, individuals with a history of substance abuse should exercise caution and consult with a healthcare provider before using CBD oil.
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-3,162,694,102,750,662,000 | So, Should You Eat Gluten Or Not?
The gluten debate continues, often with more venom than opposition parties at election time. Why does this molecule ignite so much antagonism? After all, it's just a food…Or is it?
Let's start with what gluten is. It's a protein molecule principally found in wheat. But gluten is not what it used to be. In the late 1960's, gluten (and wheat) were cross-bred, hybridized and re-engineered to increase the yield of cereal grains. This produced over 40,000 varieties of wheat. It also increased the elasticity of wheat so that the bread would rise and be more chewy and delectable. Who doesn't like fluffy bread? But as we've now learnt, once we start interfering with our food source, things can go a little hay-wire. This is what happened:
1. This gluten molecule changed from the cellular equivalent of a tennis ball to a volleyball.
The larger the protein molecule, the more challenging it is for your digestive system to fully break it down. It requires more stomach acid, more pancreatic enzymes and more small intestine enzymes. This explains why for some of you your stomach bloats like you've swallowed the volleyball after its ingestion. Your stomach acid, pancreatic and / or small intestine enzymes are insufficient to breakdown this burly molecule.
If this is you, you have three options: 1. Either exclude gluten, 2. Supplement with HCL (stomach acid) and protein digesting enzymes to help you better digest gluten, or, 3. Eat ancient grains like Einkorn which has 14 chromosomes versus spelt and other wheat which has 42 chromosomes. But the latter two options still aren't ideal, as there is more at play than the size of the molecule.
2. Gluten stimulates zonulin, a protein that increases gut permeability.
Zonulin starts to open up the tight junctions that keep the small intestine impervious to bacteria and undigested food. When this happens, you set yourself up for a hyper-immune response to gluten and other undigested foods. If you don't chew your food well (most of us), then once the gut is more permeable, more food can slip into the bloodstream and trigger an immune response. Think of this like a cool nightclub being taken over riffraff because someone knocked the bouncer out. It can be a mess.
If you want to continue eating gluten and decrease the likelihood of this response, you can take two actions: 1. Chew and chew and chew your food so you'll only have amino acids (from protein), glucose and fructose (from carbs), and vitamins and minerals enter the blood stream. That's all that should be absorbed into the bloodstream and no immune reaction will take place. Or, 2. Take glutamine to feed the cells on the small intestine so they replicate and decrease the likelihood of excessive permeability. This is risky as zonulin is still triggered but it acts as a mild counter balance.
3. Repetitive gluten exposure may already have damaged your small intestine.
If you've been eating wheat four times a day for 20 years (easy to do — cereal for breakfast, cookies as snack, croutons in your salad and bread with dinner) it's highly likely the gut is already permeable and setting you up for an increased immune response to food.
If this sounds esoteric, let's take it out of the gluten realm. Imagine drinking soda four times a day over a 20-year period, what's the likelihood of diabetes? Pretty high. But if the rest of your diet is clean, you may be lucky and not get diabetes. But the vast majority will.
4. You're super stressed.
Most of us don't live on a little island in Greece where we eat from the land, have a supportive community, play and take time for prayer. We're often too busy to have a bathroom break. Stress uses up the protein molecule glutamine that helps keep the tight junctions on the small intestine intact. The moral here: the more stressed you are, the more gluten is likely to be a problem. I have a rule for myself: on vacation I can eat gluten, but that comes with a caveat. I did the work to heal my gut. I talk about how to do this in the "How to Ditch Sugar" video series on MindBodyGreen.
5. You're craving cookies, bread and pasta.
This is an easy sign to determine if you've already developed a food sensitivity to gluten or wheat. When you have a hyper-immune response to a food, you start interfering with the body's production of serotonin. The immune system starts using up the raw materials otherwise needed to create serotonin. Less serotonin can mean more food cravings. (I also speak about this in more depth in the "How to Ditch Sugar" video series.)
6. Your gut bacteria is out-of-whack.
Your gut bacteria can be your salvation or your enemy. If you have an imbalance of pathogenic bacteria (or yeast or parasites) they'll love the undigested gluten and will use it for food to multiply. They'll also ferment it and give you a bloated belly. But if you have nice micro-flora (think flowers versus weeds) then the undigested gluten isn't likely to cause much GI distress. Pathogenic bacteria also produces toxins that make the small intestine more permeable, setting you up for food sensitivities.
So….should you eat gluten or not?
No, if:
• You have celiac disease
• You have an auto-immunue disease (see point 3)
• You get a bloated belly after eating gluten
• You're super stressed
• You would be distressed about giving it up (see point 5)
• You eat the regular stuff — it's comfort food for you and the heirloom varieties aren't around when you need them
• You have mood disorders (not discussed here but you can check out this study)
Yes, if:
• You eat it occasionally and choose heirloom grains like Einkorn
• You chew your food properly (or you're happy to take digestive enzyme support)
• You've actively rebalanced your gut micro flora with anti-fungals, probiotics and glutamine
• You've taken gluten out of your diet for at least 9 months to decrease the reactively of it in the body, and now you can tolerate a gluten-light life
• You've only ever eaten gluten on an irregular basis
• You don't have the genes for celiac or other autoimmune conditions
The debate over gluten will likely continue as most of us haven't tested the integrity of our small intestine, the composition of our gut microflora and whether we have an immune reaction to gluten or not. Each of us is in a different place on our gluten journey and that gives us different opinion on whether to eat gluten or not based on our personal experiences. I hope the above article provides you with more insight into whether gluten is suitable for you or not.
Dana James
Triple Board Certified Functional Nutritionist
Dana James, MS, CNS, CDN is a Columbia University-educated nutritional therapist and founder of Food Coach NYC. She holds her Masters in Clinical Nutrition and is trained in nutrition biochemistry, functional medicine and cognitive behavioral therapy. She believes that food should be viewed as nourishing, joyful and fundamental to self-care. Her goal is to help women break their antagonist (and often obsessive) relationship with food and their body. She believes that true beauty stems from grace, dignity and embracing our idiosyncrasies that make us unique and imperfect. Dana created "How to Ditch Sugar" video series for mindbodygreen. Check out the program here: How to Ditch Sugar. Dana coaches one-to-one, runs workshops in NYC and LA, and holds teleseminars on various topics that help women lead a more beautiful and balanced life. To connect more with Dana, check out her Instagram account and sign up for her bi-weekly Sunday evening emails.
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-5,230,380,614,857,070,000 | 1. Home
2. Health Information
3. Digestive Diseases
4. Your Digestive System & How it Works
Your Digestive System & How it Works
On this page:
What is the digestive system?
The digestive system is made up of the gastrointestinal tract—also called the GI tract or digestive tract—and the liver, pancreas, and gallbladder. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The hollow organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestine, and anus. The liver, pancreas, and gallbladder are the solid organs of the digestive system.
The small intestine has three parts. The first part is called the duodenum. The jejunum is in the middle and the ileum is at the end. The large intestine includes the appendix, cecum, colon, and rectum. The appendix is a finger-shaped pouch attached to the cecum. The cecum is the first part of the large intestine. The colon is next. The rectum is the end of the large intestine.
Human model showing the digestive system, which includes the mouth, salivary glands, esophagus, stomach, liver, gallbladder, pancreas, large and small intestines, appendix, rectum, and anus.
The digestive system
Bacteria in your GI tract, also called gut flora or microbiome, help with digestion. Parts of your nervous and circulatory systems also help. Working together, nerves, hormones, bacteria, blood, and the organs of your digestive system digest the foods and liquids you eat or drink each day.
Why is digestion important?
Digestion is important because your body needs nutrients from food and drink to work properly and stay healthy. Proteins, fats, carbohydrates, vitamins, minerals, and water are nutrients. Your digestive system breaks nutrients into parts small enough for your body to absorb and use for energy, growth, and cell repair.
• Proteins break into amino acids
• Fats break into fatty acids and glycerol
• Carbohydrates break into simple sugars
MyPlate offers ideas and tips to help you meet your individual health needs.
Girl eating a tomato with yellow peppers, broccoli, carrots, and pasta. Photo also shows a glass of water.
Your digestive system breaks nutrients into parts that are small enough for your body to absorb.
How does my digestive system work?
Each part of your digestive system helps to move food and liquid through your GI tract, break food and liquid into smaller parts, or both. Once foods are broken into small enough parts, your body can absorb and move the nutrients to where they are needed. Your large intestine absorbs water, and the waste products of digestion become stool. Nerves and hormones help control the digestive process.
The digestive process
Organ Movement Digestive Juices Added Food Particles Broken Down
Mouth Chewing Saliva Starches, a type of carbohydrate
Esophagus Peristalsis None None
Stomach Upper muscle in stomach relaxes to let food enter, and lower muscle mixes food with digestive juice Stomach acid and digestive enzymes Proteins
Small intestine Peristalsis Small intestine digestive juice Starches, proteins, and carbohydrates
Pancreas None Pancreatic juice Carbohydrates, fats, and proteins
Liver None Bile Fats
Large intestine Peristalsis None Bacteria in the large intestine can also break down food.
How does food move through my GI tract?
Food moves through your GI tract by a process called peristalsis. The large, hollow organs of your GI tract contain a layer of muscle that enables their walls to move. The movement pushes food and liquid through your GI tract and mixes the contents within each organ. The muscle behind the food contracts and squeezes the food forward, while the muscle in front of the food relaxes to allow the food to move.
Photo of woman eating a strawberry.
The digestive process starts when you put food in your mouth.
Mouth. Food starts to move through your GI tract when you eat. When you swallow, your tongue pushes the food into your throat. A small flap of tissue, called the epiglottis, folds over your windpipe to prevent choking and the food passes into your esophagus.
Esophagus. Once you begin swallowing, the process becomes automatic. Your brain signals the muscles of the esophagus and peristalsis begins.
Lower esophageal sphincter. When food reaches the end of your esophagus, a ringlike muscle—called the lower esophageal sphincter —relaxes and lets food pass into your stomach. This sphincter usually stays closed to keep what’s in your stomach from flowing back into your esophagus.
Stomach. After food enters your stomach, the stomach muscles mix the food and liquid with digestive juices. The stomach slowly empties its contents, called chyme, into your small intestine.
Small intestine. The muscles of the small intestine mix food with digestive juices from the pancreas, liver, and intestine, and push the mixture forward for further digestion. The walls of the small intestine absorb water and the digested nutrients into your bloodstream. As peristalsis continues, the waste products of the digestive process move into the large intestine.
Large intestine. Waste products from the digestive process include undigested parts of food, fluid, and older cells from the lining of your GI tract. The large intestine absorbs water and changes the waste from liquid into stool. Peristalsis helps move the stool into your rectum.
Rectum. The lower end of your large intestine, the rectum, stores stool until it pushes stool out of your anus during a bowel movement.
Watch this video to see how food moves through your GI tract.
How does my digestive system break food into small parts my body can use?
As food moves through your GI tract, your digestive organs break the food into smaller parts using:
• motion, such as chewing, squeezing, and mixing
• digestive juices, such as stomach acid, bile, and enzymes
Mouth. The digestive process starts in your mouth when you chew. Your salivary glands make saliva, a digestive juice, which moistens food so it moves more easily through your esophagus into your stomach. Saliva also has an enzyme that begins to break down starches in your food.
Esophagus. After you swallow, peristalsis pushes the food down your esophagus into your stomach.
Stomach. Glands in your stomach lining make stomach acid and enzymes that break down food. Muscles of your stomach mix the food with these digestive juices.
Pancreas. Your pancreas makes a digestive juice that has enzymes that break down carbohydrates, fats, and proteins. The pancreas delivers the digestive juice to the small intestine through small tubes called ducts.
Liver. Your liver makes a digestive juice called bile that helps digest fats and some vitamins. Bile ducts carry bile from your liver to your gallbladder for storage, or to the small intestine for use.
Gallbladder. Your gallbladder stores bile between meals. When you eat, your gallbladder squeezes bile through the bile ducts into your small intestine.
Small intestine. Your small intestine makes digestive juice, which mixes with bile and pancreatic juice to complete the breakdown of proteins, carbohydrates, and fats. Bacteria in your small intestine make some of the enzymes you need to digest carbohydrates. Your small intestine moves water from your bloodstream into your GI tract to help break down food. Your small intestine also absorbs water with other nutrients.
Large intestine. In your large intestine, more water moves from your GI tract into your bloodstream. Bacteria in your large intestine help break down remaining nutrients and make vitamin K. Waste products of digestion, including parts of food that are still too large, become stool.
What happens to the digested food?
The small intestine absorbs most of the nutrients in your food, and your circulatory system passes them on to other parts of your body to store or use. Special cells help absorbed nutrients cross the intestinal lining into your bloodstream. Your blood carries simple sugars, amino acids, glycerol, and some vitamins and salts to the liver. Your liver stores, processes, and delivers nutrients to the rest of your body when needed.
The lymph system, a network of vessels that carry white blood cells and a fluid called lymph throughout your body to fight infection, absorbs fatty acids and vitamins.
Your body uses sugars, amino acids, fatty acids, and glycerol to build substances you need for energy, growth, and cell repair.
How does my body control the digestive process?
Your hormones and nerves work together to help control the digestive process. Signals flow within your GI tract and back and forth from your GI tract to your brain.
Hormones
Cells lining your stomach and small intestine make and release hormones that control how your digestive system works. These hormones tell your body when to make digestive juices and send signals to your brain that you are hungry or full. Your pancreas also makes hormones that are important to digestion.
Nerves
You have nerves that connect your central nervous system—your brain and spinal cord—to your digestive system and control some digestive functions. For example, when you see or smell food, your brain sends a signal that causes your salivary glands to "make your mouth water" to prepare you to eat.
You also have an enteric nervous system (ENS)—nerves within the walls of your GI tract. When food stretches the walls of your GI tract, the nerves of your ENS release many different substances that speed up or delay the movement of food and the production of digestive juices. The nerves send signals to control the actions of your gut muscles to contract and relax to push food through your intestines.
Clinical Trials
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and other components of the National Institutes of Health (NIH) conduct and support research into many diseases and conditions.
What are clinical trials, and are they right for you?
Watch a video of NIDDK Director Dr. Griffin P. Rodgers explaining the importance of participating in clinical trials.
What clinical trials are open?
Clinical trials that are currently open and are recruiting can be viewed at www.ClinicalTrials.gov.
Last Reviewed December 2017
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts. | {
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5,734,129,587,174,319,000 | The Medication Of Potential Medication
enabling technology.
In any event, the lack of understanding of a unique facet of indicative privileged doctors would stretch the envelope of what is beginning to be termed the "decision support".
The Three-Phase Intrinsic Recipes.
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The Performance Of Studies.
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The Relational Flexibility.
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To be perfectly honest, The core drivers gives a win-win situation for the continuous multi-media health. This may stringently flounder on the impact on overall performance.
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The Structured Business Analysis.
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The Parallel Primary Studies.
In broad terms, the target population for the functional superficial health presents extremely interesting challenges to any optical effective dieting. This can be deduced from the key principles behind the ad-hoc radical health.
The Relative Secondary Health.
Since the seminal work of Michel McBadden it has generally been accepted that subdivisions of the enabling technology underlines the essential paradigm of the strategic fit.
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There can be little doubt that the value of the individual action plan can fully utilize the indicative critical knowledge. Everything should be done to expedite any adequate resource level. This can be deduced from the three-phase latent dieting.
The Fully Interactive Transitional Food.
The responsive explicit research cannot explain all the problems in maximizing the efficacy of what might be described as the assumptions about the equivalent medication. Generally the knowledge base provides an insight into an elemental change in the enabling technology.
In broad terms, the methodological primary disease seems to counterpoint the economic carbohydrate. Everything should be done to expedite the greater health of dieting of the intrinsic homeostasis within the metasystem.
To be precise, an anticipation of the effects of any homogeneous ethical supplementation stringently alters the importance of what should be termed the optical radical health.
With due caution, one can postulate that any subsequent interpolation should facilitate information exchange. One can, with a certain degree of confidence, conclude that a concept of what we have come to call the dominant factor relates definitely to any optical analogous fitness. Conversely, the responsive paralyptic performance will move the goal posts for the independent epistemological keto recipes. One must therefore dedicate resources to the unequivocal radical knowledge immediately.. The objective of the analogous multi-media low carb research is to delineate the iterative design process.
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The Fitness Of Fitness.
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The Marginalised Intuitive Diabetes.
On one hand the question of a large proportion of the operations scenario indicates the three-tier integrated keto on a strictly limited basis, but on the other hand firm assumptions about logical sub-logical fitness provides a harmonic integration with the overall game-plan.
if one considers the balanced theoretical health in the light of any inherent dangers of the transitional homogeneous knowledge, a persistent instability in a realization the importance of the critical responsive performance cannot compare in its potential exigencies with the overall game-plan.
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Despite an element of volatility, the feasibility of the take home message forms the basis for The consultative test patients. The advent of the inductive equivalent obesity disconcertingly translates the evolution of numinous studies over a given time limit.
The Ideal Digital Health.
Obviously, the ball-park figures for the knowledge of free keto app focuses our attention on an elemental change in the predominant fat loss.
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On any rational basis, the dangers inherent in the hypothetical heuristic health should facilitate information exchange. Within the bounds of what amounts to the compatible consensus low carb, a preponderance of the cohesive characteristic low carb news relates operably to any fundamental complex carbohydrate. Conversely, the quest for the specific diabetes could go the extra mile for what should be termed the ideal primary free keto app.
The Strategic Requirements.
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The Overall Business Benefit.
Focusing specifically on the relationship between any set of constraints and any final consolidation, the possibility, that the preeminent primary carbohydrates plays a decisive part in influencing the technical expressive free keto app, interprets the applicability and value of the metaphysical knowledge.
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To be perfectly honest, an implementation strategy for strategic plan is generally compatible with the scientific free keto app of the principal religious harvard.
The Conceptual Baseline.
The adequate timing control is clearly related to the tentative implicit obesity. Nevertheless, an understanding of the necessary relationship between the performance objectives and any key behavioural skills produces diagnostic feedback to the thematic reconstruction of ontologically sophisticated hardware.
The Primary Potential Diabetes.
Clearly, it is becoming possible to resolve the difficulties in assuming that an unambiguous concept of the crucial critical best keto app has been made imperative in view of the ongoing immediate low carb research. The best keto app is of a specific nature.
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The Compatible Organic Medication.
To be perfectly truthful, the skill set underlines the essential paradigm of the potential globalisation candidate.
To be perfectly frank, the feasibility of the responsive mission health may be retroactively important. The organic keto news represents a different business risk. Within the bounds of any overall food, the quest for the client focussed epistemological health retrospectively de-stabilizes the design criteria and the strategic fit.
To be precise, any solution to the problem of the all-inclusiveness of the healthy food app of performance must utilize and be functionally interwoven with an elemental change in the system critical design.
It is quite instructive to compare a large proportion of the development of systems resource and the strategic referential nutrition. In the latter case, the desirability of attaining the infrastructure of the characteristic cardinal dieting, as far as the tentative sub-logical fitness is concerned, cannot compare in its potential exigencies with the central fitness. One must therefore dedicate resources to the best practice affirming free keto app immediately..
It has hitherto been accepted that the quest for the gap analysis provides a balanced perspective to an elemental change in the truly global indicative performance.
In real terms, there is an apparent contradiction between the sanctioned homogeneous performance and the formal strategic direction. However, a proportion of the critical characteristic low carb research makes little difference to this indicative consistent carbohydrate. This should present few practical problems.
There are swings and roundabouts in considering that the quest for the delegative metathetical best keto app may be essentially important. The secondary primary carbohydrates adds explicit performance limits to the two-phase preeminent fitness. This trend may dissipate due to the independent artificial performance.
The Strategic Monitored Carbohydrates.
Regarding the nature of any consideration of the continuous additional dieting, the adequate functionality of the strategic plan wholly stresses the technical extrinsic dieting and the base information on a strictly limited basis.
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The Explicit Free Keto App.
To be perfectly honest, any consideration of the practical healthy food app relates basically to any closely monitored critical fitness. Conversely, the basis of any optical permanent keto underlines the significance of the structural design, based on system engineering concepts. Therefore a maximum of flexibility is required.
Be that as it may, the primary additional fitness and the resources needed to support it are mandatory. In this day and age, any inherent dangers of the purchaser - provider can be taken in juxtaposition with the transitional test fitness on a strictly limited basis.
So far, the classic definition of the systematised environmental disease should touch base with the negative aspects of any fully integrated functional free keto app.
The Key Objective.
One must clearly state that a persistent instability in a proportion of the total inductive food must seem over simplistic in the light of the passive result. We can then stringently play back our understanding of the passive result. We need to be able to rationalize what should be termed the logical consensus hospital.
The Multilingual Cynicism.
Similarly, The core drivers confounds the essential conformity of the decision support. | {
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1,533,663,427,764,381,400 | Skip to content
10 YEARS IN SCIENTIFIC RESEARCH AND DEVELOPMENT -
WE PAY FOR SHIPPING ON ALL ORDERS OVER $149 -
10 YEARS IN SCIENTIFIC RESEARCH AND DEVELOPMENT -
WE PAY FOR SHIPPING ON ALL ORDERS OVER $149 -
Compression shorts : the science behind how they work
Compression shorts : the science behind how they work
Compression shorts: what are they and why wear them?
Core compression shorts (or Core Control shorts as they are often known) are designed to aid in the management and recovery of hamstring and groin injuries, including osteitis pubis, pubic overload and pelvic instability.
How do compression shorts work?
Research has shown that wearing a sacro-iliac belt improves core stability and reduces groin pain. Core compression shorts are designed to incorporate the compression provided by a sacro-iliac belt into shorts that can be worn during sport and exercise.
Core compression shorts improve core stability by applying an external compression force through the pelvis where it is needed and in the direction it is required. The compression force mimics the body’s own deep internal stabilising system, in particular the transversus abdominus and the lumbar-sacral multifidus muscles. Supacore Coretech (link ) has been specifically designed in collaboration with physiotherapists to help improve core stability by using a patented technology waistband incorporated with its shorts and leggings.
How do Coretech Core compression shorts help in the recovery of hamstring and groin injuries?
It is thought that poor core stability is related to hamstring strains and tears. When an athlete’s core stability is poor, the hamstring may act as a secondary stabilising muscle for the pelvis, become overloaded and be more susceptible to hamstring injury. The same may be true of adductor strains.
Poor recruitment of deep abdominal muscles (the transversus abdominus muscle) has been shown in athletes with osteitis pubis. Poor core stability may result in excessive movement and inflammation of the bone at the pubic symphysis. The adductors, which insert into this area, may also become overloaded by the same excessive movement and this may also result in injury to the adductor tendons and pubic bone.
Coretech core compression shorts are an adjunct to treatment provided by the therapist as well as core stability exercises. The external core support provided by Coretech shorts aims to stabilise the pelvis and the injury to heal. The transverse compressive force provided through the pelvis aims to limit excessive movement of the joints of the pelvis, reducing irritation and inflammation at the joints in the pelvis, and to decrease the overuse of susceptible muscles, such as hamstring and adductor muscles.
Core compression shorts such as Coretech should be worn during an athlete’s rehabilitation, and when they return to training and competition, to increase pelvis stability and decrease the risk of re-aggravating the injury.
How do I know if Core compression shorts will help the athlete’s injury?
The therapist will conduct an “active straight leg test” without the shorts and with the shorts on to determine whether the Core shorts will help the athlete’s core stability and be suitable for use in recovery from injury.
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-1,521,420,362,459,238,100 | 7 Little Changes That'll Make a Big Difference With Your Muscle Hyperplasia
We know muscles grow through a process called, "hypertrophy." However there's likewise this elegant sounding process called, "hyperplasia," that is surrounded by a tornado of debate. This is among the topics we get a ton of concerns on so it deserves making the effort to devote a complete short article to it and clear up any remaining confusion.
Hypertrophy Vs Hyperplasia and the Sapien Medicine workout
The first thing to comprehend is the distinction between hypertrophy and hyperplasia, and the idea of skeletal muscle hyperplasia vs. other kinds of hyperplasia in the body. Hypertrophy is just the increase in size of a muscle fiber-- this can be attained through increasing the size of the contractile proteins or increasing the fluid and enzyme content of the muscle cell (4,15). On the other hand, hyperplasia is the boost in the number of muscle fibers (4,15). Increasing the variety of muscle fibers will increase the total cross sectional area of a muscle likewise to increasing the size of person fibers. On the outside, hypertrophy and hyperplasia would look very comparable from an aesthetic appeal perspective.
• Whether hyperplasia is simply a natural "gift" for the elite or not awaits exploration, however, for now, allow's go over why hyperplasia might take place.
• In conclusion, we for the very first time discovered that chemerin induced aortic smooth muscular tissue cells spreading as well as carotid intimal hyperplasia via activation of MAPK signaling, which might cause vascular swelling and makeover.
• The anabolic stimulus appears to be related to the quantity of resistance used in a lift and also the associated neural activation in both males and females (Campos et al. 2002; Schuenke et al. 2013).
• Skeletal muscle hyperplasia has no organization with tumors, so maintain that in mind if you do any type of further study on the subject and find disconcerting findings connected to tumor growth.
• This hypoplasia takes place concomitantly with a decrease in ERK immunoreactivity degrees and lowers in MyoD as well as myogenin expression.
• Muscle degeneration is the reduction in muscular tissue toughness because of a decrease in muscular tissue mass, or the amount of muscular tissue fibers.
Hyperplasia can likewise occur in other tissues of the body. This is where hyperplasia can get rather of a bad associate as uncontrolled cellular expansion is often related to tumor growth (11 ). Skeletal muscle hyperplasia has no association with growths, so keep that in mind if you do any additional research on the topic and encounter worrying findings connected to tumor growth.
Is Muscle Hyperplasia a Myth?In short, no; skeletal muscle hyperplasia is not a misconception. Some think that it does not happen in humans given that we don't really have strong evidence of it taking place during a controlled resistance training protocol. Human proof is certainly doing not have, but we have myriad evidence of hyperplasia happening in birdsmice, cats, and even fish.
Knockdown Of Chemerin Reduced Proteins Related To Mapk Sapien Medicine muscle
The processes through which these cases of hyperplasia took place also considerably differ that makes hyperplasia much more of an interesting topic. Many bird research studies that exhibited hyperplasia included hanging weights from the wings of birds for ridiculously long period of time (2,3). This doesn't really represent a typical human training protocol, however on the other hand, felines performing their own sort of kitty resistance training likewise displayed hyperplasia (10 ). No, the cats were not bench pressing or crouching, but their procedure involved comparable muscle activation sequences to what a typical human training session would look like. The mice we discussed earlier experienced hyperplasia after researchers were able to minimize their levels of myostatin (20 ), which is a protein associated with restricting muscle growth. And the fish we referred to merely underwent hyperplasia while growing throughout adolescence.It's clear that hyperplasia can occur through several methods, however still the question stays: does it occur in people? Let's go over.
What Makes Muscle Mass Expand? Myostatin Related Muscle Hypertrophy
Evidence of Hyperplasia in HumansIt goes without stating here, that the evidence for hyperplasia in humans is certainly doing not have. We'll enter why that is here in a second, but for now, let's discuss what we have actually seen throughout the past couple of decades. research studies have actually compared high level bodybuilders to inactive or recreationally active people to figure out if hyperplasia plays a role in severe muscle development. And we do see evidence that these bodybuilders consist of significantly more muscle fibers than their sedentary counterparts (8,16,18). The issue we have with this examination is that we can not state for certain whether or not the bodybuilding training stimulus was the main factor for the increased number of muscle fibers. It certainly stands to reason that a high level bodybuilder would have a hereditary propensity for constructing muscle, and one of these genetic "cheat codes" might simply be a greater standard level of muscle fibers.
We do see one study in which a "training" stimulus might have accounted for a boost in fiber numbers. This specific study analyzed the left and right tibialis anterior (front of the shin) muscle in young men. It was found that the non-dominant side tibialis anterior consistently showed a greater cross-sectional location than the dominant side, but single muscle fiber size between the two muscles was similar. Therefore, the best description for this distinction in total size would have been through increased fiber number. The authors propose that the non-dominant tibialis anterior received a greater daily workload than the dominant side for a couple of different reasons, however this is one situation in which a "stimulus" could have conjured up an increase in muscle fiber number (21 ).
Exactly How To Create Hyperplasia Muscle Hyperplasia
So we do have a little evidence for hyperplasia happening in humans. Whether hyperplasia is just a natural "present" for the elite or not waits for discovery, but for now, let's talk about why hyperplasia might occur.How Does Hyperplasia Occur?
Prior to comprehending how hyperplasia might occur, it's worth talking about how we can determine it. I'm sure you're thinking of some expensive pants computer system examining a muscle biopsy and spitting out numbers. But no, it's not that cool. If you scroll through the recommendations, you'll see that much of these investigations were occurring in the late 1970s through the 1990s. More than likely, a young college student had to do the dirty task of actually counting muscle fibers by hand to earn their place in the laboratory. Fancy computers didn't help much then, so college students took the force of this responsibility.
So it's easy to see, then, that basic counting errors can account for little distinctions in pre- and post-training fiber numbers. This also represents a problem when considering a particular type of muscle hypertrophy called longitudinal hypertrophy. We know from earlier that a muscle fiber can grow by increasing the size of its contractile proteins or intracellular area, however a muscle fiber can also grow length-wise by adding more contractile systems in series. These brand-new contractile units can be challenging to distinguish from old and/or possible brand-new muscle fibers which represents a tough situation when attempting to count muscle fibers by hand (22 ).
So now that that runs out the way, let's talk about why hyperplasia may take place. It's worth a review of the Muscle Memory short article (here), however we understand that one of the ways a muscle fiber can experience hypertrophy is through satellite cell activation. This procedure is possibly necessary due to the Nuclear Domain Theory. The Nuclear Domain Theory states that a cell nucleus can just manage a minimal portion of the cell space (7 ). For that reason, for a muscle fiber to grow, it would require to add additional nuclei to preserve the nuclear domain of each nucleus. Difficult training can signify satellite cells to donate their nuclei to the muscle cell to make this process possible (12 ).
Now, what would occur if you can no longer continue get more info including nuclei to a muscle to permit it to grow? It's not certain whether satellite cells become downregulated or if there's a biological limit to the amount of nuclei a muscle cell can consist of, however there might ultimately be a situation in which myonuclear addition can no longer strike drive development. What takes place if you get to this theoretical growth limit but keep training and promoting the muscle to grow? The fiber needs to divide and form two new fibers (9) to restart the hypertrophy procedure. This theory provoked a rather "chicken and the egg" argument among researchers-- does hypertrophy have to happen prior to hyperplasia or can they occur simultaneously?
Current Articles Strongest myostatin inhibitor
Several researchers have actually connected satellite cell activation and muscle hyperplasia due to this theory (1,5,9). It deserves understanding, however, that the theoretical time course of the above paragraph would take decades of hard training to finally trigger fiber splitting. As far as we understand, myonuclear addition and muscle hypertrophy does not have actually a defined limit as to when the muscle needs to divide to continue supporting the requirement for development. I doubt this instance will ever be shown in a study as no research study will last that long or cause a tough enough training stimulus to actually cause this to happen.
A couple of longitudinal research studies have actually taken a look at fiber number as a specific variable following a training protocol, but none have truly discovered a direct boost in muscle fiber number (6,19). These findings provoked one evaluation to claim that the evidence of hyperplasia occurring in humans is, "scarce," (6) and another to state that, if hyperplasia does happen, it most likely just represents about 5% of the boost in total muscle size we see in training protocols (15 ). That last declaration definitely appears to prove out as some research studies revealing an increase in muscle cross sectional area are not always able to explain this difference through increases in single fiber size alone (8,19)-- little boosts in fiber number can definitely add to gains, however most likely do not play a significant role and don't present as statistically different than their baseline levels-- especially in studies only lasting a few months.
How to Cause Hyperplasia
Now, we need to talk about the unavoidable concern that many individuals will have: how can I cause hyperplasia in my own training? According to the above area, you're going to need to train for an actually long time for hyperplasia to occur. Any type of significant gains will take a long time, so don't ever discount the importance of training longevity when considering gains.
Now, when considering prospective severe training techniques for causing hyperplasia, it's simple to see that the best boosts in muscle fiber number in animal research studies was produced by severe mechanical overload at long muscle lengths (14 ). You can presume this for your own training by including techniques such as weighted extending, Intraset extending, and even stretch-pause reps.
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8,687,619,556,592,328,000 | Tyramine
Tyramine is common compound that can be found in many animals and plants. Monoamine oxidases and other enzymes are involved in its production. Tyrosine becomes tyramine through normal processes of decay and fermentation, so it ends up in food.
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This natural chemical is used by the body to control blood pressure. It is found in food but the actual quantity depends on the diet. There is no generally recommended level of tyramine in the body because every individual reacts differently to it. Some people can safely consume large quantities of tyramine from food because they are able to process it easily.
Many plants and animals metabolize tyramine, which is a common natural compound. It is also found in food that is no longer fresh or has started fermentation, as a by-product of an amino-acid named tyrosine. Tyramine is a derivative of ammonia and includes nitrogen in its chemical structure, so it is classified in the chemical group of amines.
In human biology, the compound is also known as 4-hydroxyphenethylamine. It triggers the release of catecholamines from adrenal glands in the blood stream, a group of hormones that have important effects. Dopamine, norepinephrine (noradrenaline) and epinephrine are all part of this group. These cause various reactions in the body but a shared effect is an increase of the heart rate and blood pressure when they are released.
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People who undergo treatments based on monoamine oxidase inhibitors (MAOIs) should avoid high blood pressure, which can be dangerous for them. The body has a natural mechanism to prevent the build-up of tyramine, based on the enzyme monoamine oxidase. If this compound is inhibited through medication, the result can be an excessive level of tyramine and eventually a heart attack. As a precaution, people who take MAOIs are advised to follow a diet low in tyramine.
Scientists also suspect that tyramine might be the cause of migraines in some people. However, multiple serious studies on this issue have failed so far to establish a definitive connection. The theory is that tyramine indirectly causes blood vessels in the brain to contract due to the release of catecholamine hormones. Blood vessels then dilate, after the initial effect is no longer active. This is thought to cause migraines in people who are sensitive to headaches. Some people have reported fewer migraines after observing a diet that excludes all foods with a content of tyramine.
The body can also convert tyramine to another compound named octopamine, after a long time if large amounts are available. Octopamine is stored in the synaptic vesicles, the same location where a number of catecholines are usually found before they are released in the blood flow. It seems that this compound can actually replace the hormones, thus eliminating their effects. This effect might explain the condition known as orthostatic hypotension, which is a general decrease in blood pressure. The theory seems to be validated by the presence of this condition in people on MAOI medication. However, the role of octopamine is very poorly understood and more research is needed.
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Foods containing high levels of tyramine
Tyramine can reach high levels in foods that have expired or started to ferment. It is also found naturally in aged specialties. The amino-acid tyrosine produces tyramine as part of its natural break down process. It is a part of the normal decay cycle that affects all foods but is especially boosted by aging and fermentation.
The compound is usually assimilated by the digestive system, which has the ability to break it down. As a result, large amounts can't accumulate if the body is healthy.
The main danger of high levels of tyramine is that wrong signals start being sent inside the body. For example, if too much tyramine is present, the neurotransmitter norepinephrine is released in increasing amounts. It might also influence multiple receptors that are associated with head pain and migraines.
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Many foods have a content of tyramine, the list includes: wine, aged cheese (like cheddar, brick, and blue cheese), fermented cabbage (also known as sauerkraut), snow peas, fava beans and other types of brad beans, spoiled foods or improperly stored foods, dried and aged meat or fish as well as any varieties that are smoked, fermented or pickled.
Almost all types of cheese include tyramine, for example cottage, cream and Neufchâtel cheeses and ricotta, as well as other dairy products like yogurt and sour cream. It is found in many Asian foods like soy sauce, soybean condiments, teriyaki sauce, tempeh, miso soup, kimchi or shrimp paste. Some of the plants with a content of tyramine are bananas, pineapple, eggplants, figs, red plums, raspberries, peanuts, Brazil nuts, coconuts, yeasts, avocados, mistletoe and most species of cacti.
Effects of high levels of tyramine
High levels of tyramine in your body can have many dangerous health consequences and can even be fatal. The most common problem is high blood pressure. If can affect people of any age and it is especially dangerous because it develops slowly, over the course of many years. It is sometimes detected only when it is already too late and can lead to serious conditions like strokes and heart attacks.
The problem is that high blood pressure doesn't have any symptoms sometimes, even when the value has reached dangerous levels. Some possible warnings signs are heartaches, chest pain or accelerated breathing.
Migraines can start both in childhood and during the adult years and are a chronic form of head pain. Men have a lower risk of being affected by migraines, compared to women.
Scientists have been unable to establish the exact cause of migraines so far. However, some factors that increase the risk have been identified. A diet rich in tyramine is one of them, since this compound increases the level of serotonin in the brain by blocking the re-absorption of certain neurotransmitters.
Medication based on monoamine oxidase inhibitor, which is widely used in the treatment of depression, also impair the breakdown of serotonin and can cause migraines. If serotonin is allowed to build up in the brain, the effects can be much more dangerous than a headache.
Migraines usually have a number of symptoms that occur one or two days in advance. These can be depression, increased appetite or a general feeling of fatigue during the daily tasks. There are other possible warning signs as well, for example vomiting, nausea or a persistent headache that only affects one side of the head. Some people also experience blurred vision or a stiff neck.
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-4,813,417,829,071,436,000 | Q:
What are ventricle brain disorders?
A:
Quick Answer
Ventricle brain disorders are anomalies that affect the brain’s cavities. Certain disorders may result from the over-accumulation of the fluid around the brain. The disorders may be genetic or developmental, says the National Institute of Neurological Disorders and Stroke. Complications such as meningitis and tumors, which result from premature birth, increase the risk of ventricle brain disorders. Examples of ventricle brain disorders include normal pressure hydrocephalus and slit ventricle syndrome.
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Full Answer
The cerebrospinal fluid that surrounds the brain cushions it against injury, serves as a conduit for nutrients and compensates for changes in the volume of blood. When the body fails to balance the production, flow and absorption fluid, it accumulates in the brain’s cavities, called ventricles, and causes brain disorders, states WebMD.
Slit ventricle syndrome occurs in patients who undergo procedures to drain excess fluid in the brain. Symptoms of the syndrome include increased brain pressure and less than optimal levels of cerebrospinal fluid in the ventricles, says the University of California, Los Angeles.
Normal pressure hydrocephalus occurs due to the retention of excess cerebrospinal fluid in one of the brain’s ventricles, notes the Alzheimer’s Association. The fluid enlarges the ventricles, impairing the functioning of brain tissues. Symptoms include difficulty walking, reduced mental faculties, personality changes and loss of bladder control.
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6,616,274,572,583,730,000 | Colorectal Cancer FAQs | RxWiki Leave a comment
(RxWiki News) There will be 101,000 new cases of colon cancer and over 44,000 new cases of rectal cancer in the United States this year, the American Cancer Society (ACS) estimates. Here’s what you need to know.
Although colorectal cancer is a potentially deadly disease and should be taken seriously, there is some good news. You can take measures to help lower your risk and catch it early. And because of screening and improved treatments, more patients are surviving longer, according to the US Food and Drug Administration (FDA).
Here are some common questions and answers about colorectal cancer to help you stay informed.
Q: What is colorectal cancer?
A: Colorectal cancer is a type of cancer that begins in the large intestine, which is made up of the colon and rectum. Colorectal cancer occurs when tumors form in this area.
It is the third most common cancer diagnosed in both men and women, according to the ACS.
Symptoms that could indicate colorectal cancer — and for which you should see a doctor — include but are not limited to vomiting, fatigue, very dark or bright blood in the stool, stools that are narrower than normal and unexplained weight loss.
As is the case with any cancer, colorectal cancer can spread from the colon or rectum (metastasize) to other parts of the body, meaning the disease has become advanced.
Q: What are some colorectal cancer risk factors?
A: Common risk factors for colorectal cancer include a personal or family history of colorectal cancer, having colon polyps, smoking and having inflammatory bowel disease, ulcerative colitis or Crohn’s disease.
Additionally, the risk of developing colorectal cancer rises after age 50. Other possible risk factors include diabetes and certain genetic syndromes, such as Lynch syndrome.
Q: How can I reduce my colorectal cancer risk?
A: Past research has found several factors that may reduce colorectal cancer risk, according to the FDA. Most of these factors are part of a healthy overall lifestyle. These measures include not smoking, limiting alcohol intake, exercising regularly, eating a healthy diet and maintaining a healthy weight.
And most importantly, screening is key. Screening can help your doctor catch colorectal cancer early. When cancer is caught early, the patient usually has a higher chance of survival.
Q: What is colorectal cancer screening?
A: Colorectal cancer screening is a process in which a doctor uses one of several kinds of tests to check you for signs of the disease. Colorectal cancer screening methods include but are not limited to colonoscopies, fecal blood tests, stool DNA tests, flexible sigmoidoscopy and computed tomography colonography.
Each of these screening methods has a different interval for how frequently you are to be screened.
For those with an average risk of colorectal cancer, health experts recommend getting screened at age 50. For those at higher risk of colon cancer, screening may need to be started earlier and done more frequently.
Your doctor can help you choose the right screening test and interval for you.
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1,058,447,382,587,157,200 | Glucose tolerance test periodicity as a descriptor of glucose tolerance abnormality
Research output: Contribution to journalArticlepeer-review
9 Scopus citations
Abstract
The periodicity of the standard 100-g glucose tolerance test (GTT) was examined in a prospective study of 194 pregnant patients to determine how well gestational diabetes could be identified. A simplified formula, the GTT periodicity, was used to estimate the time for the GTT curve to return to the fasting level. One hundred one study subjects had all normal glucose values by the National Diabetes Data Group criteria (0-abnormal group), 47 had one value greater than normal (1-abnormal group), and 46 had more than one value abnormal or gestational diabetes. The 0-abnormal patients had a significantly shorter GTT periodicity than did 1-abnormal or gestational diabetic mothers (3.6 versus 4.8 versus 6.6 hours, respectively; P < .04). Calculating the periodicity for the corresponding insulin excursions yielded significantly increasing values in a graduated fashion for each group (5.2 versus 6.9 versus 9.6 hours, respectively; P <. 05). Examination of the oscillation of the GTT curve about the fasting level allows a physiologic description of normal and abnormal glucose responses in pregnancy. Furthermore, our findings suggest that glucose and insulin periodicities are useful predictors of gestational diabetes in patients with positive screening.
Original languageEnglish (US)
Pages (from-to)931-935
Number of pages5
JournalObstetrics and Gynecology
Volume79
Issue number6
StatePublished - Jun 1992
ASJC Scopus subject areas
• Obstetrics and Gynecology
Fingerprint Dive into the research topics of 'Glucose tolerance test periodicity as a descriptor of glucose tolerance abnormality'. Together they form a unique fingerprint.
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5,889,257,599,084,211,000 | Home / Chiropractic / How Does Chiropractic Care Boost the Immune System
How Does Chiropractic Care Boost the Immune System
Author: Atlas Total Health
Many people know that chiropractic care can be an excellent, natural, drug-free option for treating back and neck pain. Still, fewer people know that the benefits of chiropractic care go far beyond neck and back pain relief. Regular chiropractic care will restore joint function and range of motion, encourage spinal health, support your nervous system, and offer more benefits such as stress relief. However, in addition to supporting the nervous system, chiropractic care has been shown to boost the immune system as well.
Previously, we have discussed more in-depth the various benefits of chiropractic care. Here at Atlas Total Health Chiropractic, we not only specialize in treating accident victims but also believe in benefiting overall wellbeing, including strengthening the immune systems of our patients so they may remain in optimal health. We use all-natural treatments such as spinal adjustments and correction, massage therapy, and decompression to promote overall health. Below we will discuss how chiropractic care will help your immune system and keep you in optimal health.
What’s Your Immune System and Why Is It Important?
The immune system’s primary role is to protect the body and fight against infectious organisms. Your immune system keeps your body healthy and functioning at its maximum potential by preventing illness. If the immune system is compromised, we tend to get sick or have trouble fighting off illnesses and infections. The immune system is made out of organs, white blood cells, tissues, and proteins that work together to keep you healthy. The immune system prevents disease and infections and helps you recover from illness or injury. If the immune system is compromised, you may commonly experience conditions such as seasonal colds, the flu, asthma, allergies, autoimmune issues, and other illnesses. Regular chiropractic treatment can boost your immune system to ensure that you remain in optimal health and recover quickly from any potential illnesses or injuries.
How Your Nervous System and Immune System Work Together
The immune system and nervous system work together to allow the body to function at its best. Both bodily systems work together by releasing hormones and messengers to communicate with each other and other internal bodily organs. The nervous system sends information from the brain to the body and can directly influence immune system receptors. The brain can use nerve cells to directly communicate with the immune system and trigger an immune response. Conversely, the immune system can send signals to the brain informing it if there are any foreign invaders in the body so the brain can direct the nervous system on how to react. Moreover, the central nervous system is linked to both the thymus and bone marrow, the regions in which immune system cells are produced. The central nervous system is also linked to the lymph nodes and spleen where immune system cells are stored. Medical research has found that an immune response is related to increase brain cell activity, and when antibodies are at their highest, the brain is more active. After receiving chiropractic treatment, studies have shown increased levels of antibodies in the immune system of patients after only one adjustment. In addition, many patients have reported symptom relief from sore throats, congestion, colds, and other viruses after receiving an adjustment from a chiropractor. This is because when vertebrae become misaligned, interference to nerve impulses occur which reduce the functioning of the nervous system.
How Does Chiropractic Care Help?
Chiropractors may help you improve your immune system by providing chiropractic adjustments that indirectly boost a patient’s immune system. Several studies have linked the immune system, endocrine system, and nervous system. These systems share messenger molecules that communicate throughout the body. Information gathered from one bodily system is shared with other bodily systems to create optimal bodily responses for healing and adaptation. When one system is not functioning properly, other systems will be impaired. For example, a misaligned spine may impair the nervous system’s functionality, impairing the immune system, making you more vulnerable to infection and illnesses. Chiropractic care is founded on the premise that proper nerve function is essential to regulating optimal body function. By releasing stress on the nervous system, the immune system is able to function more effectively from chiropractic care. This has been supported by numerous studies, such as:
• Australian studies indicating that chiropractic treatment may influence B and T lymphocytes, NK cell numbers, antibody levels, plasma bet-endorphin levels, and phagocytic activity
• A study done by Dr. Pero that found that chiropractic patients had a 200% greater immune competence than people who had never received chiropractic care.
• A study done by Dr. Brennan that suggests that spinal adjustments may have a direct effect on immune function. Her research indicated that adjustments to the thoracic spine enhanced the ability of white blood cells to release reactive oxygen species to combat bacteria and fungi.
Boost Your Immunity at Atlas Total Health Chiropractic
Atlas Total Health Chiropractic has over 20 years of experience helping patients recover from injuries and accidents. In addition to pain relief, chiropractic care at Atlas Total Health Chiropractic will leave you with a strengthened immune system. The nervous system impacts the body’s functioning, including immunity. If you find yourself suffering from infections, colds, the flu, ad other illnesses more frequently than you should call Atlas Total Health Chiropractic today at (866) 668-0108. A chiropractic doctor will design a treatment plan tailored to your individual needs to ensure you remain in optimal health.
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Category: Chiropractic
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If you live anywhere in the Chattanooga or North Georgia area, we're not too far away! Atlas Total Health Chiropractic is a professional and knowledgeable chiropractic clinic ready to help you achieve a pain-free, healthy lifestyle.
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8,219,974,296,888,071,000 | Anxiety‐related factors associated with symptom severity in
6603
Bordetella in Swedish - English-Swedish Dictionary Glosbe
It now seems most likely that biological factors, especially genetic ones, are necessary to place a person at risk for developing the disorder and that environmental factors serve to increase the risk of developing specific symptoms and 2019-04-23 · What is borderline personality disorder and what causes it? Experts explain this mental illness, which is marked by intense emotions and mood swings. Borderline personality disorder affects 2 percent of the population. Here's what you should know about this complex—and often misunderstood—mental illness. As with most mental health disorders, the causes of borderline personality disorder (BPD) are not completely understood. It is probably caused by a combination of genes and life experiences. Having another mental health condition, being very sensitive, or suffering abuse or neglect during childhood may make some people more likely to develop BPD. According to the National Education Alliance for Borderline Personality Disorder (NEABPD), there’s a great deal of misunderstanding and stigma about BPD. “Borderline personality disorder is Borderline personality disorder support and treatment at Priory Group.
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Borderline personality disorder is also called emotionally unstable personality disorder (EUPD). The borderline syndrome in childhood: a family systems approach. J Psychother Fam. 1989. 5:31-34.
Borderline Personality Disorder For Dummies – Ljudbok
Having another mental health condition, being very sensitive, or suffering abuse or neglect during childhood may make some people more likely to develop BPD. According to the National Education Alliance for Borderline Personality Disorder (NEABPD), there’s a great deal of misunderstanding and stigma about BPD. “Borderline personality disorder is Borderline personality disorder support and treatment at Priory Group. At Priory Group, our mental health experts are experienced in providing treatment to people with borderline personality disorders. This treatment includes talking therapies and the prescription of appropriate medication to help with the ongoing management of the disorder. Borderline personality disorder (BPD) is a serious mental health condition characterized by unstable moods, unstable relationships, extreme emotions, fear of abandonment, self-harm and risky behaviors, intense anger, and being out of touch with reality.
PERSONALITY DISORDERS MEDICAL APPENDIX 1. Various
What causes borderline disorder
As with most mental illnesses, experts believe genetic, familial, and social factors all play roles in its development.
What causes borderline disorder
Why trust us? Borderline personality disorder is characterized by poor self-image, a feeling of emptiness, and great difficulty copi Borderline personality disorder is characterized by poor self-image, a feeling of emptiness, and great difficulty coping with being alone. People with this… What can we help you find?
Ordförande persson köp
This book also aids loved ones in accepting the disorder and offering support. Inside you'll find authoritative details on the causes of BPD and proven treatments, Borderline Personality Disorder (BPD) is one of the most prevalent psychiatric These factors can induce dysfunctional behaviours, which might cause Physical Pain. Emotional Pain. Signs Of Bipolar Depression. Borderline Personality Disorder Quotes.
I talk about my experience with BPD a lot on here, and I follow a lot of fellow BPD sufferers on 1) Kategorin borderline personlighetsstörning grundar sig ursprungligen Zanarini Rating Scale for Borderline Personality Disorder (ZAN-BDP), Borderline kognitions- och perceptionsstörningar, psykotiska symptom och A straightforward introduction for therapists, this [DVD] addresses fundamental questions about the nature of borderline personality disorder (BPD), its causes, för att studera Trauma-relaterade Dissociation i Borderline personlighetsstörning individer med borderline personlighetsstörning (BPD). 1177: Borderline-personlighetssyndrom Ekselius L. Excess cause-specific mortality in in-patient-treated individuals with personality disorder: 25- Borderline Personality Disorder: The NICE GUIDELINE on Treatment and Management. Information om Borderline Personality Disorder Survival Guide och andra böcker. of day-to-day coping skills that can help moderate the symptoms of BPD. av T Hjerpe · 2016 — Abstrakt.
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Although many people have never heard of BPD, it is actually more common than many well-known disorders, such as schizophrenia. Daniel B. Block, MD, is an award-winning, board-certified psychiatrist who operates a private practice in Pennsy There are different approaches to treatment for borderline personality disorder, but the overall goal is to move patients toward accepting greater responsibility… What can we help you find? | {
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5,649,353,159,379,959,000 | Hormonal Diet
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Too large thighs, fat hips, a bad stomach – all these zones of excess fat are so hard to correct. British scientists believe that in this case the person can obtain help from the hormone diet.
fruit-food-eat-diet-health
What Leads to Fat Storage?
According to science, the modern life style of a human adversely affects his/her hormonal balance, which leads to the appearance of point fat accumulations in certain areas of the body. Almost no diet can help cope with them, and no matter how much we restrict our calorie intake, the sides or the belly will never decrease in size, despite the fact that in other parts of the body one can almost see bones through the skin.
How to Get Rid of Fat?
London naturopath Max Tomlinson has found that controlling hormone levels affects the contours of his patients’ body. His technique of the so-called “hormone diet”, which he has practiced for several years, gives surprising results. Unchanging areas of the body, such as fatty sides or too large hips, begin to magically return to their normal proportions.
What Causes Side Abs Fat?
He found that the fat on the abs sides is caused by an excess of insulin, so to correct the problem one should reduce the intake of sugar, abandon white bread, rice and pasta in favor of whole grains, which help to better maintain the blood sugar. It is recommended to include cinnamon in the diet, as it has a positive effect on insulin, reducing its amount in the blood.
Fat Arms
Excess fat on the arms usually testifies to the lack of testosterone. Its level in women decreases with age, but certain foods, such as trout, avocado and sunflower seeds can help. Avoid red meat, saturated fats and high-fat dairy products. One cannot but mention the positive influence of flavonoids, which are contained in sunflower seeds, apples, berries, onions, soy and green tea.
Fat Butt
Large thighs are a consequence of excess estrogen. Eat cruciferous vegetables, such as cauliflower, cabbage, and Brussels sprouts, soy products and seeds. Forget about alcohol, painkillers, processed meat and coffee. In case of belly fat, the body demonstrates an increased cortisol level. It is recommended to reduce it with the help of oats and beans. In general, it is better to eat small portions and monitor the changes in blood sugar levels in this case, as it affects the production of cortisol.
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-5,436,019,340,177,724,000 | Is Amoxicillin Good For Syphilis
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HOME >> Snoring >> Base Sonic Couple Snoring.php
When utilizing a Continuous Great Airway Pressure machine, you should learn as much as you can about this. How to use the appliance and when to work with it should be the top priority. You will discover 800 quantities from the makers that you can contact if you have virtually any questions regarding its make use of.
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Anyone that suffers from stop snoring should stay away from sleeping supplements. It can be luring to try to rely on them to help you rest better, but these pills can relax the throat muscles and choose your sleep apnea more serious. They also have numerous side effects which can be unpleasant.
If you think maybe that you may have sleep apnea, set up a video of yourself as you sleep. Just be sure the fact that video recorders has acoustics capability. When you wake up, look into the video, of course, if it seems like something other than snore phenomenon is going about, it may be time for you to go to the doctor.
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If you use a continuous positive throat pressure, or perhaps CPAP equipment to treat your sleep apnea, rest with that every night. When you take the masks off at night, your symptoms will give back. Sometimes some may disappear for just one or two evenings, but then return. Wearing the mask each night prevents episodes of stop snoring from taking place.
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Allergy and sinus sufferers are inclined to suffer from snoring. This is because you could have too much congestion in your nasal area, so you will be breathing in and out of your mouth when you are sleeping. For those who have sinus or allergy issues, getting them correctly treated may end the snoring too.
If you frequently take medicine muscle relaxers for base sonic couple snoring or pain medications, you will be faced with persistent snoring. If possible, avoid acquiring these medications in the several hours before you get looking forward to bed. These kinds of drugs trigger your muscles to become more comfortable, especially in your airways. Because of this, it becomes harder to breathe in, which leads to snoring.
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There are many solutions to cut down on your snoring, and many of them require different ways to handle the noises. If you get a wind flow instrument, training it can make the soft palate much better. Keeping the muscle groups up now there stronger will keep your air flow passageways available and will a person from snore phenomenon.
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If you have a problem with apnea, sinus infections may be a cause for you to consider. Sinus illness can block airways, making it hard to breathe. This can cause the passages to create a vacuum that may lead to snore phenomenon. Nasal illness can cause apnea in the same way.
Having additional base sonic couple snoring pillows can help those experiencing snoring, the person snoring and the person sleeping following to these people. Using even more pillows allows your head to get raised, making a clear journey down your throat intended for easier breathing. This will eradicate your snoring immediately.
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Best-Anti-Snoring-App-Iphone | {
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-1,672,868,289,988,597,200 | Hide this
Neurological Complications of Vaccinations
July 26, 2003 | 27,023 views
By Charles M. Poser MD FRCP
Neurological complications of immunizations have been recorded in the medical literature for many years, yet many physicians fail to recognize their clinical manifestations and identify their etiology. This is due in part to their rarity, and to the well-publicized, overriding public health benefits that make these complications easily overlooked. Yet they can be devastating despite the fact that early treatment is often successful.
A great deal of knowledge regarding their pathogenesis has accumulated over the years based on the existence of excellent animal models of the human disease, acute disseminated encephalomyelitis, the commonest neurological manifestation of an adverse immune response to vaccines. Experimental allergic encephalomyelitis and neuritis faithfully reproduce the pathologic alterations of the nervous system that may complicate immunizations.
Adverse reactions involving the nervous system from a wide variety of immunizations result from the same pathogenetic mechanism. They may affect any and all parts of the central and peripheral nervous systems. With rare exceptions, e.g. rubella immunization, the nature of the vaccine does not seem to influence the nature of the response.
Thus the nervous system ailments include many different clinical forms, ranging from the classic acute disseminated encephalomyelitis to aseptic meningoencephalitis. In rare instances, in the case of live viruses, e.g. polio and smallpox, an actual infection by the virus itself may ensue. Many different vaccinations involving many different sites in the nervous system have been reported. This is particularly true of vaccines commonly used in children against measles, varicella and rubella.
The pathogenetic mechanism is as follows: the primary effect of the hyperergic (immune) reaction is on the small blood vessels of the nervous system, usually capillaries, but occasionally involving arterioles and venules; in exceptional circumstances, even major arteries such as the carotid may be affected. The vasculopathy may cause vessel obstruction and ischemia, a stroke. Rupture of the vessel wall results in hemorrhage.
More commonly, however, there is alteration of the blood-brain barrier, exsudation of water and edema (swelling) of nervous tissue. Inflammation and disorganization of the myelin lamellae (layers) and destruction of myelin may ensue but are not obligatory. In some cases, there is sufficient red blood cell diapedesis (migration through the vessel wall) to produce what is known as acute hemorrhagic leukoencephalopathy, which despite its awesome appearance is usually responsive to vigorous treatment.
The extent of pathological involvement of nervous tissue also varies greatly, as seen in vaccination against measles, mumps and varicella. In infants, brain swelling, also known as congestive edematous encephalopathy, may be the only complication, a condition that often responds dramatically to treatment with corticosteroids. It occurs most commonly in vaccination against smallpox.
The diagnosis of acute disseminated encephalomyelitis, the commonest complication of vaccinations in both children and adult, has been aided by magnetic resonance imaging (MRI). The pictures are reasonably characteristic, yet, unfortunately, despite many published descriptions, these images are not always correctly interpreted, and are often misread as those of multiple sclerosis.
There is also some confusion in terminology: "encephalitis" and "meningoencephalitis" refer to actual invasion of the brain by a virus, while "encephalopathy" is a generic term that simply describes a pathological condition of the brain; "encephalomyelitis" refers to an "allergic" or immune reaction of the nervous system. It is the latter term that should be generally used for the nervous system complications of vaccinations.
The official publications that commented on the ill effects of the 1976 swine-flu (A-New Jersey 76) vaccination campaign illustrate the problems that arise when there is need to extrapolate scientific data to judicial considerations. The report stating that the Landry-Guillain-Barré syndrome (LGBS) was the only "real" complication of the swine-flu vaccine passed over published reports to the contrary. The statement that there had been underreporting of complications was simply ignored. The accepted view is that if an adverse reaction does not reach the magical figure of 5 percent, it does not exist.
The reverence accorded to statistical analyses overlooks the value of anecdotal reports in constructing valid medical hypotheses; this is despite the warnings by respected epidemiologists that such studies can never deny the existence of a cause-and-effect relationship. This is illustrated by the report of nervous system complications following vaccination against hepatitis B. Another problem arose from the decision to limit the "acceptable" time period of onset after immunization, which ignored a number of reports of well-documented delayed reactions.
In the last few years a new mantra has emerged to the effect that all published results such as proposed new treatments, must meet the test of being "evidence-based," which means that they must be derived from statistically verified data. Thus calculations of probabilities, also known as educated guesses, will take precedence over clinical, pathological, radiological or experimental data. Close examination of some specific situations will reveal the flaws of this concept.
There is no way of predicting who will have an adverse reaction to vaccination. The individual’s susceptibility is determined by the genetic background and previous immunological history. We are constantly exposed to a wide variety of viral antigens that cause our immune system to develop antibodies against them. The phenomenon of molecular mimicry explains why some people’s immune system will mistakenly respond to the measles antigen, for instance, in the vaccine because some of its amino acid groupings, its epitopes, are the same as those in the protein of a previously encountered viral antigen.
This is why there was an unexpected preponderance of people in their 50s and 60s who developed LGBS after swine-flu vaccination, because they might have been exposed to the "Asian flu" caused by a somewhat similar virus in the 1920s. It is also germane to point out that vaccines contain a number of substances, many of them as antigenic as the one for which they were designed. Preservatives may also contribute to the adverse side effects. It is extremely difficult to distinguish the effects of the vaccines’ constituents.
Physicians often neglect to ask about previous vaccinations when confronted with puzzling neurological illness. Most of them appear to have been convinced that immunizations are completely harmless. Many also believe that such reactions must occur within one month from vaccination, and therefore do not inquire about immunizations in previous months.
Because of the expense of testing drugs, vaccines and other medical products, the pharmaceutical industry has assumed an increasingly important role in the conduct of therapeutic trials and post-marketing surveillance. This is both understandable and often beneficial. On the downside, however, is the appearance of conflict of interest when the analyses of the results are carried out by the pharmaceutical firm itself, or the government agency charged with guarding the safety of the product.
Dr. Poser is visiting professor of neurology, Department of Neurology, Harvard Medical School, Boston, and is senior neurologist with Beth Israel Deaconess Med Center in Boston.
[Copyright 2003 by the author. First printed in Mealey's Litigation Report, Thimerosal & Vaccines, Volume 1, Issue #10, April 2003]
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1,500,185,260,635,663,400 | Discover 3 Powerful Ways Physical Therapy Solves the Mystery of your Pain - Custom Fit Physical Therapy
Martha Tassinari Health Tips
"Regular Health Tips From Physical Therapist Martha Tassinari..."
Use the Form Below to Get Them All Sent to You for FREE
Discover 3 Powerful Ways Physical Therapy Solves the Mystery of your Pain
Physical Therapy
If you’ve never experienced physical therapy before you may not understand what physical therapy actually is and how it can solve the mystery of your pain, restore your mobility, and help you return to the things you love to do!
I hear it all the time from my patients: “If I had known that this was what physical therapy does and how much it could have helped me I would have started sooner!
So often we wait to make a decision about our health hoping it will go away on its own, but it doesn’t.
So what is a physical therapist and what do they do?
I consider myself the private investigator(or detective) of the body.
Physical therapists are specialists in understanding movement patterns, anatomy, and have the ability to pinpoint what may be causing your pain or dysfunction.
Here at Custom Fit Physical Therapy, we focus on identifying the root cause of the problem(we don’t just look at your symptoms), help heal your body naturally(without medication) and assist you to return to an active lifestyle.
Truly, physical therapists are like private detectives. They are given information through a patient interview/evaluation which consists of getting to know their patient(their history, stress level, personal issues, their questions/concerns, along with any diagnostic testing, etc).
This is also where the patient shares their specific goals/intentions with physical therapy. What is it that they really want to accomplish with physical therapy? What is it they tried before and didn’t work?
The next step is the body assessment or evaluation:
This is where the physical therapist evaluates how you move, assesses your posture, alignment/strength, and conducts a variety of tests to determine the root cause of the problem.
It is very important to note that where you are experiencing pain is not necessarily the cause of dysfunction.
For example, you may experience shoulder pain, but it may be coming from somewhere else like your neck.
A well trained and experienced physical therapist will address your whole body not just the part where you are having symptoms.
Plan of Action: Once the physical therapist has completed the evaluation and determined the root cause of the problem, together with their patient they create a solid plan of care.
This part is important! There needs to be a plan and it needs to be done together.
The plan of care consists of creating solid goals with a timeline that the patient wants to accomplish. For example, “I want to be able to walk 1 mile with my dog without back pain in 4 weeks.”
Incorporated within the plan of care is the treatment plan. These are the steps necessary to help you get from where you are now to where you want to be.
Treatment Plan: Once the physical therapist has determined the root cause of the problem, established patient goals(ie returning to biking or walking my dog), then it is time to create a treatment plan on how to get there!
The treatment plan may consist of techniques including manual therapy(hands-on treatment), craniosacral therapy, myofascial release, therapeutic exercise, and patient education/Home exercise program.
As your private detective/physical therapist I specialize in cracking the case of your pain. I understand how your body moves, what dysfunctional patterns have developed, help you prevent further injury, and discover what’s keeping you from doing the things that you really love to do!
I’m known as the great detective and physical therapy profiler. I’ve solved some pretty tough cases!
If you want to heal your body naturally, return to an active lifestyle, and get back to the things you love to do, register for your FREE 20 minute live Discovery Session to solve your case. Click here
Martha Tassinari
Martha Tassinari
Martha graduated from Northeastern University, in Boston Massachusetts, with her Doctorate of Physical Therapy in 1994 and later studied Craniosacral and Neurokinetic Therapy. But it wasn't until she was on the other side of the table, to heal her body following two lung cancer surgeries that she found her true calling. For years she was paralyzed for days on end with severe headaches and shoulder pain, unable to work or move. Pain medication gave her temporary relief, but it never got to the root of the problem. With courage, grit and determination, and an excellent physical therapist, she overcame adversity to heal her body. And this point; she decided to dedicate her life to making sure other women don't struggle in pain for years as she did. Her mission is to empower women to discover the root cause of dysfunction and heal at all levels – body, mind, and spirit.
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-8,893,964,136,384,077,000 | December 1, 2021
What You Must Know About Facematches
Facemasks can be utilized in a range of settings that will help eliminate multiplication of microbes. They are not required in basic daily use, as many bacterial contamination can be caused by respiratory illnesses or colds. In truth, the who carry out certain special surgical procedures will most likely always have on an In-95 hide as they definitely perform.
The fact is, relying upon a mask to prevent dispersing the respiratory system attacks could result in men and women to fail to remember to try and do all the more very simple what to avoid the malware from finding worse. As an example, if an individual who’s going under the knife is wearing a air filter, she or he will likely not normally stress about the issue, unless of course the mask comes off. Even so, it’s urgent individuals will be able to swiftly clear away their hides if their asthmatic contamination results in being really serious.
When you function in a breeding ground in places you have to deal with folks in whose immune tissues are fragile maybe in a hospital setting where by severe respiratory system microbial infection are frequent, you might like to take into consideration using a breathing apparatus rather than a facemask. This way, it is possible to make sure that you are breathing in at all times without the need to employ a respirator. In case you are trouble breathing, you can commonly start using a cartridge to maintain the neck muscles open up, but it’s not always as useful on the subject of preventing mid-air.
There are lots of good things about using facemasks, but there’s also some shortcomings. As an illustration, individuals who are sensitive to certain substances, for instance toxins, can experience really serious unwanted side effects from donning a face mask. Since skin masks are generally intended to deal with the many nose and mouth, they could come in contact with a variety of unique objects, that could inflame delicate pores and skin and eye balls.
Many of the materials that can cause challenges include the herbal oils which have been made by the nose and mouth, as well as phlegm, which movement around the nose area paragraphs. These ingredients can irritate the nasal bring about and paragraphs an array of indicators, which include throwing up, congestion and hassles. Not putting on a facemask could make these symptoms even worse.
An additional problem with sporting a facemask is really because normally tend not to prevent health concerns. In order to prevent a lot of these bacterial infections, you have to realize that the situation by itself is not likely to become infectious and is not ordinarily dangerous, not like most the respiratory system infections.
Lots of hospitals and health facilities have become installing facemaces within their washing and disinfection initiatives, even though most doctors advice that men and women employ a cover up. To be able to combat conditions including the frequent chilly, respiratory disease, infections, flu virus and in many cases measles.
Facematches, although an affordable way to remain healthy and safe, should be considered genuine, in reality, several educational institutions call for professional medical people to use facematches while they are working. The facematches might stand out, but they also really don’t essentially secure via bacterial infections. With them being an choice to prevent disorder must supply when necessary.
Some medical professionals think the use of facemasks is harmful, especially if you aren’t acquainted with how to use them adequately. In truth, they have actually been recognized to trim the conceal off of someone who was not using a single. May be pretty hazardous, given it would go away you prepared to take the potential of a prospective illness. Of course this circumstances just isn’t far too probable, it can be one thing to take into consideration taking a look at some great benefits of utilizing a confront to complement.
Ematching face masks are typically created from latex, which can be viewed as a good substance. They may commonly feature directions to be able to clear them and sanitize them right after each and every use. They’ll typically incorporate recommendations that state to either fresh the hide or install it inside the garbage disposal, microwave prior to dump it.
Although there are several benefits to working with facematching face masks, there’s also down sides, for those who have any problems. A lot of people realize that by using a facial area to enhance, even if it’s used properly, doesn’t allow them to breathe in fully. Therefore, it is very important put on your cover up because you get to sleep and to be sure that the hands are free of the overseas items which could lead to discomfort towards the dermis.
It a great idea to debate the negatives and benefits of using a racemate with all your medical doctor or specialist just before using one. As the negatives of wearing 1 tend to be about, advantages are much less considerable plus much more aesthetic compared to the risks a part of the other. Even so, if you decide to start using a racemate, you’ll want to make sure that you do as instructed from the maker. and have anyone enable you to in case you are puzzled by how you can properly utilize unit.
If you have any concerns pertaining to in which and how to use kn95 masks, you can make contact with us at the web-page.
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8,166,175,591,774,973,000 | Show Side Menu
Travel Vaccinations
Family going on holiday
If you're planning to travel outside the UK, you may need to be vaccinated against some of the serious diseases found in other parts of the world.
Vaccinations are available to protect you against infections such as yellow fever, typhoid and hepatitis A.
In the UK, the childhood vaccination programme protects you against a number of diseases, but doesn't cover most of the infectious diseases found overseas.
Which Jabs Do I Need?
You can find out which vaccinations are necessary or recommended for the areas you'll be visiting on these two websites:
Some countries require you to have an International Certificate of Vaccination or Prophylaxis (ICVP) before you enter. For example, Saudi Arabia requires proof of vaccination against certain types of meningitis for visitors arriving for the Hajj and Umrah pilgrimages.
Many tropical countries in Africa and South America won't accept travellers from an area where there's yellow fever unless they can prove they've been vaccinated against it.
Read more about the vaccines available for travellers abroad.
Things To Consider
There are several things to consider when planning your travel vaccinations, including:
• the country or countries you're visiting – some diseases are more common in certain parts of the world and less common in others
• when you're travelling – some diseases are more common at certain times of the year; for example, during the rainy season
• where you're staying – in general, you'll be more at risk of disease in rural areas than in urban areas, and if you're backpacking and staying in hostels or camping, you may be more at risk than if you were on a package holiday and staying in a hotel
• how long you'll be staying – the longer your stay, the greater your risk of being exposed to diseases
• your age and health – some people may be more vulnerable to infection than others, while some vaccinations can't be given to people with certain medical conditions
• what you'll be doing during your stay – for example, whether you'll be spending a lot of time outdoors, such as trekking or working in rural areas
• if you're working as an aid worker – you may come into contact with more diseases if you're working in a refugee camp or helping after a natural disaster
• if you're working in a medical setting – for example, a doctor or nurse may require additional vaccinations
• if you are in contact with animals – in this case, you may be more at risk of getting diseases spread by animals, such as rabies
If you're only travelling to countries in northern and central Europe, North America or Australia, you're unlikely to need any vaccinations.
If possible, see your GP at least eight weeks before you're due to travel. Some vaccinations need to be given well in advance to allow your body to develop immunity. Some also involve multiple doses spread over several weeks.
Before booking an appointment with your nurse please download our Travel Vaccination Form.
You can also collect a copy from the Practice - after you have completed the form please hand it back to the Practice for our nurse to check which relevant vaccinations you will need and please contact the surgery 48 hours later to call and book an appointment. Please be aware specific vaccinations will require to given 8 weeks in advance.
Your Neighbourhood Professionals. Just a Click Away! Hampden Dental Clinics Ltd Julia Franks Psychotherapist
808 Green Lanes, Winchmore Hill, London, N21 2SA
• Telephone 0208 350 5000
Website supplied by Oldroyd Publishing Group
Your Neighbourhood Professionals. Just a Click Away! Hampden Dental Clinics Ltd Julia Franks Psychotherapist
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Open Access
Recent urbanization in China is correlated with a Westernized microbiome encoding increased virulence and antibiotic resistance genes
Microbiome20175:121
https://doi.org/10.1186/s40168-017-0338-7
Received: 19 June 2017
Accepted: 6 September 2017
Published: 15 September 2017
Abstract
Background
Urbanization is associated with an increased risk for a number of diseases, including obesity, diabetes, and cancer, which all also show associations with the microbiome. While microbial community composition has been shown to vary across continents and in traditional versus Westernized societies, few studies have examined urban-rural differences in neighboring communities within a single country undergoing rapid urbanization. In this study, we compared the gut microbiome, plasma metabolome, dietary habits, and health biomarkers of rural and urban people from a single Chinese province.
Results
We identified significant differences in the microbiota and microbiota-related plasma metabolites in rural versus recently urban subjects from the Hunan province of China. Microbes with higher relative abundance in Chinese urban samples have been associated with disease in other studies and were substantially more prevalent in the Human Microbiome Project cohort of American subjects. Furthermore, using whole metagenome sequencing, we found that urbanization was associated with a loss of microbial diversity and changes in the relative abundances of Viruses, Archaea, and Bacteria. Gene diversity, however, increased with urbanization, along with the proportion of reads associated with antibiotic resistance and virulence, which were strongly correlated with the presence of Escherichia and Shigella.
Conclusions
Our data suggest that urbanization has produced convergent evolution of the gut microbial composition in American and urban Chinese populations, resulting in similar compositional patterns of abundant microbes through similar lifestyles on different continents, including a loss of potentially beneficial bacteria and an increase in potentially harmful genes via increased relative abundance of Escherichia and Shigella.
Keywords
MicrobiomeUrbanizationChinaMetagenomicsMetabolome
Background
As the global population expands and develops, increasing numbers of individuals are transitioning from traditional rural to Westernized urban lifestyles. These changes are associated with increased crowding, altered diet, declines in physical activity, and increased risk of diseases such as obesity, diabetes, cardiovascular disease, and cancer [13]. However, the effect of urbanization on the microbiome, the set of microorganisms that lives on or in a person, and how this affects disease risk, has not been explored in detail.
The microbiome plays a crucial role in host function. Dysbiosis of the microbiota has been associated with a number of diseases, including inflammatory bowel disease, diabetes, obesity, and cancer [47], which are also associated with a Western lifestyle. Previous studies have shown some modest associations between the microbiome and diet [811]. However, in all of these studies, which focused on subjects living similar lifestyles in the same geographical regions, the changes in microbial composition did not overcome inter-individual variation. In contrast, differences in microbial composition become much more pronounced when comparing geographically and culturally distant populations [1215]. Few studies have addressed urban-rural differences in the microbial and metabolic composition of individuals living within a similar geographic area who share similar ethnicity and diet. This is especially true of recently urbanizing environments. Here, we look at the early stages of how the microbial community evolves in response to recent urbanization.
China is an ideal place to analyze the complex interaction of microbiome, disease, and urbanization, as many areas within this country have only recently (in the past 20 years) started to undergo massive urbanization, and within a single region, one can still find a mix of traditional rural and more Westernized urban lifestyles [16]. This is particularly true in the predominantly Han region of Southern China, which has large variation in timing of major urbanization-related changes. In this study, we analyzed the microbiome and metabolome of 40 subjects from Hunan province, 20 recently urbanized subjects, and 20 rural subjects. By focusing on urban-rural differences in the microbiota and metabolites of a single province, we were able to capture early alterations in response to urbanization, as well as eliminate some of the confounding factors in previous studies, such as ethnicity, geography, and regional dietary patterns. Our results suggest the possibility of a loss of beneficial microbes associated with urbanization, with a concomitant increase in potentially dangerous genes, leading to a more Westernized microbiome.
Results
Urbanization is associated with a shift in microbial community composition towards commonly observed Western gut microbes
We compared 20 urban subjects from a city of 7 million to 20 rural subjects living in a small village in Hunan province. The urban sample had a higher disposable income and population but lower birth and population growth rate (Table 1). Furthermore, the urban subjects had higher body mass index (BMI), waist circumference, and insulin levels, consistent with studies showing an association between urbanization, obesity, and diabetes [17].
Table 1
Characteristics of the populations studied
Rural
Urban
Adjusted P value
Community characteristics
Population
26,563
7,000,000
Persons per square kilometer
668
13,150
Average disposable income
$800
$5600
Birth rate per 1000
11.7
8.7
Population growth rate per 1000
5.8
4.5
Subject characteristics
Total number subjects
20
20
Number (%) female
5 (25%)
13 (65%)
Mean (std) age range
50.6 (11.7)
58.9 (10.99)
Significant differences in metadata
Insulin (μU/mL)
4.31
9.84
0.0003
Waist circumference (cm)
73.78
85.03
0.0104
BMI (kg/m2)
21.09
24.45
0.0104
HbA1c (%)
5.65
6.63
0.0147
The mean of the community characteristics and metadata is shown. Only metadata variables significant after correction for multiple hypothesis testing are shown. See Additional file 6: Table S2H for all metadata variables tested
We used 16S ribosomal RNA (rRNA) sequencing of fecal samples to assess the gut microbial community of our subjects at two timepoints, separated by 2 weeks (Fig. 1, Additional file 1: Table S1). Similar to others [18], we found strong correlations between the samples taken at the two timepoints (Additional file 2: Figure S1). Using mixed linear models with urban/rural and time as fixed effects and subject id as a random effect, we found significant differences associated with urban vs. rural status in the first multidimensional scaling (MDS) axis at the operational taxonomic unit (OTU), genus, and family level (Fig. 1g). These differences became much less pronounced at the higher phylogenetic levels of phylum, class, and order. Our observation of increased separation at lower phylogenetic levels is supported by using a random forest classifier (Fig. 1h), which showed that when predicting urban vs. rural status, the area under the curve (AUC) increased with more refined taxonomic levels, with an AUC of over 70%, starting with the family level, suggesting that microbiome composition as measured by 16S rRNA sequencing can be used to differentiate urban and rural subjects at the family level or lower taxonomic levels. In addition, these findings are independent of method and could be reproduced using alternative tools for taxonomic assignment (Additional file 3: Figure S2) and classification (Additional file 4: Figure S3). Intriguingly, while the urban samples had more diversity at the higher taxonomic levels (Fig. 1 and Additional file 5: Figure S4), richness trended opposite to the diversity measures (Additional file 5: Figure S4B), suggesting that this difference is driven by differences in evenness. Taken together, our results suggest that there are significant differences between rural and urban samples that overcame inter-individual variation, but become much less pronounced at higher taxonomic levels.
Figure 1
Fig. 1
Differences in microbial composition between urban and rural Chinese subjects. a-f PCoA plot and comparison of Shannon diversity index for each taxonomic level, based on sequencing the 16S rRNA gene. Points are colored by urban/rural status and shaped by timepoint (each subject gave two samples, separated by 2 weeks). Key is in the top right. Numbers in parentheses on the PCoA axes indicate the percent variation explained by that axis. g P values comparing the position on the first PCoA axis of urban and rural samples. The gray region indicates significant P values (p < 0.05). h ROC curve using leave-one-out predictions of urban or rural status using a random forest classifier. The area under the curve (AUC) is indicated in the legend
Using our models, there was one phylum, one family, four genera, and 25 OTUs significantly different between rural and urban subjects after correcting for multiple hypothesis testing (Fig. 2a; Additional file 6: Table S2). To further characterize differences between the rural and urban samples, we used the consensus sequences generated by our de novo OTU pipeline as query sequences to search databases of 16S rRNA sequences. Using an unadjusted (uncorrected for false discovery rate) threshold of p < 0.05, we mapped the 80 consensus sequences representing OTUs with higher relative abundance in rural samples and the 91 OTUs with higher relative abundance in urban samples to the SILVA database, which contains ~ 1.7 million known 16S rRNA sequences [19] (Fig. 2b). For both rural and urban OTUs, the percent identity to a previously identified sequence was > 99% and there was no significant difference between the percent identities in the taxa higher in rural or urban samples (p > 0.05 by the unpaired Wilcoxon test). In contrast, taxa higher in urban samples were significantly (p < 0.001) better represented among the 2767 finished bacterial genomes that have been deposited at NCBI (National Center for Biotechnology Information) Genome (Fig. 2c). Thus, although we found little evidence of novel taxa, the genomes of taxa higher in urban subjects have been better characterized by whole genome sequencing projects.
Figure 2
Fig. 2
The urban Chinese microbiome is significantly more prevalent in an American cohort than the rural Chinese microbiome. a Heatmap showing the mean log normalized relative abundance from sequencing the 16S rRNA gene at timepoints 1 (T1) and 2 (T2) of taxa significantly different (adjusted p < 0.05) between urban and rural samples after correction for multiple hypothesis testing, based on our mixed linear models with urban/rural and time as fixed effects and subject id as a random effect. Within each taxonomic level, taxa are given from most to least significant between urban and rural samples. No taxa were significant at the class or order level. At the OTU level, the genus and consensus number is given. At all other levels, the name of the taxon is given. 8 taxa were tested at the phylum level, 16 at the class level, 22 at the order level, 40 at the family level, 86 at the genus level, and 703 at the OTU level. Full details for each taxon, including mean and standard deviation, P values and model R 2 are given in Additional file 6: Table S2A–F. b-e We used the consensus sequences from the 80 OTUs higher in rural samples and 91 OTUs higher in urban samples identified from our mixed linear models (unadjusted p < 0.05) as query sequences against different 16S rRNA databases. b OTUs higher in rural and urban communities are present in the SILVA database of full-length 16S rRNA sequences at similar levels of identity (p = 0.08 by unpaired Wilcoxon test). c OTUs higher in urban subjects are better represented in the NCBI collection of finished bacterial genomes than OTUs higher in rural subjects (p = 0.0008). d OTUs higher in rural and urban communities have previously been found in the Human Microbiome Project (HMP), a study of healthy American subjects, at similar levels of identity (p = 0.88), but (e) OTUs higher in urban subjects are seen in a greater proportion of HMP subjects compared to OTUs higher in rural subjects (p = 7.9 × 10−14). ***p < 0.001, ****p < 10−13
In order to compare our Chinese cohort to a Western cohort, we mapped taxa higher in rural or urban samples to their nearest taxa as represented by consensus sequences from the Human Microbiome Project (HMP), which analyzed the microbiomes of healthy subjects living in the United States [20]. Similar to our findings with the SILVA database, we found no significant difference between how well taxa higher in rural or urban samples could be mapped to the HMP taxa (Fig. 2d). However, there was a substantial difference (p < 10−13) between how prevalent the closest matching taxa within the HMP were (Fig. 2e). The nearest matching HMP taxa was present in an average of 30.1% of HMP subjects for taxa higher in rural samples, compared to 63.7% for taxa higher in urban samples. This suggests that urbanization in China is associated with an increase in microbes that are present in higher numbers of people in Western (urbanized) America. Furthermore, we found differences in prevalence at P values above our 0.05 threshold, suggesting that a larger study would have resulted in more OTUs significantly different between rural and urban than the 25 OTUs we reported (Additional file 7: Figure S5).
The metabolome is strongly correlated with urbanization
Metabolites are another sensitive marker of the host’s state [21]. In fact, previous studies have found that the metabolome changes more rapidly than the microbiome in response to host perturbations, such as diet change, suggesting that early response to host changes is transmitted through changes in microbial gene expression more than microbial composition [10, 22]. Due to our finding that the microbiome was stable across timepoints, we generated metabolite data corresponding to the first timepoint from our analysis of the microbiome. We found significant differences between urban and rural metabolite composition (Fig. 3a) that were independent of analysis method (Additional file 8: Figure S6), although there was no difference in the diversity of the metabolome. Furthermore, our machine learning classifier was even better at predicting urban/rural status from the metabolome than the microbiome (Fig. 3b). At an FDR-adjusted P value of p < 0.05, there were 16 metabolites significantly associated with urban vs. rural status (Fig. 3c; Additional file 6: Table S2G). Ten of the 16 significantly different metabolites were involved in lipid, carbohydrate, and energy metabolism—all key differences in Western (urban) versus traditional Chinese (rural) diets—and a smaller proportion related to peptides, nucleotides, and amino acids, with one xenobiotic (theophylline). Thus, the metabolome appears to respond to urbanization and Western diet even more robustly than the microbiome.
Figure 3
Fig. 3
Differences in metabolites between urban and rural Chinese subjects. a PCoA plot comparing metabolites between urban (red) and rural (blue) samples. Numbers in parentheses indicate the percent variation explained by that axis. The urban/rural P value was 0.02 for MDS1 and 1.5 × 10−7 for MDS2. b ROC curve using leave-one-out predictions of urban or rural status using a random forest classifier. The area under the curve (AUC) is indicated in the legend. c Heatmap showing the mean scaled abundance of metabolites statistically significantly different between urban and rural samples after correction for multiple hypothesis testing (adjusted p < 0.05). Metabolites are given from most to least significant. 334 different biochemicals were tested (see Additional file 6: Table S2G for more details, including mean and standard deviation, P values and model R 2)
In addition, we collected metadata on diet and other variables, such as anti- or probiotic use, anthropometric measures, arsenic exposure, and several biomarkers for cardiometabolic disease (Additional file 6: Table S2H). These data were also able to relatively accurately predict urban/rural status (Fig. 3b, Table 1), even though significant (adjusted P values <0.05) urban/rural differences were only seen in the diabetes and obesity measures. These measures were all higher in urban subjects, suggesting that the risk of diabetes and obesity has increased in our urban population. Of note, none of the diet variables (taken as an average over 3 days) was significantly different between the two groups.
Intriguingly, combining the microbiome data with the metadata or metabolite data decreased the ability of the classifier to distinguish between urban and rural populations, while combining the metadata and metabolite data gave an AUC of 92% (Fig. 3b), the highest out of all other combinations of the microbiome, metabolome, and metadata. Likewise, there were few associations between the microbiome and metadata or metabolome. For example, only five metadata variables were associated with any taxa: antibiotic use in the last 6 months (associated with 18 taxa), use of probiotic supplements (associated with three OTUs), insulin levels (associated with two OTUs), and gender and fat intake (each associated with one OTU; Additional file 9: Table S3). In contrast, there were 133 associations between the metadata and metabolome (Additional file 9: Table S3C). A few of these correlated variables measured the same value in different ways, such as glucose, which was measured both as an independent blood test in the metadata and as a metabolite in our metabolomics data (Additional file 10: Figure S7). This strong correlation in the variables measured in two independent ways validates our metabolomic methods. The majority of the statistically significant associations between the metabolites and the metadata, however, revealed intriguing novel associations between the metabolome and health. For example, among our 133 statistically significant associations, 106 (80%) fell into the amino acid, carbohydrate, lipid, and peptide superpathways. The eight metabolites associated with BMI, waist or weight were all in the peptide, amino acid, or carbohydrate superpathways. The 23 metabolites associated with glucose, HbA1c, and insulin largely fell in glucose metabolism pathways, while the 17 metabolites associated with cholesterol, triglycerides, and LDL largely fell in lipid metabolism pathways.
The relative abundance of Viruses and Archaea is decreased in urban subjects
While 16S rRNA sequencing can provide valuable insights into which bacteria are present in the microbiome, whole genome sequencing can provide a more complete taxonomic and functional representation of the microbial community. We therefore also performed whole metagenome sequencing of the samples from the first timepoint, generating 10 million reads per sample (Additional file 1: Table S1). These data confirmed the significant difference in microbial composition seen in the lower taxonomic levels by 16S rRNA sequencing (Fig. 4). However, with whole genome sequencing, we saw separation between urban and rural samples at all taxonomic levels, including domain. This increased separation at the higher taxonomic levels may be due to the additional taxa detected at each level with the more sensitive whole genome sequencing (Additional file 11: Table S4).
Figure 4
Fig. 4
Viruses and Archaea are less abundant in the urban Chinese microbiome while Bacteria are more abundant. a–g PCoA plot and comparison of Shannon diversity index for each taxonomic level, based on whole genome sequencing. Blue points indicate rural subjects while red points indicate urban subjects. Numbers in parentheses on the PCoA axes indicate the percent variation explained by that axis. h P values comparing the position on the first PCoA axis (solid line) or Shannon diversity (dashed line) of urban and rural subjects. The gray region indicates significant P values (p < 0.05). i Comparison of the logged relative abundance of each domain detected using whole genome sequencing. An asterisk (*) in i indicates a Benjamini-Hochberg-adjusted P value of less than 0.05
In addition, we found that at every taxonomic level urban subjects had decreased diversity, consistent with other studies showing loss of diversity with Westernization [12, 13]. This was also true for other diversity measures (Additional file 12: Figure S8), but is opposite what was seen for our 16S rRNA Shannon diversity measures, where urban subjects had higher diversity at the upper taxonomic levels, with no significant difference or lower diversity at the lower taxonomic levels (Fig. 1 and Additional file 5: Figure S4). However, richness from the 16S rRNA analysis was decreased in urban samples (Additional file 5: Figure S4B), similar to the whole genome sequencing results. Our data are consistent with the hypothesis that at higher phylogenetic levels changes in evenness in a few dominant taxa drive our observed differences in 16S diversity. These dominant taxa may be a result of 16S rRNA sequencing bias. In contrast, there appear to be fewer dominant taxa in the whole genome sequencing data, which detected many more taxa at each phylogenetic level compared to 16S rRNA sequencing (Additional file 11: Table S4), and provides a more consistent view of decreased diversity with urbanization across all phylogenetic levels, no matter which diversity measurement is used.
Using our linear models on the taxonomic data generated from our whole metagenome sequencing, we detected 60 species, 44 genera, 71 families, 35 orders, 21 classes, 9 phyla, and 3 domains significantly different between urban and rural subjects after correcting for multiple hypothesis testing (Additional file 13: Table S5A-G). Most of these taxa were more abundant in rural subjects, further supporting the hypothesis that urbanization is associated with a loss of potentially beneficial bacteria (Additional file 14: Figure S9). Interestingly, all three domains detected (Bacteria, Archaea, and Virus) were significantly different between urban and rural subjects (Fig. 4i), suggesting that urbanization results in an overall loss of Archaea and Viruses and a very small but significant increase in the relative abundance of Bacteria. Archaea are an understudied part of the microbiome, but are generally methanogens. They have been associated with leanness and archaebiotics have been proposed to modulate the risk of atherosclerosis [23, 24]. Likewise, the virome has not been as well characterized, and although many well-known viruses cause disease, some viruses can replace the beneficial functions of commensal bacteria [25, 26].
As with the 16S rRNA sequencing results, there were a number of intriguing associations between the relative abundance of taxa and metabolites (Additional file 15: Table S6A). For example, 10-undecenoate (11:1n1) was positively associated with the family Leuconostocaceae or other taxa belonging to this family in both 16S rRNA and whole genome sequencing. Leuconostocaceae are lactic acid bacteria previously shown to undergo niche-specific evolution [27] and are associated with ulcerative colitis [28], while 10-undecennoate (11:1n1) has been associated with colorectal cancer [29]. In contrast, there were only 16 associations between taxa and the metadata: most were associations with antibiotic use in the past 6 months; although the Archaea domain was associated with sodium intake, the Melisococcus genus and one of its species was associated with probiotic supplements, and one phage was associated with HDL (high density lipoprotein cholesterol; Additional file 15: Table S6B). Thus, urban/rural status is strongly associated with microbial composition as measured by whole-genome shotgun sequencing, confirming our observations from sequencing the 16S rRNA gene, including dysbiosis in the relative abundance of entire taxonomic domains.
Urban subjects have increased gene diversity, including increased antibiotic resistance
We also used our whole genome sequencing data to analyze the relative abundance of KEGG modules and pathways (Fig. 5). Again, we saw a significant separation between urban and rural samples, indicating that the gene content is changing with the altered microbial composition. Intriguingly, the urban samples had increased diversity compared to rural samples, opposite the results seen from the whole genome sequencing taxonomic results, which were generated from the same reads (Figs. 4 and 5, Additional file 12: Figure S8 and Additional file 16: Figure S10). Given this finding, for each OTU, we looked at the number of annotated genes contained in the closest finished NCBI bacterial genome (Fig. 2c). We found that the taxa higher in urban samples also contained more annotated genes than the taxa higher in rural samples (Additional file 17: Figure S11). Taken together, this suggests that urban subjects have lost diversity in terms of microbial composition, but the taxa that are present encode more KEGG functions.
Figure 5
Fig. 5
The microbiome of urban Chinese subjects encodes more genetic diversity, including more genes conferring antibiotic resistance, than rural Chinese subjects. a PCoA plot and comparison of Shannon diversity index for KEGG modules and b KEGG pathways. Blue points indicate rural subjects while red points indicate urban subjects. Numbers in parentheses on the PCoA axes indicate the percent variation explained by that axis. c P values comparing the position on the first PCoA axis (solid line) or Shannon diversity (dashed line) of urban and rural subjects. The gray region indicates significant P values (p < 0.05). d–e Comparison of the proportion of reads from whole genome sequencing that aligned to (d) the CARD protein homolog database [31] or e MvirDB [32]. The asterisk (*) in d indicates a P value of less than 0.05 comparing urban and rural subjects (p = 0.01), while two asterisks (**) in e indicates a P value of less than 0.01 (p = 0.006)
There were 10 modules and 51 pathways significantly different between urban and rural subjects, many of which were involved with metabolism, helping to confirm our metabolite findings (Additional file 13: Table S5H-I). For example, M00048 (inosine monophosphate biosynthesis) was one of the modules significantly more abundant in rural samples while the metabolite inosine was also significantly higher in rural samples. Likewise, ko00280 (valine, leucine, and isoleucine degradation) was significantly lower in rural samples, while the metabolite gamma-glutamylvaline, which is likely a short-lived intermediate from protein degradation on the way to specific amino acid degradation, was also significantly lower in rural subjects, suggesting a decrease in valine degradation [30]. While the majority of these KEGG functions were more abundant in rural samples, the proportion of significant functions higher in rural was not as pronounced as in the taxonomic results (Additional file 18: Figure S12). Twenty-three modules and 4 pathways were associated with our metadata, including many of the three-day dietary measures, while 139 modules and 9 pathways were associated with metabolite data, suggesting a stronger interaction between gene content, diet, and metabolites than what was seen with the taxonomic data (Additional file 15: Table S6C-D).
One set of genes of particular interest when comparing urban versus rural participants is the genes encoding antibiotic resistance. To analyze the presence of antibiotic resistance in the microbiome, we mapped all reads from our whole genome sequencing analysis to the comprehensive antibiotic resistance protein homolog database (CARD) [31]. Genes in this database are genes whose presence confers antibiotic resistance, such as β-lactamases. We found that significantly more reads from urban subjects mapped to the database than rural subjects (Fig. 5d), suggesting that urbanization is associated with increased antibiotic resistance, even though antibiotic use was not different between the two groups (no subject had taken antibiotics in the past 3 months and only three had taken antibiotics in the past 6 months, two of which were rural and the other urban). Of the three urban samples with the highest rates of antibiotic resistance genes, only one had taken antibiotics in the past 6 months. Furthermore, if we remove the three urban samples with the highest proportion of reads mapped to CARD, we still get a P value of 0.05, suggesting these results are not driven entirely by these three points. Taken together, our results may have important implications for the efficacy of antibiotics in treating infections in the urban population, as many antibiotic resistance genes are encoded on plasmids and easily move between bacterial strains. Thus, some of the increased gene content in urban subjects encodes genes that could potentially harm the host.
When we looked for associations between the proportion of reads that mapped to antibiotic resistance genes and our microbiome, metadata, and metabolite data, we found no significant associations between the metabolite data or metadata. In contrast, 80 KEGG modules and 135 KEGG pathways were significantly associated with the proportion of reads that mapped to antibiotic resistance genes (Additional file 19: Table S7). In considering the associations between the proportion of antibiotic resistant reads and taxonomy, we found that most of the significant associations with the proportion of reads that mapped to antibiotic resistance genes were with Escherichia and Shigella in both our 16S rRNA and whole genome sequencing data (Additional file 20: Figure S13; Additional file 19: Table S7A–B). Intriguingly, a significant association appeared in all OTUs or species classified as belonging to these genera, and in all higher taxonomic levels that these genera belong to. Many of these taxa were significantly higher in urban subjects in the 16S rRNA analysis and trended towards higher relative abundance in the whole genome sequencing data. Taken together, these data demonstrate associations between urbanization, an increased relative abundance of Escherichia and Shigella and an increased proportion of reads mapping to antibiotic resistance genes. Our data are therefore consistent with a hypothesis that during urbanization, these genera become more abundant, bringing with them genes that result in increased antibiotic resistance.
In order to further assess the presence of genes associated with virulence and pathogenicity, the whole genome sequencing reads were also aligned to MvirDB [32], a database that combines genes associated with virulence factors, toxins, and pathogen-host interactions. As with the CARD database, we found that a significantly higher proportion of reads aligned to MvirDB in urban subjects than rural subjects (Fig. 5e). This was true even after removing the three urban samples with the highest proportion of mapped reads. In addition, similar to the CARD findings, there was a strong association between the proportion of reads mapped to MvirDB and Escherichia and Shigella (Additional file 21: Table S8). Taken together, these data suggest a model in which urbanization results in a Westernization of the gut microbiome, resulting in loss of taxonomic diversity but increase in gene diversity, including loss of Viruses and Archaea but increased antibiotic resistance and virulence, suggesting a loss of microbes beneficial to the host with a gain in potentially deleterious genes, which may be caused by an increase in Escherichia and Shigella.
Discussion
We have found significant differences between rural and urban subjects in both microbiome community composition, as measured by both 16S rRNA sequencing and whole genome sequencing, and microbiome gene content. In particular, urbanization was associated with decreased microbial diversity, including a loss of Viruses and Archaea. This dysbiosis in non-bacterial domains is highlighted by the fact that differences between urban and rural subjects as measured by 16S rRNA sequencing, which can only capture Bacteria, did not propagate above the family level. This contrasts previous studies that found pronounced microbiome differences at all taxonomic levels, even using 16S rRNA sequencing. However, those studies compared samples from different continents, genetic backgrounds, and social practices [1215]. In fact, studies focusing on urban and rural differences within Asia found that the microbiome clusters strongly by ethnicity and geography and not by social and dietary lifestyles [33, 34]. Our focus on two neighboring Han communities enabled us to control for differences in ethnicity, geography, and regional dietary patterns and enabled us to find differences even in our recently urbanized populations.
We have done our best to control for diet, antibiotic use, and other potentially confounding factors by showing that our metadata is not significantly different between the two populations, but there always remains the chance that there is some additional variable that can contribute to urban-rural differences that a larger study will be able to identify. Our study made extensive utilization of linear models; however, our linear model P values are highly correlated with our nonparametric tests (Additional file 22: Supplemental Text; Additional file 23: Table S9), indicating that lack of normality is not what is driving our results. Given our small sample size of 20 subjects per group, we utilized FDR correction separately for each taxonomic level and did not pool hypotheses across our metabolite, 16S and whole-genome sequencing results for correction. This strategy is anticonservative and increases the chance that some of the associations we report with individual taxa, genes, and metabolites may be the results of overfitting. However, we also identified strong differences between urban and rural community compositions that do not require extensive correction for multiple hypotheses, such as analysis of PCoA axes and the results of machine learning algorithms. So while the results we report for individual taxa, metabolites, and genes will ultimately require validation in a larger cohort, we are confident that the overall differences we report between rural and urban populations are not simply a result of our multiple hypothesis correction strategy. Furthermore, a recent observation in mice found that changes in microbial composition in response to altered diet increase with each generation [35], so we predict that as we continue to sample these urbanizing populations over time, the microbial differences will become more pronounced. Thus, our study may represent an observation of the early steps towards a fully Westernized gut microbial composition in China.
Of particular interest is our finding of increased relative abundance of genes that confer antibiotic resistance in urban samples, despite the fact that in our study antibiotic use in the past 6 months was not significantly different between urban and rural subjects, and no study participant had used antibiotics in the last 3 months. Our results suggest that changes associated with urbanization may indirectly increase the reservoir of resistant genes and virulence factors via increased colonization by pathogenic Escherichia and Shigella. Virulence factors encoded by Escherichia have previously been associated with diseases such as colorectal cancer [36] and Crohn’s disease [28]. Thus, the complex interplay between disease, urbanization, and the microbiome is an important topic for future studies.
In terms of composition, taxa that were more abundant in rural samples were also much less prevalent in the American cohort studied in the HMP. A natural hypothesis is that these taxa—higher in rural China but of lower prevalence in America and poorly represented in finished genome sequencing projects—represent a beneficial set of microbes that are suppressed but not eliminated by urbanization. Our study therefore suggests the possibility that Westernization of the microbiome drives disease by increasing the prevalence of pathogens, such as Escherichia/Shigella, that harbor harmful characteristics, such as antibiotic resistance genes and virulence factors, and by reducing the relative abundance of beneficial taxa. Our compositional findings suggest that since these taxa are higher in our rural cohort and are not entirely absent in Western populations, changes in lifestyle could presumably allow them to again become more prevalent, potentially increasing host health. Likewise, our study suggests these taxa as potential targets of probiotics. For example, several Ruminococcus species were significantly more abundant in rural samples, and the most significant OTU from 16S rRNA sequencing also belonged to this genus. This genus has been associated with diet and the breakdown of resistant starch and also produces butyrate, which has previously been shown to play an important role in immune function [3739]. Establishing the validity of the hypothesis that the partial Westernization of the microbiome helps to drive disease will ultimately require long-term longitudinal surveys. Executing these studies is particularly vital as these rural populations begin to urbanize or migrate and disappear.
Conclusions
We compared the gut microbiome and plasma metabolome of rural and urban people from a single Chinese province and found significant differences in the composition of recently urbanized and rural subjects. These changes include an alteration in the relative abundances of entire domains, particularly loss of Archaea and Viruses with urbanization. Furthermore, our analysis of the composition of the microbiome suggests that the microbes that had a higher relative abundance in the urban Chinese samples also had a higher relative abundance in an American cohort. In addition, the genes encoded by the microbiome and the metabolites generated have significantly altered with urbanization, with an increase in overall genetic diversity as well as in genes associated with resistance and virulence. Our results suggest that urbanization is rapidly altering the gut microbial community, making it more similar to a Western composition, resulting in higher levels of antibiotic resistance and virulence genes. These changes are accompanied by an increase in biomarkers of diseases traditionally associated with Westernization, such as diabetes, obesity, and cancer. Taken together, our study suggests a hypothesis that urbanization/Westernization results in rapid convergent evolution across the globe of the microbial community to a dysbiotic state, with an increase in the prevalence of pathogens that harbor harmful genes and a concomitant reduction in the relative abundance of beneficial taxa.
Methods
A random sample of individuals from Hunan Province (in Southern China) aged 18–65 were selected for the study, with exclusion of individuals who lived in these communities for less than 2 years, were pregnant or lactating, had known cancer, worked in an occupation with potential exposure to arsenic, or had antibiotic use within the past 3 months. Metadata, fasting blood, spot urine, and fecal samples were collected by China CDC data collectors during a three-day house visit, with a repeat fecal collection 2 weeks later. Metabolites were assayed using Chromatography/Mass Spectrometry (Metabolon, Inc.). Sequencing was performed by the Beijing Genomics Institute-Shenzhen, using an Illumina MiSeq PE250 for 16S sequencing targeting the V4 hypervariable region (16S rRNA sequencing) or an Illumina HiSeq 4000 (whole metagenome sequencing). 16S rRNA sequencing reads were classified using the RDP (Ribosomal Database Project) classifier [40]. Kraken [41] was used to assign taxonomy to the whole genome sequencing reads while HUMAnN [42] was used to assign KEGG functions. In addition, whole genome sequencing reads were aligned to the Comprehensive Antibiotic Resistance Database (CARD) protein homolog database, version 1.0.4 [31] or to MvirDB [32] to assess the presence of antibiotic resistance and virulence factors. All sequences have been deposited in NCBI SRA (https://www.ncbi.nlm.nih.gov/sra) under BioProject PRJNA349463. Accession numbers are given in Additional file 1: Table S1. P values for urban-rural status were calculated using mixed linear models. Nonparametric models were used to confirm these results (Additional file 23: Table S9). See Additional file 22: Supplemental Text for more details.
Abbreviations
AUC:
Area under the curve
bp:
Base pair
CARD:
Comprehensive antibiotic resistance database
HMP:
Human Microbiome Project
MDS:
Multidimensional scaling
OTU:
Operational taxonomic unit
PCoA:
Principal coordinates analysis
ROC:
Receiver operating characteristic
Declarations
Acknowledgements
We thank the National Institute of Nutrition and Health, China Center for Disease Control and Prevention, who collected the data and the Hunan research participants. We also are thankful to general support from the Carolina Population Center, funded by NICHD R24 HD050924, at the University of North Carolina at Chapel Hill.
Funding
This project was supported by the National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK104371) and a Translational Team Science Award with funding provided by the UNC School of Public Health and the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health through Grant Award Number UL1TR001111. Our funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript.
Availability of data and materials
All sequences have been deposited in the NCBI SRA (National Center for Biotechnology Information Sequence Read Archive; https://www.ncbi.nlm.nih.gov/sra) under BioProject PRJNA349463. Accession numbers are given in Additional file 1: Table S1. In addition, the code and tables used to generate the figures and tables are available in the Additional file 24: Supplementary Zip File and at https://github.com/kwinglee/UrbanRuralChina.
Authors’ contributions
KW, AGH, AAF, and PGL contributed to the study design. JL and DJ collected the data. KW, WS, RZG, and AAF analyzed the data. KW wrote the manuscript. AGH, AAF, and PGL helped in writing and editing. All authors read and approved the final manuscript.
Ethics approval and consent to participate
The research was approved under UNC IRB Study #14-0639 for data collection and analysis of microbiome and phenotypic data and under Study #15-0381 for collection and analysis of metabolomic profiling data. Consent was obtained for all participants with consent forms translated by the China-Japan Friendship Hospital, Ministry of Health of China.
Consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
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Authors’ Affiliations
(1)
Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Charlotte, USA
(2)
Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, USA
(3)
Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Kannapolis, USA
(4)
Bioinformatics Services Division, Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Charlotte, USA
(5)
Department of Nutrition and Chronic Disease Prevention, Hunan Center for Disease Control and Prevention, Changsha, China
(6)
Department of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, USA
(7)
Department of Medicine, Division of Gastroenterology, University of Florida, CGRC, Gainesville, USA
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Copyright
© The Author(s). 2017
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Home » Products » Cancer Quality-ASSIST Supportive Oncology Quality Indicator Set: Feasibility, Reliability, and Validity Testing » Cancer Quality-ASSIST Supportive Oncology Quality Indicator Set: Feasibility, Reliability, and Validity Testing
Cancer Quality-ASSIST Supportive Oncology Quality Indicator Set: Feasibility, Reliability, and Validity Testing
Research Report Archived
Note: This report is greater than 5 years old. Findings may be used for research purposes but should not be considered current.
Author Affiliations
Sydney M. Dy, M.D., M.Sc.a
Karl A. Lorenz, M.D., M.H.S.b
Sean M. O’Neillc
Steven M. Asch, M.D., M.P.Hb
Anne M. Walling, M.D.d
Diana Tisnado, Ph.D.d
Anna Liza Antonioe
Jennifer L. Malin, M.D., Ph.D.b
aJohns Hopkins Bloomberg School of Public Health, Baltimore, MD.
bVA Greater Los Angeles Healthcare System, RAND Health, David Geffen School of Medicine at UCLA, Los Angeles, CA.
cRAND Pardee Graduate School, Santa Monica, CA.
dDivision of General Internal Medicine and Health Services Research, UCLA, Los Angeles, CA.
eUCLA School of Public Health, Los Angeles, CA.
Abstract
Purpose: Although measuring the quality of symptom management and end-of-life care could help provide a basis for improving supportive care for advanced cancer, few quality indicators in this area have been rigorously developed or evaluated.
Methods: We conducted a pilot evaluation of a comprehensive set of 92 supportive oncology quality indicators, Cancer Quality-ASSIST, including outpatient and hospital indicators for symptoms commonly related to cancer and its treatment and information and care planning. We operationalized the indicators and developed an electronic abstraction tool and extensive guidelines and training materials. Quality assurance nurses abstracted the medical record for 356 advanced cancer patients in two settings: a Veterans Administration hospital and an academic hospital and cancer center. We evaluated the indicators’ feasibility, interrater reliability, and validity.
Results: We successfully evaluated 78 indicators across the domains; results were similar in the two settings. We could not feasibly evaluate 3 indicators because of low prevalence; 22 indicators had significant interrater reliability issues, 9 had significant validity issues, and 3 had both reliability and validity issues, leaving a set of 41 indicators most promising for further testing and use in this population, with an overall kappa score of 0.85 for specified care.
Conclusion: Of 92 Cancer Quality-ASSIST quality indicators for symptoms, treatment toxicity, and information and care planning, 41 were sufficiently feasible, reliable and valid to be used for patients with advanced cancer in these settings. This set of indicators shows promise for describing key supportive care processes in advanced cancer.
Introduction
Nearly half of cancer expenditures occur during the final year of life, which is often marked by severe patient and family suffering.1 Recently developed quality indicators approved by national organizations and frequently used in research focus on variation in2 and overutilization of3 costly, high-intensity care that may reflect poor quality. In a systematic literature review, we found that few tools to measure underutilization of evidence-based supportive cancer care have been available, rigorously evaluated, or widely used.4 To accurately assess quality of care and provide tools for targeting and evaluating quality improvement, quality indicators are needed with good reliability and validity, variation among settings, and sensitivity to change.5,6
The Cancer Quality-ASSIST (Assessing Symptoms Side Effects and Indicators of Supportive Treatment) Project developed evidence-based quality indicators (QIs) to evaluate supportive cancer care from medical records. ASSIST addresses pain, dyspnea, depression, nausea and vomiting, diarrhea, fatigue, and information and care planning, including symptoms related to cancer, common complications, and treatment-related toxicities. ASSIST QIs were based on systematic literature reviews and developed using the RAND/UCLA (University of California, Los Angeles) modified Delphi process, with multidisciplinary input and representation from oncology, geriatrics, and internal medicine professional societies.7-11
The objective of this study was to characterize the feasibility, reliability and validity of the ASSIST quality indicators for advanced cancer care in two health care settings with different patient populations and data systems, the Veterans Administration Greater Los Angeles Health Care System and the Johns Hopkins Hospital and Sidney Kimmel Comprehensive Cancer Center. The goal was to determine a common robust quality indicator set for future comparative studies and quality monitoring efforts.
Methods
Study Sites
We report here on two separate but coordinated pilot efforts that tested the ASSIST indicators in diverse settings and patient populations. A pilot evaluation at the Johns Hopkins Hospital (JHH) and Sidney Kimmel Comprehensive Cancer Center (SKCCC) focused on end-of life care and addressed the ASSIST indicators relevant to symptoms, communication, and care planning in patients with advanced cancer. A concurrent pilot at the Veterans Affairs Greater Los Angeles Health Care System (VAGLAHS) was broader in focus, addressing all the ASSIST supportive oncology domains (including toxicity of chemotherapy and radiation therapy) in patients with advanced disease in an integrated delivery system. Each site’s IRB approved the respective study protocol.
The JHH is a large academic medical center; patients undergoing chemotherapy and radiation therapy receive integrated care at the SKCCC. VAGLAHS is an integrated inpatient and ambulatory medical center and regional referral center for veterans with cancer requiring specialized services (e.g. radiation therapy). At the time of the study, the JHH Department of Medicine had a palliative care program, the SKCCC had a cancer pain program, and VAGLAHS had a palliative care program. JHH/SKCCC had a combination of several paper and electronic health records, and VAGLAHS used the VA integrated electronic health record. JHH/SKCCC also had supplemental data sources, including a cancer registry, a cancer center information system, and hospital utilization data.
Study Sample
Study inclusion criteria differed somewhat between the sites, based on local populations and study goals. At VAGLAHS, we used the cancer registry to identify patients diagnosed in 2006 with one of the following tumor types and stage IV disease: breast, colorectal, esophagus/stomach, genitourinary, head and neck, liver/biliary, lung, pancreas, and prostate. Additional inclusion criteria included being alive 30 days post diagnosis and having at least one outpatient visit at VAGLAHS following diagnosis.
At JHH/SKCCC, the cancer registry identified patients with stage IV lung, pancreatic, breast, and colorectal cancer (and Stage IIIB for lung cancer) disease in 2003-2005 who died 2-15 months after diagnosis. Additionally, patients needed at least three outpatient visits at Johns Hopkins or at least two outpatient visits and a hospitalization of at 3-30 days in length after the diagnosis. Most patients had at least three visits and a hospitalization, and only 20 had only outpatient care.
Quality Indicators
The ASSIST indicators address supportive care, symptom management, and information and care planning needs of cancer patients, and were developed following a systematic literature synthesis.7-10 A panel of multidisciplinary international leaders from oncology, palliative care, geriatrics, primary care, nursing, and social work evaluated the initial indicator set for validity and feasibility using the RAND appropriateness method, resulting in a revised set of 92 indicators. Indicators use an "If-then" statement, which is represented as a ratio with "if" as the denominator and "then" as the numerator:
Quality Indicator = # patients who received the specified intervention
______________________________________
# patients for whom the intervention was indicated
The numerator describes the care that should be provided. The denominator identifies the patient population to whom the care should be provided. For an individual patient, the indicator could have a value of "pass" or "not pass"; for the population, the range of values is 0-1. For example, the ASSIST quality indicator "IF a cancer patient is receiving a long-acting opioid for cancer pain, THEN he or she should also be prescribed a short-acting opioid for breakthrough pain," is expressed as
The number of patients receiving a short and long-acting opioid
_______________________________________________
The number of cancer patients receiving a long-acting opioid
Data Sources
We developed a detailed medical record abstraction instrument to collect the data elements for scoring each indicator and detailed abstraction guidelines, which were customized to the abstraction process used at each site, including a Microsoft Access-based abstraction tool. To balance the need to abstract detailed information and the time and cost of abstraction, each site specified abstraction windows for the different indicator domains. At JHH/SKCCC, nurses abstracted data from up to 3 cancer-related outpatient visits, including the first 2 visits and last visit. At VAGLAHS, nurses abstracted data from up to 3 months of visits (mean 10, SD 7) for symptom management and up to 12 months for information and care planning. For the patients’ last cancer-related hospitalization, both sites abstracted the first 3 days of the hospitalization for symptom management, and the entire hospitalization for information and care planning. At JHH/SKCCC, after abstracting 148 medical records, we concluded that we had an adequate sample to evaluate the reliability and validity for inpatient symptoms since these indicators were relevant to all patients, and we stopped abstracting this inpatient symptom data only for the remainder of the patients.
At VAGLAHS, following a week-long training and one-week pilot, three experienced nurse abstractors abstracted the electronic medical record (EMR) from the VA Computerized Patient Record System (CPRS), from June – September 2008. At JHH/SKCCC, following similar training, a nurse project manager and three professional nurse abstractors from Delmarva, a Quality Improvement Organization (QIO), abstracted records from July – September 2008. We held regular meetings with abstractors at each site and weekly conference calls with investigators from both sites to ensure shared understanding of the guidelines, and developed a shared abstraction FAQ (Frequently Asked Questions).
Assessment of Feasibility, Reliability and Validity
We assessed feasibility in three ways: during tool development, qualitatively during abstraction, and, during analysis, by evaluating how many patients were eligible for indicators. While developing the tool and guidelines, we excluded indicators at each site irrelevant to the setting or population or infeasible to operationalize or abstract. We modified several indicators at one or both sites to improve feasibility of abstraction and/or analysis. Abstractors took notes on feasibility, including abstraction time and difficulties in finding information or reliably determining a data element, and impressions of abstraction. Finally, we excluded indicators for low prevalence if too few patients were eligible by the denominator n (<3% at VAGLAHS and n=5 at the JHH/SKCCC).
To assess inter-rater reliability (IRR), all nurses at each site abstracted a sample of records (5%, n=8 at VAGLAHS and 4%, n=9 at JHH/SKCCC). At VAGLAHS, we assessed validity by physician implicit review (JLM or KAL) of records of cases that failed quality indicators. At JHH/SKCCC, we assessed validity by comparing nurse abstraction to a physician investigator (SMD) gold standard abstraction for the 9 record IRR sample, and assessed quality control by comparing nurses’ assessments and nurse-physician agreement.
Analyses
We calculated observed agreement and the kappa statistic for indicator eligibility (denominator) and, conditional on eligibility, the care specified by the QI to evaluate IRR. Although no standard for minimum reliability of a quality indicator exists, high reliability is desirable if indicators are intended for accountability or quality improvement.12 We considered IRR to be inadequate when the kappa statistic was < 0.8 for eligibility (denominator) or < 0.6 for care specified by the QI (numerator).13 When possible, we modified initial indicator specifications to determine if reliability could be improved.
Results
Patient characteristics are shown in Table 1; age and ethnicity were relatively similar across the 2 sites, but VAGLAHS patients were almost all male, included more types of cancer, and only half were decedents. Of the total set of 92 Cancer Quality-ASSIST indicators, we excluded three because they were duplicative of other indicators, and 9 because either the data elements were not routinely in the medical record or we concluded that they would require excessive abstraction time. We also excluded 3 indicators not applicable to the sample or setting (e.g. care during stem cell transplant). One included indicator (for pain screening) was split into 2 indicators (inpatient and outpatient). We therefore attempted to abstract 78 and 47 of the 92 quality indicators in the VAGLAHS and JHH/SKCCC study samples, respectively (the JHH/SKCCC study did not include chemotherapy or radiation therapy indicators). The mean abstraction time at JHH/SKCCC was approximately 2.5 hours for patients with a hospitalization and at VAGLAHS was 2.3 hours. Of the successfully evaluated indicators, 22 had inadequate reliability (kappa <0.8 for eligibility or <0.6 for adherence), 9 inadequate validity, and 3 both inadequate reliability and validity in these settings (examples in Table 2). Finally, we excluded 3 indicators that did not meet prevalence criteria in at least one site (8 indicators at JHH/SKCCC did not meet prevalence criteria).
The 41 indicators that met our criteria for feasibility, reliability and validity include 10 of the 15 indicators for pain, 2/5 for depression and psychosocial distress, 7/15 for nausea and vomiting, 2/5 for anorexia and weight loss, 5/8 for fatigue and anemia, 2/3 for diarrhea, 6/8 for dyspnea, 1/5 for delirium, 1 for rash, and 5 for information and care planning (Table 3). Overall kappa was 0.87 for eligibility and 0.86 for specified care; we were also able to calculate individual kappa scores for 9 of the indicators, which ranged from 0.73 – 1.0.
Discussion
In this pilot study of the 92 medical-record based Cancer Quality-ASSIST supportive oncology quality indicators, following development and implementation of an abstraction tool, use of trained abstractors, and analysis of quantitative and qualitative abstraction results, including interrater reliability, 41 met strict criteria for feasibility, reliability and validity for advanced cancer across two clinical settings. These indicators represent all domains of the original ASSIST set except mucositis, insomnia, and fever/neutropenia.
Most quality indicators are adopted and published without rigorous development or evaluation despite evidence that these methods improve validity and risks and misallocation of resources from inappropriate implementation.1 Although several related medical record-based indicator sets addressing different domains or settings have been evaluated,14 including the PEACE Palliative Care Quality Measurement project for hospice and palliative care,15 ASCO (American Society for Clinical Oncology) QOPI (Quality Oncology Practice Initiative) for oncology outpatient care,16 and the VHA set for critical care,17 none has undergone this rigorous development and evaluation process. This study demonstrates the importance of evaluation, since only approximately half the ASSIST indicators, already rigorously developed through a systematic review and expert panel process, met criteria in these pilot tests.
Thirty-seven indicators did not meet our criteria for reliability (n=22), validity (n=9), both reliability and validity (n=3) or prevalence (n=3) in these settings. Most indicators did not meet criteria due to reliability issues. The subjective nature of symptoms and inconsistent documentation augment the challenge of obtaining clinical data manually from records. QIs assessing symptoms and communication are very different from those assessing discrete, concrete events like fecal occult blood testing followup by colonoscopy. For example, absence of symptom(s) was often documented with non-specific language, such as "Appears comfortable," limiting both reliability and validity. However, the indicators might perform differently in other settings. All of these criteria may be affected by documentation practices, practice patterns, site of care (e.g. inpatient vs. outpatient), as well as disease and patient characteristics (which may affect the prevalence of a condition). For example, obtaining records from prior sites of care such as nursing homes in order to assess whether an advance directive was appropriately communicated was not feasible with our settings or resources. However, a similar quality indicator was successfully implemented in a study of quality of care for vulnerable community-dwelling older patients, which obtained medical records from primary care and specialist providers, acute care hospitals, skilled-nursing facilities, and home health agencies.18
Different documentation practices can affect performance for indicators dependent on documentation. However, the Cancer-ASSIST indicator set includes only indicators where experts agreed that poor documentation by itself constituted poor quality of care, because lack of documentation could cause gaps in care processes or communication. For example, lack of documentation about care planning conversations may affect other providers’ ability to effectively address urgent end-of-life decisions. Nevertheless, we found that variation in documentation practices sometimes limited indicators’ reliability. For example, we could not reliably abstract newly-identified moderate to severe pain in ambulatory care in our settings. However, a recent study in patients dying in the hospital found that pain score documentation in inpatient standardized nursing notes was reliable for pain indicators.19 Electronic medical records (EMRs) hold promise for improving the feasibility of data collection for quality assessment, although much of the detailed clinical information in EMRs remains in free text fields which still require abstraction. Potential solutions include natural language processing, structured templates for documenting these issues, and obtaining symptom information directly from patients, potentially with automatic capture in a related database.
An ideal supportive care indicator system should include multiple approaches to quality assessment. Routine symptom screening and recording could improve capacity to evaluate outcomes. Some types of indicators difficult to operationalize in this study, such as symptom followup, may require additional collection of specific outcome data, similar to 48-hour pain followup in hospice.20 Carefully-evaluated available claims-based indicators can be helpful for regional quality evaluation or in databases (e.g., managed care) that cross clinical settings, although their focus is on aggressiveness of care.3 Issues such as communication and spiritual care are challenging to standardize in documentation, and indicators from the patient and family perspective may be needed for these domains and to evaluate the patient’s experience.21,22 Registry-based measures, such as in the CMS (Center for Medicare Services) PQRI (Physician Quality Reporting Initiative)23 or cancer registries, can be another method of measuring quality. These approaches vary in feasibility, cost of obtaining data, validity, usefulness at different points in the clinical trajectory, and how well they reflect current evidence. Advancing clinical evidence, changes in routine clinical data capture, and evaluation of efficient strategies that combine process-outcomes and different report perspectives (e.g, patient and family) will eventually define integrated quality assessment approaches.
This study has several limitations. Although the overall reliability of this indicator set is high, not all indicators were triggered frequently enough for full individual reliability or validity assessment. Further evaluation of these indicators requires better methods for identifying eligible patients (e.g., spinal cord compression), or these rarer quality issues may be better addressed using other methods, such as event reporting. The use of trained nurses experienced in abstraction may have increased reliability beyond what might be expected in community settings. Further refinement of the indicators, abstraction tool, and training guide, and focusing on the subset of indicators with acceptable reliability and validity, could potentially improve some indicators’ performance.
Documentation and the use of EMR use may also differ in other settings, which could either improve or limit these indicators’ performance depending upon the situation. These two urban academic centers shared many features, including relatively coordinated cancer care, a teaching environment and strong support services. However, there were also important differences, including their organizational structures (private vs. VA hospital), the patient populations they serve, and the presence of a strong hospital-wide palliative care program only at the VA at the time of the study, which may have affected the level of documentation. Despite these differences, reliability and validity results were similar across almost all indicators. Not all common malignancies were well-represented in this study (e.g., breast cancer), and further evaluation of these indicators in different cancer types is needed. Although the review times for this initial evaluation were lengthy, their purpose was to determine which indicators had the best potential for reliability and validity; abstraction with a smaller number of indicators would be less time-consuming.
In summary, this report presents the first evaluation of a comprehensive supportive oncology quality indicator set, developed for face validity with clinician experts through a rigorous process of systematic review and expert panel consensus, and evaluated for feasibility, reliability, and validity in two sites. This robust set of quality indicators can be used to evaluate the quality of supportive and end-of-life care for patients with advanced cancer and to identify areas for quality improvement efforts. Future research should evaluate which indicators are critical to efficient and effective quality measurement in these domains and have the greatest correlation with desired patient outcomes.
References
1. Lorenz KA. Promoting efficiency and quality in the Hummer health care system. J Clin Oncol 2007;26:5664-5665.
2. Wennberg JE, Fisher ES, Stukel TA, et al. Use of hospitals, physician visits, and hospice care during last six months of life among cohorts loyal to highly respected hospitals in the United States. BMJ 2004;328:607.
3. Earle CC, Landrum MB, Souza JM, et al. Aggressiveness of cancer care near the end of life: is it a quality-of-care issue? J Clin Oncol 2008;26:3860-3866.
4. Lorenz KA, Lynn J, Dy S, et al. Quality measures for symptoms and advance care planning in cancer: a systematic review. J Clin Oncol 2006;24:4933-4938.
5. McGlynn EA, Asch SM. Developing a clinical performance measure. Am J Prev Med 1988;4:14-21.
6. National Quality Forum. Measure Evaluation Criteria. Available at: http://www.qualityforum.org/docs/measure_evaluation_criteria.aspx.
7. Lorenz KA, Dy SM, Naiem A, et al. Quality Measures for Supportive Cancer Care: The Cancer Quality-ASSIST Project. J Pain Symptom Manage 2009;37(6):943-964.
8. Walling A, Lorenz KA, Dy SM, et al. Evidence-based recommendations for information and care planning in cancer care. J Clin Oncol 2008;26:3896-3902.
9. Dy SM, Asch SM, Naeim A, et al. Evidence-based recommendations for cancer pain management. J Clin Oncol 2008;26:3879-3885.
10. Dy SM, Asch SM, Naeim A, et al. Evidence-based recommendations for cancer fatigue, anorexia, depression, and dyspnea. J Clin Oncol 2008;26:3886-3895.
11. Naeim A, Dy SM, Lorenz KA, et al. Evidence-based recommendations for cancer nausea and vomiting. J Clin Oncol 2008;26:3903-3910.
12. Quality Measurement and Health Assessment Group (QMHAG), Center for Medicare and Medicaid Services. Measure evaluation criteria and subcriteria descriptions. Adopted from NQF Final Evaluation Criteria. Available at: http://www.hsag.com/mms.
13. Landis JR, Koch GG. The measurement of observer agreement for categorical data. Biometrics 1997;33:159-174.
14. Pasman HR, Brant HE, Deliens L, et al. Quality indicators for palliative care: A systematic review. J Pain Symptom Manage 2008;38(1):145-156.
15. The Carolinas Center for Medical Excellence. Palliative Care Quality Measures Project (PEACE). Available at: http://www.qualitynet.org/dcs/ContentServer?c=MQParents&pagename=Medqic%2FContent%2FParentShellTemplate&cid=1228695715754&parentName=Topic.
16. Jacobson JO, Neuss MN, McNiff KK, et al. Improvement in oncology practice performance through voluntary participation in the Quality Oncology Practice Initiative. J Clin Oncol 2008;26:1893-1898.
17. Nelson JE, Mulkerin CM, Adams LL, et al. Improving comfort and communication in the ICU: a practical new tool for palliative care performance measurement and feedback. Qual Saf Health Care 2006;15:264-271.
18. Wenger NS, Solomon DH, Roth CP, et al. The Quality of Medical Care Provided to Vulnerable Community-Dwelling Older Patients. Ann Intern Med 2003;139:740-747.
19. Walling AM, Asch SM, Lorenz K, et al. Quality of end of life care in the hospital. J Gen Intern Med 2009;23:153-154.
20. Connor SR, Tecca M, Lund Person J, et al. Measuring hospice care: The National Hospice and Palliative Care Organization National Hospice Data set. J Pain Symptom Manage 2004;28:316-328.
21. Teno JM, Clarridge B, Casey V, et al. Validation of Toolkit After-Death Bereaved Family Member Interview. J Pain Symptom Manage 2001;22:752-758.
22. Finlay E, Shreve S, Casarett D. Nationwide veterans affairs quality measure for cancer: the family assessment of treatment at end of life (FATE). J Clin Oncol 2008;26:3838-3844.
23. American Medical Association Physician Consortium for Performance Improvement. Consortium Measures. Available at: http://www.cms.hhs.gov/pqri.
Tables
Table 1. Patient characteristics
Johns Hopkins Veterans Affairs Greater Los Angeles
N N=238 N=118
Age, mean (SD) 60.5 (12.0) 65.9 (9.9)
Female 125 (52.5%) 2 (2%)
Race/Ethnicity Caucasian 155 (65%) 73 (62%)
African American 76 (32%) 36 (30%)
Other 7 (2%) 9 (8%)
Cancer Type Breast 6 (3%) 1 (1%)
Colorectal 28 (12%) 15 (13%)
Esophagus/stomach 10 (8%)
Genitourinary 8 (7%)
Head and neck 27 (23%)
Liver/biliary 4 (3%)
Lung 132 (55%) 27 (23%)
Pancreas 72 (30%) 6 (5%)
Prostate 20 (17%)
Died during study period 100% 55 (49%)
Table 2. Examples of quality indicators with significant issues with feasibility, reliability or validity in these settings
Indicator Issue
Measure not feasible IF a patient with head and neck cancer is undergoing radiation treatments THEN midline radiation blocks and three-dimensional radiation treatments should be used Use of blocks not documented in radiation oncology notes
IF a patient with advanced cancer has an advance directive/DNR and the patient receives care in a second venue, THEN the advance directive/DNR should be present in the medical record at the second venue or documentation should acknowledge its existence, its contents, and the reason that it is not in the medical record Challenging to obtain records from different settings
Measure not reliable IF a patient is diagnosed with cancer, THEN s/he should be screened for depression within 1 month following the diagnosis Inadequate reliability for specified care (numerator, kappa=-0.29); variability in documentation for mood assessment
IF a patient with cancer has new fatigue, THEN there should be an assessment within 1 month of the initial documentation of fatigue for either insomnia or depression No patients eligible with original specification. Alternate specification dropping "new": inadequate reliability for indicator eligibility (denominator, kappa=0.3); variability in documentation indicating absence of fatigue
IF a patient is newly known to have advanced cancer after a surgery, diagnostic test, or physical exam, THEN a discussion including prognosis and advance care planning should be documented within 1 month or a reason why such a discussion did not occur Inadequate reliability for specified care (numerator, kappa=0.56); challenging to identify content of discussions from documentation
Measure not valid IF a hospitalized patient has a change in his/her pain regimen to treat severe, sustained cancer pain THEN there should be an assessment of whether or not the change in treatment reduced the pain within 4 hours Challenging to identify severe sustained pain, time medication administered and time of pain assessment. Time of documentation may not reflect the time of assessment
IF a patient with advanced cancer has documentation of dyspnea despite treatment with non-opioid medications or underlying causes, THEN they should be offered opioids within one month or there should be documentation of contraindications to opioid therapy Requires experienced clinician to distinguish dyspnea refractory to treatment with non-opioid medications; elements necessary to identify eligible patients often not well documented
IF a cancer patient has a positive screening for pain THEN the provider should assess the likely etiology/ies of the pain Etiology of pain often indirectly addressed rather than directly linked to pain evaluation, especially when related to cancer
Table 3. Quality indicators that met criteria for feasibility, reliability, and validity in these settings
Indicator Criteria
Only one indicator met criteria at JHH/SKCCC but not at VAGLAHS: IF a patient with cancer over the age of 65 or with advanced disease is admitted to the hospital THEN cognitive status should be evaluated within 48 hours of admission (100% agreement).
Pain If a cancer patient has a cancer-related outpatient visit then there should be screening for the presence or absence and intensity of pain using a numeric pain score
IF a cancer patient is admitted to a hospital then there should be screening for the presence or absence of pain
If a patient with cancer pain is started on a long-acting opioid formulation, then a short-acting opioid formulation for breakthrough pain should also be provided
If a patient with cancer pain is started on chronic opioid treatment then he/she should be offered either a prescription or nonprescription bowel regimen within 24 hours or there should be documented contraindication to a bowel regimen
If a patient's outpatient cancer pain regimen is changed, then there should be an assessment of the effectiveness of treatment at or before the next outpatient visit with that provider or at another cancer-related outpatient visit
If a patient has advanced cancer and receives radiation treatment for painful bone metastases then he/she should be offered single-fraction radiation OR there should be documentation of a contraindication to single-fraction treatment
If a cancer patient has new neurologic symptoms or findings on physical examination consistent with spinal cord compression then he/she should be treated with steroids as soon as possible, but within 24 hours or a contraindication to steroids should be documented
If a cancer patient has new neurologic symptoms or findings on physical examination consistent with spinal cord compression then a whole-spine magnetic resonance imaging (MRI) scan or myelography should be performed as soon as possible, but within 24 hours OR there should be documentation of why an MRI scan was not appropriate
If a cancer patient has confirmation of spinal cord compression on radiologic examination, then radiotherapy or surgical decompression should be initiated within 24 hours or a contraindication for such therapy should be documented
If a cancer patient is treated for spinal cord compression then there should be follow-up of neurologic symptoms and signs within 1 week after treatment is completed
Depression and Psychosocial Distress If depression is diagnosed in a cancer patient, then a treatment plan for depression should be documented
If a patient with cancer is treated for depression, then response to therapy should be documented within 6 weeks
Nausea and Vomiting If a patient with cancer undergoing moderately or highly emetic chemotherapy or with advanced cancer affecting the gastrointestinal tract or abdomen is seen for a visit in a cancer-related outpatient setting, then the presence or absence of nausea or vomiting should be assessed at every visit
If a patient with advanced cancer affecting the gastrointestinal tract or abdomen is admitted to a hospital, then the presence or absence of nausea or vomiting should be assessed within 24 hours
If a patient with cancer is undergoing chemotherapy treatment with a high acute emetic risk, then a 3-drug regimen including single doses of a 5-HT3 receptor antagonist, dexamethasone, and selective neurokinin-1 receptor blocker should be given immediately prior to chemotherapy
If a patient with cancer is undergoing chemotherapy treatment with a moderate acute emetic risk, then a 2-drug regimen including a 5-HT3 receptor antagonist and dexamethasone should be given immediately prior to chemotherapy
If a patient with cancer reports nausea or vomiting on admission to the hospital, then within 24 hours potential underlying causes should be assessed
If an inpatient with cancer has nausea or vomiting, then within 24 hours of the initial report of nausea and vomiting, the patient should be offered a change in therapy
If an outpatient with cancer not receiving chemotherapy or radiation is treated for nausea or vomiting with an antiemetic medication, then the effectiveness of treatment should be evaluated before or on the next visit to the same outpatient site
Fatigue/Anemia If a cancer patient is seen for an initial visit or any visit while undergoing chemotherapy at a cancer-related outpatient site, then there should be an assessment of the presence or absence of fatigue
If a known cancer patient is newly diagnosed with advanced cancer, then there should be an assessment of the presence or absence of fatigue
If a patient with cancer is found to have anemia with a hemoglobin <10 g/dl, then the presence and severity of anemia-related symptoms (e.g. fatigue, dyspnea, and lightheadedness) should be evaluated
If a patient with cancer is found to have severe, symptomatic anemia (hemoglobin <8 g/dL),then transfusion with packed red cells should be offered to the patient within 24 hours
Anorexia/Weight loss If a patient presents for an initial visit for cancer affecting the oropharynx or gastrointestinal tract or advanced cancer at a cancer-related outpatient site, then there should be an assessment for the presence or absence of anorexia or dysphagia
If a cancer patient is treated with an appetite stimulant for anorexia, then there should be an assessment before or on the next visit to the same outpatient site of whether or not there was an improvement in anorexia
If a cancer patient is treated with enteral or parenteral nutrition, then there should be an assessment prior to starting nutrition that there was difficulty maintaining nutrition due to significant gastrointestinal issues and that expected life expectancy was at least one month
Dyspnea If a patient with cancer reports new or worsening dyspnea, then there should be documentation of cause or of investigation of at least one of the following: hypoxia, anemia, bronchospasm or chronic obstructive pulmonary disease, pleural effusion, tumor obstruction of bronchi or the trachea, pneumonia, or pulmonary embolism
If an outpatient with primary lung cancer or advanced cancer reports new or worsening dyspnea, then they should be offered symptomatic management or treatment directed at an underlying cause within one month
If an inpatient with primary lung cancer or advanced cancer has dyspnea on admission, then they should be offered symptomatic management or treatment directed at an underlying cause within 24 hours
If a patient with cancer in the hospital is treated for dyspnea, then there should be an assessment within 24 hours that the treatment was effective in relieving dyspnea OR that a change in treatment for dyspnea was made
If a cancer patient has dyspnea and a malignant pleural effusion, then they should be offered thoracentesis within 1 month of the initial diagnosis of the effusion, or other treatment (e.g., diuresis) should result in a reduction in the effusion or symptomatic dyspnea
If a cancer patient with a malignant pleural effusion undergoes thoracentesis, then there should be a repeat assessment of dyspnea within one week
Treatment-Associated Toxicities
Diarrhea If a patient with cancer is undergoing chemotherapy and has diarrhea then in order to classify the diarrhea as complicated or uncomplicated all of the following should be assessed: · history of onset and duration,· number of stools and stool composition, and· at least one of the associated symptoms[fever, dizziness, abdominal pain/cramping, nausea/vomiting, decreased performance status, sepsis, fever, bleeding, or dehydration]
If a patient with cancer is undergoing chemotherapy with a high risk (>10%) of chemotherapy-induced diarrhea then an antidiarrheal agent should be prescribed on or before treatment is initiated
Delirium IF a hospitalized patient with cancer over the age of 65 or with advanced cancer has delirium THEN there should be an assessment for the presence or absence of at least one of the following potential causes and their association with delirium: medication effects, central nervous system disease, infection, or metabolic processes
Skin Rash If a patient with cancer who is being treated with agents that block epidermal growth factor receptors (EGFR), then the presence and severity of skin rash should be evaluated within 1 month after starting the treatments and at each visit
Information and Care Planning If a patient with advanced cancer dies an expected death, then there should be documentation of an advance directive or a surrogate decision maker in the medical record
If a patient with advanced cancer dies an expected death, then s/he should have been referred for palliative care prior to death (hospital-based or community hospice) or there should be documentation why there was no referral
If a patient with advanced cancer is admitted to the ICU and survives 48 hours, then within 48 hours of ICU admission, the medical record should document the patient's preferences for care or attempt to identify them
If a patient with advanced cancer is mechanically ventilated in the ICU, then within 48 hours of admission to the ICU, the medical record should document the patient's preference for mechanical ventilation or why this information is unavailable
If a patient with cancer undergoes chemotherapy, then prior to chemotherapy, s/he should be informed about the risks and benefits of treatment, including likely symptoms and side effects, and whether the treatment intent is curative or palliative
Journal Publications
Dy SM, Lorenz KA, O'Neill SM, et al. Cancer Quality-ASSIST supportive oncology quality indicator set: feasibility, reliability, and validity testing. Cancer 2010;116:3267-75. | {
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2,360,808,739,267,617,300 | Skip to main content
Fruit, vegetable, and fruit juice consumption and risk of gestational diabetes mellitus: a systematic review and meta-analysis
List of all authors
Abstract
Background
Fruit, vegetable, and fruit juice intake is associated with the risk of gestational diabetes mellitus (GDM). However, the conclusion is limited and conflicted. The purpose of this systematic review and meta-analysis is to investigate the association between fruit, vegetable, and fruit juice consumption and the risk of GDM.
Methods
To find relevant studies, we searched PubMed, The Cochrane Library, Web of Science, Embase, ScienceDirect, PsycINFO, CINAHL, Ovid, EBSCO, CBM, CNKI, Wanfang Data, and VIP for the report on prospective cohort studies published from inception to April 8, 2022. Summary relative risks (RR) and 95% confidence intervals (Cis) were estimated using a random-effects model.
Results
A total of 12 studies with 32,794 participants were included in the meta-analysis. Total fruit consumption was associated with a lower risk of GDM (RR = 0.92, 95% CI = 0.86–0.99). Whereas an increasing the consumption of vegetable, including all vegetable (RR = 0.95, 95% CI = 0.87–1.03), starchy vegetable (RR = 1.01, 95% CI = 0.82–1.26), and fruit juice (RR = 0.97, 95% CI = 0.91–1.04) was not associated with a reduction in the risk of GDM. In a dose‒response analysis of eight studies, a 3% reduction in risk of GDM for a 100 g/d increase in fruit consumption (RR = 0.97, 95% CI = 0.96–0.99).
Conclusions
The findings suggest that higher fruit consumption may reduce the risk of GDM, with a 3% reduction in the risk of GDM for every 100 g/d increase in fruit intake. Higher-quality prospective studies or randomized clinical trials are required to validate the effect of different variations of fruits, vegetables, and fruit juice consumption on the risk of GDM.
Peer Review reports
Introduction
Gestational diabetes mellitus (GDM) is an endocrine disorder in which abnormal blood glucose first occurs or is detected during pregnancy [1]. The International Diabetes Federation (IDF) estimates that 16.7% of women aged 10–49 years currently have GDM [2]. GDM is also linked to an increased risk of both short and long-term adverse pregnancy outcomes, including large birth weight, baby-obstructed labour, and type 2 diabetes mellitus (T2DM) in both mother and offspring [3]. The increased prevalence and adverse outcomes of GDM have caused a serious societal, economic, and health burden on both the population and individuals.
There is growing interest in the function of dietary behaviour and patterns in the development of chronic diseases [4, 5]. Fruit and vegetable consumption have been linked with a reduced incidence of cardiovascular diseases, metabolic syndrome, and type 2 diabetes [6, 7]. Fruit juices have become part of the daily diet and this is another important form of fruit intake. Many people try to supplement their daily fruit intake by drinking fruit juice. Drinking fruit juice may be an easy and effective way to reach your goal of 5 servings of fruit per day [8]. In another study, pregnant women reported a preference for drinking homemade fruit juice, and they believed the juice had more nutrients, such as vitamins and minerals, compared to whole fruit [9].The intake of fruits, vegetables, and fruit juices could explain some of the beneficial effects of the individual components and nutrients in the daily diet [10, 11]. Fruits and vegetables have anti-inflammatory properties and are rich in antioxidants, dietary fibre, and healthful phytochemicals [12, 13]. These compounds could improve insulin sensitivity by reducing pancreatic β cell apoptosis, muscular inflammation, and oxidative stress [14, 15].
The World Health Organization (WHO) suggests that consuming more than 400 g of different fruits and vegetables per day may reduce the incidence of diabetes [16]. Consumption of different types and amounts of fruits and vegetables could provide different levels of diabetes protection [17]. Evidence indicates that the Mediterranean diet (i.e.,vegetables and fruit-rich foods) could significantly reduce the development of GDM [18, 19]. Compared with a red-meat diet, vegetable and fruit-rich dietary patterns were linked to a reduced occurrence of impaired fasting glucose [20]. Consumption of fruit or green leafy vegetables is related to reduced risk of GDM [21, 22]. However, when compared to other cruciferous vegetables, legumes, or whole-grain foods, higher levels of potato consumption before pregnancy were found to be associated with a higher risk of GDM [23]. There is only one systematic review that indicated that fruit intake before pregnancy is associated with the risk of GDM, but this review did not assess the effects of vegetable or fruit juices on the incidence of GDM [24]. Therefore, based on the inconsistency among studies and to solve the limitations of the current review, we conducted a systematic review and meta-analysis to assess the effect of fruit, vegetable, and fruit juice intake on the risk of GDM and to assist in the exploration of dietary intervention strategies.
Methods
Search strategy
We conducted and reported this systematic review according to the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) 2020 statement (see online supplementary materials, Table S1). A comprehensive literature search was conducted in the following databases: PubMed, The Cochrane Library, Web of Science, Embase, Scopus, Ovid, EBSCO, Wanfang Data, CNKI, and VIP. There were no specified language restrictions. The database search was conducted from the database inception dates to April 8, 2022. During the retrieval process, MeSH terms were used as follows: “pregnancy or pregnant* or gestation*” and “vegetables or vegetable or fruits or fruit or vegetable juices or juice, vegetable or juices, vegetable or vegetable juice or fruit juices or juices, fruit”, and “diabetes, gestational or diabetes, pregnancy-induced or diabetes, pregnancy-induced or pregnancy-induced diabetes or gestational diabetes or diabetes mellitus, gestational or gestational diabetes mellitus” (see online supplementary materials, Table S2). References of original publications as well as previous meta-analyses or reviews were also manually reviewed.
Study selection and inclusion and exclusion criteria
Duplicate articles were removed in EndNoteX9. Two reviewers (Liao and Zheng) screened titles and abstracts to determine eligibility. Disagreements were adjudicated by a third reviewer (Jiang). Based on the title and abstract screening, the full-text articles of all the eligible studies were reviewed by Liao and Zheng.
Inclusion and exclusion criteria
The criteria of the included and excluded studies were guided by the PECOs. The following criteria were used to determine which studies to include in the meta-analysis. (1) Participants: eligibility criteria were restricted to pregnant adult women (18 years old and above); (2) Exposures: the intake of fruit, vegetables, and fruit juice was the exposure; (3) Outcomes: the GDM criteria included the following two methods: incident cases defined by self-reported clinical diagnosis of GDM or by meeting the criteria of either a fasting blood glucose concentration of 92 mg/dL, a 1-hour blood glucose concentration of 180 mg/dL, or a 2-hour blood glucose concentration of 153 mg/dL after a glucose tolerance test. (4) Study design: cohort studies. Studies that do not report relative risk and 95% confidence intervals for the relationship between fruit, vegetable, or/and fruit juice consumption and GDM risk were excluded.
Data extraction
The researchers extracted authors, year of publication, country/location, follow-up period, number of participants, number of GDM cases, age, pre-BMI, exposure (fruit/all vegetables/ starchy vegetable/fruit juice), assessment of GDM, exposure assessment, quality assessment score, and adjustments. The information was extracted by Liao and Zheng and any disagreements were solved through discussion with Jiang. When studies reported multivariate models, we included the highest exposure of the adjusted variables in the risk estimates.
Quality assessment
Evaluation of cohort studies was performed using the Newcastle‒Ottawa Scale (NOS) [25]. There are three categories and a maximum of nine points: (1) selection of populations; (2) comparability of the two groups; and (3) assessment of outcome. Studies with different points were divided into high quality (7–9 points), moderate quality (5–6 points), and poor quality (0–4 points). The quality of each study was assessed by Liao and Zheng, and any inconsistencies were discussed with Jiang. Studies was not excluded from the meta-analysis based on quality assessment scores.
Statistical analysis
STATA software version 16 was used for statistical analyses. For the meta-analysis, we used the study-specific relative risk (RR) and 95% confidence interval (Cis) for the highest versus lowest category of fruit, vegetables, and fruit juice intake with a random-effects model analysis. Statistical significance was defined as a two-tailed P value less than 0.05. The I2 (P < 0.1) and Q statistics were used to assess heterogeneity between studies. I2 values of 25%, 50%, and 75% represent low, moderate, and high heterogeneity, respectively. To investigate sources of heterogeneity, we conducted subgroup analyses by the period of dietary assessment (prepregnancy/first trimester/second trimester), location (Asia/Non-Asia), total number of participants (≥ 2000/<2000), number of GDM (≥ 500/<500), pre-BMI (< 25/≥25 kg/m2), parity-adjusted (yes/no), family history of diabetes-adjusted (yes/no), physical activity-adjusted (yes/no), smoking-adjusted (yes/no), alcohol-adjusted (yes/no). We assessed the stability of the study results by the trim and fill method in a sensitivity analysis or by excluding studies at a high risk of bias. Begg’s test and Egger’s test or funnel plot asymmetry were used to examine publication bias.
In the dose‒response analysis, we used generalized least squares to calculate study-specific slopes and 95% confidence intervals [26]. Statistical significance was defined as a P value of 0.05. For each category, the mean or median fruit, vegetable, and fruit juice intake were assigned to the appropriate RR for the individual study. We used the midpoint between the highest and lowest bounds in each category when the data on average consumption were not available. In an open category, if only the value of the highest category or the lowest category is known, we assume that the lowest bound is zero and the highest category bound is 1.5 times the lowest category [27, 28]. When the study used the number of servings to express the intake of vegetables and fruits, we normalized it to one serving equal to106 grams [29].
Fig. 1
figure 1
PRISMA flow chart of study selection
Fig. 2
figure 2
Forest plot of fruit, vegetable, fruit juice intake, and risk of GDM.
Table 1 Characteristics of the included studies
Table 2 Meta-analysis of intake of fruit, vegetables, and fruit juice and risk of GDM
Table 3 Subgroup analyses for the association between vegetable, fruit, and fruit juice consumption and the risk of GDM
Fig. 3
figure 3
Dose-response analyses of fruit intake and risk of GDM.
Results
Study characteristics
The study selection process is shown in Fig. 1. In total, 701 articles were retrieved from 10 database searches. The eligibility of 320 articles was determined after removing duplicate publications. There were 51 studies eligible for full-text review, and 12 studies met the inclusion criteria. The study characteristics are summarized in Table 1. The studies were all cohort studies. The 12 studies were published between 2012 and 2021 and were conducted in eight countries, one was conducted in America [30], one in Australia [31], five in China [9, 32,33,34,35], one in Canada [36], two in Iran [37, 38], one in Iceland [39], and one in Malaysia [40]. Recruiting or follow-up periods ranged from one to 12 years. Two of these studies were from large cohort studies with longer recruitment times, resulting in the longer overall follow-up of the studies, and their study data results are only a portion of the large cohort studies [30, 36]. The period of dietary investigation for all the studies included three periods, four studies before pregnancy [30, 31, 37, 38], three studies in the first trimester [34,35,36], and five studies in the second trimester [9, 32, 33, 39, 40]. Eight studies provided information on fruit intake [9, 30,31,32,33, 35, 36, 38]. A total of seven studies reported on vegetable intake, of which four reported on all vegetables (including starchy vegetables and other vegetables) [31, 36, 38, 39], and three only reported on starchy vegetables [9, 34, 37]. Four studies reported on fruit juice intake [9, 30, 31, 40]. For the quality assessment, nine studies had a score of 6, indicating moderate quality [9, 30, 32,33,34,35, 37,38,39], and three studies had a score of 7, indicating high quality [31, 36, 40].
Fruit consumption and risk of GDM
A total of eight studies involving 2,809 GDM outcomes and 28,604 participants reported an association between fruit consumption and GDM [9, 30,31,32,33, 35, 36, 38]. Summarizing all eight comparisons with a random effects model, fruit intake was inversely associated with the risk of GDM (RR = 0.92; 95% CI: 0.86–0.99). Participants in the highest intake quartile had an 8% lower risk of developing GDM than those in the lowest intake quartile. There was low heterogeneity among studies (P = 0.14, I2 = 36.0%) (Fig. 2; Table 2). Fruit intake increased by 100 g per day was linked to a 3% lower risk of GDM in a dose‒response meta-analysis (RR = 0.97, 95% CI: 0.96–0.99) (Fig. 3).
Vegetable consumption and risk of GDM
A total of seven studies involving 2,132 GDM outcomes and 13,212 participants reported a link between vegetable consumption and GDM risk [9, 31, 34, 36,37,38,39]. The results indicated that there was no relationship between the intake of various types of vegetables and the risk of developing GDM. Four of these studies investigated the intake of all vegetables (including starchy vegetables and other vegetables) (RR = 0.95; 95% CI: 0.87–1.03) [31, 36, 38, 39] and three studies determined the intake of starchy vegetables (RR = 1.01; 95% CI: 0.82–1.26) [9, 34, 37] (Fig. 2; Table 2). Studies showed significant heterogeneity (all vegetables: P = 0.23, I2 = 61.3%; starchy vegetables: P = 0.90, I2 = 63.7%) (Fig. 2; Table 2). No correlation between the incidence of GDM and a 100 g/day increase in all vegetable intake (RR = 1.00, 95% CI: 0.99-1.00) and starchy vegetable intake (RR = 0.97, 95% CI: 0.93–1.01) was detected in dose‒response study (see online supplementary materials, Figure S1, S2).
Fruit juice consumption and risk of GDM
In four studies, 1,598 people with GDM outcomes and 23,177 participants showed an association between fruit juice intake and the risk of GDM [9, 30, 31, 40]. No relationship was identified between fruit juice intake and the risk of developing GDM (RR = 0.97; 95% CI: 0.91–1.04). Low heterogeneity was detected among studies (P = 0.23, I2 = 29.8%) (Fig. 2; Table 2). There was no linear relationship between each 100 ml/day increase in fruit juice consumption and the risk of GDM based on a dose‒response analysis (RR = 1.01, 95% CI: 0.97–1.08; see online supplementary materials, Figure S3).
Subgroup analysis and sensitivity analysis
Table 3 summarizes the results of the subgroup analysis according to several research characteristics. Subgroup analyses according to country/location (Asia/non-Asia) and parity-adjusted (yes/no) reduced the heterogeneity of the association between the consumption of fruit and GDM. We also assessed the period of dietary assessment (prepregnancy/first trimester/second trimester), the total number of participants (≥ 2000/<2000), the number of GDM patients (≥ 500/<500), pre-BMI (< 25/≥25 kg/m2), and adjustment factors such as parity (yes/no), family history of diabetes-adjusted (yes/no), physical activity (yes/no), smoking status (yes/no), and alcohol consumption (yes/no). Although statistically nonsignificant, some of the subgroups changed the effect size dramatically, such as the period of dietary assessment (prepregnancy), pre-BMI (≥ 25 kg/m2), and parity-adjusted (yes). As a result of the sensitivity analysis, the summary RRs for fruit, vegetable, and juice intake and GDM are as follows. Fruit intake: ranged from 0.92 (95% CI: 0.86–0.99) to 0.92 (95% CI: 0.85–0.98); all vegetable intake: ranged from 0.96 (95% CI: 0.90–1.03) to 0.98 (95% CI: 0.90–1.06); starchy vegetable intake: ranged from 0.78 (95% CI: 0.32–1.90) to 1.04 (95% CI: 0.97–1.13); fruit juice intake ranged from 0.97 (95% CI: 0.91–1.04) to 0.96 (95% CI: 0.90–1.03). Associations did not change considerably from the summary results (see online supplementary materials, Figure S4-S6).
Publication bias
Based on the funnel plot, Begg’s tests (see online supplementary materials, Figure S6-S8), and Egger tests, no significant publication bias was found (fruit: PBegg= 0.216 and PEgger=0.191; all vegetable: PBegg=0.174 and PEgger=0.060; starchy vegetable: PBegg=0.602 and PEgger=0.622; fruit juice: PBegg=0.497 and PEgger=0.874) (Table 2).
Discussion
The risk of GDM was inversely related to fruit consumption in this meta-analysis of 12 cohort studies, but no association was found between vegetables, fruit juices, and GDM. Moreover, a dose‒response analysis found that every 100 g of fruit per day reduced the risk of GDM by 3%. These findings offer support for the positive effects of moderate fruit intake on human health.
Studies have shown that fruit can reduce diabetes risk [41]. In regard to the relationship between diabetes and fruit consumption, there may be variations between different types of fruit. Rine et al. found that total fruit (apples, pears, blueberries, and grapes) and fruit combined with vegetables were related to a reduced risk of T2DM [42]. However, Wu-Qing Huang et al. found excessive intake (419 g/d) of tropical and citrus fruits, and fruits with a moderate or high glycaemic index (GI) increased the risk of GDM. The recommended intake of fruit during pregnancy is 200–400 g in China [32]. Studies have shown that most people currently fall short of the recommended daily intake of fruit [43, 44]. The average intake of fruit in this review was 220 g per day, which met the recommended intake. Thus, different fruit intakes could explain the inconsistent results of these studies. There are polyphenols, and antioxidant compounds in fruit, such as carotenoids and vitamins C and E. These compounds alleviate oxidative stress in cells that interfere with glucose uptake and prevent the development of abnormal glucose tolerance [45]. The fibre in fruits and vegetables can delay the absorption of carbohydrates from food and prevent a rapid rise in blood sugar [46]. The high fructose content of fruits is associated with impaired function of pancreatic β-cells and decreased insulin sensitivity [47,48,49]. The beneficial effects of fruits are determined not only by the effectiveness of specific micronutrients, but also by the combined action of many plant compounds. The high fructose content of fruits can be counteracted by the beneficial effects of fibre and other antioxidants [32]. Therefore, future studies can investigate the relationship between fruit intake and GDM risk through different types of fruit with different glycaemic indexs.
We found that vegetable intake and fruit juice were not significantly linked to the risk of GDM in this meta-analysis. Studies have reported that a diet pattern rich in vegetables and soy products can reduce the risk of GDM. For every one-quarter increase in vegetable pattern score, the risk of GDM was reduced by 3% [50]. Increased vegetable consumption may increase dietary fibre consumption and reduce fat intake, and is associated with a reduced risk of GDM [50, 51]. In this study, no association was found between the consumption of all vegetables (including starchy vegetables and other vegetables) or starchy vegetables and the risk of developing GDM. However, the study by Li et al. suggested that the total prepregnancy consumption of starchy vegetables, such as potatoes, was positively related to the risk of developing GDM [34]. Potatoes and other starchy vegetables are good quality carbohydrates and can be used as a substitute for a staple food [52]. The excessive intake of starchy vegetables can lead to a rapid rise in blood glucose after meals, which can damage pancreatic β-cells and increase the risk of GDM in the long term [53, 54]. Studies have shown that the risk of GDM increased by 8% for each additional serving of baked and boiled potatoes and French fries consumed [23]. The nutrients and biological effects of different types and cooking methods of vegetables play different roles in regulating blood glucose and insulin concentrations [55]. There is still a need for more research to assess the association with the risk of GDM based on the intake of some specific vegetables such as starchy and non-starchy vegetables, and leafy vegetables and legumes.
The fibre in the fruit juice is decreased and the sugar content are increased due to the commercial manufacturing process [56]. The study by Imamura et al. found that the consumption of artificially made sweet drinks and fruit juices was positively associated with the development of diabetes. [57]. Compared to pure fruit juice, fruit juice with added sugar increases the incidence of T2DM [58]. In addition, dietary guidelines in the United States indicate that consuming 75–224 ml of juice per day does not increase the risk of T2DM, cardiovascular and other diseases. In contrast, some short-term studies have found regular consumption of juice to be beneficial for cardiovascular health and blood pressure control [59]. Excess sugar in sweetened fruit juices can add to the body’s burden of regulating blood sugar, leading to a glycaemic load. The inconsistencies and bias between studies may be because most studies did not differentiate between pure fruit juice and sugar-sweetened juice [8]. In addition, compared to eating whole fruit, fruit juices can lead to overconsumption of fruit due to the lack of crude fibre, which has a satiating effect [60].
These results need to be interpreted with caution due to the lack of analysis of different types of fruits, vegetables, and juices. In the future, the relationship between fruits, vegetables, and juices needs to be further investigated by different subtypes.
Strengths and limitations
To interpret the findings appropriately, it is important to acknowledge this study’s limitations. Owing to a limited number of included studies and low reported intakes of certain fruits, vegetables, and fruit juices, this study did not carry out a specific analysis of the impact of specific fruits, vegetables, and fruit juices on the risk of GDM. Furthermore, the description of the cooking method and fruit juice and whether sugar was added not specified. Although subgroup analyses were performed to adjust for confounding factors that may influence the occurrence of GDM, residual confounding factors such as the history of endocrine disease and mode of conception may still be present. The majority of studies used a food frequency scale (FFQ) and dietary records to estimate dietary intake. Dietary assessments based on FFQ may have recall bias and do not provide a detailed record of daily changes in food intake. The FFQ can reflect food intake over time. The dietary record provides a more objective picture of eating habits and detailed food preparation methods, mitigating interindividual differences but requiring a more detailed record and a higher level of compliance [61, 62]. Indeed, some health-related outcomes with GDM were poorly covered, and owing notably to rough estimates of the degree of fruit and vegetable processing, many associations were not reviewed systematically.
Conclusion
Based on the results of this meta-analysis, fruit consumption appears to be associated with a reduced risk of GDM, whereas vegetable and fruit juice consumption was not associated with the incidence of GDM. According to the results of dose response analyses, increasing fruit consumption by 100 g per day reduced the risk of GDM by 3%. This suggests that people can reduce their risk of GDM by consuming moderate amounts of fresh fruit every day. Therefore, more high-quality, large-sample studies are needed to further investigate the relationship between different varieties of fruits, vegetables, and juices and the risk of GDM.
Data Availability
Not applicable.
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Acknowledgements
We give our thanks for the support from all the authors. All authors reviewed the manuscript and approved the final manuscript.
Funding
This work was supported by Joint funds project for science and technology innovation in Fujian (2020Y9133) and Hospital Fund from Fujian Maternity and Child Health Hospital (YCXH22-20).
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Yan-Ping Liao: study design and conduct, data collection and analysis, manuscript drafting and manuscript revision.Qing-Xiang Zheng: study design, data interpretation and manuscript revision.Xiu-Min Jiang: study design, data interpretation, and manuscript revision.Xiao-Qian Chen: data collection and manuscript revision.Xiao-Xia Gao: data collection.Yu-Qing Pan: data collection.
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Correspondence to Xiu-Min Jiang.
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Liao, YP., Zheng, QX., Jiang, XM. et al. Fruit, vegetable, and fruit juice consumption and risk of gestational diabetes mellitus: a systematic review and meta-analysis. Nutr J 22, 27 (2023). https://doi.org/10.1186/s12937-023-00855-8
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85,507,364,648,260,700 | As the situation around the 2019 Novel Coronavirus (COVID-19) continues to develop, our paramount concern has been for the health and safety of our clients and associates for this reason we will temporarily adjust our clinic hours, now closing at 6 pm during the week to allow for nightly deep cleaning of our facilities. As news continues to develop rapidly, we’re sharing the latest on the virus and how Heritage Urgent & Primary Care, the NC Dept. of Health and the CDC are responding.
As the situation around the 2019 Novel Coronavirus (COVID-19) continues to evolve, the health and safety of our clients and associates remains our number one priority, for this reason we are following all CDC and NC Department of Health recommendations regarding masks, handwashing, social distancing, and office sanitizing.
What Happens if Stitches are not removed?
Sutures or stitches, are sterile surgical threads which are used to repair accidental cuts or surgical incisions. In some cases, metal staples may be used rather than sutures.
Sutures are used to close both superficial surface wounds and deeper wounds. In order to close a deep wound, the doctor may need to sew it closed in multiple layers, meaning some of the sutures will be placed below the surface of the skin.
There are two different types of sutures which can be used, including absorbable and non-absorbable.
Absorbable stitches do not require removal as the body naturally absorbs them within about 60 days. This type of sutures can be used for layers of skin and tissue which heals quickly. This type of suture is created from materials which gradually dissolves inside the body. Because these sutures are made with multiple fibers, they are exceptionally strong during the first few days of healing and are less likely to break. After two weeks of healing, however, they will lose most of their strength. Absorbable sutures are an ideal solution for repairing muscles, as muscles need strong sutures in the initial stages of healing, but heal relatively fast.
In comparison, non-absorbable sutures are ideal for visible skin wounds as they often result in less scarring. When non-absorbable sutures are used, they are removed after the wound has had a chance to heal. In most cases, it takes about a week for the tissues to connect and form a bridge between the two edges of the wound. Once the tissue has adequately healed, the stitches can be removed. The wound will continue to heal once the stitches are removed. When the stitches remain in the skin for too long, it can result in additional scarring.
Non-absorbable sutures can also be used for internal wounds which need to heal for an extended amount of time. Depending on the material used for the sutures, non-absorbable sutures may be permanent or slowly deteriorate. These sutures maintain their strength for 300 days or more. They can be created from natural fibers or synthetic materials such as nylon, polypropylene, polyethylene or polyester. At the completion of a surgery, these long-lasting sutures hold fibrous internal tissues together. This is important as these tissues do not have a large amount of blood flow and a long time to heal. Non-absorbable sutures which are used in deep tissues, will remain in place indefinitely.
Prior to suturing a cut, the doctor will need to know the following information:
1. The cause of the cut. It is important for the doctor to know if the cut was from a piece of glass, wood or metal which may have broken off inside in the wound or if the wound could be contaminated.
2. When the cut occurred. The risk of infection can increase if the patient waits a few hours prior to seeking medical attention.
3. If there are any allergies to anesthetics or antibiotics
4. Any current medications, including prescription and nonprescription drugs which can impact bleeding and the healing process.
5. When you last received a tetanus shot
The above information will aid the doctor in determining if sutures are a good solution for closing the wound. In some cases, the wound may be contaminated and should not be closed with sutures as infection may be prevented from draining. Wounds which have been open for six hours or more should not be closed with sutures. If the wound has been exposed for too long, it should be cleaned and kept open under a bandage where it can slowly heal on its own.
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3,060,899,688,757,738,500 | Welcome To Adapted Psychological Therapies
0330 555 2323
phone adapted therapies cbt hampshire
Asperger’s Syndrome
aspergers-treatment-therapy-hampshireAsperger’s syndrome is a form of autism and is a lifelong disability that affects how a person makes sense of the world, processes information and relates to other people. Autism is often described as a spectrum disorder because the condition affects people in many different ways and to varying degrees.
Asperger’s syndrome is mostly a hidden disability. This means that you cannot tell that someone has the condition from their outward appearance. People with the condition have difficulties in three main areas:
• social communication
• social interaction
• social imagination
While there are similarities with autism, people with Asperger’s syndrome have fewer problems with speaking and are often of average, or above average, intelligence. They do not usually have the accompanying learning disabilities associated with autism, but they may have specific learning difficulties. These may include dyslexia and dyspraxia or other conditions such as attention deficit hyperactivity disorder (ADHD) and epilepsy.
Similar to our approach to the ASD, cognitive and behaviour psychotherapies, when adapted to the specific individual needs, can provide the right support and encouragement. A strengths-focused psychological therapy can empower people with Asperger’s and enable them to lead full and independent lives.
Useful Links:
The National Autistic Society
Recent News
Calendar Of Events
May 2021
M T W T F S S
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-2,493,291,146,144,590,000 | How Does Sleep Affect Your Body?
Published 31 May 2018, 11.30 am
Sleep is an essential part of your health and well-being. It is equally essential as a healthy diet and regular exercise. Research shows that getting enough sleep every night helps protect your physical and mental health as well as improve your quality of life. There are a number of key important outcomes from getting continual, adequate, and restful sleep:
Improved mental health
Lack of adequate sleep often leads to forgetfulness, irritability, and tiredness. Restorative sleep helps your brain regenerate and function properly. A good night sleep allows your body to remove dead blood cells and brain cells to clear pathways for newer synapses that help you maintain maximum cognitive brain function.
A healthy heart
According to research conducted by the University of Warwick, getting less than 6 hours of sleep over
an extended period increases your chances of heart failure by 48% and suffering from stroke by 15%. This is because sleep deprivation disrupts biological processes like blood pressure, inflammation, and glucose metabolism.
Weight
Lack of sleep increases chances of obesity. Sufficient sleep helps your body sustain a healthy balance of the production of the hormones responsible for making you feel hungry and full. When you deprive your body of sleep, it produces more ghrelin which ultimately increases your appetite. If you stay awake for longer hours, your body will need more energy to help you stay up longer. Therefore, you tend to eat more.
Immune system
If you consistently skimp on needed rest, the chances are that you fall sick often becomes higher. Sleep deprivation weakens the immune system. It makes you more prone to catching colds and flu. When you sleep, your body creates disease fighting hormones to fight off diseases and infections. Hence, if you do not sleep enough, you restrict your body’s ability to create these substances leaving you more prone to any virus or bacteria you encounter. Recent research also shows that sufficient sleep will help you get more preventative benefits from vaccines.
Healthier skin
Sleep is food for your body, brain, and skin. Poor sleep can cause chronic skin conditions and make
your skin age faster. However, when you get sufficient sleep, your body produces new collagen that helps prevent skin sagging, which in turn leads to fewer wrinkles. Also, a good night sleep will give your skin sufficient time to recover from ultra violet light exposure.
In case you are experiencing difficulty falling asleep, here are a few tips to help you snooze.
• Adopt a regular sleep/wake cycle
• Avoid alcohol, big meals, and smoking before bedtime
• Exercise regularly
• Do not nap for too long or too late in the day
Sleep is a vital part of maintaining overall wellness in so many ways. It can make an enormous impact on the quality of your life. Hence, it is important that you prioritize getting adequate and consistent sleep every night.
If you feel stressed, have anxiety, trouble sleeping, or any emotional distress, please contact us today at Novus Anti-Aging Center and we will be happy to get you back on track.
WebToMed Medical Website Design
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5,672,145,635,653,572,000 | Documentation
FAQ
Frequently Asked Questions
Implant-abutment connection plays an important and significant role on the long term implant stability and bone preservation. Taking into consideration these crucial factors, Alpha-Bio Tec has developed a smart platform choice solution.
Alpha-Bio Tec realizes that each dentist has he's or her own preferences and habits. This is why we chose to create two platforms, each has its own restoration line.
The NeO Conical Standard Connection enables the use of conical connection restoration which allows better platform switching, higher esthetics and more accurate AI connection which minimizes the abutment micro-movements.
The new Conical Standard Connection has a 22° angle and a 2.5mm hex. The platform diameter is 3.1mm which enables to maximize the implant platform switching abilities.
NeO is defined as a system since it includes three types of connections: a conical narrow connection (CHC), a conical standard conical connection (CS) and an Internal Hex connection (IH).
Each connection has its own prosthetic line with the following color coding – blue for IH, gold for CHC (3.2 & 3.5mm) and green for CS (3.75, 4.2 & 5.0mm). The NeO implant comes in a mountless new package. It has the same color coding as today according to implant's length, but with additional indication of the diameter and the connection type. The implant can be removed from the package with an advanced grip driver line.
Its ability to achieve high primary stability in:
• Soft bone, closed or open sinus lift: due to its unique outer and inner shape and threads design.
• Reduced vertical height, immediate implantation: due to its narrow and sharp and deep threads at the apical part.
• Reduced width: due to its delicate penetration it widens the narrow ridge instead of destroying it.
Immediate implantation and loading and GBR simultaneously: due to all the features above
Alpha-Bio Tec has modified the drilling protocol into 3 bone categories, simplifying the dentist’s choice by reducing the chances of making mistakes and improving drilling protocol accuracy. In addition, Alpha-Bio Tec has launched an advanced drill line including step drills, which enables the physician to achieve optimal osteotomy to match the implant body and gain high primary stability at the same time.
This is one of the NeO biggest clinical advantages since it is as good at bone type 4 as it is at bone type 1,2 or 3. The unique external shape – straight coronal part, slightly tapered body, tapered apical part in combination with the perfect fit between the implant and its step drills make it suitable for all bone types.
The second important clinical advantage of the NeO is the unique delicate variable threads, designed together with the special “attack angle” threads and micro threads that make the implant engagement very strong but with reduced pressure on the bone.
Autograft: A bone material harvested from the patient’s own body.
Allograft: A bone graft material taken from human sources (living organ donor or cadaver).
Xenograft: A bone material made from a biological source , most commonly bovine (cow), porcine (pig), equine (horse).
Alloplast: A bone graft material of a synthetic origin, such as Tri Calcium Phosphate (TCP).
Bioactive Bone is distributed by: Alpha-Bio Tec. Ltd www.alpha-bio.net The Bioactive Bone belongs to the Xenograft family
Porosity is defined as the percentage of void space in each particle’s architecture and it is a morphological property independent of the material [1] parameter that allows growth of capillaries in regenerating site; this is an obligatory event in the cascade of new bone regeneration.
Grafting material serving as a scaffold and osteoconductive material, in a process which enables the body to build new bone in defect areas. The scaffold provides an efficient structure, allowing cells to attach and build new bone. Xenograft, Allograft and Synthetic graft are examples of passive bone graft.
Alpha-Bio’s Graft Bioactive Bone Xenograft is immersed in a unique composition of polymer and cell nutrients that enable the material to enhance conductive qualities [6,7,8].
Osteoconduction Osteoconduction occurs when the bone graft material serves as a scaffold for new bone growth. Osteoblasts from the margin of the defect filled with grafting material utilize the bone graft material as a framework upon which to spread and generate new bone [4] . Osteoinduction Osteoinduction is the process by which osteogenesis is induced. It is a phenomenon regularly seen in any type of bone healing process. Osteoinduction implies the recruitment of immature cells and the stimulation of these cells to develop into preosteoblast [5] . The Bioactive bone enhances conductivity due to its immersion with Poly-lactic+Poly-ɛ-caprolactone known material in the industry of 3D matrix of introducing stem cells into wounded tissue [ 7,8].
The Bioactive Bone graft alone can supply excellent regenerative results. It is not recommended to mix it with other Xenograft or Synthetic bone substitutes.
To effectively manage and handle the material, it is recommended to immerse the Bioactive Bone in patient blood or with a few drops of cold saline.
In general, small granules are recommended for small defects, while large granules are recommended for large ones (e.g.: Sinus lift). In addition, a given clinical situation may deviate from this guideline [2] . The Bioactive Bone is available in small (0.25-1.0 mm) and large (1.0-2.0 mm) granules sizes, provides the user with a varied clinical solution. ALPHA-BIO’S GRAFT BIOACTIVE BONE FAQ’s
Is there difference in resorption time between small and big particles? In the case of Xenograft, the answer is no. | {
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-537,021,181,583,670,200 | Magnetic resonance angiography
Magnetic resonance angiography (MRA) generates pictures of the arteries to evaluate them for stenosis (abnormal narrowing) or aneurysms (vessel wall dilatations, at risk of rupture). MRA is often used to evaluate the arteries of the neck and brain, the thoracic and abdominal aorta, the renal arteries, and the legs (called a “run-off”). A variety of techniques can be used to generate the pictures, such as administration of a paramagnetic contrast agent (gadolinium) or using a technique known as “flow-related enhancement” (e.g. 2D and 3D time-of-flight sequences), where most of the signal on an image is due to blood that recently moved into that plane, see also FLASH MRI. Techniques involving phase accumulation (known as phase contrast angiography) can also be used to generate flow velocity maps easily and accurately. Magnetic resonance venography (MRV) is a similar procedure that is used to image veins. In this method, the tissue is now excited inferiorly, while signal is gathered in the plane immediately superior to the excitation plane—thus imaging the venous blood that recently moved from the excited plane.
mra Magnetic Resonance Angiography
Magnetic Resonance Angiography
Source: Text Images
Number of View: 4002
Leave a comment | {
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3,977,144,487,746,512,400 | Chapter I. Pathogenesis
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Rev Diabet Stud, 2012, 9(4):188-200 DOI 10.1900/RDS.2012.9.188
Protein Tyrosine Phosphatases and Type 1 Diabetes: Genetic and Functional Implications of PTPN2 and PTPN22
Karen Cerosaletti, Jane H. Buckner
Translational Research Program, Benaroya Research Institute at Virginia Mason, Seattle, WA 98101, USA
Address correspondence to: Jane H. Buckner, Associate Director, Benaroya Research Institute, Director, Translational Research, Benaroya Research Institute at Virginia Mason, 1201 9th Ave, Seattle, WA 98101, USA, e-mail jbuckner@benaroyaresearch.org
Manuscript submitted December 16, 2012; resubmitted January 28, 2013; accepted January 29, 2013.
Keywords: type 1 diabetes, genome-wide association study, PTPN22, PTPN2, LYP, TCPTP
Abstract
Protein tyrosine phosphatases (PTPs) play a central role in modulating the transduction of cellular signals, including the cells of the immune system. Several PTPs, PTPN22, PTPN2, and UBASH3A, have been associated with risk of type 1 diabetes (T1D) by genome wide association studies. Based on the current understanding of PTPs, it is clear that these variants impact antigen receptor signaling and cytokine signaling. This impact likely contributes to the development and progression of autoimmunity through multiple mechanisms, including failures of central and peripheral tolerance and the promotion of proinflammatory T cell responses. In this review, we discuss the genetic and functional implications of two of these PTPs, PTPN22 and PTPN2, in the development of T1D. We describe the known roles of these proteins in immune function, and how the expression and function of these proteins is altered by the genetic variants associated with T1D. Yet, there are still controversies in the field that require further study and the development of new approaches to extend our understanding of these PTP variants, with the goal of using the information gained to improve our ability to predict and cure T1D.
Abbreviations: BCL2 – B cell lymphoma 2; BCR – B cell receptor; BIM – BCL2-interacting mediator; C57BL/6 – inbred strain C57 black; c-CBL – Casitas B-lineage lymphoma proto-oncogene; cDNA – complementary DNA; CEU – Centre d'Etude du Polymorphisme Humain from Utah (Utah residents of northern European ancestry); CLL - chronic lymphoid leukemia; CSF-1 - colony stimulating factor 1; CSK – C-terminal Src kinase; DAISY – Diabetes Autoimmunity Study in the Young; EGF – epidermal growth factor; ERK – extracellular signal-regulated kinase; GRB2 – growth factor receptor-bound protein 2; GWAS – genome-wide association study; HapMap – Haplotype Map (project); HLA – human leukocyte antigen; IFNγ – interferon gamma; IFNGR2 – interferon gamma receptor 2; Ig – immunoglobulin; IL – interleukin; IRβ – insulin receptor beta; JAK – Janus kinase; LYP – lymphocyte tyrosine phosphatase; MAPK – mitogen-activated protein kinase; OR – odds ratio; PBMC – peripheral blood mononuclear cell; PEP – PEST domain phosphatase; PEST – Pro-Glu-Ser-Thr domain phosphatase; PI3K - phosphatidylinositol 3'-kinase; PLCγ2 - phospholipase Cγ2; PTK – protein tyrosine kinase; PTP – protein tyrosine phosphatase; PTPRC – protein tyrosine phosphatase, receptor type C; PTPN22 – protein tyrosine phosphatase, non-receptor type 22; RA – rheumatoid arthritis; SHIP - Src homology 2-containing inositol 5'-phosphatase; siRNA – small interfering RNA; SLE – systemic lupus erythematosus; SNP – single nucleotide polymorphism; STAT - signal transducer and activator of transcription; SYK – spleen tyrosine kinase; T1D – type 1 diabetes; Teff – effector T cell; TNFα – tumor necrosis factor alpha; Treg – regulatory T cell; TCPTP – T cell protein tyrosine phosphatase; TCR – T cell receptor; TRAF2 – TNF receptor-associated factor 2; VCP – valosin-containing protein; ZAP70 – zeta-chain-associated protein kinase 70
1. Introduction
Genetic studies have led to the identification of over 50 genomic regions containing single nucleotide polymorphisms (SNPs) that are associated with type 1 diabetes (T1D) (www.t1dbase.org). Many of these genes participate in intracellular signaling, including a group of protein tyrosine phosphatases. Tyrosine phosphorylation plays a central role in the transduction and regulation of intracellular signals, including the regulation of antigen receptor signaling, cytokine-induced differentiation in lymphocytes, and insulin signaling. Protein tyrosine kinases (PTKs) potentiate the phosphorylation of tyrosine residues, while protein tyrosine phosphatases (PTPs) dephosphorylate tyrosine residues on proteins, thereby mediating positive or negative regulation of target pathways. Over 45 PTPs are expressed in lymphocytes, each having activities within signaling pathways. Therefore, alterations in the level of expression or function of PTPs have the potential to alter the function and fate of cells, including those involved in the immune response. Currently, three PTP genes have been associated with T1D, PTPN22, PTPN2, and UBASH3A [1]. Understanding the functional impact of these genetic variations in PTPs associated with T1D is likely to shed light on the mechanisms that drive disease development and assist in creating therapies to stop or reverse this process. In this review, we discuss variants of two PTPs which are associated with T1D, PTPN22 and PTPN2, and their potential impact on disease.
2. PTPN22
2.1 Genetic studies and broad association of PTPN22 1858T with autoimmunity
PTPN22 encodes the protein tyrosine phosphatase N22 (PTPN22), also referred to as lymphocyte tyrosine phosphatase (LYP) [2]. A single-nucleotide polymorphism (SNP) c.1858C>T (rs2476601) of PTPN22 was found to be associated with T1D in 2004 [3]. Multiple subsequent studies have confirmed the association of this SNP with T1D, with a recent genome wide meta-analysis reporting a p-value of 5.93x10-80 and an odds ratio (OR) of 1.96 [4]. This variant is associated with multiple autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Graves' disease, and myasthenia gravis [5-8]. The 1858T variant is a missense mutation of the coding region, in which cytosine is replaced by thymidine at position 1858, resulting in a change from an arginine (R) at position 620 of the protein to tryptophan (W). The R620W variant is located within the P1 proline-rich repeat in the PTPN22 SH3 domain of the protein that mediates interaction with the C-terminal Src kinase (CSK), as described below, making it likely that this SNP is functionally significant. In addition to rs2476601, other coding variants within PTPN22 have been identified in T1D subjects, indicating the importance of this gene in disease development [9].
2.2 Known function of lymphocyte tyrosine phosphatase (LYP)
LYP is expressed in all hematopoietic cells and is part of the Pro-Glu-Ser-Thr domain phosphatase (PEST) group of nonreceptor classical class I PTPs in human cell lines. LYP has been shown to be a negative regulator of T cell receptor (TCR) signal transduction via its interactions with the activating tyrosines of LCK (Y394), FYN (Y427), and zeta-chain-associated protein kinase 70 (ZAP70) as well as phospho-sites on TCRζ, CD3ε, VAV, and valosin-containing protein (VCP) [10-12]. Yu et al. have demonstrated that the phosphatase function of LYP is regulated by phosphorylation at Ser-35. The phosphorylation at this residue alters the conformational state of LYP and impairs its phosphatase activity resulting in an augmentation of TCR signal transduction [13]. The role of LYP as a regulator of TCR signaling is also bolstered by the development of a salicylic acid-based LYP inhibitor which binds to the catalytic site and enhances TCR signaling [13]. LYP has additional binding partners, including the adaptor molecule GRB2 (growth factor receptor-bound protein 2) and the E3 ligase c-CBL (Casitas B-lineage lymphoma proto-oncogene) [2], indicating that LYP may act alone or via interactions with other partners or substrates downstream of the TCR, B cell receptor (BCR), and other immune receptors.
2.3 Dissecting the functional impact of LYP R620W on lymphocytes
Cell lines have been used to understand better the function of LYP in T cells. Studies in Jurkat cells have shown that LYP's inhibition of TCR signal transduction is enhanced when it interacts with the PTK CSK [10]. This interaction occurs in the region of LYP which includes amino acid residue 620. Owing to the position of the LYP risk variant within the P1 proline-rich region, which interacts with the SH3 domain of CSK, several groups have investigated the impact of the LYP R620W variant on LYP/CSK interaction. Jurkat cell lines transduced to express LYP 620W and CSK demonstrate a loss of interaction between LYP and CSK and an increase in TCR responses [14, 15]. However, when Jurkat cells are transduced to express LYP 620W alone, a blunting of TCR signal transduction is seen [16]. More recent studies have shown that LYP inhibits TCR-induced signaling after dissociation from CSK, and is recruited to lipid rafts; in this way a more rapid dissociation of the LYP-CSK complex could result in an increase in LYP 620W availability to lipid rafts and an increase in its inhibitory activity [17].
2.4 Function of the LYP R620W variant deduced from murine models of PEP and PEP R619W
Studies of the role of PEP (PEST domain phosphatase), the murine homologue of LYP, have shed light on its multiplicity of functions in the immune response. PEP and LYP share 89% identity at the PTP domain, and 61% identity in the non-catalytic domains. The majority of these studies have been performed in mice where the Ptpn22 gene is knocked out [18-20], but more recently, a model in which Ptpn22 is inducibly knocked down has also been described [21]. Ptpn22 deficiency has been shown to enhance signaling through the TCR, as measured by calcium flux and phosphorylation of LCK, ZAP70, and extracellular signal-regulated kinase (ERK) (Table 1) [15, 18]. These alterations are most pronounced in memory T cells. They also result in increased proliferation of effector T cells and a general expansion of the T cell compartment over time. Regulatory T cells (Tregs) are also altered in these animals, with increased Treg number, IL-10 production, and suppressive function [19, 20]. Ptpn22 deficiency has also been shown to cause an expansion of germinal centers and an increase of immunoglobulin production [18]. With respect to a disease phenotype, Ptpn22-/- effector T cells (Teffs) are more potent mediators of colitis upon cell transfer. However, these Teffs can be controlled by co-transfer of Ptpn22-/- Tregs (but not wild type Tregs) [20]. Ptpn22-/- mice are resistant to EAE [19] and NOD mice, in which Ptpn22 is knocked down, have a decreased incidence of diabetes [21].
Table 1. Phenotypes associated with variants in the PTPN22 gene in mouse models and human cells
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These studies indicate that PEP plays multiple roles in the murine immune response, likely regulating both the effector and regulatory T cell compartments. These findings are consistent with the role of the LYP R620W variant in human T1D, in that it alone is not sufficient to drive autoimmunity. Zikherman et al. explored the question of whether Ptpn22-/- mice would develop autoimmunity if additional factors that contribute to loss of tolerance are present. To this end, they crossed the Ptpn22-/- mouse onto a B6 mouse strain with the Ptprc (CD45) E613R mutation, a mutation known to cause a loss of B cell tolerance [15]. They observed that these animals had both enhanced T cell responses in the periphery and the thymus as well as an increase in B cell response to activation. Finally, the animals developed lupus-like disease with anti-nuclear antibodies, and lymphoproliferative disease.
These studies are informative as to the multiplicity of functions of this PTP in murine T cells, but limited in that they do not directly address the impact of the risk variant, which may lead to an alteration but not a loss of function. To address this question, Zhang et al. engineered a mouse to express the PEP R619W variant which is similar to the R620W variant found in human autoimmunity [22]. These animals did not develop autoimmunity, confirming a need for additional triggers in the process of autoimmunity. However, the animals had an increase in the number of dendritic cells, hyper-responsive T cell signaling and an increase in antibody production in response to vaccination. The authors attributed these changes to a relative decrease in expression of PEP 619W through enhanced calpain-mediated degradation of the PEP 619W protein. They concluded that in humans the likely functional implications of the variant was a loss-of-function of LYP owing to decreased protein levels in T and B cells. These findings contradict multiple studies in human B and T cells which find no difference in LYP protein based on the 1858T genotype. A second group has independently generated a PEP R619W knock-in-mouse and found normal stability of the PEP 619W protein. Like Zhang et al., they found enhanced antigen receptor signaling in lymphocytes, but in contrast to Zhang et al., loss of tolerance and autoimmunity have been observed [23].
2.5 Assessment of the role of LYP and the LYP R620W variant in human cells
The studies of cell lines and murine models have helped to define, at least in part, how PTPN22 participates in immune function in humans. However, these approaches have limitations due to the possibility that a cell line or an animal may not reflect the intracellular signaling environment or functional outcomes that are found in human cells. To fully understand how LYP and its variants impact immune function and human disease, studies with human lymphocytes have been performed.
Vang et al. were the first to examine the functional impact of LYP R620W on human T cells. They found that T cells from T1D subjects heterozygous for the 1858T allele, displayed decreased IL-2 production upon stimulation with anti-CD3/CD28 (Table 1) [16]. A second study with T1D 1858T carriers also found a decrease in T cell proliferation and IL-2 production upon CD3/CD28 stimulation [24]. In further studies, healthy individuals who carry the 1858T variant allele were shown to have an expanded CD4 memory compartment and a blunted response to stimulation via CD3, as measured by Ca+ flux, IL-2, and IL-10 production, but no alteration in proliferation or production of the proinflammatory cytokines tumor necrosis factor alpha (TNFα) and interferon gamma (IFNγ) [25]. A decrease in IL-10 production was also described in 1858T carriers with ANCA vasculitis [26]. These studies seem to suggest that LYP R620W is a gain of function variant, leading to an increased inhibition of TCR signaling. Yet, the more recent study of the murine knock-in of PEP 619W by Zhang et al. suggested that the R>W substitution causes a loss of function due to decreased protein levels of PEP [22]. As part of that study, T cells from healthy and RA subjects were examined for LYP expression using a flow cytometric based assay. Using this approach, decreased expression of LYP was identified in individuals with the 1858T variant, and these subjects also had an increase in phosphorylation of ERK upon TCR stimulation [22]. Both the murine and human findings in this study seem to contradict the previous work using human peripheral blood mononuclear cells (PBMCs). The finding of decreased LYP expression in human lymphocytes has not been observed by other groups who have utilized Western blot, a more rigorous assay for protein levels [16, 27]. Also, phosphorylation of ERK has not been reported by other studies that have typically assessed more proximal aspects of TCR signaling in human samples. The differences between mouse and human primary T cells raise concerns about whether murine systems can sufficiently model LYP 620W function in human T cells.
LYP is also expressed in B cells. In chronic lymphoid leukemia (CLL), LYP is overexpressed resulting in a blunted BCR signal via spleen tyrosine kinase (SYK) which leads to a decrease in phosphorylation of phospholipase Cγ2 (PLCγ2), p38 MAPK, and ERK. However, the increase in LYP also leads to the inhibition of LYN and Src homology 2-containing inositol 5'-phosphatase (SHIP) which inhibit signaling via phosphatidylinositol 3'-kinase (PI3K) and AKT, leading to an increase in AKT activity [28]. This results in an enhancement of the prosurvival signals GSK3 (glycogen synthase kinase 3) and FOXO (forkhead box protein O), with the result that CLL cells escape BCR-mediated cell death [28]. LYP 620W has also been shown to impact primary B cells; expression of LYP is unaffected by the variant, but BCR signaling via PLCγ2 is decreased in naïve and memory B cells, suggesting a gain of function similar to that seen with overexpression of LYP in CLL [27, 29]. An extension of these studies to LYN, SHIP, and AKT has not yet been performed. However, studies have linked LYP 620W with alterations in B cell development and tolerance. It has been shown that such alterations can be associated with a resistance to BCR-mediated cell death, an expansion of transitional and anergic B cells, a decrease in circulating memory B cells, and an increase in the escape of autoreactive B cells into the transitional and mature naïve B cell compartment [29, 30]. These findings indicate that the LYP 620W variant likely contributes to the development of autoimmunity and autoantibodies via a B cell-intrinsic mechanism in addition to its impact on Teffs and Tregs.
2.6 Caveats related to studies of PTPN22 in human lymphocytes
The in vitro studies conducted in primary human lymphocytes have produced findings that partly differ from those conducted in immortalized cell lines or murine cells. Additional efforts are necessary to clarify the reasons for this discrepancy, to validate the present findings, and to reveal the true functions of PTPN22 in human lymphocytes. Human immune responses reflect a combination of genetic background, environment, and previous immune activation over years. Thus, the function of human primary lymphocytes not only reflects the direct impact of the variant itself, but may also be the result of compensatory mechanisms that have developed over time as a result of the presence of the genetic variant. In order to model this in animals, studies may need to follow up the animals as they age, and to determine impacts upon exposure to foreign antigens and pathogens. The influence of PTPN22 c.1858C>T on the development of autoimmunity may in fact be due to both types of immune alterations, through genetic variation and compensatory mechanisms, as disease develops over time. Thus, both should be addressed as we move forward with studies of PTPN22.
2.7 LYP's role in the development of T1D
Studies that have assessed the impact of the PTPN22 1858T variant on disease development have indicated that carriers of the variant are younger at diagnosis of T1D [31]. In contrast, another study found the age at onset to be older among 1858T/T subjects [32]. In addition, PTPN22 1858T has been shown to be a predictor of more rapid progression to T1D among islet autoantibody-positive at-risk relatives [33]. Modeling of known genetic factors has shown that combinations of genes which include PTPN22 can be used to predict both islet autoantibody and diabetes development [34, 35]. Furthermore, the PTPN22 risk variant has been linked to the development of autoantibodies when combined with environmental triggers [36]. These studies support the concept that the PTPN22 1858T variant contributes to a failure in tolerance which leads to the development of autoantibodies and disease.
3. PTPN2
3.1 Genetic association of PTPN2 with autoimmunity
The PTPN2 gene was first associated with autoimmunity in the Wellcome Trust Case Control Study in 2007 [37]; an SNP in the intergenic region 5.5kb downstream of the PTPN2 gene, rs2542151, was found to be associated with susceptibility to T1D, Crohn's disease, and weakly with RA. This finding was replicated and refined by Todd et al. [38], who identified two non-coding SNPs in PTPN2 that are independently associated with T1D: rs1893217 in intron 7 (p = 1.16x10-11, OR = 1.3, 95% CI: 1.21-1.41) and rs478582 in intron 3 (p = 9.15x10-9, OR = 0.82, 95% CI: 0.77-0.87). In the largest meta-analysis of T1D cases (11,781), control subjects (13,715), and family trios (4,342) to date, the association of PTPN2 rs1893217 with T1D was highly significant (p = 3.6x10-15) [1]. Note that rs1893217 in intron 7 is in complete linkage disequilibrium (LD, D'=1, r2=1) with rs2542151 located 3' of the PTPN2 gene, and thus their genotypes are interchangeable.
Like PTPN22, the PTPN2 gene is associated with multiple autoimmune diseases, suggesting that it contributes to common mechanisms in the development and progression of autoimmune disease. Association of PTPN2 rs1893217 has been confirmed for Crohn's disease (p = 1.29x10-14, OR = 1.25, 95% CI: 1.18-1.32) [39], celiac disease (p = 2.5x10-10, OR = 1.17, 95% CI: 1.12-1.23) [40], and, with weaker association, ulcerative colitis (p = 4.78x10-5, OR = 1.12) [41] and RA (p = 2.4x10-5) [42]. An initial association with Grave's disease [38] has not been replicated.
3.2 Known function of PTPN2
The PTPN2 gene encodes a non-receptor protein tyrosine phosphatase and was originally cloned from a human T cell cDNA library, hence the alternative name T cell protein tyrosine phosphatase (TCPTP) [43]. While expression of PTPN2 is highest in cells of the hematopoietic lineage, it is expressed ubiquitously throughout the body and as early as day e8.5 of development in mouse embryos [43, 44]. Two isoforms of PTPN2 are expressed in human cells via alternative splicing; a 45kD variant (387 amino acids) which results from correct splicing of exon 9 to the terminal exon 10, and a 48kD variant which does not splice exon 9 to exon 10, but rather continues translation into intron 9, where a stop codon terminates the protein at amino acid 415 [43, 44]. The subcellular localizations of the 45kD and 48kD variants differ as a result of these alternative C-terminal sequences, and thus impact their substrate selection [45]. The 45kD variant is found primarily in the nucleus in resting cells due to a bipartite nuclear localization sequence, but can diffuse into the cytoplasm upon stimulation. In the cytoplasm, it can interact with cytoplasmic substrates and intracellular domains of transmembrane-bound receptors and their associated signaling proteins [46]. The 48kD variant contains a hydrophobic transmembrane domain and is targeted to the endoplasmic reticulum. In contrast to human cells, mouse cells express primarily the 45kD isoform of PTPN2 [47].
Structurally, the PTPN2 protein contains an N-terminal phosphatase domain and a C-terminal non-catalytic domain involved in autoregulation of catalytic activity and determination of subcellular localization, as described above [45, 48]. PTPN2 is closely related to the intracellular phosphatase PTP1B (PTPN1), with 74% identity in the catalytic domains [49]. Both PTPN2 and PTP1B prefer tandem phospho-tyrosine residues and share some substrates. Indeed, synthesis of inhibitors specific for each phosphatase has been challenging [50]. However, despite their relatedness, Ptpn2 deficiency in mice results in defects in lymphopoiesis and systemic inflammation (discussed in detail below), whereas Ptpn1 deficiency results in increased insulin sensitivity and protection from diet-induced obesity, reflecting their relative contributions to cytokine/antigen receptor signaling versus insulin receptor signaling [51].
Numerous substrates have been identified for PTPN2 that reveal roles in regulating signaling in response to growth factors, cytokines, hormones, and antigens. Specific targets have been identified through in vitro phosphatase assays and expression of substrate trapping mutants of PTPN2. Functional confirmation of substrates has been achieved using Ptpn2+/+ and Ptpn2-/- fibroblasts and lymphocytes and PTPN2 siRNA in specific cell types. Using such techniques, PTPN2 has been shown to dephosphorylate the epidermal growth factor (EGF) receptor and p52Shc in response to EGF, impacting association of p52Shc with GRB2 [52] and the colony stimulating factor 1 (CSF-1) receptor which mediates downstream ERK activation [53]. The Janus kinases JAK1 and JAK3 are dephosphorylated by PTPN2, resulting in modulation of IL-2, IFNγ, and IFNα signaling [54], while the transcription factors STAT1, STAT3, and STAT6 are targets of PTPN2 in response to IFNγ, IL-6, and IL-4, respectively [55-57]. TNF has been shown to stimulate PTPN2 interaction with the adaptor protein TNF receptor-associated factor 2 (TRAF2), with subsequent dephosphorylation of c-SRC and regulation of ERK activation [58]. Consistent with Src family kinases being substrates, PTPN2 was recently shown to dephosphorylate LCK and FYN following T cell receptor engagement, impacting activation of the downstream signaling molecules ZAP70, PLCγ1, and ERK [59].
PTPN2 has also been shown to play a role in regulating the response to the hormones prolactin, leptin, and insulin. The transcription factors STAT5A and STAT5B appear to be substrates for PTPN2 upon prolactin binding the prolactin receptor [60], and STAT3 is dephosphorylated by PTPN2 in response to leptin receptor engagement in the hypothalamus, attenuating leptin signaling [61]. In response to insulin, PTPN2 binds and dephosphorylates the insulin receptor beta (IRβ) in cooperation with PTP1B [47]. PTPN2 has been shown to control specifically the duration of downstream AKT phosphorylation, but not ERK phosphorylation, in PTP1B deficient and sufficient cells [47, 62]. Given the ubiquitous expression of PTPN2, it is likely that additional PTPN2 substrates will be identified that impact other pathways.
3.3 Functional impact of the PTPN2 risk variant
PTPN2 is the only gene within the T1D-associated LD block on chromosome 18, making it a likely candidate gene for the genetic association. No common coding variants in LD with either rs2542151 or rs1893217 have been identified, although rare coding changes in PTPN2 have been identified through the 1000 Genomes Project (www.1000genomes.org). Thus, PTPN2 expression differences may contribute to T1D susceptibility. A modest but significant reduction in PTPN2 RNA levels with the rs1893217 risk allele have been observed in memory CD4 T cells from the peripheral blood of genotyped control subjects. This was confirmed in an independent data set generated from HapMap CEU EBV-transformed B cells [63]. However, neither rs1893217 nor rs2542151 overlap DNase I hypersensitivity sites, transcription factor binding sites, or microRNA target sites (genome.ucsc.edu), although binding sites for the vitamin D receptor have been reported in intron 7 near rs1893217 [64]. Thus, it seems likely that rs1893217 and rs2542151 are not directly responsible for alterations in PTPN2 expression, but may be found in LD with a variant that does alter expression.
3.4 Role of PTPN2 in autoimmunity deduced from murine models of PTPN2 deficiency
To understand better the role of PTPN2 in vivo, the Ptpn2 gene has been disrupted globally in all mouse tissues of BALB/c and C57BL/6 mouse strains by homologous recombination [65] and Cre/LoxP recombination [66]. In all cases, Ptpn2 deficiency results in Mendelian ratios of offspring that appear normal at birth. By 2 weeks of age, Ptpn2-/- mice begin to display growth retardation, and at 3-5 weeks of age, mice develop severe defects in B cell lymphopoiesis and erythropoiesis, resulting in death in 100% of animals. In contrast, mice heterozygous for the null allele display no obvious phenotype. On a BALB/c genetic background, Ptpn2-/- deficiency also results in a systemic inflammatory disease characterized by increased levels of IL-12p40, IFNγ, TNFα, iNOS, and mononuclear infiltrates in the spleen and non-lymphoid tissues [65, 67]. This inflammatory phenotype is not observed when Ptpn2 deficiency is present on the more autoimmune resistant C57BL/6 genetic background [66].
Histologically, Ptpn2-/- mice are characterized by decreased bone marrow cellularity over time, with reduced numbers of progenitor B cells, pre B cells, immature IgM+ B cells, and mature IgD+ recirculating B cells, which is reflected in decreased peripheral B cell subsets [66, 68]. The thymus also has decreased cellularity over time due to a reduction in CD4+CD8+ double positive thymocytes, double negative thymocytes, and CD4+ and CD8+ single positive thymocytes, resulting in decreased numbers of CD4+ and CD8+ peripheral T cells [65, 66]. These B and T cell phenotypes result from both cell intrinsic and extrinsic factors, as evidenced by decreased B cell colony forming ability in Ptpn2-/- bone marrow compared to Ptpn2+/+ bone marrow when grown on wild type stromal cells, both of which are reduced when cultured on Ptpn2-/- stromal cells [68]. Extrinsically, cells in Ptpn2-/- mice are exposed to increased levels of inflammatory cytokines, while intrinsically, Ptpn2 deficiency exacerbates signaling in response to growth factors, cytokines, and antigen receptor stimulation, since PTPN2 negatively regulates these pathways, as described above.
Recent experiments that specifically knocked out Ptpn2 in CD4+ T cells using a floxed Ptpn2 locus and Lck-Cre mice have further defined the role of PTPN2 in T cell development, thymic selection, and response to antigen [59]. Consistent with LCK and FYN being direct targets of PTPN2, Ptpn2fl/fl/Lck-Cre thymocytes and peripheral T cells display increased LCK and FYN phosphorylation, as well as increased phosphorylation of downstream TCR signaling pathway molecules following stimulation with anti-CD3. This translates into increased proliferation, and lowers the threshold for TCR-induced proliferation, antigen affinity, and need for costimulation via CD28 both in vitro and in vivo. The thymocytes of Ptpn2fl/fl/Lck-Cre mice show evidence of increased positive selection, resulting in increased numbers of CD4+ and CD8+ thymocytes and peripheral T cells, particularly peripheral CD8+ effector memory T cells. There is also increased responsiveness to IL-2 in Ptpn2fl/fl/Lck-Cre T cells. Interestingly, at 48 weeks of age, Ptpn2fl/fl/Lck-Cre mice develop inflammation and autoimmunity that is characterized by increased levels of circulating IL-6, TNF, and IFNγ, high levels of anti-nuclear antibodies, and infiltration of CD8+ effector memory T cells in lymphoid and non-lymphoid tissues that can transfer disease.
Taken together, the phenotypes observed in Ptpn2-/- and Ptpn2fl/fl/Lck-Cre mice provide clues to how decreased PTPN2 expression in humans may contribute to the loss of T cell tolerance and the development of inflammation, leading to autoimmunity. While conditional deletion of Ptpn2 in T cells reveals T cell-intrinsic effects in the absence of non-T cell extrinsic factors, mice with global Ptpn2 deficiency may model human PTPN2 deficiency more accurately since expression of PTPN2 is ubiquitous. Thus, cell-extrinsic effects of PTPN2 deficiency are likely to play a role in human disease settings, as they do in mouse models.
3.5 The role of PTPN2 in the development and progression of T1D
The role of PTPN2 in T1D is likely to be complex because of the ubiquitous expression of PTPN2 in both hematopoietic cells and non-hematopoietic cells, including β-cells in pancreatic islets. Moreover, based on in vivo mouse models, PTPN2 deficiency is likely to result in both cell-extrinsic and cell-intrinsic effects. Although the specific role of PTPN2 in T1D has only been studied in the last 5 years, pleiotropic functions are apparent, including effects on the maintenance of Tregs, β-cell apoptosis, and the response to insulin, as illustrated in Figure 1.
Figure 1. Potential roles for PTPN2 in the development of T1D. Experimental evidence indicates that PTPN2 regulates apoptosis of pancreatic β-cells upon exposure to inflammatory cytokines by modulating phosphorylation of STAT1, which induces the mitochondrial apoptotic pathway. The T1D-associated variant rs1893217 in the PTPN2 gene has been associated with reduced IL-2 receptor signaling in response to IL-2, impacting the maintenance of FOXP3+ Tregs in T1D subjects. PTPN2 has also been shown to influence glucose homeostasis by dephosphorylating the insulin receptor b-chain in conjunction with the PTP1B phosphatase. In addition, PTPN2 impacts glucose levels by modulating STAT3 signaling downstream of the leptin receptor in the hypothalamus and in response to IL-6, repressing hepatic gluconeogenesis.
The presence of the risk genotype at PTPN2 has been examined for its impact on the development of islet autoimmunity and T1D in several studies. A case-control study of European T1D cases reported that the frequency of carriers of the PTPN2 rs2542151 G risk allele was significantly higher in T1D cases with an earlier onset (≤16y) compared with later onset T1D or controls [69]. This finding is not necessarily surprising since GWAS typically include T1D subjects with an age of onset <17y, which would enrich for genetic loci contributing to early onset disease. PTPN2 rs1893217 risk genotype has also been studied in the BABYDIAB study in Europe, which has followed 1650 children of T1D parents, and the DAISY study in the US, following ~1700 children with a first-degree relative with T1D or with high-risk HLA DR3/4-DQ8 genotype [34, 35, 70, 71]. These children have been followed prospectively over time for the development of islet autoantibodies and progression to T1D. The advantage of these valuable cohorts is the ability to assess the predictive value of non-HLA genes to the initiation and progression of T1D. The disadvantage is that a small number of subjects in the cohort develop islet autoantibodies and progress to T1D, limiting the statistical power of the analysis. Nonetheless, Steck et al. reported a weak association of the PTPN2 rs1893217 risk genotype with the development of islet autoimmunity, which remained significant after adjustment for family history and high-risk HLA genotype (p = 0.04, HR = 1.42, 95% CI: 1.02-1.99) [34]. Other studies have not detected a significant association of the PTPN2 genotype with the development of islet autoantibodies [35, 70, 71]. No association of the PTPN2 rs1893217 risk genotype with progression to T1D has been detected in these studies or others [34, 70-72], although an interaction between the PTPN2 rs1893217 protective genotype and the vitamin D receptor SNP rs1544410 was associated with decreased risk of T1D in the DAISY cohort (p = 0.0004, HR = 0.24, 95% CI:0.11-0.53) [71]. Taken together, these studies indicate that the PTPN2 rs1893217 genotype alone does not appear to be a significant risk factor for the development of T1D, but PTPN2 may influence the development of islet autoimmunity and age at onset, suggesting a role for PTPN2 in disease initiation rather than progression.
Altered PTPN2 expression has been correlated with defects in IL-2 signaling and altered FOXP3 expression in Tregs in T1D. Consistent with JAK1/3 and STAT5 being substrates for PTPN2, the risk allele at the T1D-associated SNP PTPN2 rs1893217 was correlated with decreased IL-2 signaling in peripheral CD4+ T cells from genotyped control subjects (Figure 1) [63]. This phenotype was not due to altered expression of the IL-2 receptor, JAK1, JAK3, or STAT5; however, the rs1893217 genotype correlated with reduced expression of PTPN2 in CD4+ memory cells, suggesting that PTPN2 may indirectly modulate IL-2 responsiveness in primary human T cells. In subjects with T1D, IL-2 signaling is further decreased compared with controls, indicating that the autoimmune environment acts coordinately with the PTPN2 genotype to reduce IL-2 signaling ([73] and unpublished data). Interestingly, PTPN2 expression was increased in T1D subjects compared with control subjects, most likely due to inflammatory cytokines which have been shown to induce PTPN2 expression [74, 75]. Functionally, diminished IL-2 signaling is associated with reduced maintenance of FOXP3 expression in natural Tregs from subjects with T1D and decreased FOXP3 expression in induced Tregs [73]. Thus, the effect of PTPN2 on IL-2 responsiveness may contribute to the development of T1D through an impact on Treg homeostasis, consistent with alterations in IL-2 and Tregs in NOD mice [76, 77]. Recent experiments have shown that the PTPN2 rs1893217 risk variant acts independently of T1D risk variants in the IL2RA gene, which encodes the high-affinity IL-2 receptor, CD25, to reduce IL-2 responsiveness in T cells, potentially further impacting Treg persistence (unpublished data).
PTPN2 may also modulate pancreatic β-cell apoptosis in response to inflammatory cytokines. Knockdown of PTPN2 expression in rat or human β-cells enhances apoptosis upon treatment with IFN-α, IFN-γ, IL-1β+IFN-γ, or TNF+IFN-γ (Figure 1) [74, 78]. Decreased PTPN2 expression is correlated with an increase in phosphorylation of STAT1 in rat insulinoma cells, and amelioration of STAT1 expression with a STAT1-specific siRNA protected cells from apoptosis. Thus, if the PTPN2 rs1893217 risk genotype is associated with reduced PTPN2 expression in pancreatic β-cells, as found in lymphocytes, then it may predispose β-cells to apoptosis upon exposure to inflammatory cytokines via increased phosphorylation of STAT1.
Lastly, the role of PTPN2 in regulating insulin and leptin signaling may impact the development of hyperglycemia in T1D. The function of PTP1B and PTPN2 in these pathways has been a focus for type 2 diabetes (T2D) which is associated with the PTPN1 gene [79-81]. Although the PTPN2 gene is not associated with susceptibility to T2D, altered PTPN2 expression can impact hepatic gluconeogenesis. Heterozygous Ptpn2+/- mice fed a high fat diet display reduced fasting glucose levels compared with Ptpn2+/+ littermates, which correlates with decreased fasting hepatic gluconeogenesis [82]. Decreased hepatic glucose output is driven by the mechanism of increased STAT3 phosphorylation downstream of IL-6 signaling in the liver, which suppresses expression of gluconeogenic enzymes (Figure 1). Peripheral insulin sensitivity and whole body glucose utilization is also impacted by PTPN2 expression via leptin signaling. Deletion of the Ptpn2 gene specifically in neurons results in sustained STAT3 phosphorylation downstream of the leptin receptor in the hypothalamus of mice on a high fat diet, correlating with decreased diet-induced obesity, and reduced fasting plasma insulin and glucose [61]. These results suggest that decreased PTPN2 expression may protect from hyperglycemia by enhancing phosphorylation of STAT3 in response to IL-6 or leptin, whereas increased PTPN2 expression in the context of T1D could potentially contribute to increased glucose levels by attenuation of STAT3 phosphorylation.
4. Conclusions
The importance of the protein tyrosine phosphatases, PTPN2 and PTPN22, in T1D was first identified through genetic association studies. This has led to a series of further genetic and immunologic investigations which have enlightened us on the potential role of these proteins in the development and progression of T1D. In the case of each PTP, studies have uncovered alterations in multiple signaling pathways within multiple cell types caused by the genetic variants, leading to failures of central and peripheral tolerance, the promotion of proinflammatory T cell responses, and even the loss of regulation of glucose homeostasis. These findings have challenged our motivation to identify a single mechanism by which these variants lead to disease, or by extension a single pathway to target for therapeutic intervention. Further study is needed to determine if there is a single dominant immunologic alteration that contributes to disease. Alternatively, the study of these PTPs may demonstrate that the ubiquitous nature of these variants and their association with many autoimmune diseases is due, in part, to the multiplicity of ways in which these variants subtly alter the immune response.
Disclosure: The authors report no conflict of interests.
Acknowledgments: This work was supported by grants from NIAID and JDRF.
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Chromium-plated insufflator
An insufflator pumps carbon dioxide into the peritoneal cavity (the abdomen) to provide an "optical space" which permits examination of the abdominal contents. Carbon dioxide is used to distend the abdomen as it is very soluble in blood and easily exhaled through the lungs. The presence of carbon dioxide distends the abdomen increasing the difficulty of spontaneous breathing, thus increasing the need for mechanical ventilation and close monitoring of the patient as compared to traditional surgeries.
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1,134,039,614,514,905,600 | Alcohol
Web Resource Last Updated: 22-10-2020
Contents
Recommended amounts
Having diabetes does not mean that you need to completely avoid drinking alcohol. In fact, government guidelines for sensible drinking are the same whether you have diabetes or not.
• Men and women are advised not to regularly drink more than 14 units of alcohol a week.
• Pregnant women are advised that no level of alcohol intake is safe in pregnancy.
• If you drink as much as 14 units a week, it is advisable to spread this over three or more days. If you have one or two heavy drinking sessions each week, this can increase the risks to your health.
The following drinks all have 14 units of alcohol:
6 medium glasses of red wine (13% ABV)
• 6 pints of lager (4% ABV)
6 medium glasses of red wine (13% ABV)
• 6 medium glasses of red wine (13% ABV)
14 single shots of spirits (40% ABV) such as rum, whisky or vodka
• 14 single shots of spirits (40% ABV) such as rum, whisky or vodka
The risk of developing a range of illnesses, including high blood pressure and certain cancers, increases if you consistently drink more alcohol than the recommended amounts.
What is a unit of alcohol?
As alcoholic drinks come in different strengths and sizes, units are a good way to tell how strong your drink is.
One unit of alcohol is 10 ml or 8 g of pure alcohol. One unit is equal to the following:
• One single pub measure (25 ml) of spirits (40% ABV)
• One half-pint of normal-strength lager, beer or cider (3.5% ABV)
• One small glass (100 ml) of wine (10% ABV)
• One glass (50 ml) of liqueur, sherry or other fortified wine (20% ABV)
Table 1 below shows how many units of alcohol there are in some common drinks.
In recent years, the alcohol content of some drinks has increased, with many wines and beers now stronger than they once were. So remember that a drink may be stronger than you think. Remember too that many measures, particularly home measures, are larger than standard sizes.
A more accurate way of calculating units is by the percentage of alcohol by volume (ABV). This is the percentage of alcohol in one litre of the drink.
For example:
• A wine of 14% ABV has 14 units in a litre.
• If you drink 125 ml you have had 1.75 units.
• If you drink 250 ml you have had 3.5 units.
The effect of alcohol on blood glucose
Alcohol can both increase and decrease blood glucose levels. If you have a drink that contains carbohydrate, such as real ale, cider, alcopops, a liqueur or a dessert wine, it is likely that you will initially notice an increase in your blood glucose level.
If, however, you have a drink that does not contain carbohydrates, such as a gin and diet tonic, a vodka and diet Coke or a glass of red wine, you may not see any change in your blood glucose level.
Alcohol: risk of hypoglycameia
When alcohol is processed in the liver, it can contribute to a drop in blood glucose levels. This is because alcohol interferes with the normal release of stored glucose from the liver, and so blood glucose levels can fall, even if you eat extra carbohydrate.
It is important to be aware of this if your diabetes is managed by insulin or sulphonylurea drugs, e.g. Gliclazide, as this could result in low blood glucose, causing a hypoglycaemic episode (a ‘hypo’). The risk of hypoglycaemia can persist for a number of hours after drinking particularly if large amounts of alcohol have been consumed. This will not occur if your diabetes is managed through diet or other types of medication.
If you are concerned about the impact of alcohol on your blood glucose, speak with your diabetes care team who will be able to give you advice based on your personal circumstances.
Ways to prevent alcohol-related hypoglycaemia
There are a few general rules to help prevent hypos when you are drinking alcohol:
• Avoid drinking on an empty stomach.
• Eat regular carbohydrate-based snacks while you are drinking alcohol and before you go to bed.
• Monitor your blood glucose levels closely.
• Always have your hypo treatment with you and make sure you keep it next to your bed.
• Make sure that the people you are with know that you have diabetes and how alcohol affects your blood glucose
• Stick to the recommended daily units of alcohol.
• Alternate alcoholic drinks with sparkling water, sugar-free lime and soda, or diet drinks.
Watching your weight
Alcohol contains 7 calories per gram. These calories usually offer no nutritional value. If you are concerned about your weight, keep the following points in mind:
• Home measures tend to be more generous.
• Check that all mixers and soft drinks are sugar-free or diet varieties.
• Drink ordinary-strength beers, lagers and ciders. Low-alcohol varieties can be higher in sugar and low-sugar versions can be higher in alcohol.
• Alcoholic drinks with high sugar content, e.g. sweet sherry, dessert wines, liqueurs and alcopops, should be drunk only occasionally.
A pint of lager is equivalent in calories to a 40g portion of chocolate cake; a small glass of sweet white wine is equivalent to a 45g portion of Tiramisu
Look at Table 1 below to see the alcohol and calorie content of some common drinks.
Table 1: Alcohol and calorie content of common drinks
Drink
Alcohol units
Calories (kcal)
Carbohydrates (g) (approx)
25 ml spirit (40% ABV)
1 unit
56
0
50 ml liqueur (17% ABV)
1 unit
118
up to 20g
275 ml alcopop (5.5% ABV)
1.5 units
170
up to 40g
330 ml lager (5% ABV)
1.6 units
135
10 - 15g
175 ml wine (13% ABV)
2.3 units
166
0g (red)
0 - 3g (white)
750 ml bottle of wine (13% ABV)
10 units
712
0g (red)
0 - 30g (white)
125 ml champagne (12% ABV)
1 unit
86
0 - 10g (dry to sweet)
Note: Calories do not equal carbohydrates!
Regularly drinking more than is recommended can increase the risk of serious health problems including certain cancers, liver disease, stroke, high blood pressure and mental health disorders.
Useful resources
For more information on how drinking alcohol can affect your diabetes, click here
Drinkaware is an independent charity that has useful information on its website.
All images used are courtesy of Carbs & Cals.
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139,888,595,362,709,760 | fbpx
molecules of the month
Icenticaftor
mutant + WT CFTR Cl channel potentiator
oral 300 mg BID , Ph. II in COPD and CF
from 1M cmpd cell-based HTS + opt.
J. Med. Chem., May 24, 2021
Millenium/Takeda, Cambridge, MA
Icenticaftor
2 mins read
The Novartis mutant and WT CFTR potentiator, icenticaftor (QBW251), is an oral Ph. II clinical candidate for chronic obstructive pulmonary disease (COPD), which is anticipated to become the 3rd leading cause of death globally. The compound had positive proof of concept studies in both cystic fibrosis and COPD, and the advancement of a WT CFTR modulator into the large COPD indication is a significant development. Since there are not good PK/PD models for cystic fibrosis, the candidate was nominated based on in vitro properties and safety studies, but has shown target engagement in humans via biomarkers such as sweat chloride. This is a great medicinal chemistry case study as the starting point for icenticaftor was objectively unattractive, with furan, aniline, and ester…
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6,226,679,777,628,420,000 | How long after a vasectomy reversal can i have intercourse?
Can ejaculating too soon after vasectomy reversal damage it?
Having sex too early after vasectomy reversal can be very uncomfortable and painful. There is also the potential for serious complications, such as ruptures, infections, or increased pain. It’s best for patients to wait until they are well and take things slowly.
How long after a vasectomy reversal can you get pregnant?
It is possible for couples to get pregnant as soon as a few weeks after a vasectomy reversal while others can take up to two years.
How long should you wait before ejaculating after a vasectomy?
Wait at least 3 days before resuming sexual activities. You may resume sexual activities then if you are not having any discomfort, but having ejaculations too soon after a vasectomy may increase the chance of minor problems developing or rejoining the tubes. 3.
How long does it take for a vasectomy reversal to work?
Does a vasectomy reversal effect sperm quality? The sperm quality should return to normal 3 to 6 months following a reversal as it takes that long for the testicles to make new sperm. However, the count and the motility may be lower after reversal due to partial blockage or scarring.
Can vasectomy reversal cause birth defects?
Early study shows more chromosomal abnormalities in sperm after these procedures. WEDNESDAY, June 21, 2006 (HealthDay News) — Men who undergo vasectomy reversal may be at significantly higher risk of producing abnormal sperm and possibly even causing birth defects in children, a new study suggests.
How can I get pregnant without a vasectomy reversal?
People who have had vasectomies can still impregnate their partners through IVF, even without a vasectomy reversal. To achieve this, a person undergoes a sperm aspiration under anesthetic. During this procedure, a doctor directly retrieves sperm from the testis or epididymis using a needle.
We recommend reading: Often asked: How fast can a 125cc dirt bike go?
How painful is a vasectomy reversal?
About 50 out of 100 men say the pain after the reversal is like after their vasectomy. Another 25 out of 100 say the pain is less than after the vasectomy, and 25 out of 100 say it’s greater. Pain bad enough to need medications rarely lasts longer than a few days to a week.
How much does a reverse vasectomy cost?
The cost for a vasectomy reversal includes a fee for anesthesia, surgeon’s fee, and hospital fee. Overall costs can range anywhere from $7,000 to $9,000, depending on your insurance coverage.
How can I get pregnant if my husband had a vasectomy?
To be able to have children after a vasectomy you can undergo a vasectomy reversal or try In vitro fertilization (IVF) and intra-cytoplasmic sperm injection (ICIS) using aspirated sperm.
Does ejaculating after a vasectomy hurt?
Your semen quality, amount, and texture won’t change noticeably after a vasectomy. The sensation of ejaculation during an orgasm shouldn’t feel any different at all. You may find that your first few ejaculations after the procedure are uncomfortable. This discomfort will diminish over time.
Does sperm taste different after vasectomy?
The fact is that noticeable differences are rarely reported. This is because only 3% of the volume of a man’s ejaculate is made up of sperm. So your ejaculate will smell, taste and look the same as before your vasectomy. And no, you will not lose your sexual function!
How many times should a man release sperm in a week?
A 2018 analysis of multiple studies by Chinese researchers found that moderate ejaculation of around 2 to 4 times a week was associated with a lower risk of prostate cancer — but that the risk did not decline by ejaculating more often than that.
We recommend reading: Often asked: How long can i take ibuprofen 800mg?
Is it difficult to reverse a vasectomy?
Vasectomy reversal is more difficult than a vasectomy and is usually done using microsurgery, in which a surgeon uses a powerful surgical microscope to magnify the vas deferens as much as 40 times its size. This type of surgery requires specialized skills and expertise.
Why do vasectomy reversals fail?
Advanced maternal age is a common reason for vasectomy reversal failure. 2. A man without prior paternity before vasectomy may have abnormal sperm quality before the vasectomy. This could be a reason why semen quality after vasectomy reversal surgery is low and a reason for pregnancy failure.
How often do vasectomies fail?
One of the most significant pros of a vasectomy is that a vasectomy is a very effective and permanent form of birth control. Only one to two in 1,000 men have a vasectomy that fails. This usually happens in the first year following the procedure.
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3,123,941,863,465,118,000 | Tuesday, September 21, 2021
General
Spinal And Processes Body Functions
Spinal is mostly brought on by wear-and-tear modifications within the spine related to aging. In extreme instances of spinal cells on the injury space and, more importantly, by modifications molecules that repress the translation of target mRNA. To grasp the mechanisms underlying gene alterations following SCI, we analyzed the microRNA expression patterns at different time factors following rat spinal cord damage. Start by mendacity on your stomach, together with your toes hips distance apart.
If find more information doing the plank in your forearms, attempt to maintain your forearms utterly parallel (like train tracks). Now flex your feet so your toes are braced towards the flooring and your heels are pointing toward the ceiling. Lift your torso and legs off the flooring so you are supporting your weight with solely your forearms and toes. Try to keep your tailbone slightly tucked to prevent your back from arching.
If you happen to discover that you’re starting to feel any ache in the lower again or you might be getting drained, you can place your knees on the flooring for assist. Try to hold for 60 seconds and remember to keep drawing your belly button in. The spinal system in our physique are present the totally different course of carried out with train and common maintenance of yoga tips and one other means of services is considered one of an important maintain the part of physique which is completed body. It has a large impact on the way the rest of our physique functions.
Therefore, this can be very and approach of one other manner of therapy which is give the right manner of health and outcomes important to maintain work on energy with the muscles across the spine so as to maintain your body wholesome. Different approach of body remedy companies with muscles, and the core of your body, is one among the primary steps in the direction of improving the health of your spine. You can think of the “well being” of your spine by thinking of your posture.
As in every part else, persistence and perseverance will additional you to your targets in a more effective approach instead of rushing issues. Once you are able to stroll a few steps in a gradual method, try utilizing different muscles of your body. Move your trunk, bend your knees a bit, transfer as in the event you have been going to jump, get the feeling of floating.
The concept is to be relaxed on the slackline and walk like a feline would, that’s to say, in a graceful and relaxed manner. Don’t overlook to breathe! Breathing deeply while slacklining helps so much, similar to yoga. Make it a meditative follow and take a deep breath, stroll a couple of steps, then exhale fully.
However, don’t get tense trying to carry the air in your lungs. just click the next site ought to really feel natural and relaxed. Take breaks from time to time. Slacklining makes use of muscles that most individuals don’t use. Once your legs and arms get drained, take a break and then start once more. Highly recommended Resource site may additionally really feel some type of psychological exhaustion after you try slacklining for a couple of hours.
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714.533.9920
Can Eyes Change Color?
Have you ever noticed a change in your eye color? Did they appear darker brown one day and look lighter the next morning? Eye color is an intriguing phenomenon. However, when one’s eyes suddenly change color, or even gradually over some time, the intriguing wonder that is the color of the human eye becomes even more fascinating.
How does the color of your eyes change? And where does eye color even come from? Do outside factors determine the color of your eyes? Or do color changes just happen naturally? The information below provides detailed answers to these questions. In addition, it will explain a few other important factors about eye color.
How Does the Color of the Eye Develop?
For a long time, most people believed they could predict their child’s eye color by looking at their grandparents’ and parents’ eye color. Grounded on the belief that blue eyes are recessive and brown ones are a dominant trait, one could get a rough idea of their kid’s eye color.
Today, we know that determining eye color is more complex than just looking at the grandparents’ and parents’ eyes. While genetics does have an important role to play in all this, eye color is not determined by a single gene. Several genes take part in helping determine the color of your eyes.
A person’s eye color is determined by the distribution and amount of melanin in their irises. Blue eyes have less melanin than brown, and there are a lot of different color shades in between. Darker-colored eyes often tend to be more dominant. However, as different genes come into play, darker colors do not always win.
A baby is likely to have blue eyes right after birth. They have this eye color because they still lack enough melanin in their system. However, once they get exposed to light, their bodies will start to produce more melanin which will, in turn, change the color of their skin, hair and, of course, eyes.
So, while two people with brown eyes have a higher chance of producing a brown-eyed child, the result is not guaranteed.
Roughly half of the United States population have brown eyes. In addition, it is also an eye color that is prevalent in places with warm climates.
Blue-eyed people lack melanin in their stroma, the iris’ front layer. This lack of pigment causes light rays to scatter once they hit the eye, giving the irises a blue appearance.
Can the Color of Your Eyes Change?
The color of a person’s eyes can change in infancy. Most children are born with blue eyes, but the color gradually changes as they develop melanin in the stroma. After the first birthday is when a child’s eye color becomes permanent.
Besides this, it is rare for the color of one’s eyes to change. They may look like they changed color when their pupils shrink or dilate, but this happens because the color pigments in the iris spread apart or come together.
In some scenarios, the color of the eyes can slightly darken during pregnancy or puberty or as one reaches their senior years. If not, you need to consider the possibility of an underlying medical condition tampering with your eye color.
Health Conditions That Affect Eye Color
Sometimes, health complications can change or affect a person’s eye color. Some of these health problems include:
• Trauma- Any eye trauma or injury can damage the iris. Any tissue loss can also change the color of your eyes.
• Neurofibromatosis- This condition affects the body’s nervous system. It can result in tiny tumors growing on nerve cells all over the body. Additionally, it can cause small nodules to appear in the iris. These are Lisch nodules and generally harmless growths. While they will not affect one’s vision, they can change their eye color.
• Fuchs’ heterochromic iridocyclitis- Also commonly referred to as FHI, this health complication is a kind of chronic uveitis. It can cause atrophy of your cataracts, iris and eye inflammation. This medical issue can also lead to the loss of pigment, resulting in a change of eye color, leading to heterochromia.
• Uveitis- Uveitis is a group of inflammatory infections and diseases that cause the eyes to swell. It can affect one’s vision and even result in permanent blindness. You might also notice a few color changes in the affected eye.
• Cataracts- Cataracts are the clouding of the lenses of the eyes, which are found behind the pupils. While a cataract does not directly affect the iris, it can change the eye color appearance of the affected eye, making it look milky or cloudy. Cataracts can affect vision and change the color of one’s eyes. However, they are more common in older people.
• Horner’s Syndrome- This is a rare medical condition that might occur because of a spinal cord injury or a stroke that damages a person’s facial nerves. Signs and symptoms include eyelid drooping, pupil constriction, and not being able to sweat on one side of your face. It can also cause iris depigmentation, which results in eye color change.
The Takeaway
According to eye specialists, the color of one’s eyes does not just change on their own. Instead, there are multiple external factors, as well as genetics, that determine how eye color appears.
Therefore, unless you have noticed sudden, drastic changes in the eyes, there is nothing you need to worry about.
However, if there has been a sudden and extreme change in your eye color, you need to consult an eye specialist as soon as possible. This rapid color change might signify something more severe that only a physician can diagnose, manage and treat.
Our establishment has qualified specialists who can accurately determine what is causing your eye color change. From young babies to seniors, we treat them all. Therefore, if you notice a sudden change in eye color, do not hesitate to visit our establishment for immediate assistance.
We offer diagnoses, and treatments, including eye surgeries that improve and preserve your vision. Get in touch today. | {
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7,814,196,545,159,944,000 | Food and Behaviour Research
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Is there an association between the consumption of ultra-processed food and adverse microbiota-gut-brain axis implications?
By Bhavana Kunkalikar
Icecream
Ultra-processed food may impact gut microbiota, potentially causing metabolic imbalances and inflammation, increasing the likelihood of disrupting the neural network.
FAB RESEARCH COMMENT:
So-called 'ultra-processed' foods (UPF) - made from highly refined and processed ingredients, and containing many artificial additives - now make up the majority of modern diets in the UK, US and some other developed countries.
High consumption of these foods is associated with, and also predicts, higher rates of almost all chronic physical health conditions (such as Type 2 diabetes, cardiovascular disease and immune disorders), as well as mental health problems including depression and anxiety. Randomised controlled trials have also shown that nutritionally matched diets made up of UPF vs minimally processed foods increase appetite and weight gain.
Determining precise mechanisms by which UPF may have negative effects on health remains a challenge - not least because there are so many possibilities.
However, this review outlines a number of ways in which features of UPF - and particularly the artificial additives that these contain - can damage gut health, by causing inflammation and disturbing gut microbial balance.
For details of this research, please see:
For further information please see:
25/04/2023 - News Medical Life Sciences
In a recent study published in the Food Research International Journal, researchers reviewed the impact of ultra-processed foods (UPFs) on the microbiota-gut-brain axis.
Background
Focus on nutrient recommendations and dietary patterns has increased due to the rise of non-communicable chronic diseases in recent years. Identifying the dietary approaches that are advantageous or disadvantageous to personal well-being is, therefore, key.
The composition and function of the gut can be influenced by diet. The gut microbiota produces metabolites that can affect brain functions, either directly or indirectly, by digesting and fermenting food.
Exposure to UPF may impact gut microbiota, potentially causing metabolic imbalances and inflammation, increasing the likelihood of disrupting the neural network.
The impact of ultra-processed food ingredients on the gut-brain axis
High sugar
Sugar affects the brain regions responsible for controlling appetite and eating habits. The hypothalamic neurons receive signals from the gastrointestinal tract and peripheral systems to monitor energy balance, while eating behaviors are driven by the motivation system/dopamine reward.
Sugar consumption triggers the mesolimbic dopamine reward system, leading to the release of opioids and dopamine, which induces pleasure feelings.
High consumption of sugary foods can cause functional changes that may lead to metabolic disorders and overeating. This can result in an increased desire for high-sugar foods and consuming more energy than necessary. Sugar cravings can also originate from the gut.
A recent study found that sugar triggers neurons in the brainstem and the vagal ganglia through the gut-brain axis, leading to an affinity for sugar and highlighting the gut's importance in sugar signaling.
High-and low-fat
Ultra-processed food is typically high in energy density and contains saturated and trans fats, which can negatively impact the gut and the brain. Research has shown that a high-fat diet (HFD) consumed over a long period can negatively affect both brain and gut function.
Lipid oxidation products are present in foods that undergo extensive thermal processing or contain high pro-oxidant levels. Lipid oxidation products can pass through the gut barrier and cause gut inflammation and neuronal membrane damage, even if the plasma does not absorb them.
Long-term high-fat diet intake leads to inflammation in both the gut and brain, resulting in memory impairment and behaviors resembling anxiety and depression. Altered gut microbiota, specifically the depletion of Akkermansia muciniphila, is associated with cognitive function impairment.
The HFD microbiota transplantation results in memory and learning deficits dependent on the hippocampus. However, treating Akkermansia muciniphila orally can reduce neuroinflammation in the hippocampus and improve memory and learning.
High salt
Dityrosine, an oxidized protein product found in high salt, can cause intestinal oxidative damage and inflammation leading to tissue damage. Dityrosine increases oxidative stress in the brain, resulting in neurotransmitter disorders and impaired learning and memory abilities.
High-salt diet-induced memory impairment is linked to oxidative stress or synaptic protein disorder. The study found that mice fed a high-salt diet for eight weeks experienced impaired memory abilities and learning.
Additionally, the abundance of certain bacteria increased while others decreased in these mice.
Food additives
Emulsifiers
Studies have shown that, aside from lecithin, the most commonly utilized dietary emulsifiers negatively affect the gut microbiota.
Several substances, including P80, glycerol monolaurate, and carrageenan, have been found to impact the composition and diversity of the microbiota and harm epithelial functions.
This can lead to the onset of obesity/metabolic syndrome and intestinal inflammation. The human body's critical micelle concentration (CMC) improved postprandial abdominal discomfort and a change in the fecal metabolome's free amino acids and short-chain fatty acids (SCFAs).
Sweeteners
Sweeteners are sugar alternatives with a sweet flavor and are typically poorly absorbed by the body. The popularity of non-nutritive sweeteners (NNS) or non-calorie artificial sweeteners (NAS) is increasing due to their low-calorie content, cost-effectiveness, and ability to regulate blood sugar levels.
Consuming sweeteners can impact how humans perceive sweetness and affect the decision to choose healthy whole foods. NAS may cause glucose intolerance by altering the composition and function of the gut microbiota.
Studies in humans have found that consuming NAS over a long period may lead to an increased risk of type 2 diabetes and weight gain.
Food preservatives
Bacteriostatic antiseptic agents have been found to impact gut microbiota composition in both in vitro and in vivo studies. This sheds light on the safety of food preservatives. The immune system of zebrafish is impacted by potassium sorbate (PS) exposure, which changes the microbiota content and metabolism.
Sulfites have been found to hinder the growth of four beneficial bacteria strains, including Streptococcus thermophilus, Lactobacillus rhamnosus, Lactobacillus casei, and Lactobacillus plantarum.
Conclusion
The study findings highlighted how UPF could disturb the gut microbiota, leading to metabolism dysbiosis, inflammation, and impaired brain function through the MGB axis.
Future studies could focus on observing intestinal health to understand the underlying mechanism better. Future research should focus on species-level changes and their corresponding metabolic functions. | {
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7,533,436,226,482,562,000 | Dr. Alex Jimenez, El Paso's Chiropractor
I hope you have enjoyed our blog posts on various health, nutritional and injury related topics. Please don't hesitate in calling us or myself if you have questions when the need to seek care arises. Call the office or myself. Office 915-850-0900 - Cell 915-540-8444 Great Regards. Dr. J
Apoptosis in Neurological Diseases
Neural cell death can occur both during the development and throughout the pathophysiology of the nervous system. Two different types of cell death, known as necrosis and apoptosis, are involved in pathological neuronal loss, however, apoptosis is the process of programmed cell death during development. All types of cells will go through apoptosis. This mechanism controls neuronal growth where an excess of neurons is produced and only those which form connections with the target structures will receive enough survival factors. The remaining neurons will then ultimately go through death and removal.
Apoptosis continues throughout life and it is the main process involved in the elimination of surplus, unwanted, damaged or aged cells. Dysregulation of apoptosis is demonstrated after damage or injury as well as in neurodegeneration and in tumorigenesis. Treatment approaches which influence the apoptotic pathway offer valuable therapeutic options in a wide variety of pathological states. The purpose of the article is to describe the significance of apoptosis in neurological diseases.
What is Apoptosis?
Apoptosis is the well-conserved and highly controlled process of cell death involved in the removal of unnecessary, surplus, aged or damaged cells. Dysregulation of apoptosis can ultimately develop mutated cells which can result in malformations, autoimmune diseases, and even cancer. Abnormal apoptosis can also result in the elimination of healthy cells which can occur in health issues such as infection, hypoxic-ischaemic injury, neurodegenerative or neuromuscular diseases, and AIDS.
Apoptosis is different from necrotic cell death. In necrosis, cell death is caused by an external factor and involves the early loss of tissue, damage to organs, and the leakage of cytoplasmic contents, leading to the recruitment of phagocytes which can cause an acute inflammatory reaction. In contrast, apoptosis is often considered cell suicide. According to research studies, cells which die due to apoptosis retain membrane and organelle structure and function until late in the process while still developing plasma membrane blebbing, reduced cytoplasmic volume, chromatin condensation, and nuclear fragmentation.
In the final phases, cell fragments wrapped in plasma membrane pull away as apoptotic bodies which are then phagocytosed by healthy cells. The removal of cell debris also occurs in the absence of an inflammatory response, and this silent, quick, and efficient elimination of apoptotic cells mean that apoptosis can be difficult to find in cells. However, as many as 50 percent of the cells in developing adulthood may go through apoptosis where less than 1 percent of cells are apoptotic at any one time.
Apoptosis in the Nervous System
Programmed cell death by apoptosis occurs in several developmental processes, such as body sculpting and removal of self-reacting resistant cells as well as sexual organ growth and gamete formation. The general principle of growth in multicellular organisms involves the development of excess numbers of cells, where the excess or unwanted cells are then removed by apoptosis through the development of functional organs. In the developing nervous system, apoptosis has been demonstrated to occur in neural tube formation and continues throughout terminal differentiation of the neural system.
A growing number of neurotrophic factors, such as nerve growth factor family, including both the neurokines and development factors like insulin-like growth variables (IGF-I and IGF-II), encourage the survival of several types of neurons. Targeted disruption of genes encoding these factors or their receptors demonstrate that neurotrophic factors are significant for the development of specific neuronal populations. Neurotrophic factors function by binding to specific receptors in the cell membrane. Moreover, the effects of NGF offer a good illustration of the subtle command the system permits.
The nerve growth factor receptor has high and low affinity components. It will function as a survival factor if it binds to the high-affinity trkA receptor but it will also cause apoptosis of retinal neurons or oligodendrocytes once it binds to the low-affinity receptor p75 in the absence of trkA. Nerve growth factor in the extracellular environment is consequently able to control neural development by both boosting the growth of several types of cells as well as the removal of other cells.
In some cases, however, concentrated genetic disruption of neurotrophic factors or their receptors may leave the central nervous system seemingly unaffected, demonstrating that these variables can ultimately become biased. According to research studies, it has now become evident that the control of neuronal survival does not only depend on the supply of trophic molecules by the targets but also on activity, humoral factors, and trophic support from glia or glial cells.
Furthermore, neurons don’t simply undergo programmed cell death during differentiation. Apoptosis appears to regulate cell numbers in systems as diverse as the disappearance of the germinal layer during the third trimester of pregnancy, the sexual differentiation of the medial preoptic nucleus where apoptosis is controlled by testosterone, lineages throughout the olfactory epithelium, oligodendrocyte development in the optic nerve, and the development of Schwann cells in the peripheral nervous system. Programmed cell death occurs in a variety of other processes in the developing nervous system.
Apoptosis in Nervous System Injuries & Diseases
Although apoptosis is a fundamental process involved in the developing nervous system, apoptosis can ultimately be involved in a variety of nervous system injuries and diseases. In most cases, the connection between a specific mutation or trauma as well as the activation of apoptotic cascades remains evasive. An overview of a developing list of neurological diseases in which apoptosis has been implicated as a significant pathological mechanism is provided below.
Neuronal Injury
Cerebral hypoxic-ischaemic injury is a cause of neurological injury and death. Magnetic resonance spectroscopy studies have demonstrated that transient hypoxia-ischemia contributes to a biphasic disturbance of cerebral energy metabolism. Related to the biphasic energy collapse, two waves of cell death appear to follow hypoxic-ischaemic injury in the developing brain. Immediate neuronal death is most likely due to necrosis resulting from the accumulation of calcium ions.
Delayed cell death caused by hypoxic-ischemic injury appears to involve further mechanisms with increasing data which demonstrates that in the delayed phase, cell death occurs by apoptosis. The amount of apoptosis is directly associated with the magnitude of ATP depletion during hypoxia-ischemia. Apoptosis can occur in the brains of newborn babies following birth asphyxia and sudden intrauterine death. Apoptosis can also be notable in white matter injury in newborn babies.
Apoptosis may continue for months after an hypoxic-ischaemic injury due to constant changes in cerebral energy metabolism in infants during the months after birth asphyxia. Following focal neural injury, apoptosis has been discovered in remote regions from the initial damage. After severe spinal cord injury in reptiles, apoptosis of oligodendrocytes occurs in distant degenerating fiber tracts and after forebrain injury in rats, apoptosis was demonstrated in the cerebellum.
The apoptotic loss of oligodendrocytes could consequently be a potential source of secondary demyelination in paraplegia and in the chronic degeneration related to multiple sclerosis. Further research studies must be performed in order to provide further evidence on the role of apoptosis in this type of injury which begins from the report of which Bcl-2 expression boosts the growth and regeneration of retinal axons. Apoptosis in neuronal injury can be demonstrated in a variety of ways.
Neural Cancers
A connection between apoptosis and the cell cycle is demonstrated in carcinogenesis where proto-oncogenes, such as c-fos, c-jun, and c-myc, can activate apoptosis and promote cell division while inactivation of the pro-apoptotic p53 tumor suppressor gene is a frequent mark of human neoplasia. By way of instance, in a number of gliomas, the reduction of wild p53 activity was connected to tumor progression, possibly leading to resistance to chemotherapy and radiotherapy.
Although there have been reports of Bcl-2 overexpression in glioma cell lines, the correlation between the anti-apoptotic effect of this gene and malignancy is not yet clear. However, a homolog of Bcl-2, the brain associated apoptosis gene (BRAG-1), is found predominantly in the brain, and it is upregulated in human gliomas as a rearranged transcript. As demonstrated above, the process of apoptosis can also be significant in the development of neural cancers, according to research studies.
Infectious Disease
Apoptosis may play a role in HIV encephalopathy. In the brain, the virus reproduces primarily in microglia which it enters through the CD4 receptor. Although the activation of microglia is believed to be the main reason for adrenal loss and demyelination, neurons die by apoptosis in HIV encephalopathies because of HIV mediated alterations in astrocyte function and aberrant stimulation of NMDA receptors or due to nitric oxide from the activation of inducible nitric oxide synthase.
In subacute sclerosing panencephalitis, widespread apoptotic death was demonstrated to develop in the brain, although no correlation was observed between viral load, lymphocyte infiltration, and the number of apoptotic cells. DNA fragmentation indicative of apoptosis was detected in scrapie-infected sheep and mice brains, suggesting a function associated with cell death in spongiform encephalopathies. Apoptosis may also ultimately be involved in another infectious disease.
Neurodegeneration
Spinal muscular atrophy is associated with mutations in the survival of motor neuron and neuronal apoptosis inhibitory protein (NAIP) enzymes. NAIP is closely related to the baculovirus inhibitor of apoptosis protein and inhibits apoptosis in many cell types. This implies that mutations in NAIP could deregulate apoptosis in spinal motor nerves, causing their death. Recent studies emphasize the importance of anti-apoptotic genes in cerebral protection which can rescue neurons.
Apoptosis has also been implicated in retinal dystrophies such as retinitis pigmentosa. In this case, apoptosis results from mutations in the three photoreceptor genes, rhodopsin, peripherin, and the β-subunit of cyclic guanosine monophosphate di esterase, resulting in photoreceptor degeneration. The absence of c-fos prevents apoptosis in those cells is unknown. Moreover, defined neurotrophins and growth factors injected intraocularly in animal models of retinal degeneration improve photoreceptor survival, suggesting that the apoptotic cascade can be obstructed by supplying exogenous survival signs.
The mutation underlying Huntington’s disease is an expanded trinucleotide which is fundamental for normal development and can be regarded as a cell survival gene. Transgenic models demonstrated increased apoptosis in the neurons of an embryonic neuroectoderm. During apoptosis, caspase-3 (apopain) is improved by a gain of function associated with the triplet expansion. This is supported by the overexpression of specific trinucleotide repeats in transgenic mice.
Most cerebellar ataxias are associated with neuronal loss. Ataxia-telangiectasia, caused by mutations in the ATM gene, is considered to have an apoptotic component. ATM shares extensive and significant homology with the DNA dependent protein kinases involved in DNA damage responses at different cell cycle checkpoints and is downregulated in most patients with ataxia-telangiectasia. The simple fact that inappropriate p53 mediated apoptosis is the major cause of death in ataxia-telangiectasia cells suggests that the mutation causes improper triggering of apoptosis by otherwise non-lethal DNA injury.
From the familial form of amyotrophic lateral sclerosis gain of function, mutations in the gene encoding copper-zinc superoxide dismutase (sod-1) develop a dominant pro-apoptotic sign. Although cell harm by the accumulation of free radicals can trigger apoptosis, these mutants can induce apoptosis both in nerve cells in culture and in transgenic mice. Mental retardation in Down’s syndrome has also been associated with abnormal apoptosis. Although cortical neurons from fetal Down’s syndrome brains are different, they then degenerate and undergo apoptosis, according to research studies.
Degeneration is blocked by treatment with free radical scavengers, suggesting that a defect in the metabolism of reactive oxygen species is the trigger for apoptosis. In Parkinson’s disease, the death of dopaminergic neurons in the substantia nigra was demonstrated to occur through apoptosis and may be obstructed by delivery of glial-derived neurotrophic factor. Alzheimer’s disease is associated with the progressive accumulation of β-amyloid protein which is the fundamental component of neural plaques. The β-amyloid peptide can cause neurons to undergo apoptosis in vitro research studies.
Inherited Metabolic Disease
Furthermore, few data suggest that the acute encephalopathy associated with maple syrup urine disease is because of the induction of apoptosis by an accumulating metabolite of leucine, α-keto isocaproic acid. This compound is a potent inducer of apoptosis in central nervous system glial cells and the result is significantly enhanced in the presence of leucine. Phenylalanine and leucine do not induce apoptosis in this system, suggesting that this result is ultimately unique.
There are two ways in which a cell can die, necrosis and apoptosis. While necrosis occurs due to an external factor which harms the cell, apoptosis follows a controlled, predictable routine. Apoptosis is generally known as programmed cell death. Apoptosis, or programmed cell death, has many fundamental functions in the developing structures of the human body, however, research studies have demonstrated that abnormal apoptosis can be associated with the development of a variety of neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Diet and Exercise for Neurological Disease
The purpose of the article above is to discuss the process of apoptosis, or cell death, in neurodegenerative diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
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Dental Implant Reviews Tijuana
How Can I Avoid Dental Implants?
There are a variety of alternative tooth restoration methods that are less expensive and do not require implants. Although these techniques can help restore lost tooth volume but they can only offer an interim solution. In addition, they could cause more harm than good, like damage to the enamel of the teeth and gum disease that leads to loose teeth and cavities. Fortunately, proper regenerative care can help restore gum health and avoid the need for dental implants.
Sugary foods
When it regards dental implants it is essential to avoid eating drinks and foods high in sugar. They can cause damage to the implants as well as your natural teeth. Also, you should avoid certain sauces, such those used on your steak. Drink plenty of water instead to keep your mouth clean and hydrated.
Candies and sweets with sugar are likely to adhere to the surface of the implant and cause it to fail, resulting in an infection. After undergoing dental implant surgery, it’s crucial to avoid eating sweet foods as well as hard food. They can cause mouth irritation which could lead to an unfavorable situation.
If you’re wondering about the foods to avoid after dental implants, consult your dentist. He or she can provide more information. You can even get an appointment for free. By calling your Cumberland dentist, you can ask about post-implant treatment. Additionally, your dentist may have some suggestions to prevent infections that can occur after dental implants.
It is important to avoid eating sticky, hard or acidic food items following dental implant surgery. All of these can disrupt the healing process of implants. Hot and acidic foods can also influence the healing process of soft tissue around the implant. After recovering from dental surgery, it is essential to stay clear of soda and other beverages that contain sugar. Those foods contain sugar and can lead to further complications.
It’s okay to indulge in soft, chewy foods however it is important not to consume too much sugar. These include muffins, cakes, as well as pies. Although they may seem innocent at first, they could cause damage to your dental implant. To avoid this from happening, you must clean your teeth frequently.
Smoking
While dental implants are extremely effective for improving dental function, smoking can negatively impact the effectiveness of dental implants. Combining smoking and dental implant treatment can increase the risk of failure. Dental Associates of New England can help you understand the risks and complications of dental implants treatment. This guide explains the reasons why smoking should be avoided by patients who undergo dental implant therapy.
Stop smoking cigarettes if considering dental implants. Smoking restricts blood flow and increases the chance of complications. Stop smoking for a minimum of two months and quit smoking one week prior to the surgery. This will allow your body to heal quicker and allow for the initial stages of the process of osseointegration.
Smoking also affects the immune system, which makes implants less secure. Additionally, smoking affects the tissues in the mouth like the gums and teeth. This can lead to tooth decay and stains on your teeth. It could also cause gum disease, and increase the chances of implant failure.
Smokers also have a higher risk of developing peri-implantitis. It is caused by the accumulation of bacteria around the implant’s base. It causes irritation to the gums as well as the bone around the implant, which weakens the osseointegration bonds. Implants that are dental may fail due to bone loss.
If you are considering having dental implants, it is crucial to quit smoking cigarettes as soon as you can. While it’s not always feasible to completely quit smoking the best option is to cut down on the amount of cigarettes you smoke. Smoking less cigarettes will greatly enhance the efficacy of dental implants, and will also boost your overall health.
High-intensity exercise
Although dental implants have an success rate of 95% percent, they carry certain dangers. They could result in the implant failing. These risks can be minimized by a dentist who makes recommendations before dental implant surgery. Patients should stay away from vigorous exercise for a minimum of 48 hours following surgery and should avoid vigorous movements. Also, they should make sure to rest more and avoid heavy lifting for a minimum of a week.
Although it is tempting to workout immediately after waking up after receiving dental implants, a high-intensity exercise routine could increase blood flow to the surgical site which could cause a delay in the healing process. Patients should consult their dentist to determine when they are permitted to exercise or engage in other strenuous activities. Each patient’s healing process will be different, and some may be able to exercise in just a few days, whereas others might need to wait several weeks or even months. Patients must listen to their bodies and stay away from exercise until their dentist has cleared them.
While physical activity and exercise are essential to a person’s overall health However, many people might not be aware of the potential dental dangers involved. Exercise that is intense should be restricted to the duration of a couple of hours per week. During this time, patients should avoid eating snacks with high sugar content. Additionally, they should continue brushing their teeth after consuming sugary snacks.
Gum disease
Gum disease can be prevented in numerous ways. One of them is proper dental hygiene. This will help you avoid the swelling, red, and bleeding gums that can happen after dental implants. Keeping your gums healthy is crucial to protect the implants as well as your remaining teeth. It will preserve your new teeth for years to come.
Brushing your teeth after each meal is a great method to remove food particles as well as plaque. It is also important to floss regularly to remove food particles and plaque from between your teeth. Regular visits to the dentist are suggested to keep your teeth in good condition. During these visits, your dentist may recommend a procedure referred to as a scale-and-polish. This procedure is designed to remove plaque and food particles from the gumline. Gum disease can also be caused by smoking, so it is important that you quit smoking before you get dental implants.
In addition to regular dental hygiene It is also important to visit a periodontist in order to ensure that your mouth is healthy enough to be able to receive implants. While most dentists are trained to treat periodontal diseases however, not all of them are qualified. It is possible to stop the disease from getting worse and to help patients get implants.
Gum disease can lead to serious issues. Gum disease may lead to tooth loss. If not treated the condition could cause an infections of implants and cause significant damage.
Smoking can interfere with healing.
Smoking cigarettes can hinder the healing process of dental implants. This is because nicotine blocks the gums from receiving oxygenated blood, which is necessary for the growth of cells and for repair. This can cause a significant delay in the healing process and eventually affect the performance of dental implants. Gum disease can also be caused by smoking cigarettes.
It is vital to be honest about your smoking habits with your dentist. Smoking is a leading cause of death and illness in the UK. About 78,000 people die each year due to smoking-related diseases. Many more suffer from smoking-related illnesses like stroke, heart disease, pneumonia, and many other cancers.
While some people can have dental implant surgery, others shouldn’t smoke for at minimum one week before the procedure. It is essential to follow the directions of your dentist during the time of recovery. This includes limiting your eating habits, smoking, drinking, and alcohol consumption. In addition to this, you should limit your consumption of caffeine, alcohol, and nicotine, as these can interfere with the healing process.
Smoke from cigarettes can cause irritation to the oral tissues and damages salivary glands. The absence of saliva will weaken the gums and bone which support dental implants. Nicotine also reduces blood flow to the area. Without enough blood flow and oxygenation these tissues will not be able to heal. The immune system is also affected by smoking cigarettes.
There are many reasons that smoking cigarettes may hinder the healing process of dental implants. Tobacco smoke, for example reduces the amount of oxygen in the bloodstream, which is vital for the growth of bone. It also weakens the immune system, making it difficult for gums and teeth to heal properly. | {
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-677,659,568,400,507,600 | Foodborne poisoning is a health problem and occurs in people who consume contaminated food and drink. Scientists discovered around 200 pathogens that can cause a foodborne disease. Unfortunately, 76 million people develop a foodborne disease annually. Many of them end up in the hospital and is estimated that a few thousands of these people die because of contaminated food or drink. To avoid getting sick, people can be more careful with their personal hygiene, the way they handle and prepare the food.
Food Poisoning
Different foodborne diseases can be caused by parasites, toxins, bacteria, and viruses. Specialists are doing their best to investigate the foodborne diseases, but in more than half of the cases they don’t have an answer. They cannot find the source of the contamination. In many cases, the cause of the foodborne disease was a virus. A virus has a short life. That doesn’t give too much time to doctors to examine its nature and to come to a satisfactory conclusion. Another cause of a foodborne disease is bacteria. Scientists conducted many studies about different types of bacteria.
The first outbreaks of foodborne diseases were caused by home-canned foods and contaminated foods that people consumed during a picnic. Doctors could help the people faster because the cause was Clostridium or Staphylococcus. Nowadays, people tend to dine outside the home (restaurants, bistros, bars, etc.), and they travel all around the world. This is the reason why the majority of the foodborne diseases occur now from external sources, and most of the time is difficult to find the contaminated source: people eat in many places, where food is handled by many people as well.
The new technology can produce food for hundreds or thousands of people. It is much easier to get sick than it was back in the days. When a person decides to travel should consider boiling, peeling and cooking of food products bought in a foreign land. Even innocent food gifts from other countries can sometimes expose people to food or drink contamination. Ships traveling from one port to another and carrying international food shipments can also be a source of contamination.
People started consuming imported food because they wanted to consume some foods when they were not in season. But the way these foods are produced and harvested is not always a controlled and supervised one. When the producers use raw manure to fertilize the soil, they can also contaminate the products. It is vital for these imported food products to be cleaned properly, and the vegetables and the fruits to be washed several times.
People who like ethnic food should be careful as well. The African American dish called chitterlings (cooked swine intestines) represents a danger to the health if it is cooked improperly. Many kids got sick with Yersinia enterocolitis because they consumed this food. People can get sick with listeriosis if they consume contaminated fresh cheese made from unpasteurized milk.[1]
Foodborne diseases are more common among very young children or older people. They can also affect people with a compromised immune system and pregnant women.
It seems like almost any food can cause a foodborne disease. Some foods are more likely to cause specific foodborne illnesses such as:
• Salmonella can be caused by poultry and eggs
• Campylobacter can be caused by chicken and unpasteurized milk
• STEC O157:H7 is caused by ground beef. When a steak that is needle-tenderized, there is the risk of exposing the center of the meat to harmful organisms. If the steak is not thoroughly cooked (which in many cases it is not), the microorganisms can survive and be responsible for causing a foodborne disease.
Water is an important source that can cause a foodborne illness. It can be contaminated with bacteria, viruses, chemicals, and parasites. Water can be contaminated during a natural disaster or when is poor sanitation. It seems like in water can survive many viruses such as caliciviruses, rotaviruses, astrovirus, enteric adenovirus and hepatitis A virus. Be careful if you go on a cruise ship. Many people got sick with gastroenteritis while being aboard. The illness was caused by different noroviruses. The most common pathogens agents involved are Shigella, Salmonella, E. coli, and Vibrio. Other parasitic organisms that can survive in water and contaminate it are Cryptosporidium and Giardia lamblia. People with a weak immune system should be careful when choosing the source of the water they drink.
Foodborne diseases have different periods of incubation:
• very brief (caused by toxins contained by staphylococcal or bacillus-contaminated food)
• short (24-48 hours), they have viral causes
• intermediate (1-5 days), they have bacterial causes
• long (more than 5 days), they have parasitic sources
What are the most common foodborne diseases?
• Botulism
• E. coli
• Trichinosis
• Campylobacter
• Listeria
• Mad cow
• Staph
• Norovirus
• Ptomaine poisoning
• Salmonella
Botulism
Everybody knows that botulism has other causes besides food. But a high percentage of all the reported cases of botulism had a contaminated food source.
Clostridium botulinum is the bacteria responsible for botulism disease. These bacteria live in the soil, with little or no oxygen at all. Many people who canned the food at home got sick with botulism. Some of these people experienced paralytic issues as well.
Symptoms of botulism:
• droopy eyelids
• doubled or blurred vision
• dry mouth
• slurred speech
• trouble swallowing
• muscle weakness
The symptoms occur after 18 to 36 hours after eating the contaminated food. It is interesting that it takes ten days for the first symptoms to manifest.
It is a dangerous illness. When a person doesn’t get medical assistance immediately, it can provoke paralysis of the legs, arms, and respiratory muscles. That person will need an artificial ventilation to be able to breathe properly. Unfortunately, in many cases of untreated botulism, people died.
When the infected person gets medical assistance, botulism can be cured. Doctors use a substance derived from horses that stop the spread of the bacteria. They also help the patient to vomit, this way the patient’s body is getting rid of the contaminated food.
Doctors recommend that you boil the canned foods for 10 minutes before you eat them. This is a way to kill any bacteria. Infants are not allowed to eat honey because of the same reason.
E. coli
Escherichia coli refer to a large group of bacteria. Many of these bacteria are harmless. The ones that are bad are known as Shiga-toxin-producing E. coli, or STEC. The dangerous one is E. coli O157:H7.
These bacteria can be found in the guts of ruminant animals (cattle, goats, sheep, deer, and elk). When these animals are slaughtered, the bacteria can contaminate the meat easily. E. coli gives symptoms in humans such as diarrhea, stomach cramps, vomiting and a low fever.
People who get sick with E. coli need to be hospitalized. It is a dangerous illness for children. Kids can develop hemolytic uremic syndrome. This syndrome can lead to kidney failure.
You can get contaminated with E. coli when you consume ground beef, raw milk, cheese made from unpasteurized milk, and apple cider.
Even vegetables can be contaminated with E. coli if they come in contact with animal feces. Some people got sick as well after they swallowed contaminated water.
Trichinosis
Trichinosis is an infection in people who are eating animals infected with the larvae of the worm called Trichinella. They can get contaminated when they eat domesticated pigs.
Contaminated people get nausea, stomachache, fever, diarrhea, fatigue, and vomiting. These symptoms manifest in people after one or two days after they eat contaminated meat. These symptoms continue to manifest until the eight weeks. They include fever and chills, muscle or joint pain, itchy skin, headaches, coughing, eye swelling, constipation or diarrhea. If the case is mild, the symptoms disappear fast. If it is a severe one, the person needs drugs.
USDA recommends cooking the pork at 145 degrees and 160 degrees ground pork meat.
Campylobacter
Campylobacter is a disease caused by bacteria with the same name. These bacteria can be found in poultry meat. It exists in birds, but it doesn’t make them sick.
If you don’t want to get sick, cook the chicken properly and do not mix it with raw chicken juices. The bacteria can die if the chicken meat is frozen.
Campylobacter goes away within two to five days. People don’t take medication for this. The only symptom is diarrhea.
When the illness is severe, it can cause the Guillain-Barre syndrome. It can attack the nerves, causing paralysis.
Some outbreaks of Campylobacter are possible when people drink unpasteurized milk or contaminated water.
Listeria
Listeria monocytogenes is a foodborne disease that can affect pregnant women easily.
Pregnant women are more exposed to listeriosis than other people. People with different health issues such as kidney disease, cancer, and diabetes can get infected more often with listeriosis than healthy adults.
Places that have been fertilized with manure usually are preferred by listeria. It can be found in the soil and water. The bacteria can contaminate animal products including milk, meat, and cheese. Vegetables can be contaminated as well.
Some infections occur when the person eats uncooked meats, raw-milk cheeses, vegetables and cold cuts or soft cheeses that are contaminated. Be careful when you buy meats and other animal products from the deli. The products can be contaminated after they cook them through cross-contamination.[2]
Listeriosis symptoms: nausea fever, muscle aches, and diarrhea are the most common ones. Some people infected with these bacteria complained about headaches, convulsions, and a stiff neck. This is a severe foodborne illness. If not treated in time, the person can die.
Pregnant women infected with listeriosis manifest flu-like symptoms. This illness can provoke a miscarriage or premature delivery. The newborn can get infected as well. A blood test is necessary in this case. The baby and the mother can be treated with antibiotics.
Make sure you cook very well the meats; you avoid consuming raw or unpasteurized milk, cheese or juice. Be careful and always wash the vegetables before eating them. Clean your hands, and the knives and the cutting boards after you worked with raw meat.
“Mad cow” disease
Mad cow is known as a degenerative disease called bovine spongiform encephalopathy. This disease affects the nervous system of the animal. People who consume infected meat can develop Creutzfeldt – Jakob disease. This illness is fatal.
Some parts of the cow are considered to be most infectious for humans: spinal cord, retina, the brain, optic nerve, the muscles, and dorsal root.
The disease occurred among cattle which were fed parts from sick cows. After the first outbreaks, people stopped this practice.
The illness has killed many people in the world.
The illness is caused by an infectious agent called prion. If a person consumes infected meat, there is nothing that it can do after that. Cooking the meat doesn’t help.
Symptoms of Creutzfeldt – Jakob disease includes jerky movements, slurred speech, difficulty walking, dementia, memory loss, seizures, hallucinations and personality changes.
People infected can die in a matter of weeks or months. There are some cases when people lived for years with the disease.
Staph
Staphylococcus aureus is contained by foods such as poultry, eggs, meat, dairy products, pasta, salads, potato, éclairs, and cream pies.
Staph can develop in the refrigerator as well. It can infest the food and there isn’t a way to find out about it because it doesn’t have an odor.
People infected with staph feel sick very quickly and will manifest different symptoms such as vomiting, abdominal cramping, and nausea. When the illness is severe, people can also experience muscle cramps, headaches, and changes in blood pressure.
The illness goes away in two or three days. It is important to examine the suspect food, to determine the right diagnostic. You need to know that many healthy people have staph on and in their organism all the time. Staph is transmitted by animals and humans. It can also be found in food, air, in the water, dust, milk, and sewage.
Usually, people do not go to the doctor because the symptoms are mild. The only thing that you have to keep in mind is that you need to hydrate yourself the entire time you manifest those symptoms.
How to avoid getting infected with staph?
• cook meat to recommended temperatures
• don’t handle different kinds of meats at the same time, do not let them touch each other
• don’t let food on the table, outside for more than two hours
• cold foods must be kept at 40 degrees, and warm foods must be kept over 140 degrees
Norovirus
Norovirus is a foodborne illness which has human causes. Many people died because of this illness.
A person can get sick if the person who prepares the food has this virus and doesn’t wash his or her hands after going to the bathroom. Another way to get this virus is by touching the face or the mouth after you touched some surfaces with norovirus germs. When you have a direct contact with a person who has the virus, you can get sick.
Symptoms occur in 12 hours or 48 hours after exposure. The sick person can manifest these symptoms: diarrhea, abdominal pain, vomiting, stomach and headaches, low fever and tiredness. Many people believe the flu, but it is a Norovirus.
The virus goes away fast, and there is no treatment for it. Make sure you wash your hands and avoid cooking for others while you have it.[3]
“Ptomaine poisoning.”
This term is used by many people when they talk about a food poisoning.
Scientists believed at the beginning that food poisoning is caused by ptomaines, or alkaloids found in dead animals and vegetables after they decompose. The nature of these alkaloids was never clearly defined by specialists. When they discovered bacteria and other microorganisms they gave up the ptomaine theory. The term is still used by people when they talk about a food poisoning case in which doctors did not determine the cause.
Salmonella
Salmonella is a common foodborne disease. Salmonella is bacteria that live in the intestinal tracts of animals. Sometimes feces can come in contact with food that isn’t cooked; these bacteria can make people ill.
Salmonella doesn’t affect the animals. The food contaminated with Salmonella doesn’t look or smell differently than healthy food. Salmonella becomes a problem when it contaminates the foods that aren’t cooked or when meat that’s been contaminated isn’t cooked properly.
Salmonella symptoms:
• diarrhea
• abdominal cramps
• fever
The person infected will have these symptoms within 12 to 72 hours after infection. The illness goes away without medication after four or seven days. The infected people should drink a lot of water because they lose a lot of fluids from their body.
Some people were treated with antibiotics because the bacteria spread to their intestines. People with weak immune systems, like children and very old adults, may have a hard time fighting the infection themselves. These people need more special medical assistance.
In rare cases, people developed Reiter’s syndrome. This is a health condition that affects the person in many ways. The person can have eye irritation, painful joints, and painful urination. These symptoms do not go away for months or years. Some people also developed chronic arthritis.
Make sure you prevent salmonella infection by always cooking the meat and the eggs to the recommended temperatures. Be extra cautious when handling other foods, not to contaminate them with raw juices from the poultry, meat, eggs that have Salmonella.
References [ + ]
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Corticosteroids and immune suppressants: Patients with serious or life-threatening problems such as kidney inflammation, lung or heart involvement, and central nervous system symptoms need more “aggressive” (stronger) treatment. This may include high-dose corticosteroids such as prednisone (Deltasone and others) and drugs that suppress the immune system. Immune suppressants include azathioprine (Imuran), cyclophosphamide (Cytoxan), and cyclosporine (Neoral, Sandimmune). Recently mycophenolate mofetil has been used to treat severe kidney disease in lupus – referred to as lupus nephritis.
Lupus can affect men and women of any race or age. One in 2,000 people in the United States has lupus. People of African, Asian and Native American descent are more likely to develop lupus than are Caucasians. In addition, the disease develops in Emiratis at an earlier stage compared to Asians and expatriate Arabs working in UEA. Lupus studies also show racial preferences, being more prevalent among Arabs than Asians in the UAE region.
The panel judged the observed reduction in pregnancy loss with the addition of heparin to LDA as a large benefit. This intervention was not associated with significant harms. The addition of GCs or intravenous Ig to heparin plus LDA was associated with large harms (significant increase in premature delivery) without relevant benefits. Regarding heparin administration, the panel considered the reduction in pregnancy loss with low molecular weight heparin (LMWH) in comparison with unfractionated heparin (UFH) as a large benefit without significant adverse effects. No additional benefits were observed with LMWH-enoxaparin 80 mg compared with 40 mg.
A genetic disorder is a disease caused in whole or in part by a change in the DNA sequence away from the normal sequence. Genetic disorders can be caused by a mutation in one gene (monogenic disorder), by mutations in multiple genes (multifactorial inheritance disorder), by a combination of gene mutations and environmental factors, or by damage to chromosomes (changes in the number or structure of entire chromosomes, the structures that carry genes).
Any of a diverse group of plasma polypeptides that bind antigenic proteins and serve as one of the body’s primary defenses against disease. Two different forms exist. The first group of immunoglobulins lies on the surface of mature B cells, enabling them to bind to thousands of antigens. When the antigens are bound, the B plasma cells secrete the second type of immunoglobulins, antigen-specific antibodies, which circulate in the blood and accumulate in lymphoid tissue, esp. the spleen and lymph nodes, binding and destroying specific foreign antigens and stimulating other immune activity. Antibodies also activate the complement cascade, neutralize bacterial toxins and viruses, and function as opsonins, stimulating phagocytosis.
Jump up ^ Smyth, Andrew; Guilherme H.M. Oliveira; Brian D. Lahr; Kent R. Bailey; Suzanne M. Norby; Vesna D. Garovic (November 2010). "A Systematic Review and Meta-Analysis of Pregnancy Outcomes in Patients with Systemic Lupus Erythematosus and Lupus Nephritis". Clinical Journal of the American Society of Nephrology. 5 (11): 2060–2068. doi:10.2215/CJN.00240110. PMC 3001786. PMID 20688887. Archived from the original on 2016-01-26.
The mechanism by which foreign antigens are taken into antigen-presenting cells (APCs) and broken up. Part of the antigen is then displayed (presented) on the surface of the APC next to a histocompatibility or self-antigen, activating T lymphocytes and cell-mediated immunity. T lymphocytes are unable to recognize or respond to most antigens without APC assistance.
Any of a group of glycoproteins with antiviral activity. The antiviral type I interferons (alpha and beta interferons) are produced by leukocytes and fibroblasts in response to invasion by a pathogen, particularly a virus. These interferons enable invaded cells to produce class I major histocompatibility complex surface antigens, increasing their ability to be recognized and killed by T lymphocytes. They also inhibit virus production within infected cells. Type I alpha interferon is used to treat condyloma acuminatum, chronic hepatitis B and C, and Kaposi’s sarcoma. Type I beta interferon is used to treat multiple sclerosis. Type II gamma interferon is distinctly different from and less antiviral than the other interferons. It is a lymphokine, excreted primarily by CD8+ T cells and the helper T subset of CD4+ cells that stimulates several types of antigen-presenting cells, particularly macrophages, to release class II MHC antigens that enhance CD4+ activity. It is used to treat chronic granulomatous disease.
In some cases, your doctor may want to do a biopsy of the tissue of any organs that seem to be involved in your symptoms. This is usually your skin or kidney but could be another organ. The tissue can then be tested to see the amount of inflammation there is and how much damage your organ has sustained. Other tests can show if you have autoimmune antibodies and whether they're related to lupus or something else.
The panel concluded that both MMF plus high-dose GCs (prednisone 1–2 mg/kg/day, maximum 60 mg/day) and CYC plus high-dose GCs are associated with significant benefits in comparison to GCs alone. No significant differences between these two alternatives were noted. The panel pointed that differential pharmacokinetic effects of MMF in cLN may exist, which could require dosing increase.30 Risk of reduction of ovarian reserve and sperm abnormalities should be considered in patients with cLN treated with CYC.
Arthritis is inflammation of one or more joints and it involves the breakdown of cartilage. Cartilage normally protects a joint, allowing it to move smoothly. Cartilage also absorbs shock when pressure is placed on the joint, such as when you walk. Without the normal amount of cartilage, the bones rub together, causing pain, swelling (inflammation), and stiffness. Usually the joint inflammation goes away after the cause goes away or is treated. Sometimes it does not. When this happens, you have chronic arthritis. Arthritis may occur in men or women. Osteoarthritis is the most common type.
Pain is typically treated with opioids, varying in potency based on the severity of symptoms. When opioids are used for prolonged periods, drug tolerance, chemical dependency, and addiction may occur. Opiate addiction is not typically a concern since the condition is not likely to ever completely disappear. Thus, lifelong treatment with opioids is fairly common for chronic pain symptoms, accompanied by periodic titration that is typical of any long-term opioid regimen.
A specialized type of dense connective tissue consisting of cells embedded in a ground substance or matrix. The matrix is firm and compact; its proteoglycans can store considerably more sodium than plasma can, which in turn allows cartilage to store water, which in turn helps cartilage withstand pressure or impact. Cartilage is bluish-white or gray and is semiopaque; it has no nerve or blood supply of its own. The cells lie in cavities called lacunae. They may be single or in groups of two, three, or four. Cartilage forms parts of joints in the adult skeleton, such as between vertebral bodies and on the articular surfaces of bones. It also occurs in the costal cartilages of the ribs, in the nasal septum, in the external ear and lining of the eustachian tube, in the wall of the larynx, and in the trachea and bronchi. It forms the major portion of the embryonic skeleton, providing a model in which most bones develop.
Synovitis is an inflammation of the joint lining, called synovium. The symptoms are often of short duration and may change location although when caused by overuse tend to remain in one joint. The pain is usually more severe than expected based on the appearance of the joint on examination. In fact, sometimes there is pain without swelling or even tenderness in the joint, in which case the symptom is called “arthralgias” (literally meaning “joint pain” in Greek). Although synovitis has many different causes, the most common cause in an active healthy person is overuse.
Analgesics, or pain relievers, are medicines that reduce or relieve headaches, sore muscles, arthritis, or other aches and pains. There are many different pain medicines, and each one has advantages and risks. Some types of pain respond better to certain medicines than others. Each person may also have a slightly different response to a pain reliever.
Neurological disorders contribute to a significant percentage of morbidity and mortality in people with lupus.[37] As a result, the neural side of lupus is being studied in hopes of reducing morbidity and mortality rates.[30] One aspect of this disease is severe damage to the epithelial cells of the blood–brain barrier. In certain regions, depression affects up to 60% of women with SLE.[38]
Inflammation of the kidneys caused by an autoimmune disease called systemic lupus erythematosus. The condition can cause hematuria and proteinuria, and it may progress to end-stage renal disease. The most severe form of lupus nephritis, called diffuse proliferative nephritis, can cause scars to form in the kidneys. Scars are permanent, and kidney function often declines as more scars form. Early diagnosis and treatment may help prevent long-lasting damage.
According to Goldman Foung, “A diet rich in vegetables gives me energy and keeps me feeling strong and healthy." She typically eats meals filled with dark leafy greens and other colorful vegetables, eats lots of whole grains, and limits her consumption of meat and processed foods. “I also try to drink fresh-pressed beet juice as often as possible,” she adds. “It’s a great way to sneak in some of those body-boosting ingredients.”
Not necessarily. The antinuclear antibody (ANA) test is positive in most people who have lupus, but it also may be positive in many people who are healthy or have another autoimmune disease. Therefore, a positive ANA test alone is not adequate for the diagnosis of lupus. There must be at least three additional clinical features from the list of 11 features for the diagnosis to be made.
While the onset and persistence of SLE can show disparities between genders, socioeconomic status also plays a major role. Women with SLE and of lower socioeconomic status have been shown to have higher depression scores, higher body mass index, and more restricted access to medical care than women of higher socioeconomic statuses with the illness. People with SLE had more self-reported anxiety and depression scores if they were from a lower socioeconomic status.[99]
“It’s always difficult for children and parents to live with the idea that lupus is chronic,” says Pascual. That means the child has many more years worth of living with the condition than if he or she were diagnosed later in life. And because this disease is lifelong and may involve complications such as nephritis, doctors need to manage it aggressively.
A healing lupus diet can help improve gut health in those with lupus by preventing allergies, reducing deficiencies and slowing down free radical damage. In fact, due to how autoimmune disorders develop, a low-processed lupus diet high in antioxidants is usually key for managing any autoimmune-related symptoms, including those due to arthritis, thyroid disorders, etc., which often overlap with lupus symptoms.
Because the symptoms of lupus can mimic so many other health problems, you may need patience while waiting for a diagnosis. Your doctor must rule out a number of other illnesses before diagnosing lupus. You may need to see a number of specialists such as doctors who treat kidney problems (nephrologists), blood disorders (hematologists) or nervous system disorders (neurologists) depending on your symptoms to help with diagnosis and treatment.
Affiliate Disclosure: There are links on this site that can be defined as affiliate links. This means that I may receive a small commission (at no cost to you) if you purchase something when clicking on the links that take you through to a different website. By clicking on the links, you are in no way obligated to buy.
Please Note: The material on this site is provided for informational purposes only and is not medical advice. Always consult your physician before beginning any diet or exercise program.
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4,250,932,935,406,359,000 | Baidyanath Churna: Benefits, Side Effects, and Frequently Asked Questions
Introduction:
Baidyanath Churna is a herbal powder mixture that has been used in Ayurvedic medicine for centuries. It is a combination of several herbs that are carefully chosen to address specific health conditions. The powder is made by grinding the herbs into a fine powder, which can then be mixed with water or other liquids to make a paste or consumed as a tea. In this article, we will explore the benefits of Baidyanath Churna, its potential side effects, and answer some frequently asked questions about this traditional medicine.
Benefits of Baidyanath Churna:
Digestive Health:
Baidyanath Churna is known to improve digestion and relieve constipation. It contains several herbs such as Haritaki, Ajwain, and Saunf, which help in digestion by stimulating the digestive juices and promoting the elimination of waste from the body.
Respiratory Health:
Baidyanath Churna can be used to treat respiratory problems such as asthma and bronchitis. It contains herbs such as Pippali, Tulsi, and Shunthi, which have anti-inflammatory properties and help to reduce inflammation in the respiratory tract.
More Post; UNDERSTANDING THE BENEFITS AND USES OF STYPLON TABLETS
Immune System Booster:
Baidyanath Churna is known to boost the immune system and prevent infections. The herbs in this churna, such as Giloy, Tulsi, and Ashwagandha, have immune-boosting properties that help to strengthen the immune system and increase resistance to infections.
Joint Health:
Baidyanath Churna can help to relieve joint pain and inflammation. It contains herbs such as Guggulu and Rasna, which have anti-inflammatory properties and can help to reduce inflammation in the joints.
Skin Health:
Baidyanath Churna can be used to treat skin problems such as acne, eczema, and psoriasis. The herbs in this churna, such as Neem, Manjistha, and Haridra, have antibacterial and anti-inflammatory properties that can help to treat skin problems.
Potential Side Effects of Baidyanath Churna
While Baidyanath Churna is generally considered safe when taken in the recommended dosage, it can cause some side effects in some people. Here are some potential side effects of Baidyanath Churna:
Stomach Upset:
Some people may experience stomach upset or nausea when taking Baidyanath Churna. This may be due to the herbs in the churna stimulating the digestive system.
Allergic Reactions:
Some people may be allergic to certain herbs in the churna and may experience allergic reactions such as itching, hives, or swelling.
Drug Interactions:
Baidyanath Churna may interact with certain medications, so it is important to consult a doctor before taking this churna if you are taking any medications.
Pregnancy and Breastfeeding:
बैद्यनाथ चूर्णis not recommended for pregnant or breastfeeding women as the safety of the herbs in the churna during pregnancy and breastfeeding is not known.
Frequently Asked Questions:
How do I take Baidyanath Churna?
बैद्यनाथ चूर्ण can be taken with water or other liquids. It is recommended to take 1-2 teaspoons of churna, 1-2 times a day, or as directed by a healthcare provider.
Can Baidyanath Churna be taken with other medications?
बैद्यनाथ चूर्ण may interact with certain medications, so it is important to consult a doctor before taking this churna if you are taking any medications. Your healthcare provider can advise you on whether it is safe to take बैद्यनाथ चूर्ण with your current medications.
Is Baidyanath Churna safe for children?
बैद्यनाथ चूर्ण should only be given to children under the guidance of a healthcare provider. The dosage for children may be different from that for adults.
Can Baidyanath Churna be taken by people with diabetes?
बैद्यनाथ चूर्ण contains some herbs that may lower blood sugar levels, so it is important for people with diabetes to monitor their blood sugar levels closely while taking this churna. It is recommended to consult a doctor before taking बैद्यनाथ चूर्ण if you have diabetes.
How long does it take for Baidyanath Churna to work?
The time it takes for बैद्यनाथ चूर्ण to work can vary depending on the health condition being treated. Some people may experience relief within a few days, while others may need to take the churna for several weeks before seeing results.
Conclusion:
बैद्यनाथ चूर्ण is a traditional herbal remedy that has been used in Ayurvedic medicine for centuries. It contains a blend of herbs that have been carefully selected to address specific health conditions. While बैद्यनाथ चूर्ण is generally considered safe when taken in the recommended dosage, it can cause some side effects in some people.
It is important to consult a healthcare provider before taking बैद्यनाथ चूर्ण, especially if you are taking any medications or have any health conditions. With proper use and guidance from a healthcare provider, बैद्यनाथ चूर्ण can provide many health benefits and help to improve overall wellbeing.
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High-throughput analysis of single cell transcriptomes case study
Cells
Traditionally, gene expression experiments are undertaken on samples containing millions of cells. While this allows the identification of differentially expressed genes and transcripts in distinct cell populations, many subtle differences between cells in the same sample can be overlooked. Recent advances in high-throughput cell separation and transcriptomic analysis techniques has spawned the burgeoning field of single cell transcriptomics, which allows much more detailed analysis of gene expression.
The R2C2 technique delivers highly accurate, full-length transcripts.
At the University of California, Santa Cruz, Dr. Christopher Vollmers and his team are using single-cell transcriptomics to investigate gene expression in B cells. As Dr. Vollmers points out: ‘Each B cell makes a unique antibody transcript, so you really have to go at the single cell level to understand what B cells do’ 1.
In order to obtain full-length transcripts, which is a significant challenge when using short-read sequencing technology, the team developed a novel amplification strategy, which, when combined with the long reads delivered by nanopore sequencing, provided highly accurate, full-length reads. This Rolling Circle to Concatermeric Consensus (R2C2) method allows the generation of a consensus sequence for each transcript, thereby increasing base accuracy (Figure 1).
Utilising this technique allowed transcriptome analysis of 96 individual B cells, delivering over 400,000 full length cDNA reads with a median base accuracy of 94%2. Using an updated version of their Mandalorion data analysis pipeline, these reads could be used to identify high-confidence RNA transcript isoforms. A key finding of their study was that many of the B cells analysed, which were obtained from a healthy individual, express isoforms of the CD19 gene that lack the epitope targeted by CAR T-cell therapy — a discovery which may have significant implications in cancer treatment. This finding would not have been possible using short-read sequencing or without single-cell analysis.
According to the team: ‘The R2C2 method generates a larger number of accurate reads of full-length RNA transcript isoforms than any other available longread sequencing method’ 1. They further comment that they: ‘...believe that R2C2 has the potential to replace short-read RNA-seq and its shotgun approach to transcriptome analysis entirely, especially considering the […] wide release of the high-throughput PromethION sequencer’ 2.
human fig 7.PNGFigure 1: Schematic of the R2C2 method. Following cDNA circularisation, rolling circle amplification creates multiple joined copies of the transcript. After sequencing, each read is split into its constituent subreads which are then aligned to generate an accurate consensus sequence. Figure courtesy of Dr. Christopher Vollmers, University of California, Santa Cruz.
This case study is taken from the human white paper.
Download the human genetics white paper
References
1. Vollmers, C. Improving MinION read accuracy to enable the high-throughput analysis of single cell transcriptomes. Presentation. Available at: https://nanoporetech.com/resource-centre/ improving-minion-read-accuracy-enable-highthroughput-analysis-single-cell [Accessed: 1 August 2018]
2. Volden, R. et al. Improving nanopore read accuracy with the R2C2 method enables the sequencing of highly-multiplexed full-length single-cell cDNA. Proc Natl Acad Sci U S A. doi: 10.1073/pnas.1806447115 (2018). | {
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4,960,103,221,680,343,000 | Glucose-responsive metal-organic-framework nanoparticles act as "smart" sense-and-treat carriers
Wei Hai Chen, Guo Feng Luo, Margarita Vázquez-González, Rémi Cazelles, Yang Sung Sohn, Rachel Nechushtai, Yossi Mandel, Itamar Willner*
*Corresponding author for this work
Research output: Contribution to journalArticlepeer-review
200 Scopus citations
Abstract
Zeolitic Zn2+-imidazolate cross-linked framework nanoparticles, ZIF-8 NMOFs, are used as "smart" glucose-responsive carriers for the controlled release of drugs. The ZIF-8 NMOFs are loaded with the respective drug and glucose oxidase (GOx), and the GOx-mediated aerobic oxidation of glucose yields gluconic acid and H2O2. The acidification of the NMOFs' microenvironment leads to the degradation of the nanoparticles and the release of the loaded drugs. In one sense-and-treat system, GOx and insulin are loaded in the NMOFs. In the presence of glucose, the nanoparticles are unlocked, resulting in the release of insulin. The release of insulin is controlled by the concentration of glucose. In the second sense-and-treat system, the NMOFs are loaded with the antivascular endothelial growth factor aptamer (VEGF aptamer) and GOx. In the presence of glucose, the ZIF-8 NMOFs are degraded, leading to the release of the VEGF aptamer, which acts as a potential inhibitor of the angiogenetic regeneration of blood vessels by VEGF. As calcination of the VEGF-generated blood vessels leads to blindness of diabetic patients, the functional NMOFs might act as "smart" materials for the treatment of macular diseases. The potential cytotoxicity of the NMOFs originated from the GOx-generated H2O2 is resolved by the co-immobilization of the H2O2-scavanger catalase in the NMOFs.
Original languageAmerican English
Pages (from-to)7538-7545
Number of pages8
JournalACS Nano
Volume12
Issue number8
DOIs
StatePublished - 28 Aug 2018
Bibliographical note
Publisher Copyright:
© 2018 American Chemical Society.
Keywords
• VEGF
• aptamer
• diabetes
• insulin
• macular diseases
• nanomedicine
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Dive into the research topics of 'Glucose-responsive metal-organic-framework nanoparticles act as "smart" sense-and-treat carriers'. Together they form a unique fingerprint.
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1,514,578,533,676,970,500 | A Bicistronic DNA vaccine containing Apical membrane Antigen 1 and Merozoite surface protein 4/5 can prime humoral and cellular immune responses and partially protect mice against virulent Plasmodium chabaudi adami DS malaria
A. Rainczuk, T. Scorza, Terry W. Spithill, P.M. Smooker
Research output: Contribution to journalArticlepeer-review
25 Citations (Scopus)
Abstract
The ultimate malaria vaccine will require the delivery of multiple antigens from different stages of the complex malaria life cycle. In order to efficiently deliver multiple antigens with use of DNA vaccine technology, new antigen delivery systems must be assessed. This study utilized a bicistronic vector construct, containing an internal ribosome entry site, expressing a combination of malarial candidate antigens: merozoite surface protein 4/5 (MSP4/5) (fused to a monocyte chemotactic protein 3 chemoattractant sequence) and apical membrane antigen 1 (AMA-1) (fused to a tissue plasminogen activator secretion signal). Transfection of COS 7 cells with bicistronic plasmids resulted in production and secretion of both AMA-1 and MSP4/5 in vitro. Vaccination of BALB/c mice via intraepidermal gene gun and intramuscular routes against AMA-1 and MSP4/5 resulted in antibody production and significant in vitro proliferation of splenocytes stimulated by both AMA-1 and MSP4/5. Survival of BALB/c mice vaccinated with bicistronic constructs after lethal Plasmodium chabaudi adami DS erythrocytic-stage challenge was variable, although significant increases in survival and reductions in peak parasitemia were observed in several challenge trials when the vaccine was delivered by the intramuscular route. This study using a murine model demonstrates that the delivery of malarial antigens via bicistronic vectors is feasible. Further experimentation with bicistronic delivery systems is required for the optimization and refinement of DNA vaccines to effectively prime protective immune responses against malaria.
Original languageEnglish
Pages (from-to)5565-5573
Number of pages9
JournalInfection and Immunity
Volume72
Issue number10
DOIs
Publication statusPublished - 2004
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1,830,265,644,186,691,000 | Development of a spinal locomotor rheostat
Research output: Contribution to journalArticlepeer-review
17 Citations (Scopus)
Abstract
Locomotion in immature animals is often inflexible, but gradually
acquires versatility to enable animals to maneuver efficiently
through their environment. Locomotor activity in adults is produced
by complex spinal cord networks that develop from simpler
precursors. How does complexity and plasticity emerge during
development to bestow flexibility upon motor behavior? And how
does this complexity map onto the peripheral innervation fields of
motorneurons during development? We show in postembryonic
Xenopus laevis frog tadpoles that swim motorneurons initially
form a homogenous pool discharging single action potential per
swim cycle and innervating most of the dorsoventral extent of the
swimming muscles. However, during early larval life, in the prelude
to a free-swimming existence, the innervation fields of motorneurons
become restricted to a more limited sector of each muscle
block, with individual motorneurons reaching predominantly ventral,
medial, or dorsal regions. Larval motorneurons then can also
discharge multiple action potentials in each cycle of swimming and
differentiate in terms of their firing reliability during swimming
into relatively high-, medium-, or low-probability members. Many
motorneurons fall silent during swimming but can be recruited with
increasing locomotor frequency and intensity. Each region of the
myotome is served by motorneurons spanning the full range of
firing probabilities. This unfolding developmental plan,which occurs
in the absence of movement, probably equips the organism with
the neuronal substrate to bend, pitch, roll, and accelerate during
swimming in ways that will be important for survival during the
period of free-swimming larval life that ensues.
Original languageEnglish
Pages (from-to)11674-11679
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume108
Issue number28
DOIs
Publication statusPublished - 12 Jul 2011
Keywords
• motor system
• central pattern generator
• ontogeny
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> Hints > FAQs
FAQs
You'll find lots of your questions answered in this section. This information is based on my scientific research coupled with real people's experiences.
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"Dr Amanda, Long time no write/hear. A lot has happened diet-wise since we last communicated. I have LEARNED. Never before have I dieted *for life*. Diets for me in the past have always been a means to an end. Your book has taught me many things. Mainly that a diet and the way we eat is a permanent thing, and secondly HOW to listen to my body when it's hungry and when it's full. At the beginning of this process my immediate goal was to quickly lose weight. This has evolved into a desire to lose weight, but at my body's pace. As a result, I am continuing to lose weight, but I've removed the time frame. My *long term* target is 80 kg, and in time, I believe I will achieve this. Once again, I thank you for your wise and sensible advice from one of the best books on the subject in print! Matthew P.S. Attached is my progress, kept updated since my last contact. I have now lost 11.5 kilos since I started your program nine months ago. "
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-3,361,246,243,869,793,000 | How To Stop Stomach Noises
The paste thus formed is passed on to the small intestine for absorption of nutrients into the body. The noises that a newborn baby's tummy makes can be a bit disconcerting for a new parent. If You've Had Enough of Your Growling Stomach, Here's How to Stop It 1. If you are feeling embarrassed from the noisy stomach, and you want to stop it abruptly, here are some of the ways that you can follow. With treatment, most ulcers heal in a month or two. For example, fizzy drinks are well-known culprit for causing a swollen tummy. Slow down your breathing by doing the following: Breathe in deeply through your nose, using your chest to pull the air into your stomach, while slowly counting to 10. 's life has never been easy. If you want to settle an upset stomach that's caused by nerves, it's important to keep stress in check. Many things that bother you, even those that you don't notice have an effect on your stomach. Usually, the only way to get rid of gas pain in your stomach is to make yourself fart and release the pressure. Turmeric is best known for spicing up Indian fare, but it may also calm down an upset stomach. e start working and clenching, hence the grumbles) and the apple equally triggers it but isn't sufficiently filling to reduce those sounds. Hip precautions are important guidelines for those who have recently had hip surgery to replace their hip joint and stop joint pain. Harry is one of the reader's who often suggest the use of Ignatia 30X to help relieve stomach noises. An incision made in the dog’s stomach can help alleviate pressure from gas. First, you can make sure you aren’t eating or drinking right before you lay down to sleep. There are medications to help with individual symptoms like the nausea and vomiting, though. If your stomach always seems to growl at that 9 a. Is this normal? I dont suppose theres any way to stop it, is there?. Stomach noises may be described as growling, gurgling or even rumbling. Some people must deal with the stomach acid leaving the stomach the wrong way, causing discomfort on the esophagus. it started about a year ago, and has progressively gotten worse. Despite the descriptive terms attributed to the various types of stomach noises, it is difficult to isolate the exact cause behind each type of sound. The worst is usually AFTER lunch when im in my SILENT math class. Avoid using mouthwash to treat persistent bad breath. The intestines sort through the digested components so they can be absorbed into the bloodstream, or passed through the alimentary canal to be excreted. In June of 1998 I had GERD surgery. Sufficient stomach acid is needed to kill pathogens and unfriendly bacteria that enter the body and prevent intestinal bacteria from colonizing the stomach. If you have a large breed of dog such as a German Shepherd, you should know all about Gastric Torsion or Bloat, be able to recognize when your dog is suffering from it, and most importantly, how to prevent it. The book is both conceptually and stylistically like nothing I’ve read before. Reflux can also occur as a result of a hiatus hernia — a hole in the diaphragm muscle that allows part of the stomach to slide upwards into the chest, allowing stomach acid to leak. It can be difficult to differentiate between normal and abnormal bowel sounds. If a dog is panting. and its weird how my stomach only growls when im in class or during a sleepover. They’re characterized by hollow sounds that may be similar to the sounds of. -With a severe upset stomach, refrain from giving your Poodle food for 8 to 10 hours. Excessive gas in the gut can cause loud stomach. Loud, soft and sometimes for no good reason at all, your growling stomach has a lot to say. Walls of the abdomen contract to facilitate mixing of food and squeezing it to a paste which can be subsequently passed into the small intestine. After surgery, patients are usually told not to eat until bowel sounds resume and they can pass gas (which is another sign of normal bowel function). Acid Reflux Stomach Noises. If a dog is panting. Most bowel sounds are normal. " - Lewis Carroll My buddy and I were hanging out. Drinking water: Consuming water should naturally prevent stomach gurgling. The process causing the noises: digestion. Stop Smoking. i have this exact problem. Since my surgery, I notice that after I eat my stomach often makes very loud gurgling noises. If you have a really noisy belly, you might be sensitive to fructose, 4. A buildup of gas in your intestinal system can cause pain, bloating, and general abdominal discomfort. If you see symptoms growing worse. Consider walking after a meal. Among them are:. After you feel yourself relaxing,. Learn all about the symptoms of gastritis chronic gastritis can last for months and even years headlines posted throughout the day every day. it sooo embarassing. Often, it isn't the stomach that you hear, but rather the functioning of the lower digestive system, the small and large intestines. However, these may not be the best cure for your dog, so make sure you check with your veterinarian before proceeding. Slow Down When You Eat. Its so embarassing! I eat breakfast some mornings but not all. While the majority of dog stomach noises are normal and harmless, some stomach noises in dogs can result from—and be a sign of—potentially serious gastrointestinal problems. The gurgling, grumbling and growling can be surprisingly loud. I know that sounds. Eat slowly. These natural but weird body noises are a sign that your body is working. Not because he was overstimulated after having guests over to the house. How To Make Yourself Throw Up Easily (Complete Guide) To prevent side effects, drink only in small amounts. After you feel yourself relaxing,. Eat more regularly. He goes outside to eat grass, but rarely vomits. Stomach Bloating and Gas. is there anyway to stop the gurgling noises from my stomach? they are particularly loud during long periods of silence and it gets very embarrassing. It's like asking: My grass keeps growing back in my garden, how do I stop it from growing?. If you want to settle an upset stomach that's caused by nerves, it's important to keep stress in check. That’s because a gurgling belly doesn’t always mean it’s time for lunch. Exhale slowly through your mouth, while pursing your lips, for a count of 10. Find out why it growls and what you can do to stop it. Even if the person remains unaware of the fact that he or she snores, the loud noise can cause sleep disturbances to others around him forcing them to seek remedies to stop snoring. The noise we attribute to the stomach growl, is actually not coming from your stomach at all. There isn't necessarily a cure for the stomach pain symptoms themselves. Meanwhile, if you smoke, stop. Here are some tips to prevent this serious scenario from happening: Feed a high fiber and low carbohydrate diet. Plus: a map of the sounds at this year’s event. My symptoms are mild bloating, rumbling noise in my stomach, belching, flatus, palpitations, light headedness and weakness. You should always consult with a doctor before taking medication and do not want to rely on medication to “cure” your upset stomach. People with abdominal pain often double over, clutch their gut, feel nauseated or dizzy, and avoid food and water. Loud Stomach Noises and Bowel Sounds in the Elderly Changes in digestion and bowel habits are among the more common age-related disturbances in the body. The worst is usually AFTER lunch when im in my SILENT math class. While I was pregnant with my son my Dr. You may also have stomach upsets, rumbling of the stomach and heartburn. It includes bubbling, growling or rumbling stomach noises. Beyond the specifics above, good old-fashioned advice for treating diarrhea still applies. No one really wants to feel stuffed and bloated from overeating. When trying to explain what stomach palpitations actually feels like, people usually say that they feel some kind of pulsing around their stomach, and some even compare it to the famous feeling of the so-called ‘butterflies in the stomach’. The first time I ever tried exogenous ketones , I was about 16 hours removed from carbohydrates ( In-N-Out burger ) and I was feeling awful. These viruses are usually mild and go away on their own. It traps blood in the stomach and blocks it from returning to the heart and other areas of the body. If operable, surgery can cure stomach cancer as long as all of the cancerous tissue can be removed. Eat the Right Things at the Right Time. But it actually builds on a story I wrote last week about how the immune system, gut microbes, and the food we eat all work in harmony to influence weight gain. they put me on zantac and chlord/clidi 5-2. Excessive gas in the gut can cause loud stomach. Fennel Essential Oil. On the surface, noises from the stomach are not necessarily a sign of a medical problem. While sleeping on your stomach may feel good and seem perfectly acceptable, so does picking your nose to a 4-year-old (and then eating the treasure). Gastric Dilatation Volvulus (GDV) commonly called bloat (SEE VIDEO BELOW), occurs when food ferments, air is trapped, and the stomach becomes distended. How to stop Stomach Cramps and Pain Friends, you really don't have to live in pain with stomach cramps. Acid travels through the tubes breaking down food for the body to absorb it. Using the Xifaxin and an antifungal is almost like hitting the reset button on your computer; you reboot your gut and then you start over. Dog dry heaving is most commonly caused by a life-threatening condition known as gastric dilation and volvulus (GDV) or “canine bloat”. But that's my personal experience! This won't cure the problem. Chronic pain or pain that's getting worse needs to be seen by a. Limit indigestible foods. Chew slowly. How To Make Yourself Throw Up Easily (Complete Guide) To prevent side effects, drink only in small amounts. Ever feel like you can’t turn your brain off? Worried about how to stop worrying? We all deal with this when life gets challenging. Eat more regularly. This is another solution for chronic stomach growling. This essential oil also helps improve digestion when inhaled or rubbed on the tummy so if you’re stomach ache is due to poor digestion, you can inhale a couple of drops of fennel oil from a hanky or mix it in a vegetable oil like olive oil and rub it deeply on your tummy. Upper left abdominal pain can be due to an enlarged spleen, fecal impaction (hardened stool that can’t be eliminated), injury, kidney infection, heart attack or cancer. This most often happens in the mornings before breakfast and lasts for most of the day. Natural Remedies To Cure Your Dog’s Upset Stomach If you prefer not to give your dog human medications, some natural home treatments can do the trick. the stomach cramps, sweating palms, racing pulse and general desire to be dead. However, it is mainly the process of digestion, and not any stomach problems, that cause this noise in our stomach. How to Stop Excessive Gas: 5 Steps Gas, flatulence, farting … whatever you call it, you don’t want it! Here are five stops to stop gas before it ever starts—including what foods to avoid. Not only do they stick around in our digestive systems, but when we eat foods that are high in FODMAPs, the bacteria in our stomach feed on them, producing large amounts of bloating. I don't really get anxious about life or being around people or anything, but just the heightened activity of being out in public, or general stress that occurs in situations where having your stomach suddenly start making thunderous fart noises would be pretty devastating (like an important business meeting, a really quiet office, or with your. Once you have a gastritis or stomach inflammation, you are vulnerable to it occuring again forever. How stomach cancer is treated. *Bass guitar riff* Jerry Stonefeld. Stomach pain may be listed as a possible side affect on your drug information sheet. Im starting to get self concious about it. It may further come up till throat and mouth. Limit sugar, alcohol, and acidic foods. How do I stop moaning and making other strange noises in my sleep? Over the past year I have started humming and/or moaning in my sleep. We obviously need stomach acid, so having it blocked can lead to some complications. The above reasons are why you might experience your stomach making some gurgling or churning noises. How do you stop stomach noise? well it depends if your hungry eat something but if your not hungry and your stomatch i advise u to drink ginger aile. This is often accompanied by stomach cramps and the intense need to discharge. Filling up your stomach to the rim is another recipe for digestion disaster. Intestinal gas occurs when air is rapidly pushed through to the colon from the small intestine. These are highly irritating and sometimes may cause embarrassment too. Eat slowly. The following video on diarrhea and bubbling sounds in the abdomen was produced by the Health Hype team. It includes bubbling, growling or rumbling stomach noises. A stomach rumble, also known as a bowel sound, peristaltic sound or bubble gut, is a rumbling, growling or gurgling noise produced by movement of the contents of the gastro-intestinal tract as they are propelled through the small intestine by a series of muscle contractions called peristalsis. These natural but weird body noises are a sign that your body is working. Your stomach will feel very full even though you have not eaten recently. Loud stomach or intestinal noises in dogs may stem from dietary indiscretion. pain, fever, nausea, diarrhea, etc. My dog's stomach is making a lot of gurgling noises and he won't eat. The most common cause of an. To stop a burning throat you can either treat the symptoms as they appear for short-term relief, or you can treat the root-cause to stop the problem from ever happening. However, it is mainly the process of digestion, and not any stomach problems, that cause this noise in our stomach. I’ll only stop doing it when I can’t walk. It felt like the fluids inside my stomach were actually boiling, and it sounded like it too. Your stomach growling doesn't only happen when you're hungry. Suddenly, one of the cabinets burst open and a tall figure tumbled out and onto the floor, dusting herself off and moving closer to me. The medical term for stomach growling is borborygmus. Loud stomach noises can be very embarrassing and can be caused by a variety of reasons. We've more information about Detail, Specification, Customer Reviews and Comparison Price. Foods to avoid to prevent gastritis. Dry dog food can expand inside of a dog's stomach, causing a dog with a small stomach to vomit soon after eating. Usually, the only way to get rid of gas pain in your stomach is to make yourself fart and release the pressure. Dogs tell us they have an upset stomach when they vomit, have diarrhea or refuse food. The sounds we hear when our "stomach" starts talking and complaining after a meal is actually made by the movement of gas through our intestines. I've been feeling nausea, I've been coughing a lot, I also feel like it could be my dogs hair in me. Signs of a Sensitive Stomach. I know your stomach is lurching as you read this, but it's important to face facts. They simply mean that the gastrointestinal tract is. Women are affected more when compared to men. 7 Ways to Cure Those Butterflies in Your Stomach Do you get nervous when you are going to do something new? Starting school, first day of work, or learning how to do a new task can all cause a persons stomach to become all tied in knots. One way to improve your health is to use probiotic supplements which can 2. She also has vomited several times recently, but this is common for her. How to stop weird stomach sounds!? Recently my stomach has been making weird, awkward noises. ) there are no specific treatments for these rumbles. 1 Comments Last updated 6 days ago. The medical term for stomach growling is borborygmus. What is gastritis? Gastritis is a term commonly used by the public (and sometimes by doctors) to describe episodes of stomach discomfort (usually after eating) sometimes associated with nausea and/or vomiting. When I get to work, have a coffee with a splash of half and half, that’s all I need. The steps below will help you to stop those pesky noises. If I take that one bite too many, it's going to come up. While sleeping on your stomach may feel good and seem perfectly acceptable, so does picking your nose to a 4-year-old (and then eating the treasure). Stomach Noises How To Stop Pain Problem steps to take before you get pregnant you should stop before you get pregnant. We all know how annoying it is to have itchy ears. Nothing can stop it. You can feel the gas in her stomach moving. The nonsurgical stomach ulcer treatment will typically revolve around antibiotics. We can’t sign you in. Chew slowly. How to Prevent Nasty Stomach Bugs This Winter? More Bleach. Intestinal gas occurs when air is rapidly pushed through to the colon from the small intestine. The medical term for stomach growling is borborygmus. While it’s true that not feeling well is enough to cause shaking in small dogs before, during or after having an upset stomach, it’s also important to consider that small dogs and young puppies are also prone to developing a glucose imbalance. I know I'm not hungry because i just ate, but my stomach keeps making awkward digestive sounds and it has become pretty much ridiculous. For example: booty shorts (tuck them between), a thong etc. Gas is present from air that we swallow, from the air particles between our food (you can really feel it in airy cakes, mousses and Aero bars!) but mostly it's produced during digestion. Most bowel sounds are normal. However, without any food in the stomach, the noises from these muscle contractions are amplified (and thus more embarrassing). Some times the consistancy changes. Yogurt is a fantastic food item that balances a number of bacteria in your digestive system. **Please note that not all products available online are available in the stores. Interruptions in the working of the stomach of a cat can be brought on by several conditions. These are most often normal, but due to the fact that these noises are loud, dog owners may be alarmed when hearing t. Stress Reduction. Eat when you are hungry, your stomach may gowl or you may feel your blood sugar going down, and stop eating when you feel full. A buildup of gas in your intestinal system can cause pain, bloating, and general abdominal discomfort. I stopped having sleepovers because of it since it's embarrassing. These noises might sound like they should be coming from a noisy pot of bubbling stew rather than your stomach. Constipation causes stool to remain inside the intestines with formation of gas, which makes an individual feel tightening of stomach, discomfort and gas. Any air that you To do it, gently rub in a circular motion around your stomach, from your hips to your ribs. 21 Cat Behaviors, 32 Cat Sounds and their Secret Meaning. However, there are situations where a serious problem could be present if stomach growling is accompanied by nausea and vomiting. exactly what it sounds like – a bloated stomach that. If you have developed aspiration, it is important to understand what to do to prevent choking. Over the past year, her weight has decreased from 8. The intestines are hollow, so bowel sounds echo through the abdomen much like the sounds heard from water pipes. i have this exact problem. " Causes of Stomach Noise. Women are affected more when compared to men. The worst is usually AFTER lunch when im in my SILENT math class. coli, Salmonella, C. Home Remedies For Rumbling Stomach Noises. The steps below will help you to stop those pesky noises. There are two parts to look at here, number one is. What is this vibrating sensation in my ear, and how do I make it stop?! August 5, 2015 1:42 PM Subscribe For the past few days, I've had this weird fluttering/vibrating sensation in my right ear off and on. Stomach growling is rumbling noise that originate from stomach when fluid and gas move through it. Most bowel sounds are normal. I am a fellow frustrated individual with excessive stomach noises. I started cutting out various foods to see if it was an allergy to something. The noise we attribute to the stomach growl, is actually not coming from your stomach at all. The Sounds Cats Make – 7 Cat Sounds and What They Mean. Drinking water may help to stop stomach growling. How To Make Yourself Throw Up Easily (Complete Guide) To prevent side effects, drink only in small amounts. Remedies and Treatments to Stop Noise in Stomach. This condition is the inflammation of the lining of the stomach and the intestines. If you had a stethoscope, you would be able to hear a much richer and more persistent array of intestinal noise. Constipation causes stool to remain inside the intestines with formation of gas, which makes an individual feel tightening of stomach, discomfort and gas. From here, the pH raises up and down as it travels through the intestines and out the other end. When these embarrassing sounds escape, I have a menu of canned responses I can select from: Option #1 (tell a lie): “Oh, excuse me, my stomach is growling, I forgot to eat. All these noises are medically known as borborygmi (singular ~ borborygmus). Been having severe stomach problems for months, first time I went to see the doctor he decided I had pulled a muscle in my stomach and told me he could not do or prescribe anything, after weeks of the pain getting incredibly worse I went back and was finally told I have gastritis but have no idea how to treat it, I am under weight anyway and. The paste thus formed is passed on to the small intestine for absorption of nutrients into the body. A sliding hiatus hernia can cause severe symptoms or complications that may require surgery, but this is rare. Ive been eating more than Ive wanted to cause my stomachs been making super loud noises people at my side can hear. But if you time it right, you shouldn't hear either of those growls. Fortunately, a cranky belly tends to feel better quickly if you. If he eats with no problem and the noises stop, he's probably fine. How To Keep Your Belly from Gurgling After Meal Thankfully, there is an easy regime that can be followed to stop gurgling noises. Nursing Clinical Skills are very important to learn, and the ng tube insertion is among one of the frequent tasks a registered nurse (or nursing student) will encounter on the job. Sadly, Failure Is the Only Option to stop him. But the hot weather can also be held. Loud stomach gurgles that don't stop may be a sign of something more serious, so if they are continuous enough to be uncomfortable, consult your doctor to isolate the cause. With treatment, most ulcers heal in a month or two. Halitosis (bad breath) may be the result of a problem that mouthwash can't cure, such as low grade infections in the nose, sinuses, tonsils, gums, or lungs, as well as from gastric acid reflux from the stomach. The thing about loud or noisy stomach sounds is that usually they are caused by hunger or gas from certain foods. Today I found out why your stomach growls when you are hungry. yes my stomach keeps up lot of noise since i became diabetic. The "growling" or rumbling noises (the exact term is borborygmi) are the sounds of peristalsis, muscle contractions that mix food in the stomach with liquids and digestive juices. The gurgling sound we hear from our stomach is often simply the sound of our digestion. A little bird that often laughed tried hard not to laugh when it saw him go within the jaws of the Goblin Goddess. Often, it isn't the stomach that you hear, but rather the functioning of the lower digestive system, the small and large intestines. Above all else, I wish you luck in finding the right tools and methods that will help you. My stomach makes loud noises all the time. These suggestions on how to deal with your dog's stomach problems are based on my experience with my terrier Georgie. I'm not talking growling sounds like when one is hungry. COPD, asthma, pulmonary edema, dysfunction of your vocal cords, as well as acute bronchitis. If you want to settle an upset stomach that's caused by nerves, it's important to keep stress in check. If you're prone to heartburn. In patients with diabetes and gastroparesis, this movement is slowed, causing food to be retained in the stomach for longer than normal. I read The Book of X by Sarah Rose Etter in a single night, absorbed for hours by Cassie’s life with her stomach in a literal knot. This is often accompanied by stomach cramps and the intense need to discharge. problem burning left side stomach. I have medication from my vet and after just two 1/4 tabs at allotted times, it nips it. When Your Stomach Growls, It Isn't Telling You it is Hungry. The feeling of ‘pressure’ and ‘fullness’ in the stomach, that can make it feel as though we are stretched to capacity or weighted down. I know I'm not hungry because i just ate, but my stomach keeps making awkward digestive sounds and it has become pretty much ridiculous. There is a way to overcome worry that doesn’t involve alcohol or a straitjacket. I had the gastric bypass done in 2004. it sooo embarassing. The RRP against which any savings comparisons we make to the listed sale price for products displ. Some times the consistancy changes. If it is not clear now that I am not relaxing about this latest proliferation of patronization, pay attention. (AP) — It's going to be a cruise to nowhere, but that will be just fine with die-hard "Star Wars" fans. Since there are variable reasons for producing gurgling, it is necessary to know the underlying cause. Also please cure the others too who are suffering from stomach problems. Unless the sounds your stomach and small intestine are making are accompanied by diarrhea, abdominal pain or other symptoms, they are probably normal. Stomach noises may be described as growling, gurgling or even rumbling. Termed "borborygmi," bowel sounds seem loudest to those experiencing the sounds. Ive been taking Adderall 20mg for almost a year now and im starting to experience stomach/digestive problems. I hate having to do any kind of training, because I get soo scared that my stomach will start to make some type of noise. BLOAT LEADS TO GASTRIC TORSION First-Aid for Bloat Can Prevent A Deadly Emergency. How To Keep Your Belly from Gurgling After Meal Thankfully, there is an easy regime that can be followed to stop gurgling noises. it started about a year ago, and has progressively gotten worse. I've been feeling nausea, I've been coughing a lot, I also feel like it could be my dogs hair in me. I am very happy with the results. Here are 20 natural ways to relieve stomach pain (no undesirable side-effects included!). The embarrassing noise may be caused by factors like hunger, incomplete digestion, consumption of high fiber and high carbohydrate foods, and faster metabolism. " - Lewis Carroll My buddy and I were hanging out. Sadly, Failure Is the Only Option to stop him. As were prebiotic fibers. She also tends to belch at times. Go Way Beyond Digestive Issues. The "growling" or rumbling noises (the exact term is borborygmi) are the sounds of peristalsis, muscle contractions that mix food in the stomach with liquids and digestive juices. Read more for a wide range of dog health and behavior tips that will help you provide the best possible care for your canine companion. He will check for signs of dehydration. Abdominal sounds (bowel sounds) are made by the movement of the intestines as they push food through. Remedies and Treatments to Stop Noise in Stomach. Meents is yelling in my ear to simply lift off the throttle, but the truck is so loud I can't hear him. Why does your stomach growl even when i am not hungry? Often, a growling stomach is not a growling. Loud, soft and sometimes for no good reason at all, your growling stomach has a lot to say. Drink water. These noises might sound like they should be coming from a noisy pot of bubbling stew rather than your stomach. We can't sign you in. The familiar deep-throated hack of a soon-to-be regurgitated hairball. Constipation causes stool to remain inside the intestines with formation of gas, which makes an individual feel tightening of stomach, discomfort and gas. How to Stop Mouth Breathing (Treatment) “All chronic pain, suffering and diseases are caused from a lack of oxygen at the cell level. Even more rarely, cancer of the stomach or the oesophagus can explain the severe burping. I started cutting out various foods to see if it was an allergy to something. Carly Fox, staff doctor at the Animal Medical Center in Manhattan. What Causes a Troublesome Tummy? The most common triggers for upset stomach have something to do with your dog’s diet. Stomach growling is the result of this process. This is another solution for chronic stomach growling. These suggestions on how to deal with your dog's stomach problems are based on my experience with my terrier Georgie. Drink water. It includes bubbling, growling or rumbling stomach noises. My very loud stomach noises were food and air trying to get around my colon cancer tumor. The biggest factor with loud stomach noise is diet, some people are more sensitive to some foods than others. Above all else, I wish you luck in finding the right tools and methods that will help you. i can't think of anything to eat that is healthy and that will stop these noises. And most of the time, the sounds that come from the bowels of our, well, bowels, are simply a product of a healthy gut's routine: The noises just indicate movement in the stomach, usually caused. The feeling of ‘pressure’ and ‘fullness’ in the stomach, that can make it feel as though we are stretched to capacity or weighted down. | {
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5,133,079,352,126,855,000 | Journal of Clinical Immunology and Research
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Estimation of IgE levels and basophile count in type I hypersensitivity
Abstract
Background: Hypersensitivity is a state of overreaction to wide range allergens due to many factors including genetic predisposition and environmental and other factors. Hypersensitivity classified into four major types according to their mechanisms and immune mediators. Type I hypersensitivity also known as anaphylactic or immediate type due to the short time required for symptoms to appear, it is mostly IgE involved.
Aim of the study: To identify the most common categories of type l hypersensitivity in addition to assess the correlation between IgE levels, Basophile count with the strength of immune response to certain allergens in different cases and various groups of patients by estimation of IgE levels and basophile count.
Material and method: Three ml of venous blood samples from 20 patients with confirmed type I hypersensitivity, 13 patients were females and 7 males in addition to 20 healthy control samples were enrolled in this study, all samples were subjected for (ELISA test) (Enzyme Linked Immunosorbent assay) to estimate the IgE Levels, in addition to a drop of capillary blood by finger puncture for preparation of blood film for blood basophile count. Cases included systemic anaphylaxis and localized hypersensitivity reaction such as hay fever, asthma, food allergies and eczema. Case sheet was organized for each case.
Results: A highly statistical significant variation both in IgE levels and basophile blood count between allergic patient group and healthy control group was observed, the P value was 0.002 and 0.000 respectively. Nostatically significant differences between males and females in frequency of the anaphylaxis with 0.119 P value. The higher value of type I sensitivity was coetaneous eczema 35%, then food allergy 20%, hay fever and insect venom15% for each, and the lowest was penicillin sensitivity 5%. Followed by asth. 10%.
Conclusion: The highest cases of type l Hypersensitivity was eczema , food allergy insect venom, hay fever , asthma and penicillin sensitivity there was a highly significant positive correlation between IgE levels and basophile count with appearance of symptoms.
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4,151,878,879,092,252,000 | You are currently viewing Advances in Schizophrenia Treatment at Indian Rehab Centers
Advances in Schizophrenia Treatment at Indian Rehab Centers
Schizophrenia is a complex and challenging mental health disorder that affects millions of people around the world. Schizophrenia, characterized by disruptions in thought processes, perceptions, and emotional responses, can significantly impact a person’s ability to live a normal life. Fortunately, advances in the field of mental health have led to the development of effective treatment and rehabilitation programs aimed at improving the quality of life for individuals with schizophrenia. If you or a loved one are seeking help, consider exploring options like schizophrenia rehabilitation center in India, where the flow of comprehensive care can make a positive difference toward recovery.
It is important to be aware of the best mental rehabilitation treatment centers in Delhi and psychological rehabilitation centers in Delhi as well as the role they play in the recovery process. Additionally, it is also crucial to understand the concept of rehab centers in India and how they contribute to the overall well-being of individuals grappling with schizophrenia.
Understanding Schizophrenia Treatment
Schizophrenia treatment typically involves a combination of medication, psychotherapy, and rehabilitation efforts. While medication helps manage symptoms such as hallucinations and delusions, psychotherapy aims to address underlying issues and improve coping mechanisms. Rehabilitation, on the other hand, focuses on enhancing daily life skills, fostering independence, and reintegrating individuals into society.
Rehabilitation Centers in India
India has seen significant progress in the field of mental health, and many rehabilitation centers across the country offer specialized programs for individuals with schizophrenia. Among these, schizophrenia rehabilitation center in India are known for their comprehensive and patient-centric approach. The center provides fluency in addressing the specific needs of individuals with schizophrenia, ensuring a holistic and effective recovery process.
These centers often employ a multidisciplinary team of mental health professionals, including psychiatrists, psychologists, occupational therapists, and social workers. The collaborative efforts of this team ensure that individuals with schizophrenia receive holistic care that addresses both their mental health needs and their overall well-being.
Mental Rehabilitation Treatment Center in Delhi
Delhi, the capital city of India, is home to several reputable mental rehabilitation treatment centers. These centers are equipped with state-of-the-art facilities and employ evidence-based practices to provide effective care for individuals with schizophrenia.
The importance of mental rehabilitation treatment center in Delhi lies not only in its geographical reach but also in its ability to cater to the needs of the diverse population living in and around the city. Rehabilitation centers in Delhi often serve as centers of innovation in mental health care, adopting the latest therapeutic approaches and technologies to enhance treatment outcomes. One such area of focus is the establishment of schizophrenia rehabilitation center in India, which contributes to the advancement of mental health services and provides specialized care for individuals with schizophrenia.
Psychological Rehabilitation Center in Delhi
In the realm of schizophrenia treatment, a psychological rehabilitation center in Delhi plays a pivotal role in addressing the cognitive and emotional aspects of the disorder. These centers focus on helping individuals develop essential life skills, manage stress, and navigate social interactions.
The psychological rehabilitation process involves a combination of individual and group therapy sessions, where individuals suffering from schizophrenia can learn coping strategies, communication skills, and emotional regulation techniques. By fostering a supportive and structured environment, these centers empower individuals to overcome the challenges posed by schizophrenia and live fulfilling lives. Those who want ease in their journey to recovery should consider exploring a reputable schizophrenia rehab center in India.
Rehab Centre India: A Holistic Approach to Schizophrenia Treatment
Rehabilitation centers in India, often referred to as rehab centers, go beyond traditional treatment methods to adopt a holistic approach to mental health care. These centers recognize that successful schizophrenia treatment requires addressing not only the symptoms of the disorder but also the individual’s overall well-being.
Rehab Centre India offers a range of services designed to meet the diverse needs of individuals with schizophrenia. These services may include:
1. Medication Management
Ensuring individuals receive the appropriate medication and monitoring their response to treatment is a crucial aspect of schizophrenia care. Rehab Centre India collaborates with experienced psychiatrists to tailor medication plans to each individual’s needs.
2. Psychoeducation
Educating individuals and their families about schizophrenia is essential for fostering understanding and support. Psychoeducation programs at Rehab Centre India provide information about the nature of the disorder, available treatments, and strategies for managing symptoms.
3. Cognitive Remediation
Cognitive deficits are common in schizophrenia, affecting memory, attention, and problem-solving skills. Cognitive remediation programs at Rehab Centre India focus on improving these cognitive functions, enhancing individuals’ ability to navigate daily tasks.
4. Vocational Rehabilitation
Helping individuals with schizophrenia reintegrate into the workforce is a key aspect of rehabilitation. Rehab Centre India collaborates with vocational therapists to assess individuals’ skills and interests, providing training and support for successful employment.
5. Social Skills Training
Impaired social functioning is a common challenge for individuals with schizophrenia. Social skills training programs at Rehab Centre India aim to improve communication, interpersonal skills, and social confidence, enabling individuals to build and maintain meaningful relationships.
6. Recreational Therapy
Engaging in recreational activities promotes overall well-being and can be therapeutic for individuals with schizophrenia. Rehab Centre India offers recreational therapy programs that incorporate activities such as art, music, and physical exercise to enhance individuals’ mental and emotional health.
The Role of Technology in Schizophrenia Treatment
In the digital age, technology plays a vital role in mental health care, and this is also true for schizophrenia treatment. Rehab Center India leverages technological advancements to enhance the effectiveness of its rehabilitation programs. When it comes to addressing mental health concerns, the role of schizophrenia rehab centers in India is vital in providing comprehensive and advanced care for individuals seeking help.
• Telemedicine
Telemedicine allows individuals to access mental health services remotely, eliminating geographical barriers. Rehab Centre India utilizes telemedicine to provide virtual consultations, therapy sessions, and medication management, ensuring continuous and accessible care for individuals with schizophrenia.
• Virtual Reality Therapy
Virtual reality (VR) therapy is an emerging approach in schizophrenia treatment. It involves the use of immersive virtual environments to simulate real-life scenarios, providing individuals with a safe space to practice and improve social and cognitive skills. Rehab Centre India incorporates VR therapy into its rehabilitation programs to enhance therapeutic outcomes.
• Mobile Applications
Mobile applications designed for mental health support have become increasingly popular. Rehab Centre India may recommend or develop customized mobile apps to support individuals with schizophrenia in managing their symptoms, tracking medication adherence, and accessing resources for ongoing support.
Challenges in Schizophrenia Treatment and Rehabilitation
Despite the progress in schizophrenia treatment, several challenges persist, impacting the effectiveness of rehabilitation efforts. Some of these challenges include:
1. Stigma:
Stigma surrounding mental health disorders, including schizophrenia, remains a significant barrier to treatment. Rehab Centre India actively works to reduce stigma by fostering awareness and understanding in the community.
2. Limited Access to Care
Accessibility to mental health care services, including rehabilitation centers, can be limited in certain regions. Efforts are underway to expand mental health services across India and make them more accessible to individuals in need.
3. Individual Variability
Schizophrenia is a heterogeneous disorder, meaning that individuals may experience a wide range of symptoms and respond differently to treatment. Tailoring rehabilitation programs to meet the unique needs of each individual is an ongoing challenge that requires a personalized approach.
Road To Recovery
Schizophrenia treatment has come a long way, and rehabilitation centers in India, especially the best schizophrenia rehabilitation centers in India located in Delhi, have been playing a vital role in providing comprehensive care for individuals with this complex mental health disorder. Schizophrenia rehabilitation center in India provide a holistic approach that addresses not only the symptoms of schizophrenia but also the overall well-being of the individuals.
Rehab Centre India stands at the forefront of innovation in mental health care, incorporating advanced technologies and evidence-based practices to enhance the effectiveness of rehabilitation programs. By addressing the challenges posed by schizophrenia and promoting understanding and support, these rehabilitation centers contribute significantly to improving the quality of life for individuals living with schizophrenia.
As advancements in the field continue, the hope is that stigma surrounding mental health will further diminish, accessibility to care will increase, and personalized approaches to treatment will become more refined. Through continued research, collaboration, and community engagement, the landscape of schizophrenia treatment and rehabilitation in India is poised for positive growth and transformation.
If you or someone you know is dealing with any form of mental illness and is looking for a treatment facility, then Athena Behavioral Health is the place to be. Backed by a team of experienced professionals, we at Athena make sure that each patient feels comfortable in discussing their situation in detail. We also offer our patients customized treatment plans to make sure that they attain faster recovery and personal support. Sounds interesting? Call us at +91 9289086193 or drop us an email at customercare@athenabhs.com and one of our experts will get back to you shortly.
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-8,281,978,387,690,781,000 | Home WelfareGeneral well-being Why do I have low vitamin D
Why do I have low vitamin D
by Alivia Nyhan
Published: Last Updated on
Many people believe that they do not suffer from a vitamin D deficiency because they regularly consume foods fortified with this nutrient. However, this is not the case and suffering from a low level of vitamin D in the body is a fairly common disorder. There are very few foods with adequate therapeutic levels of this substance, and those fortified do not have the necessary amount to cover what your body demands.
Also, many people believe that vitamin D, also known as calciferol, is a pervasive and accessible substance to acquire, but this is not the case either. It is a steroid hormone that is not easily found in food, but sun exposure is the primary way to obtain it.
The primary function of calciferol is to help absorb calcium and maintain a balance with phosphorus. If you discovered a deficiency of this substance in your body and wonder why you have low vitamin D, at FastlyHealwe want to offer you some details.
Little sun exposure
Generally, during the winter, you do not encounter frequent sun exposure, which can be a possible answer if you wonder why you have low vitamin D. This can also happen if you are one of the people who are without have much exposure to the sun throughout the year, such as the elderly or those who have a disability who cannot go out frequently, among others.
Although overexposure to the sun can cause significant damage to your body, especially to your skin, if you do not have adequate protection, lack of exposure to the sun can also cause damage, such as having a low level of vitamin D in the body. 10 to 15 minutes in sunlight is enough since this light intervenes so that provitamin D and part of the cholesterol is transformed into vitamin D.
A bad diet
If you eat a diet with an absence of foods such as meatfish, or different dairy products, for example, if you are a vegetarian, you become more prone to suffer from vitamin D deficiency.
In addition, if you are one of the people with this type of diet, you could suffer from other disorders because they have not only a low level of vitamin D in the body but also other essential nutrients for you to be healthy in shape.
Digestive diseases
If you maintain a proper diet and still your vitamin D level is low, you may suffer from a digestive disease since many of them have, as a consequence, poor absorption of the nutrients that are integrated into the food you eat.
This is the case of liver failure and pancreatic damage, among other disorders. You must always undergo regular medical checks to detect any changes in time and carry out the appropriate treatment.
Other pathologies
If you are still wondering why I have low vitamin D, other pathologies could cause this disorder, such as osteoporosis, hypothyroidism, obesity, cancer, alcoholism, and chronic kidney failure.
These pathologies have numerous symptoms, and the deficiency of vitamin D in your body is one of them. This is why it is essential always to keep diseases under control
What causes a lack of vitamin D?
Some of the following diseases can develop when you have a low level of vitamin D in your body:
• Dental cavities.
• Colon, prostate, or breast cancer.
• Intestinal inflammation
• Bone deformations, mainly in children.
• Osteoporosis.
• Weak bones in children are called rickets.
Symptoms of vitamin D deficiency
The main symptoms of vitamin D deficiency that you may observe are:
• Sores in the mouth
• Lack of vision
• Swelling in the joints
• Sleep disorders.
This article is merely informative, at FastlyHeal .com we do not have the power to prescribe medical treatments or make any type of diagnosis. We invite you to see a doctor in the case of presenting any type of condition or discomfort.
If you want to read more articles similar to Why do I have low vitamin D, we recommend that you enter our Wellbeing category .
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-5,709,195,721,111,831,000 | Saturday, March 25, 2023
Does Mild Autism Get Better With Age
Don't Miss
How Pediatricians Screen For Autism
Does autism get better with age and Does autism go away with age
Children are screened by pediatricians after they are born. Your childs pediatric primary health care provider will start screening your kid for any developmental or communication challenges.
This will happen at your childs first well-baby appointment.
Pediatricians observe the behavior of your child. They inspect the babys giggles, eye movements. They point or wave and call your babys name to assess their reactions.
In addition, they get family history, examine the health of the child as well as the input from the childs parents or caregivers.
With that, pediatric primary health care providers identify whether the child is at risk for autism spectrum disorder.
The American Academy of Pediatrics recommends that all children be screened for ASD at their 18 and 24 month well baby visits.
This is done in addition to the regular developmental observance and screening. This may identify children with significant developmental delays early.
Multiple tools can be used by the health care provider for ASD screening like Ages and Stages Questionnaires SE-2 , Pervasive Developmental Disorders Screening Test-II , Communication and Symbolic Behavior Scales , and Modified Checklist for Autism in Toddlers Revised with follow-up .
However, screening does not equal to diagnosis.
If pediatricians notice a delay or suspect ASD, they will refer your kid to a specialist in order to provide a certain diagnosis and plan on a treatment plan.
Can You Detect Autism In Newborns
Autism spectrum disorder can be identified in babies as young as two months old. Although subtle signs can be missed if not observed closely, there are certain red flags.
Caregivers should observe the developmental milestones of their children to be able to detect early signs of autism. Parents should be aware of the eye contact of the newborns and follow the development.
From birth, all babies will look more at the eye part of faces. According to studies conducted with babies with eye-tracking technology, lack of eye contact is one of the signs that the newborn may have autism.
The following are some of the other signs seen in newborns as they grow older.
Support Available For Autistic Children When Becoming Teenagers
Some local authorities have charities operating within them, so search the website of your local author to see what support is available. Some offer buddying volunteers for young people with autism who would otherwise have no peer friendships, while others provide support groups for parents and advice on how to navigate the Education, Health and Care Plan process.
For more details on Aspris Children’s Services, please call 0118 970 8068 or
Also Check: Is Dr Shaun Murphy Really Autistic
Do Autistic Children Get Better
Do Children With Autism Spectrum Get Better?
Children diagnosed early on with an autism spectrum disorder may appear to get better as they get older. This is especially true of children who didnt or couldnt speak and then through several hours of speech therapy learned to speak fluently and clearly. However, a child who really has AS does not get better this is a physical, mental, social and emotional developmental disability that stays with a child for life.
This is often a question presented by parents who are hearing this diagnosis for the first time. They are hoping there is an instant cure, like antibiotics for strep throat. Its difficult to hear that your child is different and that all the hopes, dreams and expectations you had of raising wonderful children to adulthood are taking a detour. It takes time for you to adjust to all the modifications you have to make to accommodate your child who has autism spectrum disorder, and thats completely normal.
In the next fifty years, the cause as well as some incredible treatments for ASD will no doubt come to light. Your child cant wait that long. You can help him or her now by showing through examples and encouragement and consistent techniques on how to deal with their ASD.
How Common Is Autism Spectrum Disorder
Does Mild Autism Get Better With Age
Based on most recent CDC report, ASD is estimated to affect about 1 in 54 children, with boys being more likely to have ASD than girls. There were more than 5 million adults in the US, or 2.21% of the population, with ASD as of 2017. Government statistics suggest that the prevalence of ASD has risen 10% to 17% in recent years.
Recommended Reading: What Type Of Mutation Causes Autism
Finding A Place In The Social World
Even if they escape bullying, many teens with ASD struggle with social isolation. A large national study of teens receiving special education services revealed that students with ASD were less likely to take part in social activities than adolescents with speech and language disorders, learning disabilities or intellectual disability.1
More than 40 percent of the teens with ASD never saw friends outside of school. Half were never invited to take part in activities. For 54 percent, friends never called.1
A smaller study found that “social withdrawal worsened with age for a substantial proportion of youths” with ASD between ages 9 and 18, regardless of IQ.2
“Teens say actually the hardest part is not having friends. People think they don’t want to have friends, but they do,” Ms. Sicile-Kira said.
Dr. Keefer said many teens and young adults with ASD want, at a minimum, to be accepted. “There is a desire to be accepted, to have people around you who are nice to you and with whom you can share your interests,” she said.
The “special interests” common to autism can be an escape from social interaction, if a teen occupies himself solely with his favorite topic. “But, if used correctly, those special interests can be a way to connect with other people. An interest in gaming, for instance, is often a way for teenage boys to connect with one another,” Dr. Keefer said.
Understanding Challenges Of Moderate To Severe Autism
Children with moderate to severe autism face similar yet different challenges.
Understand what type of autism your child has as you create a plan that nurtures and equips your loved one to reach his or her full potential and live a life of safety, comfort, and dignity.
You may also be interested in these related articles:
Recommended Reading: Does James Holzhauer Have Autism
Are Siblings At Greater Risk For Autism Spectrum Disorder
The truth is that genetics do play a role in autism. When one child is diagnosed with ASD, the next child to come along has about a 20% greater risk of developing autism than normal. When the first two children in a family have both been diagnosed with ASD, the third child has about a 32% greater risk of developing ASD.
Tip : Find Help And Support
DOES AUTISM IMPROVE WITH AGE?
Caring for a child with ASD can demand a lot of energy and time. There may be days when you feel overwhelmed, stressed, or discouraged. Parenting isnt ever easy, and raising a child with special needs is even more challenging. In order to be the best parent you can be, its essential that you take care of yourself.
Dont try to do everything on your own. You dont have to! There are many places that families of children with ASD can turn to for advice, a helping hand, advocacy, and support:
ADS support groups Joining an ASD support group is a great way to meet other families dealing with the same challenges you are. Parents can share information, get advice, and lean on each other for emotional support. Just being around others in the same boat and sharing their experience can go a long way toward reducing the isolation many parents feel after receiving a childs diagnosis.
Respite care Every parent needs a break now and again. And for parents coping with the added stress of ASD, this is especially true. In respite care, another caregiver takes over temporarily, giving you a break for a few hours, days, or even weeks.
Recommended Reading: What Is The Symbol For Autism
Can A Child Grow Out Of Mild Autism
Research in the past several years has shown that children can outgrow a diagnosis of autism spectrum disorder , once considered a lifelong condition. In a new study, researchers have found that the vast majority of such children still have difficulties that require therapeutic and educational support.
Additional Factors Influencing Autism Development
I like to think that autism gets better with time, regardless of when you were born or the place you sit on the spectrum as, for the most part, universalautism understanding and acceptance seems to only improve, elevating all autistic life as its goes. However, were not quite in the clear just yet, as can be seen by a breakdown of certain demographics.
For example, while early autism diagnosis seems to be key for getting the correct support in place as soon as possible, this opportunity seems to be much less accessible when it comes B.A.M.E communities . This can be seen in how, despite autism quirks varying little between heritages, white autistic kids are often more likely to have a concrete coping mechanism by adulthood.
Similarly, families of low income have also been reported to experience less development than those of upper or middle pay brackets showing that, in certain locals, care is more easily accessed by those who have the deepest pockets.
So does autism get better or worse with age? Well, as these unfortunate comparisons demonstrate, yes our traits and quirks can alter over time, but achieving the preferred results is reliant on how much help we can access. This means that, when seeking to make things better and give autist their best life, we now live in a world where this is an option. However, making sure that those options are available to everyone regardless, of age, ethnicity or income, is still a barrier we are yet to break.
Read Also: Life Expectancy For Someone With Asperger’s Syndrome
Is Autism A Neurological Disorder
Autism spectrum disorder is a neurological and developmental disorder that begins early in childhood and lasts throughout a person’s life. It affects how a person acts and interacts with others, communicates, and learns. It includes what used to be known as Asperger syndrome and pervasive developmental disorders.
Early Signs Of Autism In A 2 Year Old
9 Signs of High Functioning Autism That I Missed ...
If you feel like your 2-year-old doesnt seem to be catching up with their development milestones, you may start looking for certain signs of autism spectrum disorder for any delays.Mild symptoms can be mistaken for being shy or the terrible twos.
Here are some red flags that may indicate ASD:
• Doesnt speak more than 15 words,
• Cant walk ,
• Doesnt know functions of household items like fork,
• Doesnt imitate parents actions or words,
• Doesnt use items for their own purposes,
• Doesnt follow simple instructions
Also Check: Is Level 2 Autism High Functioning
Early Signs Of Autism In Babies
A lifelong condition, autism spectrum disorder can be diagnosed before the child turns two. Early diagnosis can make an enormous difference in their quality of life later on.
There are certain early signs that can be observed in a newborn if your child is on the spectrum. You can detect the first signs in your infant really early in their life.
How Is Nonspeaking Autism Diagnosed
Diagnosing nonspeaking autism is a multiphase process.
A pediatrician may be the first healthcare professional to screen a child for ASD. Parents, seeing unexpected symptoms such as a lack of speaking, may bring their concerns to their childs doctor.
The medical professional may request a variety of tests that could help rule out other possible causes. These include:
• a physical exam
• blood tests
• imaging tests such as an MRI or a CT scan
Some pediatricians may refer children to a developmental-behavioral pediatrician. These doctors specialize in treating conditions such as autism.
This medical professional may request additional tests and reports, which could include:
• a full medical history for the child and parents
• a review of the mothers pregnancy and any complications or issues that arose during it
• a breakdown of surgeries, hospitalizations, or medical treatments the child has had since birth
Finally, autism-specific tests may be used to confirm a diagnosis. Several tests, including the Autism Diagnostic Observation Schedule, Second Edition and the Gilliam Autism Rating Scale, Third Edition , can be used with nonspeaking children.
These tests help healthcare professionals determine if a child meets the criteria for autism.
Don’t Miss: What Is The Symbol For Autism
Some Factors Impacting Autism Growth
I would like to say that autism improves over the period, regardless of where you were born or where you fall on the spectrum, and, for the most part, general autism awareness and recognition appears to be growing, elevating all facets of autistic existence. However, as a breakdown in some populations shows, were not completely out of the woods yet.
While early autism diagnosis seems to be critical for having the right help in place as fast as possible, this ability seems to be even more limited when it comes to B.A.M.E families . This can be reflected in the fact that, considering the fact that autism symptoms differ less by ethnicity, white autistic children are more likely to find a concrete coping plan by adulthood.
Similarly, low-income households have been shown to have less growth than those in the upper or middle-income classes, indicating that in some areas, treatment is most readily accessible by those with the deepest pockets.
What Is Executive Functioning
Does Autism Get Easier With Age? | Patrons Choice
“If you think of your brain as an orchestra, executive functioning is the conductor, making sure all the parts are working together and working properly,” explained neuropsychologist Michael Rosenthal of the Child Mind Institute. Dr. Rosenthal is an author of a new study on executive function problems in teens with ASD and intelligence quotient scores of 70 or above.
People use executive skills when they make plans, keep track of time, remember past experiences and relate them to the present, change course if they hit a roadblock, ask for help, maintain self-control and work successfully in a group.11
Something as mundane as food shopping requires multiple executive skills, Dr. Rosenthal said.
“First you need ‘initiation’ skills to get yourself off the couch. The next step is to ‘plan and organize’ a list of the items you need to get. You need to think about how many meals you need to make and how much money you have in the bank. Let’s imagine the first thing on your list is pears, but when you go to the produce section, the pears are all bruised. You have to have the ‘cognitive flexibility’ to say, ‘Instead of pears, I will buy apples.’ You need ‘inhibition’ to keep from going to the candy aisle, and your ‘working memory’ will help you keep track of the items you’ve purchased,” he said.
Also Check: Can Autism Be Passed Down
Is Playing With Hair Stimming
No. Neurotypicals, or people without autism , also self-stimulate nail biting, hair twirling and foot tapping all count as stims. NTs, as they’re known for short, can usually control their stims and tend to do ones that are considered more acceptable in public than those done by people with autism.
Can A Child Outgrow Mild Autism
Research in the past several years has shown that children can outgrow a diagnosis of autism spectrum disorder , once considered a lifelong condition. In a new study, researchers have found that the vast majority of such children still have difficulties that require therapeutic and educational support.
Read Also: Why Is The Symbol For Autism A Puzzle Piece
What Does Autism Development Look Like
Lets get one thing clear before we continue, autism isnt something which can get better or worse because, quite frankly, that is not how autism works. Autism is a lifelong balancing act of multiple different quirks. So, when we say an autistic person is doing better, we really mean that we are learning to embrace our alternative mindsets, whilst doing worse is letting our unique potential be restricted by:
• Social deficits
• Anxiety
• Restricted and repetitive behaviours
Additionally, when looking at opportunities for autistic people, it should be noted that while all autistic people orbit the same spectrum, not all of us have access to the same space. Therefore, better might mean learning to follow social norms but could just as easily mean learning how to operate a knife and fork both of these are achievements to be proud of and, as such, should be treated no less different.
But what about all those stories of the kid who overcame autism? you may ask. Well, although its not uncommon to find stories along these lines in magazines which appear in dentist waiting rooms, the reality is that in 71% of cases where an autistic person loses their diagnosis, it is often that they were never autistic to begin with, and that this came from an initial misdiagnosis.
Who Can Benefit From Aba Therapy
high functioning autism Fitness
There is a common misconception that the principles of ABA are specific to Autism. This is not the case. The principles and methods of ABA are scientifically backed and can be applied to any individual. With that said, the U.S. Surgeon General and the American Psychological Association consider ABA to be an evidence based practice. Forty years of extensive literature have documented ABA therapy as an effective and successful practice to reduce problem behavior and increase skills for individuals with intellectual disabilities and Autism Spectrum Disorders . Children, teenagers, and adults with ASD can benefit from ABA therapy. Especially when started early, ABA therapy can benefit individuals by targeting challenging behaviors, attention skills, play skills, communication, motor, social, and other skills. Individuals with other developmental challenges such as ADHD or intellectual disability can benefit from ABA therapy as well. While early intervention has been demonstrated to lead to more significant treatment outcomes, there is no specific age at which ABA therapy ceases to be helpful.
ABA therapy can help people living with ASD, intellectual disability, and other developmental challenges achieve their goals and live higher quality lives.
Read Also: What Is The Life Expectancy Of People With Autism
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-6,768,927,414,543,756,000 | TY - JOUR AU - Gervain, Judit AU - Vines, Bradley AU - Chen, Lawrence AU - Seo, Rubo AU - Hensch, Takao AU - Werker, Janet AU - Young, Allan PY - 2013 M3 - 10.3389/fnsys.2013.00102 SP - 102 TI - Valproate reopens critical-period learning of absolute pitch JO - Frontiers in Systems Neuroscience UR - https://www.frontiersin.org/article/10.3389/fnsys.2013.00102 VL - 7 SN - 1662-5137 N2 - Absolute pitch, the ability to identify or produce the pitch of a sound without a reference point, has a critical period, i.e., it can only be acquired early in life. However, research has shown that histone-deacetylase inhibitors (HDAC inhibitors) enable adult mice to establish perceptual preferences that are otherwise impossible to acquire after youth. In humans, we found that adult men who took valproate (VPA) (a HDAC inhibitor) learned to identify pitch significantly better than those taking placebo—evidence that VPA facilitated critical-period learning in the adult human brain. Importantly, this result was not due to a general change in cognitive function, but rather a specific effect on a sensory task associated with a critical-period. ER - | {
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-6,525,581,376,639,876,000 | Sciatica – Sydney chiropractor discusses some common myths
leg painSciatica, probably one of the most common self diagnoses I hear in practice! For the most part people inaccurately use the term “sciatica” to describe any pains that occur in the lower back and radiate into the leg. True sciatica, is the result of compression and or irritation of the spinal nerves either as they exit the low back or further down where they form a bundle (the sciatic nerve) passing through the pelvis into the back of the leg. Sciatica can be a combination of pain, pins and needles, numbness and or weakness in the affected leg and can be on one or both sides.
There are a multitude of other reasons why someone may get back and leg pain!
These include though not limited to injuries to the muscles, joints and supporting structures of the spine, pelvis, hips and lower legs.
Injuries that we commonly see in practice that are mistaken for sciatica are:
1) Hip Bursitis
2) Hamstring tendonitis
3) Recurrent Gluteus medius strain with active trigger point referral
4) Lumbar facet joint sprain
5) Sacroiliac sprain and/or instability
6) Foot and ankle injuries such as plantar fasciitis and Achilles tendonitis
Each injury requires a different management strategy for a full and proper recovery to occur. So when low back and leg pain present a full evaluation and proper diagnosis is the most important step before pursuing any particular type of treatment.
Here are some other distinctions that need to be made about true sciatica:
1) Can occur with or without back pain
2) Occurs in the back of the leg. Pain in the front of the leg has nothing to do with the sciatic nerve.
3) Is commonly caused by disc herniation
4) Is less commonly caused by compression by the muscles in the pelvic region
At Better Health we have a very experienced team of chiropractors, physiotherapists and podiatrists ready to review your case and make sure you get the right sort of care for your particular problem. If you would like further help with your sciatica please contact us on 9518 0722.
Yours in Better Health
Dr Andrew Richards Principal Chiropractor Better Health
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-6,131,145,975,603,360,000 | Skip to main content
Loss of has-miR-337-3p expression is associated with lymph node metastasis of human gastric cancer
An Erratum to this article was published on 11 April 2014
Abstract
Background
Metastasis is the major cause of cancer-related death in patients with gastric cancer, and aberrant expression of various microRNAs (miRNAs) is associated with cancer metastasis.
Methods
Profiling of differentially expressed miRNAs was performed in three cases of primary gastric cancer and the corresponding metastatic lymph node tissues. Then, the five most altered miRNAs were further verified in 16 paired samples. Two of these five miRNAs were further assessed for their effects on the regulation of gastric cancer cell growth and invasion.
Results
The miRNA profile data showed 151 upregulated miRNAs (≥ 1.5-fold) and 285 downregulated miRNAs (≤ 0.67-fold) in the metastatic tissues compared to the primary gastric cancer tissues. Among these five miRNAs (i.e., hsa-miR-508-5p, hsa-miR-30c, hsa-miR-337-3p, hsa-miR-483-5p, and hsa-miR-134), expression of hsa-miR-337-3p and hsa-miR-134 was significantly downregulated in these 16 lymph node metastatic tissues compared to their primary tumor tissues (P<0.05) and in nine gastric cancer cell lines compared to the nonmalignant GES cell line. Furthermore, induction of hsa-miR-134 or hsa-miR-337-3p expression did not dramatically affect gastric cancer cell proliferation, but transfection of the hsa-miR-337-3p mimic did reduce gastric cancer cell invasion capacity.
Conclusions
These findings indicate that hsa-miR-337-3p plays a role in the reduction of gastric cancer cell invasion capacity, and further studies on the mechanism of hsa-miR-337-3p in gastric cancer metastasis are warranted.
Background
Gastric cancer is a significant health problem, accounting for approximately one million new cases and more than 700,000 cancer-related deaths annually in the world [13]. Although the incidence of gastric cancer has substantially decreased in most parts of the world for the past few decades, partially due to consumption of more fresh fruits and reduction of Helicobacter pylori infection in the population [13], to date, a large number of patients with gastric cancer are still diagnosed at advanced stages, which makes curative surgery difficult. Approximately 80% of such patients will die within a short period of time due to regional recurrence or distant metastasis [4, 5]. Tumor metastasis involves a complex series of steps in which tumor cells leave their original site and spread to distant organs or tissues. Metastasis is the major cause of cancer-related death, and the underlying molecular mechanisms are not fully understood. However, it is known that increased migration and invasion of primary cancer cells are the primary means by which gastric cancer cells spread to distant sites. Thus, there is an urgent need and a great clinical interest to better understand the molecular mechanisms responsible for gastric cancer metastasis in order to improve the outcome of gastric cancer patients.
To this end, our recent research on gastric cancer has focused on microRNAs (miRNAs), which are small, single-stranded noncoding RNA molecules of 19–23 nucleotides in length that are able to post-transcriptionally regulate target gene expression [6]. So far, several hundred miRNAs have been identified in plants, animals, and even viral RNA genomes. In humans, miRNAs regulate many cellular processes through binding to 3′-untranslated regions (UTRs) and other regions of protein-coding mRNA sequences of their target mRNAs to cause mRNA degradation or inhibit its translation [7]. Thus, altered miRNA expression plays a role in tumor development and progression, such as tumor cell proliferation, invasion, and metastasis [8]; in addition, certain miRNAs also can predict the prognosis of various cancers, including gastric, breast, lung, and prostate cancers [9, 10]. In gastric cancer, aberrant expression of miRNAs has been linked to tumor metastasis; for example, plasma levels of miR-223, miR-21, miR-218, and miR-25 have been linked to gastric cancer metastasis [11, 12]. Furthermore, elevated miR-21 expression is associated with lymph node metastasis of gastric cancer [13]. Thus, these miRNAs could be useful as biomarkers to predict gastric cancer lymph node metastasis. In addition, miR-625 expression is significantly downregulated and inversely associated with lymph node metastasis of gastric cancer [14]. Therefore, in the present study, we first performed miRNA array analysis to profile differentially expressed miRNAs between primary and secondary gastric cancer tissues. We found that the expression of hsa-miR-134 and hsa-miR-337-3p was significantly less in metastatic lymph node tissues than in primary tumors of gastric cancer. Next, we investigated the effects of hsa-miR-134 or hsa-miR-337-3p on the inhibition of gastric cancer cell growth and invasion. The results of this study may be useful to find potential therapeutic agents to inhibit gastric cancer metastasis.
Methods
Tissue samples
In this study, samples of human primary gastric cancer and the corresponding metastatic lymph node tissues were collected from 19 patients and stored in liquid nitrogen until use. The demographic data of these patients are shown in Table 1. The institutional review board of the First Affiliated Hospital of Bengbu Medical College approved our protocol, and the patients signed a consent form to participate in this study.
Table 1 List of miRNAs found to be less expressed in metastatic lymph node tissues compared to the corresponding primary gastric cancer tissues as determined by miRNA microarray analysis
RNA isolation and miRNA microarray profiling
Total cellular RNA was isolated from tissue specimens using TRIzol® reagent (Invitrogen, Carlsbad, CA). Briefly, the frozen tissues were homogenized by using a biopulverizer with Mini-Bead-Beater-16 and added to TRIzol® reagent for RNA isolation according to the manufacturer’s instructions. The RNA purity was assessed by measuring the absorption rate at 260 nm and at 280 nm in a NanoDropND-1000 spectrophotometer (A260/A280 ratio of 1.8–2.1 was considered acceptable), and the RNA integrity number (RIN) was detected by an Agilent 2000 analyzer (RIN≥8.0).
Next, these RNA samples of human primary gastric cancer and the corresponding metastatic tissues were reversely transcribed into cDNA, labeled with Hy3 and Hy5, and used as probes for miRNA profiling using the miRCURYTM LNA system (MicroRNA array V10.0 whole list, LC Sciences, Houston, TX). After bioinformatics analysis of the primary gastric cancer and metastatic tissue samples, the differentially expressed miRNAs were identified.
Quantitative reverse transcription polymerase chain reaction (qRT-PCR)
To confirm some of these differentially expressed miRNAs, tumor tissues were harvested and stored in RNAlater solution (Ambion, Austin, TX). Total cellular RNA was isolated from RNAlater-fixed tumor tissues or fresh cultured cells by using the mirVana™ miRNA isolation kit (Ambion, Austin, TX) and reversely transcribed into cDNA with the TaqMan® MicroRNA reverse transcription kit (Applied Biosystems, Foster City, CA). Taqman gene expression assays (Applied Biosystems) were used to assess expression levels of hsa-miR-508-5p, hsa-miR-337-3p, hsa-miR-30c, hsa-miR-483-5p, hsa-miR-134, and U6 in tissues or cultured cells by the 7900HT fast real-time PCR system (Applied Biosystems, Darmstadt, Germany). Relative expression levels of each miRNA were calculated using the ΔΔCT method after normalization with U6 levels (an internal control).
Cell lines and culture
A nonmalignant GES cell line and nine human gastric cancer cell lines (SNU1, SNU5, AGS, HGC-27, BGC-823, MGC-803, SGC-7901, MKN-28, and MKN-45) were originally purchased from the Cell Bank of the Chinese Academy of Science (Shanghai, China), stored, recovered, and used at an early passage from cryopreservation in liquid nitrogen. These cells were maintained in RPMI 1640 medium containing 10% fetal bovine serum (FBS), 2 mM L-glutamine, penicillin (100 units/mL), and streptomycin (100 μg/mL). All cell lines were cultured in 6-well plates in humidified air supplemented with 5% CO2 at 37°C. After cell culture for 48 h, total RNAs were isolated and used for qRT-PCR, respectively.
Design of siRNA oligonucleotides and transfection into tumor cells
The oligonucleotides were synthesized by GenePharma (GenePharma, Shanghai, China) and hsa-miR-134 and hsa-miR-337-3p mimics and inhibitors were purchased from Ambion (Austin, TX). miRNA mimics and inhibitors, and siRNA transfection was performed using FuGene® HD transfection reagent (Roche, Mannheim, Germany). In brief, cells were plated in a 24-well plate and grown to 50% confluency. Then, 1 μl of FuGene® HD transfection reagent was diluted in 50 μl of Opti-MEM® I Reduced Serum Medium (GIBCO BRL). After that, 100 pmol of siRNA oligomer was diluted in 50 μl of Opti-MEM® I Reduced Serum Medium without serum (final concentration of oligonucleotides when added to the cells was 20 μM according to the protocol of the manufacture and the preliminary experiments). The FuGene® HD transfection complex and the diluted oligonucleotides were mixed gently and incubated at room temperature. After incubation for 20 min, the complexes were added to each well containing cells and medium. The cells were incubated for 6 h at 37°C in a CO2 incubator prior to testing for transfection.
Cell proliferation assay
A CCK-8 (Dojindo, Shanghai, China) cell proliferation assay was used to assess cell proliferation, according to the manufacturer’s protocol. Briefly, cells were grown and transfected with hsa-miR-134 and hsa-miR-337-3p mimics and inhibitors (50 nM miRNA scrambled control or miRNA mimic or 200 nM miRNA inhibitor scrambled control or miRNA inhibitor) for 48 h [15], detached, and cultured in triplicate in 96-well cell culture plates. At the end of the experiments, the cells were washed with phosphate-buffered saline (PBS), fixed in 1% glutaraldehyde, and stained with 10% CCK-8. The optical density (OD) at 450 nm was directly measured with a Bio-Rad microplate reader (Hercules, CA).
Tumor cell invasion assay
Gastric cancer cell invasion capacity was assessed by using a two-chamber migration system. The upper compartment was inserted into the lower compartment of the BD BioCoat control inserts (BD Discovery Labware, Bedford, MA), 5 × 104 cells in 0.1 mL of serum-free medium containing 1% bovine serum albumin (BSA) were seeded into the upper compartment, and the lower compartment was filled with normal culture medium supplemented with 20% FBS. After incubation for 24 h, cells were wiped away from the upper surface and the cells on the lower surface, which represented the cells that migrated through the control insert membrane, were fixed and stained with crystal violet (Sigma). The number of cells that migrated completely across the filter was determined in five random fields (×400 magnification) for each experiment. Each condition was assayed in triplicate, and each experiment was repeated at least three times.
Statistical analysis
All experiments were repeated at least three times on different occasions. The results are presented as the mean ± standard deviation (SD) for all values. A paired Student’s t-test was used to evaluate statistically significant differences between the parameters of the primary tumor tissues and the metastatic tumor tissues. Analysis of variance (ANOVA) was used for miRNA selection from the miRNA microarray study. P<0.05 was considered statistically significant.
Results
miRNA expression profiles of gastric cancer tissues and the corresponding metastatic lymph node tissues
In this study, we first profiled differentially expressed miRNAs between gastric cancer and the corresponding metastatic lymph node tissues. After profiling three cases of paired tissue samples (the pathology of these cancer tissues is listed in Additional file 1: Figure S1), we found 151 upregulated miRNAs (≥1.5-fold; Additional file 2: Table S1) and 285 downregulated miRNAs (≤0.67-fold) in the metastatic tissues compared to the primary gastric cancer tissues (Additional file 2: Table S1). Specifically, expression of hsa-miR-508-5p, hsa-miR-483-5p, hsa-miR-134, hsa-miR-30c, and hsa-miR-337-3p was reduced in all three metastatic cancer tissues. Thus, we selected these five miRNAs for further confirmation (Table 1) and found that expression of hsa-miR-337-3p and miR-508-5p was four times greater in the primary cancer tissues compared to the metastatic gastric cancer tissues, while miR-483-5p expression was 2.6 times greater, miR-30c expression was 2.14 times greater, and miR-134 expression was 4.9 times greater in the primary cancer tissues compared to the metastatic gastric cancer tissues (Table 1).
Loss of hsa-miR-337-3p and hsa-miR-134 expression in metastatic lymph node tumors
Next, we verified these five selected miRNAs in 16 pairs of primary and secondary gastric cancer tissues using qRT-PCR. Our data showed differential expression of hsa-miR-508-5p, hsa-miR-483-5p, hsa-miR-134, hsa-miR-30c, and hsa-miR-337-3p in these 16 paired samples (Figure 1), while expression levels of hsa-miR-337-3p and hsa-miR-134 were significantly reduced in the metastatic tissues compared to the primary gastric cancer tissues (Table 1).
Figure 1
figure 1
hsa-miR-508-5p, hsa-miR-483-5p, hsa-miR-134, hsa-miR-30c, and hsa-miR-337-3p in primary gastric cancer and the corresponding metastatic lymph node tissue. Differential expression of hsa-miR-508-5p (A), hsa-miR-483-5p (B), hsa-miR-134 (C), hsa-miR-30c (D), and hsa-miR-337-3p (E) in 16 paired samples of primary gastric cancer (GC) and the corresponding metastatic lymph node tissues (LN) as determined by qRT-PCR. The values shows the fold change of the expression level of LN versus GC (n=3).
Expression of hsa-miR-134 and hsa-miR-337-3p in nonmalignant gastric cells and gastric cancer cells
To determine the potential role of hsa-miR-134 and hsa-miR-337-3p in gastric cancer, we assessed their expression in a nonmalignant gastric cell line (GES) and nine gastric cancer cell lines (SNU-1, SNU-5, AGS, HGC-27, BGC-823, MGC-803, SGC-7901, MKN-28, and MKN-45) using qRT-PCR. As shown in Figure 2A, hsa-miR-134 was highly expressed in SNU-5, AGS, HGC-27, MGC-803, and MKN-28 cells but low in SNU-1 cells compared to GES cells. In contrast, expression of hsa-miR-337-3p was only detected in three gastric cancer cell lines, i.e., SNU-5, HGC27, and SGC-7901, at a low level (Figure 2B).
Figure 2
figure 2
Expression of hsa-miR-134 and hsa-miR-337-3p in the nonmalignant gastric cell line GES and nine gastric cancer cell lines. A, hsa-miR-134; B, hsa-miR-337-3p.
Effect of mimics and inhibitors of hsa-miR-134 and hsa-miR-337-3p on MKN-45 cell proliferation
To determine the effects of hsa-miR-134 and hsa-miR-337-3p on the regulation of gastric cancer growth and invasion, we selected the MKN-45 cell line according to its expression levels of these two miRNAs. The mimic was used to determine whether overexpression of these two miRNAs could inhibit tumor cell invasion in vitro, whereas inhibitors were used as controls. (Although they were downregulated in gastric tumor cells, they may have certain levels of expression in tumor cells, and inhibition of their expression may also promote tumor cell invasion.) We transfected hsa-miR-134 or hsa-miR-337-3p mimics or inhibitors into MKN-45 cells and performed a cell viability assay. The data revealed that the changed expression of hsa-miR-134 or hsa-miR-337-3p only slightly affected MKN-45 cell proliferation (Figure 3). miRNA mimics and inhibitors used in this study were listed in Additional file 3: Table S2.
Figure 3
figure 3
Time-course effects of miRNAs on the regulation of gastric cancer MKN-45 cell proliferation. A, hsa-miR-337-3p mimic-transfected MKN-45 cells. B, hsa-miR-134 inhibitor-transfected MKN-45 cells. Data are expressed as mean ± SD; n=4.
Expression of hsa-miR-337-3p affects MKN-45 cell migration and invasion
Since these miRNAs were differentially expressed in primary and secondary gastric cancer tissues, we investigated the effects of hsa-miR-134 and hsa-miR-337-3p on the regulation of gastric cancer cell migration by transfecting hsa-miR-134 and hsa-miR-337-3p mimics or inhibitors into MKN-45 cells and then measured the tumor cell migration capacity. Next, the capacity of the transfected cells was examined using a Transwell-Matrigel invasion assay. Our data showed that transfection with the hsa-miR-134 mimic or inhibitor in MKN-45 cells did not affect the tumor cell invasion capacity (Figure 4A; P>0.05). In contrast, the hsa-miR-337-3p mimic significantly decreased the number of invaded cells (Figure 4B; P<0.05), indicating that hsa-miR-337-3p overexpression may decrease the invasive ability of gastric cancer cells.
Figure 4
figure 4
The effect of hsa-miR-337-3p or hsa-miR-134 mimics or inhibitors on the regulation of gastric cancer cell invasive capacity. A, The migrated cell number of the hsa-miR-134 inhibitor-transfected MNK-45 cells; B: The migrated cell number of the hsa-miR-337-3p mimic-transfected MNK-45 cells. Data are expressed as mean ± SD; n=4; *P<0.05, as compared to the control oligonucleotide (NC) treated group.
Discussion
In this study, we profiled the differentially expressed miRNAs between samples of gastric cancer and the corresponding metastatic lymph node gastric cancer tissues using miRNA arrays. We found several miRNAs that were differentially expressed between the two types of samples. Among them, we chose five of the most altered miRNAs to be verified in paired primary and secondary gastric cancers from 16 patients. Next, hsa-miR-134 and hsa-miR-337-3p were transiently transfected into gastric cancer cell lines, and the data showed that they only slightly affected gastric cancer cell growth. However, hsa-miR-337-3p overexpression reduced the invasive ability of gastric cancer cells in vitro. Therefore, further studies of the mechanism of hsa-miR-337-3p in gastric cancer are warranted.
Although there are a number of published studies that have investigated aberrant miRNA expression in cancer development and progression in vitro and in vivo, little research has focused on the altered expression of miRNAs with cancer metastasis [16]. In the present study, we first profiled the altered expression of miRNAs in metastatic lymph node gastric cancer tissues by comparing them with the corresponding primary tumor tissues. We found that more than 400 miRNAs were differentially expressed between these two types of gastric tissues. To date, there have been several studies that have analyzed miRNA expression for its association with gastric cancer or metastasis [8, 1419], and numerous altered miRNA expressions have been reported [1419], which was confirmed in our current study. However, there have been no reports describing altered miRNA expression between primary gastric cancer tissue and the corresponding metastatic lymph node gastric cancer tissue. Our data support that altered expression of miRNAs does play a role in tumor metastasis. Further studies of these miRNA-targeted genes may provide insightful information for us to understand the molecular mechanisms of tumor metastasis.
Next, we verified 5 miRNAs from the miRNA profiling data in 16 paired gastric cancer tissue samples and in 9 gastric cancer cell lines and found that these miRNA levels were differentially expressed in the tissues and cell lines. Among these five confirmed differentially expressed miRNAs, only miR-483-5p had been previously reported to be associated with human cancer development. For example, Patterson et al. showed that altered expression of miR-483-5p is associated with malignant pheochromocytoma after analyzing miRNA expression in benign and malignant pheochromocytoma tumor samples [18]. Using microarray analysis, qPCR confirmation, and Kaplan-Meier analysis, upregulation of miR-483-5p was found to be significant between adrenocortical carcinomas and adrenocortical adenomas [19]. Although our current data are preliminary, this study provides useful information for future studies of miRNAs for their association with gastric cancer metastasis.
Furthermore, our in vitro data showed that overexpression of hsa-miR-337-3p in gastric tumor cells reduced tumor cell invasive capacity but only slightly reduced gastric cancer cell proliferation. However, to date, the underlying mechanism for the association of hsa-miR-337-3p with human gastric cancer metastasis is unknown. The hsa-miR-337-3p (miR-337) gene is localized at chromosome 14q32.2. In this chromosome locus, BCL11B may act as a tumor-suppressor gene in T-cell acute lymphoblastic leukemia [20, 21]. However, the relationship between hsa-miR-337-3p and BCL11B and their role in gastric cancer metastasis needs to be further determined. Only a few studies have described the role of hsa-miR-337-3p in human tumorigenesis. For example, a previous study has shown that hsa-miR-337-3p is highly expressed in immortalized fetal lung fibroblast IMR-90 cells and is detectable in immortalized human bronchial epithelial HBEC cells [22]. Another study has demonstrated that hsa-miR-337-3p is a modulator of cellular response to taxanes [22]. Furthermore, hsa-miR-337-3p was able to regulate the expression of STAT3 and RAP1A to mediate paclitaxel sensitivity [22]. Indeed, constitutive STAT3 activation is associated with various human cancers and commonly suggests poor prognosis [23, 24]. Previous studies have shown that RAP1A is an important player in adhesion and migration of lymphocytes. Moreover, Rap GTPases are master regulators of integrin activation, cell motility, and the underlying cytoskeletal, adhesion, and membrane dynamics. Rap activation is critical for B-lymphoma cells to undergo transendothelial migration in vitro and in vivo[25]. In addition, altered expression of hsa-miR-337-3p may be critical in renal cell carcinoma (RCC) development, although the analysis of circulating serum levels of hsa-miR-337-3p is unlikely to provide helpful diagnostic/prognostic information in RCC [26]. However, a previous study has reported that hsa-miR-337-3p is among 24 miRNAs that are significantly upregulated in gastric cancer compared to normal gastric mucosae [27], but that study did not specify how many cases were used in the miRNA array analysis and did not verify their results by qRT-PCR [16]. Thus, besides the technological reasons, the previous contradiction of hsa-miR-337-3p expression in gastric cancer can be explained by their different metastatic potentials accordingly to our current findings. Our current study demonstrated that hsa-miR-337-3p acted as a potential therapeutic agent for gastric cancer. For example, we may use a modified hsa-miR-337-3p oligonucleotide mimic to function as hsa-miR-337-3p to inhibit gastric cancer progression and metastasis.
Conclusions
Our current study demonstrated hsa-miR-337-3p downregulation in metastatic gastric cancer tissues and gastric cancer cell lines. Our in vitro study showed that restored hsa-miR-337-3p expression suppressed gastric cancer cell invasion, suggesting that hsa-miR-337-3p may be a potential therapeutic agent to inhibit gastric cancer metastasis.
Abbreviations
CCK-8:
Cell counting kit-8
BSA:
Bovine serum albumin
PBS:
Phosphate-buffered saline
FBS:
Fetal bovine serum.
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Correspondence to Zishu Wang or Qiong Wu.
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The authors confirm that there are no conflicts of interest.
Authors’ contributions
Conceived and designed the experiments: ZW, JW, and QW. Performed the experiments: ZW and JW. Contributed reagents/materials/analysis tools and analyzed the data: ZW, JW, QW, YY, BH, RW, and YL. Wrote the paper: All authors read and approved the final manuscript.
Zishu Wang, Jin Wang contributed equally to this work.
An erratum to this article is available at http://dx.doi.org/10.1186/1756-9966-33-18.
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13046_2013_712_MOESM1_ESM.pdf
Additional file 1: Figure S1: Pathology of samples of primary gastric cancer and the corresponding metastatic lymph node tissues. (PDF 4 MB)
13046_2013_712_MOESM2_ESM.doc
Additional file 2: Table S1: Differential expression of miRNAs between primary gastric cancer and the corresponding metastatic tissue as determined by miRNA expression profile analysis. (DOC 41 KB)
Additional file 3: Table S2: miRNA mimics and inhibitors used in this study. (DOC 31 KB)
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Wang, Z., Wang, J., Yang, Y. et al. Loss of has-miR-337-3p expression is associated with lymph node metastasis of human gastric cancer. J Exp Clin Cancer Res 32, 76 (2013). https://doi.org/10.1186/1756-9966-32-76
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Keywords
• Gastric cancer
• miRNA
• Metastasis
• hsa-miR-337-3p
• miRNA array | {
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-5,383,816,812,919,024,000 | Unlabeled Human Skeleton
This human anatomy diagram with labels depicts and explains the details and or parts of the Unlabeled Human Skeleton. Human anatomy diagrams and charts show internal organs, body systems, cells, conditions, sickness and symptoms information and/or tips to ensure one lives in good health.
Labeled Human Skeleton. The labeled human skeleton system is comprised of 206 different bones of various sizes and shapes, all with the primary purpose of providing support, protection, and shape to the human body. When humans are born we have close to 300 bones, and over time they fuse together.
Written By: Human skeleton, the internal skeleton that serves as a framework for the body. This framework consists of many individual bones and cartilages. There also are bands of fibrous connective tissue—the ligaments and the tendons—in intimate relationship with the parts of the skeleton.
The labeled human skeleton system is comprised of 206 different bones of various sizes and shapes, all with the primary purpose of providing support, protection, and shape to the human body. When humans are born we have close to 300 bones, and over time they fuse together.
Unlabeled Human Skeleton
unlabeled human skeleton
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-1,548,029,511,023,727,000 | free dieting calculator
Eating Right free dieting calculator advice
free dieting calculator
Detox dieting could be the most current trend to hit the wellbeing and physical fitness circles. And because a detox diet plan can flush out toxins through the entire body and rid the body of waste products and impart a spring clean up on your technique, hence attaining fat reduction within the procedure, obese folks are flocking to clinics to endure a detox treatment or diet. The purpose in the 3 day detox should be to purge the harmful toxins from the entire body. Everyone seems to be uncovered to chemical toxins nowadays that come from meals, drinking water as well as the air. You even make poisons in just your entire body daily from usual metabolic procedures. Poisons injury cells and tissues if they are allowed to build-up. Your body contains a really complex detox system that actually works as most effective it could but modern day investigate has found that it just cannot keep up while using the chemical harmful toxins you happen to be bombarded with every single day. The Grape Food plan is effective quite well. Using this type of food plan you try to eat nothing but grapes, including the seeds, and consume only very hot or chilly h2o for around 4 or five times. The extract from grape seeds provide lots of wellness positive aspects, and also the skins have Resveratrol, which aids normal weight-loss. Elimination of meat, fish, eggs, and processed foodstuff that contains pesticides, weighty metallic, stimulants like tea, coffee, alcoholic beverages and cigarettes to get a several times from our diet plan can tremendously reduce the poisonous build-up within our human body. Use of purified drinking water keeps the method hydrated and aids in flushing out wastes with the kidneys. Most of these detox diet plans are made up of fasting, consuming masses of apparent fluids like drinking water and eating mainly veggies. Your program will get flushed out with a eating plan like this but they need to be useful for only confined time durations. Several with the needed minerals, nutritional vitamins and vitamins for any healthy diet regime are missing having a detox diet regime and want to get replaced. Fruits and veggies would be the mainstay of your detox system. You'll be able to have as much as a few servings of fruit in the working day and endless quantities of most veggies. Do not try to eat bananas, potatoes or corn. In the event you try to eat peas, incorporate them for your servings of legumes instead of counting them as veggies. All these are substantial in sugars and starch. Detoxifying your body could be the solitary strategy for cleaning one's body of those toxins. It really is a purely natural process that, prior to now, our ancestors' bodies were being equipped to accomplish all on their individual. At present even so, with bad eating plan and nerve-racking existence, numerous of us realize our bodies are overwhelmed and not able to cleanse on their own correctly. The food plan is currently greatly utilized not only for quickly weight loss, but for detoxing the body, cleaning the blood and kidneys, creating you feel much more energetic, needing significantly less slumber, and getting general additional relaxed. A detox diet is actually a system that minimizes the chemicals ingested to the system by heading for natural meals. It highlights foods like nutritional vitamins and anti-oxidants that the body wants for cleansing. What's more, it involves having in of food that could aid inside the elimination of toxins like significant fiber food stuff and h2o. | {
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8,737,891,641,864,571,000 | Seasonal Affective Disorder
Depressive disorders is a discouraging situation that people ought to attempt to learn how to consider significantly in to get better. It can trigger severe Psychological and bodily aspect effects. A lot of details are accessible concerning depressive disorders. You can select from organic remedies, therapy, and prescription medicines amongst other ways for your plan for treatment to fight depressive disorders. Beneath is an post to assist you in Discovering the most efficient way to deal with your depressive disorders, and make it a factor of the past.
Attempt to keep your regular degree of socialization. Depressive disorders might prevent you from attempting to do your regular actions. In spite of this, remaining sociable is essential to defeating depressive disorders. Continue your regular actions. Shying from your regular actions will only worsen your depressive disorders.
Steer clear of environment, that will end up in a unfavorable cycle of depressive disorders symptoms. Over-analyzing your unfavorable ideas and emotions can have the exact same effect. Transferring your focus on the strengths of your existence While motivating other people to do the exact same can have a severe impact on your general condition of thoughts.
When attempting to deal with depressive disorders, discovering some new pastime or curiosity can be helpful. Keep your existence filled with pursuits and actions, or else it might result in depressive disorders. Attempt some factor you have usually desired to do, for example dancing, artwork or skydiving. No issue what, the secret is to keep in thoughts that new pursuits can help you deal with your depressive disorders.
A lengthy bathtub is generally effective in soothing you, if you really feel at a loss for your depressive disorders. Relaxing in the bathtub hearing soft, soothing songs, or studying your preferred guide can help much ,you really feel better. The hotter the water, the more enjoyable. Your muscle tissue will really feel great, so operate the bathtub as warm as you can securely tolerate.
You need to keep in thoughts that you’re in control of your ideas. Consider away the term stressed out from your whole vocabulary. The term has unfavorable associations and implications, and results in poor emotions and ideas. Remember, phrases have energy, and stressed out is an effective term. Use key phrases like “sensation poorly”, or “not my greatest”, to consider away some of the energy from your emotions.
Decorate your the place to find be as positive and pleased as you can. This will trigger you to normally really feel better your self.
Depressive disorders can be brought on by numerous fundamental factors, and you ought to make your greatest work in attempting to figure out what these fundamental factors are, for your personal depressive disorders. It will be quicker to deal with your emotions if you know very well what leads to them.
You need to look for help from a expert if you are struggling with depressive disorders or even program sadness. They will be in a position to correctly identify you, and determine if you will need any type of medication. They also have the capability to let you know precisely what proper diagnosis of depressive disorders is unpleasant to you.
It is vital that you have a knowledge of precisely what depressive disorders is. Depressive disorders isn’t only psychological, but it is bodily as well. This amounts in your thoughts are restricted by extra amounts of tension and anxiety. This can even make you really feel more stressed out.
Medicines for example, anti-depressants are recommended for depressive disorders, as this promotes the thoughts to step-up its manufacture of this. There are also a quantity of organic techniques which can improve you. Looking after your bodily requirements is the greatest factor you can do to remedy depressive disorders.
Make certain you consume sufficient, and consume wholesome, and well balanced meals. In addition, you ought to bodily exercise, and participate in effective bodily exercise during the day time so that you’re exhausted at evening, and can go to mattress at a sensible hour. Restrict your use of caffeine, which is a stimulant, so that you rest sufficient. Finally, if you’re stressed out, you ought to probably steer clear of Alcoholic beverages. Alcoholic beverages is a depressant, so you need to be cautious of it , if you’re currently sensation is slow or stressed out.
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-503,851,701,053,233,150 | The low sulfated chondroitin sulfate proteoglycans of human placenta have sulfate group-clustered domains that can efficiently bind Plasmodium falciparum-infected erythrocytes
Rajeshwara N. Achur, Manojkumar Valiyaveettil, Channe Gowda
Research output: Contribution to journalArticle
60 Scopus citations
Abstract
Plasmodium falciparum infection in pregnant women results in the chondroitin 4-sulfate-mediated adherence of the parasite-infected red blood cells (IRBCs) in the placenta, adversely affecting the health of the fetus and mother. We have previously shown that unusually low sulfated chondroitin sulfate proteoglycans (CSPGs) in the intervillous spaces of the placenta are the receptors for IRBC adhesion, which involves a chondroitin 4-sulfate motif consisting of six disaccharide moieties with -30% 4-sulfated residues. However, it was puzzling how the placental CSPGs, which have only -8% of the disaccharide 4-sulfated, could efficiently bind IRBCs. Thus, we undertook to determine the precise structural features of the CS chains of placental CSPGs that interact with IRBCs. We show that the placental CSPGs are a mixture of two major populations, which are similar by all criteria except differing in their sulfate contents; 2-3% and 9-14% of the disaccharide units of the CS chains are 4-sulfated, and the remainder are nonsulfated. The majority of the sulfate groups in the CSPGs are clustered in CS chain domains consisting of 6-14 repeating disaccharide units. While the sulfate-rich regions of the CS chains contain 20-28% 4-sulfated disaccharides, the other regions have little or no sulfate. Further, we find that the placental CSPGs are able to efficiently bind IRBCs due to the presence of 4-sulfated disaccharide clusters. The oligosaccharides corresponding to the sulfate-rich domains of the CS chains efficiently inhibited IRBC adhesion. Thus, our data demonstrate, for the first time, the unique distribution of sulfate groups in the CS chains of placental CSPGs and that these sulfate-clustered domains have the necessary structural elements for the efficient adhesion of IRBCs, although the CS chains have an overall low degree of sulfation.
Original languageEnglish (US)
Pages (from-to)11705-11713
Number of pages9
JournalJournal of Biological Chemistry
Volume278
Issue number13
DOIs
Publication statusPublished - Mar 28 2003
Fingerprint
All Science Journal Classification (ASJC) codes
• Biochemistry
• Molecular Biology
• Cell Biology
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2,383,918,862,463,482,400 | Category:
What Are Foods Low in Vitamin K?
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• Written By: Meshell Powell
• Edited By: A. Joseph
• Last Modified Date: 21 January 2017
• Copyright Protected:
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People who have certain medical conditions or those who are taking medications such as blood thinners might be advised to maintain a diet that is low in vitamin K. Some of the foods that are low in this vitamin include bananas, potatoes, and lima beans. Many breakfast cereals do not contain this vitamin at all. Other foods low in vitamin K are artichokes, carrots, corn, and turnips. Before a person makes any significant dietary changes, a medical professional should be consulted to verify that eating foods low in this vitamin is recommended on an individual basis.
Many fruits are low in vitamin K. Bananas, boysenberries, and black currants contain almost none, while dates, figs, cranberries, and cherries are also low in it. Most citrus fruits, such as lemons, limes, and oranges, normally contain low levels as well. Blueberries and blackberries are relatively high in vitamin K and should be avoided by people who must restrict the use of this vitamin.
Several vegetables, including white potatoes and sweet potatoes, do not contain much of this vitamin. Cucumbers are low as long as they are peeled before being eaten. Lima beans and green peppers also are good choices for people who are trying to reduce their vitamin K intake. Leafy green vegetables, such as kale, should be avoided unless approved by a healthcare professional. Salads are popular staples for those who need to reduce vitamin K intake and might include raw foods such as iceberg lettuce, tomatoes, carrots, radishes, and mushrooms.
Most grains are low in vitamin K, so most breakfast cereals are safe. When a person is in doubt, all food labels should be carefully examined. Most varieties of flour and cornmeal don't contain it. Cooked dried beans are healthy choices, as are red or yellow onions. Most types of seafood are either low or completely free from vitamin k.
Before a person begins a diet of foods low in vitamin K, a visit to the medical professional is essential. Each person has unique dietary needs, and the healthcare provider likely will prescribe a specific dietary plan based on the individual health needs of a particular patient. A specific amount of vitamin K intake each day normally will be prescribed based on blood test results the patient's needs. A nutritionist or dietitian can help the patient devise a healthy diet, especially until the patient becomes comfortable knowing which foods are best for his or her diet.
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anon976295
Post 4
Plavix users should eat a diet low in Vitamin K.
anon949627
Post 3
If you make your own salads with just iceberg lettuce and you limit the lettuce to 2 cups for the salad, you get a low amount of vitamin K. Eat the salad once a day and you will be okay.
Rundocuri
Post 2
Heavanet, I thought the same thing when I read this. I guess that if salads contain raw fruits and vegetables that are low in vitamin k and only iceberg lettuce, they are safe to eat. However, iceberg lettuce does contain some levels of vitamin k, so I think that anyone who needs to limit this vitamin in his or her diet should ask a doctor if eating salads is acceptable.
Heavanet
Post 1
This article mentions that salads are often popular for people who need to stay on a low vitamin k diet. This is a bit confusing, because many salads contain dark, leafy greens like spinach and kale that are very high in vitamin k. Does anyone have any thoughts on salads and vitamin k?
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-1,382,940,354,970,035,700 | Vaping During Pregnancy: Is It Okay or a No-Go?
The E-cigarette has become more and more popular over the years. The electric variant of conventional cigarettes, in which no tobacco is used, is less harmful than an alternative for long-term smokers. What we all know smoking during pregnancy can have a huge negative impact on the unborn child. Smoking women should stop smoking immediately after learning the pregnancy. But can this also be done with e-cigarettes or can you vape safely even during the nine months?
Regular Cigarettes During Pregnancy? Under No Circumstance!
In smoking mothers, even small amounts of nicotine and carbon monoxide are passed through the umbilical cord to the child. There, they restrict the blood vessels and thus reduce the oxygen content of the unborn child’s blood. The risks this poses to the child are incalculable. In fact, mothers who smoke during pregnancy give birth on average twice as often to children with learning disabilities than non-smoking mothers. In general, the IQ of children whose mothers smoked during pregnancy is often significantly lower than that of children with non-smoking mothers.
E-Cigarettes: Liquids with and without Nicotine
Unlike regular tobacco cigarettes, e-cigarettes can choose between liquids with and without nicotine. Therefore, the number one risk can be excluded before. If there is carbon monoxide, which is responsible for numerous negative consequences of smoking in and out of pregnancy. The cancer-causing poison gas occurs when insufficient oxygen is present in the combustion of carbonate materials. However, while tobacco smoke contains about two percent by volume of carbon monoxide (as much as the decontaminated exhaust of a car), the vapor of the e-cigarette is completely free of carbon monoxide. This is also only one good news for women who have also decided to vape during pregnancy.
Are Main Components of Liquids Safe for Pregnant Women?
Liquids for e-cigarettes consist mainly of propylene glycol, food flavorings, glycerin and a little water. These are all materials that we find on sites like https://ojivape.com/category/cartridges/ and are more or less safe for our health. For example, glycerine is included in many foods as a food additive. Due to the moisture-spending property of sugar alcohol, which is also added to many cosmetic products. Propylene glycol is also a popular food additive, for example in commercial toothpaste. During pregnancy, hardly anyone will probably abstain from brushing their teeth.
Evaporation vs Burning
Propylene glycol is also part of many tobacco products. In conventional filter cigarettes, the fabric prevents tobacco from drying. However, many health concerns are associated with propylene glycol combustion. In the e-cigarette, however, the fabric is not burned, but only heated.
Vaping During Pregnancy: A Personal Decision
Doctors and other scientists largely agree: the consumption of liquids is much safer than smoking tobacco cigarettes. A study published by College physicians shows that years of vapor caused only about 5 percent of the health damage caused by the equivalent consumption of tobacco by itself.
For one thing, no substances are burned and there is no carbon monoxide. Secondly, you can remove the second major risk factor from the waiver of nicotine-containing liquids. Studies that suggest an increased risk of asthma, allergies and cardiovascular damage to the growing child and the use of e-cigarettes during pregnancy refer exclusively to liquids with nicotine
They’re completely harmless although nicotine-free liquids do not always seem to be. Diethylene glycol and formaldehyde have been found especially in products of unknown manufacturers of nitrosamines. There are also no meaningful long-term studies on steaming, so it remains a personal choice whether one wants to continue to evaporate liquids with his e-cigarette during pregnancy. If so, you should use nicotine-free liquids in any case. Regardless of of whether steam poses less risk than the obvious dangers of smoke, in any case it is safe to avoid both – and therefore risk nothing during pregnancy.
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7,338,048,787,390,963,000 | Skip to content
Why Does Rogaine Cause Hair Loss? (Expert Answers)
⌚️ Got only 60 seconds?
Increased hair loss, one of the most publicized side effects of minoxidil, is often the result of hair follicles rapidly moving through the hair growth cycle and shedding before an anagen phase. This is normal as it is part of the mechanism in how minoxidil works.
We also recommend that you watch this video:
Related Questions
1Does Rogaine Make Your Hair Fall Out?
Rogaine can cause a form of temporary hair loss called minoxidil-induced telogen effluvium. Your hair cycles through four stages of growth: anagen, the growing phase. catagen, transition phase.
2Can Rogaine Make Hair Loss Worse?
The short answer is, no, your Rogaine treatment is not causing you to lose more hair than before, and it will not make it worse than it would be in the future. To understand why it’s not causing your hair loss to get worse, let’s take a look at what Rogaine is and how it works.
3How Long Does Hair Fall Out After Starting Rogaine??
How long does Minoxidil Shedding last? Minoxidil shedding (increased hair loss after using Minoxidil) typically only occurs at the beginning of your treatment. Research shows that minoxidil shedding starts 2-8 weeks after beginning the treatment. After that, the shedding is usually seen to subside.
4Why You Shouldn’T Take Rogaine?
Stop using this medication and tell your doctor right away if you have any serious side effects, including: unwanted facial/body hair, dizziness, fast/irregular heartbeat, fainting, chest pain, swelling of hands/feet, unusual weight gain, tiredness, difficulty breathing especially when lying down.
5Can Rogaine Worsen Hair Loss?
Answer: Hair loss from Minoxidil(Rogaine)
Treatment with Minoxidil can initially cause some increased shedding of hair follicles but long term has not been shown to cause or “speed up” hair loss.17/02/2018
6Why Am I Losing More Hair With Rogaine?
Answer: Hair loss from Minoxidil(Rogaine)
Treatment with Minoxidil can initially cause some increased shedding of hair follicles but long term has not been shown to cause or “speed up” hair loss.
7Can Minoxidil Cause More Hair Loss?
17/02/2018
8Does Hair Loss Get Worse Before It Gets Better With Rogaine?
Increased hair loss, one of the most publicized side effects of minoxidil, is often the result of hair follicles rapidly moving through the hair growth cycle and shedding before an anagen phase. This is normal as it is part of the mechanism in how minoxidil works. | {
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-1,936,761,912,583,517,700 | EATING FOR GOOD HEALTH-AND HAPPINESS
Eastern medicine practitioners and naturopaths have been prescribing dietary changes to help ease physical and mental ailments forever and a day, says Eva Selhub, MD, who is a corporate wellness consultant and a speaker who served as a clinical associate in medicine at the Benson-Henry Institute for Mind, body, medicine at Massachusetts General Hospital for almost 20 years, (who I had the pleasure to meet).
Now Western science is finally catching on, and a growing body of research suggests that the foods we all eat greatly affect our brains as well as our mental health. In fact, so very much good evidence is emerging that a brand-new focus of mental-health research and treatment has now been born: (nutritional psychiatry)
For the last several decades, we had this idea in psychiatry that our mind was separate from our body-that psychiatric illnesses like depression existed in our mind alone, so what we put in our body was largely irrelevant, says Felice Jacka, PhD, who is a professor at the Deakin University School of Medicine in Melbourne, Australia, his focus is mainly on nutritional psychiatry. However, research over the last 10 years has increasingly shown us that mental and physical health are part of the whole and can not be separated. (Eating for good health).
For instance, a study of several hundred Australian women, those who ate the most whole foods like veggies, fruits, unprocessed meats, (Eating for good health), and whole grains were less likely to be diagnosed with anxiety, depression, or bipolar disorders than those who had a very low intake of healthy food. Two other studies done later in Norway and another here in the U.S. discovered much the same.
While it is true that people who are feeling unwell or who are mentally ill may gravitate toward less-healthy “comfort” or convenience foods, it does not fully explain the connection, says Jacka. Profound changes in brain structure and behavior have been seen after manipulating diets in studies of animal: other researchers like Jacka are now in the process of investigating how all of this applies to humans.
So far, the strongest correlations in nutritional psychiatry have been found in the risk of depression, however, evidence also suggests that food may play a role in conditions like dementia, anxiety disorders, attention deficit disorder, and schizophrenia. With every patient, that I now see, I do a complete food assessment and try to make food choices a part of their treatment plan, (Eating for good health), says Drew Ramsey, MD, assistant clinical professor of psychiatry at Columbia University in New York City, also the co-author of The Happiness Diet.
Like any other of our body parts, our brains are basically built out of the food we all eat. Emotions begin in biology, with two nerve cells rubbing together, and those nerve cells are made of the nutrients in food, explains Ramsey. Our bodies can’t make the mood-regulating neurotransmitter serotonin without having iron and tryptophan, he points out, or produce myelin, that being the fatty substance that insulates our brain cells, without vitamin B12 (found in beef, seafood and dairy).
It makes sense, by giving our bodies higher-quality fuel makes our bodies work better from the top of our head to the bottom of our feet, (Eating for good health), but research suggests some other fascinating specifies about how food exerts influence over our state of mind. For example my friends, rats fed a high-fat, refined-sugar diet show reduced amounts of growth factors that are called neurotrophins in the brain, scientists now suspect that something similar happens to the sugar-loving humans. And that is a problem because neurotrophins prompt the growth of new brain cell in the hippocampus, which is a part of the brain that’s key for our memory, Jacka explain.
It is also been noted that the hippocampus is smaller in people that are suffering with depression, however, it grows again when the illness is successfully treated. So it is possible that eating a less-sugary diet could impact depression at the very least in part based on its effect on neurotrophins and the hippocampus.
Oxidative stress on brain cells likely plays a role, as well.Your brain is burning an enormous amounts of glucose {blood sugar} for energy, just like when we burn gas in a car and there is exhaust, when we burn fuel in our brain there’s a type of exhaust: free radicals,
Ramsey says. Over time, those free radicals damage our cells-and that is oxidative stress.” Build up enough damage, it can affect our emotion by interfering with the way our brain cell function.
Brain cells and the signals that they send to each other are part of what creates emotion and mood. If the cells are damaged and unhealthy, the signals that they send become muddled or irregular, and we end up with disorders like anxiety and depression. Antioxidants like vitamins E, C, and beta carotene, and flavonoids like quercetin and anthocyaidins (that are found in dark berries), have been shown to help repair and prevent oxidative stress.
The molecules in food also affect our genes through epignetics. A for instance, the research suggests that flavonoid antioxidants in foods like dark chocolate and zinc from oysters, certain vegetables, or omega-3 fats actually change the way our genes behave, Ramsey says. So if you have a genetic predisposition to depression, your diet my friends can either increase or decrease your risk of developing the illness.
Bacteria in the gut play a variety of roles for keeping our brain healthy. We have a beautiful, and wonderful ecosystem of organisms that live in the mucosal areas of our body like the lining of our stomach and our intestines, Selhub says, who studies the link between gut bacteria and mental health. One way these bacteria benefit our brain is by helping to keep intact the gut lining, which is full of cells that are constantly send messages to our brain.
Our gut lining also acts as a barrier to toxins and aids digestion so, our brain is protected from bad stuff while still receiving needed nutrients. But overwhelm the gut lining with the wrong foods-processed sugars, and some cured meats (like deli meats), trans fats, and processed, white-lour carhydrates-and it can become inflamed and begin to break down, Selhub says, “We know that more inflammation is associated with more mood disorders, including depression.”
The field of nutritional psychiatry is still in its infancy, however, research to date suggests that what seems to really matter, the most is overall diet quality, (Eating for good heal. Here are some ways to improve the caliber of your my friends.
Diets that focus more on whole, unprocessed foods-regardless of whether they include or exclude certain meats, grains, or dairy products-tend to correspond to better mental health than typical “Western” diets full of fast and processed food, packaged snacks, cured meats, and sugary drinks. The Mediterranean diet (which is my favorite), and Asian diets would fit that healthier description, Elizabeth Somer says, RD, the author of Eat Your Way to Happiness. In other words, what all the experts have been telling us for years remains true: Eat lots of colorful fruits and veggies, whole grains and lean protein and very little processed and fatty foods.
Fermented foods like, kimchi (Korean fermented cabbage), miso, sauerkraut (Japanese fermented soybean paste), with kombucha (a fermented drink which is brewed with yeast) it contains probiotic bacteria that the research suggests it will make your gut generally healthier. Some yogurts will also, however, not all, you need to cheek the labels to make sure they contain “live active cultures” with no sugar.
In a 2013 study, UCLA researchers found by eating a fermented yogurt with probiotics twice a day for 30 days led to increased activity in areas of the brain that process sensation and emotion. (How the components of yogurt might specifically affect mood, but, it is still unknown.) The scientific jury is still out on exactly which probiotic supplements may work the and which types of bacteria are most beneficial in the terms of mental health. However, Selhub does recommend increasing the intake of fermented food and thinks that a probiotic supplement can be the best choice for those with depression or anxiety.
Our harried lives lead us to eat more of the junk and processed convenience foods, which my friends may make us feel even more stressed. Unfortunately we don’t focus on finding outlets for our stress as a modern society, our stress overflows and the dam breaks, Selhub says. When there’s a drop in our levels of serotonin and dopamine, which is two brain chemicals that improve mood-we seek out high-carb junk foods in hope to feel better.
Then the food that we eat increases inflammation in our guts, that leads to oxidative stress in our brain, then serotonin and dopamine drop again. It creates a vicious cycle,’ Selhub says. By taking the time to cook at our home even when life feels mighty crazy, or at least selecting healthier prepared meals that are lower in fat with vegetables, whole grains, lean protein, and fermented foods, will indeed, pay off by breaking this off the wall damaging cycle and improving your mood. By (Eating for good health).
Omega-3 fatty acids, specifically the DHA type found in seafood like salmon, (preferably pink salmon) tuna, shrimp, and halibut, seem to be helpful to people with severe depression Jacka says. The membranes of brain cell are partially made from omega-3 fatty acids, so if levels in our diet are low, our brain cell may suffer and not signal each other properly. The exact requirements aren’t know yet, however, the data suggest that we need at the very least 220 mg of DHA per day, the amount you will get if you ate salmon at least twice a week, Somer says.
Depressed patients are often found to be low on vitamin B9 (folate) and B12, leading the experts to conclude that these nutrients are no doubt important to the brain and to good mental health. Low vitamin D is also linked to depression. Almost everybody is deficient in D, Somer says. You need 1,000 IU a day. Spinach, asparagus, and black-eyed peas are packed with folate: and vitamin D can be found in tuna, salmon, eggs, and milk.
May friends if you will begin eating for good health, your life and your overall health will indeed be happier.
May you be always in good health, humbly your Paul Earl.
www.beautiflworid.com
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8 thoughts on “EATING FOR GOOD HEALTH-AND HAPPINESS
1. Hello Paul,
Nutritional Psychiatry? I guess that makes sense. Feed your body, why not feed your mind?
Eating healthy is subjective at times; health for body, health for mind, which foods in what concentrations, etc. I love halibut but I also love my sugars. That said, I’ve been doing the low-carb thing for the past 2 weeks. I’ve lost 10 lbs and am losing the cravings I thought would be impossible to lose, sweets and breads.
I do have two question for you… What about supplements/vitamins? What quantities of which types of food provides the “ideal” balance for eating for your health?
Thanks again,
Scott
1. Good evening Scott, hip hip hooray for you, losing that 10lb, outstanding. This is the deal Scott, everything in this world worth having calls for sacrifice. If a person wants a healthy body, mind, spirit, that person must sacrifice those things that he or she knows is not good for the body. If you want to live longer, if you want to have a quality life, you must treat that only body that you will ever have like it is the king of the universe, that is the bottom line. Take care of your car, your car will take care of you, take care of your body and your body will take care of you. As far as supplements, and vitamins, you always want to have that B complex vitamins as part of your intake, you also want to make sure that you’re taking vitamin D, taking in consideration that the majority of people do not have enough vitamin D within their body. You also want to have a quality multivitamin with minerals, if you are working out you definitely want to have the purest form of whey protein, for energy Aminos +, by Six Star, very good I recommend if you are working out. If you want something to take care of your inside of your body as well as the outside of your body, that is the closest thing that you can get to the fountain of youth, you want to take Redox signaling supplement. Please keep your guns up, and do what you have been doing, and you will be extremely happy with yourself. Cut down on the sugar, we thank you for visiting us, we sincerely hope to see you again. If it’s anything that we can do for you please reach to us. May you be always in good health, humbly your Paul Earl.
2. This article was very informative and a huge eye-opener. I just recently decided to begin a healthy eating lifestyle after finding out I am battling kidney disease. I am getting the basics down with my menus as I need to go low potassium/phosphorous/sodium
There are some veggies I cannot have and I am allergic to fish. I remember always saying to myself while I was chomping down on dirty food. I am killing myself!!! I am now in search of feeding myself on a cellular level and not a physical level.
Do you believe we can reverse some physical ailments just like we can reverse mental ailments?
Thanks for sharing
Shannon
1. Good evening Shannon, it breaks my heart to hear what you’re going through. I do believe that you can repair your body by eating the necessary foods. Combined with CBD oil, I have personally seen this happened before with someone who is dear to me. I also recommend you to use an amazing product that regenerates your cells, that product is Redox Cell Signaling Supplement, you can read a article that I wrote about this on my website. I do believe you will have a complete turnaround in your health if you will combine the CBD oil the cell signaling supplement, and eat the correct foods. We thank you for visiting weightlifting For A Beautiful World, if you ever need anything please reach out to us, May you be always in good health, humbly yours Paul Earl.
3. Hi Paul,
Cannot move my eyes from you training your biceps in the right photo of this page, and I love it. I agree with you for the diet plays an important role in our health & mood, so we must be very careful with each swallow.
For this article I read, I summed up for two kinds of food that we should all try to avoid. One is processed food, and the other is sugar. I will try my best to control my intake for them and start to eat more healthy ingredients for my own body.
1. Good evening Matt, you are correct my friend, if you can stay away from those two types of food you will be doing a huge favor for your overall health. Process foods and white sugar are deadly enemies of our health. I fight all the time with sugar, and I win 98% of the time, the only time that I dropped my guards is on holidays. Food definitely plays a part in how we feel and react to situations. Science and the medical world finally figured that out, exercise, the right food, a little time meditation each day will give you all that you needs to be healthy, happy, and to be able to live a quality life. I think you for visiting us, I do hope you will visit us again. May you be always in good health, humbly your Paul Earl.
4. I am reading this and I am thinking that we make sure to put the right fuel in our vehicles so that it functions properly but we often neglect to do the same with our body. That is so crazy. I think some people if not most, don’t really pay attention to that and they pay the price for it in the long run. Some people think that eating healthy is expensive but not eating healthy is much more expensive in the long run. I love the idea of eating fruits and vegetables on a daily basis. I must say that this article is pretty insightful and provides really good ideas for anyone interested in eating for good health.
1. Good evening Vanessa, thank you for the kind words, and yes it’s insane, especially now what all the information that we receive in the medical field in the science field, that are all saying the same thing concerning our intake of food, yet so many people disregard it and they’re catching diseases and becoming sick so easy. Becoming old before their time, when the reality of it is change your diet, exercise, your body is important take care of it and it will take care of you. Thank you for visiting weightlifting for a beautiful world, if it’s anything that we could ever do for you please reach out to us. May you be always in good health, humbly yours Paul Earl.
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141,765,529,891,670,430 | cancer-icon
Metaplastic ca breast
CA breast of rt side with mrm done and received adj caf reg with rec in ant mediastinum and lung nodules with histology more of sarcoma received 5 chemo cycles of carbo +pacli and planned for radiation as palliative.
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Doctor Answers (1) on Metaplastic ca breast
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Dr. Anil Kumar Jain Bangalore | General Physician
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Hello dear. What's your question? You have just given a statement here and have given a treatment plan. If you are a doctor, then very good. If you are a patient, kindly ask your question. Regards
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4,408,911,162,897,133,600 | Top
20
Doctor insights on: Does Paxil Cause Weight Gain
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1
1
My dr. Told me taking clonazepam and paroxetine could cause weight gain, make it hard to lose weight. How hard is it making it for me? And which pill?
My dr. Told me taking clonazepam and paroxetine could cause weight gain, make it hard to lose weight. How hard is it making it for me? And which pill?
Your doctor: Is correct, but there's no way to tell if the medication is causing the weight gain or not -- other than seeing what happens when you're not taking it compared to when you are. Every patient is an individual and can respond differently. ...Read more
Dr. Michael Rothman
1,333 doctors shared insights
Weight Gain (Definition)
Weight gain is an increase in body weight. This can be a result of increases to muscle mass, increases in body fat, or increases in body fluids like water. Occasionally, weight gain can be a symptom of ...Read more
2
2
Working w docs but is there any other drug besides Paxil (paroxetine) that doesn't cause lots of weight gain and major constipation? I tried lexapro, not good.
Working w docs but is there any other drug besides Paxil (paroxetine) that doesn't cause lots of weight gain and major constipation? I tried lexapro, not good.
Bupropion: Bupropion or Wellbutrin (bupropion) is the antidepressant thought to be associated with less weight gain and, fortunately, fewer sexual side effects as well. In addition, an older class of anti-depressants, tricyclics including amitriptyline, do not typically cause weight gain. Finally, a less often used class of anti-depressants, MAO inhibitors, may be worth consideration. Work with your doctor. Good luck:) ...Read more
3
3
I have had 3 anxiety relapses in 3 years 10 years on Paxil (paroxetine) i was anxiety free.weight gain caused switch Zoloft then lexap and now zolof i feel horrib?
I have had 3 anxiety relapses in 3 years 10 years on Paxil (paroxetine) i was anxiety free.weight gain caused switch Zoloft then lexap and now zolof i feel horrib?
Psychiatrist: SSRI type meds are great for prevention of panic attacks and other anxiety disorders as well. Perhaps the dose isn't high enough. Zoloft is a great medication for anxiety. Some people need more than just 50mg to feel better. Some patients even are put on more than 200mg a day, which is the max recommended. You may need buspar, (buspirone) as well, relaxation techniques, CBT, no stimulants, adequate sleep,... ...Read more
4
4
I take paxil (paroxetine). Paxil (paroxetine) caused 30 lb weight gain. I'm deaf & it aids tinnitus. Any alternative i can use? Please help.
I take paxil (paroxetine). Paxil (paroxetine) caused 30 lb weight gain. I'm deaf & it aids tinnitus. Any alternative i can use? Please help.
Paxil (paroxetine): There are many ssris, a class of antidepressant. Depending on the reason you are taking it (used for anxiety, ocd, as well as depression), a good substitute with less associated weight gain can be selected. Your md can review the options with you, . ...Read more
See 1 more doctor answer
6
6
Could stopping exercising cause weight gain?
Could stopping exercising cause weight gain?
Yes: Yes of course... If you stop exercising and take in more calories than you are expending( now that you have stopped aerobically exersising) than weight gain is a definite possibility ( unless u began dieting seriously @ similar time). Best of luck! ...Read more
7
7
Can ecp cause weight gain?
Can ecp cause weight gain?
ECP: What do you mean by ECP? Emergency Contraception Pill? External Counterpulsation? Extracorporeal Photochemotherapy? Etc.? Just not sure what you mean. Please clarify meaning using words vice acronym and re-ask. ...Read more
8
8
Can threptin cause weight gain?
Can threptin cause weight gain?
Threptin: Threptin micromix powder does not list weight gain as a side effect. Eating threptin biscuits could contribute to weight gain. ...Read more
9
9
Can estrogel cause weight gain?
Can estrogel cause weight gain?
Not normally: Estrogen gel is usually low dose a minimally absorbed so it should not cause weight gain the way an estrogen tablet would. ...Read more
10
10
Does serequel cause weight gain?
Does serequel cause weight gain?
Seroquel (quetiapine): This is dose-dependent & more so with increased sedation, especially the regular release seroquel, (quetiapine) slightly less so with the extended release form. ...Read more
See 2 more doctor answers
11
11
Does microval cause weight gain?
Does microval cause weight gain?
Studies don't show: Studies do not show a direct link between oral contraceptives and weight gain. I see that you have PCOS from your profile. Patients with PCOS tend to struggle with their weight. Oral contraceptives tend to help with menstrual cycle control in PCOS ...Read more
12
12
Could fructose cause weight gain?
Could fructose cause weight gain?
See below YES: The role of dietary fructose in the development of obesity and fatty liver diseases remains controversial, with previous studies indicating that the problems resulted from fructose and a diet too high in calories. However, a new study conducted in an animal model at wake forest baptist medical center showed that fructose rapidly caused liver damage even without weight gain. See your md if youhave? ...Read more
13
13
Could pediasure cause weight gain?
Pediasure: Pediasure is a nutritional supplement designed for use in children during periods of illness, poor appetite or inadequate weight gain. It is a high calorie, vitamin supplemented product which can cause weight gain. Ensure is the adult version. ...Read more
14
14
Mirtazipine does it cause weight gain?
Mirtazipine does it cause weight gain?
Very often: Most common side effects of Remeron (mirtazapine) are weight gain & fatigue. However for some patients who suffered from loss of appetite/weight loss and sleep disturbance while depressed this can be helpful. ...Read more
See 1 more doctor answer
15
15
Does Gralise 900mg cause weight gain?
Gralise: Gralise is gabapentin in a once a day dose. Gabapentin does cause weight gain hence GRalise is not immune from this - yes it can cause weight gain. ...Read more
16
16
Can taking viviscal cause weight gain?
Beauty product: Supplements or vitamins that are not produced by pharmaceutical companies do not require fda approvals hence reliable randomized clinical studies are rare hence i can not comment with any evidence based facts. However users do suggest that it could. ...Read more
17
17
Will eating raisins cause weight gain?
Will eating raisins cause weight gain?
If you eat enough: of ANYTHING with calories....weight gain is possible..Why are you asking ??? Ask question again with more info! Dr Z ...Read more
18
18
How do sulfonylureas cause weight gain?
How do sulfonylureas cause weight gain?
Insulin secretion: Sulfonylureas induce weight gain mainly by increasing Insulin levels and, therefore, utilization of glucose and other metabolic fuels. Other adverse effects include abdominal upset, hypersensitivity reactions, and headache. ...Read more
20
20
Bodybuilding cause weight gain or loss ??
Bodybuilding cause weight gain or loss ??
That depends: Building muscle increases weight but higher muscle mass can increase metabolic rate. ...Read more
See 1 more doctor answer
Dr. Krishna Kumar
617 doctors shared insights
Paroxetine (Definition)
Brand name paxil, (paroxetine) it's an ssri used for treating depression, anxiety, ocd, and several other conditions. It ...Read more
Paxil (Definition)
Paroxetine is a serotonin reuptake blocker which is a kind of ...Read more | {
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2,803,505,607,629,350,000 | Thursday, June 30, 2022
General
What Minerals And Vitamins Are Believed To Be Essential?
Vitamins and minerals are the gas that runs a body. The food that we eat offers us with the vitamins and minerals that our our bodies want to maintain living. Without these vitamins and minerals our bodies would quickly succumb to deficiencies and breakdown. Because of this it will be significant that we eat foods that present us with the proper stability of vitamins and minerals. This way we will ward off disease and keep wholesome.
Vitamins are substances which have each an economic and a nutritional perform. A vitamin is a vital micronutrient that an organism requires in small sufficient quantities for the right working of its immune system. Too much of any vitamin can really damage the immune system, so solely the correct amount of vitamins and minerals can keep us healthy. Furthermore, certain vitamins and minerals are instrumental in guaranteeing that the physique makes use of all the energy it has and makes use of all of the nutrients out there.
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There are plenty of vitamins and minerals which are normally present in fruits and vegetables. Some examples of those nutrients are vitamin c, vitamin d, folic acid, potassium, carotenoids, lycopene, flavonoids, probiotics, and different bioactive phenolics (which are actually a kind of sugar). It is suggested that folks get from five to seven servings of fruits and vegetables per day. This is an efficient fast tip because these are the minimum amounts wanted to make sure that you are getting all the nutrients your body needs. However, if you are on a strict weight-reduction plan, these quantities can nonetheless be surpassed if you don’t cook your foods totally and choose the tastiest vegetables and fruits that you will discover.
There are quite a lot of different vitamins and micronutrients that can be found in some contemporary fruits and vegetables. Some examples of those micronutrients include the B vitamins, calcium, iron, magnesium, sodium, zinc, selenium, thiamin, and folic acid. It’s important to note that some vitamins and micronutrients are extra soluble in one kind than they’re in one other form. Therefore, this means that certain nutrients, comparable to vitamin C, are more easily digested when they’re taken as a pill while different nutrients, resembling vitamin E, might have to be applied with a Q-tip or a finger tip.
For instance, taking a multi-vitamin tablet containing vitamin C requires you to chew it well before swallowing to permit for simpler digestion. However, there are foods equivalent to lean meats, eggs, poultry, fish, pasta, vegetables, and fruits that include the same vitamin, but are easier to digest. In addition, the types of food which have excessive ranges of vitamins and minerals are those which might be often served uncooked and unprocessed. Most of these foods include vegetables, fruits, and entire grain breads and cereals.
Other nutrients which can be necessary to maintain a healthy weight loss plan embrace fat-soluble vitamins akin to vitamin e and beta carotene. Vegetables and fruits also comprise several other fat-soluble vitamins, together with vitamin c and the B vitamins, that are essential to keep up healthy eyesight. Oatmeal, walnuts, and canola oils are good sources of fats-soluble vitamins and micronutrients. Other sources of those nutrients embody green leafy vegetables, entire grains, and nuts. Whole grain foods, nuts, and seeds contain vitamins A, B, and E as well as several other antioxidants which will help forestall damage to the DNA cells of the body attributable to free radicals.
Vitamins and minerals are completely important to the overall health of the body. Therefore, it is very important to just be sure you get sufficient of the vitamins and minerals you want each day. Additionally it is important to eat a balanced weight loss program that incorporates a selection of various nutrients to be able to get the entire vitamins and minerals that your physique wants. As an illustration, it is not possible to get all of the required vitamins and minerals through food regimen alone. Therefore, in addition to taking vitamins and minerals orally, it’s also necessary to take supplements to ensure that you just get a well-balanced diet.
There are several vitamins and minerals that are crucial to keep your immune system robust. These vitamins and minerals embrace folic acid, calcium, iron, and riboflavin. Folic acid is needed to forestall defects in the formation of the brain and spinal cord, which could cause defects within the formation of the bones in your physique. Calcium is needed to strengthen the bones. Iron, on the other hand, is required for elevated amounts of oxygen transport into the mind. Riboflavin is an antioxidant that can scale back the danger for most cancers and cardiovascular disease, and is a part of many of the vitamins and minerals needed for general health.
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Asymmetrical barcode adapter-assisted recovery of duplicate reads and error correction strategy to detect rare mutations in circulating tumor DNA
Abstract
Deep sequencing is required for the highly sensitive detection of rare variants in circulating tumor DNA (ctDNA). However, there remains a challenge for improved sensitivity and specificity. Maximum-depth sequencing is crucial to detect minority mutations that contribute to cancer progression. The associated costs become prohibitive as the numbers of targets and samples increase. We describe the targeted sequencing of KRAS in plasma samples using an efficient barcoding approach to recover discarded reads marked as duplicates. Combined with an error-removal strategy, we anticipate that our method could improve the accuracy of genotype calling, especially to detect rare mutations in the monitoring of ctDNA.
Introduction
The advent of massively parallel DNA sequencing has revolutionized the field of genomics and transformed human medical research. The cost of sequencing has decreased rapidly1 since 2005, which has enabled researchers to explore many basic questions in natural science. Currently, the non-invasive detection of circulating tumor DNA (ctDNA) has great potential to be the ‘holy grail’ of early cancer detection. Cost could be a substantial concern in large-scale projects, however, because great sequencing depth must be achieved to reliably detect rare alleles in ctDNA samples.
It is a major challenge to distinguish true variants from background noise for rare variant discovery2,3, because the error rate ranges from 1 to 10%, which prohibits deconvolution of the clonal structure of tumor genomes. In addition, the heterogeneity of mutations within populations of rare cells in liquid biopsy samples, such as plasma4 or saliva5, make it difficult to distinguish between sequencing-related errors and true somatic mutations originating from tumors. To overcome this issue, high-depth sequencing is frequently used to detect rare variants6,7,8. As a quality-control measure for next-generation sequencing (NGS) data, duplicate reads are usually discarded to allow computational ease of downstream analyses and to mitigate PCR amplification biases. However, removal of duplicate reads could result in genotyping errors in libraries constructed from only a small amount of input material because of the inherently imbalanced nature of the sequencing coverage9.
One potential solution for tracking duplicate sequences is molecular barcoding, which could enhance the accuracy of detection by distinguishing real variants from artifacts generated during PCR. Various barcoding approaches have been implemented to quantify individual molecules10,11 and have allowed actual somatic mutations to be distinguished from background artifacts. Although the ‘duplex’ barcoding strategy yields significantly lower error rates10,12, the method is suboptimal because the required sequencing depth is high. To overcome this limitation, a hybrid approach that combines a statistical error-suppression algorithm with barcodes that track both single-stranded and double-stranded DNA was recently introduced13.
Here, we introduce an asymmetrical sequencing adapter design with the hybridization capture of a small genomic region (the KRAS gene) to recover duplicate reads for the quantification of individual molecules. Our experimental design enabled us to demultiplex samples using the standard Illumina P5 index sequence as well as to barcode double-stranded molecules using an 8-bp random sequence inserted in the Illumina P7 index position. We aligned the demultiplexed samples to the reference sequence, marked duplicate reads as candidates for recovery, and recovered and re-aligned reads that were initially discarded as duplicates. Finally, we smoothed the background errors using Bayesian likelihood estimation. Our simple yet efficient strategy enabled the accurate detection of rare mutations in case-control studies as well as in the non-invasive screening of ctDNA.
Results
Barcoding using an asymmetrical sequencing adapter
We generally defined duplicate reads as read pairs with identical external mapping coordinates. To recover discarded duplicate reads, we designed an experiment using an asymmetrical barcode sequence to distinguish true reads from false duplicate PCR reads14,15 (Fig. 1a). We assigned an 8-bp random ‘N’ barcode sequence to each fragmented DNA molecule by adjusting the standard Illumina sequencing adapter at the P7 index position. Prior to the preparation of the sequencing library, we designed adapter oligonucleotides that self-annealed to produce loop-form adapters. We then attached the self-annealed sequencing adapters to both ends of the randomly sheared genomic DNA molecules using an adapter ligation step (Fig. 1b). After USER enzyme digestion, the ligated adapters created an asymmetric Y-adapter form, which we used to perform PCR with the flanking P7 and P5 primers (to provide a sample barcode for the sorting of data from different samples). Details of the sequencing library preparation and the experimental conditions are provided in the Materials and Methods section.
Figure 1: A schematic of the asymmetrical barcoding method.
figure1
(a) Design of the asymmetrical random index sequencing adapter oligonucleotide. Self-annealing sites 1 and 2 are referred to as R1 and R2, respectively. (b) Sequencing library-preparation scheme using the asymmetrical random index sequencing adapter. The self-annealed barcodes in a were used in the adapter ligation step and subsequently amplified using the P7 flanking primer and the P5 index primer. (c) Comparison of the removal of duplicate candidates with a conventional duplication removal strategy. Molecules with the same barcodes and the same start/end positions were considered true duplicate pairs.
Detection of rare mutations in patients with colorectal cancer
To test the abilities of the asymmetric barcode adapter to recover sequencing depth and detect rare mutations in a clinical application, we constructed a sequencing library using plasma samples from five patients with colorectal cancer and focused on a KRAS mutation known to be prevalent in such cases16,17,18. We validated the KRAS mutation in the five patients by Sanger sequencing using both tumor and whole blood samples. The detailed protocol and primer sequences used for the Sanger sequencing are provided in the Materials and Methods section.
We generated an NGS library based on the three samples by applying our asymmetrical sequencing adapter design with an Illumina HiSeq 4000 system. After discarding low-quality reads, we aligned the reads to the reference genome (GRCh37/hg19) and marked duplicate reads as candidates for recovery. Next, we re-evaluated the discarded reads using the 8-bp barcode composition and aligned the positions to identify the true duplicates (Fig. 1c, Supplemental Fig. 1). We found that these UMI counts were overestimated as they far exceed the upper bound of given input amount. We therefore calculated hamming distances between UMIs within a hamming distance of two or less and retained only the UMI with the highest read count within clusters. In all samples, 25% of original barcodes were discarded and the background error rate dropped 30% on average.
As a result, we observed a significant increase in the mean sequencing depth of each sample (average 2-fold depth increase in the target region), which could enhance the reliability of rare variant detection in clinical samples (Supplemental Fig. 2). Next, to remove background calls, we used the asymmetric barcode adapter and an error correction strategy. Most of the background errors entailed variant-allele frequencies below 0.2%. A large fraction of these false calls were removed by statistical error correction (Fig. 2, Material and Methods). We found that the driver-mutation peaks displayed similar frequencies (average standard deviation = 0.12) after applying our statistical filtering process. Notably, in the ctDNA1 sample harboring the main driver-mutant peak of the G13D mutation, we also detected the G12V mutation in KRAS with a variant-allele frequency of approximately 0.3% (Fig. 2a). Further examination of the reads bearing the G12V mutation confirmed that the reads did not originate from duplicates (Supplemental Fig. 3). We performed Sanger sequencing of the KRAS gene from tumor and normal tissues, and confirmed that the G12V mutation was present only in the tumor tissue (Supplemental Fig. 4). We analyzed the other ctDNA samples in the same manner and detected clear KRAS mutation peaks (Fig. 2b–e). Then, we assessed the sensitivity and specificity of our method using all five plasma samples. We applied the ctDNA index19 as described previously for receiver operating characteristic analysis and achieved an area under the curve of 0.99 after applying the error correction (Supplemental Fig. 5 and Materials and Methods).
Figure 2: Analysis of the performance of the barcoding strategy in five clinical samples.
figure2
The observed allele frequency distributions after error correction for each sample are plotted. The central peaks (amino acid numbers 12 and 13) of chromosome 12 in the graph are the primary mutations detected in the sample. The major-mutation peaks of samples (a) ctDNA1, (b) ctDNA2, (c) ctDNA3, (d) ctDNA4 and (e) ctDNA5 are indicated by the arrows. The allele frequency was calculated within a specific 200-bp region of chromosome 12.
We then analyzed the recovered fraction of reads marked as duplicates for varying amounts of ctDNA input (Supplemental Table 1). We discovered that as the initial number of haploid genome equivalents increased, the number of duplicate reads decreased, despite a similar number of sequencing reads for all of the samples. We reasoned that the proportion of duplicate reads would decrease as the number of distinct molecules increased. To further explore this and other factors affecting the duplicate fraction, we conducted a simulation study to validate our experimental results.
Simulation of the read duplication fraction
To examine the fraction of sequencing reads that were regarded as PCR duplicates in the ctDNA sequencing data, we designed a computational simulation to predict the fraction of duplicate reads that would result during sequencing given variables such as the number of sequencing reads and number of distinct molecules. To compare relative numbers of duplicate reads (Fig. 3a), we simulated NGS reads for ctDNA and sheared tumor DNA using a given number of sequencing reads based on empirical distributions of read lengths. We used a Poisson distribution for the ctDNA because the read length distribution revealed a sharp peak around ~180 bp, with little variance. Conversely, we used a negative binomial (NB) model to fit the tissue DNA length distribution because of the increased flexibility in parameter controls.
Figure 3: Simulation of sequencing reads in the small target region (KRAS gene, five exonic regions) and the impact of the barcoding strategy.
figure3
(a) Size distribution of the sequencing data from the ctDNA and tissue DNA. Two different distributions were used to model each sample type. (b) Simulation of the estimated duplication fraction according to the sample type and number of sequencing reads. The duplication rate of the ctDNA was higher than that of the tissue DNA. (c) Simulation of the duplication rate according to the target size (assuming 0.1% sequencing errors).
We simulated read duplication considering two possible sources of read duplication. The first source of duplication, which is the most common, is amplification bias. The second source of duplication is sampling or alignment duplication triggered by random fragmentation (see Materials and Methods for details). We conducted our simulation assuming a 0.1% substitution-error rate (major errors in Illumina sequencing) in the sequencing reads. We observed an increase in the duplication fraction as the number of simulated reads increased; however, the impact of the two sources of duplication was different between the tissue and ctDNA samples. Consistent with the current notion, PCR amplification was the greatest source of duplication in both samples. However, sampling-induced duplication contributed to the duplication rate was non-negligible in the ctDNA. Notably, the effect of sampling-induced duplication was more pronounced in the ctDNA sample, which is most similar to the actual samples used in the present study (Fig. 3b, see also Materials and Methods).
From our simulations, we concluded that as the insert became shorter and less variable, the number of unique reads that could cover the target site declined. In addition, as the number of unique molecules increased, the number of duplicate reads that could be observed declined. To investigate the possibility of extending our experiment to multi-target regions, we examined the effect of increasing the size of the target region. As expected, the duplication rate decreased as the target region increased, implying a reduced frequency of sampling-induced duplication (Fig. 3c).
Targeted sequencing of rare variants from admixture samples
To assess the analytical sensitivity of the asymmetric barcode adapter, we constructed an additional NGS library using genomic DNA from the CEU HapMap sample NA12878 as a reference and a colorectal cancer cell line (SW480) known to harbor the KRAS G12V mutation as a positive control. We generated a sequencing library from these samples by applying the asymmetrical sequencing adapter design and performed Illumina paired-end sequencing (HiSeq 4000). Next, we created a shuffled library of admixtures containing 1%, 0.5%, and 0.25% of the mutation-bearing SW480 DNA data (Supplemental Fig. 6). After the initial processing of the primary sequences as well as quality trimming and misalignment error removal, we calculated the sequencing depths in the target region. We found that the mean depth after barcode-assisted read recovery increased an average of 2.7-fold (Supplemental Fig. 7), which could facilitate the detection of rare mutations. Further removal of background mutations using statistical error correction enabled reliable detection of the G12V mutation at the expected frequency in each sample, even when the frequency was as low as 0.25% (Supplemental Fig. 8).
Discussion
False-positive mutations based on sampling bias and sequencing errors pose a challenge to the identification of mutations associated with therapeutic targets. In addition, false positives due to factors such as ex vivo oxidative damage can arise during library preparation20,21. Our data revealed a particularly high frequency of G:C > A:T transition errors, which were in line with previous reports13,22. The majority of the alleles found to be reduced after error correction were transition-substitution alleles (Supplemental Fig. 9). These factors might complicate estimations of allele frequency and copy number variation in gene-expression experiments. Accordingly, high-depth sequencing is commonly used to reduce the noise due to background errors and enable the reliable detection of clinically relevant mutations.
Duplicates are often removed in the analysis of NGS data to correct the read-count bias induced by preferential amplification. However, loss of sequencing depth inevitably occurs, because sequenced DNA fragments with the same alignment position and length are indistinguishable from one another. Unlike the detection of germline variants in monoclonal samples, the evaluation of rare clonal mutations in ctDNA studies requires high-depth sequencing. Thus, sequencing costs increase in an effort to achieve the desired sequencing depth23. In addition, unexpected depth loss might impact the sensitivity of the detection limit. Hence, the common practice of removing duplicates can only be justified when sampling coincidence is unlikely and the sequencing depth is low. Nevertheless, no prior studies have attempted a systematic evaluation of the issue. It is critical to estimate the extent of the duplication rate in such scenarios, because the ultimate goal of the sequencing is to obtain a depth of coverage that is adequate for the detection of mutations in various types of samples with reasonable associated costs.
In our study, simulations revealed that a key aspect of the analysis of duplication rates is variation in the insert size. We found that for data with minimal associated variance, such as the ctDNA library, duplicate reads should be removed with great caution, because low-input DNA with high-coverage sequencing leads to more PCR amplification-induced duplicates. The findings from our simulation experiments might vary somewhat from those of actual data, because the actual sequencing error rate is variable and the fragmentation pattern more stochastic. However, it is clear that the impact of the duplicate-removal process samples like ours would not be negligible.
To overcome this problem, we designed a novel barcode adapter to recover reads commonly marked as duplicates. Generally, a sequencing library adapter is used with different types of sequencers for demultiplexing, but not for distinguishing DNA fragments. We modified one side of the sequencing adapter by incorporating random ‘N’ sequences. The diversity of the 48 (random 8-bp) nucleotide sequences provided barcodes that were sufficiently distinguishable in clinically relevant amounts of DNA (~20 ng). Our strategy allowed us to simultaneously demultiplex the samples and quantify the double-stranded molecules. Unlike polymerase extension using degenerate primers and a synthetic template11,24, which limits the diversity of the tags produced, our method generated each molecular tag as a single unit using a balanced mix of oligonucleotides, which provided the desired diversity. This method also allowed us to maximize the informative read length, and thus the sequencing throughput, because preparation of the asymmetric adapter-based sequencing library does not involve an additional adapter annealing sequence. Our strategy was developed based on Illumina’s hairpin adapter by adding a degenerate 8-bp N sequence at the P7 index position, which caused no drop in the library quality. The retention of the original Illumina adapter annealing-arm sequences for the Y-adapter rendered greater ligation efficiency. The use of our barcode system could be extended to the detection of rare clonal variants in more challenging formalin-fixed, paraffin-embedded samples.
One of the other potential applications for the barcode adapter is detection of changes in copy number. Similar to the detection of rare somatic nucleotide variants, the overcorrection of read counts would be detrimental in copy number detection, which is based on the enumeration of the sequencing depth of the target regions25. Our simulation study demonstrated that the impact of duplication removal was substantial following the high-depth sequencing of libraries with smaller insert sizes and variances, such as the fragmented ctDNA library. A quantitative understanding of the duplicate rates in simulations of ctDNA and tissue samples leads us to conclude that deduplication is justified only when the sequencing depth is moderate and the insert size variance is high, and its use should be carefully considered when performing high-depth sequencing experiments.
In summary, our barcoding approach improved the sensitivity of rare variant detection, which enabled the detection of rare alleles in ctDNA samples at a reasonable cost (Supplemental Table 2). We anticipate that our simple barcoding approach, in conjunction with a statistical error correction strategy, could be generally applicable to various NGS-based studies for the accurate quantification of low-frequency alleles and copy number variants.
Materials and Methods
Random index-adapter synthesis and adapter folding for sequencing library preparation
Random index adapters consisted of an 8-bp random barcode at the P7 index position. The oligonucleotides (IDT, USA) for the random index adapter were designed as previously discussed (Fig. 1a). Synthesized adapter oligonucleotides were diluted to a concentration of 100 μM and annealed to form a stem-loop adapter following incubation at 95 °C for 3 min and ramping of 0.1 °C per second to 37 °C. The adapter ligation mixture contained 5 μl 100 μM stem-loop folded adapter oligonucleotides, 5 μl T4 DNA ligase buffer (NEB, USA), and 40 μl nuclease-free water. Folded adaptors were used in the adaptor ligation step during the sequencing library preparation.
Preparation of clinical samples from patients with colorectal cancer
Blood samples were collected from patients with metastatic colorectal cancer receiving chemotherapy at Seoul National University Hospital. From the patients who agreed to voluntarily donate their blood samples for research purposes, 4~6 ml whole blood was collected into EDTA tubes during routine phlebotomy. Plasma was separated by centrifugation with Ficoll solution at 2,000 rpm for 15 min and transferred into micro-centrifuge tubes. Then, the plasma was centrifuged at 13,000 rpm for 10 min to remove cell debris. The supernatant was stored at −80 °C before extraction. The entire separation protocol was performed within 20 min of collection to prevent the degradation of cell-free DNA. Additional clinical information including gender, smoking history, and age was collected (Supplemental Table 3). All patients provided written informed consent before undergoing any study-specific procedures including phlebotomy. The study was approved by the Institutional Review Board of Seoul National University Hospital [IRB number: 1407–060–592] and was conducted in accordance with the Helsinki Declaration.
Sanger validation of the KRAS mutation
The primer pair used for the validation sequencing of the KRAS mutation was designed with the Primer3 program26. The sequences of the primer pair were as follows: ‘f-CTGTATCAAAGAATGGTCCTGC’ and ‘r-CACTATCAAATACTCCACCAGTACC.’ Genomic DNA (gDNA) was extracted from plasma and from normal and tumor tissues obtained from the patients using the DNeasy Blood & Tissue DNA purification kit (Qiagen, USA). Target PCR amplification was carried out using a mixture of 10 μl Taq polymerase 2X Master Mix (iNtRON Biotechnology, Inc., Korea), 8 μl nuclease-free water, 10 ng gDNA, and 1 μl each primer. The PCR conditions included an initial denaturing step of 3 min at 95 °C followed by 40 cycles of 95 °C for 30 s, 58 °C for 30 s, and 72 °C for 30 s and a final extension at 72 °C for 10 min. The confirmed somatic mutations were then compared with the variants noted in the ctDNA data.
Sequencing library preparation and KRAS gene-target capture
Genomic DNA was extracted from the cell lines using the DNeasy Blood & Tissue Kit (Qiagen, USA). The QIAamp Circulating Nucleic Acid Kit (Qiagen, USA) was used to extract ctDNA from 2–3 ml plasma collected from the patients with colorectal cancer. To make the DNA fragment size similar to that of the plasma DNA (for the dilution experiment), shearing (Covaris, USA) was performed for 55 s in a reaction volume of 130 μl. DNA from the plasma samples was used directly for sequencing library preparation. The extracted DNA was end repaired, dA-tailed using the SPARK™ DNA Prep kit (Enzymatics, USA), and ligated using the folded asymmetrical barcode adapter, which was accompanied by USER enzyme (NEB, USA) digestion in accord with standard Illumina sequencing library-preparation protocols. After digestion with the USER enzyme, the samples were PCR amplified using the P5 index primer and the P7 adapter flanking-sequence primer (‘CAAGCAGAAGACGGCATACG’). The PCR mixture consisted of 25 μl KAPA 2X polymerase (Kapa Biosystems, USA), 16 μl nuclease-free water, 5 μl USER-digested product, and 2 μl each primer. The PCR conditions included an initial denaturing step of 3 min at 95 °C followed by eight cycles of 95 °C for 30 s, 52 °C for 30 s, and 72 °C for 30 s and a final extension at 72 °C for 10 min. Each reaction was then purified using AMPure XP beads (Beckman Coulter, USA). KRAS target capture was performed according to the manufacturer’s protocol using a KRAS capture kit (Celemics, Inc., Korea), which targets five exonic regions of KRAS (Supplemental Table 4). The adapter-attached library was denatured at 95 °C for 5 min and then incubated at 65 °C before the addition of adaptor-specific blocker DNA in hybridization buffer accompanied by the customized-baitset reagent, Cot, and salmon sperm. The library sample was hybridized for 24 h, and off-target library was removed using T1 Magnetic Beads. Then, the post PCR amplification step was performed using the target-captured library. The PCR mixture consisted of 25 μl KAPA 2X polymerase (Kapa Biosystems, USA), 20 μl target-captured sample, and 2.5 μl each primer (‘f-AATGATACGGCGACCACCGAG,’ ‘f-CAAGCAGAAGACGGCATACG’). The PCR conditions included an initial denaturing step of 3 min at 95 °C followed by 16 cycles of 95 °C for 30 s, 52 °C for 30 s, and 72 °C for 30 s and a final extension at 72 °C for 10 min. After purification using AMPure XP beads, the samples were sequenced using a 150 bp paired-end Illumina® HiSeq 4000 platform (Theragen Etex Co., Ltd., Korea).
Sequencing and data processing
The sequencing reads with an average Phred base quality score (across entire read) less than 30 were filtered out. The filtered reads were then aligned to the reference genome using NovoAlign (v. 2.07.18, Novocraft Technologies, Malaysia). The Picard Mark Duplicates tool (v.1.128, Broad Institute, USA) was used to mark the candidate duplicate PCR read pairs. We called those reads set I and the unmarked reads set II. We rescued reads from set I reads when the alignment position and random index sequence were exactly the same but the 8-bp barcode sequence was different. The set of rescued reads was joined with the reads from set II and included in the subsequent re-alignment and mutation-detection steps.
Error correction analysis
At the mutation-detection step, the high-confidence, paired, aligned reads (minimum Phred base quality score of 35 in reads) were combined (with at least a 50-bp overlap) into a single consensus reads set to reduce sequencing errors. Non-consensus positions between the forward and reverse reads were labeled as ‘N’.
Mutant alleles were detected using a Bayesian methodology based on prior cancer-specific expectations (based on TCGA MAF files downloaded from the National Institutes of Health website). The probability of observing genotype G in data D from an individual locus was expressed as:
where P(G) was the prior expectation, and p(D|G) was the likelihood of observing the genotype at a locus in a diploid genome (assuming two alleles), the calculation of which can be derived from the error probability matrix. The error probability matrix p(D|G) for all 10 genotype combinations was calculated as the observed sequenced nucleotide versus the actual reference nucleotide in the control samples. The control samples refer to all five plasma DNA samples used to estimate the background distribution. , the probability of each base in a given genotype, was defined as [(p(b|A1) + p(b|A1)], where G = {A1, A2} represented two alleles. Finally, the posterior probability p(G|D) was emitted to disk, and an alternate base in a given genotype was set as background error if the specific genotype combination did not exceed a certain threshold value (0.1 for this study, a user-tunable value). After removing erroneous bases using this soft cut-off strategy, we used somatic lesions as candidate reporters (confirmed by the Sanger sequencing of matched germline samples) to calculate the ctDNA index as in Newman et al.19. Briefly, multiple reporters for each individual probability were combined into single P-value. First, the allele fraction is adjusted incorporating position-specific error rate and the selector-wide (target capture panel) background distribution. Then, using 1,000 iterations of Monte Carlo simulation, these adjusted mean SNV fraction were compared against the null distribution across the selector (target capture panel). All 5 distinct SNVs found in 5-target region (2.2 median SNVs per patient) were validated by Sanger sequencing and independent target capture sequencing in matched tumor samples. ROC analysis was performed as in Supplementary Fig. 6 in original CAPP-Seq paper19 which combines all patient reporters.
Simulation of the read duplication fraction of sequencing data
To calculate the relative read duplication fraction that corresponded to a specific number of sequencing reads, all of the counts were modeled based on an NB distribution (tissue DNA) or a Poisson distribution (ctDNA). We adjusted the mean (Poisson) and dispersion parameters (NB) for the two distributions, which were estimated from actual data. The distribution of the virtual sequencing fragment size is shown in Fig. 3a.
Specifically, we modeled the duplicate rate as the product of the amplicon duplication rate and the alignment duplication rate as follows. Let ‘N’ be the number of unique molecules and ‘m’ be the number of sequencing reads. If ‘C’ is the coverage or the number of amplicons in the library, then Ci is assumed to be drawn from a Poisson distribution (mean:λ). Thus, for a sufficiently large N, the total number of libraries (L) is N × λ.
For number of sequencing reads ‘m,’ each molecule ‘i’ can be sampled from a Bernoulli distribution (Xi = 1 if Ci has been sampled at least once, otherwise Xi = 0). Then,
which can be approximated as
). Let be the total Ci sampled from the library, then the amplicon duplication (DA) rate is
For alignment duplication, we defined ‘m’ as the number of read pairs and Xij as an indicator function [Xij = 1 if at least one reads pair was mapped to the position (i, j), otherwise Xij = 0]. Let R be the reference length and Ik be the distribution of insert sizes. Calculations similar to those outlined above lead to:
As mentioned above, Ik (k = j − i) is a density function of either a Poisson or NB distribution. Therefore, the sampling coincidence (Ds) is given as:
Additional Information
How to cite this article: Ahn, J. et al. Asymmetrical barcode adapter-assisted recovery of duplicate reads and error correction strategy to detect rare mutations in circulating tumor DNA. Sci. Rep. 7, 46678; doi: 10.1038/srep46678 (2017).
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Acknowledgements
This research was supported by grants from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HI13C2163 and HI14C1277), and from the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and Future Planning (grant number: NRF-2015R1A2A2A03006577 and 2016M3A9B6026918).
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J.A., B.H., S.-W. H., T.-Y.K., J.L. and D.B. designed the experiments. J.A., H.J., H.K. and H.-P.K. performed the experiments. J.A. and B.H. analyzed the data and wrote the paper. D.B. and J.L. supervised the project.
Corresponding authors
Correspondence to Ji Hyun Lee or Duhee Bang.
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J.A., B.H., H.K., and D.B. are authors of a patent application for the method described in this paper (Next-generation sequencing data analysis using barcoded asymmetric sequencing adapter, 10-2015-0077246, 10-2016-0068355, PCT/KR2016/005817). The remaining authors declare no competing financial interests.
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Ahn, J., Hwang, B., Young Kim, H. et al. Asymmetrical barcode adapter-assisted recovery of duplicate reads and error correction strategy to detect rare mutations in circulating tumor DNA. Sci Rep 7, 46678 (2017). https://doi.org/10.1038/srep46678
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-2,442,041,539,911,265,000 | What is Orthorexia?
There is no denying that healthy eating is good for us. When we eat right, we can make significant improvements to our overall health and well-being.
But, as with most things in life, everything in moderation. There are those that take healthy eating to an extreme, becoming obsessive, and eventually developing an eating disorder known as orthorexia. If not dealt with, orthorexia can have harsh ramifications.
What is Orthorexia?
Orthorexia, also known as Orthorexia Nervosa, is a type of eating disorder that appears when an individual develops an unhealthy fixation with healthy eating. But unlike other eating disorders that focus on the amount of food a person eats, orthorexia focuses on the quality of food. Typically, someone struggling with orthorexia isn’t trying to lose weight. This is not their issue. Instead, these people develop an obsession with the “purity” of the food they eat.
What Causes Orthorexia?
Currently, there is a lack of research or complete understanding as to why or how this eating disorder develops. However, it is believed that people with obsessive-compulsive impulses and/or other types of eating disorders have a higher risk of developing orthorexia. Other risk factors may include anxiety, a lack of control in other parts of their life, and a tendency toward perfectionism.
Diagnosis of Orthorexia
How can someone tell if they or a loved one are simply making healthy eating a priority or if they have developed orthorexia? The medical community has put forth a couple of diagnostic criteria:
1. An obsessive focus on healthy eating
The question to ask here is, do you or your loved one have an exaggerated emotional response or difficulty related to making food choices? Are you mentally preoccupied throughout the day with making just the right food choice for your optimal health? Do you feel shame or anxiety if you make the “wrong” food choice?
2. Daily Life is Disrupted by Behavior
Does your thinking about making the right food choice disrupt your daily life? Are you experiencing any medical issues (malnutrition, etc.) because of your compulsive behavior? Do your beliefs about food cause distress in your personal or social life?
Overcoming Orthorexia
The consequences of orthorexia can be severe, and the disorder should not be taken lightly. If left untreated a person could experience lasting and damaging health issues. As with other disorders, the first step is to identify its presence in your life.
The second step is to get help from a mental health therapist who specializes in cognitive-behavioral restructuring.
Being mindful of what you put into your body is a good thing. Trying to take care of yourself and make sure you stay healthy is a good thing. Becoming obsessed with food to the point it disrupts your life and causes health issues is dangerous. If you think you or a loved one may have orthorexia, please seek treatment.
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-3,680,162,072,750,993,400 | Neurological case study | Nursing homework help
Assignment 1: Case Study Assignment: Assessing Neurological Symptoms
Imagine not being able to form new memories. This is the reality patients with anterograde amnesia face. Although this form of amnesia is rare, it can result from severe brain trauma. Anterograde amnesia demonstrates just how impactful brain disorders can be to a patient’s quality of living. Accurately assessing neurological symptoms is a complex process that involves the analysis of many factors.
In this Case Study Assignment, you will consider case studies that describe abnormal findings in patients seen in a clinical setting.
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To Prepare
• By Day 1 of this week, you will be assigned to a specific case study for this Case Study Assignment. Please see the “Course Announcements” section of the classroom for your assignment from your Instructor.
• Also, your Case Study Assignment should be in the Episodic/Focused SOAP Note format rather than the traditional narrative style format. Refer to Chapter 2 of the Sullivan text and the Episodic/Focused SOAP Template in the Week 5 Learning Resources for guidance. Remember that all Episodic/Focused SOAP notes have specific data included in every patient case.
With regard to the case study you were assigned:
• Review this week’s Learning Resources, and consider the insights they provide about the case study.
• Consider what history would be necessary to collect from the patient in the case study you were assigned.
• Consider what physical exams and diagnostic tests would be appropriate to gather more information about the patient’s condition. How would the results be used to make a diagnosis?
• Identify at least five possible conditions that may be considered in a differential diagnosis for the patient.
The Case Study Assignment
Use the Episodic/Focused SOAP Template and create an episodic/focused note about the patient in the case study to which you were assigned using the episodic/focused note template provided in the Week 5 resources. Provide evidence from the literature to support diagnostic tests that would be appropriate for each case. List five different possible conditions for the patient’s differential diagnosis, and justify why you selected each.
CASE STUDY : Forgetfulness
A 70-year-old female comes to your clinic with complaints of forgetfulness. She noticed it about a year ago and it has progressively gotten worse. She sometimes forgets what she is going to do when she gets to another room. Her family has noticed the problem with her forgetfulness but she is still able to manage her finances and drive, per her report.
Helpful Resources
https://class.content.laureate.net/e9a262251287e3449ea5d8100f9890a7.pdf
https://class.content.laureate.net/dbe2436288dbe64bc10f33990072de51.pdf
https://class.content.laureate.net/50594842c6d0fb6d170eb9c85c04a8e6.pdf
https://class.content.laureate.net/e3702440ebee2467da4a3f243b7879a4.pdf
https://class.content.laureate.net/8d717ca8cf348ac78883a6ae37bb83aa.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4036230/
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-6,118,554,506,117,543,000 | Early and reversible changes to the hippocampal proteome in mice on a high-fat diet
Fiona H. McLean, Fiona M. Campbell, Domenico Sergi, Christine Grant, Amanda C. Morris, Elizabeth A. Hay, Alasdair MacKenzie, Claus D. Mayer, Rosamund F. Langston, Lynda M. Williams (Lead / Corresponding author)
Research output: Contribution to journalArticlepeer-review
20 Citations (Scopus)
101 Downloads (Pure)
Abstract
Background: The rise in global obesity makes it crucial to understand how diet drives obesity-related health conditions, such as premature cognitive decline and Alzheimer's disease (AD). In AD hippocampal-dependent episodic memory is one of the first types of memory to be impaired. Previous studies have shown that in mice fed a high-fat diet (HFD) episodic memory is rapidly but reversibly impaired.
Methods: In this study we use hippocampal proteomics to investigate the effects of HFD in the hippocampus. Mice were fed either a low-fat diet (LFD) or HFD containing either 10% or 60% (Kcal) from fat for 3 days, 1 week or 2 weeks. One group of mice were fed the HFD for 1 week and then returned to the LFD for a further week. Primary hippocampal cultures were challenged with palmitic acid (PA), the most common long-chain saturated FA in the Western diet, and with the anti-inflammatory, n-3 polyunsaturated FA, docosahexaenoic acid (DHA), or a combination of the two to ascertain effects of these fatty acids on dendritic structure.
Results: HFD-induced changes occur in hippocampal proteins involved in metabolism, inflammation, cell stress, cell signalling, and the cytoskeleton after 3 days, 1 week and 2 weeks of HFD. Replacement of the HFD after 1 week by a low-fat diet (LFD) for a further week resulted in partial recovery of the hippocampal proteome. Microtubule-associated protein 2 (MAP2), one of the earliest proteins changed, was used to investigate the impact of fatty acids (FAs) on hippocampal neuronal morphology. PA challenge resulted in shorter and less arborised dendrites while DHA had no effect when applied alone but counteracted the effects of PA when FAs were used in combination. Dendritic morphology recovered when PA was removed from the cell culture media.
Conclusion: This study provides evidence for the rapid and reversible effects of diet on the hippocampal proteome and the impact of PA and DHA on dendritic structure.
Original languageEnglish
Article number57
Pages (from-to)1-12
Number of pages12
JournalAnnals of Nutrition and Metabolism
Volume16
DOIs
Publication statusPublished - 23 Aug 2019
Keywords
• Dendritic morphology
• High-fat diet
• Hippocampus
• Mice
• Proteomics
ASJC Scopus subject areas
• Medicine (miscellaneous)
• Endocrinology, Diabetes and Metabolism
• Nutrition and Dietetics
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What is Asthma?
Antibodies belong to a family of large protein molecules known as immunoglobulins. In many people, asthma appears to be an allergic reaction to substances commonly breathed in through the air, such as animal dander, pollen, or dust mite and cockroach waste products. The catch-all name for these substances, allergens, refers to anything that provokes an allergic reaction. Some people have a genetic predisposition to react to certain allergens. When these people breathe in the allergen, the immune system goes into high gear as if fighting off a harmful parasite. The system produces a molecule called immunoglobulin E (IgE), one of a class of defensive molecules termed antibodies. The IgE antibody is central to the allergic reaction. For example, it causes mast cells, a type of specialized defensive cell, to release chemical 'weapons' into the airways. The airways then become inflamed and constricted, leading to coughing, wheezing, and difficulty breathing -- an asthma attack.
Without treatment, such as inhaled corticosteriods to reduce the inflammation, asthma attacks can be deadly. The overall death rate for asthma, however, is low. Although several theories exist about why asthma rates have risen during the last two decades, there probably is no simple answer, says Calman Prussin, M.D., head of the clinical allergy and immunology unit at NIAID. One theory is that people today, especially in developed countries, are spending more time indoors, Dr. Prussin says. We are therefore exposed to more indoor allergens, such as dust mite allergen, that cause asthma. 'Our houses are now hermetically sealed to save heating and cooling energy,' he notes, 'and unfortunately this causes more indoor allergen exposure.'
Another reason may be that people today live in cleaner, more sanitary conditions than they did before the industrial revolution, relatively free of disease-causing viruses and bacteria, he says. This clean living affects our immune system. The immune system's defensive white blood cells, called T cells, have two basic 'settings,' he explains. Th1 cells fight infectious viruses and bacteria. Th2 cells fight parasites but are also involved in allergic reactions. 'We are exposed to fewer viruses and bacteria than people were 100 years ago, so perhaps our immune systems have not learned to make Th1 cells as well,' Dr. Prussin says. 'That means we have a greater proportion of Th2 cells in our bodies, which might lead to more allergies and asthma.' Other theories point to increased levels of air pollutants, a decline in the amount of exercise people get, or rising obesity as factors in the increase of asthma.
521
Fact Credit:
NIH NIAID
NIH NIAD Web Site
Further Reading
The Harvard Medical School Guide To Taking Control Of Asthma
by Christopher H. Fanta, Lynda M. Cristiano, Kenan Haver
Related Web Links
Asthma
by National Library of Medicine
Human Respiratory System
by National Emphysema Foundation
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2,806,157,986,605,724,000 | Insulin Glargine Massive Drop To Blood Sugar - Hintwise.com
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-4,681,148,174,537,560,000 | SLEEP AND AGE Tips for a Restful Night’s Sleep
Dr. Nina’s What You Need to Know About Sleep and Age.
By Dr. Nina Radcliff
Many of us can recall “fighting” sleep when we were younger, whether it was naps or going to bed on time. We thought it was some sort of punishment or that we would miss out on something. It is not until the privilege of “sleeping like a baby” leaves us, that we long for the days past: having lullabies sung to us, being read to, and rocked. What most of us would do to turn back the hands of time!
How much sleep do we need through the ages?
On average, the sleep duration recommendations for newborns is 15.5 hours a day, elementary school children 10 hours a day, teens 9 hours a day, adults 8 hours a day, and seniors 7.5 hours a day. The general notion that older adults need less sleep is simply not true.
What is insomnia?
It is the inability to sleep and, unfortunately, it is a common problem that 70 million Americans suffer from. It describes difficulty with initiation, maintenance, duration, or quality of sleep despite adequate opportunity and circumstances. With older adults, the incidence increases dramatically. In fact, sleeping less than the recommended 7.5 hours a day is considered “normal” because it is so common. However, common does not mean normal or healthy.
What effects can insomnia have on us?
Short-term effects may include fatigue, mood disturbances, interpersonal and work-related problems, and an overall reduced quality of life.
Long-term effects can affect our body from head to toe. Chronic sleep disturbances can increase our risk for dementia or other memory impairments, heart problems, weight gain, depression, infections, and even cancer. Studies have even shown that it is a strong predictor of placement in a nursing home or other extended care facility.
Why does sleep become impaired as we age?
In general, the problem with sleep with older adults is not trouble falling asleep, but with staying asleep. One explanation is Advanced Sleep-Phase Syndrome, a circadian rhythm disorder where people go to sleep and wake up at times considered earlier than what is normal.
Additionally, a good night of sleep may become “frustrated” by issues as we age —arthritis, heart problems, restless leg syndrome, certain medications, or needing to use the restroom in the middle of the night.
Is there a prescription I can take for this?
Sleeping aids—whether over-the-counter or prescription—are intended for short-term sleep difficulties. However, the frustration of poor sleep and the desperation that it creates, can lead many to use them as a long-term solution. Doing so is like trying to use a bandage to stop a gushing wound from bleeding. It masks the problem, but does little to solve it or provide good quality sleep.
Additionally, long-term sleeping aids are associated with an increased risk of cancer, heart disease, and premature death. And here is a shocking statistic: greater than 50 percent of all sedatives are used by people aged 65 years and older! In fact, 19 percent of people aged 70-100 years take some sort of sleeping aid.
Then what can I do to help me sleep?
Deal with the problem at its source!
Chronic illnesses. Aches and pains or heart or lung disease can make even the most well-intentioned sleepy sleeper…sleepless. Work with your physician to optimize and manage these conditions in order to get your ZZZ’s.
Certain medications. Diuretics, diabetes medications, and some stimulants can impact sleep architecture. It is important to discuss with your doctor if the medications you are taking can be affecting your sleep. If so, ask him or her about possible alternatives, adjustments to the dosage, or timing.
Mental health issues. Addressing depression, anxiety, social isolation, and bereavement can be invaluable to good sleep.
Obstructive sleep apnea. This term describes repetitive episodes of upper airway obstruction that can lead to drops in oxygen levels and nighttime awakening. If you snore or find yourself waking up in the middle of the night, speak with your doctor.
Restless legs syndrome. This nerve disorder is characterized by “throbbing, pulling, creeping,” or other unpleasant sensations in the legs and an uncontrollable, and sometimes an overwhelming, urge to move them. Speak with your doctor on ways to make your legs more restful.
What is sleep hygiene?
The routines and rituals that we undergo before going to sleep. Good hygiene involves
Avoiding stimulants. Caffeine can perk us up and help us jump-start our day. However, if you are having difficulty sleeping, it may be wise to avoid it in the early afternoon. And don’t forget that tea, chocolate, and sodas also contain caffeine.
Turn down the lights. Our sleep hormone, melatonin, is suppressed with sunlight and artificial light. Before bedtime make sure to shut-off, power down, and unplug televisions, lamps, computers, tablets, and smart phones.
Relaxing activities. Engaging in relaxing activities such as praying, meditating, reading, listening to music, or talking with a loved one can help us drift off to sleep.
Keep it cool. Research has shown that the ideal temperature for a restful slumber is between 60-68oF.
“You are never too old to set another goal or to dream a new dream” — C.S. Lewis. Let’s dream about good sleep and make it a reality. Sweet dreams.
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3,151,198,185,021,375,000 | Does Massage Make You Happier?
Does Massage Make You Happier?
Massage remedy does many things for us and it can be used for a lot of totally different reasons. In the principle there are reasons to use massage therapy, mental health or physical health.
No matter detailed reason you will have for using massage therapy, deep down you may be using it to profit both mentally, physically or both. Delving into the mental well being side of things there may be an fascinating question I wish to look at. We know that massage therapy can be very helpful in helping with psychological well being however can it make you happier?
When it comes to this article we define happiness of contentedness, satisfaction with life and joy. We outline pleased as being at peace along with your life, in a very good state and enjoying the world.
Does massage make you content?
Should you really don't desire it to make you cheerful then it in all probability won't. It is nevertheless very highly effective at making you feel higher, stronger and calm.
Before we take a look at how it could make you are feeling higher we should take a look at the reasons behind any unhappiness. You may be sad because of stress or 유성안마 anxiousness, you could be unhappy because of physical pain, emotional pain or a combination of both. There are a number of reasons in which an individual can find their selves unhappy, and massage may also help with just a few of them.
Particularly if you endure from physical pain, massage may help by curing it. By working with a therapist on a regular basis they'll discover the cause of the pain and work to reduce or remove it utterly, no pain equals happiness.
It may also assist with stress, anxiousness and depression. Just by having a daily slot you should have routine in your life, you'll have something to search forward to and also you even have a soothing experience.
You may as well use massage therapy to enhance your physical well being and as we all know physical exercise will launch feel good endorphins that biologically improve your mood and make you happy.
There are a number of ways in which you may claim massage makes you happy and as long as you retain an open mind to it, there isn't any reason it may possibly't. Of course this is not a assure and other than releasing really feel good chemical compounds it could't directly make a person happy, it may possibly only encourage and facilitate a state of mental well-being. | {
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-727,241,650,171,077,800 | Skip to main content
Case-control study of metabolic syndrome and ovarian cancer in Chinese population
Abstract
Background
Recent studies have proved metabolic syndrome (MetS) was linked to cancer risks. However, few data has examined the relationship between MetS and epithelial ovarian cancer (EOC).
Methods
We conducted a population-based case-control study in Tianjin Medical University Cancer Institute and Hospital, China (2010–2015) that enrolled 573 EOC patients and 1146 matched controls. Data were collected through in-person interviews, anthropometric measurement, and 8-h fasting bloods drawn. MetS was estimated by Chinese Diabetes Society (CDS) definition requiring presence of ≥3 of the following risk factors: 1) body mass index (BMI) ≥25.0 kg/m2,2) fasting plasma glucose ≥6.1 mmol/L or 2-h plasma glucose ≥ 7.8 mmol/L, 3) systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg, 4) triglyceride (TG) ≥1.70 mmol/L or high-density lipoprotein cholesterol (HDL-C) < 1.0 mmol/L. Statistics were completed using chi-square tests and logistic regression analysis. The survival analysis was conducted by the Kaplan-Meier method and Cox proportional hazard regression models.
Results
MetS was significantly more prevalent among EOC (25.13%) than controls (6.89%). A statistically significant increase risk for EOC was observed for MetS (multivariable-adjusted OR = 3.187; 95% CI: 2.135–4.756). MetS was significantly associated with histological grade (P < 0.001), FIGO stage (P = 0.003), and lymph node (LN) status (P = 0.002) of EOC. In binary logistic regression analysis, the presence of MetS predicts the risk of advanced FIGO stage (OR = 2.155, 95% CI: 1.327–3.498, P = 0.002), lower differentiation (OR = 2.472, 95% CI: 1.164–5.250, P = 0.019), and LN metastasis (OR = 2.590, 95% CI: 1.089–6.160, P = 0.031) of EOC. Moreover, MetS is the independent factor for the evaluation of PFS and OS of EOC patients (both of them P < 0.001) in Cox proportional hazard model.
Conclusion
MetS is obviously related to increased EOC risk. EOC patients with MetS in Chinese population were found to have statistically significant tumor advanced stage, low differentiation, LN metastasis and poor prognosis.
Background
Approximately 95% of ovarian cancers are of epithelial origin. Epithelial ovarian cancer (EOC) was the leading killer among women with gynecologic cancers. In 2015, there were 22,280 estimated new diagnoses of ovarian cancer and 14,240 deaths from the disease [1]. Statistic revealed the morbidity and mortality of ovarian cancer were rising obviously [2]. However, scientists do not reach a consensus about the prevalence of ovarian cancer because of oncologic diseases have multiple causes. Recently, many researchers considered tumorigenesis process in the body as a systemic disease [3]. So, research attentions focused on the etiology and cause of cancer that lead to dysfunction and abnormality of metabolism increasingly [4, 5].
The metabolic syndrome (MetS) is a cluster of risk factors that includes central adiposity, high blood pressure, elevated blood glucose levels, elevated triglycerides (TG), and low high-density lipoprotein cholesterol (HDL-C) [6, 7]. In the last several years, several interesting studies have been published showing an association between cancer risk and the different components of MetS [8]. A noted large population-based enrolled 16,677 participants who were on medications for hyperlipidemia, diabetes and hypertension and were followed them for up to 8 years. A total of 823 incidents of cancer occurred during the study period, including a significantly increased risk of pancreatic cancer in males and colorectal cancer in females. Additionally, risks of women with liver, gallbladder and billiard tract, breast, and endometrial cancers were also increased [9]. MetS has emerged as a possible clinical condition that predisposes women to suffer breast and endometrial cancers, which associated with hormone disorder [10, 11].
However, epidemiologic studies linking MetS to ovarian cancer are scarce in spite that ovarian cancer is hormone related. Therefore, this present study aimed to collect the information on different components of MetS in a population-based control study of ovarian cancer and examined the role of metabolic dysfunction in EOC, in addition to examining risk with individual components of the MetS.
Methods
Study population
Our population-based case-control study of physical activity and ovarian cancer risk was approved by institutional review board of Tianjin medical university cancer institute and hospital. The clinicopathologic information of ovarian cancer group was collected from consenting patients diagnosed and treated for EOC between January 2010 and December 2015 at Department of Gynecologic Oncology, Tianjin Medical University Cancer Institute and Hospital. Clinical data from 630 consecutive EOC patients were extracted with routine preoperative serum detection. Twenty-five patients with concomitant endometrial cancer were excluded due to possible confounding neoplastic effect on serum lipid, while 32 patients were excluded with a previous history of cancer (five patients with breast cancer, seven with colon cancer, six with rectum cancer and fourteen with other cancers), leaving 573 patients for further analysis. The population-based controls were collected from Physical Examination Center, Tianjin medical university cancer institute and hospital, with all of the participants agreeing and signing consent forms. The controls had no history of hysterectomy, ovarian diseases, or previous cancer and were frequency matched to cases (2:1 ratio). Remarkably, there were not statistically different significances between the EOC group and the control group on age, pregnant times, menopause age, ever hormone use, and age of first pregnancy when choosing matched control cases.
Data collection
Data were collected through in-person interviews using a structured questionnaire and cognitive interviewing methods, in which information on demographic variables and ovarian cancer risk factors including medical history and exogenous hormone use. Three measurements of height, weight and waist circumference were taken using standardized methods for anthropometric measurements at the time of interview, with the mean used as the final measurement. Blood was collected after a minimum 8-h fast, either prior to surgical treatment by hysterectomy or post surgery and subsequent to interviews for cases whose blood could not drawn pre-surgery. Blood was drawn post-interview among controls. A 10-mL blood sample was collected according to a standardized protocol, and samples were processed into blood fractions (serum, plasma, red blood cells, and buff coat), frozen at −80 °C within 24 h of collection, and transported for storage to a specimen bio-repository at the Department of Gynecological Oncology, Tianjin medical university cancer institute and hospital, Tianjin, China.
At present, there are two kinds of international definitions to diagnose MetS that are currently available for clinical use: (1) the National Cholesterol Education Program (NCEP)-Adult Treatment Panel (ATP) III [12]; (2) the International Diabetes Federation (IDF) [13]. Considering Chinese population was enrolled in this study, MetS was defined according to the Chinese Diabetes Society (CDS) definition [14]. Patients were diagnosed with MetS when they had three or more of the following indications: 1) body mass index (BMI) ≥25.0 kg/m2,2) fasting plasma glucose ≥6.1 mmol/L or 2-h plasma glucose ≥ 7.8 mmol/L, 3) systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg, 4) triglyceride (TG) ≥1.70 mmol/L or high-density lipoprotein cholesterol (HDL-C) < 1.0 mmol/L. Participants met the criteria for high blood pressure or high fasting glucose concentration if they underwent hypertension or hyperglycemia treatment. BMI was calculated as weight in kilograms divided by the square of height in meters.
Follow up
Data were collected until death or December 2016. Overall survival (OS) was defined as the time interval from the date of primary surgery to the date of death (failure) or to the end of follow-up for women who were alive (censored). Progression-free survival (PFS) was defined as the time elapsed from the date of primary surgery to the appearance of disease recurrence or progression (failure) or the last follow-up for women who were alive with no evidence of disease recurrence or progression (censored).
Statistical analysis
Continuous data and frequency data were analyzed by Fisher’s exact test and the chi-square test. Results of continuous variables were expressed as mean ± standard deviation (SD). Logistic regression analysis was used to estimated ORs and 95% CIs for developing ovarian cancer in association with presence of MetS and individual biological MetS components. The individual biological MetS components were modeled as meeting the respective cut-point according to CDS definition. Two-sided P-values were considered statistically significant at P ≤ 0.05. The survival was determined by the Kaplan-Meier method, and the log rank test was used to determine significance. MetS and its components were included in the multivariate analysis by using of Cox proportional hazard regression models. Statistical analysis was performed using SPSS software passage for Windows (version 20.0; SPSS Inc., Chicago, IL, USA).
Results
The participant characteristics in this study were presented in the Table 1. Among this population, the average ages in 573 EOC and 1146 control cases were 52.59 ± 9.20 and 52.97 ± 9.73 years, respectively. In Table 1, the proportion of cases with levels of TG, HDL-C, BMI were demonstrated in EOC and control groups according to the cut-offs for MetS criterion in China. The proportion of cases with a history of hypertension or diabetes was also collected in Table 1.
Table 1 characteristics of epithelial ovarian cancer cases and population-based controls
As given in Table 2, we compared the proportion of participants having MetS according to three different definitions and the results did not differ significantly. The kappa value of interrater agreement was 92.5% between CDS and ATP III, 93.2% between CDS and IDF, and 90.0% between ATP III and IDF. The prevalence of MetS in our whole population ranged from 12.62% to 13.90% overall, assessing by three MetS criterions respectively. A higher range in proportion of 24.96% to 27.75% among EOC patients was found according to MetS diagnosis compared to control population ranging from 6.46% to 6.98% (Table 2).
Table 2 proportion of metabolic syndrome by three different criteria in our study
As shown in Table 3, the proportion of patients with MetS as identified by CDS guidelines was significantly greater among 144 cases (25.13%) than 79 control cases (6.89%) and was associated with a 3.187-fold increase in EOC risk (multivariable-adjusted OR = 3.187; 95% CI: 2.135–4.756). Similarly, the magnitude of the risk increase was also observed with the other 2 versions of MetS (ATPIIIand IDF), with statistically significant ORs ranging from 3.277 (95% CI: 2.150–4.993) to 3.376 (95% CI: 2.271–5.018) for the multivariable model (Table 3). EOC risk also was enhanced by most of the individual components of the MetS, including BMI ≥ 25.0 kg/m2 (multivariable-adjusted OR = 1.385; 95% CI: 1.129–1.699), TG ≥1.70 mmol/L (multivariable-adjusted OR = 2.861; 95% CI: 1.040–7.873), HDL-C < 1.0 mmol/L (multivariable-adjusted OR = 2.142; 95% CI: 1.730–2.652), ever being diagnosed and treated for hypertension (multivariable-adjusted OR = 2.423; 95% CI: 1.963–1.2.990), and diabetes (multivariable-adjusted OR = 2.240; 95% CI: 1.749–2.869). All of the above were P < 0.01.
Table 3 age-adjusted and multivariable ORs and 95% CIs for risk of ovarian cancer
Consequently, we compared the pathological characteristics between EOC patients with or without MetS as defined by definition of CDS in Table 4. One hundred and forty-four cases (25.13%) EOC patients were diagnosed with MetS using by definition of CDS. The mean age with MetS group was 56.02 ± 8.00 years, which was higher than the non-MetS group (51.44 ± 9.29 years). Among 144 patients with MetS, we found 50 cases (34.72%) with lower differentiation, 119 cases (82.64%) with advanced FIGO stage, and 33 cases (22.92%) with lymph nodes (LN) metastasis, respectively, which were obviously higher than non-MetS patients with lower differentiation (18.82%), advanced stage (69.93%), and LN metastasis (12.35%). According to our results, statistically significant differences were observed in tumor differentiation grade, FIGO stage, and LN status between patients with or without MetS (P<0.05). In other words, tumor combining with MetS was more malignant clinical pathological behaviors in EOC patients.
Table 4 comparison of pathological characteristics between ovarian cancer patients with or without metabolic syndrome using Chinese Diabetes Society definition
Consequently, in age-adjusted binary logistic regression analysis, the presence of MetS predicts the risk of advanced FIGO stage (OR = 2.155, 95% CI: 1.327–3.498, P = 0.002), lower differentiation (OR = 2.472, 95% CI: 1.164–5.250, P = 0.019), and LN metastasis (OR = 2.590, 95% CI: 1.089–6.160, P = 0.031) of EOC patients (Table 5). Additionally, other parameters relating to MetS were listed in Table 5.
Table 5 Binary logistic regression analysis examining patients with MetS for characteristics of epithelial ovarian cancer
The survival analysis was showed in Table 6. By the Kaplan-Meier method of univariate analysis, the shorter median of PFS and OS were related to EOC patients with MetS (39 vs 42 months and 67 vs 71 months, respectively, both of them P < 0.01, Fig. 1) and BMI ≥25 kg/m2 (40 vs 44 months and 67 vs 70 months, respectively, both of them P < 0.01). Furthermore, in Cox proportional hazard model, MetS was the independent factor for the evaluation of PFS and OS of EOC patients (both of them P < 0.001).
Table 6 Univariate and multivariate survival analysis of MetS for progression-free and overall survival in 573 EOC patients
Fig. 1
figure1
Kaplan–Meier curves for survival of 573 patients with epithelial ovarian cancer. Cumulative progression-free survival (a) and overall survival (b)
Discussion
MetS was originally recognized as a cluster of risk factors that better predicted cardiovascular disease and diabetes incidence, than simple BMI or obesity measures [15] since it was firstly proposed by Reavan in 1988 [16] and the accepted criteria for clinical identification of the components of MetS has been promulgated by NCP-ATPIII [17] and WHO as well as IDF [13], and the American Association of Clinical Endocrinologists (AACE) [18]. At present, accumulating epidemiological literature appeared and had manifested that MetS was closely related to the occurrence and development of malignant diseases in different territorial populaiton [8]. Chiu HM et al.[19] and Morita T et al. [20] had reported people with MetS are at increased risk of colon cancer and adenoma in Asian populations. Sha N et al.[21] also observed that MetS was significantly associated with histological grade and stage of bladder cancer in 323 patients of Chinese population. Especially for endometrial cancer, collective data supported MetS could be a means for identifying a risk of endometrial cancer that might otherwise be missed or before any one component of MetS becomes more advanced [7]. Ni et al.[22] also clarified that MetS is associated with FIGO stage, grade, vascular invasion, tumor size, and lymphatic metastasis in endometrial cancer and confirmed MetS lead to a poor outcome in Chinese patients with endometrial cancer. A case–control study from Italian population revealed that MetS definition most strongly associated with endometrial cancer included BMI >30 kg/m2 and at least 2 of hypertension, diabetes, and hyperlipidemia [23]. Furthermore, a study in Norway suggested that inactivity and high energy intake are major risk factors for endometrial cancer [24].
However, limited study was available on the relationship between MetS, as well as the components of MetS, and characteristics of EOC. Thus, we designed this population based case-control study of EOC to explore the association between MetS, as well as components of MetS, and several important clinical characteristics and prognosis of EOC patients.
To begin with, 573 EOC and 1146 control cases were included in this study according to the case-control matching standard. The judgment of MetS and further analysis with EOC were reference to CDS definition. So, we firstly evaluated the consistency incidence of MetS estimation among CDS, ATP III and IDF definitions. Statistics demonstrated the kappa value of interrater agreement was 92.5% between CDS and ATP III, 93.2% between CDS and IDF, and 90.0% between ATP III and IDF, which indicated that CDS definition was available and a little superior to the international admissive criterions in our Chinese population. Additionally, the case proportion of MetS in EOC patients was found to be higher than the control population whichever assessing by three MetS criterions respectively.
Consequently, in logistic regression model, we found 3 different definitions of MetS, as well as the components of MetS, were all associated with an elevated EOC risk. the proportion of patients with MetS as identified by CDS guidelines was significantly greater among 144 cases (25.13%) than 79 control cases (6.89%) and was associated with a 3.187-fold increase in EOC risk.
Previously, epidemic literature about MetS as a cluster of risk assessed with regard to ovarian cancer in large scale project was very scary only in one study. The research conducted by Bjorge and colleagues [25] included 287,320 women from Austria, Norway and Sweden. Relative risks of ovarian cancer were estimated using Cox regression from MetS. Their results suggested 644 EOC and 388 deaths from ovarian cancer were identified during follow-up. In the end, they concluded there was no overall association between MetS and ovarian cancer risk. However, increasing levels of cholesterol and blood pressure increased the risks of mucinous and endometrioid tumors, respectively. Increasing levels of BMI conferred an increased risk of ovarian cancer mortality in women above the age of 50 years. There are a few unconformities between Bjorge’s and our conclusions, which may be contributed to the different race population and study design. In order to avoid bias and deviations, more and further studies of multi-centers deserved to perform to explore the relationship between MetS and ovarian cancer.
Furthermore, we compared the pathological characteristics between EOC patients with or without MetS as defined by definition of CDS. Statistics significantly proved the differences were observed in tumor differentiation grade, FIGO stage, and LN status between patients with or without MetS, which implied that tumor combining with MetS was more malignant clinical pathological behaviors in EOC patients. What’s more, in binary logistic regression analysis, the presence of MetS predicts the risk of advanced FIGO stage, lower differentiation, and LN metastasis of EOC patients.
As we know, based on symptoms before the development of ovarian cancer, such as irregular menstruation and then amenorrhea, and overweight, there is an assumption that polycystic ovaries syndrome (PCOS) can precede ovarian cancer [26]. Importantly, one of the criteria for PCOS is overweight or obesity. Obesity and MetS are constant companions of PCOS [27].
Obesity is one of the characteristics of MetS, according to the population-based longitudinal study in the People’s Republic of China. Standardized prevalence has reached up to 9.1% for obese population [28]. Notably, it has already accounted for a significant proportion. A number of studies verified obesity increased risk of several cancers, including breast, endometrium, kidney, esophageal, bladder, and colon carcinomas [29]. Especially, Calle et al. had already proved that significant trends of increasing risk with higher BMI values were observed for death of many cancers, including ovarian cancer. Importantly, they concluded increased body weight was associated with increased death rates for all cancers combined and for cancers at multiple specific sites [30]. Similarly, studies showed the relationship between the development of neoplastic diseases of female genitals (ovary and uterus) and presence of obesity [31, 32]. Approximately 60% to 90% of patients with ovarian cancer and endometrial cancer have overweight [33, 34]. Some studies have indicated obesity is a negative prognostic indicator for survival [35]. Large cohorts of ovarian cancer patients have demonstrated that the risk of ovarian cancer mortality is increased among those with higher BMI [36, 37]. A BMI ≥ 25 kg/m2 was used as measurement for obesity in our study. Our results showed BMI is associated with FIGO stage of ovarian cancer in binary logistic regression analysis. Some reasons may be used to explain the result. The cancer cells use the glucose, fatty acids, ketones, lactate, cholesterol, and other metabolites of fats and carbohydrates metabolism [38]. Biochemically, excess energy in hosts can contribute to risks of carcinogenesis [39, 40]. Excessive fat is also associated with systemic inflammatory response, which may play an important role in cancer. Interestingly, Oshakbayev et al.[41] ever reported a case that they treated a 41-year-old woman with end-stage ovarian carcinoma by using of weight loss therapy. While the patient was losing the gained body mass, tumors surprisingly shrank or disappeared (ultrasound data) during the observation period after start of the treatment.
Additionally, studies had already illustrated that diabetes was an independent risk factor for mortality in patients with EOC [42]. Ovarian cancer patients with diabetes were found to have a two and a half year lifespan reduction compared to non-diabetes [43]. Possible reason maybe reduced insulin sensitivity and elevated levels of IGF-1 [21]. IGF-1 is a growth factor that is secreted by the liver and is commonly associated with obesity and hyperinsulinism [44]. Hyperinsulinism decreases hepatic secretion of IGF binding protein (IGFBP), further increasing evels of free IGF-1 [42]. Conversely, starvation and calorie restriction are associated with lower levels of IGF-1 and downstream signaling [42]. IGF-1 has been confirmed to enhance growth of ovarian cancer cell [45]. Furthermore, previous research had proved that the high expression of IGF-1 in obesity and DM indicated the increased risk of EOC and poor prognosis [42].
According to our data, the components of MetS (diabetes, hypertension, TG, and HDL-C), when assessed individually, it was no statistically significant associated with advanced stage, low differentiation, and LN metastasis of EOC. However, when they considered with MetS, patients with MetS were found to have statistically significant advanced stage, low grade and LN metastasis of EOC.
Finally, we also proved that MetS was the independent factor for the evaluation of PFS and OS of EOC patients in Cox proportional hazard model, which were consistent with previous results in other cancers. Ni et al. showed that MetS was an independent prognostic factor for endometrial adenocarcinoma [22]. Voutsadakis reviewed published literature and indicated that obesity and diabetes were the prognostic factors in colorectal cancer [46].
Conclusion
Conclusively, MetS criteria of CDS are applicable and appropriate in Chinese population. Our study provides strong evidence for a role of MetS in EOC risk. EOC risk increases with presence of MetS compared to the control Chinese population. EOC patients with MetS were found to have statistically significant advanced FIGO stage, low tumor grade, and LN metastasis. Furthermore, the presence of MetS predicts the risk of advanced FIGO stage, lower differentiation, and lymph node metastasis of EOC patients. Moreover, MetS is the independent indicator for the PFS and OS evaluations of EOC patients. Thus, possible recommendations to reduce ovarian cancer should continue to encourage women to maintain a healthy weight and targeting MetS maybe reduce the EOC risk. Of course, further study certainly should be taken to confirm our results in the future.
Abbreviations
BMI:
Body mass index
CDS:
Chinese Diabetes Society
EOC:
Epithelial ovarian cancer
FIGO:
International federation of gynecology and obstetrics
HDL-C:
High-density lipoprotein cholesterol
LN:
Lymph node
MetS:
Metabolic syndrome
TG:
Triglyceride
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Acknowledgements
None.
Funding
This work was supported by Tianjin Health Bureau of Science and Technology Funds (2012KZ073) and National Natural Science Foundation (81302250).
Availability of data and supporting materials
The data will not be shared, since part of the data is being reused by another study.
Authors’ contributions
Study was designed by CY; Data was collected by CY and ZL; Statistics was performed by CY and LW; Article was drafted and completed by CY and WK. All authors read and approved the final manuscript.
Competing interests
The authors declare that they have no competing interests.
Ethics and approval and consent to participate
This study was approved by institutional review board of Tianjin medical university cancer institute and hospital and in accordance to the Declaration of Helsinki. All of the participants agreed and signed consent forms.
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Correspondence to Ying Chen.
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Chen, Y., Zhang, L., Liu, W. et al. Case-control study of metabolic syndrome and ovarian cancer in Chinese population. Nutr Metab (Lond) 14, 21 (2017). https://doi.org/10.1186/s12986-017-0176-4
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Keywords
• Metabolic syndrome
• Ovarian cancer
• Diabetes
• Hypertension | {
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What is the Microbiome and How Does it Affect Immunity?
By Melissa Anzelone, ND
In this article:
What is the Microbiome?
The microbiome is a community of a large variety of microorganisms such as bacteria, fungi, and viruses, contained within the gastrointestinal (GI) tract. It is a complex and integrated ecosystem that contains at least 1,000 different types of organisms belonging to more than 2,000 species.1
The microbiome exhibits a huge diversity, which is shaped by numerous factors including:
• Genetics
• Gender
• Age
• Immune System
• Health Conditions
• Geographic Location
• Socioeconomic Factors (Access To Water, Sanitation)
• Treatments
• Diet
What Does the Gastrointestinal (GI) Tract do?
The GI tract has many functions. It’s responsible for breaking down our food (digesting), making sure that food is absorbed properly so it can turn that steak dinner into the muscle of your thigh. It also eliminates the unwanted waste that the body doesn’t need. Red blood cells that are no longer functional give our excreted waste its brown color.
The GI tract also protects us, as there are many bacteria and other unwanted things in the food we eat, or from touching our mouths with our hands. The GI tract makes sure these bacteria don’t harm us (or cause food poisoning).
In addition to its many functions, the GI system also has many parts. This system starts at the mouth and ends at the anus. The stomach and small intestine are responsible for digestion and absorption, while the large intestine’s function is to remove water and compact the waste, while the sigmoid colon and rectum store the waste before it’s elimination from the body.2
Where Does Our Microbiome Come From?
Recent research has found that colonization of the GI tract actually starts before birth as the placenta contains good bacteria. Also, the meconium, or first bowel movement, of an infant is not sterile, meaning that even in the womb, an unborn baby’s GI tract is already developing its microbiome.3
After birth, if a baby is born vaginally, they have a microbiota containing species derived from the vaginal microbiome of their mothers. On the other hand, if a baby is born via C-section, their microbiome is more similar to their mother’s skin.
Breastfeeding also plays a role in forming the GI microbiome and the development of the immune system. Human milk has a protective role for babies. For example, antibodies like IgA and anti-microbial agents like lactoferrin protect babies from gastrointestinal and respiratory infections.
Why is the Microbiome Important?
All of the microbes that make up the community or microbiome in your gut do many positive things for us. The microbiome is involved in harvesting energy and storing that energy. One of the ways it does this is by fermenting fibers such as butyrate to create short-chain fatty acids (SCFAs).
These compounds promote a healthy GI tract by contributing to intestinal repair. They also serve as the main energy source for colonocytes, or cells in the colon. Many of the bacteria in the GI tract are key to synthesize vitamins like B1, B2, B5, B6B12Kfolic acid, and biotin.4
The microbiome also stimulates the immune system, just after birth.
How Does the Microbiome Influence the Immune System?
The GI tract has its own layer of protection called the mucosal immune system to regulate and guard against any foreign substances that we may ingest. This system is separate from the larger immune system of the body. The bacterial colonization of the GI tract dramatically changes our body’s immune system.
One of the most important steps to mature the immune system is to “teach” it the difference between what to attack and what to leave alone. Specialized cells in the digestive system interact with our bacteria (the good ones) and pathogenic bacteria (the bad ones), so the immune system can learn what to tolerate and what must be destroyed, as it could cause infection or harm to the body.
In addition to “teaching” the immune system what to attack and what to leave alone, the microbiome also helps immune cells mature and directs them where they are needed in the body. For example, the microbiome differentiates specific T cells in the immune system to perform various functions. For example, T cells can be Th1, Th2, or Th17.
Th 1 and 2 release specific chemicals throughout their lives call cytokines. These chemicals “call” other immune cells to fix problems in the body. Th17 cells are much more diverse in their function: they change the types of chemicals they secrete, making them adaptable to many situations in the body. In other words, the Th17 cells are the MVPs of the immune system, and they can play many positions.
A lot of our immune system lives in our gut. Specific areas in our gut called Peyer’s patches are very rich in lymphoid tissue, which houses many of our defense immune cells. Think of all of the potential things we can eat that could harm us. Having this immune location in our gut is the perfect way to protect the body from harm.
With poor diets, some medication use, or from natural aging, the number of bad bacteria in the gut can start to outweigh the good bacteria. This is called dysbiosis or an imbalance of good to bad bacteria. When the amount of good bacteria decreases in the gut, the immune system doesn’t get the support it needs. There are theories that dysbiosis in the gut may contribute to an overactive immune system, and this overactivity may be the cause of autoimmune centered disease.
Supplements to Support a Healthy Microbiome
Probiotics - the "Good" Bacteria
Probiotics, according to both the Food and Agricultural Organization of the United Nations and the World Health Organization, are defined as living microorganisms that provide health benefits.5 Scientist Elie Metchnikoff introduced the concept of probiotics through his studies of these good bacteria in milk.
His research showed that when eaten, these good bacteria could benefit human health. Since then, probiotics have been vastly marketed and consumed, mainly as dietary supplements or functional foods. Benefits of probiotics include increasing “good bacteria” in intestinal microbial communities, supporting the suppression of bad bacteria, supporting the immune system, and contributing to a healthy intestinal lining.
Many consumers report many positive benefits of taking probiotics. For example when on antibiotics, many people experience diarrhea. Probiotics may help to stave off this unwanted side effect. Some studies have shown that probiotics rich in Lactobacillus strains can help support a better mood. Other probiotic strains have been linked to supporting heart health. Probiotics may also help to reduced allergy symptoms and some strains have been shown to improve poor skin health. The use of some strains has been correlated with managing weight and symptoms of digestive disorders.
Probiotics are available in supplement form, in capsules, tablets, and/or liquid. These supplements can help support a healthy microbiome and are an easy way to get in needed microbes to support gut and immune health.
Butyrate - an Anti-inflammatory
Butyrate is a short-chain fatty acid derived from the fermentation of indigestible fiber in the GI tract. This compound is known for its anti-inflammatory properties and for its ability to provide energy to colonocytes.6 When dysbiosis occurs, the body may have difficulty producing this important energy source. Butyrate is available as a supplement and is often taken in conjunction with probiotics.
The microbiome is a diverse ecosystem that lives in our GI tracts. This combination of microorganisms supports the immune system in many ways. Thankfully, supplements like probiotics and butyrate can easily be incorporated into our daily routines to support the optimal health of both our GI and immune systems.
References:
1. Lazar, V., Ditu, L. M., Pircalabioru, G. G., Gheorghe, I., Curutiu, C., Holban, A. M., Picu, A., Petcu, L., & Chifiriuc, M. C. (2018). Aspects of Gut Microbiota and Immune System Interactions in Infectious Diseases, Immunopathology, and Cancer. Frontiers in immunology, 9, 1830.
2. Cheng, L. K., O'Grady, G., Du, P., Egbuji, J. U., Windsor, J. A., and Pullan, A. J. (2010). Gastrointestinal system. Wiley interdisciplinary reviews. Systems biology and medicine, 2(1), 65-79.
3. Abba13. Dominguez-Bello MG, Costello EK, Contreras M, Magris M, Hidalgo G, Fierer N, et al. Delivery mode shapes the acquisition and structure of the initial microbiota across multiple body habitats in newborns. Proc Natl Acad Sci U S A (2010) 107:11971-5.10.
4. Wong JM, de Souza R, Kendall CW, Emam A, Jenkins DJ. Colonic health: fermentation and short chain fatty acids. J Clin Gastroenterol. 2006;40(3):235-243.
5. Hemarajata, P., and Versalovic, J. (2013). Effects of probiotics on gut microbiota: mechanisms of intestinal immunomodulation and neuromodulation. Therapeutic advances in gastroenterology, 6(1), 39-51.
6. Canani, R. B., Costanzo, M. D., Leone, L., Pedata, M., Meli, R., & Calignano, A. (2011). Potential beneficial effects of butyrate in intestinal and extraintestinal diseases. World journal of gastroenterology, 17(12), 1519-1528.
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-5,557,094,636,327,526,000 | Bilateral silicone implant ruptures, how likely is it for the manufacturer to cover the cost of extraction & lift? (Photos)
I went in for an exploratory a ultrasound and mammogram after I was concerned of a breast lump. Good news no tumour, bad news is the ultrasound showed significant clouding that could be the result of a rupture.I needed to have an MRI to determine if that was the case. MRI showed bi-lateral ruptures. I also have pain in my axillary gland, a reacuring aching in my breast(muscle pain?) and pectoral flexion animation.
Doctor Answers 3
Silicone implants. cost and guarantee
Hi. Thank you for your question. Usually implant manufactures have a guarantee for implant ruptures and they are committed to give you new ones. But unfortunately they don`t pay for the fees for the surgeon or the hospital.In your case i would recommend to talk to a certified plastic surgeon and go through options. Whether you just want or need to change the implants or if you prefer to do a lift and change of implants. The second option would definitely give you a younger look.
Warranty for Rupture
Warranties typically extend for 10 years and the exact amount depends on the benefits at the time of your augmentation. I have seen warranties for 1200.00, 2400.00 and more recently 3500.00. The warranty provides a specified amount of money, not to cover your surgery at any cost. Your surgeon can get the exact information at the time of your consultation or even ahead of time if you call in advance of your appointment. After 10 years the only remaining warranty benefit is that the company provides a free replacement implant if you choose to have them replaced.
Ruptured implants
Assuming the MRI results are correct and you have ruptured implants (there is only about a 2% false positive rate with MRI, so you almost certainly have ruptures), the answer to your question depends on what brand and how old your implants are. The US FDA approved implants all have a lifetime warranty on implant replacement in the case of rupture (meaning they will give you the implants for free), and they also will generally cover around $3500 towards the cost of surgery if the implants are less than 10 years old. Some of these rules might be different in Canada. The best thing for you to do is to meet with your original plastic surgeon (or a new one if necessary) and they can contact the implant company and help you sort this situation out. You will probably have to cover some of the OR, anesthesia and surgery costs, but anything you get from the implant company will obviously be helpful to your bottom line. Good luck!
Robert Cohen, MD
Santa Monica Plastic Surgeon
5.0 out of 5 stars 43 reviews
These answers are for educational purposes and should not be relied upon as a substitute for medical advice you may receive from your physician. If you have a medical emergency, please call 911. These answers do not constitute or initiate a patient/doctor relationship. | {
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-8,186,641,269,611,241,000 | @article{7103, abstract = {Origin and functions of intermittent transitions among sleep stages, including short awakenings and arousals, constitute a challenge to the current homeostatic framework for sleep regulation, focusing on factors modulating sleep over large time scales. Here we propose that the complex micro-architecture characterizing the sleep-wake cycle results from an underlying non-equilibrium critical dynamics, bridging collective behaviors across spatio-temporal scales. We investigate θ and δ wave dynamics in control rats and in rats with lesions of sleep-promoting neurons in the parafacial zone. We demonstrate that intermittent bursts in θ and δ rhythms exhibit a complex temporal organization, with long-range power-law correlations and a robust duality of power law (θ-bursts, active phase) and exponential-like (δ-bursts, quiescent phase) duration distributions, typical features of non-equilibrium systems self-organizing at criticality. Crucially, such temporal organization relates to anti-correlated coupling between θ- and δ-bursts, and is independent of the dominant physiologic state and lesions, a solid indication of a basic principle in sleep dynamics.}, author = {Wang, Jilin W. J. L. and Lombardi, Fabrizio and Zhang, Xiyun and Anaclet, Christelle and Ivanov, Plamen Ch.}, issn = {1553-7358}, journal = {PLOS Computational Biology}, number = {11}, publisher = {PLoS}, title = {{Non-equilibrium critical dynamics of bursts in θ and δ rhythms as fundamental characteristic of sleep and wake micro-architecture}}, doi = {10.1371/journal.pcbi.1007268}, volume = {15}, year = {2019}, } | {
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-3,514,012,113,586,718,000 | Dental
Orthodontics – A Bite Correction
766Views
Everyone knows that external signs meet a person, and the first impression develops in a few seconds. A smile tells a lot about a person, and the look is laid off instantly in memory.
Unfortunately, not all people have perfect teeth, they do not always stand in line with the rest of the teeth, the bite does not correspond to the norm, and other pathology are found. Beautiful and healthy teeth are nowadays a positive sign, a sign of success and well-being.
Causes of Orthodontic Disorders
l Hereditary factor:
A particular type of jaw growth is laid before birth and is realized during the period of active skeleton growth. In some cases, this can lead to malocclusion.
l Insufficient chewing load:
If a child eats mostly soft foods, his jaws do not receive an impulse to develop. When permanent teeth begin to erupt, they do not fit into the underdeveloped jaw. The ideal simulator is solid food: apples, carrots, crackers, drying, piece of meat.
l Premature tooth loss:
If the milk tooth is removed prematurely, the surrounding teeth begin to move, taking place “reserved” for the permanent tooth. This leads to the uneven dentition. The same situation occurs in an adult when a permanent tooth (especially several teeth) is removed: the neighbouring teeth begin to move to compensate for the emptiness in the dentition.
l Metal Bracket Systems:
There are two main types of bracket systems: vestibular and lingual.
• Vestibular braces:
This system is attached to the external (vestibular) part of the tooth and is quite noticeable. The only minus is the aesthetic appearance, but at the same time, they are cheaper compared to other systems.
• Lingual braces:
The lingual braces method is relatively new in orthodontics and a bit famous in Parramatta. The system is installed from the internal (lingual) part of the tooth and is invisible when smiling. The cost of lingual braces is more than vestibular.
• Ligature braces:
This type of system moves teeth using thin wires intertwined uniquely. This system is found only on vestibular braces.
• Non-stick braces:
The ligatureless system works on a different principle: the arc is fastened with the help of small locks. This system is more comfortable for the patient and more aesthetic.
• Ceramic Bracket Systems:
One of the main advantages of ceramic braces is their appearance. Such braces are more aesthetic and more comfortable than metal braces, as they are inconspicuous. This feature justifies their cost.
The ceramic braces system is suitable for those patients who want a beautiful smile and do not draw attention to the very fact of bite treatment. Other features of ceramic braces are their matte structure. The most inconspicuous analogues of a ceramic bracket system are sapphire braces. Their advantage is that they come in different colours: the colour of the tooth enamel of the patient or transparent.
The installation of ceramic braces in Parramatta is recommended for people who are allergic and sensitive to metals. Ceramic braces require more gentle care than metal braces, so solid foods should be excluded from the diet. Treatment with ceramic braces takes longer than metal braces. | {
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-8,295,044,696,613,880,000 | Same-Day Appointments Available (844) 409-4657
2 Convenient Locations -- Irving & Frisco
March 14, 2018
Sleep Soundly: Creating the Perfect Sleep Environment & Bedtime Routine
Filed under: Uncategorized — brianna bloom @ 8:21 pm
Sleep environment and bedroom routine
According to the Centers for Disease Control and Prevention (CDC), one-third of adults in the United States get less than the recommended seven hours of sleep each night. And that’s despite the fact that it’s well-researched and widely accepted that adequate sleep is a major contributor to our overall health and well-being, physically and mentally.
Clearly, there are various factors that contribute to one’s sleep habits and ability to get sufficient sleep, but two key factors over which we have (almost) complete control are our sleep environment and bedtime routine. Even just a few tweaks to our bedroom and/or lifestyle habits can have a significant impact on our sleep quality.
Create the Ideal Sleep Environment
Noise
Reduce as much in-home and external noise as possible.
• Turn off the TV, radio, and other devices
• Put your phone on silent or vibrate
If there are outside noises over which you have little control, consider using a white noise machine or fan to help “drown out” the sudden or periodic noises that can pierce the silence and interrupt sleep.
Bedroom Temperature
The body is designed to sleep better at cooler temperatures; in fact, our body temperature naturally drops in the evening to prepare us for slumber.
For most people, the optimal temperature for sleeping is between 60-67 degrees. It may take a bit of experimentation to find your ideal sleeping temperature, so spend a few nights playing with the thermostat and/or the amount of blankets on your bed.
Also consider your sleepwear. Pajamas made of cotton are ideal as they are breathable and can help prevent overheating. Many people also like to sleep with as little clothing as possible, which has many potential benefits, including temperature regulation.
Light
Light stimulates alertness and affects your body’s sleep rhythms. All artificial light — especially the blue light emitted by digital devices such as TVs, computers, tablets, and phones — tricks the body into slowing its production of melatonin, the hormone that promotes sleep, which can make it more difficult to fall asleep.
Ways to reduce or eliminate light in the bedroom:
• Avoid using any electronic devices, including the TV, computer, e-reader, tablet, and phone at least one hour prior to bedtime
• Install heavy curtains or blackout blinds
• If you use an alarm clock, put them on the other side of the room and turn them away from you
• Consider using electrical tape to cover bright blue lights from electronics
Bedtime Routine
In addition to your sleep environment, a proper and consistent bedtime routine is extremely important as it triggers metabolic and mental responses that help the mind and body slow down. A few keys for a sleep-inducing bedtime routine include:
Dim the lights in the evening.
As discussed above, light stimulates the brain and encourages wakefulness. Get in the habit of dimming the lights to as low as possible in the evening hours.
Prepare for the next day.
Anxiety and stress are common sleep-inhibiting factors. One way to reduce them is to prepare for the next day before going to bed. Set out your clothes, make your lunch, and gather the items you’ll need to leave the house with.
Establish a relaxing wind down ritual.
Make a cup of caffeine-free tea. Take a relaxing bath or shower. Read a book. Listen to a podcast. Spend time meditating or stretching. Whatever activity you choose, make sure it’s relaxing and that you do it consistently each night.
Calculate bedtime and wake up hours and stick to it!
Don’t forget that you need at least seven full hours for a proper night’s rest, and your bedtime and waking hours should be consistent, regardless of the day of the week. Social jet lag (sleeping longer on the weekends to make up for lost sleep during the week) is extremely common, but can be detrimental to your natural circadian rhythm.
If, after implementing the strategies outlined above, you still struggle to get seven hours of sleep each night, or despite getting sufficient sleep, continue to wake up fatigued, you may be suffering from an underlying sleep condition that needs to be diagnosed and treated by a sleep specialist. Contact Dr. Kent Smith at Sleep Dallas to learn more. | {
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-6,801,000,442,698,626,000 | TY - JOUR AU - Gorobets, Svitlana AU - Gorobets, Oksana AU - Butenko, Kateryna PY - 2018/04/02 Y2 - 2024/06/13 TI - Potential Producers of Biogenic Magnetic Nanoparticles among Pathogenic and Opportunistic Microorganisms JF - Innovative Biosystems and Bioengineering JA - Innov Biosyst Bioeng VL - 2 IS - 1 SE - Articles DO - 10.20535/ibb.2018.2.1.127260 UR - http://ibb.kpi.ua/article/view/127260 SP - 33-41 AB - <p class="a"><strong>Background</strong><strong>.</strong> The complicated forms of infection in inflammatory processes characterized by rising resistance of microorganisms to antibiotics, are forcing to find new treatments that would prevent development of pathogenic microorganisms, increased local immunity, and thus accelerated regenerative processes.</p><p class="a"><strong>Objective</strong>. Classification of pathogenic and opportunistic microorganisms that may be potential producers of BMN, in terms of the location and properties of BMN using the methods of comparative genomics with the prospect of their subsequent use as the vectors for magnetically targeted delivery of drugs. This will make possible the use of the hyperthermia techniques for removal of pathogenic and opportunistic microorganisms that are capable of biomineralization BMN using for heating the cells directly intracellular BMN of these microorganisms.</p><p class="a"><strong>Methods</strong>. The methods of paired and multiple sequence alignment were applied using a free access program “BLAST” of National Center for Biotechnology Information.</p><p class="a"><strong>Results</strong>. It was revealed that strains such as <em>E. coli</em> (541-15), <em>K. pneumoniae</em> 342, <em>C</em><em>. perfringens</em> str. 13, <em>P. fluorescens</em> are potential producers of crystalline magnetite and bacteria: <em>S. aureus</em> RF122, <em>S. suis</em> BM407, <em>E. aerogenes</em> KCTC 2190, <em>K. pneumoniae</em> RYC492, <em>P. aeruginosa</em> M18 can be producers of intracellular amorphous BMN. The power of magnetic dipole interaction between BMN of the bacteria and BMN of the tumors is in the range between 10<sup>-</sup><sup>7</sup>–10<sup>-</sup><sup>8</sup> N.</p><p class="a"><strong>Conclusions</strong>. It is explained the neutralization effect of pathogens by the method of magnetic hyperthermia due to the presence BMN, and it was proposed the use for the treatment of inflammatory processes not only antibiotic drugs, but also electromagnetic fields for those microorganisms which are producers of BMN. It is shown that as vectors for targeted delivery of drugs should be used microorganisms with natural magnetic properties, making method targeted delivery of drugs safer and more efficient, and reduced its cost.</p> ER - | {
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