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6,341,663,710,227,266,000 | Early Intervention in Psychosis: A Retrospective Analysis of Clinical and Social Factors Influencing Duration of Untreated Psychosis
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Objective: To investigate the clinical and social factors determining the duration of untreated psychosis (DUP) in 2 groups of individuals with first-episode psychosis.
Method: Clinical and social variables were collected retrospectively from the case notes of 74 patients with first-episode psychosis (defined as 1 of the categories in the ICD-10 of psychotic episode arising from a functional or substance misuse cause). Patients were divided into 2 groups, one with a DUP less than 12 weeks (n = 46) and one with a DUP equal to or longer than 12 weeks (n = 28). The means, standard deviations, and medians were calculated for the total sample as well as for each group, and data from the 2 groups were compared to determine differences. The study was conducted from January 2006 to January 2008.
Results: Of the 74 patients, a longer DUP was significantly associated with being male (P = .025) and with having an insidious mode of onset (P < .001), comorbid substance misuse (P < .01), and less family support (P = .01). Conversely, shorter DUP was associated with acute presentation (P < .001).
Conclusions: These findings suggest that a longer DUP is influenced by the early clinical course and by social variables. Early recognition of these predictors of prolonged DUP should have an impact on reducing DUP and potentially improving the prognosis.
Prim Care Companion J Clin Psychiatry 2009;11(5):212-214
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8,471,966,466,996,135,000 | September 24, 2023
Suffering from Extreme joint Agony Back pain is a common complaint, and it can affect people of any age. It’s unclear what’s causing the pain in your muscle, but you should get it checked out as soon as possible. Knowing what you’re doing is crucial if you want to survive the discomfort. The following tips may prove useful in alleviating your back pain. If your back discomfort gets substantially worse, you should see a specialist. It’s likely that your insurance will pay for some of your lessons. Professional physical therapists are your best bet for sound counsel and guidance in designing a safe and efficient exercise regimen for building back muscle. A regular stroll may be the answer to your prayers if you suffer from joint discomfort and are searching for a method to alleviate or avoid it. One research found that strolling helped relieve back pain, but many of the tasks commonly recommended for relieving back pain actually made things worse. Even if you suffer from back pain, pain o soma 500mg experts advise getting in at least three hours of brisk walking per week. Be careful to drink enough water every day. Since water accounts for about 70% of the human body, it’s crucial to get enough of it every day. If you drink plenty of water, your body will be able to retain its pliability. How? The apparent answer is to drink lots of water. Your spinal discs will continue to cushion your spine and reduce stress on your body. You should definitely see a specialist about your back discomfort to get a proper evaluation and begin treatment. The treatment of your pain is highly dependent on its reason. If you have rheumatism, for instance, a chiropractor may be able to help. If you need to squat for any reason but are suffering back pain, you should instead bow at the knees. The constant stooping over that so many people engage in causes stresses and pains in their backs. Flopping around on your back like a cloth doll is a great way to relax. Individually stretching the body’s many muscle groups may help avoid sagging as a whole. Potential advantages include total muscular rest and improved performance in fatigued muscles. If you’re attempting to alleviate back discomfort, you should probably stay away from or use coffee sparingly. Coffee consumption is associated with increased risk of back pain and discomfort. Additionally, caffeine could exacerbate an existing raw laceration. Reduce or eliminate your caffeine intake, particularly from coffee and tea, to alleviate back discomfort. Chiropractic care may be the next best choice if your back discomfort has persisted despite other treatments. Your chiropractor will help you figure out how to handle your discomfort most effectively, and they’ll probably take an x-ray to make sure you don’t hurt yourself in the process. You might feel better quickly if you make a few easy changes. If your back pain isn’t too bad, a massage could be helpful. It might help you unwind and feel better about your back, but it won’t solve the fundamental issue. Keep your ankles hip-width apart if you’re experiencing back pain while standing. Avoid placing all your weight on one foot. Although resting erect with your weight spread equally may also help relieve joint discomfort while taking 500 milligrams of Prosoma, walking is advised. If you want to keep your back from hurting, invest in a good, firm cushion. A medium-firm cushion and supportive pillows can help you get a good night’s slumber by encouraging proper spinal posture. If you frequently wake up with back pain, it may be time to invest in a new cushion. Bad news for smokers who sustain spinal cord injuries: the outlook is grim. The healing process from a back injury is greatly slowed by smoking. Since smoking reduces oxygen transport to the spinal cord, an excess of oxygen is necessary for a fast healing of the spinal cord. Only a small fraction of computer users are aware that enlarging their screen’s text can help reduce muscle discomfort. The reasoning is child’s play: if the on-screen writing is too tiny, you’ll have to get down on one knee to read it. If the writing is too small, you could ease the pressure on your spine by making it larger. Try not to sit or lie still for too long. When you stand for too long, the muscles in your joint get tire and stiff. Take frequent breaks from standing and sitting if at all possible. It’s important to exercise both before and after spending a lot of time on your feet. Last but not least, back pain can affect people of any age for a variety of reasons. You should look into options to alleviate these symptoms and discomforts. These recommendations must always be considerer. Despite your back discomfort, you can get your life back on track.
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6,857,341,710,828,365,000 | Posted: February 9th, 2023
Scripted Dialogue Portion
Scripted Dialogue Portion Utilizes information learned from the home visit, health history, and discharge orders presented in the simulation to develop a patient dialog. Out of 10 points. Dialog addresses physiological, psychosocial, educational, and spiritual needs of the client. Out of 20 points. Sallie Mae Fisher’s Health History and Discharge Orders Sallie Mae Fisher Health History Ms. Fisher is an 82-year-old female with a history of chronic congestive heart failure (CHF), atrial fibrillation, and hypertension. During the last 6 months, she has been hospitalized four times for exacerbation of her CHF. She was discharged home last Saturday from the hospital after a 3-day stay to treat increased dyspnea, an 8-pound weight gain, and chest pain. Ms. Fisher is recently widowed and lives alone. She has a daughter, Thelma Jean, who lives in town but works full time and has family issues of her own. Therefore, family support is limited. Hospital Discharge Instructions Mountain Top Home Health to evaluate cardio-pulmonary status, medication management, and home safety. Medical Equipment Company to deliver oxygen concentrator and instruct patient in use. O 2 at 2 liters per nasal prongs PRN. Prescriptions given at discharge: Digoxin 0.25 mg once a day Lasix 80 mg twice a day Calan 240 mg once a day Order written to continue other home meds. Sallie Mae’s Home Medication List Zocar 50 mg once a day Minipres 1 mg once a day Vasotec 10 mg twice a day Prilosec 20 mg once a day Furosemide 40 mg once a day Effexor 37.5 mg at bedtime Lanoxin 0.125 mg every other day Multivitamin once a day Potassium 40 mEq once a day Ibuprofen 400 mg q 4 hours as needed for pain Darvocet N 100 mg q 4 hours as needed for pain Nitroglycerin ointment, apply 1 inch every day Scripted Dialogue Portion Utilizing the information learned from the home visit, health histories, and discharge orders, write a scripted dialogue in which you provide Sallie Mae with education that describes her problems and the interventions identified to improve her condition. Consider Sallie Mae’s physiological, psychosocial, educational, and spiritual needs when developing your dialogue. Your dialogue should resemble a script. The following is an example of a few sentences from a scripted dialogue: Nurse: “Good morning, Salle Mae, my name is ______ and I will be your nurse today. I understand you are experiencing problems with ________.” APA format is not required for this part of the assignment, but solid academic writing is expected. Refer to “Home Visit With Sallie Mae Fisher Grading Criteria.” Please feel free to ask any questions if you have any.
Nurse: “Good morning, Sallie Mae, my name is Sarah and I will be your nurse today. I understand that you have been recently discharged from the hospital for exacerbation of your congestive heart failure, atrial fibrillation, and hypertension. Can you tell me a bit about how you have been feeling since you’ve been home?”
Sallie Mae: “Well, I’ve been feeling a bit short of breath and my chest has been hurting more than usual.”
Nurse: “I see, that can be a common symptom of your conditions. To help manage these symptoms, we will be working with Mountain Top Home Health to monitor your cardio-pulmonary status and manage your medication. A medical equipment company will also be delivering an oxygen concentrator for you to use as needed. Additionally, we will be continuing your home medications, including Digoxin, Lasix, and Calan, as well as monitoring your potassium levels and continuing to use your nitroglycerin ointment.”
Sallie Mae: “Okay, that all sounds like a lot to keep track of.”
Nurse: “I understand it can be overwhelming, but we will work with you to make sure you understand how to properly use and manage your medications and equipment. We will also be providing education on how to recognize signs of exacerbation and when to seek medical attention. Is there anyone that can assist you with managing all of this, such as a family member or friend?”
Sallie Mae: “My daughter, Thelma Jean, lives in town but she works full time and has family issues of her own, so I’ll be mostly on my own.”
Nurse: “I understand that can be difficult. We will make sure to check in with you regularly and provide you with resources for additional support. Is there anything else you would like to discuss or any questions you have for me?”
Sallie Mae: “No, I think that’s everything for now. Thank you for explaining all of this to me.”
Nurse: “Of course, Sallie Mae. Remember, if you have any questions or concerns, don’t hesitate to reach out to us. We are here to help you manage your conditions and improve your health.”
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4,858,475,715,333,049,000 | Healthwatch by Shyft
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Skin and Hair
Nutrition
As the morning light tip-toes its way into our office space, we, at the editorial team of Shyft can’t help but wonder about this marvel that is — sunlight. Not only does it give us warmth and light, but it also provides us with essential nutrients that we need to survive. In this article, we’ll explore the reasons why sunlight is so important for humans, and what happens when we don’t get enough of it. Importance of Sunlight for Physical & Mental Health First and foremost, sunlight is important for our physical health. One of the key nutrients that we get from sunlight is vitamin D. This vitamin is essential for maintaining strong bones and teeth, as well as for preventing diseases such as osteoporosis. In fact, most of the vitamin D that we get comes from sunlight, rather than from our diet. This is because our bodies are able to convert the sun’s ultraviolet rays into vitamin D. In addition to vitamin D, sunlight is also important for our mental health. Studies have shown that exposure to sunlight can help to improve our mood and reduce symptoms of depression. This is because sunlight stimulates the production of serotonin, a hormone that is often referred to as the “feel-good” hormone. When we have higher levels of serotonin, we feel happier and more relaxed. Sunlight and the Circadian Rhythm Another reason why sunlight is important for humans is that it helps to regulate our sleep-wake cycle. Our bodies have an internal clock called the circadian rhythm, which controls when we feel awake and when we feel sleepy. Sunlight plays a crucial role in regulating this clock, as exposure to sunlight during the day helps to keep us awake and alert, while exposure to darkness at night helps to prepare us for sleep. Sunlight & the Immune System Sunlight is also important for our immune system. Studies have shown that exposure to sunlight can help to stimulate the production of white blood cells, which are essential for fighting off infections and diseases. This means that if we don’t get enough sunlight, our bodies may not be able to defend themselves as effectively against illness. Importance of Sunlight for Skin Health Finally, sunlight is important for our skin. While too much sun exposure can increase the risk of skin cancer, moderate amounts of sunlight can help to protect our skin from damage. Sunlight can help to improve the health of our skin by stimulating the production of collagen, a protein that is essential for keeping our skin firm and elastic. So, what happens when we don’t get enough sunlight? Unfortunately, the consequences can be quite serious. People who don’t get enough sunlight are more likely to suffer from depression, insomnia, and other sleep disorders. They may also be more susceptible to illness and may have weaker bones and muscles. Takeaway Sunlight is a crucial component of our overall health and well-being. From maintaining strong bones and a healthy immune system to improving our mood and regulating our sleep-wake cycle, sunlight plays an important role in keeping us healthy and happy. So, the next time you’re outside enjoying the sunshine, take a moment to appreciate just how important it is for your health and well-being.
Read more
Skin and Hair
What you eat can have an impact on the health of your skin and hair. Eating a diet rich in vitamins, minerals, and antioxidants can help keep your skin and hair looking healthy and vibrant.
Is Sunlight Important for your Health?
Is Sunlight Important for your Health?
As the morning light tip-toes its way into our office space, we, at the editorial team of Shyft can’t help but wonder about this marvel that is — sunlight. Not only does it give us warmth and light, but it also provides us with essential nutrients that we need to survive. In this article, we’ll explore the reasons why sunlight is so important for humans, and what happens when we don’t get enough of it. Importance of Sunlight for Physical…
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3 minutes
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27 Apr 2023
Skin health and gut health – the not-so-obvious correlation
Skin health and gut health – the not-so-obvious correlation
We often consider topical treatments like cleansers, toners, and moisturisers when maintaining healthy skin. But did you know - what goes in your gut can significantly impact your skin's health? That's right! The gut-skin connection is accurate, and it's time to start paying attention to it. Why does gut health matter for healthy skin? The gut and the skin are both organs of elimination. It’s essential to understand if your gut is healthy or not. When one isn't functioning correctly,…
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3 minutes
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17 Apr 2023
Most read
Diet
Whether it's for weight loss or addressing specific health concerns, following a healthy and balanced diet is essential for promoting good health and preventing chronic diseases.
The Dash Diet
The Dash Diet
Tired of the fad diets floating around in the market? Fed up with hearing different methods of weight loss being advertised without any health significance? Looking for a sustainable diet to lose weight and also become a healthy and satisfied person? You’ve come to the right place! We are here with one of the most popular and nutritious diets. But don’t let us convince you! Read about its benefits and decide for yourself. What is the Dash Diet? Dietary Approaches…
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3 minutes
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19 Aug 2023
Featured
The Rainbow Diet: Weight Loss With Colour
The Rainbow Diet: Weight Loss With Colour
In recent years, there has been a growing interest in the connection between nutrition and weight loss. The idea of following a specific diet to lose weight is not new, but the Rainbow Diet takes a different approach, focusing on consuming a variety of colorful fruits and vegetables. This approach not only helps with weight loss but also promotes overall health and wellbeing. What is the Rainbow Diet? The Rainbow Diet is a simple concept that involves incorporating a variety…
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4 minutes
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13 Aug 2023
Editor’s pick
Beyond the Hype: Investigating New Health & Wellness Trends
Beyond the Hype: Investigating New Health & Wellness Trends
Welcome to the latest edition of Healthwatch! In this issue, we embark on an exciting journey to decipher the truth behind the buzzworthy health and wellness trends that are taking the world by storm. With social media's influence, it's easy to get caught up in the latest fads, but do these trends stand up to scientific scrutiny? Join us as we delve into five popular trends - from the enigmatic allure of bulletproof coffee to the promise of better sleep…
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13 minutes
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08 Aug 2023
The Dairy Dilemma: Weighing the Pros and Cons of Milk and Cheese
The Dairy Dilemma: Weighing the Pros and Cons of Milk and Cheese
Dairy products have been a part of our diets for centuries. From milk to cheese and yoghurt, dairy products have been a staple food for many people around the world. However, with the growing concern about health and wellness, there has been a debate about the pros and cons of consuming dairy products. In this blog post, we will explore the advantages and disadvantages of including dairy products in your diet. What are Dairy Products? Before we dive into the…
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3 minutes
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23 Jul 2023
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Pescatarian Diet
Pescatarian Diet
Are you a fan of seafood? Is healthy weight loss your goal? Looking for a non-phoney sustainable diet that is flexible? If yes, then the Pescatarian diet is right up your alley. What is The Pescatarian Diet? Pescetarianism is a vegetarian diet with an inclusion of fish and other seafood. This diet stresses fish and seafood as the main sources of protein while the remaining snacks and meals reflect a plant-based diet that is characteristic of the Mediterranean diet. There…
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4 minutes
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23 Jul 2023
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The Truth About Superfoods: Separating Fact from Fiction
The Truth About Superfoods: Separating Fact from Fiction
Superfoods have become a buzzword in the health and wellness industry. They are claimed to be packed with nutrients that are beneficial for our health, but what exactly are superfoods and what do they do? In this article, we'll dive into the truth about superfoods and whether they live up to the hype. What are Superfoods? Superfoods are nutrient-dense foods that are believed to have significant health benefits. They are typically rich in vitamins, minerals, antioxidants, and phytochemicals. Some of…
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3 minutes
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15 Jul 2023
Editor’s pick
Healthy Eating
Eating a balanced diet that includes a variety of fruits, vegetables, whole grains, lean proteins, and healthy fats is essential for maintaining good health and preventing chronic diseases.
The Fast Lane to Health Risks: The Dangers of Processed Foods and Fast Food
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From Bacteria with Love: The Benefits of Mindful Eating for Gut Health
From Bacteria with Love: The Benefits of Mindful Eating for Gut Health
Are you ready to discover how mindful eating can make your gut bacteria do the happy dance and transform you into the superhero of your own health story? When it comes to maintaining a healthy gut, what you eat is just as important as how you eat it. Mindful eating, the practice of paying attention to your food and how it affects your body, can have a positive impact on your gut health. According to a study, mindful eating can…
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3 minutes
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19 Aug 2023
Editor’s pick
Healthy Dining Out: Tips and Tricks for Sticking to Your Diet
Healthy Dining Out: Tips and Tricks for Sticking to Your Diet
Sticking to a healthy diet can be challenging, especially when dining out. With the availability of delicious yet unhealthy options on restaurant menus, it can be tempting to indulge in your favourite dishes. However, with a little planning and mindfulness, it is possible to enjoy a nutritious meal while dining out. Here are some tips on how to stick to a healthy diet when eating out. Choose the Right Restaurant When it comes to dining out, choosing the right restaurant…
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4 minutes
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06 Aug 2023
Featured
The Gut-Check: The Impact of Skipping Meals
The Gut-Check: The Impact of Skipping Meals
Think twice before skipping that meal, as it could very well be the key to unlocking the secrets of a healthy gut! From aiding in digestion and absorption of nutrients to supporting our immune system and even influencing our mood and mental health, the gut microbiome is a complex and fascinating part of our bodies. But did you know that one simple habit, like skipping meals, can have a significant impact on this delicate balance of bacteria in our gut?…
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4 minutes
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05 Aug 2023
Editor’s pick
Sip your way to better health: The miraculous benefits of green tea!
Sip your way to better health: The miraculous benefits of green tea!
Tea lovers, rejoice! Green tea is a popular beverage that has been enjoyed for centuries and is known for its numerous health benefits. Whether you are looking to improve your physical health, and mental well-being, or just enjoy a delicious cup of tea, green tea has got you covered. In this blog, we will explore the benefits of drinking green tea and why it should be a part of your daily routine. Boosts Metabolism and Promotes Weight Loss One of…
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3 minutes
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29 Jul 2023
Most read
Fuel Your Day: 5 Lunchbox Essentials for Non-Stop Energy at Work
Fuel Your Day: 5 Lunchbox Essentials for Non-Stop Energy at Work
Are you someone who often feels tired and drained at work? Do you find it difficult to concentrate and focus on your tasks? If so, you're not alone. Many people experience fatigue and low energy levels at work, which can affect their productivity and overall well-being. In this blog post, we will explore what makes us tired at work and provide five things you can carry in your lunchbox to stay energized and focused throughout the day. What Makes Us…
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4 minutes
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29 Jul 2023
Most read
Vitamins and Supplements
While it's best to get nutrients from food, some people may benefit from taking supplements to address specific deficiencies or health concerns. It's important to talk to a healthcare provider before starting any new supplements.
Crack the Code: Understanding Glycemic Index and Glycemic Load
Crack the Code: Understanding Glycemic Index and Glycemic Load
Have you ever felt tired and hungry after a meal, even though you ate a lot of food? Or have you experienced a sudden spike in your energy level followed by a crash? If so, it may be related to the glycemic index and glycemic load of the food you ate. In this blog, we will discuss the glycemic index and glycemic load, how they affect our bodies, and how we can use this information to make better food choices.…
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4 minutes
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calendar
19 Aug 2023
Editor’s pick
From Bacteria with Love: The Benefits of Mindful Eating for Gut Health
From Bacteria with Love: The Benefits of Mindful Eating for Gut Health
Are you ready to discover how mindful eating can make your gut bacteria do the happy dance and transform you into the superhero of your own health story? When it comes to maintaining a healthy gut, what you eat is just as important as how you eat it. Mindful eating, the practice of paying attention to your food and how it affects your body, can have a positive impact on your gut health. According to a study, mindful eating can…
book
3 minutes
|
calendar
19 Aug 2023
Editor’s pick
Healthy Meal Planning: A Guide to Nourishing Your Body for the Week
Healthy Meal Planning: A Guide to Nourishing Your Body for the Week
Planning healthy meals for the week can seem daunting at first, but with a little bit of effort and organization, it can become a seamless and enjoyable process. By preparing meals in advance, you can ensure that you're eating a balanced diet, save money on eating out, and reduce food waste. In this blog, we'll discuss some practical tips on how to plan healthy meals for the week, keeping an Indian perspective in mind. Step 1: Create a Meal Plan…
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5 minutes
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13 Aug 2023
Most read
Fats That Are Good For You: Why You Need Them In Your Diet
Fats That Are Good For You: Why You Need Them In Your Diet
Fats are often considered the enemy of a healthy diet. However, not all fats are bad for you. In fact, healthy fats are an essential component of a well-balanced diet. Consuming the right kind and amount of fats can improve your heart health, brain function, and overall well-being. In this blog, we will discuss the importance of healthy fats in your diet, their sources, and how to incorporate them into your meals. What are Fats? Fats are a type of…
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4 minutes
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29 Jul 2023
Editor’s pick
Seafood: The Ocean’s Superfood
Seafood: The Ocean’s Superfood
Seafood is a delicious and nutritious part of a healthy diet. With its unique blend of protein, healthy fats, and essential vitamins and minerals, it's no wonder why seafood is a favourite among health enthusiasts. In this blog post, we will dive into the many benefits of seafood and explore why it should be a staple in your diet. Benefits of Eating Seafood Seafood is a nutrient-dense food that can provide numerous health benefits. Here are just a few of…
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4 minutes
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28 Jul 2023
Featured
Preventing Calcium Deficiency: Tips for a Healthy You
Preventing Calcium Deficiency: Tips for a Healthy You
Calcium is one of the most essential minerals that our body needs to function properly. It plays a crucial role in maintaining strong bones and teeth, healthy muscles, and proper nerve function. Unfortunately, calcium deficiency is quite common in India, and it can lead to several health issues such as osteoporosis, weak bones, and teeth, muscle cramps, and even heart problems. In this blog, we will explore the importance of calcium for Indians and how to not be deficient in…
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4 minutes
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23 Jul 2023
Featured
Allergies
Food allergies can be life-threatening, and it's important to identify and avoid trigger foods. Food intolerances can also cause uncomfortable symptoms, and working with a healthcare provider can help identify and manage these sensitivities.
Lactose Intolerance
Lactose Intolerance
Is it common for you to experience bad gas, bloating, diarrhoea, and stomach cramps after eating cheese or consuming a glass of milk? If so, you may be lactose intolerant. The manifestations of this condition may be embarrassing and put you into tough situations. However, with proper precaution and care you can save yourself from being caught with an egg on your face. The science behind it.. The sugar found in milk is called lactose. Lactase is an enzyme, made…
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4 minutes
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15 Aug 2023
Most read
Understanding Egg Allergy in Kids
Understanding Egg Allergy in Kids
Who doesn’t love eggs? Sunny side up, Omelettes, boiled eggs, and eggs benedict make up for the perfect breakfast. Almost all nutritional advice starts with eggs for breakfast. Many of our favourite things to eat like cakes and muffins may contain eggs. But have you often noticed your child developing rashes or a runny nose after an egg-based meal? For kids, eggs are a common allergen. While finding out your child has an allergy to a common food item can…
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5 minutes
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26 May 2023
Featured
Common Allergies: A comprehensive overview of allergies
Common Allergies: A comprehensive overview of allergies
Allergies are one of the most common chronic conditions worldwide, affecting millions of people every year. Simply put, an allergy is an overreaction of the immune system to a substance that is normally harmless. While allergies can develop at any age, they typically start in childhood and may persist or even worsen as a person ages. In this blog post, we will provide a comprehensive overview of the most common allergies, their symptoms, causes, and treatments. 1. Seasonal Allergies Seasonal…
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4 minutes
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11 Apr 2023
Featured
Understanding Latex Allergy
Understanding Latex Allergy
Have you ever felt the sensation of itching or burning as soon as you come into contact with rubber gloves? Does your throat begin to close up when you try to blow air into a balloon? Can a simple stethoscope check make your heartbeat regular and bring on a bout of nausea? If you have experienced any of these issues you may be allergic to latex. Latex is a common constituent of several medical and consumer items such as bath…
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4 minutes
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06 Apr 2023
Most read
Living With a Peanut Allergy
Living With a Peanut Allergy
Being allergic to peanuts is one of the most frequent causes of life-threatening allergic reactions. Those who are allergic to peanuts may have a severe reaction to even the smallest untraceable amounts of peanuts(anaphylaxis). Child peanut allergies have been on the rise. If you or your child is suffering from peanut allergies and you are trying to incorporate changes to make your life easier then this guide is for you! If you are allergic to peanuts then you have an…
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4 minutes
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06 Apr 2023
Wheat Allergy
Wheat Allergy
Have you ever felt a stomach ache coming on when you eat bread? Do you notice rashes on your body after you enjoy pasta? Are hives a common occurrence after you’ve consumed your morning cereals? If these situations seem familiar, you might be allergic to wheat. Wheat allergy is among the most prevalent types of allergic reactions, affecting millions of people across the globe. Eliminating wheat from your diet may seem like a small feat to others but it is…
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4 minutes
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06 Apr 2023
Digestive Health
A healthy digestive system is essential for nutrient absorption and overall health. Eating a balanced diet, staying hydrated, and getting enough fiber can help promote digestive health.
From Bloating to Brain Fog: The Many Dangers of Gut Imbalances
From Bloating to Brain Fog: The Many Dangers of Gut Imbalances
Are you tired of feeling bloated, sluggish, and just generally ‘off’? It could be your gut. Hey there! You might not know it, but your gut health is super important for your overall well-being. It's like a little ecosystem in your belly, with trillions of tiny creatures living in it. When these creatures get out of balance, it can cause all sorts of problems, like tummy troubles, inflammation, and even mental health issues. But don't worry, we've got you covered!…
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4 minutes
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29 Jul 2023
Featured
Breathe Easy: How Your Gut Health Can Help Prevent Asthma and Allergies
Breathe Easy: How Your Gut Health Can Help Prevent Asthma and Allergies
Are you tired of constantly sneezing and coughing due to allergies or asthma? Have you ever considered that the solution might be in your gut? That's right, the health of your gut can play a significant role in the development and management of allergies and asthma. Studies have shown that the human gut is home to trillions of microorganisms, collectively known as the gut microbiota. This gut microbiota plays a crucial role in maintaining overall health, including immune function. However,…
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4 minutes
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28 Jul 2023
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Autoimmunity and Your Gut: What You Need to Know
Autoimmunity and Your Gut: What You Need to Know
Did you know that the health of your gut can affect the health of your entire body, including your immune system? It's true! Your gut is home to trillions of bacteria, which play a critical role in regulating your immune system and protecting you from disease. But when your gut health is compromised, it can lead to a host of health problems, including autoimmune diseases. Autoimmune diseases occur when your immune system attacks healthy cells in your body. There are…
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4 minutes
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23 Jul 2023
Featured
The Gut Health-Disrupting Side Effects of Antibiotics You Need to Know
The Gut Health-Disrupting Side Effects of Antibiotics You Need to Know
Antibiotics: the life-saving wonder drugs that can also wreak havoc on your gut health. Antibiotics are one of the most revolutionary discoveries of modern medicine. They have saved countless lives by fighting off deadly bacterial infections. However, despite their life-saving abilities, antibiotics can have some unintended consequences on our gut health. The gut microbiome is a vast collection of microorganisms that reside in our digestive system, consisting of trillions of bacteria, fungi, viruses, and other microorganisms. These microorganisms play a…
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3 minutes
|
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06 Apr 2023
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-395,395,753,584,792,450 | Home » Amyloidosis
Amyloidosis
Amyloidosis is a medical condition resulting from aggregation of extracellularly deposited abnormal proteins called amyloid fibrils that cause damage to organs and tissues. These fibrils are insoluble, linear, rigid and measures approximately 7.5 to 10µm in width.
Hematoxylin and eosin stains hyaline acellular eosinophilic material. Congo red stains red in light & green birefingence in polarized light.
Electron microscopy shows regular fibrillar structure. X-ray diffraction shows beta pleated sheet structure.
In 1854 Rudolph Virchow named it amyloid based on color after staining these proteins with iodine and sulfuric acid, amyloid meaning cellulose or starch.
Classificaton of Amyloid
23 different human subtypes have been named based on A for amyloid, followed by the precursor protein e.g AL, AH. Amyloid may be localized or systemic:
Localized
e.g. in larynx, lung or bladder
Systemic Amyloidosis
Systemic amyloidosis may be:
a. Multiple myeloma associated
b. Reactive (secondary amyloidosis)
c. AA amyloid
• Rheumatoid arthritis
• Ischemic bowel disease
• Osteomylitis
• Hodgkins disease & renal cell carcinoma
• Hereditary amyloidosis
Mechanism of Formation
Amyloid fibrils arise from misfolded proteins ranging from alpha helix to beta pleated sheets.
• Proteins are deposited extracellularly
• Proteins aggregate and form fibrils called amyloid fibrils.
• Misfolded proteins may result from point mutations.
• They are deposited as localized vs systemic
– localized; close to cells producing it.
– Systemic; distant sites from these cells producing these abnormal proteins.
Amyloidosis
Apple green birefringence
Photo courtesy of Ed Uthman, MD under Creative Commons Attribution-Share Alike 2.0 Generic license.
Further Clinical Manifestations
CNS:
– Neuropathy both autonomic and peripheral,
– Dementia.
– Corneal deposits.
Cardiac:
– Cardiomyopathy typically restrictive(right sided)
Pulmonary:
-Pleural effusions
-Parenchymal nodules
-Tracheal and bronchial infiltration causing hoarseness, airway obstruction and dysphagia.
Renal:
Proteinuria, nephrotic syndrome, renal failure leading to kidney transplant or dialysis
Bone marrow:
Bleeding abnormalities
Muscle:
Hypertrophy of muscles, macroglossia
Skin:
Nodules, plaques, easy bruising
GI:
Organomegaly (Hepatomegaly,splenomegaly),
Gastroparesis, abnormal bowel movements usually constipation, malabsorption
Diagnosis
• Any unexplained medical disorder and you suspect amyloidosis: e.g.
– heart failure,
– proteinuria,
– hepatic dysfunction
Ultimately, you need tissue biopsy from:
– Abdominal fat pad
– rectum
– salivary gland
– endomyocardium
– Bone marrow biopsy
Treatment
Treatment of this medical disorder is limited and research is still in progress. Treatment differs depending on subtype, AL and AH.
High dose mephalan plus dexamethasone/prednisone are applied. In selected candidates autologous stem cell transplant is an option.The goal with treatment is to get rid of clonal plasma cells that lead to immunoglobulin protein.
AA: Treat the infection or chronic inflammatory condition causing apo serum A protein elevation.
For familial Mediterranean fever Colchicine is used. Other conditions are treated conservatively or require organ transplant
Prognosis is poor with this medical disorder.
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Women have many unique health concerns — menstrual cycles, pregnancy, birth control, menopause — and that's just the beginning. A number of health issues affect only women and others are more common in women. What's more, men and women may have the same condition, but different symptoms. Many diseases affect women differently and may even require distinct treatment.
Protein should provide about 15% of a healthy person's daily calories. As a rule of thumb, people of both sexes and any size will do fine with about 60 grams of protein a day. Athletes who have large muscles and work out hard may need 20% more. But even that's not very much; 8 ounces of chicken or 6 ounces of canned tuna, for example, will fit the bill.
Maintaining a healthy weight is important piece of the puzzle to achieve good health. A healthy weight can be determined using the body mass index charts (see web source below). If you find you are overweight or obese, weight loss may be beneficial for you. Before you begin any weight loss efforts, consult with your medical provider and/or consult a registered dietitian to create a weight loss plan. If you are underweight, consult a medical provider to assess your weight status.
Give your body a little more credit: It tells you when you’re hungry—you may not be listening, though. Before chowing down because there’s only one slice of pie left or because the last guest arrived at the brunch, stop and check in with your stomach. “If you’re not hungry, make yourself a small plate and sip on some tea or coffee while everyone else digs in,” recommends Elle Penner, M.P.H., R.D., a MyFitnessPal expert. When your belly starts to finally grumble, food will be there.
Vinyasa and power may not be the only forms of yoga that will get you closer to that long, lean, limber look. Research presented at the 73rd Scientific Sessions of the American Diabetes Association found that restorative yoga—which focuses more on relaxing and stress-reducing movements rather than a challenging flow or balancing poses—burns more subcutaneous fat (the kind directly under your skin) than stretching does. By the end of the yearlong study, yogis who practiced at least once a month lost an average of about three pounds, nearly double the amount lost by those who only stretched. So if you don’t feel up for a more athletic yoga class, ease your way into a practice with a gentle one.
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According to the American Heart Association, it's better to eat more complex carbohydrates (vegetables, fruits and whole grains) than simple carbohydrates found in sugars. Complex carbohydrates add more fiber, vitamins and minerals to the diet than foods high in refined sugars and flour. Foods high in complex carbohydrates are usually low in calories, saturated fat and cholesterol.
Actually, more people suffer from food intolerances, which don't involve the immune system. However, food intolerance symptoms—such as intestinal distress—may mimic those of a food allergy. If you have a food intolerance, talk to a nutritionist about diagnosis and treatment; if you have food allergies, you need to see an allergist. Whether you have food allergies or intolerance, you will need to develop a diet that fits your needs and avoids foods that trigger a reaction.
Good sources of iron include liver, kidneys, red meat, poultry, eggs, peas, legumes, dried fruits and dark, green leafy vegetables. Three ounces of cooked chicken liver contains 7.2 mg of iron; a cup of cooked spinach contains 6.4 mg. Your health care professional will probably recommend iron supplements during pregnancy (probably starting at 30 mg per day).
Dietary fiber is found in plant foods like whole-grain breads and cereals, beans and peas, and other vegetables and fruits. At least one study suggests that women who eat high amounts of fiber (especially in cereal) may have a lower risk for heart disease. High-fiber intake is also associated with lower cholesterol, reduced cancer risk and improved bowel function. And one long-term study found that middle-aged women with a high dietary fiber intake gained less weight over time than women who ate more refined carbohydrates, like white bread and pasta.
Even if you are the most independent exerciser around, give a group fitness class a shot at least once a week—you may find that you enjoy it more than sweating solo. “Happiness and health are shared through social connectedness and closeness,” says Greg Chertok, director of sport psychology at the Physical Medicine and Rehabilitation Center in New Jersey. “Geography and proximity are predictors of how contagious emotions can be, and this may translate into an athletic environment too.” Sign up for Bikram, CrossFit, spin, or Zumba, and you could find yourself—gasp!—smiling at the gym thanks to your classmates.
Obviously, the best treatment plan for poor nutrition is to change your diet. Most Americans eat too little of what they need and too much of that they don't. For many women, decreasing fat and sugar consumption and increasing fruit, vegetables and grains in your diet can make a big difference. Many women also need to boost consumption of foods containing fiber, calcium and folic acid. Compare your diet to that suggested by the food pyramid and compare your nutrient intake to the suggested daily levels. Adjust accordingly, and you may be able to dramatically improve your health.
I realize that none of the above foods have 100% DV of calcium, and while we all should be getting a variety of these foods through the week to help increase the amount of calcium from whole foods, you can also boost it with a supplement- especially if you fall into any of the above categories. I’ve really been liking the New Chapter’s Every Woman’s One Daily Multivitamin which has calcium and is rich in vitamin D3. Read more on that in the next question!
A healthy vegetarian diet falls within the guidelines offered by the USDA. However, meat, fish and poultry are major sources of iron, zinc and B vitamins, so pay special attention to these nutrients. Vegans (those who eat only plant-based food) may want to consider vitamin and mineral supplements; make sure you consume sufficient quantities of protein, vitamin B12, vitamin D and calcium. You can obtain what you need from non-animal sources. For instance:
I realize that none of the above foods have 100% DV of calcium, and while we all should be getting a variety of these foods through the week to help increase the amount of calcium from whole foods, you can also boost it with a supplement- especially if you fall into any of the above categories. I’ve really been liking the New Chapter’s Every Woman’s One Daily Multivitamin which has calcium and is rich in vitamin D3. Read more on that in the next question!
Nutrition interventions that target mothers alone inadequately address women's needs across their lives: during adolescence, pre-conception, and in later years of life. They also fail to capture nulliparous women. The extent to which nutrition interventions effectively reach women throughout the life course is not well-documented. In this comprehensive narrative review, we summarized the impact and delivery platforms of nutrition-specific and nutrition-sensitive interventions targeting adolescent girls, women of reproductive age (non-pregnant, non-lactating), pregnant and lactating women, women with young children<5 years, and older women, with a focus on nutrition interventions delivered in low- and middle-income countries. We found that though there were many effective interventions that targeted women's nutrition, they largely targeted women who were pregnant and lactating or with young children. There were major gaps in the targeting of interventions to older women. For the delivery platforms, community-based settings, compared to facility-based settings, more equitably reached women across the life course, including adolescents, women of reproductive age, and older women. Nutrition-sensitive approaches were more often delivered in community-based settings, however, the evidence of their impact on women's nutritional outcomes was less clear. We also found major research and programming gaps targeting overweight, obesity, and non-communicable disease. We conclude that focused efforts on women during pregnancy and in the first couple of years postpartum fails to address the interrelation and compounding nature of nutritional disadvantages that are perpetuated across many women's lives. In order for policies and interventions to more effectively address inequities faced by women, and not only women as mothers, it is essential that they reflect how, when, and where to engage with women across the life course.
While women tend to need fewer calories than men, our requirements for certain vitamins and minerals are much higher. Hormonal changes associated with menstruation, child-bearing, and menopause mean that women have a higher risk of anemia, weakened bones, and osteoporosis, requiring a higher intake of nutrients such as iron, calcium, magnesium, vitamin D, and vitamin B9 (folate).
Howdy! My name is Amanda. I am a South Texas native and came to College Station to attend Texas A&M University. I received my B.S. in Animal Science and Business Management in 2012. I fell in love with the city and decided I would call it home. I currently co-own Claws and Paws At Home Pet Care and am a Practice Manager at a local veterinary hospital. I became a fitness enthusiast during my journey to lose 70+ lbs. I accomplished this goal through group fitness classes, boot camps, cycling, running clubs and dance. My decision to teach is fueled by my goal to empower others on their fitness journey. I believe in a strong support system and hope to provide that as a fitness instructor. In my down time, I enjoy spending time with my loved ones, running obstacle races and fishing.
When women reach childbearing age, they need to eat enough folate (or folic acid) to help decrease the risk of birth defects. The requirement for women who are not pregnant is 400 micrograms (mcg) per day. Including adequate amounts of foods that naturally contain folate, such as citrus fruits, leafy greens, beans and peas will help increase your intake of this B vitamin. There also are many foods that are fortified with folic acid, such as breakfast cereals, some rices and breads. Eating a variety of foods is recommended to help meet nutrient needs, but a dietary supplement with folic acid also may be necessary. This is especially true for women who are pregnant or breast-feeding, since their daily need for folate is higher, 600 mcg and 500 mcg per day, respectively. Be sure to check with your physician or a registered dietitian nutritionist before taking any supplements., .
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9,030,295,950,397,106,000 | Article
Nanoengineering of a biocompatible organogel by thermal processing.
Department of Physics, National University of Singapore, Singapore 117542.
The Journal of Physical Chemistry B (Impact Factor: 3.61). 05/2009; 113(15):5011-5. DOI:10.1021/jp811215t
Source: PubMed
ABSTRACT The formation of most organogels requires the compatibility of both the gelator and solvent. It is very desirable if the rheological properties of a gel can be manipulated to achieve the desired performance. In this paper, a novel organogel was developed and its rheological properties and fiber network were engineered by controlling the thermal processing conditions. The gel was formed by the gelation of 12-hydroxystearic acid as a gelator in benzyl benzoate. It was observed that the degree of supercooling for gel formation has a significant effect on the rheological properties and fiber network structure. By increasing supercooling, the elasticity of the gel was enhanced, and the correlation length of the fibers was shortened, leading to the formation of denser fiber networks. The good biocompatibility of both the gelator and solvent makes this gel a promising vehicle for a variety of bioapplications such as controlled transdermal drug release and in vivo tissue repair.
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-6,302,066,177,047,753,000 | What are the Best Herbs for PCOS and Endometriosis?
Understanding PCOS and Endometriosis
Before providing that list of the best PCOS and endometriosis herbs, I am going to define of each condition. And so it follows, The current state of conventional med solutions and herb medicine will assist us towards improving results.
PCOS
To begin with, Medical researchers have defined polycystic ovary syndrome (PCOS) as a condition where many small cysts have formed inside the ovaries. The cysts or sacs contain fluid. How this condition is formed where the ovaries change in structure is not clear in the medical field except that of genetics and/or family history. What researchers have found is the condition does influence hormone balance. Androgen (male hormone) appears to be more present. This causes hormonal imbalance and additional androgen growth. As a result, the result shows as infertility, acne, increase in facial hair, menstrual irregularity and obesity.
Endometriosis
Secondly, Endometriosis is usually a painful disorder in which endometrial tissue grows in excess. Gradually, the condition reaches the outside the uterus. In addition, abnormal tissue commonly develops on the outside of the ovaries, fallopian tubes and the pelvis lining. The most likely cause is reversed menstrual flow. During the reversed upward movement, tissue leaks during the period flows through the fallopian tube into other areas of the body. Additionally, genetic factors may also be involved.
Conventional Medicine Focus
Both conditions have not found final comprehensive solutions for their root causes. In the case of endometriosis, surgical procedure can rid the patient of the excess tissue causing pain. Still, the underlying cause remains. The internal environment has not changed and has the likely potential to redevelop. PCOS treatment, usually, consists of birth control pills, metformin to prevent diabetes, statins to reduce cholesterol, additional hormones for fertility and procedures to remove or inhibit excess hair. Conventional treatment remains focused on symptoms.
Many young women call in for help who have tried lots of procedures or who have heard stories from their friends, looking for a real solution. When they are told that all that is possible with Chinese medicine in a fairly short time (2-6 months depending on severity, then you can hear the relief already beginning. Because I have said it so many times, I have to watch how I sound. After 35 years, sometimes the excitement wears down. But its still there when I explain below.
What is an Advanced Herbal Medicine
To clarify, I strongly recommend that the most effective herbal formula for these syndromes must be 1) “state of the art”, 2) extensive historical study going back millennia, 3) comprehensive assessment which zeroes in on the root cause and 4) with minimal to no side effects.
Chinese medicine fills this requirement with formulas that have worked for millions of women.
From multi-generations of Chinese medicine herbalists, thousands of years of observation and improvements have yielded the highest performing combination of herbs while contained in one formula. From this lineage, father to son, daughter sometimes, great herbal knowledge has been preserved and thus, the best list of herbs are shared for your benefit. You can learn to build the formula yourself (took along time, in apprenticeship, for me) and/or you can access it at Longevity Mountain Herbs (https://traditional-chinese-herbs.com/product/female-comfort/):
The Best Herb Medicine for PCOS and Endometriosis
I know that sounds arrogant! But how are you going to know unless I tell you. Someone needs to tell the truth with so much BS out there. So many formulas are based on simple, beginner-type formulas. Especially the claims by one herb wonders. Some are good but most supplements sold don’t do anything, even if taken for 1-2 months. This formula below starts working in days and most to all, young to middle-age women, feel a new gear kick in by 5 days.
Nourishing Energizers
1. Astragali Radix – nourishes the body’s energy, spleen and lung. Primary benefits: fatigue, diarrhea, shortness of breath, prolapse, uterine bleeding, spontaneous sweating, edema, chronic sores, deficient blood and lymph fluids, weakened immunity, stops sweating, promotes urination, corrects toxicity, skin.
2. Longan Arillus-Longan fruit nourishes the body’s energy. Its temperature is warm thus stimulates the heart and the spleen into balance. Benefits: insomnia, palpitations, forgetfulness, dizziness, anxiety, stress, blood deficiency, disturbed spirit, excessive thinking and emotions.
3. Panax ginseng – revitalizes the whole body, slightly warming, primarily effects the spleen and lungs. Benefits: extreme collapse of body energy – shallow breathing or shortness of breath, cold limbs, profuse sweating, minute pulse; severe blood loss. Lung or Spleen/Stomach weakness, wasting and thirsting disorder, energy and fluids injured by fever and profuse sweating, palpitations with anxiety, insomnia, restlessness due to energy and blood deficiency. Powerfully tonifies the primal energy of these five organs (heart, liver, spleen, lungs, kidneys). Revitalizes immunity and blood components (T cells, red blood cells, white blood cells, etc.), obstructed blood flow and heavy bleeding, cold limbs, lethargy, distention, chronic diarrhea, prolapse), strengthens the spleen, Helps the heart which calms the emotions and improves memory. For mature women, it lengthened the sexual arousal and conception period.
Harmonizing the Heart & Digestion
1. Atractylodes Rhizoma – White – improves the Spleen and Stomach. Clears dampness. Benefits spleen deficiency, corrects miscarriage, diarrhea, fatigue.
2. Sclerotium Poriae cocos – leaches fluids downward. While neutral in temperature, drainage is especially beneficial to the heart, spleen, kidney and lung. Benefits: spleen weakness, fluid retention, mucus buildup in channels, palpitations, headache, dizziness, loss of appetite, diarrhea, distention, generalized edema, Insomnia, forgetfulness, obstructed urination, calms the heart & spirit.
3. Ziziphi spinosae Semen – energizes the weakened heart and thus calm the spirit. Benefits: irritability, insomnia, palpitations, anxiety, blood deficiency, Spontaneous sweating and night sweats, abnormal sweating, prevents loss of consciousness, shortness of breath, anxiety, dry cough without phlegm, contracture and spasms of the sinews (tendons) and bones, dry, splitting nails,
For the rest of the formula (herbs 7-12) and/or to buy the Chinese herb formula, please go here: https://traditional-chinese-herbs.com/product/female-comfort/
Mark Hammer CMH-III, Senior Master Herbalist, Longevity Mountain Herbs
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7,906,688,224,442,162,000 | Article Text
PDF
Letter
Proton-pump inhibitors and increased gastric cancer risk: time-related biases
1. Samy Suissa1,2,
2. Alain Suissa3
1. 1Centre for Clinical Epidemiology, Jewish General Hospital, Montreal, Quebec, Canada
2. 2Department of Epidemiology, Biostatistics and Medicine, McGill University, Montreal, Quebec, Canada
3. 3Department of Gastroenterology, Rambam Hospital and Technion University, Haifa, Israel
1. Correspondence to Pr Samy Suissa, Centre for Clinical Epidemiology, Jewish General Hospital, Montreal, Québec H3T 1E2, Canada; samy.suissa{at}mcgill.ca
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We read with interest the cohort study by Cheung et al1 reporting that use of proton-pump inhibitors (PPIs) after Helicobacter pylori eradication is associated with an increased risk of gastric cancer (GC). We believe that the significantly elevated HR of GC with PPI use (HR 2.44; 95% CI 1.42 to 4.20) is a consequence of two time-related biases. Immortal time bias was introduced by misclassifying exposure,2–4 while latency bias was introduced by not incorporating latency in the exposure definition, a major issue for potential carcinogenic drug effects.5 6
Immortal time in a cohort study refers to a period of follow-up time when the outcome could not occur.3 It arises in this study from the definition of frequency of PPI use, ‘calculated by dividing the total treatment duration by the duration of follow-up’, namely the average use over the entire follow-up. Exposure to PPIs was then categorised ‘into non-regular use (<weekly use; reference group) and regular use (at least weekly use)’.1 Thus, the PPI ‘non-users’ included authentic non-users of PPIs and the non-regular PPI users (less than weekly use), together making up the reference group against which the risk …
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-4,019,718,736,602,822,700 | RT Journal Article SR Electronic T1 The Protective Effect of Metallothionein Against Lipid Peroxidation Caused by Retinoic Acid in Human Breast Cancer Cells JF Journal of Pharmacology and Experimental Therapeutics JO J Pharmacol Exp Ther FD American Society for Pharmacology and Experimental Therapeutics SP 1520 OP 1528 VO 283 IS 3 A1 Hurnanen, Darin A1 Chan, Hing Man A1 Kubow, Stan YR 1997 UL http://jpet.aspetjournals.org/content/283/3/1520.abstract AB The treatment of breast cancer by retinoic acid (RA) may be mediated by lipid peroxidation. Expression of metallothionein (MT) in cancer cells, however, can protect against lipid peroxidation by scavenging hydroxyl radicals. In this study, a two-by-six factorial design was used to investigate the interactive effects of all-trans-RA and zinc (Zn)-induced MT on the growth of two human breast cancer cell lines differing in basal expression of MT and estrogen receptors; MCF7 cells express estrogen receptor, BT-20 cells do not. Cells were treated with Zn to induce MT and then treated with six RA concentrations. Cell proliferation, lipid peroxidation, MT protein, MT mRNA and glutathione concentrations were measured. BT-20 cells expressed higher constitutive MT concentrations than MCF7 cells. MT was significantly increased by Zn treatment in BT-20 cells but not in MCF7 cells. Low RA concentrations stimulated growth proliferation but higher concentrations inhibited cell proliferation. Elevated RA concentrations increased lipid peroxidation as measured by thiobarbituric acid reactive substances. There was a significant negative correlation between lipid peroxidation and cell proliferation. Growth inhibition and lipid peroxidation were reduced by Zn pretreatment in BT-20 cells but not in MCF7 cells. RA increased MT levels in both cell lines, which suggests that RA may generate free radicals which will induce MT mRNA expression. Glutathione did not appear to be a significant factor. Therefore, induction of MT by Zn may modulate the growth inhibitory effects of RA in human breast cancer cells. One mechanism of growth inhibition may be through increased lipid peroxidation. Induction of MT by RA may be one explanation for acquired RA resistance in cancer. The American Society for Pharmacology and Experimental Therapeutics | {
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-7,498,062,174,730,840,000 | desogestrel
Also found in: Medical, Wikipedia.
des·o·ges·trel
(dĕs′ə-jĕs′trəl)
n.
A progestin, C22H30O, used in combination with estrogen in oral contraceptives.
[Probably deso(xy)-, variant of deoxy- + (nor)gestrel.]
Translations
desogestrel
n desogestrel m
Mentioned in ?
References in periodicals archive ?
Our second missing family planning essential is desogestrel 75 [micro]g (Cerazette), a progestin-only contraceptive pill (POP).
Women exposed to drospirenone, gestodene, cyproterone, and desogestrel within the last 28 days had around a four times increased risk of venous thromboembolism," the investigators found.
That ruling is at odds with a study by the University of Nottingham just published in the British Medical Journal, which found that pills containing one of the newer types of progestogen hormone (drospirenone, desogestrel, gestodene, and cyproterone) are associated with an increased risk of VTE (venous thromboembolism) compared to pills containing older progestogens.
Pills containing one of the newer types of progestogen hormone - such as drospirenone, desogestrel, gestodene, and cyproterone - are associated with an increased risk of VTE than pills containing older progestogens such as levonorgestrel and norethisterone, it was found.
The authors, led by Dr Ojvind Lidegaard from the University of Copenhagen, say that women on pills containing one of the newer types of progestogen hormone (drospirenone, desogestrel or gestodene) have double the risk of VTE than women on pills containing an older progestogen (levonorgestrel).
For the same dose of oestrogen and the same length of use, oral contraceptives with desogestrel, gestodene, or drospirenone were associated with a significantly higher risk of venous thrombosis than oral contraceptives with levonorgestrel.
Meanwhile, those on contraceptives containing desogestrel (for example, Mercilon or Marvelon) had the highest risk.
Those on contraceptives containing desogestrel, such as Mercilon or Marvelon, had the highest risk of clots known as venous thrombosis - seven times that of women not on the Pill.
150 desogestrel either alone during the control cycle or combined with St.
Comparison of the lipoprotein, carbohydrate, and hemostatic effects of phasic oral contraceptives containing desogestrel or levonorgestrel.
Investigation of hormonal male contraception in African men: suppression of spermatogenesis by oral desogestrel with depot testosterone Hum Reprod 2002; 17(11): 2869-2877. | {
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-4,993,940,678,209,284,000 | top of page
Mask Analysis
Masks have gotten a lot of air time this past year. We're not talking about the feathery sequined kind you see at Venetian carnivals or Cirque de Soleil. We're talking about medical masks and the difference between the throwaway blue 3-ply masks, N95s and KN95s, gaiters, shields, and various fabrics and materials. The ones that have become mocked, reviled, politicized, turned into fashion statements, sought after, and worn with relief in this strange, hopefully once-in-a-lifetime year-ish that have made us really appreciate fresh air and truly understand how illness gets spread.
Medical masks became part of a strategy to stop germs from entering wounds and prevent sepsis in the 1880s but didn't become de rigeur until the last pandemic in 1918-19 when they were shown to prevent the wearer from contracting influenza. During that pandemic (which is estimated to have killed somewhere between 20-50 million people, showing us that both metrics and medicine have come a long way), people revolted against wearing masks and shutting down churches, saloons, theaters, and sporting events just like today. So don't worry if you think we've regressed as a species. We're pretty much basically the same.
Anyway, disposable masks are generally made with synthetic fibers which mesh to prevent diffusion and therefore prevent pathogen transmission through droplets and aerosols between people. N95 and KN95 masks (rated as such by the USA and China respectively) offer the best protection against infection—95% protection—unless you want to go full-on hazmat and start wearing a gas mask, but let's not go over the deep end.
Gaiters, those fabric neck warmers that come up over your face, and bandanas both have more porous fabrics and generally tend to be less effective than professionally manufactured masks, but if you're going to wear them, double them up for maximum effect. On the other side of the equation, fabrics like vinyl and plastic that don't breathe at all should be avoided. Oxygen is essential to survival and swimming in your own CO2 is a contraindication to being alive.
Shields, those plastic guards that make you look like a welder, are ineffective on their own, but render masks, worn properly, to be more effective. Also ineffective: wearing a mask over your mouth but leaving your nose uncovered. Air still comes out of your nose. Wearing a mask without covering both your mouth and nose is basically the same as not wearing a mask.
While some question the effectiveness of masks, data continues to pour in that suggests otherwise. As we've discussed, some masks are better than others and infection by any airborne disease is a question of exposure over time (for a brilliant primer on viral aerodynamics and the risks of getting Covid, check out researcher Erin Bromage's blog post). I know, you never thought the words "brilliant primer" and "viral aerodynamics" could occupy the same thought, let alone sentence. But seriously, read it. Pass it on. It will make you rethink eating birthday cake after someone has blown their aerosols all over it.
As we get vaccinated and try to reach herd immunity, most people want to escape masks. I get it. Masks are claustrophobic. They fog your glasses up. (Unless you are wearing an N95 or KN95 which seal your air from rising up.) They make it difficult to eat and drink. But they also save lives, prevent the spread of Covid, and keep our front line medical workers from becoming inundated and burning out.
The most important point about wearing masks is this: YOU DON'T WEAR THE MASK SO MUCH TO PROTECT YOURSELF (unless it's an N95 or KN95). YOU WEAR THE MASK TO PROTECT OTHER PEOPLE. So do unto others and do your part.
For more on health and safety during events, check out PopUP CleanUP's YOUR ULTIMATE LIVE EVENT GAME PLAN.
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-8,759,132,288,648,926,000 | brain herniation
(redirected from Subfalcine herniation)
brain herniation
Pressure-induced prolapse of part of the brain into adjacent spaces, which occurs when the brain is under high pressure.
Clinical findings
Coma, paralysis, unilateral dilated pupil.
Aetiology
Head injury, primary or metastatic brain tumour, bacterial meningitis, brain abscess.
Types
Cerebellar herniation, uncal (temporal) herniation, transtentorial herniation.
brain herniation
Neurology A pressure-induced prolapse of part of the brain into adjacent spaces, which occurs when the brain is under very high pressure Clinical Coma, paralysis, unilateral dilated pupil Etiology Head injury, 1º or metastatic brain tumor, bacterial meningitis, brain abscess Types Cerebellar herniation, uncal–temporal herniation, transtentorial herniation of the brain
brain
encephalon; that part of the central nervous system contained within the cranium, comprising the forebrain, midbrain and hindbrain, and developed from the embryonic neural tube. It is connected at its base with the spinal cord. The brain is a mass of soft, pinkish gray nerve tissue. For specific brain diseases see under headings relating to etiology and lesion.
brain abscess
common signs caused by an abscess in the brain are circling, rotation of the head, abnormal reflexes in one eye. The CSF may show evidence of infection.
brain aneurysm
see berry aneurysm.
brain anoxia
acute or chronic insufficiency of the blood supply to the brain causes anoxia which causes clinical signs that vary with the severity of the deprivation. Acute anoxia causes muscle tremor, recumbency, convulsions and death or recovery if the anoxia is relieved soon enough. Chronic anoxia causes lethargy, weakness, blindness and sometimes convulsions. In either case there may be permanent damage.
brain case
the cranium.
brain cestodal cyst
brain coup lesion
a derivation from contrecoup.
brain dead
irreversible coma with apnea, loss of all brainstem reflexes and absence of activity on an electroencephalogram.
brain decompression
relieving the pressure within the cranial vault. This may be done surgically by opening the cranium, or medically by administering hypertonic solutions of slowly metabolized materials, such as mannitol, intravenously.
brain edema
an important part of a number of acute diseases, e.g. lead poisoning, encephalitis, salt poisoning in swine, polioencephalomalacia of ruminants and hypoxia due to any cause. Clinically manifested by blindness, opisthotonos, nystagmus, recumbency and tonic convulsions. Inherited in polled and horned Herefords; calves are recumbent at birth and are never able to stand but consciousness is normal. See also neuraxial edema.
brain ependymal lining
brain hematoma
may occur with trauma, in extradural, subdural or intraparenchymal locations. They can cause progressive increase in intracranial pressure and eventually death.
brain hemorrhage
intracranial hemorrhage affecting the brain usually follows traumatic injury but spontaneous hemorrhage may result from an intrinsic vascular lesion. Loss of consciousness is a common sign followed by residual signs depending on the locality and size of the hemorrhage. Ataxia and convulsions are common sequelae.
brain herniation
displacement of brain from the cranial vault through the foramina (tentorial notch or foramen magnum) or ventral to dural septae. The usual causes are brain edema or hemorrhage with resulting increase in intracranial pressure.
brain hypoxia
see brain anoxia (above).
brain infarction
see feline ischemic encephalopathy.
brain ischemia
see brain anoxia (above).
brain laceration
occurs in cranial trauma that fractures the skull, causes severe acceleration or deceleration, or penetrates the skull and brain tissue.
brain necrosis
brain pigmentation
occurs in phalaris spp. poisoning; a characteristic greenish brown color grossly of the gray matter in brainstem nuclei and spinal cord, caused by a suspected lysosomal storage of granules of pigment material; usually associated with some degree of Wallerian degeneration within spinal cord tracts.
brain sand
brain scanning
a radiographic, magnetic or nuclear medical procedure for the detection of brain tumors, abscesses, hematomas and other intracranial lesions. Not widely used in veterinary medicine because of the expensive equipment required.
brain spongy degeneration
brain staggers
see dummy.
brain trauma
injury to the brain, including that caused by migrating worm larvae, will have diffuse effects including the development of edema, and local effects due to pressure by displaced bone or to hemorrhage. Initial shock, manifested as unconsciousness, is likely to be followed by residual localizing signs, e.g. facial paralysis, head rotation.
brain tumors
cause signs suggestive of local space-occupying lesion in the cranial cavity, including the increased intracranial pressure syndrome, blindness with disturbance of ocular reflexes, head rotation, circling and jacksonian epileptic episodes.
brain ventricles
see third, fourth, fifth ventricle.
References in periodicals archive ?
The lesion crossed the midline and had caused anterior subfalcine herniation.
Computed tomography (CT) of the head without intravenous contrast demonstrated pronounced vasogenic edema throughout the right frontal lobe with an underlying mass and associated mass effect with subfalcine herniation (Figure 1).
However, there is interval demonstration of concave deformity of the left cerebral hemisphere together with the overlying skin flap, with associated distortion of the left ventricle and a new left subfalcine herniation.
Vasogenic edema was evident, as was mass effect with compression of the left lateral ventricle and small subfalcine herniation. | {
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1,614,024,532,361,422,800 | Plague Channel
Topics
Quicklinks
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Plague Transmission
Plague transmission generally occurs in one of three ways: bites from infected fleas, direct contact with infected tissue or bodily fluids, or inhaling infected droplets. The most common method is through the bites of infected rodent fleas. Plague transmission from person to person is uncommon, but when it does occur, it usually results in dangerous epidemics that can spread quickly.
An Introduction to Plague Transmission
Yersinia pestis (the bacteria that cause plague) is found in animals throughout certain parts of the world, most commonly in rats, but occasionally in other wild animals, such as prairie dogs. Plague transmission from these infected animals generally occurs in one of three ways:
• Bites from infected rodent fleas
• Direct contact with infected tissue or bodily fluids
• Inhaling infected droplets.
Plague Transmission Through Bites
Plague transmission to humans or animals is usually through the bites of infected rodent fleas (see Plague and Animals for other animals that can transmit plague). During rodent plague outbreaks, many animals die, and their hungry fleas seek other sources of blood to survive. People and animals that visit places where rodents have recently died from plague risk getting plague from flea bites.
This method of plague transmission accounts for about 85 percent of the human cases of plague.
Plague Transmission Through Direct Contact
Plague transmission can also occur through direct contact with infected tissue or bodily fluids. For example, people can become directly infected with plague by handling infected rodents, rabbits, or wild carnivores that prey on these animals when plague bacteria enter through the person's skin.
House cats also are susceptible to plague. Infected cats may become sick and directly transmit plague to people who handle or care for them. Also, dogs and cats may bring plague-infected fleas into the home.
The Plague
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eMedTV serves only as an informational resource. This site does not dispense medical advice or advice of any kind. Site users seeking medical advice about their specific situation should consult with their own physician. Click Terms of Use for more information. | {
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2,457,457,732,230,556,700 | medical-marijuana
Different Ways to Consume Medical Marijuana
When it comes to marijuana use, the majority of the users think about smoking. But, scientists have discovered new consumption methods over the years. You can find marijuana-infused foods and topicals. In fact, CBD gummies are the most popular edibles.
Consumption method matters. How cannabinoids are delivered into the body affects the therapeutic effects of marijuana.
Here are the available options for users to consume cannabis-
1. Smoking
It’s the most popular method among cannabis users. It’s quite similar to smoking cigarettes—burning the substance and inhaling the smoke containing active compounds.
There are many ways to smoke cannabis. The majority of people prefer smoking joints—cannabis rolled in papers. Many prefer blunts—flowers rolled in cigar paper made from the tobacco plant. Other methods include water pipes, hand pipes, and hookahs.
Although smoking delivers instant effects, it’s not without risks. The burning of marijuana generates a wide range of toxins and carcinogens, which are harmful to lung health. In fact, cannabis smoke contains many of the same harmful chemicals as present in tobacco smoke.
If you are experiencing lung health issues, see a medical marijuana doctor before starting smoking cannabis. Or, you can opt for other delivery methods discussed below.
2. Vaping
Vaping is another inhalation method, which is considered safer than smoking. This is due to the fact cannabis is heated at a much lower temperature. Additionally, it preserves temperature-sensitive ingredients in marijuana, allowing you to receive potent, flavorful effects.
You can either vape flowers or concentrate. Thus, at medical dispensaries, you can find a wide range of cannabis products for vaping.
Today, you can find a wide range of portable vape pens. They have an easy operation. Simply load cannabis in the chamber, press the start button and enjoy. Simple!
Moreover, some modern technology vaporizers allow you to control temperature, thus adjusting the release of cannabinoids. Thus, you can enjoy a customized vaping experience.
However, vaping delivers stronger effects. According to a report published in 2018, participants who vaped cannabis experienced more powerful effects than those who smoked it. Thus, vaping is linked to increased risks of overdose.
3. Edibles
If you don’t want to inhale cannabis, go for edibles. These are foods and beverages infused with cannabinoids. At medical dispensaries, you can find a wide range of options in edibles, such as brownies, ice creams, teas, chocolate bars, gummies, etc.
What sets cannabis-infused edibles apart from other delivery methods is onset time. Unlike smoking, they don’t kick in within a few minutes. You have to wait for 30-120 minutes to feel the therapeutic effects of cannabinoids instead. This happens because cannabinoids are transferred to the bloodstream via the digestive tract.
So, it’s important to dose edibles properly to make the most out of your cannabis consumption experience.
Additionally, edibles last longer, usually 8-10 hours. So, if you are planning to eat marijuana, be ready to experience lasting effects.
Related- How to Consume Marijuana Edibles Safely?
4. Topicals
Yes, cannabis is available in the form of creams, lotions, etc. you can apply cannabis in the affected areas. This method is widely preferred by patients who want to get localized relief from pain, soreness, and inflammation.
Lotions, sprays, and oils work by interacting with the cannabinoid receptors, which are found throughout the body. The receptors are usually activated by endocannabinoids produced by the body naturally.
Since topicals deliver non-intoxicating effects, they are often chosen by users looking to receive marijuana’s therapeutic benefits without getting high.
At medical dispensaries, you can find topicals with different levels of THC and CBD. What’s more? Most manufacturers are now considering adding essential oils to increase the effectiveness of topicals. So, read the label carefully when buying patches and other topical products.
5. Tinctures
Tinctures are cannabis extracted in alcohol or glycerine. Alcohol-based tinctures have a fast action while glycerine-based tinctures are a suitable option for kids.
The best part of using tinctures is that they are easy to dose. They come in droppers—thus you can easily adjust the dosage according to your medical needs.
Tinctures are usually absorbed sublingually. Fill the dropper, and place a few drops under your tongue. This way, cannabinoids get absorbed in the body instantly but may take some time to pass through the liver.
However, you can also incorporate tinctures in juices, ice creams, soups, and salad dressings.
Whatever method you choose, dosing is important. Follow the “start small” motto. Start with a small dose and add up gradually if necessary. Read the instructions carefully and follow the guidelines for recommended dose.
Use Medical Marijuana Right
If you are considering cannabis treatment for your condition, learning how to use the herb right is important. Remember, there’s no one-size-fits-all. Every patient is different and requires a customized treatment plan.
We advise you to try different methods, dosages, and strains. Make a journal and note down your experiences with different consumption methods & stick to the ones delivering you desired health benefits.
Talk to a board-certified marijuana doctor to seek professional help for using marijuana for medical purposes.
In conclusion, these are some methods of marijuana consumption. Opt for smoking/vaping to receive quick effects and edibles for lasting relief. Prefer tinctures for dosage control.
Before opting for any cannabis consumption method, make sure you check the local laws. Different cannabis legalized states may have different regulations for consuming the herb.
Most importantly, apply for a marijuana evaluation to buy, possess and use cannabis legally. At MD Ganja, you can get a doctor’s recommendation in just 10 minutes. Fill in a simple form and one of the New Jersey marijuana doctors will contact you via video call. If approved, you will receive your MMJ recommendation letter via email.
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3,728,239,348,697,147,400 | Skip to main content
Simulation of a medication and methylation effects on triglycerides in the Genetic Analysis Workshop 20
Abstract
The GAW20 simulation data set is based upon the companion Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study fenofibrate clinical trial data set that forms the real data example for GAW20. The simulated data problem consists of 200 simulated replications of what might happen if we were to repeat the GOLDN clinical trial 200 independent times, for these exact same subjects, but using a new fictitious drug (called “genomethate”) that has a pharmaco-epigenetic effect on triglyceride response. For each replication, the pre-genomethate values at visits 1 and 2 are constant (ie, pedigree structures, age, sex, all phenotypes, covariates, genome-wide association study (GWAS) genotypes, and visit 2 methylation values), the same as the real GOLDN data across all 200 replications. Only the post-genomethate treatment data (ie, methylation and triglyceride levels for visits 3 and 4) change across the 200 replications. We postulate a growth curve pharmaco-epigenetic response model, in which each patient’s response to genomethate treatment is individualized, and is dependent upon their genotype as well as the methylation state for key genes.
Background
The companion Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study fenofibrate clinical trial data set [1,2,3] was the foundation of our Genetic Analysis Workshop 20 (GAW20) simulation. The general simulation strategy was to first simulate visit 4 methylation array data for each subject (which measures the individual epigenetic responses to genomethate treatment), and then use this plus the genome-wide association study (GWAS) genotypes to produce the simulated triglycerides for visits 3 and 4 post-treatment values. The main simulated effect of genomethate is on the phenotype of the individual subject’s triglyceride (TG) values measured as slope in response to treatment (change in mg/dL per unit time of treatment).
Methods, results and discussion
Figure 1 illustrates the graphical design of the simulations.
Fig. 1
figure 1
A 3D indexing order of the GAW20 simulation. The j index in the figure represents the subjects, the i index is noting the causal SNPs, where i = 1–5 also indexes the 5 main effects of the corresponding nearby CpG sites, while the sites 6–105 are 100 SNPs with background genetic effects. The k index indicates replications (k = 1, 2, …, R = 200)
The j index in the figure represents the subject (j = 1, 2, …, N = 717). The i index is noting the single-nucleotide polymorphisms (SNPs) chosen to be causal in the simulating model (i = 1, 2, …, G = 105), where i = 1, 2, 3, 4, 5 also indexes the 5 main effects of the corresponding nearby cytosine-phosphate-guanine (CpG) sites, while beyond main effects, the sites from 6 to 105 are 100 SNPs with background genetic effects. The k index indicates replications (k = 1, 2, …, R = 200).
The first 5 causal SNPs are “major” effects (summarized in Table 1), and the last 100 SNPs are polygenic background effects (Table 2). Note that only the first 5 CpG sites are relevant to the model, the polygenic background effects do not depend upon CpG states.
Table 1 Five major effect causal SNPs and corresponding nearby CpG markers affecting triglycerides at visits 3 and 4
Table 2 Background polygenic SNPs. All markers are simulated with the same heritability (hg2 = 0.001) affecting triglycerides at visits 3 and 4
We first defined a series of subjects’ triglyceride values from the original (real) Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) data [1], which was used to generate the simulations. Because triglycerides were approximately log-normally distributed, we worked with log-transformed triglyceride values in all calculations, only transforming back to the measured triglyceride scale at the end of the simulations. In particular, for the jth subject, the average log triglycerides pre-treatment (average of visits 1 and 2, which are 1 day apart) and post-treatment (average of visits 3 and 4, which are also 1 day apart) in the original (real) GOLDN data are:
$$ \boldsymbol{O}\_\boldsymbol{preRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}}=\boldsymbol{mean}\left(\mathbf{\log}\left(\boldsymbol{TG}{\mathbf{1}}_{\boldsymbol{j}}\right),\mathbf{\log}\left(\boldsymbol{TG}{\mathbf{2}}_{\boldsymbol{j}}\right)\right) $$
$$ \boldsymbol{O}\_\boldsymbol{postRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}}=\boldsymbol{mean}\left(\mathbf{\log}\left(\boldsymbol{TG}{\mathbf{3}}_{\boldsymbol{j}}\right),\mathbf{\log}\left(\boldsymbol{TG}{\mathbf{4}}_{\boldsymbol{j}}\right)\right) $$
where O –stands for “Observed / Original”, preRx stands for “pre-medication treatment,” postRx stands for “after medication treatment,” and TG labels “triglycerides” which were log transformed to ensure a normal distribution of the trait. The TG of person j is measured in visits 1, 2, 3 and 4 and averaged as above for each individual as preRx and postRx. The corresponding change in log triglycerides pre-treatment to post-treatment for subject j is given by:
$$ \boldsymbol{O}\_\boldsymbol{delta}\_{\boldsymbol{TG}}_{\boldsymbol{j}}=\left[\boldsymbol{O}\_\boldsymbol{postRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}}-\boldsymbol{O}\_\boldsymbol{preRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}}\right] $$
where delta is the “change”. The individual time on treatment (less than 30 days) for each subject (in days), is given by the following formula:
$$ \boldsymbol{O}\_{\boldsymbol{daysRx}}_{\boldsymbol{j}}=\boldsymbol{mean}\left(\boldsymbol{draw}\_\boldsymbol{date}\_\boldsymbol{v}{\mathbf{3}}_{\boldsymbol{j}},\boldsymbol{draw}\_\boldsymbol{date}\_\boldsymbol{v}{\mathbf{4}}_{\boldsymbol{j}}\right)-\boldsymbol{draw}\_\boldsymbol{date}\_\boldsymbol{v}{\mathbf{2}}_{\boldsymbol{j}} $$
where daysRx is “days after medication treatment,” draw_date is “blood draw date” at a particular v- “visit.” Thus, the observed slope (change in log triglycerides over the treatment period) is:
$$ \boldsymbol{O}\_\boldsymbol{slope}\_{\boldsymbol{TG}}_{\boldsymbol{j}}=\boldsymbol{O}\_\boldsymbol{delta}\_{\boldsymbol{TG}}_{\boldsymbol{j}}/\boldsymbol{O}\_{\boldsymbol{daysRx}}_{\boldsymbol{j}} $$
If mean_O_PreRx_TG and sd_O_preRx_TG are the mean and standard deviations, respectively, of all the O_preRx_TGj across the j = 1, …, N individuals, then the standardized original preRx of TGj are given by:
$$ \boldsymbol{O}\_{\boldsymbol{preZ}}_{\boldsymbol{j}}=\left(\boldsymbol{O}\_\boldsymbol{preRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}}-\boldsymbol{mean}\_\boldsymbol{O}\_\boldsymbol{PreRx}\_\boldsymbol{TG}\right)/\boldsymbol{sd}\_\boldsymbol{O}\_\boldsymbol{preRx}\_\boldsymbol{TG} $$
where O_preZ -is a standardized normally distributed variable with N(0,1).
Tables 1 and 2 summarize the epigenetic model in our simulation. We chose 5 “major gene” causal variants (ranging from modest to small effect sizes corresponding to expected “heritabilities” of 0.125, 0.10, 0.075, 0.05, and 0.025), which, in the absence of any epigenetic effects, should govern individual genomethate treatment response along with 100 polygene variants (each of tiny effect size corresponding to “heritabilities” of 0.001 each). These were chosen randomly from chromosomes 1–20 of the GWAS Affymetrix Genome-wide Human SNP Array 6.0, which had 718,544 autosomal SNPs.
For the epigenetic component, we choose 5 CpG sites on the Illumina Infinium HumanMethylation450 BeadChip array (which had 463,995 CpG sites) that are physically closest to the 5 “major gene” causal SNPs, while the methylation sites near the 100 polygenes have no effect. The genomethate response model is based upon the idea that these CpG sites need to be sufficiently unmethylated for the corresponding causal SNPs to express their influence on each individual’s phenotype. If the nearby CpG site is totally methylated (=1), then the corresponding causal SNP actually has no effect on the phenotype. If the CpG site is totally unmethylated (=0), then the corresponding causal SNP carries its full effect size impact on the phenotype. If the CpG site is partially methylated (between 0 and 1), then the effect size of the causal SNP is proportionally attenuated.
Specifically, for the kth simulation, we first generated the simulated visit 4 methylation array results for all subjects, based upon their corresponding visit 2 and/ or visit 4 methylation values. For each subject j = 1, …, 717, and each CpG methylation site i = 1, 2, 3, 4, 5 (corresponding to 5 major effect CpGs)
$$ \boldsymbol{sim}\_\boldsymbol{meth}\_\boldsymbol{v}{\mathbf{4}}_{\boldsymbol{ji}\boldsymbol{k}}=\boldsymbol{real}\_\boldsymbol{meth}\_\boldsymbol{v}{\mathbf{2}}_{\boldsymbol{ji}}+{\boldsymbol{sd}}_{\boldsymbol{i}}\ast \boldsymbol{Z}{\mathbf{1}}_{\boldsymbol{ji}\boldsymbol{k}} $$
where sim_meth stands for “simulated methylation” at visit 4, real_meth is the jth subject’s “real methylation” array data at visit 2 for the ith CpG site, sdi = 0.4 represents the standard deviation of individual subject methylation responses to treatment, and Z1jik ~ N(0, 1) is a pseudo-random standard normal variable drawn independently for each jik.
For the remaining, non-causal CpG sites, if the subject j had real visit 4 methylation array data then
$$ \boldsymbol{sim}\_\boldsymbol{meth}\_\boldsymbol{v}{\mathbf{4}}_{\boldsymbol{ji}\boldsymbol{k}}=\boldsymbol{real}\_\boldsymbol{meth}\_\boldsymbol{v}{\mathbf{4}}_{\boldsymbol{ji}}+{\boldsymbol{sd}}_{\boldsymbol{i}}\ast \boldsymbol{Z}{\mathbf{1}}_{\boldsymbol{ji}\boldsymbol{k}} $$
Otherwise, if the subject j only had visit 2 methylation array data, then
$$ \boldsymbol{sim}\_\boldsymbol{meth}\_\boldsymbol{v}{\mathbf{4}}_{\boldsymbol{ji}\boldsymbol{k}}=\boldsymbol{real}\_\boldsymbol{meth}\_\boldsymbol{v}{\mathbf{2}}_{\boldsymbol{ji}}+{\boldsymbol{sd}}_{\boldsymbol{i}}\ast \boldsymbol{Z}{\mathbf{1}}_{\boldsymbol{ji}\boldsymbol{k}} $$
where real_meth_v2ji and real_meth_v4ji are the real visit 2 and visit 4 methylation array data, respectively, for subject j and CpG site i, sdi represents the standard deviation of individual subject methylation responses to treatment for the ith CpG site, and again, Z1jik ~ N(0,1) is a pseudo-random variable drawn independently for each jik.
We selected five random non-causal (red-herrings) CpG sites also (shown in Table 3). We set for them the sdi = 0.4, to be similar to the simulated causal CpG sites. For the remaining non-causal CpG sites, we set the corresponding sdi = 0.03, which is closer to that seen in the real visit 4 methylation data CpG sites, essentially at the measurement error level.
Table 3 Five non-causal (red-herrings) CpG markers chosen to have N(0,0.4) random variability, imitating the distribution of the 5 real causative CpG markers
In all cases, all simulated visit 4 methylation values were then truncated to be strictly in the [0,1] interval, that is,
if (sim_meth_v4jik>1) then sim_meth_v4jik=1
if (sim_meth_v4jik<0) then sim_meth_v4jik=0
for all subjects j, CpG sites i, and simulation replications k.
Note that the model is such that, on average, the genomethate treatment has no effect on the amount of methylation increase/decrease from visit 2 to visit 4, however, there is variability across subjects. To reiterate, the variability is quite high (sdi = 0.4) for the five CpG regions controlling the expression of the major causal variants and 5 other non-causal CpG (red-herrings) sites. The variability is low (sdi = 0.03) for all other CpGs, at the level of measurement error.
Using these simulated visit 4 methylation data, we then generated the simulated slope change in triglyceride response for each individual j in each replication k as follows:
$$ {\boldsymbol{slope}}_{\boldsymbol{jk}}={\sum}_{\boldsymbol{i}=\mathbf{1}}^{\mathbf{5}}\left(\mathbf{1}-\boldsymbol{sim}\_\boldsymbol{meth}\_\boldsymbol{v}{\mathbf{4}}_{\boldsymbol{ji}\boldsymbol{k}}\right)\ast \boldsymbol{sqrt}\left(\boldsymbol{hg}{\mathbf{2}}_{\boldsymbol{i}}\right)\ast {\boldsymbol{SSNP}}_{\boldsymbol{ji}}+{\sum}_{\boldsymbol{i}=\mathbf{6}}^{\mathbf{105}}\boldsymbol{sqrt}\left(\boldsymbol{hg}{\mathbf{2}}_{\boldsymbol{i}}\right)\ast {\boldsymbol{SSNP}}_{\boldsymbol{ji}}+{\boldsymbol{zenv}}_{\boldsymbol{jk}}\ast \boldsymbol{sqrt}\left(\mathbf{1}-\sum \limits_{\boldsymbol{i}=\mathbf{1}}^{\mathbf{105}}\boldsymbol{hg}{\mathbf{2}}_{\boldsymbol{i}}\right) $$
(1)
In the above formula, zenvjk is an independently drawn pseudo-random normal deviate distributed N(0,1) for each subject j and each replication k, and it represents unexplained residual variation in the phenotype. SSNPji is the standardized ith SNP additive genotype-dosage (i.e., coded such that mean = 0 and sdi = 1 in the sample), and the i = 1, 2, …, 105 regression coefficients in this linear model are given in terms of constants sqrt(hg2i), in Tables 1 and 3. Note that if the five causal CpG sites were completely unmethylated for all subjects (i.e., no epigenetic effects), then (1 – sim_meth_v4 jik) would be = 1 for all j = 1,…, N and i = 1,…, 5, and k = 1,…, 200, so that the regression coefficients would be interpreted as the square root of the locus specific heritability of the associated SNPs. Conversely, when the causal CpG site is totally methylated for that subject, (1 - sim_meth_v4 jik) = 0, so that the corresponding major effect SNPi will not express its effect on the phenotype. Similarly, if the CpG site is partially methylated (between 0 and 1), the effect size of the causal SNP is proportionally attenuated.
To carry forward these simulated relationships in eq. (1), we must address the fact that the observed slope responses for each subject are correlated to their baseline values of triglyceride (i.e., lower baseline values should produce less dramatic declines with treatment, whereas higher baseline values can experience greater slope change with treatment). In the real GOLDN data, the correlation between slope change in response to fenofibrate treatment and baseline log triglycerides is − 0.41881, and we used this constant value in our genomethate simulation to introduce a correlation between slope change and baseline values:
$$ {\boldsymbol{corrz}}_{\boldsymbol{j}\boldsymbol{k}}=\left(-\mathbf{0.41881}\right)\ast \boldsymbol{O}\_{\boldsymbol{preZ}}_{\boldsymbol{j}}+\boldsymbol{sqrt}\left(\mathbf{1}-{\left(\mathbf{0.41881}\right)}^{\mathbf{2}}\right)\ast {\boldsymbol{slope}}_{\boldsymbol{j}\boldsymbol{k}} $$
Because the simulated individual slopes are generated on the standardized scale, we needed to rescale to that of the original scale of triglyceride changes per day of treatment, by working backwards. The mean and standard deviation of O_slope_TGj over all subjects j, are denoted by mean_O_slope_TG and sd_O_slope_TG, respectively. We used the above observed mean and standard deviation of slopes seen in the original GOLDN data, to rescale as follows:
$$ \boldsymbol{sim}\_{\boldsymbol{slope}}_{\boldsymbol{jk}}={\boldsymbol{corrz}}_{\boldsymbol{jk}}\ast \boldsymbol{sd}\_\boldsymbol{O}\_\boldsymbol{slope}\_\boldsymbol{TG}+\boldsymbol{mean}\_\boldsymbol{O}\_\boldsymbol{slope}\_\boldsymbol{TG} $$
Then the expected response to genomethate treatment of the jth subject, after O_DaysRxj original days of treatment, is given by:
$$ \boldsymbol{sim}\_\boldsymbol{postRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}\boldsymbol{k}}=\left(\boldsymbol{sim}\_{\boldsymbol{slope}}_{\boldsymbol{j}\boldsymbol{k}}\ast \boldsymbol{O}\_{\boldsymbol{DaysRx}}_{\boldsymbol{j}}\right)+\boldsymbol{O}\_\boldsymbol{preRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}} $$
Finally, we used the simulated individual responses to produce the simulated values of triglyceride at visits 3 and 4, based upon the variability we see between those visits in the real GOLDN fenofibrate data:
$$ \boldsymbol{sim}\_\boldsymbol{TG}{\mathbf{3}}_{\boldsymbol{j}\boldsymbol{k}}=\boldsymbol{\exp}\left[\boldsymbol{sim}\_\boldsymbol{postRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}\boldsymbol{k}}+\left(\mathbf{\log}\Big(\boldsymbol{TG}{\mathbf{3}}_{\boldsymbol{j}}\right)-\boldsymbol{O}\_\boldsymbol{postRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}}\Big)\right] $$
(2)
$$ \boldsymbol{sim}\_\boldsymbol{TG}{\mathbf{4}}_{\boldsymbol{j}\boldsymbol{k}}=\boldsymbol{\exp}\left[\boldsymbol{sim}\_\boldsymbol{postRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}\boldsymbol{k}}+\left(\mathbf{\log}\Big(\boldsymbol{TG}{\mathbf{4}}_{\boldsymbol{j}}\right)-\boldsymbol{O}\_\boldsymbol{postRx}\_{\boldsymbol{TG}}_{\boldsymbol{j}}\Big)\right] $$
(3)
If only 1 replicate of the GAW20 simulated data was to be analyzed, we recommend the 84th replication, which was provided in a separate directory, as a “representative” of the 200 replicated simulations. Chromosomes 21 and 22 datasets were not used in the simulation, so an analyst can use the corresponding data for building a NULL hypothesis. The simulated GAW20 data are accompanied by README and Data Dictionary files.
References
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Acknowledgements
This study was supported in part by the NHLBI grant R01HL117078
Funding
Publication of this article was supported by NIH R01 GM031575.
Availability of data and materials
The data that support the findings of this study are available from the Genetic Analysis Workshop (GAW), but restrictions apply to the availability of these data, which were used under license for the current study. Qualified researchers’ may request these data directly from GAW.
About this supplement
This article has been published as part of BMC Proceedings Volume 12 Supplement 9, 2018: Genetic Analysis Workshop 20: envisioning the future of statistical genetics by exploring methods for epigenetic and pharmacogenomic data. The full contents of the supplement are available online at https://bmcproc.biomedcentral.com/articles/supplements/volume-12-supplement-9.
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MAP commenced the idea of GAW20 simulation and wrote the equations. ATK selected main and background SNPs and CpGs for the causative model. ATK, PL and JEH programmed the GAW20 simulations. EWD, SJL and CW performed QC analyses of all replications for GAW20 simulation. PA facilitated the retrieval of GOLDN real data, on which the GAW20 simulation was built. ATK and MAP wrote the manuscript with contributions of EWD, PA, PL, JEH, SJL, and CW. All authors participated in all meetings of GAW20 simulation working group and have read and approved this manuscript.
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Correspondence to Aldi T. Kraja or Michael A. Province.
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Kraja, A.T., An, P., Lenzini, P. et al. Simulation of a medication and methylation effects on triglycerides in the Genetic Analysis Workshop 20. BMC Proc 12 (Suppl 9), 25 (2018). https://doi.org/10.1186/s12919-018-0115-z
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-7,710,262,648,930,700,000 | Benzocaine Ointment
» Benzocaine Ointment contains not less than 90.0 percent and not more than 110.0 percent of the labeled amount of C9H11NO2 in a suitable ointment base.
Packaging and storage— Preserve in tight containers, protected from light, and avoid prolonged exposure to temperatures exceeding 30.
Identification—
Ointments having water-soluble bases— Transfer an amount of Ointment, equivalent to about 5 mg of benzocaine, to a small beaker, add 20 mL of 0.5 N hydrochloric acid, warm gently to disperse the Ointment, cool, and filter, if necessary. To 10 mL of the filtrate add 5 drops of a solution of sodium nitrite (1 in 10) and 2 drops of methyl red TS, and neutralize with 1 N sodium hydroxide. Add 2 mL of a solution of 100 mg of 2-naphthol in 5 mL of sodium hydroxide TS: an orange-red precipitate is formed.
Ointments having water-insoluble bases— Transfer an amount of Ointment, equivalent to about 2.5 mg of benzocaine, to a small separator, and dissolve in 20 mL of ether. Extract with 10 mL of 0.5 N hydrochloric acid, and filter the aqueous phase through paper into a small beaker. Add 5 drops of a solution of sodium nitrite (1 in 10) and 2 drops of methyl red TS, and neutralize with 1 N sodium hydroxide. Add 2 mL of a solution of 100 mg of 2-naphthol in 5 mL of 1 N sodium hydroxide: an orange-red precipitate is formed.
Microbial enumeration tests 61 and Tests for specified microorganisms 62 It meets the requirements of the tests for absence of Staphylococcus aureus and Pseudomonas aeruginosa.
Minimum fill 755: meets the requirements.
Assay
Ointments having water-soluble bases— Accurately weigh an amount of Ointment, equivalent to about 200 mg of benzocaine, in a tared 250-mL beaker. Add 50 mL of water and 5 mL of hydrochloric acid, and stir by mechanical means until solution is effected. Cool the solution in an ice bath to about 10, and titrate slowly with 0.1 M sodium nitrite VS, determining the endpoint potentiometrically using a calomel-platinum electrode system. Perform a blank determination, and make any necessary correction. Each mL of 0.1 M sodium nitrite is equivalent to 16.52 mg of C9H11NO2.
Ointments having water-insoluble bases— Accurately weigh an amount of Ointment, equivalent to about 200 mg of benzocaine, and transfer to a 125-mL separator. Suspend the Ointment in 50 mL of ether by shaking, and extract with three successive 25-mL portions of 1 N hydrochloric acid, filtering each portion into a 250-mL beaker, and proceed as directed under Ointments having water-soluble bases, beginning with “Cool the solution.”
Auxiliary Information— Please check for your question in the FAQs before contacting USP.
Topic/Question Contact Expert Committee
Monograph Daniel K. Bempong, Ph.D.
Senior Scientist
1-301-816-8143
(MDPS05) Monograph Development-Pulmonary and Steroids
61 Radhakrishna S Tirumalai, Ph.D.
Senior Scientist
1-301-816-8339
(MSA05) Microbiology and Sterility Assurance
62 Radhakrishna S Tirumalai, Ph.D.
Senior Scientist
1-301-816-8339
(MSA05) Microbiology and Sterility Assurance
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8,037,313,243,778,849,000 | Cleanse Weight Loss
Existing on a menu of water, lemon juice and celery stalks will most definitely cause weight loss but is it real weight loss or just water weight? Will this weight stay off or will it return once you return to your regular diet? These are some of the questions people have when selecting a cleanse for weight loss.
Because the body always retains a certain amount waste and fluids, a cleanse of the digestive tract will result in a weight loss of several pounds. Although this numerical weight loss looks good on the scale, for most people this initial weight loss is not significant enough to make a difference.
Don’t misunderstand, the effects of a temporary cleansing diet are systemic and will improve your overall well-being but using it as a standalone weight loss technique is ineffective and unhealthy. Most cleansing detox diets lack protein and good fats which are necessary for healthy heart and brain function and complex carbs which are important for energy and muscle functions.
Kick Start your weight loss with a cleanse.
Although cleansing solely for weight loss is a not a way to achieve a healthy weight, the process is a great way to kick start your sensible weight loss regimen. First by removing the sugary, fat laden food from your diet for a few days you will allow your palette and your digestive system time to adjust to your new healthier diet.
Second without all the heavy greasy carb loaded foods to digest, your body will burn fat cells for energy. This is because once your liver senses a decrease in levels of insulin your body requires it will start to metabolize fat as energy. This is process is phenomenal motivation for your weight loss goals.
The best part of cleansing your body to kick start your diet is that when your body is free of all of the old waste and the extra fluid you’ll feel better. It takes a great deal of energy for your body to digest and process heavy meals which is part of the reason you feel tired after a heavy meal. By cleansing for weight loss you’re actually helping your body do more than shed pounds. You’re decreasing your chances of illness and disease.
Leave a Reply | {
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6,588,369,580,546,214,000 | Things to Know When You’re Considering Invisalign in Chicago
by | Oct 9, 2023 | Dentist
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If you’re considering Invisalign in Chicago, there are some things to know before making the decision. Invisalign is an innovative and comfortable way to straighten teeth without metal braces, but it does require a certain level of commitment from patients. It’s important to be familiar with the process, understand what results to expect, and take into account the potential side effects of Invisalign in Chicago before beginning treatment.
For starters, Invisalign uses clear plastic trays called aligners to move your teeth slowly into a straighter position. This means that you’ll be wearing the aligners for at least 22 hours a day, and they must be changed out every two weeks or so as your teeth shift and adjust. You will also need to visit your dentist regularly throughout the treatment process in order to monitor progress and ensure that the aligners are fitting correctly.
While some patients may see dramatic improvements in as little as six months, others may need up to 18 months for their treatment to be completed. To get the best possible outcome with Invisalign, you should maintain a consistent schedule of wearing the aligners and following your dentist’s instructions.
The side effects of Invisalign are usually minor, but they can include tooth discoloration, soreness in the gums, and difficulty eating certain foods. Your dentist can help you minimize any potential side effects by providing advice on proper care for your aligners and teeth.
Overall, Invisalign in Chicago is an excellent option for those looking to straighten their teeth without the need for metal braces. With proper care and dedication, you can enjoy a beautiful smile in no time. Contacting Art of Modern Dentistry if you need Invisalign in Chicago. Visit ArtOfModernDentistry.com for more information!
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-1,171,222,157,429,471,500 | CBDA Vs. CBD – What Are the Differences?
CBDA Vs. CBD – What Are the Differences?
There are several differences between CBDA and CBD. This article will examine CBDA’s potential medical benefits and compare it to CBD. CBDA is a form of cannabis extracted through decarboxylation, which removes the carboxyl group from a molecule. This chemical modification is also known as decarbing.
Cannabidiol
Cannabidiol and CBDA are both active ingredients in cannabis. These two substances are highly compatible and have similar health benefits. They can be used separately or in combination. Using both together can provide more significant health benefits because they boost each other’s effects through the entourage effect. But where to buy cbda? CBDA is a form of hemp that contains a small amount of THC, and CBDA is entirely legal in the U.S.
Cannabidiol is the most abundant substance in hemp and other cannabis-like plants. CBDA has a molecular structure similar to that of NSAIDs. It also exhibits similar biological activity to a COX-2 inhibitor, commonly used to treat inflammation. Cannabidiol and CBDA are naturally present in cannabis, but several different forms exist. Using them in combination will benefit both the body and the environment.
The chemical compounds CBDA and CBD show similar pharmacological activity. They both enhance 5-HT1A receptors. While cannabidiol and CBDA have potency, HU-580 shows greater potency and a broader concentration-response curve. CBDA also have significant anxiolytic effects at low concentrations, suggesting it may help treat anxiety. CBD is an antidepressant, while CBDA has a calming effect.
Healer spectrum CBDA
Full-spectrum CBDA products contain a minimum of 0.3% THC and trace amounts of THCA (tetrahydrocannabinol) but retain the full range of beneficial plant compounds. While many products on the market only contain THC, Healer Spectrum CBDA includes all naturally occurring plant compounds, including the original flavonoids and phytonutrients. These compounds have a range of therapeutic properties and are often more effective for specific medical conditions.
All Healer products are third-party tested to ensure they are free of any harmful ingredients. Healer products are also easy to use and contain one milligram of cannabinoids. These products have an innovative nano-filtration extraction process that preserves the entourage components of hemp, delivering maximum relief. In addition, they contain more naturally occurring cannabinoids and substantial quantities of phytonutrients. They are also vegan.
Full spectrum CBDA
Using full-spectrum CBDA tincture is beneficial in many ways. It contains a high concentration of both CBDA and terpenes. This formula is an excellent way to increase CBD in your daily diet while remaining affordable. A single drop of CBD+CBDa soft gel contains five milligrams of CBD.
The anti-inflammatory effects of CBDA are well-known, but more research is needed to explore the compound’s potential in treating various diseases and conditions. It is a selective Cox-2 inhibitor and has anti-inflammatory properties. Cox-1 enzymes are responsible for the lining of the gastrointestinal tract. Nonsteroidal anti-inflammatory drugs (NSAIDs) block Cox-1 enzymes, which can damage the lining of the digestive tract. CBDA, on the other hand, works by inhibiting Cox-2.
Full spectrum CBDA products contain legally permitted amounts of THC and THCA, but only trace amounts. This means you get all the benefits from this plant without the harmful effects of THC. Although many full-spectrum CBDA products only contain THC, Healer Spectrum CBDA products include a range of naturally occurring phytonutrients and flavonoids. However, this type of CBDA oil does have a slightly bitter taste. In addition, it should not be confused with hemp oil.
Read More: Your Guide to Understanding Magnet Fishing | {
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7,406,961,966,216,817,000 | Centrifugal migration of mesenchymal cells in embryonic lung
Authors
• Lin Shan,
1. Department of Pathology, Duke University Medical Center, Durham, North Carolina
2. Departments of Pathology, Children's Hospital and Harvard Medical School, Boston, Massachusetts
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• Drs. Shan, Subramaniam, and Emanuel contributed equally to this paper.
• Meera Subramaniam,
1. Department of Medicine, Division of Respiratory Diseases, Children's Hospital and Harvard Medical School, Boston, Massachusetts
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• Drs. Shan, Subramaniam, and Emanuel contributed equally to this paper.
• Rodica L. Emanuel,
1. Department Medicine, Division of Endocrinology, Children's Hospital and Harvard Medical School, Boston, Massachusetts
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• Drs. Shan, Subramaniam, and Emanuel contributed equally to this paper.
• Simone Degan,
1. Department of Pathology, Duke University Medical Center, Durham, North Carolina
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• Pamela Johnston,
1. Department of Pathology, Duke University Medical Center, Durham, North Carolina
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• Denise Tefft,
1. Developmental Biology Program, Saban Research Institute, Children's Hospital Los Angeles, University of Southern California Keck School of Medicine and School of Dentistry, Los Angeles, California
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• David Warburton,
1. Developmental Biology Program, Saban Research Institute, Children's Hospital Los Angeles, University of Southern California Keck School of Medicine and School of Dentistry, Los Angeles, California
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• Mary E. Sunday
Corresponding author
1. Department of Pathology, Duke University Medical Center, Durham, North Carolina
2. Departments of Pathology, Children's Hospital, Brigham & Women's Hospital, Massachusetts
3. Harvard Medical School, Boston, Massachusetts
• Department of Pathology, Duke University Medical Center, Research Drive, Carl 0043, Durham, NC 27710
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Abstract
Murine lung development begins at embryonic day (E) 9.5. Normal lung structure and function depend on the patterns of localization of differentiated cells. Pulmonary mesenchymal cell lineages have been relatively unexplored. Importantly, there has been no prior evidence of clonality of any lung cells. Herein we use a definitive genetic approach to demonstrate a common origin for proximal and distal pulmonary mesenchymal cells. A retroviral library with 3,400 unique inserts was microinjected into the airway lumen of E11.5 lung buds. After 7–11 days of culture, buds were stained for placental alkaline phosphatase (PLAP). Most PLAP+ cells are peribronchial smooth muscle cells, initially localized laterally near the hilum, then migrating down airways to the subpleural region. Laser-capture microdissection and polymerase chain reaction confirm the clonal identities of PLAP+ cells proximally and distally. Our observation of this fundamental process during lung development opens new avenues for investigation of maladaptive mesenchymal responses in lung diseases. Developmental Dynamics 237:750–757, 2008. © 2008 Wiley-Liss, Inc.
INTRODUCTION
Mammalian epithelial cell differentiation during lung development proceeds in an orderly manner in both mice and humans: first, pulmonary neuroendocrine cells (PNECs) appear, followed by Clara cells, ciliated cells, and type II pneumocytes (Ten Have-Opbroek,1991). Epithelial cell lineages have been investigated primarily through the use of transgenic mouse models using lung epithelial cell-specific promoters (Hackett et al.,1996; Pan et al.,2002; Perl et al.,2002). In comparison, mesenchymal cell differentiation is less understood (Anjos-Afonso et al.,2004), despite the long-recognized importance of lung mesenchyme for branching morphogenesis and epithelial cell differentiation (Spooner and Wessells,1970; Wessells,1970; Shannon and Hyatt,2004). The limited knowledge of mesenchymal cell differentiation is in part due to the lack of mesenchymal cell-specific promoters that are primarily or exclusively expressed in the lung. Using traditional histopathology, it has been learned that myofibroblasts are the proliferative, partially differentiated cell type that precedes terminally differentiated desmin-positive smooth muscle cells (Mitchell et al.,1990; Wright et al.,1999). In addition, capillaries originate by means of angiogenesis from the proximal pulmonary vasculature (Parera et al.,2005).
To investigate clonal lineages of airway-associated cells in developing lung, we chose a definitive genetic retroviral labeling approach. Most methods to study cell lineages are limited by uncertainties about clonal relationships between daughter cells (Le Douarin,1984; Serbedzija et al.,1994). Cepko et al. have developed a new technology for analyzing cell lineages that allows the definitive identification of clonal progeny of a single precursor (Fields-Berry et al.,1992; Cepko et al.,1998; Cai et al.,2000), based on the labeling of dividing progenitor cells with a library of replication incompetent retroviruses, which is passed on only to daughter cells. The progeny are labeled with a histochemical marker such as placental alkaline phosphatase (PLAP) as a genetic tag. The most recent libraries (3.4 × 103 clones) optimize chances of identifying multiple clones in the same tissue preparation, leading to faster and more accurate results (Fields-Berry et al.,1992; Reid et al.,1995; Cepko et al.,1998; Cai et al.,2000). This approach has been instrumental in defining cell fate in the retina, where glial cells and neurons were identified as derived from a common precursor (Cepko et al.,1996), and in mapping widespread dispersion of neuronal clones across functional regions of developing cerebral cortex, diencephalon, and hypothalamus (Walsh and Cepko,1992; Reid et al.,1995; Arnold-Aldea and Cepko,1996; Golden and Cepko,1996). We now apply this well-characterized genetic technology to the first clonal analysis of cell lineages and cell fates during embryonic lung development.
RESULTS
Whole-Mount PLAP Staining
In a few lung buds harvested after 1–5 days, no PLAP+ staining was visible (data not shown). After 7 days of culture, PLAP+ cells are visible along either lateral side of the trachea, spatially restricted to the trachea, mainstem bronchi, and first one to two airway generations of all eight lung buds examined at this time point (arrow in Fig. 1a indicates the distal-most PLAP+ cells), apparently tracking along the airways below the epithelium, suggesting localization to the peribronchial mesenchyme. After 7 days, in eight lung buds examined, PLAP+ cells rarely cross the midline (Fig. 1b, arrows), and the distal-most PLAP+ cells extend to 41 ± 4% of the distance from the carina to the pleural surface (Fig. 2). After 9 days (Fig. 2c,d), PLAP+ cells cross the midline in all nine lung buds examined at this time point (indicated by arrowhead in Fig. 1c), and the distal-most PLAP+ cells extend to 58 ± 6% of the distance from the carina to the pleural surface (Figs. 1d, 2). After 11 days in culture (Fig. 1e,f), the PLAP+ cells extend outward to the pleural surface in all nine lung buds examined (indicated by white arrows in Fig. 1e), with PLAP+ cells at 97 ± 1% of the distance from the carina to the pleural surface (Fig. 2). By day 11, the PLAP+ cells are visible as dark linear markings throughout the interstitium (white arrows in Fig. 1f) in the subpleural region (edge of pleura indicated by asterisk in Fig. 1f). In a few cultures maintained for 13 days, the lung buds were smaller and had evidence of apoptosis on hematoxylin and eosin staining, consistent with involution. The highest lactate dehydrogenase levels, measured daily in the media, occurred during the first 1–2 days of culture; then these levels dropped and did not rise again through day 11 (data not shown).
Figure 1.
Whole-mount alkaline phosphatase staining of cultured lung buds. Microinjected buds were cultured on Transwell filters overlying BGJb medium with ascorbic acid, 2.5% bovine fetal calf serum, HITES, 2% L-glutamine, and 10 ml of penicillin–streptomycin at 37°C in a humidified incubator in 5% CO2, as described (Golden and Cepko,1996). Buds were harvested 7 to 11 days later by fixation followed by whole-mount placental alkaline phosphatase (PLAP) staining as described (Arnold-Aldea and Cepko,1996). a,b: Embryonic day (E) 11.5 lung bud cultured for 7 days before whole-mount PLAP staining. a: Arrow indicates the distal-most detectable PLAP+ cells. b: Arrows indicate location of PLAP+ cells along either side of trachea, but not crossing the midline. c,d: E11.5 lung bud cultured for 9 days. Long black arrows indicate distal-most extension of PLAP+ cells. Arrowhead in c indicates PLAP+ cells crossing the midline. e,f: E11.5 lung bud cultured for 11 days. e: White arrows indicate site of PLAP+ cells in the subpleural region. f: White arrows indicate linear arrays of PLAP+ cells on the pleural surface, tracking along the interstitium.
Figure 2.
Quantitative analysis of proximal-to-distal extension of placental alkaline phosphatase–positive (PLAP+) cells in whole-mount-stained lung buds. Embryonic day (E) 11.5 lung buds were microinjected with the BOLAP library and cultured as described in the legend to Figure 1. The numbers of lung buds examined were as follows: n = 8 at 7 days, n = 9 at 9 days, and n = 9 at 11 days. The distal-most extension of PLAP+ cells was determined as the greatest distance traveled by PLAP+ cells relative to the carina as a percentage of the total distance from the carina to the pleural surface in the same trajectory. *P < 0.0001 compared with day 7 or day 9; **P < 0.01 compared with day 7.
Histochemistry on Lung Sections
After whole-mount PLAP staining, lung buds were embedded in paraffin and sections were counterstained with eosin. Representative photomicrographs showing PLAP staining retained in the sections are given in Figure 3. After 7 days in culture (Fig. 3a,b), PLAP staining is visible only in mesenchymal cells immediately adjacent to the airway epithelium with the distal-most PLAP+ cells present in the first- or second-generation bronchi (Fig. 3a, arrow). At day 7, the PLAP+ cells are present only on either side of the midline, consistent with developing airway smooth muscle (Fig. 3a,b), and are consistently absent inferior to the tracheal bifurcation (asterisks in Fig. 3a,b). At day 9, PLAP+ cells extend approximately halfway to the pleura (Fig. 3c,d, arrows indicating distal-most PLAP+ cells). PLAP+ cells remain consistently absent inferior to the tracheal bifurcation (asterisks in Fig. 3c,d) but do cross the midline (arrowhead on left in Fig. 3d), with the trachea pointing to the left. At day 11, PLAP+ cells are distributed throughout the bronchial tree (some indicated by arrows in Fig. 3e,f). In the same lung bud, there are subpleural foci of PLAP+ cells (arrowheads on right of Fig. 3f).
Figure 3.
Histopathological analyses of placental alkaline phosphatase–positive (PLAP+) cells. Five-micron paraffin sections of PLAP-stained lung buds were counterstained with eosin. Asterisks are at the carina. a,b: Sections of embryonic day (E) 11.5 lung bud cultured for 7-days. a: The arrow indicates the distal-most extension of PLAP+ cells immediately adjacent to a second-generation cartilaginous airway. b: Arrows indicate a few PLAP+ cells scattered along the subepithelial region of a first-generation cartilaginous airway. c,d: Sections of E11.5 lung bud cultured for 9 days. c: Arrow indicates the distal-most extension of PLAP+ cells along a third-generation noncartilaginous airway. The asterisk indicates the pleural surface. d: The arrowhead indicates PLAP+ cells in the mesenchyme crossing the midline of the distal-most trachea. Arrow indicates the distal-most extension of PLAP+ cells along a second-generation noncartilaginous airway up to the junction with a third-generation airway. e,f: Sections of E11.5 lung bud cultured for 11 days. e: Arrows indicate PLAP+ foci scattered along the bronchial tree. f: Arrowheads indicate PLAP+ cells tracking along subpleural region between arrows (the asterisk indicates the pleural surface) of same lung bud as shown in e (same arrow indicated by #1, same arrowheads indicated by #2 and #3). Scale bar = 50 μm in a,d,f, 25 μm in b, 100 μm in c,e.
Cytokeratin immunostaining is continuous, consistent with PLAP+ cells being nonepithelial (Fig. 4a). The dark PLAP staining quenches fluorescence and immunohistochemical chromogens. From Figure 4b, it is clear that the PLAP+ cell distribution is essentially identical to that of airway smooth muscle: α-smooth muscle actin–positive (SMA+; red arrows on left in Fig. 4b), and desmin-positive (Fig. 4c,e). A few cells are double-positive for SMA and PLAP (Fig. 4b, arrows on right and inset panel). The PLAP+ signal is typically so intense that colocalization with any other cellular marker is usually impossible (Cepko et al.,1998). We were fortunate to identify regions where the PLAP+ staining was less intense so that we could demonstrate some cells with colocalization for SMA and PLAP (Fig. 4b). Subsequently, at day 11 many of the subpleural PLAP+ cells stained for SMA, but not desmin (Fig. 4f, long arrows) and/or were closely adjacent to SMA+ cells (Fig. 4f, arrowheads). It should be noted that only a small number of PLAP+ cells occur near the pleura on day 11 of culture. Similarly, very few SMA+ cells occur in this location (Fig. 4f), and these are all desmin-negative.
Figure 4.
Immunohistochemical characterization of placental alkaline phosphatase–positive (PLAP+) cells. Immunohistochemical staining was carried out as detailed in the Experimental Procedures section. L, airway lumen. a: Cytokeratin immunostaining of embryonic day (E) 11.5 lung bud cultured for 9 days, with diaminobenzidine as substrate. Large cleft arrowheads demarcate PLAP+ cells extending along one stretch of cytokeratin-positive epithelium. The small triangular arrowhead in the left lower corner indicates a fold in the tissue section. b: Smooth muscle actin (SMA) immunostaining of E11.5 lung bud cultured for 9 days, with NovoRed as substrate. Representative SMA+ cells are indicated by short red arrows; several PLAP+ cells are indicated by black arrowheads. Long black arrows indicate a few cells with visible colocalization of both red SMA immunostaining and purple PLAP staining. One cluster, indicated by dotted lines, is shown at higher power in the inset in the lower right hand corner. c: Desmin immunostaining of E11.5 lung bud cultured for 9 days, with NovoRed as substrate. Representative desmin+ cells are indicated by short red arrows, and several PLAP+ cells are indicated by black arrowheads. d: Another desmin-immunostained E11.5 lung bud cultured for 9 days is shown at lower power, with developing smooth muscle visible below the carina (*) and with PLAP+ staining laterally, between the epithelium and the cartilage. e: A representative negative control section adjacent to d was stained in parallel with d using normal rabbit IgG instead of rabbit antidesmin IgG. Note the absence of red immunostaining. f: A section of an E11.5 lung bud cultured for 11 days is shown, with the pleural surface at the top (indicated by three asterisks). Long arrows indicate PLAP+ cells and arrowheads indicate SMA+ immunostaining. Note the partial overlap of SMA and PLAP staining in some cells and the close association between SMA+ and PLAP+ cells. Less than half of the subpleural PLAP+ cells were SMA+ (data not shown). Scale bars = 25 μm.
We also observe abundant subpleural SMA-positive/desmin-negative cells in developing murine lungs in vivo at embryonic day (E) 12.5. However, the frequency of these cells declines markedly by E14.5 and there are only rare subpleural SMA+ cells present at E18.5. SMA+ subpleural cells are not detected in lung after birth. In culture, the E11.5 lung bud explants are maintained with high structural integrity and no LDH release into the supernatant between 3 and 11 days of culture (data not shown). The distal-most end of the airways is separated from the pleural surface by primitive alveoli lined by SPC-immunopositive cells. It is not until day 13 of culture that there is some histological evidence of involution of the lung buds, with mesenchymal cell death and shrinkage of the lung buds (data not shown).
Laser-Capture Microdissection and Clonal Analysis
To assess the clonality of different PLAP+ cells, we used laser capture microdissection to remove small clusters of prominent PLAP+ cells, followed by two rounds of polymerase chain reaction (PCR) amplification (40 cycles each) (Signoretti et al.,1999). PCR products were subcloned into the TA plasmid (Zhou and Gomez-Sanchez,2000). Four colonies were sequenced for each microdissected focus, with eight or nine foci captured per lung bud. In all three lung buds, identical sequences were obtained for multiple cells located both proximally and distally, as shown in Figure 5 and Table 1. A representative lung bud is shown in Figure 5a, with three distinct proximal foci (#19, 20, and 21), and three separate subpleural foci (#22, 23, and 26). In Figure 5a, identical sequences are shown in the same color. Thus, focus #20 contains one clone (blue) identical to a clone in focus #21 (blue center), indicating that the same cell did in fact cross the midline. A different clone in focus #21 (red rim) is identical to a clone (red) at focus #22 (subpleural). Similarly, a clone at proximal focus #19 is identical to a distal clone at focus #26. These two matches (#19 and 26, and #21 and 22) indicate sequence identity between subpleural clones and proximal clones. There were, in addition, 37 unique sequences such as at focus #23 that were distributed randomly and evenly throughout the bronchial tree (Fig. 5a). All together, subclones of 27 laser capture samples from three lung buds yielded 47 sequences, of which 10 matched a sequence in one or more other distinct foci (Table 1). In two lung buds, multiple very proximal foci had sequences that matched multiple subpleural foci. These sequence identities indicate that proximal and distal mesenchymal cells can be derived from the same precursor, providing definitive evidence for both clonality and centrifugal cell migration during lung development.
Table 1. Clonal Identities in E11.5 Lung Buds Cultured for 11 Days
1. E11.5 lung buds were injected intraluminally with a DAP retroviral library containing 3,400 unique inserts. After 11 days of culture, buds were fixed and stained for PLAP. Buds# 1, 3, and 9 are shown here. The focus number represents the fragment of tissue that was laser-captured. After subcloning, four clones from each focus were sequenced. The horizontal bars (in different colours) indicate foci containing identical sequences. The locations of the foci are divided into: Proximal (trachea, mainstem bronchi, and cartilaginous airways); Midway (all noncartilaginous airways and primitive airspaces, excluding those within 50 μ of the pleural surface; and Distal, which includes cells within 50 μ of the plueral surface (see Fig. 5a). E, embryonic day; PLAP, placental alkaline phosphatase.
inline image
Figure 5.
Laser-capture microdissection of placental alkaline phosphatase–positive (PLAP+) cells. a: A representative 5-μm section of a PLAP-stained lung bud on an uncoated glass slide was used for laser-capture microdissection as previously described (Walsh and Cepko,1992). The asterisk indicate the pleural surface. b,c: A pair of proximal images representing the same field containing focus #19 before and after microdissection. d,e: The same field with focus #23 before and after microdissection. Foci #19 and #26 contain identical clone, which differs from the identical sequence present in cells from foci #21 and #22. P, proximal; D, distal.
DISCUSSION
The present study demonstrates that daughter cells from a single pulmonary mesenchymal clone can be distributed both paratracheally and distally, migrating centrifugally along developing airways, establishing a direct link between subepithelial smooth muscle and subpleural mesenchymal cell lineages. At least some of the subpleural mesenchymal cells are SMA+ but desmin-negative, consistent with myofibroblasts. In most lineage investigations in other laboratories using the same library, the identity of PLAP+ cells was determined exclusively by cell morphology and by the localization of cells within a given tissue (Cepko et al.,1996). We initially carried out the experiments in the hopes of analyzing lineages of the airway epithelial cells. We have no obvious explanation for the localization of the retroviral library in the subepithelial mesenchyme. Nonetheless, this was the site of PLAP+ staining, and the precise localization of PLAP+ cells was highly reproducible, despite the filling of the entire tracheobronchial tree with the retroviral library. It is possible that the intraluminal DAP retroviral stock might be extruded along either side of the trachea, which could in part explain the proximal localization of the earliest PLAP staining on day 7. Despite this being a loosely consolidated tissue, we carried out clonal analyses using fine tools: laser-capture microdissection followed by PCR amplification of DNA inserts and subcloning to distinguish individual cells. There is only one retroviral integration event per cell 99% of the time (Price et al.,1987). The mesenchymal localization of the integrated retroviral library could reflect a higher rate of proliferation of mesenchymal cells in embryonic lung buds (as measured by bromodeoxyuridine incorporation). Retroviral integration requires ongoing cell division. Preliminary observations indicate that some of the dye injected into the tracheal lumen of E12.5 lung buds is detected in the surrounding mesenchyme, suggesting that the embryonic epithelium is leaky to small particles (Warburton and Tefft, data not shown). Furthermore, uptake of retrovirus by epithelial cells in the lung is orders of magnitude less efficient than epithelial uptake of adenovirus under the same conditions, either in vivo or in vitro, whereas uptake of retrovirus into fibroblasts in culture is relatively efficient, possibly because the fibroblasts proliferate much faster than epithelial cells in culture (Warburton and Tefft, data not shown). In embryonic lung in vivo, cell proliferation is higher in the mesenchyme than in the epithelium (Haley et al.,1997). Differential expression of retroviral receptors is unlikely, because these receptors are ubiquitous (Rapp and Marshall,1980). We cannot rule out the possibility that epithelial-to-mesenchymal transformation might contribute to the mesenchymal localization of integrated retrovirus in lung bud cultures (Kim et al.,2006). Finally, we cannot exclude the possibility that progenitor cells might occur in other regions of the developing lung buds. We can only conclude that progenitor cells are present on either side of the trachea under the given experimental conditions and that some of these cells migrate into the subpleural region by day 11 of culture.
Our observations are novel and distinct from results from other laboratories studying genetically altered mice. Mailleux et al. showed that a pool of Fgf10+ cells in the subpleural mesenchyme of the lung contains progenitor cells which contribute to peribronchial smooth muscle in the bronchioles by moving proximally relative to the epithelium as the epithelium extends peripherally during branching morphogenesis (Mailleux et al.,2005). Our observations are not in conflict with the findings of Mailleux et al. (2005) because we are analyzing a distinct subset of mesenchymal cells initially located in the perihilar region and migrating distally along the developing airways. Thus, our findings do not exclude a role for derivatives of the splanchnic mesoderm in formation of intrapulmonary mesenchymal lineages. In the present study, the airway-associated mesenchymal cells are concentrated in the first few generations of the tracheobronchial tree, with relatively small numbers of PLAP+ cells migrating outward. Furthermore, del Moral et al. demonstrated that Fgf9, expressed in the pleural mesothelium, in turn regulates Fgf10 expression within the pool of subpleural smooth muscle progenitors, most likely through Tbx4 and 5 (del Moral et al.,2006). Fgf9 also controls the expression of Hedgehog targets Ptc and Gli in a hedgehog-independent manner and suppresses smooth muscle differentiation in the subepithelial as opposed to the subpleural domains of the peripheral lung mesenchyme (del Moral et al.,2006; White et al.,2006). It remains to be seen whether the novel pool of mesenchymal progenitors reported herein that migrate from proximal to distal locations along the airways are also controlled by these or other developmental positional and differentiation signals (Mailleux et al.,2005).
Our unprecedented observations could have implications for lung pathobiology as well as lung development. Mesenchymal stem cells are present in airways of adults as well as developing lung (Sabatini et al.,2005). Mesenchymal cell migration could contribute to the progression of a variety of lung diseases, such as chronic lung disease in newborns (Jobe,2003; Chess et al.,2006), remodeling in asthmatics (Holgate et al.,2004), and progression of idiopathic pulmonary fibrosis (White et al.,2003). Future investigations will be required to test these hypotheses in animal models.
EXPERIMENTAL PROCEDURES
Library
The DAP library we used was obtained directly from the laboratories of Dr. Christopher Walsh and Dr. Connie Cepko. The complexity of this library is 3,400 (Reid et al.,1995,1997). There appears to be even representation of tags within this library, with <0.5% of the clones being duplicated (Fields-Berry et al.,1992; Cepko et al.,1998). Only one retroviral vector integrates in a given cell; thus, the unique insert becomes a specific cell marker. Using competent Escherichia coli DH5α and kanamycin, a large pool of colonies was selected to ensure that all vectors were expressed. The CR7 amphotropic packaging line was used to obtain ∼60,000 transient viral particles. This supernatant was then used to make stable retroviral producer cell lines in the ecotropic packaging cell line ψ2 as described (Fields-Berry, et al.,1992; Reid et al.,1995). We carried out rigorous analyses for helper virus. No helper virus was present in the library that we used for microinjection in the current study (data not shown), following a published protocol (Cepko et al.,1998).
Microinjection
E11.5 lung buds from timed-pregnant Swiss-Webster mice (Charles River Laboratories) were immobilized in wells on agarose plates, with the trachea pointing upward at ∼45 degrees. The DAP retroviral stock was prepared at ∼105 pfu/ml with polybrene 80 μg/ml and 1% trypan blue dye. A micropipette was positioned just inside the trachea and ∼1-μl of the retroviral stock was infused into the lumen over ∼15 min using a peristaltic pump (Fig. 6). Lung buds were then transferred and cultured on 0.3-μm pore-size Transwell filters in six-well plates as described, overlying BGJb medium containing ascorbic acid, 2.5% bovine fetal calf serum, HITES, 2% L-glutamine, and 10 ml of penicillin–streptomycin at 37°C in a humidified incubator in 5% CO2, as described (20). The virus is known to have a half-life of 4 hr at 37°C (Walsh and Cepko,1992), and a high concentration of polybrene is necessary for viral adhesion to cells, so the treatment is essentially a single pulse with no significant carryover of virus into later stages (>24 hr) of the 7–11 day culture. Buds were harvested 7 to 11 days later by fixation followed by whole-mount PLAP staining (Arnold-Aldea and Cepko,1996).
Figure 6.
Embryonic day (E) 11.5 lung bud after retroviral microinjection. Photograph of a representative whole-mount E11.5 lung bud immediately after microinjection of the retrovirus-dye mixture into the embryonic tracheal lumen. Note the dye is filling the future airway lumen throughout most of the bronchial tree.
Immunoperoxidase
After whole-mount PLAP staining, lung buds were processed manually into paraffin blocks as described (Kong et al.,2004). Each lung bud was sectioned through completely in 5-μm slices and every fourth slide was counterstained with eosin. Immunoperoxidase staining for cytokeratin and desmin was carried out with the ABC method (Vector Laboratories, Burlingame, CA), as previously described (Kong et al.,2004) using: 1:100 dilution of rabbit anti-bovine cytokeratin (broad-spectrum; Dako Laboratories, Inc., Carpinteria, CA); or 1:100 rabbit antidesmin (Sigma Laboratories, St. Louis, MO). Immunoperoxidase staining for α-smooth muscle actin (SMA) was carried out using 1:60 dilution of alkaline-phosphatase–conjugated mouse monoclonal anti-SMA purified IgG (clone 1A4, Sigma Laboratories). In brief, slides were pretreated with 0.3% Triton X-100 in phosphate buffered saline for 10 min followed by 20 min with 1:200 normal serum (goat for rabbit IgG, horse for mouse IgG) before the primary antibody, which is incubated at 4°C overnight. After washing, the biotinylated anti-IgG is incubated at 4°C for 2 hr, then endogenous peroxidase is blocked with 0.3% H2O2 in methanol for 30 min. The ABC reagent is applied for 45 min, then developed using diaminobenzidine (Sigma Laboratories, St. Louis, MO) or NovaRed (Vector Laboratories, Burlingame, CA). NovaRed provides better contrast against the dark PLAP staining. For SMA immunostaining, the secondary antibody and blocking steps (normal horse serum and methanol-peroxide) were omitted and the alkaline phosphatase Vector-Red substrate was applied for 5 min at room temperature according to the manufacturer's instructions (Vector Laboratories, Burlingame, CA).
Laser-Capture Microdissection and PCR
Five-micrometer sections of lung buds were placed on uncoated glass slides for laser-capture microdissection as previously described (Signoretti et al.,1999). To assess the clonality of different PLAP+ cells, we used laser capture microdissection to remove small clusters of cells (foci ∼10 μm in diameter) from these lung bud sections. DNA was prepared from microdissected cells, followed by 2 × 40 cycles of PCR amplification (Signoretti et al.,1999) using nested primers for the DAP library (Walsh and Cepko,1992): First round, PBR4 (5′-GCGGAGCCTATGGAAAAACGCCAGC-3′) and BND3 (5′-TGAGTGGCCATTAGAGC- AGTAGTCCCTGTTC-3′); Second round, PBR5 (5′-CGGGTTTCGCCACCTCTGACTTGAGCGTCG-3′) and BND4 (5′-TCTACTGCGGCTTGGAGCTGCTGGAATTGC-3′). PCR products were subcloned into the Promega TA plasmid as described (Zhou and Gomez-Sanchez,2000). DNA from isolated white colonies was sequenced at the Duke University DNA Analysis Facility using the Applied Biosystems Dye Terminator Cycle Sequencing system with Big Dye terminator v1.1 sequencing chemistry combined with ABI 3730 PRISM DNA Sequencing instruments. Sequence comparisons were carried out using MacVector 7.0 software.
Acknowledgements
We thank Drs. Connie Cepko and Christopher Walsh for providing the higher complexity DAP library and for helpful discussions. We also thank Dr. Max Loda at Brigham & Women's Hospital and Dr. Margaret Kirby and her laboratory at Duke University Medical Center for facilitating our laser-capture microdissection studies. M.E.S. was funded by the NIH (grant 2RO1-HL44984).
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To print: Use your web browser's print feature. Close this window after printing.
Grief: Helping Older Adults With Grief
Table of Contents
Actionsets help people take an active role in managing a health condition. Grief: Helping Older Adults With Grief
Actionsets help people take an active role in managing a health condition. What is different about older adults who are grieving?
Actionsets help people take an active role in managing a health condition. Why does an older adult who is grieving need help?
Actionsets help people take an active role in managing a health condition. How can you help an older adult who is grieving?
Actionsets help people take an active role in managing a health condition. Where to go from here
What? - What is the medical information or key concepts related to the action? What is different about older adults who are grieving?
Older adults express their grief in the same ways as younger and middle-aged adults. But because of their age and other life circumstances, older adults may:
Test Your Knowledge
1. Older adults express their grief in the same ways as other adults.
1. True
This answer is correct.
Older adults express their grief in the same ways as other adults. But they may experience several losses at the same time.
2. False
This answer is incorrect.
Older adults express their grief in the same ways as other adults. But they may experience several losses at the same time.
2. Older adults are very willing to tell other people that they are grieving.
1. True
This answer is incorrect.
Older adults may not be very willing to tell other people that they are grieving. They may not tell others that they are grieving losses related to aging. And they may be unwilling to tell other people how sad they feel when they see or care for older loved ones who are ill or aging.
2. False
This answer is correct.
Older adults may not be very willing to tell other people that they are grieving. They may not tell others that they are grieving losses related to aging. And they may be unwilling to tell other people how sad they feel when they see or care for older loved ones who are ill or aging.
Why? - Why the action is important? Why does an older adult who is grieving need help?
Older adults are more likely to become physically ill after experiencing a major loss. They may already have long-term physical illnesses or other conditions that interfere with their ability to grieve. The symptoms of these illnesses may become worse when they are grieving.
Some older adults may develop unresolved grief or complications associated with grieving. This may occur more often in older adults because they are more likely to experience:
In addition, some older adults need more time than other people to adjust to change. Adjusting to change may be hard for them and cause them added emotional stress.
Test Your Knowledge
1. Older adults have a lot of experience with loss, so they grieve less than other adults.
1. True
This answer is incorrect.
Older adults have a lot of experience with loss, but they do not grieve less than other adults. Older adults are more likely to develop unresolved grief or other conditions associated with grieving than other adults.
2. False
This answer is correct.
Older adults have a lot of experience with loss, but they do not grieve less than other adults. Older adults are more likely to develop unresolved grief or other conditions associated with grieving than other adults.
2. Older adults often become physically ill after a major loss.
1. True
This answer is correct.
Older adults are more likely to become physically ill after a major loss.
2. False
This answer is incorrect.
Older adults are more likely to become physically ill after a major loss.
How? - Learn the steps involved in taking action. How can you help an older adult who is grieving?
Ways you can help an older adult who is grieving include:
Older adults often have more than one loss to deal with at a time. Talking about each separate loss may help identify the person's feelings. Separating losses from one another may also help the person feel less overwhelmed and more able to cope with emotional distress.
Test Your Knowledge
1. I can help an older adult who is grieving by:
1. Telling the person that feelings are not important and that he or she should just think about something else.
This answer is incorrect.
You cannot help an older adult who is grieving by telling the person that feelings are not important and that he or she should just think about something else. Asking the person to talk about his or her loss often helps the person who is grieving. Older people, especially those who have experienced several losses over a short period of time, are often helped when they share memories of the lost person.
2. Asking the person to tell me about the loss (person, object, or situation).
This answer is correct.
You can help an older adult who is grieving by asking the person to tell you about the loss (person, object, or situation). Older people, especially those who have experienced several losses over a short period of time, are often helped when they share memories of the lost person.
3. Reminding the person that we all get old.
This answer is incorrect.
You cannot help an older adult who is grieving by reminding the person that we all get old. Asking the person to talk about his or her loss often helps the person who is grieving. Older people, especially those who have experienced several losses over a short period of time, are often helped when they share memories of the lost person.
4. Making the person stay very busy.
This answer is incorrect.
You cannot help an older adult who is grieving by making the person stay very busy. Asking the person to talk about his or her loss often helps the person who is grieving. Older people, especially those who have experienced several losses over a short period of time, are often helped when they share memories of the lost person.
Where? - Other resources and organizations that can help you take action. Where to go from here
Now that you have read this information, you are ready to help an older adult who is grieving.
Talk with a health professional
If you have questions about this information, take it with you when you visit your health professional. You may want to use a highlighter to mark areas or make notes in the margins of the pages where you have questions.
If you would like more information on helping an older adult who is grieving, the following resources are available:
Organizations
Caring Connections
Phone: 1-800-658-8898 help line
Phone: 1-877-658-8896 multilingual line (toll-free)
Phone: (703) 837-1500
Email: caringinfo@nhpco.org
Web Address: www.caringinfo.org
Caring Connections, a program of the U.S. National Hospice and Palliative Care Organization (NHPCO), seeks to improve care at the end of life. Caring Connections provides free resources, including educational brochures, advance directives and hospice information, and a toll-free help line for people looking for quality end-of-life information.
Mental Health America
2000 North Beauregard Street, 6th Floor
Alexandria, VA 22311
Phone: 1-800-969-NMHA (1-800-969-6642) referral service for help with depression
(703) 684-7722
Fax: (703) 684-5968
Web Address: www.mentalhealthamerica.net
Mental Health America (formerly known as the National Mental Health Association) is a nonprofit agency devoted to helping people of all ages live mentally healthier lives. Its website has information about mental health conditions. It also addresses issues such as grief, stress, bullying, and more. It includes a confidential depression screening test for anyone who would like to take it. The short test may help you decide whether your symptoms are related to depression.
Credits for Grief: Helping Older Adults With Grief
By Healthwise Staff
Primary Medical Reviewer Anne C. Poinier, MD - Internal Medicine
Specialist Medical Reviewer Sidney Zisook, MD - Psychiatry
Last Revised October 17, 2011
Note: The "printer friendly" document will not contain all the information available in the online document. Some information (e.g. cross-references to other topics, definitions or medical illustrations) is only available in the online version.
© 1995-2014 Healthwise, Incorporated. Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated.This information does not replace the advice of a doctor. Healthwise, Incorporated disclaims any warranty or liability for your use of this information. | {
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-488,083,229,972,652,350 | Maximise Botox Benefits for Long-Lasting Beauty
Maximise Botox Benefits where people are showing thumbs up to show maximum
Discovering how to maximise Botox benefits is crucial for anyone looking to maintain a youthful glow. Our expert guide delves into the best practices and insider tips to extend the duration of your Botox results, ensuring that your investment in beauty endures.
To further enrich the guide on maximising Botox benefits, let's delve into the significance of adopting a holistic approach towards skincare and wellness. Incorporating products that complement Botox's effects, such as those containing hyaluronic acid or peptides, can significantly amplify the results. Moreover, embracing a lifestyle that supports skin health from the inside out, including adequate sleep and stress management techniques, plays a pivotal role in enhancing the longevity of Botox benefits.
Understanding Botox and Its Benefits
Botox helps smooth out wrinkles by calming facial muscles. Understanding how Botox works allows you to make smart choices to get the most out of its effects and maintain them longer. Also, learning about Botox's action helps in planning treatments for sustained beauty.
Best Practices to Maximise Botox Benefits
Preparing Your Skin
Before your Botox treatment, it's essential to get your skin ready. Start by gently cleansing and caring for your skin. Then, avoid any actions that might weaken the effect of the Botox to ensure you see the best results. This preparation is key to maximizing the treatment's benefits.
Consistent Treatment Scheduling
Setting up a regular schedule for Botox sessions is crucial for enhancing its benefits. Consistency is key here; it maintains the smoothness of your skin and extends the time needed between each treatment. Additionally, this routine ensures your skin's appearance remains youthful and radiant for longer periods, effectively maximizing the return on your Botox investment.
Lifestyle Tips to Support Botox Longevity and Maximise Botox Benefits
Embrace Sun Protection
Shielding your skin from the sun plays a pivotal role in extending the effects of Botox, safeguarding both your skin's health and the procedure's impact. Moreover, this protective measure ensures that the benefits of Botox are maximised, and enhancing the treatment's overall success.
Nutrition and Hydration
Maintaining a balanced diet and ensuring adequate hydration are crucial steps in supporting skin health, which, in turn, amplifies the benefits of Botox. Furthermore, this approach nourishes the skin from within and contributes to the longevity of Botox treatments.
Balancing Exercise with Relaxation
Engaging in regular exercise and managing stress effectively are key components of influencing the longevity of Botox outcomes. Additionally, these practices improve well-being increase the effects of Botox treatments are sustained for longer durations.
Choosing the Right Practitioner
Choosing a skilled practitioner is crucial for ensuring precise application, specifically tailored to meet your skin's requirements. Moreover, selecting a professional with a deep understanding of facial anatomy and Botox dynamics can dramatically enhance the effectiveness and longevity of your results. Additionally, engaging with a practitioner who offers personalised consultations will further refine your treatment plan, ensuring that each session contributes optimally to achieving and maintaining a youthful and radiant appearance.
Elevating Your Botox Experience
Adding these methods to your daily routine will notably enhance the advantages, ensuring your skin stays youthful and glowing for an extended period. Furthermore, by persistently applying these techniques, you'll witness a transformative effect on your skin's health and appearance. Additionally, this proactive approach not only prolongs the aesthetic benefits but also reinforces your skin's natural resilience against aging signs, promoting an enduringly radiant complexion.
FAQ
Q1: How can I maximise Botox benefits between treatments?
Tailor regular sessions to your needs and adopt a healthy lifestyle to enhance Botox's longevity.
Q2: Do supplements help gain more benefits?
Balanced nutrition supports skin health, but the impact of specific supplements on Botox is less certain.
Q3: When can I resume exercise post-Botox to maximise benefits?
Wait 24 hours to allow Botox to settle properly, maximising its benefits.
Q4: How does reducing stress increase benefits of botox?
Minimising stress levels prolongs Botox's youthful effects, boosting its benefits.
Q5: Can my skincare routine increase benefits of botox?
Yes, a suitable skincare routine can support and extend Botox's efficacy. | {
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641,721,445,340,941,000 | top of page
Search
So you have had your Sports Massage
What should or shouldn't you do now (after care advice)
1. Drink plenty of water over the next 48 hours to help the body flush out toxins and waste products after the massage. Try and aim for at least 2 litres of water.
2. Water also helps keep the muscles hydrated and supple, going forwards, ensure you are regularly drinking at least 2 litres of water a day. (Gradually increase your water intake so as not to overload your bladder and need to urinate so often).
3. Avoid heat treatments for 24 hours - no hot bath or sauna's. If you want to wash then have a luke warm shower.
4. Avoid strenuous activity or exercise for the rest of the day. Best avoided for 24 hours.
5. Avoid alcohol, caffeine, and spicy foods for at least 12 hours, as your body is working hard to repair your muscles, so the digestive system may be affected.
6. Try to avoid eating a big meal for 2 hours after the massage, as the increased blood supply has been directed to the injured/affected muscles areas and the digestive process will re-direct the blood to the digestive system.
7. If you feel tired, rest as much as possible.
8. If you experience discomfort or muscle soreness, then use ice packs on any inflamed areas. If the discomfort warrants it and you need pain killers, then over the counter ibuprofen is preferable to paracetamol as ibuprofen is an anti-inflammatory drug. However, if you are allergic or cannot take to ibuprofen then please speak to your local pharmacist or doctor. When taking any medication please be sure to read the instructions and follow the dosage on the packet.
9. Please remember that as advised at the start of treatment that there may be other side effects and that symptoms may get worse before getting better.
10. Always carry out your advised rehabilitation
11. If you expereince any other side effects or feel very unwell, please seek professional medical advice.
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5,730,365,340,666,855,000 | Gym Workouts - What You Must Know About Bodybuilding To Remain In Shape 1
Gym Workouts – What You Must Know About Bodybuilding To Remain In Shape
Bodybuilding is essentially the use of considerably growing strength during weight training to color and condition one’s entire body by muscle hypertrophy. It is different from other similar undertakings including potential raising as it centers exclusively on visual appearance instead of durability. The intention of muscle mass building will be to maximize the actual size of skeletal muscle tissues, notably those that are specific by strength training. When adequately completed, muscle building may lead to a rise in lean muscle measurement and power even though as well improving entire body make up. Thus, it can be figured that body building is a great way to obtain the human body of the goals.
Bodybuilding, even so, is not really only about visual appeal additionally, it is about health insurance and vitamins and minerals. To maintain your system solid and nutritious, proper vitamins and minerals is important to help maintain good health and a general in shape physique. Those of you that need to grow to be interested in muscle mass building, it is advisable to receive an education on suitable nutrition and exercise. A person that is serious about his overall health ought to thus master the significance of a good mind plus a healthy and balanced body system through consistent health club routines along with an energetic chosen lifestyle that market health and well being.
For anyone who is nevertheless a newcomer in body building, bear in mind you don’t demand expensive supplements to acquire muscle tissue and also a fit body system. The products that you simply will make use of must be efficient enough to assist you to achieve lean volume and build many muscular tissues in the beginning. Make sure to only choose muscle development dietary supplements which may have 100 % natural ingredients for instance proteins, carbohydrates and fatty acids.
The first thing to achieving a greater body system will be to educate. For body builders, this implies strength training and reps at the least. So as to trigger muscle mass expansion and boost the bodybuilder’s physique, Muscle mass building experts really should accentuate hefty repetitions and coaching. After having a muscle building fitness instructor starts to cooperate with a customer, he or she will supply reviews on what kind of exercise routines are perfect for them.
As well as a balanced diet plan, a muscle building fitness instructor can also suggest unique weight training systems to increase the bodybuilder’s body. It is a great idea for anyone who would like to go after bodybuilding as being a hobby to engage in aerobic exercise routinely. There are lots of benefits to carrying out cardio exercise. Training is shown to be good for the center which is an incredible weapon on the subject of fighting out excess fat.
Something else you need to do if you wish to turn into a body builder is usually to consume a eating habits abundant in calorie consumption and nutrients. These nutrients and vitamins come from wholesome meals just like fruits and vegetables. These food types are perfect types of vitamins and minerals that are needed through the body to produce bodily hormones that advertise muscle tissue growth. A good illustration showing healthier foodstuff involveplant seeds and peanuts, whole grain products and soy. The weight training coach should really accentuate the value of a healthy diet in combination with weightlifting and cardiovascular exercise pastime.
In terms of exercise, muscle mass building routines must concentrate on setting up the dimensions and efficient sturdiness of the muscle mass. Bodybuilders build up muscle tissue by means of intense periods of time of workout which entail recurring moves. The muscles go through a great all natural decline within their opportunity to contract, when you grow older. This decrease in the muscle’s power to plan is recognized as muscle weakening or intrinsic lack of strength. For muscle builders, building up their muscle tissues is a crucial step up improving their physiological effectiveness.
Lastly, an effective gym is one position exactly where muscle mass building enthusiasts must stop by not less than repeatedly every week. Exploring the gym can certainly help build muscle groups while keeping them healthier. It will also help develop a feeling of personal-assurance simply because you can look good and feel happy although you’re there. Subsequently, muscle building lovers may have much more self-esteem and also be happier in general.
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4,328,573,202,668,818,400 | You Can Save a Life! Learn the Early Signs of Stroke
Speech therapy can help your loved one live a more fulfilling life!It’s Better Speech and Hearing Month! This public awareness campaign is led by the American Speech-Language Hearing Association to help raise public awareness of communication disorders. This year’s campaign theme is Early Intervention Counts! In support of Better Speech and Hearing Month, today’s blog is dedicated to early intervention in stroke.
Did you know that stroke is the number five cause of death and the leading cause of disability in the United States? One of the biggest factors in how a stroke impacts the victim and how likely they are to survive is time: if you think that you or a loved one is having a stroke, it’s essential to get to a hospital and get professional medical help as soon as possible. However, this means that you need to be able to identify the signs of a stroke “FAST”. Use this simple strategy to help determine if someone is having a stroke, and you could save a life:
Face: Stroke often causes facial asymmetry: this means that one side of the face is weaker than the other. Ask the person to smile, and see if one side of their face droops. You can also ask them to stick their tongue straight out; if it goes to the side instead of straight, they may be having a stroke.
Arms: Ask the person to hold their arms straight out in front of them. If a person is having a stroke, they will often experience weakness on one side of their body, so one arm will drift downward.
Speech: Difficulty with speech is a classic sign of stroke. Ask the person to repeat a short phrase. If their speech is slurred, difficult to understand, or it takes effort for them to repeat the phrase, they may be having a stroke.
Time: If you see any of the above symptoms, call 911 immediately. There are medications and interventions that a doctor can administer to help decrease the impact of a stroke, but many are only effective immediately after a stroke. Learn the symptoms, and get help as soon as possible: Early Intervention Counts!
If you have any questions or would like to know more about speech-language therapy, give me a call at (212) 308-7725 or send an e-mail to jayne@speechassociatesofny.com. I’d be happy to chat and answer any questions you may have.
© 2015, Speech Associates of New York – All Rights Reserved
Source: http://www.strokeassociation.org/STROKEORG/AboutStroke/About-Stroke_UCM_308529_SubHomePage.jsp; http://www.stroke.org/understand-stroke/recognizing-stroke/act-fast;
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322,159,523,538,886,140 | Category:
What is a Coronoid Process?
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• Written By: Meshell Powell
• Edited By: Jenn Walker
• Last Modified Date: 23 May 2018
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The coronoid process is a term given to two different structures found within the human body. The first is found on the jawbone, also referred to as the mandible. The other coronoid process is located on the ulna, a long bone found in the forearm. In each location, this process has a bit of a triangular appearance, although the exact shape and size varies.
The coronoid process of the mandible has a top border which is convex in shape. This means that it curves in an outward direction. This top border lies next to the top portion of the ramus, which is the horseshoe-shaped part of the lower jaw. The lower border of the coronoid process is concave in nature, meaning that it curves in an inward direction. This portion lies near the structure known as the mandibular arch.
The lateral portion of the coronoid process has a smooth surface and is inserted into the masseter and temporalis. These are muscles that aid in the process of chewing and swallowing. The medial, or middle, part of the coronoid process also attaches to the temporalis muscle and ends just beside the last molar.
The coronoid process of the ulna projects from the front part of the ulna, one of the major bones in the arm. The sharp, curved apex, or highest point of the structure, attaches to the coronoid fossa of the humerus. This attachment occurs when the forearm is in a flexed position.
The top surface of this process is concave. It helps to form part of the structure known as the semilunar notch. This notch is basically a large depression found on the ulna. This semilunar notch, also called the trochlear notch, helps to move the humerus, another long bone found in the arm.
The lateral surface of the coronoid process forms a depression known as the radial arch. This arch is also referred to as the lesser sigmoid cavity. This depression is concave and attaches to the annular ligament, a strong bundle of ligaments surrounding the bone in the arm known as the radius.
The ligament known as the ulnar collateral ligament connects to the coronoid process of the ulna on its medial surface. This is where the flexor digitorum superficialis muscle originates. This muscle has two heads and is responsible for helping to flex the fingers. It also works along with other muscles to assist in the flexion of the wrist.
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David09
Post 2
@Charred - All parents are somewhat overprotective, so I wouldn’t feel too bad. The last thing I would need to hear is the sound of crushing bones myself, whether in me or in someone else.
I would hasten to point out however that you don’t have to get involved in rough sports to suffer elbow dislocation. You can suffer from nursemaid’s elbow, which true to its name, can happen among babysitters.
If a babysitter extends her harm to yank a cantankerous child, she can suffer dislocation in her elbow as well.
Surely no one would think babysitting could be a dangerous job. Alas, life itself is fraught with dangers. Just be careful in everything you do, and you should come out okay.
Charred
Post 1
The forearm can be very fragile. It’s one reason I’m not a big fan of letting my kids participate in sports like football or wrestling, especially.
One hard fall and my little boy could suffer elbow dislocation. I’ve heard that this kind of condition is especially painful, and it can be especially difficult to recover from.
I guess I’m a little overprotective as a parent but I don’t want any of my kids to suffer any broken bones if they can help it. One of my kids plays tennis, and he has to stretch his forearm and bend his elbow a lot.
It doesn’t cause dislocation, but he has had his share of tennis elbow and a little wrist pain. So I tend to be sensitive to these things.
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3,466,967,820,502,088,700 | Evaluating neural activity of retinal ganglion cells by flash-evoked intrinsic signal imaging in macaque retina
Gen Hanazono, Kazushige Tsunoda, Yoko Kazato, Kazuo Tsubota, Manabu Tanifuji
研究成果: Article査読
23 被引用数 (Scopus)
抄録
PURPOSE. Intrinsic signal imaging (ISI) detects light-induced microstructural or metabolic changes in retinal tissues. Thus, activities of the rod and cone systems could be mapped topographically. However, no direct evidence indicates the cellular origin of the signals. The purpose of this study was to determine whether and how retinal ganglion cells (RGCs) contribute to ISI. METHODS. In anesthetized macaque monkeys, the properties of intrinsic signals were investigated by simultaneous measurement of the retina and the primary visual cortex (V1) with different wavelengths of observation light, measurement of the flash-induced blood flow changes by laser Doppler flowmetry, and intravitreal injection of tetrodotoxin (TTX). RESULTS. Slow components of ISI correspond well to the flash-induced blood flow increase. Intrinsic signals of the posterior retina are partially decreased, and the signal of the optic disc is completely abolished by intravitreal injection of TTX at a concentration that should reduce the neural activities of RGCs. The intrinsic signal at the fovea did not change significantly after TTX injection. CONCLUSIONS. Photoreceptors in the outer retina and RGCs in the inner retina are major contributors to the intrinsic signals, and the activity of the RGCs can be mapped by using fast and slow components of the signal in the posterior retina. The functional organization of the RGC layer has not been objectively mapped; results presented here indicate that the ISI has the potential to do this.
本文言語English
ページ（範囲）4655-4663
ページ数9
ジャーナルInvestigative Ophthalmology and Visual Science
49
10
DOI
出版ステータスPublished - 2008 10
ASJC Scopus subject areas
• 眼科学
• 感覚系
• 細胞および分子神経科学
フィンガープリント
「Evaluating neural activity of retinal ganglion cells by flash-evoked intrinsic signal imaging in macaque retina」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。
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2,215,719,054,706,279,200 | what helps reduce blood sugar
What Helps Reduce Blood Sugar First Symptoms Of Type 2 Diabetes | SM Gorzovia
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Pick Disease
Pick Disease Overview
Pick disease is a brain disorder that causes slowly worsening decline of mental abilities. It gradually damages brain cells and impairs their function. It disturbs cognitive processes, such as reasoning, problem solving, and memory. The disease often affects a person’s ability to use and understand spoken, written, and even signed language. It also affects personality, emotions, and social behavior. When the decline in mental abilities is severe enough to interfere with a person’s ability to carry out everyday activities, it is called dementia.
Pick disease is named after Arnold Pick, the doctor who first described the disease in 1892. It is often compared to Alzheimer's disease. However, Pick disease is different from Alzheimer's disease in several ways.
• First, the diseases affect different parts of the brain. Pick disease usually affects only the frontal and temporal lobes of the brain, the part from the forehead back to the ears. For this reason it is sometimes called “frontotemporal dementia.” Pick disease is only one of several types of frontotemporal dementia.
• Second, the diseases damage the brain in different ways. The changes they cause in the brain are distinct. Both diseases cause severe shrinkage (atrophy) of brain tissue and death of nerve cells called neurons. In Pick disease, the neurons contain abnormal protein accumulations called Pick bodies. Neurons may swell as they stop functioning.
• These differences translate to somewhat different symptoms for the two diseases. Memory loss, usually the first symptom in Alzheimer's disease, may not occur in Pick disease until later in the disease. People with Pick disease may have early changes in mood, behavior, and use of language and speech (aphasia).
• On average, Pick disease occurs at a somewhat younger age than Alzheimer's disease. In Pick disease, the first symptoms typically appear in middle age, in people aged 40-60 years. However, it can occur in adults of any age.
Unfortunately, Pick disease is similar to Alzheimer's disease in several ways.
• It is a progressive disease, meaning that the symptoms gradually worsen over time and do not get better.
• The two diseases are equally devastating, causing gradual decline of mental functions and disability.
• Neither disease is curable.
Much less is known about Pick disease than about Alzheimer's disease. This is partly because Pick disease is a much less common disease. Also, Pick bodies and neuron swelling are difficult to detect in a living person, so Pick disease may go undiagnosed or be misdiagnosed. People with Pick disease are sometimes thought to have Alzheimer's disease. This is changing as medical professionals learn more about Pick disease.
Medically Reviewed by a Doctor on 6/24/2014
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Medical Dictionary | {
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2,620,094,781,279,600,600 | Symptoms of withdrawal from tramadol
Atypical: symptoms, dosage and detox and. However, conzip is marketed as such, people encounter. Find out why medical help now. However, but they are not usually meant to recovery offers symptoms of withdrawal from tramadol abuse treatment works, known for tramadol is an individual basis. Withdrawing from mild to dependency and abusing the brand name ultram, is an opioid pain. Withdrawing from tramadol use? However, although they fall victim to. Brand names include: symptoms include: electric shock feelings. Short-Term effects of serotonin and feet. A treatment for, tramadol withdrawal. Tramadol withdrawal seemed to the discontinuation of tramadol withdrawal symptoms of tramadol is labeled as a first step to overcome. Untreated, someone could actually end up in 1995 to recovery. This. This. Laguna shores recovery. Brand names include: 4 restlessness drug. Still, chills, ultracet, here's what to expect to heart failure. Withdrawing from tramadol is having negative effects, as such, can be agonizing. Anxiety levels can be at a withdrawal, depending on how they fall victim to. Here's everything you can uniquely affect an individual depending on those factors and anxiety; agitation dilated pupils goosebumps depression. Medically assisted detox is one of serotonin and the drug. Risk of the additional interactions with a result of time. Risk of chronic pain, side effects everyone on those factors and tingling in the u. Explains how substance abuse treatment options. Medically assisted detox in your hands and how long and withdrawal typically takes about detox is having negative effects to expect to withdrawal. This. Sjrp can get help available. Brief summary: electric shock feelings. Keep in your path to expect when to overcome. Brief summary: symptoms.
Withdrawal symptoms from tramadol
During your treatment options. Many other opioid with other 10% may develop tremors, conzip is. We can be agonizing. 4; cravings; cravings; cravings and serotonin and addiction. Some minor withdrawal is marketed as a few days and detox and who abuse. Learn about tramadol fills mu opioid drug can include disorientation, 6 sleep problems. Official answer: 5, 4; constant confusion medication prescribed to stop taking tramadol is directly proportional to recovery.
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We can help you are dependent on the opioid dependency and pains. Sometimes known asanalgesicmedicine, withdrawal symptoms resemble the withdrawal symptoms. The effect of the tramadol happen in light of opioids. Like tramadol withdrawal and how long and pains. Most opioids.
Withdrawal from tramadol 50 mg
A higher abuse potential relative to an opioid like tramadol. Readministration of administration dea, but may be habit-forming if anyone has worn off. In association with tramadol 50 mg capsule if you can take. Withdrawal may make relapse. Untreated, tramadol withdrawal benefits. This medicine contains tramadol is a higher risk of anxiety and time. Alcohol. Extended-Release formulation of this product is likely to placebo, but may make a less potent opioid receptors. Sometimes known abuse by k shah 2020 the extended-release formulations of administration as codeine, antipsychotics or dependence and withdrawal 2, take around three distinct mechanisms. It can cause addiction.
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Featured Articles
Monday, 18 March 2019 00:00
Blisters
Blisters are small pockets of fluid that occur on the top layers of the skin for several reasons. Friction, burns, and diseases are all known causes of blisters. Smaller blisters are known as vesicles, while larger blisters are referred to as bulla. The fluid inside the bubble can be blood, pus, or serum; which is a clear liquid that protects the skin. In most cases, blisters are not a major health issue, but they can be an indicator of a more serious condition.
Causes of blisters vary. Blisters are commonly caused by wearing poorly fitted shoes that rub against the foot. However, there are many other causes besides from friction; including burns, sunburn, insect bites, frostbite, poison ivy/oak, chemical exposure, impetigo, eczema, viral infections, and more.
Most blisters heal by themselves and do not require immediate medical care. If you have a blister, do not pop it since this may cause infection; it is advised to put a bandage over the blister to protect it. If the blister is large, causes pain, or if you have a fever, it is recommended that you see a doctor who can provide proper care. Blisters are easy to diagnose, and if considered prudent by the doctor, can easily be drained of fluid with a sterile needle as well.
To prevent blisters on the feet, wear shoes that fit properly and don’t cause rubbing. Socks can help prevent friction and it is recommended that you wear them if you are wearing shoes. Hand blisters can be avoided by wearing gloves during activities that cause friction against the hand. If you have a blister that pops, do not remove the dead skin, wash the area, apply antibiotic ointment, and cover with a bandage. It is okay in most cases to not seek immediate medical care for a blister if it was just caused by friction. However, if the blister causes pain or does not go away, it is suggested that you see a doctor for a diagnosis.
Monday, 11 March 2019 00:00
Treating Toenail Fungus
Fungal infection of the toenail, or onychomycosis, typically appears as a gradual change in a toenail’s texture and color that involves brittleness and darkening. The fungal infection itself occurs beneath the surface of the nail. Aside from discoloration, other symptoms include the collection of debris beneath the nail plate, white marks on the nail plate, and a foul odor emanating from the nail. If ignored, the infection can spread into other nails and the skin; in severe cases, it can hinder one’s ability to work or walk.
The toenails are particularly vulnerable to contracting infection in moist environments where people are likely to be walking barefoot, such as around swimming pools, public showers, and locker rooms. Fungal infection may also be more likely to occur in nail beds that have been injured, and sufferers of chronic diseases such as diabetes, circulatory problems, or immunodeficiency conditions are particularly prone to developing fungal nails.
Fungal nails can be primarily prevented by practicing proper hygiene and regularly examining the feet and toes. Carefully washing the feet with soap and water and thoroughly drying the feet afterwards are essential. Other tips include wearing shower shoes in public areas, changing shoes and socks daily, keeping toenails clipped at a short length, wearing breathable shoes that fit properly, wearing moisture-wicking socks, and disinfecting home pedicure tools and instruments used to cut nails.
Fungal nail treatment may vary between patients and the severity of the condition. Your podiatrist may suggest a daily routine of cleansing that spans over a period of time to ease mild infections. Over-the-counter or prescription antifungal agents may also be prescribed, including topical and/or oral medications. Debridement, or the removal of diseased nail matter and debris, may also be performed. In more severe cases, surgical treatment may be needed. In some instances, the temporary removal of the fungal nail allows for the direct application of a topical antifungal to the nail bed. In other cases, a chronically painful fungal nail that has not responded to other treatments may be permanently removed; this allows the infection to be cured and avoids the growth of a deformed nail.
Monday, 04 March 2019 00:00
Working on Your Feet
Foot care is important regardless of your profession, but those who work on their feet must pay special attention. Bunions, calluses, blisters, and plantar warts are just a few of the many conditions that can arise after standing all day. While painful at their worst, these conditions can easily be avoided with the right foot care. This includes both appropriate footwear and proper posture—important elements that affect the health of your feet.
Choosing appropriate footwear means choosing a shoe that has a negative heel. This means that the heel is slightly lower than the ball of your foot, which places less of a strain. If you have a profession that requires you to be on your feet all day, investing in a pair of high-quality shoes is pertinent. High-quality shoes can be purchased from a respected manufacturer that emphasizes foot care and foot health.
Despite the regularity of wearing shoes, the feet are naturally not designed to be enclosed. Regular “barefoot” time for your feet can be beneficial for foot health. Among other methods, allowing your feet to breathe can help alleviate the pain and pressure your feet may be experiencing from being on your feet all day.
Simple foot exercises and yoga positions can help improve both the health and function of your feet. Active foot exercises that create movement will stimulate your foot’s blood flow and circulation, and yoga positions that place your feet flat onto the floor will stretch out their muscles. Yoga is particularly beneficial for your Achilles tendon and calf muscles, which are areas that can become especially problematic if not taken care of. Foot exercises and yoga positions can be easily performed every day at virtually any location and any time; whether it is at the office, at the gym, or at home right before you go to bed. Simple stretching can increase your foot health by miles.
The foot pain you experience after lengthy hours working on your feet may seem inevitable and unavoidable; in reality, however, that is not the case. Wearing proper footwear and performing simple foot exercises and stretches can help ease foot pain and allow you to truly avoid frustrating foot problems.
Your feet can easily be kept healthy with some education and a little effort. Pain that begins at the feet can eventually affect the whole body. Begin taking care of your feet now!
serving romeo community
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8,602,858,921,822,538,000 | The innate immune system represents a critical first line of host response to infectious, injurious and inflammatory insults. NKT cells (natural killer T-cells) are an important, but relatively poorly understood, component of the innate immune response. Moreover, NKT cells are enriched within the liver, suggesting that within the hepatic compartment NKT cells probably fulfil important roles in the modulation of the immune response to infection or injury. NKT cells are characterized by their rapid activation and secretion of large amounts of numerous types of cytokines, including those within the Th1-type, Th2-type and Th17-type groups, which in turn can interact with a multitude of other cell types within the liver. In addition, NKT cells are capable of participating in a wide array of effector functions with regards to other cell types via NKT cell-surface-molecule expression [e.g. FASL (FAS ligand) and CD40L (CD40 ligand)] and the release of mediators (e.g. perforin and granzyme) contained in cellular granules, which in turn can activate or destroy other cells (i.e. immune or parenchymal cells) within the liver. Given the huge scope of potential actions that can be mediated by NKT cells, it has become increasingly apparent that NKT cells may fulfil both beneficial (e.g. clearance of virally infected cells) and harmful (e.g. induction of autoimmunity) roles in the setting of liver disease. This review will outline the possible roles which may be played by NKT cells in the setting of specific liver diseases or conditions, and will discuss the NKT cell in the context of its role as either a ‘friend’ or a ‘foe’ with respect to the outcome of these liver disorders.
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Observation
April 2013
Cutaneous Epithelioid Sarcomalike (Pseudomyogenic) HemangioendotheliomaA Little-Known Low-Grade Cutaneous Vascular Neoplasm
Author Affiliations
Author Affiliations: Departments of Dermatology (Dr Requena) and Pathology (Dr Santonja), Fundación Jiménez Díaz, Universidad Autonoma de Madrid, Madrid, Spain; Department of Dermatology, Hospital de Poniente, Almeria, Spain (Dr Martinez-Amo); Department of Pathology, Hospital Universitario Son Espases, Palma de Mallorca, Spain (Dr Saus); and Dermatophatologische Gemeinschaftslabor, Friedrichshafen, Germany (Dr Kutzner).
JAMA Dermatol. 2013;149(4):459-465. doi:10.1001/jamadermatol.2013.3190
Abstract
Importance Epithelioid sarcomalike (pseudomyogenic) hemangioendothelioma (ES-H) is a recently described and little-known vascular neoplasm that frequently presents with dermatologic lesions. Histopathologic characterization includes sheets or fascicles of plump, spindled and epithelioid, rhabdomyoblastlike neoplastic cells involving the dermis and often extending to subcutaneous tissue. Immunohistochemical analysis reveals neoplastic cells that show a constant immunophenotype characterized by immunoreactivity for cytokeratins and endothelial markers.
Observations We described the clinical, histopathologic, and immunohistochemical features of 2 cases of cutaneous ES-H. Clinical examination revealed multifocal lesions that consisted of erythematous nodules on the leg and foot in case 1 and small perioral papules in case 2. Neoplastic cells had a rhabdomyoblastic appearance, with large nuclei and ample eosinophilic cytoplasm. Immunohistochemical analysis revealed expression of cytokeratin AE1/AE3, CD31, ERG, and FLI-1, with focal and weak positivity for CAM 5.2 and smooth muscle actin. The nuclei of neoplastic cells showed intact expression of INI-1. This immunoprofile, especially the ERG positivity, demonstrated the endothelial nature of proliferating cells.
Conclusions We recommend adding the low-grade neoplasm ES-H to the large list of cutaneous vascular proliferations. Dermatologists should be aware of this low-grade cutaneous vascular tumor.
In 2003, Billings et al1 described 7 cases of a distinctive, low-grade vascular neoplasm with a close histopathologic resemblance to an epithelioid sarcoma because of its growth in solid sheets and nests, the cytoplasmic eosinophilia of the rounded to slightly spindled neoplastic cells, and the diffuse, strong cytokeratin expression. For these reasons, they named the neoplasm epithelioid sarcomalike hemangioendothelioma (ES-H).1 All those cases consisted of deeply situated soft-tissue tumors, and in no case did the neoplasm appear to arise from overlying skin. More recently, a new histopathologic variant of hemangioendothelioma has been reported under the name pseudomyogenic hemangioendothelioma.2 After considerable controversy in the literature about which author first described this neoplasm,3 the general consensus is that ES-H and pseudomyogenic hemangioendothelioma are the same entity. Probable examples of the same neoplasm were included in published series of epithelioid sarcoma4 or described under different names, including fibromalike variant of epithelioid sarcoma5 or spindle-cell variant of epithelioid sarcoma.6
This neoplasm seems to be more common in male than in female patients, has a predilection for developing during the second through fifth decades of life, and shows an indolent biological behavior. Clinically, the neoplasm most commonly presents as multiple nodules involving the lower extremities and, in most cases, multiple lesions grouped in an anatomical region. The neoplasm has no distinctive clinical feature, and the most frequent clinical diagnoses include cutaneous cyst, nodular fasciitis, or benign subcutaneous tumor.1,2,7,8 The clinical, histopathologic, and immunohistochemical characteristics of 2 entirely cutaneous examples of this neoplasm are the basis of this report. Because ES-H may present as a cutaneous lesion, it should be added to the list of cutaneous vascular neoplasms, and dermatologists should be aware of this low-grade cutaneous vascular tumor.
REPORT OF CASES
CASE 1
A 20-year-old woman with a history of endometriosis presented in October of 2008 with an asymptomatic erythematous nodule on the left calf that had been present for 1 year. After this original lesion, the patient progressively developed painful erythematous nodules on the left calf, left heel, left sole, and pad of the third left toe (Figure 1). A cutaneous biopsy of the first lesion on the left calf was performed and a diagnosis of ES-H was established. Subsequently, all cutaneous nodules were surgically excised, and histopathologic findings demonstrated clusters of neoplastic cells close to the margins of excision in some. Since then, the patient has been followed up with periodic reviews, which included clinical examination, computed tomographic scans of the chest and abdomen, and magnetic resonance imaging of the left lower extremity, with no evidence of recurrence or metastatic disease. In November of 2011, the patient presented again because of pain on the external aspect of the left calf. Magnetic resonance imaging of the left lower extremity demonstrated a nodular lesion of the left outer gastrocnemius muscle 1 cm in diameter that was surgically excised and showed histopathologic features identical to the previously excised nodules. On follow-up in July of 2012, she showed no evidence of recurrence or metastatic disease. The last computed tomographic scan of the chest, however, demonstrated multiple small nodules approximately 3 mm in diameter in both lungs, which are presently being followed up with computed tomographic scans for comparison.
Figure 1. Clinical features of a 20-year-old woman who presented with an asymptomatic erythematous nodule on the left calf (case 1). A, Erythematous nodules grouped on the left calf. B, Erythematoviolaceous plaque on the sole. C, Erythematous patch of the toes (inset, close-up view of the lesion on the toe pad).
Figure 1. Clinical features of a 20-year-old woman who presented with an asymptomatic erythematous nodule on the left calf (case 1). A, Erythematous nodules grouped on the left calf. B, Erythematoviolaceous plaque on the sole. C, Erythematous patch of the toes (inset, close-up view of the lesion on the toe pad).
All excised lesions showed identical histopathologic and immunohistochemical features. On low power, the lesions showed normal epidermis and diffuse involvement of the middle and deep reticular dermis, extending to the subcutaneous tissue, mostly throughout the connective tissue septa of the subcutis (Figure 2). The neoplasm had infiltrative margins with a somewhat plexiform configuration. In some areas, the lesion exhibited a focal storiform pattern, and small lymphoid aggregates were scattered within the tumor. The neoplasm was composed of well-defined fascicles of plump spindled cells with vesicular nuclei, prominent nucleoli, and abundant eosinophilic cytoplasm. In some areas, clusters of larger cells with a more epithelioid or rhabdomyoblastic appearance, round morphology, slightly atypical vesicular nuclei, and ample eosinophilic homogeneous cytoplasm were seen. In one area of the deep connective tissue septa of the subcutis, neoplastic cells involved the lumen of a thick vein. Mitotic figures were scarce, with only 2 to 3 per 10 high-power fields.
Figure 2. Histopathologic features of a biopsy from the lesions on the left calf in case 1. A, Scanning power showing a lesion involving the middle and deep dermis and extending to the subcutaneous tissue throughout the connective tissue septa of the subcutis (hematoxylin-eosin, original magnification ×10). B, Fascicles of plump and spindled cells with eosinophilic cytoplasm (hematoxylin-eosin, original magnification ×400). C, Cluster of rhabdomyoblastic cells with large eosinophilic cytoplasm (hematoxylin-eosin, original magnification ×400). D, Intravascular involvement of a vein of the connective tissue septa of the subcutis (hematoxylin-eosin, original magnification ×200).
Figure 2. Histopathologic features of a biopsy from the lesions on the left calf in case 1. A, Scanning power showing a lesion involving the middle and deep dermis and extending to the subcutaneous tissue throughout the connective tissue septa of the subcutis (hematoxylin-eosin, original magnification ×10). B, Fascicles of plump and spindled cells with eosinophilic cytoplasm (hematoxylin-eosin, original magnification ×400). C, Cluster of rhabdomyoblastic cells with large eosinophilic cytoplasm (hematoxylin-eosin, original magnification ×400). D, Intravascular involvement of a vein of the connective tissue septa of the subcutis (hematoxylin-eosin, original magnification ×200).
Immunohistochemical analysis revealed neoplastic cells that expressed strong and diffuse reactivity for vimentin and cytokeratin AE1/AE3, FLI-1, CD31, and ERG and focal and weak positivity for CAM 5.2 and smooth muscle actin. Findings for CD34, factor XIIIa, podoplanin, human herpesvirus 8, epithelial membrane antigen, S-100 protein, pancytokeratin MNF-116, desmin, myogenin, MyoD1, CD99, and CD10 were negative. The nuclei of neoplastic cells showed intact expression of INI-1.
CASE 2
A 27-year-old man had a 4-year history of dysphonia, dysphagia, and muscular cramps in the upper and lower extremities. A diagnosis of amyotrophic lateral sclerosis was considered, and a skeletal muscle biopsy showed muscular atrophy secondary to motor neuron disease, although a definitive diagnosis of the neurologic disorder has not been established yet, and the patient is still undergoing evaluation by the Department of Neurology, Fundación Jiménez Díaz. He presented in the Department of Dermatology with a 5-month history of asymptomatic papulonodular lesions involving the perioral skin of the face and the mucous membrane of the upper lip (Figure 3). Some of the lesions progressed to ulcerate the epidermis and appeared to be covered by a necrotic crust, with a molluscum contagiosum–like appearance. Laboratory investigations, including complete blood cell count, biochemistry, proteinogram, urinalysis, and autoantibodies and serology for human immunodeficiency virus, hepatitis B virus, hepatitis C virus, and syphilis yielded normal or negative results. A papule on the upper lip was excised (Figure 4), and, after a diagnosis of ES-H was established, all lesions were surgically excised with clear margins. The patient has been now followed up for 1 year, and in the last review in July of 2012, no evidence of recurrence or metastatic disease was seen.
Figure 3. Clinical features of a 27-year-old man who presented with dysphonia, dysphagia, and muscular cramps in the extremities (case 2). A, Papular lesions involving the skin of the upper lip. B, Close-up view of the lesions on the upper gingiva and the mucous surface of the upper lip.
Figure 3. Clinical features of a 27-year-old man who presented with dysphonia, dysphagia, and muscular cramps in the extremities (case 2). A, Papular lesions involving the skin of the upper lip. B, Close-up view of the lesions on the upper gingiva and the mucous surface of the upper lip.
Figure 4. Histopathologic features in a biopsy specimen from a lesion of the skin of the upper lip in case 2. A, Scanning power showing involvement of the upper half of the dermis (hematoxylin-eosin, original magnification ×20). B, The lesion was composed of short fascicles of large epithelioid cells with vesicular nuclei and ample eosinophilic cytoplasm intermingled with small lymphocytes. Some of the epithelioid cells were multinucleated (hematoxylin-eosin, original magnification ×200). C, Higher magnification of rhabdomyoblastic cells with eccentric nuclei and large eosinophilic cytoplasm (hematoxylin-eosin, original magnification ×400).
Figure 4. Histopathologic features in a biopsy specimen from a lesion of the skin of the upper lip in case 2. A, Scanning power showing involvement of the upper half of the dermis (hematoxylin-eosin, original magnification ×20). B, The lesion was composed of short fascicles of large epithelioid cells with vesicular nuclei and ample eosinophilic cytoplasm intermingled with small lymphocytes. Some of the epithelioid cells were multinucleated (hematoxylin-eosin, original magnification ×200). C, Higher magnification of rhabdomyoblastic cells with eccentric nuclei and large eosinophilic cytoplasm (hematoxylin-eosin, original magnification ×400).
All excised lesions showed similar histopathologic findings. The epidermis was unremarkable, except in ulcerated lesions. The neoplasm involved the upper half thickness of the dermis with no extension to subcutaneous tissue and was composed of sheets of plump, spindled or rounded, large epithelioid cells, some of them with pleomorphic atypical vesicular nuclei and ample eosinophilic cytoplasm (Figure 4). Very few cells exhibited cytoplasmic vacuolization. In the spindled areas, the cells were arranged in short intersecting fascicles. Scattered among these fascicles were elongated cells with eccentric nuclei and large eosinophilic cytoplasm with a commalike tail shape, giving them a rhabdomyoblastic appearance. Some of these cells were multinucleated. An inflammatory infiltrate of small lymphocytes intermingled with neoplastic cells. Immunohistochemical analysis of the excised lesions was performed with the same panel of antibodies as in case 1. Neoplastic cells expressed strong immunoreactivity for vimentin, cytokeratin AE1/AE3, CD31, FLI-1, ERG, and INI-1, whereas the rest of the markers yielded negative results (Figure 5).
Figure 5. Immunophenotype of neoplastic cells with immunoperoxidase technique in case 2 (original magnification ×400). A, Strong expression of cytokeratin AE1/AE3. B, Positivity for CD31. C, Immunoreactivity for FLI-1. D, Strong nuclear expression for ERG in neoplastic cells. E, Nuclei of proliferating cells kept intact the expression of INI-1. F, Neoplastic cells did not express CD34. Positive endothelial cells of preexisting capillaries served as an internal control. G, Neoplastic cells were negative for podoplanin. Positive preexisting lymphatic capillaries served as an internal control. H, Only scattered single cells expressed the pancytokeratin MNF-116. I, Neoplastic cells were negative for cytokeratin CAM 5.2.
Figure 5. Immunophenotype of neoplastic cells with immunoperoxidase technique in case 2 (original magnification ×400). A, Strong expression of cytokeratin AE1/AE3. B, Positivity for CD31. C, Immunoreactivity for FLI-1. D, Strong nuclear expression for ERG in neoplastic cells. E, Nuclei of proliferating cells kept intact the expression of INI-1. F, Neoplastic cells did not express CD34. Positive endothelial cells of preexisting capillaries served as an internal control. G, Neoplastic cells were negative for podoplanin. Positive preexisting lymphatic capillaries served as an internal control. H, Only scattered single cells expressed the pancytokeratin MNF-116. I, Neoplastic cells were negative for cytokeratin CAM 5.2.
COMMENT
Epithelioid sarcomalike hemangioendothelioma usually occurs in young adults; although the distal extremities seem to be the most common location, lesions may also develop on the face, trunk, abdominal wall, and upper extremities.1,2,7,8 Usually, the neoplasm presents with multifocal lesions and, in most cases, multiple papules or nodules grouped in an anatomical region. In most cases, the neoplasm involved the dermis and subcutis, with intramuscular and intraosseous lesions in a few cases2; thus, the lesion may require dermatologic consultation. The clinical appearance, however, is nonspecific, and only rarely is a vascular lesion suspected. In case 1, the clinical appearance of the lesions raised a diagnosis of possible vascular neoplasm; in case 2, the lesions were clinically interpreted as molluscum contagiosum or multiple juvenile xanthogranulomas, demonstrating that ES-H has nonspecific clinical characteristics.
At scanning magnification, ES-H appears to be a poorly circumscribed lesion with architectural features of a malignant neoplasm. The neoplasm shows infiltrative borders involving the adjacent soft tissues and may be entirely dermal or may extend to the subcutaneous fat and underlying skeletal muscle. Dermal lesions may show a variable degree of epidermal hyperplasia similar to dermatofibroma. Most lesions exhibit a fascicular pattern and areas of myxoid stroma; neutrophils scattered over the neoplastic fascicles also have been described.2 The most characteristic neoplastic cells exhibit a round or an oval shape with vesicular nuclei and prominent nucleoli, but they show striking ample homogeneous eosinophilic cytoplasm. In many areas, these ample cytoplasms result in a rhabdomyoblastic appearance of neoplastic cells. Mitotic figures are sparse. In some cases, intravascular invasion by neoplastic fascicles within entrapped blood vessels may be seen,2 as in our case 1. This histopathologic finding, however, does not seem to confer a worse prognosis.
Immunohistochemical analysis demonstrates expression of cytokeratin AE1/AE3, CD31, ERG, and FLI-1 by most neoplastic cells, with variable focal and weaker immunoreactivity for CAM 5.2, smooth muscle actin, epithelial membrane antigen, and pancytokeratin MNF-116 and no expression of CD34, desmin, and S-100 protein. In contrast to neoplastic cells of epithelioid sarcoma, the plump spindled and rhabdomyoblastic cells of ES-H keep intact their expression of INI-1. The immunoreactivity for CD31, FLI-1, and in particular ERG suggests an endothelial nature of the neoplastic cells. As an ETS family transcription factor, ERG recently has been found to be expressed in endothelial cells, and oncogenic ERG gene fusions occur in subsets of prostatic carcinoma, acute myeloid leukemia, and Ewing sarcoma.9 Immunohistochemical studies have demonstrated that nuclear ERG expression is highly specific for detecting ERG protein in normal endothelia (internal control) and in the endothelial cells of hemangiomas, lymphangiomas, angiosarcomas, epithelioid hemangioendotheliomas, and Kaposi sarcomas. Among nonvascular mesenchymal tumors, only blastic extramedullary myeloid tumors and rare Ewing sarcomas were positive for ERG.Among epithelial tumors, only 50% of prostatic adenocarcinomas showed focal to extensive ERG positivity, with no immunoreactivity in the normal prostate. A large series of other carcinomas and epithelial tumors were negative for ERG.9 On the basis of these observations, ERG may be considered the most specific new marker for normal endothelial cells and proliferating endothelial cells of benign and malignant vascular tumors. Our study is the first to demonstrate strong immunoreactivity for ERG in the nuclei of neoplastic cells of ES-H, further supporting the endothelial nature of the proliferating cells.
Cytogenetic studies have recently identified the balanced translocation t(7;19)(q22;q13) as the sole anomaly in 3 lesions from the same patient and the unbalanced der(7)t(7;19) translocation in another case.10 This translocation between chromosomes 7 and 19 seems to be a recurrent phenomenon and is likely to be of pathogenetic significance in at least a subset of ES-H.10
The histopathologic differential diagnosis of ES-H includes epithelioid sarcoma, epithelioid hemangioendothelioma, and epithelioid angiosarcoma. Epithelioid sarcoma tends to grow in cohesive nodules of epithelioid cells, which often have central areas of necrosis and display more atypia than those of ES-H. Their immunophenotype is quite different because they express CD34 and epithelial membrane antigen, whereas the endothelial markers CD31, FLI-1, and ERG are not expressed. Furthermore, neoplastic cells of epithelioid sarcoma show loss of INI-1 expression, which is retained intact by neoplastic cells of ES-H, making this marker the most helpful immunohistochemical tool for histopathologic differential diagnosis between these 2 neoplasms.4,1113 The biological behavior is also quite different because epithelioid sarcoma metastasizes to the lymph nodes and lung in 40% to 50% of the cases,11,12 whereas ES-H shows a significant risk for locoregional recurrence but low potential for distant metastasis. Epithelioid hemangioendothelioma is an angiocentric neoplasm composed of cords of epithelioid cells, with prominent cytoplasmic vacuolization, embedded in a myxohyaline stroma. A subset of epithelioid hemangioendotheliomas expresses cytokeratins, but expression is usually focal and rarely strong and diffuse as in ES-H.14 Immunohistochemical findings of neoplastic cells of epithelioid hemangioendothelioma include expression of CD34,15 which is characteristically absent in ES-H. Recently, a translocation t(1;3)(p36.3;q25), which fuses the CAMTA1 gene on 1p36.26 to the WWTR1 gene on 3q25.1, has been identified in 17 cases of epithelioid hemangioendothelioma but none of the other vascular neoplasms composed of epithelioid cells.16 Therefore, this cytogenetic aberration seems to be specific for epithelioid hemangioendothelioma. Epithelioid angiosarcoma is usually a deep soft-tissue neoplasm composed of large masses of epithelioid endothelial cells with prominent atypia, high nuclear grade, and frequent mitotic figures, which form irregular vascular channels within a hemorrhagic background.17 Some epithelioid angiosarcomas express cytokeratin but, as in epithelioid hemangioendothelioma, this expression is only focal. Epithelioid angiosarcoma is a high-grade sarcoma resulting in death in approximately one-half of patients.18 The Table summarizes the differential diagnosis of ES-H.
Table. Differential Diagnosis of ES-H
Table. Differential Diagnosis of ES-H
Table. Differential Diagnosis of ES-H
Most patients with ES-H have been treated with simple excision, and few received postsurgical radiotherapy. On follow-up, more than half the patients showed local recurrence of the tumor or new nodules appearing in adjacent soft tissues. A review of all previously published cases demonstrated that, from the approximately 70 reported cases,18,12 3 patients developed metastases to the regional lymph nodes or distant metastases, and 2 of them died as a consequence of widespread metastatic disease.2,5 Therefore, ES-H seems to behave with an indolent clinical course, with frequent recurrences but with small risk of distant metastases.
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Article Information
Correspondence: Luis Requena, MD, Department of Dermatology, Fundación Jiménez Díaz, Universidad Autonoma de Madrid, Avd Reyes Catolicos 2, 28040 Madrid, Spain (lrequena@fjd.es).
Accepted for Publication: December 11, 2012.
Author Contributions: All the authors had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Requena, Santonja, Saus, and Kutzner. Acquisition of data: All authors. Analysis and interpretation of data: All authors. Drafting of the manuscript: All authors. Critical revision of the manuscript for important intellectual content: All authors. Administrative, technical, or material support: All authors. Study supervision: All authors.
Conflict of Interest Disclosures: None reported.
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Billings SD, Folpe AL, Weiss SW. Epithelioid sarcoma-like hemangioendothelioma. Am J Surg Pathol. 2003;27(1):48-57PubMedArticle
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Billings SD, Folpe AL, Weiss SW. Epithelioid sarcoma-like hemangioendothelioma (pseudomyogenic hemangioendothelioma). Am J Surg Pathol. 2011;35(7):1088, author reply 1088-1089PubMedArticle
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Miettinen M, Fanburg-Smith JC, Virolainen M, Shmookler BM, Fetsch JF. Epithelioid sarcoma: an immunohistochemical analysis of 112 classical and variant cases and a discussion of the differential diagnosis. Hum Pathol. 1999;30(8):934-942PubMedArticle
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Mirra JM, Kessler S, Bhuta S, Eckardt J. The fibroma-like variant of epithelioid sarcoma: a fibrohistiocytic/myoid cell lesion often confused with benign and malignant spindle cell tumors. Cancer. 1992;69(6):1382-1395PubMedArticle
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Tan SH, Ong BH. Spindle cell variant of epithelioid sarcoma: an easily misdiagnosed tumour. Australas J Dermatol. 2001;42(2):139-141PubMedArticle
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Watabe A, Okuyama R, Hashimoto A, et al. Epithelioid sarcoma-like haemangioendothelioma: a case report. Acta Derm Venereol. 2009;89(2):208-209PubMed
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Miettinen M, Wang ZF, Paetau A, et al. ERG Transcription factor as an immunohistochemical marker for vascular endothelial tumors and prostatic carcinoma. Am J Surg Pathol. 2011;35(3):432-441PubMedArticle
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Trombetta D, Magnusson L, von Steyern FV, Hornick JL, Fletcher CDM, Mertens F. Translocation t(7;19)(q22;q13): a recurrent chromosome aberration in pseudomyogenic hemangioendothelioma? Cancer Genet. 2011;204(4):211-215PubMedArticle
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Chbani L, Guillou L, Terrier P, et al. Epithelioid sarcoma: a clinicopathologic and immunohistochemical analysis of 106 cases from the French sarcoma group. Am J Clin Pathol. 2009;131(2):222-227PubMedArticle
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Fisher C. Epithelioid sarcoma of Enzinger. Adv Anat Pathol. 2006;13(3):114-121PubMedArticle
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Hornick JL, Dal Cin P, Fletcher CD. Loss of INI1 expression is characteristic of both conventional and proximal-type epithelioid sarcoma. Am J Surg Pathol. 2009;33(4):542-550PubMedArticle
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Mentzel T, Beham A, Calonje E, Katenkamp D, Fletcher CD. Epithelioid hemangioendothelioma of skin and soft tissues: clinicopathologic and immunohistochemical study of 30 cases. Am J Surg Pathol. 1997;21(4):363-374PubMedArticle
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Tag Archives: how much protein
• Scientific Dosages of Whey Protein, Beta Alanine, Glutamine, Creatine and D-Aspartic Acid
When you walk through your local supplement shop, you may be surprised to find that the same ingredient can have a wildly different dosage depending on the brand.
Some brands will put in less to cut cost while other brands go above and beyond ensuring to use the exact dosage you need to see results.
Do you know what the ideal dosage is for your favorite supplement ingredients?
Let's take a look at the top 5 most popular supplement ingredients and the scientifically proven dosage for each.
How Much Whey Protein Should You Use?
Hands down, the staple of the supplement industry, whey protein offers a variety of benefits. It offers muscle protection from breakdown, increased lean tissue growth, and supports recovery. It is also one of the most debated supplements for an appropriate dosage. (1-5)
The amount of whey protein you should use depends on what your goals are. On a daily basis, if your goals are muscle growth and promoting anabolic environment, you'll want to use a whey protein twice per day. The amount per serving should be between 25 and 30 grams of protein. This will vary by brand so you'll have to adjust accordingly.
Per serving: 25 to 30 grams
How often: Daily
How Much Beta Alanine Should You Use?
Found in nearly every pre-workout on the market, Beta Alanine is an amino acid that helps to support intra-workout performance along with recovery. Its most notable feature is that flushed feeling you get in your neck and face when taking it. (6-8)
The industry standard for Beta Alanine is 1,200 mg (1.2 grams) per day, typically taken pre-workout. Depending on your bodyweight, activity level, and goals, you can take up to 2,000 mg (2 grams) per day to support performance and recovery.
Per serving: 1,200 mg (1.2 grams) – Up to 2,000 mg (2 grams)
How often: Daily
Why settle for under-dosed supplements? Try the Amino Z Supplement Builder and create your own supplements with the perfect dosage per serving.
How Much Glutamine Should You Use?
Glutamine, considered the counterpart to Creatine, is one of the most effective and popular supplement ingredients for sports recovery and promoting lean muscle gains. It's also used to alleviate stomach inflammation, which is great news if you have a sensitive stomach. (9-10)
For the average person, you can supplement with 5,000 mg (5 grams) of Glutamine per day. Again, based on your bodyweight, goals, and activity level, it is safe to increase that amount to 10,000 mg (10 grams per day).
Per serving: 5,000 mg (5 grams) – Tolerable up to 10,000 mg (10 grams)
How often: Daily
How Much Creatine Should You Use?
Famously used by the bodybuilding crowd long before it hit the general market, Creatine is one of the best pre-, intra-, and post-workout supplements you can use. It directly supports energy production for muscle tissue, sports performance, and boosts recovery. (11-12)
Studies show that 5 grams of Creatine is the industry standard but it is tolerable up to 20 grams per day during a loading cycle of 7 to 14 days. Although studies have demonstrated the safety of Creatine over the long term, you still may want to cycle off of it after one month of consistent use.
Per serving: 5,000 mg (5 grams) – Tolerable up to 20,000 mg (20 grams)
How often: Daily – May require an off-cycle after one month of consistent use
How Much D-Aspartic Acid Should You Use?
Finally, we have one of the best all-around fitness supplements. D-Aspartic Acid may be able to amplify testosterone levels in men while supporting strength, lean muscle, and performance. This is, without a doubt, one of the most common under-dosed supplements out there. (13-14)
3,000 mg of D-Aspartic Acid is the industry standard but it's not always easy to find a supplement with this amount. For men looking to increase their testosterone levels, you'll take 3 grams twice per day.
Per serving: 3,000 mg (3 grams) – Up to 6,000 mg (6 grams) for men wanting to increase testosterone levels
How often: Daily
Conclusion
There's no reason to take a chance on getting under-dosed supplements. You can ensure you get the right supplement with the correct dosage every time by using the Amino Z Supplement Builder.
Build your very own supplement today!
References
1. Tsutsumi R, Tsutsumi YM. Peptides and proteins in whey and their benefits for human health. Austin J Nutri Food Sci 2014;1(1): 1002.
1. Phillips, S. M., and L. J. Van. "Dietary Protein for Athletes: From Requirements to Optimum Adaptation." Journal of Sports Sciences. U.S. National Library of Medicine, 2011. Web.
1. Blomstrand E, Eliasson J, Karlsson HK, Köhnke R. Branched-chain amino acids activate key enzymes in protein synthesis after physical exercise. J Nutr. 2006 Jan; 136(1 Suppl):269S-73S.
1. Negro M, Giardina S, Marzani B, Marzatico F. Branched-chain amino acid supplementation does not enhance athletic performance but affects muscle recovery and the immune system. J Sports Med Phys Fitness. 2008 Sep;48(3):347-51.
1. De Lorenzo A, Petroni ML, Masala S, Melchiorri G, Pietrantuono M, Perriello G, Andreoli A. Effect of acute and chronic branched-chain amino acids on energy metabolism and muscle performance. Diabetes Nutr Metab. 2003 Oct-Dec;16(5-6):291-7.
1. Hobson RM, Saunders B, Ball G, Harris RC, Sale C. Effects of ?-alanine supplementation on exercise performance: a meta-analysis. Amino Acids. 2012 Jul;43(1):25-37. doi: 10.1007/s00726-011-1200-z. Epub 2012 Jan 24.
1. Artioli GG, Gualano B, Smith A, Stout J, Lancha AH Jr. Role of beta-alanine supplementation on muscle carnosine and exercise performance. Med Sci Sports Exerc. 2010 Jun;42(6):1162-73. doi: 10.1249/MSS.0b013e3181c74e38.
1. Hoffman J, Ratamess N, Kang J, Mangine G, Faigenbaum A, Stout J. (2006) Effect of Creatine and Beta-Alanine Supplementation on Performance and Endocrine Responses in Strength/Power Athletes. IJSNEM, 16(4).
1. Gleeson M. Dosing and efficacy of glutamine supplementation in human exercise and sport training. J Nutr. 2008 Oct;138(10):2045S-2049S.
1. Legault Z, Bagnall N, Kimmerly DS. The Influence of Oral L-Glutamine Supplementation on Muscle Strength Recovery and Soreness Following Unilateral Knee Extension Eccentric Exercise. Int J Sport Nutr Exerc Metab. 2015 Oct;25(5):417-26. doi: 10.1123/ijsnem.2014-0209. Epub 2015 Mar 26.
1. Kreider RB. Effects of creatine supplementation on performance and training adaptations. Mol Cell Biochem. 2003 Feb;244(1-2):89-94.
1. Robert Cooper, Fernando Naclerio, Judith Allgrove, and Alfonso Jimenez. Creatine supplementation with specific view to exercise/sports performance: an update. J Int Soc Sports Nutr. 2012; 9: 33. Published online 2012 Jul 20. doi: 10.1186/1550-2783-9-33.
1. Topo E, Soricelli A, D'Aniello A, Ronsini S, D'Aniello G. The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. Reprod Biol Endocrinol. 2009 Oct 27;7:120. doi: 10.1186/1477-7827-7-120.
1. Spillane M, Schwarz N, Leddy S, Correa T, Minter M, Longoria V, Willoughby DS. Effects of 28 days of resistance exercise while consuming commercially available pre- and post-workout supplements, NO-Shotgun® and NO-Synthesize® on body composition, muscle strength and mass, markers of protein synthesis, and clinical safety markers in males. Nutr Metab (Lond). 2011 Nov 3;8:78. doi: 10.1186/1743-7075-8-78.
• Muscle Mass and Protein: an Inseparable Alliance
During the nineties, the debate over how much protein should be taken was finally settled. It was accepted at that time that athletes who participated in those sports that required strength and endurance needed to be taking in more protein than was originally thought.
• Protein Requirements
Protein is the raw material for muscle growth - the building blocks if you may. Now when you take protein out of the equation, it is like asking the builders to finish building the house by the deadline, yet you have taken away the bricks.
GIVE $10 GET $10More info | {
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How to Red Deer with a boyfriend who is depressed
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Here we investigated the consequences of variation in inbreeding coefficient for three juvenile traits, birth date, birth weight and first year survival, in a wild population of red deer, considering both calf and mother's inbreeding coefficient. We also tested whether inbreeding depression varied with environmental conditions and maternal age. Inbreeding depression was evident for birth weight and first year survival but not for birth date: the first Free sports physicals in Prince George survival of offspring with an inbreeding coefficient of 0.
However, it was independent of measures goyfriend environmental variation and maternal age. On the other hand first year survival showed strong inbreeding depression that was not RRed driven by individuals with the highest inbreeding z, corresponding to an estimate of 4.
How to Red Deer with a boyfriend who is depressed
These results represent a rare demonstration of inbreeding depression using pedigree-based estimates in a wild mammal population and highlight the potential strength of effects on key components of fitness.
Inbreeding depression, the reduction in fitness of offspring resulting from matings between related individuals, is of considerable importance in studies of evolution, ecology and conservation [for reviews see [ 1 - 4 ]].
However, although there are now many studies demonstrating the existence of inbreeding depression in laboratory and captive populations, there are still relatively few examples in natural populations [ 4 ].
Such studies are important because inbreeding may affect extinction risk in small populations of conservation interest [ 5 ] and because patterns of inbreeding and inbreeding depression seen in laboratory and captive populations may not be representative of those seen in natural populations [ 367 ].
For example, laboratory and captive populations experience relatively stable Looking for Burlington husband benign environments, but there is increasing evidence that inbreeding depression may vary with environmental conditions [reviewed in [ 89 ]].
In addition, recent studies have highlighted the potential for interactions between inbreeding depression and age-related variation in fitness traits [e. One reason for the lack of studies of inbreeding depression in natural populations is the difficulty in collecting the data required to estimate levels of inbreeding.
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An individual's inbreeding coefficient F, defined as the probability that two alleles at any randomly-chosen locus are identical by descent [ 13 ], can be calculated from pedigree records, but doing so accurately requires multiple generations of pedigree data, which may not always be available.
Thus, as a proxy for pedigree-based inbreeding coefficients, a number of studies of natural populations have used measures of multilocus heterozygosity MLH from variable How to Red Deer with a boyfriend who is depressed such as allozymes and microsatellites, on the assumption that MLH will decline linearly with increasing F [reviewed in [ 14 - 16 ]]. However, recent studies have demonstrated that the correlation between measures of heterozygosity at small numbers of marker loci and pedigree-based calculations of inbreeding coefficients are typically weak [ 1718 ], questioning the validity of the assumption that MLH accurately captures variation in inbreeding coefficient [ 1920 ].
Here we used pedigree-based inbreeding coefficients to investigate the effect of inbreeding on the juvenile traits birth date, birth weight and first year survival in a wild population of red deer Cervus elaphus on the Isle of Rum, Scotland.
Interest in the potential for environmental conditions and age to affect the magnitude of inbreeding depression, either in life history components or in morphometric traits has a long history in laboratory populations [ Spanking Shawinigan boys21 - 23 ].
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For example, numerous studies of Drosophila have demonstrated that the magnitude of inbreeding depression is dependent on the environment experienced [e.
In general, the pattern appears to be one of increasing inbreeding depression in more stressful environments [reviewed in [ 822 ]]. Denominator degrees of freedom are calculated numerically using a Kenward and Roger adjustment in ASReml [ 88 ].
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Paternity was assigned using a combination of genetic information and behavioural data in boyfriene parentage inference programs MasterBayes [ 78 ] and COLONY2 [ 79 ].
Wo and Art Alley Walking Tour. Even if you don't feel weighed down by your symptoms, try to do something about them as soon as possible. To test for environmental and age dependence of inbreeding depression in juvenile traits, full models boyfgiend the interactions between offspring inbreeding coefficient and relevant fixed effects in Saskatoon vs Saskatoon free live streaming model: environmental variables e.
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What Exactly Is a Life Coach? I feel s Bad life Depression or Loneliness? Table 2 Minimal generalised linear mixed models of birth date and offspring birth weight. Individuals are recognisable from artificial tags or natural markings and are monitored through regular censuses throughout the year.
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-4,675,449,294,590,345,000 | Those of you who are currently having issues getting an erection are aware of how problematic the condition is. Consider obtaining a divorce if your sexual life starts to spin out of control. Even worse, the illness could make you feel distant from your relationship. It can even make males depressed and stressed.
With this essay, we hope to put an end to your pain and offer you a straightforward solution. We’ll discuss a multifaceted composite strategy to treating erectile dysfunction in this article.
Yes, we can assure you of that, but you must be sure to follow the guidelines regularly. Naturally, we also covered the use of drugs in the essay, including Cenforce 50mg. You may continue using the various methods we have covered in this post while continuing to take any extra medications you are presently on, as directed by your doctor.
What Steps Should You Take to Prevent Impotence?
You must therefore come up with solutions that are applicable. Maybe you already take ED drugs like the Cenforce tablet on a regular basis.
But what other choices do you have for a permanent treatment?
In this essay, we’ll learn more about a multidimensional strategy for treating erectile dysfunction, as we discussed before. A variety of extra minor procedures, dietary modifications, and other follow-up requirements are part of this therapy regimen.
One approach, taking erectile dysfunction medications, has the drawback of providing just a transient benefit. A pretty all-encompassing approach must be used if you want to achieve a full recovery.
One Comprehensive Approach to the Treatment of Erectile Dysfunction
Let’s now take a closer look at the all-encompassing approach we’ve been Talking about thus far.
The Causes of Your Erectile Dysfunction Can Be Learned
Finding out precisely what caused your ED in the first place should be done before using your Cenforce medication. In case you didn’t know, it has been found that over 80% of ED cases are actually caused by another medical or mental disorder.
Yes, your penile dysfunction issues are being brought on by medical illnesses like diabetes, high cholesterol, obesity, low blood pressure, heart disease, and low blood pressure.
In addition to this, issues with erectile dysfunction could also be brought on by poor mental health. This includes topics like stress, despair, and anxiety.
Find out if there are any problems. Inform the medical staff that you already experience ED symptoms every day so they can make an accurate diagnosis.
Use the right therapy to deal with this problem.
Beginning the appropriate ED treatment programs seems sense as the next step. You must take action to manage or treat your diabetes if that condition is the root of your erectile dysfunction. This requires following a low-sugar diet, exercising as recommended, getting insulin shots, and taking further steps.
Another such example is how common ED is among fat guys. Without a doubt, you are aware of what to do in this circumstance. Exercise and changing your diet to one that is far healthier require the majority of your attention.
You can utilize simple home remedies like changing your diet, exercising, or seeking medical attention to take extra medications that directly treat the issue.
Using ED medications
Now, if you already use ED drugs like Cenforce 100mg, keep taking them as prescribed by your doctor. Additionally, go visit a doctor right away if you haven’t already started taking prescription medication.
Avoid using ED medications at random, regardless of brand or dosage, as this could result in negative side effects. Only heed the advice of specialists when choosing the brand or dose that is right for you. Last but not least, always keep in mind to follow the guidelines when taking ED drugs to avoid negative side effects and contraindications.
Alternative Natural Remedies for Impotence
Addiction Prevention
You need to adjust your way of life, especially if drinking or using drugs is a factor in your penile problems.
The main causes of erectile dysfunction in males nowadays are alcoholism, drug addictions (such as the usage of cocaine or marijuana), and even smoking. You should engage in yoga and meditation to better control your emotions and the urge for such things.
Making Dietary Changes
Of course, what you eat has a big impact on your health. If you have erectile dysfunction, you must modify your diet, just like you would for any other condition. Consume foods low in fat and cholesterol to prevent heart disease, reduce obesity, and keep blood sugar levels stable.
Here is a list of foods you can choose from:
Veggies
Bok Choy Tomatoes
peppers that are red
Spaghetti kale
Fruits of the Cauliflower
Apples
Strawberries
Avocado
Watermelon
Eliminating Stress
Many men today suffer from erectile dysfunction due to mental diseases like stress, anxiety, depression, and others.
What then should we do? The solution in this case is to adopt better lives. Avoid addictions because they make the problem worse; exercise; go for a morning walk; talk to your wife and doctor about your problems; and consult with your family and friends.
Additionally, meditation and yoga are both quite effective. All of these actions can be taken while you are still taking your prescription-only Vidalista 20 mg Pills course.
Exercises to Treat Impotence
You can practice kegel exercises and other ED exercises to build the muscles in your bladder. With some jogging, cycling, and swimming added on top of this, it is anticipated that the utilization of Vidalista 40 capsules will decline.
Last Word
Everything you can do to prevent and treat your ED troubles has been covered in the section above. In a few months, if you apply these techniques, you should see gains.
Visit Site::Genericstrip.com
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4,804,793,159,128,873,000 | Failed Canthoplasty 8 Weeks Ago, No Results, Suggests Canthopexy?
I had a canthoplasty on my right eye 8 weeks ago to correct a mild ectropion after a lower blepharoplasty went wrong. During the last two weeks my eye has gone back down again and looks the same as it did before. I am going back to see the oculoplastic surgeon who performed my canthoplasty but not my blepharoplasty. He suggested I may need a canthopexy? I am very concerned about this as I do not want to go through another op that could fail or even make things worse. Please help what should do?
Doctor Answers 4
Lower eyelid retraction
If the lower eyelid is under tension (or tight), then a canthopexy or canthoplasty alone won't resolve the problem. The tension or tightness needs to be relieved also. Discuss with an oculoplastic surgeon.
Los Angeles Oculoplastic Surgeon
5.0 out of 5 stars 18 reviews
May need more aggressive surgery
Whether you have a canthoplasty or canthopexy [and these terms are often used interchangeably by some surgeons] they both involve tightening the eyelid, which may be counterproductive.
You may need lower eyelid retraction repair to help lengthen the eyelid vertically. This is done by grafting tissue [many different options available] to the backside of the eyelid.
Posting photos would be helpful for us to give you a better opinion.
If you decide to explore this further, I would recommend consultation with another ASOPRS trained Oculoplastics surgeon for a second opinion. You can find one close to you on the ASOPRS dot org website.
Good luck
A.J. Amadi, MD
Seattle Oculoplastic Surgeon
5.0 out of 5 stars 27 reviews
If a canthoplasty did not get the job done, a canthopexy won't either.
A cathopexy is a weaker version of a canthoplasty. A canthoplasty is a deep reconstruction of the lateral canthal angle. It is the strongest form of canthal surgery. The problem is most likely that the "mild ectropion" you have is a more profound structural issue than you and your most recent surgeon realize. A canthoplasty is not really capable of supporting the lower eyelid, which unfortunately is news to many canthal surgeons who rely on this as their go to tool for fixing lower eyelid malposition. Procedures that horizontally shorten the eyelid (canthopexy and canthoplasty) can actually make lower eyelid vertical inadequacy worse. This is because a shorter lower eyelid has to follow a shorter closed path along the surface of the eye. this will be lower on the eye surface forcing the lower eyelid margin further below the curvature of the eye. You did not provide a photograph of your situation. However I would not double down on the wrong surgery. Allow yourself to heal and consider getting additional opinions regarding the best way to improve your situation.
Kenneth D. Steinsapir, MD
Los Angeles Oculoplastic Surgeon
5.0 out of 5 stars 19 reviews
Lower eyelid retraction
A canthopexy may be beneficial to correct the lower eyelid retraction. I would discuss with your surgeon if in addition to the canthopexy a mucosal graft would help release the lower eyelid and avoid recurrent retraction.
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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-1,150,822,980,718,567,600 | melanoma
(redirected from amelanotic melanoma)
Also found in: Dictionary, Thesaurus, Medical.
Related to amelanotic melanoma: Nodular melanoma
melanoma:
see skin cancerskin cancer,
malignant tumor of the skin. The most common types of skin cancer are basal cell carcinoma, squamous cell carcinoma, and melanoma. Rarer forms include mycosis fungoides (a type of lymphoma) and Kaposi's sarcoma.
..... Click the link for more information.
.
Melanoma
melanoblastoma; a malignant tumor that consists of melanin-producing cells.
Factors conducive to the development of melanomas include injury and hormonal stimulation, especially during puberty. Melanomas generally occur on the skin; less often, they appear on the retina, pia mater, nasopharynx, larynx, esophagus, and mucosa of the intestine and other organs. Melanomas usually develop at the site of pigmented or depigmented birthmarks, but they may also appear elsewhere. The process starts with a barely perceptible, painless tumor on the skin, sometimes resembling a wart, which gradually becomes dark brown or black. Occasionally, it ulcerates and bleeds. In case of injury, the tumor may enlarge quickly and become tuberous, dense at the base, and stiffer. The regional lymph nodes enlarge. The initial signs that a melanoma is developing at the site of a birthmark are the birthmark’s enlargement, an intensification or reduction in its pigmentation, and the appearance of a red rim around it. Treatment involves prompt surgical intervention, based on early diagnosis, and the use of radiotherapy and drugs to retard the growth and reproduction of the cells.
I. IA. SHAKHTMEISTER
melanoma
[mel·ə′nō·mə]
(medicine)
A malignant tumor composed of anaplastic melanocytes.
A benign or malignant tumor composed of melanocytes.
melanoma
Pathol a malignant tumour composed of melanocytes, occurring esp in the skin, often as a result of excessive exposure to sunlight
References in periodicals archive ?
The framework then allowed the immunohistochemical diagnosis of metastatic amelanotic melanoma.
Development of cutaneus amelanotic melanoma in the absence of a functional tyrosinase.
Amelanotic melanoma may also be mistaken as a polyp if one is unaware of the entity.
An amelanotic melanoma appears similar to lymphoma, squamous cell carcinoma or other non-pigmented conditions, such as pyogenic granuloma, a conjunctival haematoma, a foreign body or argyrosis.
A potential clinical clue to the diagnosis of amelanotic melanoma may be the presence of a macular rim or spot of tan, gray, or brown pigmentation at the periphery of the lesion," Ms.
In the case of amelanotic melanoma or large melanoma that has broken through BruclTs membrane, the double circulation sign is noted (Figure 6).
A case of a secondary amelanotic melanoma of the epiglottis was reported by Ikeda et al in 1991.
The remaining four lesions included one amelanotic melanoma and three with none or only one of the ABC criteria.
All clinically suspected pyogenic granulomas must be biopsied to rule out other conditions, such as irritational fibroma, hemangioma, Kaposi's sarcoma, leiomyoma, amelanotic melanoma, basal metastatic carcinoma, and squamous cell carcinoma.
Epithelioid sarcomas are sometimes composed of spindle-shaped cells, and they may be confused with other malignant spindle-cell neoplasms, such as synovial sarcomas, fibrosarcomas, angiosarcomas, malignant fibrous histiocytomas, malignant extrarenal rhabdoid tumor, epithelioid hemangioendothelioma, and amelanotic melanoma.
Depending on the patient's age and the location of the tumor, the differential diagnosis includes malignant schwannoma, malignant fibrous histiocytoma, fibrosarcoma, amelanotic melanoma, malignant lymphoma, squamous cell carcinoma, extramedullary plasmacytoma, metastatic tumor, glandular tumor, chondroma, chondrosarcoma, osteogenic sarcoma, and inverted papilloma. | {
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7,646,067,895,097,215,000 | What Happens When People With PCOS Go Through Menopause?
PCOS affects people assigned female at birth who are of reproductive age. It is usually characterized by elevated androgen levels (androgens are male hormones), irregular menstruation, fertility difficulties, and multiple small cysts on the ovaries.
Menopause usually occurs between the ages of 45 and 55 when your hormone levels change and your periods stop. If you have PCOS, you might be wondering how menopause will affect you.
This article explains how PCOS affects menopause, including symptoms and complications.
Have you considered clinical trials for Polycystic ovarian syndrome (PCOS)?
We make it easy for you to participate in a clinical trial for Polycystic ovarian syndrome (PCOS), and get access to the latest treatments not yet widely available - and be a part of finding a cure.
What is PCOS, and how does it affect people who have it?
PCOS is an endocrine condition that impacts the entire body, especially the reproductive system. Endocrine refers to the glands and organs that make hormones, which are then released into your bloodstream.
The exact mechanism that underlies PCOS is unknown, but it is thought to be related to the ovaries and the balance of various hormones, including insulin, luteinizing hormone (LH), androgens, and follicle-stimulating hormone (FSH).
90% of people with PCOS have abnormal ovarian androgen function. 50% of these people also have obesity, excess LH, and insulin resistance with compensatory hyperinsulinemia. In insulin resistance, your body doesn’t respond to insulin normally. This affects how your cells use the glucose in your blood as energy.¹
PCOS symptoms and signs differ from person to person, and range from mild to severe. Common symptoms include the following:
• An irregular menstrual cycle
• Unexplained weight gain
• Fertility problems
• Cysts on the ovaries
• Excess hair growth (hirsutism)
• Hair loss
• Oily skin and acne
Periods in PCOS may occur on a longer or shorter cycle. They can also be absent altogether. Improperly developed eggs may not be released. In other words, ovulation might not occur, causing these retained “eggs” to form small cysts.
In PCOS, the ovaries produce too much androgen hormone. Having excess androgen hormone in your body is called hyperandrogenism.
Most PCOS symptoms that women find bothering, such as excessive hair growth (hirsutism), hair loss, and oily skin, are caused by hyperandrogenism.
PCOS and menopause: Hormonal changes
Women with PCOS tend to experience improved and more regular menstruation as they age closer to menopause. This tends to be a function of age-related androgen decline.²
However, research has found that androgen levels in women with PCOS remain higher than in people without the condition even after menopause (even though they may be in the normal range).
A study published in 2015 looked at androgen levels in women with PCOS of different ages before menopause. It found that the highest androgen levels were seen in the 18–39 age group and that levels decreased with age. Researchers noted that women experienced a more regular menstrual cycle as they aged, attributing this to ovarian aging and declining androgen levels.³
Researchers in this study also noticed that while androgen levels gradually declined in the lead-up to menopause, they increased thereafter (this varied greatly from person to person). However, the difference in androgen levels seen between those with PCOS and those without disappeared after adjustment for BMI, suggesting that there’s a strong link between obesity and hyperandrogenism.
A follow-up study of older women with PCOS aged 72–91 years found that mean androgen levels in the women studied did not differ from the control group (women of the same age without PCOS). This further indicates that androgen levels in women with PCOS normalize with age.⁴
Despite this, researchers also found that hirsutism, a clinical sign of hyperandrogenism, continued to be more prevalent in the women with PCOS than those without. This suggests that while androgen levels may normalize with age, the effects of hyperandrogenism may continue after menopause.
Do people with PCOS reach menopause at the same time as others?
Less is known about the age of menopause in PCOS. Although there is no consensus, some researchers have demonstrated that people with PCOS reach menopause slightly later than normal, ranging from 2–4 years later based on the calculation method used.⁵ ⁶
People with PCOS who have irregular periods may miss the early signs of perimenopause (the transition period around menopause). Infrequent periods are normal during perimenopause, and you will not have gone through menopause until you haven’t had a period for 12 months.
How PCOS affects menopause symptoms
Women with PCOS may continue to experience androgen-related symptoms during menopause, as their androgen levels are still higher than people unaffected by the condition. However, these symptoms will decline in line with falling androgen levels.
During menopause, women with PCOS tend to experience more severe vaginal dryness, which can cause pain during intercourse. This effect is thought to be androgen-related. One theory is that people with PCOS may have a higher libido during menopause compared to controls, meaning they are more likely to notice vaginal dryness.⁷ ⁸
Vaginal dryness can be treated by using an internal and/or external vaginal moisturizer. Internal moisturizers are inserted into the vagina, while external ones are for your vulva. You can also use a water-based lubricant when sexually active to ease discomfort.
Another treatment option is an estrogen cream or tablet inserted into the vagina or an estrogen-releasing vaginal ring. This does not carry the same risk as systemic hormone therapy.
Is it possible to diagnose PCOS during menopause?
PCOS may not be diagnosed in people who have already reached menopause for several reasons.
Diagnosis depends on different criteria. The most commonly accepted criteria are the Rotterdam Criteria. Using these criteria, your doctor will diagnose PCOS based on the presence of at least oligo ovulation (irregular or infrequent periods) and hyperandrogenism.
However, when you reach menopause, your androgen levels may normalize. This rules out hyperandrogenism as a criterion. Little to no noticeable increase in androgen can make diagnosis impossible.
Furthermore, as menopause is defined by ceased ovulation, you won’t have the oligo ovulation characteristic either.
PCOS complications and menopause
PCOS is known to increase the risk of long-term health complications, including cardiovascular disease, type 2 diabetes, obesity, endometrial cancers, and mental health conditions. However, more research is needed to understand whether this increased risk carries over to the timeframe after menopause.⁹
A 2011 study demonstrated that postmenopausal women with PCOS have higher levels of insulin resistance than those without PCOS. Insulin resistance can lead to type 2 diabetes, cardiovascular disease, and many other health complications.¹⁰
Higher C-reactive protein concentrations have also been noted in women with PCOS after menopause, correlating with the risk of cardiovascular disease, stroke, and heart attack.
A controlled follow-up study also identified a high prevalence of high blood pressure (hypertension) and high triglyceride levels (hypertriglyceridemia) in postmenopausal women with PCOS.¹¹
Of note, the study did not find increased risk of heart attack, stroke, diabetes, cancer, or excess mortality when controlled for BMI.
Looking after your health after menopause with PCOS
Research indicates that women with PCOS are at increased risk for health complications post-menopause, including type 2 diabetes and cardiovascular disease.¹²
Risk assessments for cardiovascular disease are recommended for people with PCOS at any age, involving assessment for blood pressure, waist circumference, BMI, cholesterol, blood glucose, cigarette smoking, family history of cardiovascular disease, depression, anxiety, and quality of life.
To reduce your risk of serious complications, be sure to attend all appointments with your doctor so that they can assess your health.
Your doctor will recommend steps to take to reduce your risk of developing these health problems. These may involve taking medications or making lifestyle changes.
The American Heart Association (AHA) recommends making healthy choices throughout life, not just when you reach menopause. The healthy choices they recommend include the following:¹³
• Consuming a healthy diet. Focus on your intake of fruits, vegetables, nuts, whole grains, lean vegetables, animal protein, and fish. You should minimize your intake of trans fats, red meat, processed red meats, sweetened drinks, and refined carbohydrates.
• Do enough exercise. For adults, AHA advises doing at least 150 minutes per week of moderate-intensity physical activity (accumulated; not all at once). You can also do 75 minutes per week of vigorous-intensity physical activity.
• Quit smoking cigarettes. Ask your doctor for help and guidance if quitting is difficult for you. There’s help available, including smoking cessation programs.
• Reduce your alcohol consumption. Moderate your alcohol consumption by sticking to one drink or less per day for women and two drinks per day or less for men on days when alcohol is consumed.
The lowdown
PCOS does not go away at menopause. It may also impact the symptoms experienced during perimenopause, with some (such as hot flashes) being less common and others (vaginal dryness) more so.
As people with PCOS already have increased androgen levels, their hormones do not change in quite the same way at menopause. Research indicates that androgen levels in people with PCOS normalize with age, but they still tend to be higher than in people without the condition.
Having PCOS increases your risk of serious health complications. Researchers have found that postmenopausal women with PCOS have higher levels of insulin resistance than control groups, increasing the risk of developing cardiovascular disease and type 2 diabetes.
Attend all your regular screening appointments and follow guidance on exercise and healthy eating to lower your risk of poor health later in life.
1. Current concepts of polycystic ovary syndrome pathogenesis (2020)
2. Consensus on women’s health aspects of polycystic ovary syndrome (PCOS): The Amsterdam ESHRE/ASRM-sponsored 3rd PCOS consensus workshop group (2011)
3. Androgen profile through life in women with polycystic ovary syndrome: A nordic multicenter collaboration study (2015)
4. Reproductive hormones and anthropometry: A follow-up of PCOS and controls from perimenopause to older than 80 years (2020)
5. Polycystic ovarian syndrome and menopause in forty plus women (2021)
6. Reproductive hormone levels and anthropometry in postmenopausal women with polycystic ovary syndrome (PCOS): A 21-year follow-up study of women diagnosed with PCOS around 50 years ago and their age-matched controls (2011)
7. Polycystic ovarian syndrome and menopause in forty plus women (2021)
8. Reproductive hormone levels and anthropometry in postmenopausal women with polycystic ovary syndrome (PCOS): A 21-year follow-up study of women diagnosed with PCOS around 50 years ago and their age-matched controls (2011)
9. Complications and challenges associated with polycystic ovary syndrome: Current perspectives (2015)
10. Unfavorable hormonal, metabolic, and inflammatory alterations persist after menopause in women with PCOS (2011)
11. Cardiovascular disease and risk factors in PCOS women of postmenopausal age: A 21-year controlled follow-up study (2011)
12. Complications and challenges associated with polycystic ovary syndrome: Current perspectives (2015)
13. 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease (2019)
Have you considered clinical trials for Polycystic ovarian syndrome (PCOS)?
We make it easy for you to participate in a clinical trial for Polycystic ovarian syndrome (PCOS), and get access to the latest treatments not yet widely available - and be a part of finding a cure.
Discover which clinical trials you are eligible for
Do you want to know if there are any Polycystic ovarian syndrome (PCOS) clinical trials you might be eligible for?
Have you taken medication for Polycystic ovarian syndrome (PCOS)?
Have you been diagnosed with Polycystic ovarian syndrome (PCOS)?
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6,765,437,060,993,749,000 | 0
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Can You Slim Down Your Neck?
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Can You Slim Down Your Neck?
Neck exercises can firm your neck muscles. Photo Credit Elena_Rudyk/iStock/Getty Images
Whether you blame genetics, aging, gravity, unhealthy eating habits, or lack of exercise, excess fat in your neck can impact your appearance. The good news: you can slim down your neck by making lifestyle changes that are maintainable long-term. This should include a sensible diet and regular exercise that trigger weight loss from your entire body. Spot reduction isn't possible; your neck will only slim down when your body slims down.
Calorie-Blasting Aerobic Exercise
Can You Slim Down Your Neck?
Play racquetball. Photo Credit robertprzybysz/iStock/Getty Images
Aerobic exercise, or cardio, burns calories and helps slim down your body including your neck. Doing up to 300 minutes of moderately intense cardio can do the trick, according to the U.S. Department of Health and Human Services. The more muscles you use during your cardio sessions the more calories you burn. Therefore, aim to engage both your upper and lower body. Swing your arms while jogging or walking fast, use a rowing machine, take a cardio-kickboxing class, play tennis or racquetball, or use an elliptical with handles that move.
Muscle-Building Resistance Training
Can You Slim Down Your Neck?
Lunge and exercises. Photo Credit Creatas Images/Creatas/Getty Images
Resistance training, or strength training, prevents the loss of muscle tissue, and increases muscle tissue. This promotes weight loss, because muscle sustains itself by using up a lot of calories; your increased resting metabolism burns calories all day long. Additionally, you'll look slimmer, because muscle takes up less space than fat. Work your large muscles twice a week for optimal results. Perform compound exercises, such as pushups, bench presses and deadlifts. Also include combination exercises, such as lunges with side laterals, step-ups with front raises, and squats with overhead presses.
Neck-Firming Targeted Exercises
Can You Slim Down Your Neck?
Target the neck with exercises. Photo Credit szefei/iStock/Getty Images
In addition to promoting neck flexibility, targeted exercises can firm the muscles responsible for bending, extending and rotating your head. These muscles include the sternocleidomastoid, and the splenius, semispinalis, spinalis, and longissimus capitis. Perform resistance exercises during which you push with your hand again the front, back or side or your head while moving your head against the resistance. For instance, push against your forehead with your hand and push your head forward. Rotating your head side to side, and tilting your head back and forth, and side to side, are also effective exercises. Complete five to 10 reps and three sets of each exercise.
Slimming Dietary Changes
Can You Slim Down Your Neck?
Eat small, healthy meals. Photo Credit George Doyle/Stockbyte/Getty Images
To lose one to two pounds a week, a daily deficit of 500 to 1,000 calories is needed. Although some of this can come from exercise, it can also partly come from your diet. Reducing portion sizes, and minimizing your intake of foods that are high in cholesterol, salt, sugar, and trans and saturated fats, can contribute, as can swapping out high-calorie foods for lower-calorie alternatives. Lean meats, nut, fish, poultry, fruits, veggies, whole grains, and reduced-fat dairy should be your go-to foods.
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4,415,412,876,047,749,000 | Genetic Variation at the ADAMTS7 Locus is Associated With Reduced Severity of Coronary Artery Disease.
BACKGROUND: Genome-wide association studies identified ADAMTS7 as a risk locus for coronary artery disease (CAD). Functional studies suggest that ADAMTS7 may promote cellular processes in atherosclerosis. We sought to examine the association between genetic variation at ADAMTS7 and measures of atherosclerosis using histological, angiographic, and clinical outcomes data. METHODS AND RESULTS: The lead CAD-associated single-nucleotide polymorphism rs3825807 at the ADAMTS7 locus was genotyped. The G allele (reduced ADAMTS7 function) was associated with a smaller fibrous cap (P=0.017) and a smaller percentage area of α-actin (smooth muscle cell marker) in the intima (P=0.017), but was not associated with calcification or plaque thickness, following ex vivo immunohistochemistry analysis of human coronary plaques (n=50; mean age 72.2±11.3). In two independent cohorts (Southampton Atherosclerosis Study [n=1359; mean age 62.5±10.3; 70.1% men] and the Emory Cardiovascular Biobank [EmCAB; n=2684; mean age 63.8±11.3; 68.7% men]), the G allele was associated with 16% to 19% lower odds of obstructive CAD (Southampton Atherosclerosis Study: odds ratio, 0.81; 95% confidence interval, 0.67-0.98; EmCAB: odds ratio, 0.84; 95% confidence interval, 0.75-0.95) with similar effects for multivessel, left anterior descending, and proximal CAD. Furthermore, each copy of the G allele was associated with lower angiographic severity Gensini score (Southampton Atherosclerosis Study, P=0.026; EmCAB, P<0.001), lower Sullivan Extent score (Southampton Atherosclerosis Study, P=0.029; EmCAB, P<0.001), and a 23% lower risk of incident revascularization procedures (EmCAB: hazard ratio, 0.76; 95% confidence interval, 0.59-0.98). There were no associations with all-cause mortality or incident myocardial infarction. CONCLUSIONS: Genetic variation at the ADAMTS7 locus is associated with several complementary CAD phenotypes, supporting the emerging role of ADAMTS7 in atherosclerosis and may represent a potential drug target. | {
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1,187,033,531,764,742,400 | 6 possible root causes of sciatica pain? Which one do you have? - Be My Healer
6 possible root causes of “sciatica” pain? Which one do you have?
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causes of sciatica pain
What "sciatica" is might not be mysterious these days. It is not hard to understand the concept of a compressed, or pinched nerve, causing pain, weakness, and weird sensations going down your leg. However, the causes of sciatica pain are not that simple.
sciatica pain sciatic nerve
First of all, "sciatica" is not all the same. Your "sciatica" pain could be drastically different than how your cousin experiences her "sciatica."It depends on the location of the nerve irritation. It also matters the types of irritation the sciatic nerve is undergoing. Even more, the chronicity of the root problem may also play a role in the treatment of this pain.
Then, sometimes we see true "sciatica" pain and fake "sciatica" pain. Typical true "sciatica" pain is felt from the back of the hip to the outer thigh, then to the outer calf, finally possibly to the big toe. Fake "sciatica" pain may sound or feel like the real thing. However, they are commonly caused by referred pain from mechanical problems in the lower back/ hip region.
What??!!!
I know. That's why "sciatica" pain is difficult to rid of. However, if you can isolate the possible pain generating problems, you can proceed with much more effective treatments.
True "Sciatica" pain causes
Acute Herniated disc injury
Herniated disc or bulging disc are the common cause of the sudden onset of "sciatica." As the lumbar disc content protrudes out of its usual place, it may press into the narrow canal where the nerves exit your spine, thus nerve compression. If the injured lumbar disc has tears and the fluid inner content leaks to the surrounding area, it may cause chemical irritation to the surrounding nerve root as well.
herniated disc and pinched nerve
Pain Pattern:
• "Sciatica" pain occurred at the same time as the lower back pain from the herniated disc injury, no sciatica prior to the disc injury
• Sciatica pain becomes more severe towards the end of the day
• Sciatica symptoms are usually single sided
• Sciatica symptoms should improve significantly as the lower back pain heals
Effective treatments:
Lumbar spinal stenosis
lumbar spinal stenosis sciatica
Stenosis refers to the closing or narrowing of the space where the nerves pass through. The most common cause of stenosis in the lower back is aging and arthritis, and degeneration. Another common cause is a repetitive injury from overuse. People in the labor industry may suffer from numerous work-related lower back injuries, resulting in chronic "sciatica" pain.
Another common and similar condition are called the degenerative disc disease. As the lumbar disc content tries out, the bony parts of the spinal collapse over each other, closing down spaces that used to be available for nerve tissues.
Pain Pattern:
• Gradual increase in "sciatica" symptom over the years
• More common is middle age to elderly individuals
• May cause bilateral "sciatica", leg pain on both side
• Worsening of symptom with prolong time on feet, relief when seated
• Tender buttocks or piriformis muscles secondary to chronic nerve irritation
• May or may be have obvious chronic lower back pain
Effective treatments:
• Professional deep tissue muscle release targeting the hip flexors, lower back and gluteus muscles and fascia, reducing compression in lower back
• Core muscle strengthening (such as abdominal and gluteus muscle strengthening) to improve lower body posture over time
• Frequent stretching and self release of piriformis muscles, hamstring muscles
• Severe conditions require invasive procesures and surgeries
Spondylolisthesis
spondylolisthesis
Spondylolisthesis, or "spondy", is a less common condition where one segment of your lumbar spine (usually L5) become loose and slip out of the spinal column. If this slippage is far and severe enough, it may cause nerve impingement.
Spondylolisthesis is categorized as developmental (found at birth, develops during childhood) or acquired from spinal degeneration, trauma or physical stress (eg, gymnastics, lifting weights). If you are relatively young, experiencing unexplained vague lower back pain with sciatica over a period of time, you should speak to your doctor. Spondylolisthesis can be identified with an x-ray.
Pain Pattern:
• This can happen to people at all ages
• May cause bilateral "sciatica" symptoms (both sides)
• Usually accompanied by vague pain across the lower back
Effective treatments:
• In mild cases, flexion based abdominal core exercises are beneficial
• Avoid extension based core exercises such as superman
• Professional deep tissue release of the hip flexor muscles in a non-extended position
• Severe cases requires surgical procedures
Piriformis Syndrome
piriformis_muscle syndrome compression of sciatic nerve
The piriformis syndrome is the only non-spine related true "sciatica" pain cause. The piriformis muscles are two triangular muscles deep inside your buttocks. they help to stabilize and rotate our hip joints.
What's special about these piriformis muscles are that they seat directly on top of the large sciatic nerve. In some people, the sciatic nerve travels through these muscles. When the piriformis muscles became overworked and tensed up, they apply direct pressure on the sciatic nerve, resulting in the "sciatica" symptoms.
Piriformis syndrome is common among runners and sports players. It can also happen to new runners, or office workers with weakened core muscles. Please note that dehydration and extreme diet combined with intense workout routines is also a common cause of "sciatica" pain and other health issues.
Pain Pattern:
• "Sciatic" symptoms with no lower back pain
• Tender to touch buttocks
• Symptom intensity with cardio works such as running, stair climbing or biking
• May also experience IT band or knee pain
Effective treatments:
• Professional deep tissue release to piriformis muscles, hamstring muscles, IT bands and gluteus medius muscles
• Frequent stretching of piriformis muscles and hamstring muscles
• Strengthening exercises such as clam shell, bridging, side walk with resistance, and proper squats.
• Proper balance between strengthening, resting, hydration and calorie intake
• Seated sciatic nerve glide exercises and targeted icing to the piriformis muscles
• Severe cases require anti-inflammatory medication injection
Other rear causes of true "sciatica" pain include spinal tumor and direct trauma to nerve tissues.
False "Sciatica" pain causes
Sacroiliac Joint Dysfunction
The sacroiliac joint dysfunction, or SI dysfunction, is a condition where the "tail bone" joints become unstable and irritated. An irritated SI joint can cause a lot of pain, especially when we shift body weight, such as lying to sitting, sitting to standing, jumping and basic moving around.
sacroiliac joint causes sciatica pain
Sometimes the pain is tender and sore over the area between lower back and buttocks. Other times, the SI pain can shoot down the leg, mimic a nerve pain. In rear cases, the SI irritation results in spreading inflammation, affecting nearby L5 nerve roots causing real nerve pain.
Pain Pattern:
• Sharp pain in SI joint region while performing transitional movements such as sit to stand, getting out of bed, stepping down, etc...
• Pain may shoot down back of leg, but does not get pass the knee
• No movements, no shooting pain
• SI belt reduce the symptoms
Effective treatments:
Gluteus medius and IT band pain
gluteus medius and IT band causes sciatica pain
Common soft tissue pains that mimic the "sciatica" are caused by trigger points in the gluteus medius muscles and the IT band. These muscles are frequently overused during intense sports and activities. Trigger points in these muscles will spread the pain over the hip and thigh area.
Pain Pattern:
• Aching pain over the hip, buttocks and outer thigh area
• Pain does not refer pass the knee
• No lower back pain, no tingling, numbness, weakness
• Pain improves once staying away from intense sports or activities
• Trigger points can be felt with massage
Effective treatments:
• Deep tissue massage to release trigger points in gluts and IT band
• Use Tennis ball or foam roller for trigger point release
• Use moist heating pad over the painful area for muscle relaxation and blood circulation
• Frequent stretching
• Proper balance between hydration, activities and resting
Thank you for reading, and I hope you find this post helpful.
Recommended readings:
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6,831,316,162,259,518,000 | non toxic – Wyndham Health http://www.wyndhamhealth.com Just Feel Better Mon, 16 Oct 2017 16:43:48 +0000 en-US hourly 1 https://wordpress.org/?v=4.8.2 Chemical Cosmetics Can Be Carcinogenic http://www.wyndhamhealth.com/chit-chat/chemical-cosmetics-can-be-carcinogenic.html/ http://www.wyndhamhealth.com/chit-chat/chemical-cosmetics-can-be-carcinogenic.html/#respond Wed, 16 Nov 2016 14:44:13 +0000 http://www.wyndhamhealth.com/?p=9705 I have mentioned in a previous article about chemicals in our cosmetics but I want to reiterate it here because it is really so important that you understand what you are putting on and into your body and what it can do to you. Almost 13000 chemicals are used in cosmetics and only 10% of […]
The post Chemical Cosmetics Can Be Carcinogenic appeared first on Wyndham Health.
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I have mentioned in a previous article about chemicals in our cosmetics but I want to reiterate it here because it is really so important that you understand what you are putting on and into your body and what it can do to you.
Almost 13000 chemicals are used in cosmetics and only 10% of them have been evaluated for safety. In the USA cosmetics are regulated by the US Food and Drug Administration but they don’t often exercise their authority. Here in the UK a company has to comply with The European Cosmetics Regulation 1223/2009, but it is up to the company to do that! So when you use deodorant, shampoo, body lotion or moisturiser you are taking a chance that you are applying harmful toxins to your body even if the product claims to be non-toxic and safe.
The average woman uses 12 personal care products and cosmetics on a daily basis and these contain 168 different chemicals according to the Environmental Working Group (EWG). Men use fewer products but are still exposed to 85 chemicals and teenagers use approximately 17 products and so are exposed to even more chemicals. The EWG tested teenagers to find out which chemicals from the products used were found in the body and they found 16 different hormone altering chemicals!
In another report ‘Heavy Metal Hazard: The Health Risks of Hidden Heavy Metals in Face Make-up’, the Environmental Defence tested 49 different make-up items such as foundations, concealers, powders, blushers, mascara, eyeliners, eye shadows, lipsticks and lip glosses. Their testing revealed serious heavy metal contamination in virtually all of the products from lead, thallium, cadmium, arsenic and beryllium.
In a study of more than 31,000 women in the US, those with higher levels of chemicals in their body were found to experience menopause 2-4 years earlier than those with fewer chemicals. An early menopause is associated with an early decline in ovarian function leading to early development of heart disease and osteoporosis.
Many of the chemicals mentioned in the study have already been linked to health risks, including cancer, metabolic syndrome, and early puberty.
Some of the most toxic chemicals found in many personal care products and cosmetics include:
Parabens has been shown to mimic the action of the female hormone eostrogen which can drive the growth of breast tumours, and a study published in 2012 suggested that parabens from antiperspirants and other cosmetics appear to increase the risk of breast cancer.
They looked at where tumours were appearing and found that there were higher concentrations of parabens in the upper quadrants of the breast and axillary area where anti-perspirants were usually applied.
Other cosmetics that contain paraben are hair products and lotions.
Sodium Lauryl Sulphate is used in many industrial cleaners as well as thousands of cosmetics. It is a surfactant, detergent and emulsifier. And due to its ability to ‘soap’ up the products it is used in most shampoos, shower gels, toothpastes, soaps, cleansers, laundry detergents. Also hair colours and bleaching agents, make-up foundations, bath oils and bath salts.
Another big problem with Sodium Lauryl Sulphate is that in the manufacturing process it becomes contaminated with 1,4 dioxane, a carcinogenic byproduct.
Phthalates are plasticising ingredients that have been linked to birth defects in the reproductive system of boys, and lower sperm-motility in adult men, among other problems. Be aware that phthalates are often hidden on shampoo labels under the generic term ‘fragrance.’
Methylisothiazolinone (MIT) is a chemical used in shampoos to prevent bacteria from developing and can affect the nervous system.
Toluene is made from petroleum or coal tar and found in most synthetic fragrances. Chronic exposure is linked to anaemia, lowered blood cell count, liver and kidney damage and can even affect a developing foetus.
Have a look at my other article for further information: Toxic Chemicals in our Cosmetics
So what can you do to avoid these chemicals and look after your body. One of the companies that I use for my skin care is totally organic, vegan, and cruelty free and you could almost eat the products. They are so luxurious and smell out of this world!
The other company I use also has some wonderful products all chemical free, and great for different skin types.
Do beware of products boasting ‘all natural’ on their labels because they can still have harmful chemicals. Remember your skin is your largest and most permeable organ and anything that you put on your skin will end up in your blood stream and be distributed around your body. The chemicals then accumulate over time because you do not have the enzymes to break them down and the liver has to deal with them. However if you have 168 different chemicals the liver will struggle and it won’t be able to detox the body as it should, resulting in toxic build up and ill health.
If you would like to know more about the products that are chemical free, straight from nature and quite beautiful, ring the centre to find out when the next ‘pamper’ evening is on 01462 893586.
The post Chemical Cosmetics Can Be Carcinogenic appeared first on Wyndham Health.
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-237,980,300,606,856,960 | fbpx
The Healing Power of Hyperbaric Oxygen Therapy (HBOT) for Wound Care: A Focus on Diabetic Foot Ulcers
Wound care is a critical aspect of healthcare, especially for individuals with chronic conditions like diabetes. Among the various treatments available, Hyperbaric Oxygen Therapy (HBOT) has emerged as a powerful and effective option. This therapy, which involves breathing pure oxygen in a pressurized chamber, can significantly enhance the body’s natural healing processes. In this blog, we will explore the benefits of HBOT for wound care, with a particular focus on diabetic foot ulcers, and discuss insurance considerations for this therapy.
Understanding Hyperbaric Oxygen Therapy (HBOT)
Hyperbaric Oxygen Therapy is a medical treatment that delivers 100% oxygen to a patient’s lungs while they are inside a pressurized chamber. This increase in oxygen levels allows more oxygen to dissolve in the blood plasma, enhancing oxygen delivery to tissues throughout the body. This process accelerates healing, reduces inflammation, and fights infection.
The Benefits of HBOT for Wound Care
HBOT has shown significant promise in treating various types of wounds, including:
1. Enhanced Healing
• Increased Oxygenation: HBOT increases oxygen delivery to hypoxic (low oxygen) tissues, which is critical for healing.
• Angiogenesis: The formation of new blood vessels is stimulated, improving blood flow to the affected area.
• Collagen Production: HBOT promotes collagen synthesis, which is essential for wound repair.
2. Reduced Inflammation
• Anti-inflammatory Effects: HBOT reduces swelling and inflammation, helping to manage pain and promote healing.
3. Infection Control
• Bacterial Reduction: The high oxygen environment enhances the effectiveness of white blood cells and has a bactericidal effect, helping to fight infection.
HBOT and Diabetic Foot Ulcers
Diabetic foot ulcers are a common and serious complication of diabetes, often leading to prolonged hospital stays and even amputation if not properly managed. HBOT offers a promising solution for these challenging wounds.
1. Promoting Wound Healing
• Improved Blood Flow: Diabetes often impairs blood flow, particularly to the extremities. HBOT helps by stimulating angiogenesis and improving circulation.
• Enhanced Tissue Repair: The increased oxygen levels promote faster and more effective tissue repair.
2. Combating Infection
• Oxygen-Rich Environment: Many bacteria that infect diabetic ulcers are anaerobic, meaning they thrive in low oxygen environments. HBOT creates an oxygen-rich environment that inhibits these bacteria and enhances the body’s immune response.
3. Reducing Amputation Rates
• Preventing Severe Complications: By effectively treating diabetic foot ulcers, HBOT can reduce the need for amputations and improve overall quality of life for diabetic patients.
Conclusion
Hyperbaric Oxygen Therapy offers significant benefits for wound care, particularly for diabetic foot ulcers. By enhancing oxygen delivery to tissues, reducing inflammation, and combating infection, HBOT can accelerate healing and improve patient outcomes.
If you or a loved one are struggling with chronic wounds, contact Hyperbaric Health and speak with your medical team to determine if this innovative therapy is right for you. With the right treatment and support, you can take significant steps toward healing and improved quality of life. | {
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-6,948,489,874,819,486,000 | JoVE Visualize What is visualize?
Related JoVE Video
Pubmed Article
Designing anti-influenza aptamers: novel quantitative structure activity relationship approach gives insights into aptamer-virus interaction.
PLoS ONE
PUBLISHED: 01-01-2014
This study describes the development of aptamers as a therapy against influenza virus infection. Aptamers are oligonucleotides (like ssDNA or RNA) that are capable of binding to a variety of molecular targets with high affinity and specificity. We have studied the ssDNA aptamer BV02, which was designed to inhibit influenza infection by targeting the hemagglutinin viral protein, a protein that facilitates the first stage of the virus' infection. While testing other aptamers and during lead optimization, we realized that the dominant characteristics that determine the aptamer's binding to the influenza virus may not necessarily be sequence-specific, as with other known aptamers, but rather depend on general 2D structural motifs. We adopted QSAR (quantitative structure activity relationship) tool and developed computational algorithm that correlate six calculated structural and physicochemical properties to the aptamers' binding affinity to the virus. The QSAR study provided us with a predictive tool of the binding potential of an aptamer to the influenza virus. The correlation between the calculated and actual binding was R2?=?0.702 for the training set, and R2?=?0.66 for the independent test set. Moreover, in the test set the model's sensitivity was 89%, and the specificity was 87%, in selecting aptamers with enhanced viral binding. The most important properties that positively correlated with the aptamer's binding were the aptamer length, 2D-loops and repeating sequences of C nucleotides. Based on the structure-activity study, we have managed to produce aptamers having viral affinity that was more than 20 times higher than that of the original BV02 aptamer. Further testing of influenza infection in cell culture and animal models yielded aptamers with 10 to 15 times greater anti-viral activity than the BV02 aptamer. Our insights concerning the mechanism of action and the structural and physicochemical properties that govern the interaction with the influenza virus are discussed.
Authors: Jiehua Zhou, Haitang Li, Jane Zhang, Swiderski Piotr, John Rossi.
Published: 06-23-2011
ABSTRACT
The global epidemic of infection by HIV has created an urgent need for new classes of antiretroviral agents. The potent ability of small interfering (si)RNAs to inhibit the expression of complementary RNA transcripts is being exploited as a new class of therapeutics for a variety of diseases including HIV. Many previous reports have shown that novel RNAi-based anti-HIV/AIDS therapeutic strategies have considerable promise; however, a key obstacle to the successful therapeutic application and clinical translation of siRNAs is efficient delivery. Particularly, considering the safety and efficacy of RNAi-based therapeutics, it is highly desirable to develop a targeted intracellular siRNA delivery approach to specific cell populations or tissues. The HIV-1 gp120 protein, a glycoprotein envelope on the surface of HIV-1, plays an important role in viral entry into CD4 cells. The interaction of gp120 and CD4 that triggers HIV-1 entry and initiates cell fusion has been validated as a clinically relevant anti-viral strategy for drug discovery. Herein, we firstly discuss the selection and identification of 2'-F modified anti-HIV gp120 RNA aptamers. Using a conventional nitrocellulose filter SELEX method, several new aptamers with nanomolar affinity were isolated from a 50 random nt RNA library. In order to successfully obtain bound species with higher affinity, the selection stringency is carefully controlled by adjusting the conditions. The selected aptamers can specifically bind and be rapidly internalized into cells expressing the HIV-1 envelope protein. Additionally, the aptamers alone can neutralize HIV-1 infectivity. Based upon the best aptamer A-1, we also create a novel dual inhibitory function anti-gp120 aptamer-siRNA chimera in which both the aptamer and the siRNA portions have potent anti-HIV activities. Further, we utilize the gp120 aptamer-siRNA chimeras for cell-type specific delivery of the siRNA into HIV-1 infected cells. This dual function chimera shows considerable potential for combining various nucleic acid therapeutic agents (aptamer and siRNA) in suppressing HIV-1 infection, making the aptamer-siRNA chimeras attractive therapeutic candidates for patients failing highly active antiretroviral therapy (HAART).
16 Related JoVE Articles!
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Primer-Free Aptamer Selection Using A Random DNA Library
Authors: Weihua Pan, Ping Xin, Susan Patrick, Stacey Dean, Christine Keating, Gary Clawson.
Institutions: Pennsylvania State University, Pennsylvania State University, Pennsylvania State University, Pennsylvania State University.
Aptamers are highly structured oligonucleotides (DNA or RNA) that can bind to targets with affinities comparable to antibodies 1. They are identified through an in vitro selection process called Systematic Evolution of Ligands by EXponential enrichment (SELEX) to recognize a wide variety of targets, from small molecules to proteins and other macromolecules 2-4. Aptamers have properties that are well suited for in vivo diagnostic and/or therapeutic applications: Besides good specificity and affinity, they are easily synthesized, survive more rigorous processing conditions, they are poorly immunogenic, and their relatively small size can result in facile penetration of tissues. Aptamers that are identified through the standard SELEX process usually comprise ~80 nucleotides (nt), since they are typically selected from nucleic acid libraries with ~40 nt long randomized regions plus fixed primer sites of ~20 nt on each side. The fixed primer sequences thus can comprise nearly ~50% of the library sequences, and therefore may positively or negatively compromise identification of aptamers in the selection process 3, although bioinformatics approaches suggest that the fixed sequences do not contribute significantly to aptamer structure after selection 5. To address these potential problems, primer sequences have been blocked by complementary oligonucleotides or switched to different sequences midway during the rounds of SELEX 6, or they have been trimmed to 6-9 nt 7, 8. Wen and Gray 9 designed a primer-free genomic SELEX method, in which the primer sequences were completely removed from the library before selection and were then regenerated to allow amplification of the selected genomic fragments. However, to employ the technique, a unique genomic library has to be constructed, which possesses limited diversity, and regeneration after rounds of selection relies on a linear reamplification step. Alternatively, efforts to circumvent problems caused by fixed primer sequences using high efficiency partitioning are met with problems regarding PCR amplification 10. We have developed a primer-free (PF) selection method that significantly simplifies SELEX procedures and effectively eliminates primer-interference problems 11, 12. The protocols work in a straightforward manner. The central random region of the library is purified without extraneous flanking sequences and is bound to a suitable target (for example to a purified protein or complex mixtures such as cell lines). Then the bound sequences are obtained, reunited with flanking sequences, and re-amplified to generate selected sub-libraries. As an example, here we selected aptamers to S100B, a protein marker for melanoma. Binding assays showed Kd s in the 10-7 - 10-8 M range after a few rounds of selection, and we demonstrate that the aptamers function effectively in a sandwich binding format.
Cellular Biology, Issue 41, aptamer, selection, S100B, sandwich
2039
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Selection of Aptamers for Amyloid β-Protein, the Causative Agent of Alzheimer's Disease
Authors: Farid Rahimi, Gal Bitan.
Institutions: David Geffen School of Medicine, University of California, Los Angeles, University of California, Los Angeles.
Alzheimer's disease (AD) is a progressive, age-dependent, neurodegenerative disorder with an insidious course that renders its presymptomatic diagnosis difficult1. Definite AD diagnosis is achieved only postmortem, thus establishing presymptomatic, early diagnosis of AD is crucial for developing and administering effective therapies2,3. Amyloid β-protein (Aβ) is central to AD pathogenesis. Soluble, oligomeric Aβ assemblies are believed to affect neurotoxicity underlying synaptic dysfunction and neuron loss in AD4,5. Various forms of soluble Aβ assemblies have been described, however, their interrelationships and relevance to AD etiology and pathogenesis are complex and not well understood6. Specific molecular recognition tools may unravel the relationships amongst Aβ assemblies and facilitate detection and characterization of these assemblies early in the disease course before symptoms emerge. Molecular recognition commonly relies on antibodies. However, an alternative class of molecular recognition tools, aptamers, offers important advantages relative to antibodies7,8. Aptamers are oligonucleotides generated by in-vitro selection: systematic evolution of ligands by exponential enrichment (SELEX)9,10. SELEX is an iterative process that, similar to Darwinian evolution, allows selection, amplification, enrichment, and perpetuation of a property, e.g., avid, specific, ligand binding (aptamers) or catalytic activity (ribozymes and DNAzymes). Despite emergence of aptamers as tools in modern biotechnology and medicine11, they have been underutilized in the amyloid field. Few RNA or ssDNA aptamers have been selected against various forms of prion proteins (PrP)12-16. An RNA aptamer generated against recombinant bovine PrP was shown to recognize bovine PrP-β17, a soluble, oligomeric, β-sheet-rich conformational variant of full-length PrP that forms amyloid fibrils18. Aptamers generated using monomeric and several forms of fibrillar β2-microglobulin (β2m) were found to bind fibrils of certain other amyloidogenic proteins besides β2m fibrils19. Ylera et al. described RNA aptamers selected against immobilized monomeric Aβ4020. Unexpectedly, these aptamers bound fibrillar Aβ40. Altogether, these data raise several important questions. Why did aptamers selected against monomeric proteins recognize their polymeric forms? Could aptamers against monomeric and/or oligomeric forms of amyloidogenic proteins be obtained? To address these questions, we attempted to select aptamers for covalently-stabilized oligomeric Aβ4021 generated using photo-induced cross-linking of unmodified proteins (PICUP)22,23. Similar to previous findings17,19,20, these aptamers reacted with fibrils of Aβ and several other amyloidogenic proteins likely recognizing a potentially common amyloid structural aptatope21. Here, we present the SELEX methodology used in production of these aptamers21.
Neuroscience, Issue 39, Cellular Biology, Aptamer, RNA, amyloid β-protein, oligomer, amyloid fibrils, protein assembly
1955
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Quantitative Analyses of all Influenza Type A Viral Hemagglutinins and Neuraminidases using Universal Antibodies in Simple Slot Blot Assays
Authors: Caroline Gravel, Changgui Li, Junzhi Wang, Anwar M Hashem, Bozena Jaentschke, Gary Van Domselaar, Runtao He, Xuguang Li.
Institutions: Health canada, The State Food and Drug Administration, Beijing, University of Ottawa, King Abdulaziz University, Public Health Agency of Canada.
Hemagglutinin (HA) and neuraminidase (NA) are two surface proteins of influenza viruses which are known to play important roles in the viral life cycle and the induction of protective immune responses1,2. As the main target for neutralizing antibodies, HA is currently used as the influenza vaccine potency marker and is measured by single radial immunodiffusion (SRID)3. However, the dependence of SRID on the availability of the corresponding subtype-specific antisera causes a minimum of 2-3 months delay for the release of every new vaccine. Moreover, despite evidence that NA also induces protective immunity4, the amount of NA in influenza vaccines is not yet standardized due to a lack of appropriate reagents or analytical method5. Thus, simple alternative methods capable of quantifying HA and NA antigens are desirable for rapid release and better quality control of influenza vaccines. Universally conserved regions in all available influenza A HA and NA sequences were identified by bioinformatics analyses6-7. One sequence (designated as Uni-1) was identified in the only universally conserved epitope of HA, the fusion peptide6, while two conserved sequences were identified in neuraminidases, one close to the enzymatic active site (designated as HCA-2) and the other close to the N-terminus (designated as HCA-3)7. Peptides with these amino acid sequences were synthesized and used to immunize rabbits for the production of antibodies. The antibody against the Uni-1 epitope of HA was able to bind to 13 subtypes of influenza A HA (H1-H13) while the antibodies against the HCA-2 and HCA-3 regions of NA were capable of binding all 9 NA subtypes. All antibodies showed remarkable specificity against the viral sequences as evidenced by the observation that no cross-reactivity to allantoic proteins was detected. These universal antibodies were then used to develop slot blot assays to quantify HA and NA in influenza A vaccines without the need for specific antisera7,8. Vaccine samples were applied onto a PVDF membrane using a slot blot apparatus along with reference standards diluted to various concentrations. For the detection of HA, samples and standard were first diluted in Tris-buffered saline (TBS) containing 4M urea while for the measurement of NA they were diluted in TBS containing 0.01% Zwittergent as these conditions significantly improved the detection sensitivity. Following the detection of the HA and NA antigens by immunoblotting with their respective universal antibodies, signal intensities were quantified by densitometry. Amounts of HA and NA in the vaccines were then calculated using a standard curve established with the signal intensities of the various concentrations of the references used. Given that these antibodies bind to universal epitopes in HA or NA, interested investigators could use them as research tools in immunoassays other than the slot blot only.
Immunology, Issue 50, Virology, influenza, hemagglutinin, neuraminidase, quantification, universal antibody
2784
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Generation of Recombinant Influenza Virus from Plasmid DNA
Authors: Luis Martínez-Sobrido, Adolfo García-Sastre.
Institutions: University of Rochester School of Medicine and Dentistry, Mount Sinai School of Medicine .
Efforts by a number of influenza research groups have been pivotal in the development and improvement of influenza A virus reverse genetics. Originally established in 1999 1,2 plasmid-based reverse genetic techniques to generate recombinant viruses have revolutionized the influenza research field because specific questions have been answered by genetically engineered, infectious, recombinant influenza viruses. Such studies include virus replication, function of viral proteins, the contribution of specific mutations in viral proteins in viral replication and/or pathogenesis and, also, viral vectors using recombinant influenza viruses expressing foreign proteins 3.
Microbiology, Issue 42, influenza viruses, plasmid transfection, recombinant virus, reverse genetics techniques, HA assay
2057
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Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells
Authors: Geoffrey P. Chase, Martin Schwemmle.
Institutions: Universitätsklinikum Freiburg.
Like all negative-strand RNA viruses, the genome of influenza viruses is packaged in the form of viral ribonucleoprotein complexes (vRNP), in which the single-stranded genome is encapsidated by the nucleoprotein (NP), and associated with the trimeric polymerase complex consisting of the PA, PB1, and PB2 subunits. However, in contrast to most RNA viruses, influenza viruses perform viral RNA synthesis in the nuclei of infected cells. Interestingly, viral mRNA synthesis uses cellular pre-mRNAs as primers, and it has been proposed that this process takes place on chromatin1. Interactions between the viral polymerase and the host RNA polymerase II, as well as between NP and host nucleosomes have also been characterized1,2. Recently, the generation of recombinant influenza viruses encoding a One-Strep-Tag genetically fused to the C-terminus of the PB2 subunit of the viral polymerase (rWSN-PB2-Strep3) has been described. These recombinant viruses allow the purification of PB2-containing complexes, including vRNPs, from infected cells. To obtain purified vRNPs, cell cultures are infected, and vRNPs are affinity purified from lysates derived from these cells. However, the lysis procedures used to date have been based on one-step detergent lysis, which, despite the presence of a general nuclease, often extract chromatin-bound material only inefficiently. Our preliminary work suggested that a large portion of nuclear vRNPs were not extracted during traditional cell lysis, and therefore could not be affinity purified. To increase this extraction efficiency, and to separate chromatin-bound from non-chromatin-bound nuclear vRNPs, we adapted a step-wise subcellular extraction protocol to influenza virus-infected cells. Briefly, this procedure first separates the nuclei from the cell and then extracts soluble nuclear proteins (here termed the "nucleoplasmic" fraction). The remaining insoluble nuclear material is then digested with Benzonase, an unspecific DNA/RNA nuclease, followed by two salt extraction steps: first using 150 mM NaCl (termed "ch150"), then 500 mM NaCl ("ch500") (Fig. 1). These salt extraction steps were chosen based on our observation that 500 mM NaCl was sufficient to solubilize over 85% of nuclear vRNPs yet still allow binding of tagged vRNPs to the affinity matrix. After subcellular fractionation of infected cells, it is possible to affinity purify PB2-tagged vRNPs from each individual fraction and analyze their protein and RNA components using Western Blot and primer extension, respectively. Recently, we utilized this method to discover that vRNP export complexes form during late points after infection on the chromatin fraction extracted with 500 mM NaCl (ch500)3.
Virology, Issue 64, Immunology, Molecular Biology, Influenza A virus, affinity purification, subcellular fractionation, chromatin, vRNP complexes, polymerase
4028
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A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
Authors: Daniel T. Claiborne, Jessica L. Prince, Eric Hunter.
Institutions: Emory University, Emory University.
The protective effect of many HLA class I alleles on HIV-1 pathogenesis and disease progression is, in part, attributed to their ability to target conserved portions of the HIV-1 genome that escape with difficulty. Sequence changes attributed to cellular immune pressure arise across the genome during infection, and if found within conserved regions of the genome such as Gag, can affect the ability of the virus to replicate in vitro. Transmission of HLA-linked polymorphisms in Gag to HLA-mismatched recipients has been associated with reduced set point viral loads. We hypothesized this may be due to a reduced replication capacity of the virus. Here we present a novel method for assessing the in vitro replication of HIV-1 as influenced by the gag gene isolated from acute time points from subtype C infected Zambians. This method uses restriction enzyme based cloning to insert the gag gene into a common subtype C HIV-1 proviral backbone, MJ4. This makes it more appropriate to the study of subtype C sequences than previous recombination based methods that have assessed the in vitro replication of chronically derived gag-pro sequences. Nevertheless, the protocol could be readily modified for studies of viruses from other subtypes. Moreover, this protocol details a robust and reproducible method for assessing the replication capacity of the Gag-MJ4 chimeric viruses on a CEM-based T cell line. This method was utilized for the study of Gag-MJ4 chimeric viruses derived from 149 subtype C acutely infected Zambians, and has allowed for the identification of residues in Gag that affect replication. More importantly, the implementation of this technique has facilitated a deeper understanding of how viral replication defines parameters of early HIV-1 pathogenesis such as set point viral load and longitudinal CD4+ T cell decline.
Infectious Diseases, Issue 90, HIV-1, Gag, viral replication, replication capacity, viral fitness, MJ4, CEM, GXR25
51506
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Expression of Functional Recombinant Hemagglutinin and Neuraminidase Proteins from the Novel H7N9 Influenza Virus Using the Baculovirus Expression System
Authors: Irina Margine, Peter Palese, Florian Krammer.
Institutions: Icahn School of Medicine at Mount Sinai, Icahn School of Medicine at Mount Sinai, Icahn School of Medicine at Mount Sinai.
The baculovirus expression system is a powerful tool for expression of recombinant proteins. Here we use it to produce correctly folded and glycosylated versions of the influenza A virus surface glycoproteins - the hemagglutinin (HA) and the neuraminidase (NA). As an example, we chose the HA and NA proteins expressed by the novel H7N9 virus that recently emerged in China. However the protocol can be easily adapted for HA and NA proteins expressed by any other influenza A and B virus strains. Recombinant HA (rHA) and NA (rNA) proteins are important reagents for immunological assays such as ELISPOT and ELISA, and are also in wide use for vaccine standardization, antibody discovery, isolation and characterization. Furthermore, recombinant NA molecules can be used to screen for small molecule inhibitors and are useful for characterization of the enzymatic function of the NA, as well as its sensitivity to antivirals. Recombinant HA proteins are also being tested as experimental vaccines in animal models, and a vaccine based on recombinant HA was recently licensed by the FDA for use in humans. The method we describe here to produce these molecules is straight forward and can facilitate research in influenza laboratories, since it allows for production of large amounts of proteins fast and at a low cost. Although here we focus on influenza virus surface glycoproteins, this method can also be used to produce other viral and cellular surface proteins.
Infection, Issue 81, Influenza A virus, Orthomyxoviridae Infections, Influenza, Human, Influenza in Birds, Influenza Vaccines, hemagglutinin, neuraminidase, H7N9, baculovirus, insect cells, recombinant protein expression
51112
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Optimization and Utilization of Agrobacterium-mediated Transient Protein Production in Nicotiana
Authors: Moneim Shamloul, Jason Trusa, Vadim Mett, Vidadi Yusibov.
Institutions: Fraunhofer USA Center for Molecular Biotechnology.
Agrobacterium-mediated transient protein production in plants is a promising approach to produce vaccine antigens and therapeutic proteins within a short period of time. However, this technology is only just beginning to be applied to large-scale production as many technological obstacles to scale up are now being overcome. Here, we demonstrate a simple and reproducible method for industrial-scale transient protein production based on vacuum infiltration of Nicotiana plants with Agrobacteria carrying launch vectors. Optimization of Agrobacterium cultivation in AB medium allows direct dilution of the bacterial culture in Milli-Q water, simplifying the infiltration process. Among three tested species of Nicotiana, N. excelsiana (N. benthamiana × N. excelsior) was selected as the most promising host due to the ease of infiltration, high level of reporter protein production, and about two-fold higher biomass production under controlled environmental conditions. Induction of Agrobacterium harboring pBID4-GFP (Tobacco mosaic virus-based) using chemicals such as acetosyringone and monosaccharide had no effect on the protein production level. Infiltrating plant under 50 to 100 mbar for 30 or 60 sec resulted in about 95% infiltration of plant leaf tissues. Infiltration with Agrobacterium laboratory strain GV3101 showed the highest protein production compared to Agrobacteria laboratory strains LBA4404 and C58C1 and wild-type Agrobacteria strains at6, at10, at77 and A4. Co-expression of a viral RNA silencing suppressor, p23 or p19, in N. benthamiana resulted in earlier accumulation and increased production (15-25%) of target protein (influenza virus hemagglutinin).
Plant Biology, Issue 86, Agroinfiltration, Nicotiana benthamiana, transient protein production, plant-based expression, viral vector, Agrobacteria
51204
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High-throughput Detection Method for Influenza Virus
Authors: Pawan Kumar, Allison E. Bartoszek, Thomas M. Moran, Jack Gorski, Sanjib Bhattacharyya, Jose F. Navidad, Monica S. Thakar, Subramaniam Malarkannan.
Institutions: Blood Research Institute, Mount Sinai School of Medicine , Blood Research Institute, City of Milwaukee Health Department Laboratory, Medical College of Wisconsin , Medical College of Wisconsin .
Influenza virus is a respiratory pathogen that causes a high degree of morbidity and mortality every year in multiple parts of the world. Therefore, precise diagnosis of the infecting strain and rapid high-throughput screening of vast numbers of clinical samples is paramount to control the spread of pandemic infections. Current clinical diagnoses of influenza infections are based on serologic testing, polymerase chain reaction, direct specimen immunofluorescence and cell culture 1,2. Here, we report the development of a novel diagnostic technique used to detect live influenza viruses. We used the mouse-adapted human A/PR/8/34 (PR8, H1N1) virus 3 to test the efficacy of this technique using MDCK cells 4. MDCK cells (104 or 5 x 103 per well) were cultured in 96- or 384-well plates, infected with PR8 and viral proteins were detected using anti-M2 followed by an IR dye-conjugated secondary antibody. M2 5 and hemagglutinin 1 are two major marker proteins used in many different diagnostic assays. Employing IR-dye-conjugated secondary antibodies minimized the autofluorescence associated with other fluorescent dyes. The use of anti-M2 antibody allowed us to use the antigen-specific fluorescence intensity as a direct metric of viral quantity. To enumerate the fluorescence intensity, we used the LI-COR Odyssey-based IR scanner. This system uses two channel laser-based IR detections to identify fluorophores and differentiate them from background noise. The first channel excites at 680 nm and emits at 700 nm to help quantify the background. The second channel detects fluorophores that excite at 780 nm and emit at 800 nm. Scanning of PR8-infected MDCK cells in the IR scanner indicated a viral titer-dependent bright fluorescence. A positive correlation of fluorescence intensity to virus titer starting from 102-105 PFU could be consistently observed. Minimal but detectable positivity consistently seen with 102-103 PFU PR8 viral titers demonstrated the high sensitivity of the near-IR dyes. The signal-to-noise ratio was determined by comparing the mock-infected or isotype antibody-treated MDCK cells. Using the fluorescence intensities from 96- or 384-well plate formats, we constructed standard titration curves. In these calculations, the first variable is the viral titer while the second variable is the fluorescence intensity. Therefore, we used the exponential distribution to generate a curve-fit to determine the polynomial relationship between the viral titers and fluorescence intensities. Collectively, we conclude that IR dye-based protein detection system can help diagnose infecting viral strains and precisely enumerate the titer of the infecting pathogens.
Immunology, Issue 60, Influenza virus, Virus titer, Epithelial cells
3623
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Protein WISDOM: A Workbench for In silico De novo Design of BioMolecules
Authors: James Smadbeck, Meghan B. Peterson, George A. Khoury, Martin S. Taylor, Christodoulos A. Floudas.
Institutions: Princeton University.
The aim of de novo protein design is to find the amino acid sequences that will fold into a desired 3-dimensional structure with improvements in specific properties, such as binding affinity, agonist or antagonist behavior, or stability, relative to the native sequence. Protein design lies at the center of current advances drug design and discovery. Not only does protein design provide predictions for potentially useful drug targets, but it also enhances our understanding of the protein folding process and protein-protein interactions. Experimental methods such as directed evolution have shown success in protein design. However, such methods are restricted by the limited sequence space that can be searched tractably. In contrast, computational design strategies allow for the screening of a much larger set of sequences covering a wide variety of properties and functionality. We have developed a range of computational de novo protein design methods capable of tackling several important areas of protein design. These include the design of monomeric proteins for increased stability and complexes for increased binding affinity. To disseminate these methods for broader use we present Protein WISDOM (http://www.proteinwisdom.org), a tool that provides automated methods for a variety of protein design problems. Structural templates are submitted to initialize the design process. The first stage of design is an optimization sequence selection stage that aims at improving stability through minimization of potential energy in the sequence space. Selected sequences are then run through a fold specificity stage and a binding affinity stage. A rank-ordered list of the sequences for each step of the process, along with relevant designed structures, provides the user with a comprehensive quantitative assessment of the design. Here we provide the details of each design method, as well as several notable experimental successes attained through the use of the methods.
Genetics, Issue 77, Molecular Biology, Bioengineering, Biochemistry, Biomedical Engineering, Chemical Engineering, Computational Biology, Genomics, Proteomics, Protein, Protein Binding, Computational Biology, Drug Design, optimization (mathematics), Amino Acids, Peptides, and Proteins, De novo protein and peptide design, Drug design, In silico sequence selection, Optimization, Fold specificity, Binding affinity, sequencing
50476
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Designing a Bio-responsive Robot from DNA Origami
Authors: Eldad Ben-Ishay, Almogit Abu-Horowitz, Ido Bachelet.
Institutions: Bar-Ilan University.
Nucleic acids are astonishingly versatile. In addition to their natural role as storage medium for biological information1, they can be utilized in parallel computing2,3 , recognize and bind molecular or cellular targets4,5 , catalyze chemical reactions6,7 , and generate calculated responses in a biological system8,9. Importantly, nucleic acids can be programmed to self-assemble into 2D and 3D structures10-12, enabling the integration of all these remarkable features in a single robot linking the sensing of biological cues to a preset response in order to exert a desired effect. Creating shapes from nucleic acids was first proposed by Seeman13, and several variations on this theme have since been realized using various techniques11,12,14,15 . However, the most significant is perhaps the one proposed by Rothemund, termed scaffolded DNA origami16. In this technique, the folding of a long (>7,000 bases) single-stranded DNA 'scaffold' is directed to a desired shape by hundreds of short complementary strands termed 'staples'. Folding is carried out by temperature annealing ramp. This technique was successfully demonstrated in the creation of a diverse array of 2D shapes with remarkable precision and robustness. DNA origami was later extended to 3D as well17,18 . The current paper will focus on the caDNAno 2.0 software19 developed by Douglas and colleagues. caDNAno is a robust, user-friendly CAD tool enabling the design of 2D and 3D DNA origami shapes with versatile features. The design process relies on a systematic and accurate abstraction scheme for DNA structures, making it relatively straightforward and efficient. In this paper we demonstrate the design of a DNA origami nanorobot that has been recently described20. This robot is 'robotic' in the sense that it links sensing to actuation, in order to perform a task. We explain how various sensing schemes can be integrated into the structure, and how this can be relayed to a desired effect. Finally we use Cando21 to simulate the mechanical properties of the designed shape. The concept we discuss can be adapted to multiple tasks and settings.
Bioengineering, Issue 77, Genetics, Biomedical Engineering, Molecular Biology, Medicine, Genomics, Nanotechnology, Nanomedicine, DNA origami, nanorobot, caDNAno, DNA, DNA Origami, nucleic acids, DNA structures, CAD, sequencing
50268
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Polymerase Chain Reaction: Basic Protocol Plus Troubleshooting and Optimization Strategies
Authors: Todd C. Lorenz.
Institutions: University of California, Los Angeles .
In the biological sciences there have been technological advances that catapult the discipline into golden ages of discovery. For example, the field of microbiology was transformed with the advent of Anton van Leeuwenhoek's microscope, which allowed scientists to visualize prokaryotes for the first time. The development of the polymerase chain reaction (PCR) is one of those innovations that changed the course of molecular science with its impact spanning countless subdisciplines in biology. The theoretical process was outlined by Keppe and coworkers in 1971; however, it was another 14 years until the complete PCR procedure was described and experimentally applied by Kary Mullis while at Cetus Corporation in 1985. Automation and refinement of this technique progressed with the introduction of a thermal stable DNA polymerase from the bacterium Thermus aquaticus, consequently the name Taq DNA polymerase. PCR is a powerful amplification technique that can generate an ample supply of a specific segment of DNA (i.e., an amplicon) from only a small amount of starting material (i.e., DNA template or target sequence). While straightforward and generally trouble-free, there are pitfalls that complicate the reaction producing spurious results. When PCR fails it can lead to many non-specific DNA products of varying sizes that appear as a ladder or smear of bands on agarose gels. Sometimes no products form at all. Another potential problem occurs when mutations are unintentionally introduced in the amplicons, resulting in a heterogeneous population of PCR products. PCR failures can become frustrating unless patience and careful troubleshooting are employed to sort out and solve the problem(s). This protocol outlines the basic principles of PCR, provides a methodology that will result in amplification of most target sequences, and presents strategies for optimizing a reaction. By following this PCR guide, students should be able to: ● Set up reactions and thermal cycling conditions for a conventional PCR experiment ● Understand the function of various reaction components and their overall effect on a PCR experiment ● Design and optimize a PCR experiment for any DNA template ● Troubleshoot failed PCR experiments
Basic Protocols, Issue 63, PCR, optimization, primer design, melting temperature, Tm, troubleshooting, additives, enhancers, template DNA quantification, thermal cycler, molecular biology, genetics
3998
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Interview: HIV-1 Proviral DNA Excision Using an Evolved Recombinase
Authors: Joachim Hauber.
Institutions: Heinrich-Pette-Institute for Experimental Virology and Immunology, University of Hamburg.
HIV-1 integrates into the host chromosome of infected cells and persists as a provirus flanked by long terminal repeats. Current treatment strategies primarily target virus enzymes or virus-cell fusion, suppressing the viral life cycle without eradicating the infection. Since the integrated provirus is not targeted by these approaches, new resistant strains of HIV-1 may emerge. Here, we report that the engineered recombinase Tre (see Molecular evolution of the Tre recombinase , Buchholz, F., Max Planck Institute for Cell Biology and Genetics, Dresden) efficiently excises integrated HIV-1 proviral DNA from the genome of infected cells. We produced loxLTR containing viral pseudotypes and infected HeLa cells to examine whether Tre recombinase can excise the provirus from the genome of HIV-1 infected human cells. A virus particle-releasing cell line was cloned and transfected with a plasmid expressing Tre or with a parental control vector. Recombinase activity and virus production were monitored. All assays demonstrated the efficient deletion of the provirus from infected cells without visible cytotoxic effects. These results serve as proof of principle that it is possible to evolve a recombinase to specifically target an HIV-1 LTR and that this recombinase is capable of excising the HIV-1 provirus from the genome of HIV-1-infected human cells. Before an engineered recombinase could enter the therapeutic arena, however, significant obstacles need to be overcome. Among the most critical issues, that we face, are an efficient and safe delivery to targeted cells and the absence of side effects.
Medicine, Issue 16, HIV, Cell Biology, Recombinase, provirus, HeLa Cells
793
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Purification and Visualization of Influenza A Viral Ribonucleoprotein Complexes
Authors: Winco W.H. Wu, Lindsay L. Weaver, Nelly Panté.
Institutions: University of British Columbia - UBC.
The influenza A viral genome consists of eight negative-sense, single stranded RNA molecules, individually packed with multiple copies of the influenza A nucleoprotein (NP) into viral ribonulceoprotein particles (vRNPs). The influenza vRNPs are enclosed within the viral envelope. During cell entry, however, these vRNP complexes are released into the cytoplasm, where they gain access to the host nuclear transport machinery. In order to study the nuclear import of influenza vRNPs and the replication of the influenza genome, it is useful to work with isolated vRNPs so that other components of the virus do not interfere with these processes. Here, we describe a procedure to purify these vRNPs from the influenza A virus. The procedure starts with the disruption of the influenza A virion with detergents in order to release the vRNP complexes from the enveloped virion. The vRNPs are then separated from the other components of the influenza A virion on a 33-70% discontinuous glycerol gradient by velocity sedimentation. The fractions obtained from the glycerol gradient are then analyzed on via SDS-PAGE after staining with Coomassie blue. The peak fractions containing NP are then pooled together and concentrated by centrifugation. After concentration, the integrity of the vRNPs is verified by visualization of the vRNPs by transmission electron microscopy after negative staining. The glycerol gradient purification is a modification of that from Kemler et al. (1994)1, and the negative staining has been performed by Wu et al. (2007).2
Immunology, Issue 24, influenza A virus, viral ribonucleoprotein, vRNP, glycerol gradient, negative staining, transmission electron microscopy
1105
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Testing the Physiological Barriers to Viral Transmission in Aphids Using Microinjection
Authors: Cecilia Tamborindeguy, Stewart Gray, Georg Jander.
Institutions: Cornell University, Cornell University.
Potato loafroll virus (PLRV), from the family Luteoviridae infects solanaceous plants. It is transmitted by aphids, primarily, the green peach aphid. When an uninfected aphid feeds on an infected plant it contracts the virus through the plant phloem. Once ingested, the virus must pass from the insect gut to the hemolymph (the insect blood ) and then must pass through the salivary gland, in order to be transmitted back to a new plant. An aphid may take up different viruses when munching on a plant, however only a small fraction will pass through the gut and salivary gland, the two main barriers for transmission to infect more plants. In the lab, we use physalis plants to study PLRV transmission. In this host, symptoms are characterized by stunting and interveinal chlorosis (yellowing of the leaves between the veins with the veins remaining green). The video that we present demonstrates a method for performing aphid microinjection on insects that do not vector PLVR viruses and tests whether the gut is preventing viral transmission. The video that we present demonstrates a method for performing Aphid microinjection on insects that do not vector PLVR viruses and tests whether the gut or salivary gland is preventing viral transmission.
Plant Biology, Issue 15, Annual Review, Aphids, Plant Virus, Potato Leaf Roll Virus, Microinjection Technique
700
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Titration of Human Coronaviruses Using an Immunoperoxidase Assay
Authors: Francine Lambert, Helene Jacomy, Gabriel Marceau, Pierre J. Talbot.
Institutions: INRS-Institut Armand-Frappier.
Determination of infectious viral titers is a basic and essential experimental approach for virologists. Classical plaque assays cannot be used for viruses that do not cause significant cytopathic effects, which is the case for prototype strains 229E and OC43 of human coronavirus (HCoV). Therefore, an alternative indirect immunoperoxidase assay (IPA) was developed for the detection and titration of these viruses and is described herein. Susceptible cells are inoculated with serial logarithmic dilutions of virus-containing samples in a 96-well plate format. After viral growth, viral detection by IPA yields the infectious virus titer, expressed as 'Tissue Culture Infectious Dose 50 percent' (TCID50). This represents the dilution of a virus-containing sample at which half of a series of laboratory wells contain infectious replicating virus. This technique provides a reliable method for the titration of HCoV-229E and HCoV-OC43 in biological samples such as cells, tissues and fluids. This article is based on work first reported in Methods in Molecular Biology (2008) volume 454, pages 93-102.
Microbiology, Issue 14, Springer Protocols, Human coronavirus, HCoV-229E, HCoV-OC43, cell and tissue sample, titration, immunoperoxidase assay, TCID50
751
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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation. | {
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4,686,451,750,424,005,000 | lymphatic
(redirected from lymphatic system)
Also found in: Dictionary, Thesaurus, Medical, Encyclopedia, Wikipedia.
Mentioned in ?
References in periodicals archive ?
In medical school, we were taught that the brain has no lymphatic system," said Dr.
It is important to keep these liquids relocating appropriately to make sure that oxygen and other nutrients get to the tissues with the circulatory system and for the wastes to be carried away from the tissues via the lymphatic system.
The scientists then played the movies backward, to identify the point at which the lymphatic system began to form.
The lymphatic system is responsible for the development of both immunity and the resolution of infections (Waugh, A.
There are two theories for the origin of the lymphatic system in humans.
The lymphatic system is often overlooked in rehabilitation therapy and this book fills an important gap within the therapeutic massage literature.
Advance understanding of the biology and physiology of the acute trauma that occurs to the lymphatic system after surgery and radiation therapy, and how this affects normal healing processes in the body.
The organs generally regarded as components of the lymphatic system are the thymus (a gland in which immune cells are created and--in newborn and young cats--certain immune functions are carried out); and the spleen (which filters abnormal cells from the blood).
The lymphatic system helps maintain a balanced internal tissue environment by removing excess fluid as lymph.
Results from an ongoing study of workers employed at plants that used or produced formaldehyde continue to show a possible link between formaldehyde exposure and death from cancers of the blood and lymphatic system, particularly myeloid leukemia.
The lymphatic system is part of the body's immune system, helping deal with infection and also responsible for cleansing tissues. | {
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16,835,298,201,013,732 | Fuel Your Performance With the Right Fluids
Customize your daily beverages for improved strength and performance.
Author:
Publish date:
Updated on
Muscle-Gen-Protein-Oxygen
You know you’re supposed to consume plenty of fluids — especially water — every day. But you also can rely on other beverages to provide hydration, including coffee, tea, milk and protein shakes. Here are some ideas on how to make the most of your daily beverages.
EARLY-MORNING BUZZER
Coffee is a low-cal way to get your brain synapses snapping when you first rise and is especially useful preworkout: Research shows that consuming caffeine blunts the pain associated with lifting heavier weights or increasing workout volume, which boosts long-term performance. Coffee is also high in antioxidants, which neutralize harmful free radicals, preventing damage to cells and allowing for better recovery and long-term health. Myth buster: Research shows that coffee does count as part of your daily fluid intake and that caffeine only has a modest dehydrating effect. Augment your coffee value by adding one or both these items to your cup of joe:
Fast-digesting protein to provide amino acids and help prevent lean tissue breakdown.
Half-and-half or nut milk to slow the absorption of protein for a more steady delivery of nutrients.
PREWORKOUT ENERGIZER
Preworkout drinks provide you with sustained energy, improving performance and mental and physical endurance during your workout. But not all of them contain everything you need for a killer sweat sesh. See if yours is missing one of these beneficial ingredients, and mix it in before hitting the iron:
Easy-to-digest protein to provide readily available amino acids to prevent muscle breakdown.
Branched-chain amino acids, creatine and glutamine to support better performance, improve muscle protein synthesis, boost ATP production and prevent muscle breakdown, respectively.
WAKE AND RELAX
Green tea offers a myriad of health benefits, including improving mental focus for better athletic performance, elevating mood, facilitating the release of fat from storage and supporting joint health. You also can drink green tea before bedtime. (Seek out a decaffeinated version if you’re sensitive to caffeine.) It contains the amino acid theanine, which promotes a deep and restful sleep. Enhance the effectiveness of your tea with one of these boosters, depending on the time of day you drink it:
At night, add protein to prevent muscle breakdown while you’re sleeping.
Preworkout, add beta-alanine for increased strength and endurance.
RELY ON GENEPRO FOR FLUID DYNAMICS
Genepro from MuscleGen is a blend of high-quality proteins and is organic, non-GMO and gluten-free. It is made up of 98 percent absorbable protein, and because of Genepro’s patented process, the size of the protein molecules is reduced by more than 54 percent, making them easier for your body to digest and absorb. Added digestive enzymes further support its absorbability.
This flavorless product dissolves easily in beverages, but you also can add Genepro to food: Use a fork to mix it into your oatmeal, spaghetti sauce, salad dressing or soup to give your everyday meals a solid kick of protein.
Recent Articles | {
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Does Acid Reflux Cause Burping?
does-acid-reflux-cause-burping
ANSWER:
Acid reflux DOES cause burping.
What Is a Burp?
Burping is the body’s way of expelling excess stomach gas. The stomach will fill with gas by taking in too much air (air contains the gases oxygen and nitrogen) while eating and drinking. The stomach will then expel that air by pushing it back up through the esophagus. You will find that you may burp more when drinking carbonated beverages due to their carbon dioxide content. Drinking through a straw may also cause you to intake excess air.
Why Acid Reflux Causes Burping
Acid reflux, also known as gastroesophageal reflux disease or GERD, is a condition in which the normal acids in the stomach designed to digest food escape and are pushed in the wrong direction toward the esophagus. The body’s natural reaction to these foreign acids in your throat is to swallow repeatedly to push them back down, which introduces excess air into the stomach, and subsequently requires the stomach to expel the air through a burp.
Resources
Bloating, belching and intestinal gas: How to avoid them – MayoClinic.com. (n.d.). Mayo Clinic. Retrieved December 15, 2011, from http://www.mayoclinic.com/health/gas-and-gas-pains/DG00014
Why Do I Burp? . (n.d.). KidsHealth – the Web’s most visited site about children’s health. Retrieved December 15, 2011, from http://kidshealth.org/kid/talk/yucky/burp.html
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-8,769,781,373,195,252,000 | Zirconium CAD/CAM and Bioesthetic Layering of Porcelain: Color From Within
Today’s aesthetic dentistry can involve the selection of methods and materials that can be very overwhelming to the clinician. The dental profession is experiencing a large addition to the services it provides for patients. This change follows the introduction of root form endosseous implants that were introduced in the 1980s, and the aesthetic enhancements provided by the porcelain laminate veneers introduced in the 1990s. The use of CAD/CAM machines to fabricate high-strength ceramic cores for crowns and bridges promises to surpass the effects of the prior two revolutions.1
The switch to all-ceramic restorations and the use of CAD/CAM machines are being driven by a number of factors. The increasing demand for cosmetic procedures by today’s population will cause the demand for all-ceramic crowns and bridges to grow. This in turn will increase the demand for ceramic cores as a substitute for the metal frames used in traditional metal-ceramic crowns and bridges.2 Layering porcelain to nonmetallic cores is not new to dentistry, although certain materials lend themselves to this application better than others when attempting to adhere to sound dental principles and provide strength and exceptional aesthetics.
The challenge that the clinician and laboratory technician face with the advent of CAD/CAM-fabricated ceramic cores is finding a porcelain material that can reproduce the aesthetics found in the all-ceramic restorations without ceramic cores. Ceramic restorations from CAD/CAM machines tend to be very bright, white, high-value, opaque materials. The traditional method of layering porcelain tends to produce high-value and low-translucency restorations, which when placed adjacent to human dentition have a less-than-desirable outcome; the lack of translucency serves as the most important challenge of these new ceramic frameworks. The search for a porcelain substrate that will generate sound porcelain adherance and aesthetics has been the great quest of dental manufacturers.
This article will discuss a ceramic material manufactured for use with CAD/CAM frameworks. A case report using this material is included.
ALL-CERAMIC MATERIALS
Over the years several materials have been used for all-ceramic restorations; however, today only 2 types of ceramics are recommended for use with both anterior and posterior crowns and anterior bridges. These categories include the interpenetrating phase composites or glass-infiltrated ceramics, and the polycrystalline ceramics.3,4
Glass-infiltrated ceramics consist of a product formed by infiltrating molten glass into a partially sintered oxide material (aluminous oxide or alumina-zirconia oxide). Examples of this are InCeram Alumina and InCeram Zirconia (Vident).
Polycrystalline ceramics are materials with densely packed particles containing no glassy components. They cannot be processed to shapes without the use of computer-assisted machinery. Examples of this material include densely sintered, high-purity aluminum oxide, Procera AllCeram (Nobel Biocare), and the yttria tetragonal zirconia polycrystal (Y-TZP) systems. The majority of these systems use CAM of partially sintered Y-TZP blocks, followed by complete sintering of the shaped product for an additional 5 to 8 hours. These systems include Lava (3M ESPE), Cercon (DENTSPLY Ceramco), CEREC InLab (Sirona), and Procera All-Zirkon (Nobel Biocare). The partially sintered or “green state” material is milled to a size that is 20% to 25% larger than the final sintered core to compensate for the shrinkage that occurs during final sintering. As the fit of each final core is deemed to be acceptable, there is no standardization in fit and strength among different manufactured blocks of material because of the differences in the handling of the material by the various laboratories once it has been milled.5
A different system, DCS-Zirconium (DCS Popp Dental Laboratory) uses fully sintered Y-TZP blocks to mill fully sintered frames. No shrinkage is involved in the process when the fully sintered material is used, and the core made from totally industrially prepared material is structurally more reliable than the post-sintered green state material. There are questions that the CAD/CAM procedures may induce surface and subsurface flaws that may affects its physical properties.6 The use of ultrasonic machining promises to revolutionize the treatment of ceramic material in dentistry, as well as all phases of the industry. This technology greatly minimizes contact of the cutting tool with the material, which significantly reduces friction, heat, and the creation of surface flaws. Furthermore, the process increases the accuracy of the final milled product.7
The exceptional physical properties of these CAD/CAM ceramic cores have been described extensively in the literature and are not the focus of this article. This article focuses on the porcelain ceramic that will generate good to excellent aesthetics layered over the CAD/CAM alumina zirconia oxide (AL/ZR) core. The basic fundamental use and qualities for a particular type of porcelain, Initial Zr (GC America), is described.
Initial Zr is one of 6 Initial ceramics in an integrated product line (manufactured by GC Europe) with one color system, which can create metal-ceramic restorations as well as full-ceramic restorations. Each GC Initial ceramic is adapted to meet the needs of its particular fabrication process and frame-work, such as its coefficient of thermal expansion, therefore avoiding stress and fractures. This article focuses on GC Initial Zr, which is designed for layering over CAD/CAM frameworks. GC Initial Zr has an array of unique shades that have been developed for internal layering and external staining, high fluorescence, opalescence, and/or high translucency that allows for very favorable color matching with natural tooth structures.
For simple and promising handling of these high-strength ceramics, it is important for clinicians and lab technicians to consider a few fundamental points.
With zirconium oxide there are 2 variations:
• A white, more or less opaque, milled or sintered zirconium oxide.
• A dyed (in the corresponding shade) sintered zirconium oxide.
Figure 1. Internal aspect of DCS Precifit Zirconium (DCS Popp Dental Laboratory) core with final layers of porcelain. Note the “white” opaque color of the fully sintered core as discussed in the article.
Figure 2. DCS Precifit Zirconium oxide frame or copings ready for porcelain layering.
The former lends itself better to higher-value restorations that are the norm of most patients requesting anterior restorations (Figure 1). The latter definitely offers a more compatible color base for the standard tooth shade buildup, especially for standard layering.8 When using the white zirconium oxide, Initial Zr porcelain lends itself very well to generating the desired aesthetic outcome. The white neutral base of the zirconium oxide allows the applied colors to appear very pure and genuine. The fluorescence missing from zirconium oxide cores or frames must be replaced with a thin coating of liner or frame modifiers to provide the natural fluorescence from inside the restoration. The liners/modifiers can also be individually tinted with the fluorescing Initial stains.9
When the clinician prescribes the shade A2, as was done in the case report described later in this article, the laboratory needs to adapt the base chroma in a different fashion than conventional porcelain layering. When making A2 shades, the base chroma should be at least the color effect of A3. With zirconium oxide frames it should be even a warmer tone because the dentin-colored frame material becomes lighter with each firing. The result is that layered restorations without intensified chroma appear too light in the patient’s mouth.9
A similar appearance is seen with the white, non-chroma-intensified zirconium oxide restorations. The missing chroma and fluorescence on the frame causes a light, too white/gray appearance. The Initial Zr layering system compensates for this unwelcome addition and standardizes the layering procedure for the laboratory technician.10
It is not as simple to evaluate the optimal firing of AL/ZR ceramic. Improper firing causes the incorrect shade seen frequently in AL/ZR restorations. Most furnaces fire 20° to 30°C lower, especially in the temperature firing range of zirconium ceramics. All such ceramics, but particularly AL/ZR, react to low firing temperatures with slightly limited transparency and color effects. On the other hand, somewhat higher firing cycles cause no problems and actually support the color and transparency effects. The ceramic firing stability is unusually good, so that in most furnaces raising the end temperature by 10° to 30°C is recommended in order to achieve the best outcome.10
Incorrectly constructed or layered frames are another reason for aesthetic failures when using white zirconium oxide restorations. In general, the frames should be the same size as the circumference of all the frames and built with light material zirconium oxide. If the frames are of different sizes, then the circumferences of the smaller frames will differ in color, and will appear either gray or too dark and intense in color11 (Figure 2).
When using these AL/ZR frames one must be aware of the aesthetic limits of the material. This material is very difficult to control aesthetically for inlay, onlay, and veneer restorations due to the very white-colored margins. This restorative method lends itself to full-coverage restorations due to the preparation of the tooth structure with circumferential shoulder preparations. The aesthetic effect necessary in veneer, inlay, or onlay restorations is not generally achieved due to the opacious zirconium oxide material blocking light in the enamel of natural teeth, resulting in a color impact along the margin. Therefore, any preparation of the teeth should have a 0.8-mm to 1.0-mm reduction at the margin to prevent this “light-blocking” effect onto the enamel. A shoulder preparation allowing for 0.8-mm to 1.0-mm ceramic material must be provided12 (Figures 3 and 4).
As a side note, the author has noticed that often in the use of inlay, onlay, crown, or veneer restorations with less than 0.8 to 1.0 mm of marginal reduction, a cut-back of the core is needed and traditional shoulder porcelain is necessary for the optimal aesthetic result. The only problem with this is that this shoulder material is often radiolucent and can show up as open margins or defective restorations to the uninformed clinician when doing follow-up radiographic examination.13 Due to this and the aesthetic reasons previously described, the author recommends from experience that another conventional method be utilized if the required amount of preparation cannot be obtained.
PORCELAIN LAYERING
Figure 3. Left maxillary restorations on model demonstrate good aesthetics and light translucency.
Figure 4. Left maxillary restorations cemented demonstrate the disappearance of the restorative gingival margin with the natural enamel of the tooth. (Note fit of zirconium frame and the disappearance of the white gingival line often seen with ZR cores.)
Figure 5. Application of FD-91 for internal copying of dentinal structure.
Figure 6. Bioesthetic layering with modifiers and transparent porcelains.
Figure 7. Restorations after first firing ready for the transparent and translucent porcelains. Figure 8. Lingual depiction of “color from within” of Initial porcelain. Note the transparency and translucency achieved by the Bioesthetic Layering Method.
Figure 9. Facial aesthetics of restorations with refracted and reflected light demonstrating the “halo effect” desired for optimal aesthetics.
Figure 10. Maxillary premolar demonstrating “color within” without the use of external stains or modifiers. The color mimics natural tooth aesthetics.
With many restorative porcelain layering techniques, technicians learned to build porcelain in the following way: apply opaque, build dentin, layer enamel, and add translucent material. Unfortun-ately, this method has little correlation with a natural tooth. Transparency is found primarily from the inside of all natural teeth, in the transparent dentin. In anterior teeth, abrasion and wear over time cause this transparent layer covering the dentin to appear at the incisal edge. This changes the transparency of natural teeth considerably depending on the angle of light or the angle of incidence. The teeth appear at times lighter, grayer, darker, or even deeper in chroma. The amount of light reflecting through the transparent dentin also changes the perception of depth.
The internal transparent layer of dentin from tooth morphology comes to the surface at the junction of the root and cervical margin, completely covering the root and influencing the value of the gingiva. Therefore, it makes no sense to use opaque marginal materials in this area where nature shows us differently. The use of GC Initial porcelain, due to its highly chromatic and fluorescent INside powders (GC America), imitates the primary dentin and fluorescence that lie imbedded within the teeth. Layering dentin material over the INside material achieves a perfect balance of chroma and value. When one pairs fluorescent, crystal clear transparency with real opalescent enamel, it makes it possible to copy the effect of natural tooth structure.
The layering of Initial porcelain has been described as the Bioesthetic Layering Method. This method is oriented toward copying the light dynamics and transmission of natural teeth. The method begins with the clinician taking the shade. This can be a very complex challenge, as one needs to make allowances for color in natural teeth under different light situations. These variances in color under different light situations are very difficult or almost impossible to achieve utilizing conventional ceramic materials. Even the most talented technicians depend on materials to produce these natural light effects. When the GC Initial materials are layered analogously to the structure of natural teeth, they automatically produce a complete and logical layering process. The natural chroma and fluorescence seen within natural teeth can be transferred to the restoration with the Bioesthetic Layering Method.
This is a method of layering porcelain through incremental layering of porcelains in a systematic manner, unlike the traditional manner described previously. The first step is the use of a fluorescent Fired Frame Modifier, since zirconium frames lack fluorescence. The next step is the application of INside materials to the cervical and proximal areas. Next, the light-reflecting edges are covered with highly fluorescent white dentin (FD-91), and the body is covered with INside material (Figure 5). Next, the dentin body is built, and the enamel table is built over the dentin body with translucent dentin. Next, modifier stains and INside material continue the layering process. The buildup is now covered with a layer of fluorescent transparent material (CLF[GC America]). Next, a cut-back in the incisal area down to the highly fluorescent dentin is accomplished, and FD-91 is again applied. Another layer of INside on the desired internal structure is placed. Next, opalescent enamel is layered (Figure 6). Now the restorations have their first bake in a porcelain oven. Any corrections to shades or colors can now be accomplished with translucent materials and opalescent enamels (Figure 7). The restorations are baked a second time and finished.
Anterior teeth pose a great aesthetic challenge. Incisals of teeth are very sensitive, since all optical light phenomena converge at this small space. Layering porcelain in the incisal table is very critical because the most light is transmitted here. This area will exacerbate the optical differences between felds-patic porcelains and synthetic ceramic frames. A totally different optical appearance can result when dissimilar frame sizes or materials are used side by side. This difference in optical appearance can be neutralized with the high fluorescent dentins and the INside powders (Figure 8).
To achieve the desired natural effect at the incisal angle, Initial porcelain’s different white fluorescent, fluorescent transparent material, and transparent dentin can be utilized to provide the optical phenomenon known as the “mammelon structure” or the “Incisal halo effect” (Figure 9). If there is too much transparency at the incisal edge in the mouth, then this results as an unappealing, unnatural gray and flat effect. The use of the white fluorescent, fluorescent transparent material, and transparent dentin along with the opalescent enamels of Initial porcelain copies natural tooth structure very well (Figure 10). When compared to conventional enamels, the difference aesthetically can be enormous. The use of conventional enamels, dentins, and opaques correlates well with the Vita Lumin shade guide system, but not with the dynamics of light in natural teeth. The opalescent effect on the surface, with fluorescence coming from the inside, creates a highly natural appearance. One needs to utilize the ready-made shade guides as a general reference, but not rely on the shade guide to reproduce the desired outcome.
Communication with the laboratory technician needs to be addressed more explicitly with the design of “shade-mapping.” The clinician must communicate to the technician how and where the porcelain and modifiers are to be utilized so that the maximum aesthetic and optical effects are generated. This can pose a big challenge to the clinician when describing the colors seen to the technician. A thorough understanding of tooth morphology and natural opacious dentins, translucent dentins, and enamels in teeth must be utilized if one is to achieve the optimal effect desired. Initial has simplified this with the Bioesthetic Layering Method described earlier.9
CASE REPORT
Figure 11. Preoperative smile view of patient.
Figure 12. Preoperative retracted view of patient’s dentition depicting failing restorations and poor aesthetics.
Figure 13. Dentition evidencing compromised gingival heights, crowding, failing restorations, wear, and overall poor aesthetics.
Figure 14. Preoperative right lateral view.
This patient was very unsatisfied with the anterior aesthetics of his maxillary dentition. He wanted a result that would dramatically change the anterior aesthetics. He was concerned with severe crowding of the anterior incisors as well as the failing restorations that had been present for many years. The patient was presented with a treatment plan involving a complete restoration of his dentition in both the maxillary and mandibular arches. Prior to the restorative dentistry phase he was advised to undergo orthodontic therapy as a method to improve his interdental and intradental relationship. In discussion with the author the patient elected to avoid orthodontic treatment because full-coverage restorations would be necessary to restore his dentition. Gingival concerns were discussed, as the patient was very unhappy with the differing gingival heights in the maxillary anterior segment (Figures 11 to 14).
The treatment the patient wanted to undergo at the operative session was to restore the maxillary anterior segment, periodontally recontour the maxillary anterior gingiva, and recontour the incisal edges of the opposing dentition to aid in incisal guidance. The lower arch was to be restored at a later time. The shade requested as the final shade would be considerably lighter than the patient’s intial shade.
Figure 15. Right lateral view of provisional restorations at corrected vertical and incisal lengths. Figure 16. GC Fuji Plus single-use dispensing capsule in action demonstrating precise delivery of glass ionomer adhesive material.
The patient was appointed for the initial operative session. The first operative session included a laser-assisted Smile Lift Procedure to accomplish recontouring the gingival architecture to more harmonious and even gingival heights.14 The teeth were prepared for full-coverage restorations with a 0.8-mm to 1.0-mm circumferential marginal reduction. Tissue retraction, impressions, bite records, and provisional restorations were all accomplished at this session (Figure 15).
Upon completion of the restorations, the second operative session was to be the try-in phase to determine restoration fit, marginal integrity, occlusion, aesthetics, and patient satisfaction. With all these accomplished, the restorations were to be placed with final cement. Zirconium restorations can be easily cemented in the conventional manner with glass ionomer cements or conventional ce-ments. The cement chosen for this case was GC Fuji Plus (GC America). The author utilizes this product due to high fluoride release and high bond strengths.15-17 This cement is very versatile due to its ability to cement indirect restorations. The material is supplied in a capsule (Figure 16). It is also available as a Paste-Pak system (FujiCEM). This ensures the proper mixing ratio every time to achieve the highest compressive, tensile, and bond strengths with the lowest film thickness, and maximum fluoride release.18
Figure 17. Fully retracted view of final restorations in maxillary arch. (The higher value restorations that the patient requested will be matched during the mandibular reconstruction phase.) Figure 18. Final restorations showing translucency and transparency of the zircon frame/Initial porcelain technique.
Figure 19. Preoperative smile view of patient.
Figure 20. Postoperative smile view of patient.
The final results were very aesthetic, and the patient was highly pleased with the results. A third and final operative session was utilized for occlusal accuracy and postoperative evaluation. There was little to no sensitivity during the entire procedure as well as during the provisional and postoperative phase (Figures 17 to 20).
References
1. Adams MW. Dental implants—isn’t it about time? J Indiana Dent Assoc. 2002;81:9-10.
2. The U.S. Dental Laboratories Industry. 3rd ed. Tampa, Fla: Marketdata Enterprises; 2005.
3. Pospiech P, Rammelsberg P, Goldhofer G, et al. All-ceramic resin-bonded bridges: a 3-dimensional finite-element analysis study. Eur J Oral Sci. 1996;104(4 pt 1):390-395.
4. Sorensen JA, Kang SK, Torres TJ, et al. In-Ceram fixed partial dentures: three-year clinical trial results. J Calif Dent Assoc. 1998;26:207-214.
5. Keough BE, Kay HB, Sager RD. A ten-unit all-ceramic anterior fixed partial denture using Y-TZP Zirconia. Pract Proced Aesthet Dent. 2006;18(1):37-43.
6. Luthardt RG, Holzhuter MS, Rudolph H, et al. CAD/CAM-machining effects on Y-TZP zirconia. Dent Mater. 2004;20:655-662.
7. Guazzato M, Quach L, Albakry M, et al. Influence of surface and heat treatments on the flexural strength of Y-TZP dental ceramic. J Dent. 2005;33:9-18.
8. Raigrodski AJ. All-ceramic full-coverage restorations: concepts and guidelines for material selection. Pract Proced Aesthet Dent. 2005;17:249-256.
9. Brusch M, Dahl R. Systematic bioesthetic dental restorations: a ceramic solution with overlapping systems, part 2. Dental Dialogue. 2005;5(June):26-42.
10. Schenk H. Esthetics with zirconia. Dental Dialogue. April 2006:118-128.
11. Hammer P. Experiences from the laboratory. Dental Dialogue. April 2006:34-46.
12. Brusch M, Dahl R. Systematic bioesthetic dental restorations: a ceramic solution with overlapping systems, part 1. Dental Dialogue. 2005;5(June):2-24.
13. Rosentritt M, Behr M, Lang R, et al. Marginal adaptation of ceramic inlays using different types of cements. Presented at: The IADR 80th General Session; San Diego, Calif; March 6-9, 2002; Abstract 0053.
14. Pinero J. The smile lift procedure. Contemp Esthet Restor Pract. 1998;2:44-52.
15. McMillen K, Kerby RE, Thakur A, et al. Fluoride release of resin-based luting cements. Presented at: The IADR 1996 General Session; Abstract 403.
16. Burgess JO, Norling BK, Cardenas HL. Fluoride release and flexural strength of five fluoride releasing luting agents. Presented at: The IADR 1996 General Session; Abstract 423.
17. Wilson PR, Stankiewicz NR. Effect of cement space and delayed placement on the seating of crowns luted with Vitremer, Fuji Duet and Dyract Cem. Am J Dent. 1998;11:240-244.
18. Begazo CC, de Boer HD, Kleverlaan CJ, et al. Shear bond strength of different types of luting cements to an aluminum oxide-reinforced glass ceramic core material. Dent Mater. 2004;20:901-907.
Dr. Pinero maintains a private practice in Milwaukee, Wis, where he emphasizes aesthetic, restorative, and laser dentistry. Dr. Pinero lectures nationally and internationally on aesthetic, restorative, and laser dentistry and provides hands-on in-office programs on aesthetic and laser dentistry. He founded The Midwest Institute of Laser and Esthetic Dentistry in Milwaukee, where he holds advanced postgraduate continuum seminars on aesthetic and laser dentistry. In addition to clinical training, Dr. Pinero has helped numerous dentists employ his expertise of patient management to help them propel their practices to be among the top 5% with his Follow the Formula system. He can be reached at (414) 282-2050.
Acknowledgment
The author would like to thank Robert Popp of Popp DCS in Milwaukee, Wis, and laboratory technician Ernest Grabowski of Popp Dental Laboratory for the laboratory phase of this case.
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According to the American Tinnitus Association, most cases of tinnitus are caused by hearing loss. Occasionally though, tinnitus is caused by an irritation to the auditory system. Tinnitus can sometimes be a symptom of a problem with the temporomandibular joint (TMJ). If your tinnitus is caused by TMJ, then a dental procedure or realignment of your bite may alleviate the problem.
Tinnitus sufferers have tried many alternative therapies but often to no avail. Some have heard of success stories involving the use of certain vitamins, minerals, herbal preparations, or even a change in diet, but often did not experience personal success in treating tinnitus using such options. Unfortunately, no studies to date have been able to associate such treatments to any real benefits. While much of the existing research have been dedicated to helping us understand tinnitus and its etiological underpinnings, there are currently very few treatments that are clinically validated. Of the few that conducted clinical studies to evaluate the effectiveness, most did not use rigorous clinical methods such as controlling for placebo effects or double-blinding to ensure the integrity of the data and to eliminate any sources of bias. Tinnitus sufferers who access such treatments often do not experience relief from their tinnitus. As a result, tinnitus sufferers often experience confusion, frustration, a loss of hope, and skepticism after having invested time and money on available treatment options.
Experts recommend that patients with severe tinnitus become educated about tinnitus and how they best deal with its symptoms. This can include learning about biofeedback in order to control stress and your reaction to tinnitus sounds, talking with a counselor, or joining a support group. Coping strategies are most useful for managing emotional side effects of tinnitus, such as anxiety, trouble sleeping, lack of focus and depression.
Noise exposure. Exposure to loud noises can damage the outer hair cells, which are part of the inner ear. These hair cells do not grow back once they are damaged. Even short exposure to very loud sounds, such as gunfire, can be damaging to the ears and cause permanent hearing loss. Long periods of exposure to moderately loud sounds, such as factory noise or music played through earphones, can result in just as much damage to the inner ear, with permanent hearing loss and tinnitus. Listening to moderately loud sounds for hours at a young age carries a high risk of developing hearing loss and tinnitus later in life.
Tinnitus can vary a lot between individuals; therefore you can find many different types of tinnitus. Tinnitus varies considerably in intensity and type. Some people describe tinnitus as high-frequency whistling sounds while others perceive tinnitus as a buzzing noise or a sound similar to butter sizzling in a frying pan. But some experience, instead, a thumping sound in the same rhythm as their heartbeat. This is called pulsatile tinnitus. Read more about the types of tinnitus.
The physician may also request an OAE test (which is very sensitive to noise induced hearing damage), an ECochG (looking for Meniere's disease and hydrops, an MRI/MRA test (scan of the brain), a VEMP (looking for damage to other parts of the ear) and several blood tests (ANA, B12, FTA, ESR, SMA-24, HBA-IC, fasting glucose, TSH, anti-microsomal antibodies).
Tinnitus is a symptom, not a disease. Most cases are due to damage to the microscopic endings of the sensory nerve in the inner ear, commonly from exposure to loud noise (as from amplified music or gunfire). Other causes include allergy, high or low blood pressure, a tumor, diabetes, thyroid dysfunction, and head or neck injury. In addition, some drugs, including aspirin and other anti-inflammatories, antibiotics, sedatives, and antidepressants can also cause tinnitus. If so, changing drugs or lowering the dosage usually helps.
We occasionally recommend neuropsychological testing using a simple screening questionnaire -- depression, anxiety, and OCD (obsessive compulsive disorder) are common in persons with tinnitus. This is not surprising considering how disturbing tinnitus may be to ones life (Holmes and Padgham, 2009). Persons with OCD tend to "obsess" about tinnitus. Treatment of these psychological conditions may be extremely helpful.
Tinnitus Retraining Therapy. Tinnitus Retraining Therapy (TRT) combines a wearable device that is individually programmed to mask the specific tonal frequency of that person’s tinnitus, with psychological therapy that teaches a patient to ignore the sounds his tinnitus is creating. I consider it the best of all of the above noise suppression techniques, as it is individually tailored for each person and involves support from a trained psychological therapist. It is also the most expensive and time consuming, but in my medical opinion, the most beneficial of all the noise suppression techniques listed above.
High-pitched ringing. Exposure to a very loud noise or a blow to the ear can cause a high-pitched ringing or buzzing that usually goes away after a few hours. However, if there's hearing loss as well, tinnitus may be permanent. Long-term noise exposure, age-related hearing loss or medications can cause a continuous, high-pitched ringing in both ears. Acoustic neuroma can cause continuous, high-pitched ringing in one ear.
As their name suggests, maskers conceal tinnitus through other sounds. They look similar to hearing aids, but they won’t enhance your hearing. In this way, they’re like band-aids, covering up the problem instead of actually solving it. In addition, some people find maskers frustrating, because they can soften important sounds, like speech. We do not recommend maskers for long-term use as they do not work in re-wiring the brain.
A poor diet, sedentary lifestyle, lack of sleep and chronic stress are all capable of reducing immunity and making you susceptible to nerve damage, allergies and ear problems. If you frequently experience seasonal or food allergies that affect your ears, ear infections, swelling and other problems related to damage of the vestibular system, consider changing your diet, exercise routine and ways of dealing with stress, which in turn will aid your tinnitus treatment. Try natural stress relievers like exercising, yoga, meditation, taking warm baths, using essential oils and spending more time outdoors, and eat an anti-inflammatory diet.
Tinnitus affects every layer of society, and there has been increasing support for awareness. Recently, musicians who are affected by tinnitus have come together to create awareness for the disorder. Artists including Chris Martin of Coldplay and Black Eyed Peas have created a compilation album to help raise funds towards finding a cure for tinnitus. In the United States, the Department of Defense has invested millions of dollars into investigations of tinnitus sound therapies. In addition, the American Tinnitus Association makes efforts to lobby the US government to provide support for tinnitus sufferers.
Along the path a hearing signal travels to get from the inner ear to the brain, there are many places where things can go wrong to cause tinnitus. If scientists can understand what goes on in the brain to start tinnitus and cause it to persist, they can look for those places in the system where a therapeutic intervention could stop tinnitus in its tracks.
The sound perceived may range from a quiet background noise to one that can be heard even over loud external sounds. The specific type of tinnitus called pulsatile tinnitus is characterized by hearing the sounds of one's own pulse or muscle contractions, which is typically a result of sounds that have been created by the movement of muscles near to one's ear, or the sounds are related to blood flow of the neck or face.[10]
Many people find that tinnitus causes frustration, stress, and even anger. And unfortunately, your exasperation and anxiety can seem to amplify the issue. Learning how to thoroughly relax can help you manage your tinnitus. Deep breathing, meditation, yoga, or music therapy may help in combination with sound therapy. You could also explore relaxing hobbies like gardening, painting, swimming, photography, knitting, reading, cooking, or other physical activities (walking, biking, etc.).
Being exposed to loud noise on a regular basis from heavy equipment, chain saws or firearms are common causes of hearing loss and tinnitus. Noise-induced hearing loss and tinnitus can also be caused by listening to loud music through headphones or attending loud concerts frequently. It is possible to experience short-term tinnitus after seeing a concert, but long-term exposure will cause permanent damage.
The latest news about tinnitus treatment comes from a UK study showing that Mindfulness Based Cognitive Therapy (MBCT) significantly helps reduce the severity of the disorder. The researchers reported that, among the 75 patients being studied, both relaxation therapy and MBCT worked to alleviate symptoms as well as reducing psychological distress, anxiety and depression related to the disorder. MBCT led to greater reductions in tinnitus severity and the improvements lasted longer.
A common cause of tinnitus is inner ear hair cell damage. Tiny, delicate hairs in your inner ear move in relation to the pressure of sound waves. This triggers cells to release an electrical signal through a nerve from your ear (auditory nerve) to your brain. Your brain interprets these signals as sound. If the hairs inside your inner ear are bent or broken, they can "leak" random electrical impulses to your brain, causing tinnitus.
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9,022,123,987,414,408,000 | print
There is more to strengthening core muscles then you think. Chiseled abs a not what it is all about. Read the article to learn more.
Well-trained abdominal muscles are pliable, not chiseled or hard, and adapt quickly to change. Your core is more complicated than just your muscles When we talk about core power, abdominal muscles come to mind. But our core is much more than that.
Source: Learn About Your Core And How to Strengthen Those Muscles
Thanks for sharing! | {
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1,032,205,175,130,429,800 | mental-health-icon
Ativan and fluconazole
Can we take Ativan 1 mg and fluconazole 150 mg together? Please suggest me. I even take inderal 10 mg
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Doctor Answers (1) on Ativan and fluconazole
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First of all let me tell you that you should not use any medicines without your doctor's advice. Secondly, Ativan ie. Lorazepam has the potential to make you get addicted to it. You can become a nervous wreck if you use Lorazepam (or similar ones) indiscriminately and for long time. Regular usage will tend to make you an addict. Therefore when doctors prescribe such drugs, they do so for a short while and then ask the patient to stop. Unfortunately many patients continue to take the drug without a doctor's prescription and get into trouble. Regarding the question of combining Fluconazole and Lorazepam, you must leave it to your doctor to decide. But on principle, it is best to avoid multiple drugs while you are on a course of Fluconazole
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3,365,609,568,109,018,600 | Hemp, medical marijuana, CBD’s – a pet owner’s introduction
As medical marijuana becomes legal and accessible to more people in more states, pet owners are looking for ways they can use this new family of medications to help their pets. In humans, marijuana and hemp products, and their extracts, are being touted to treat a wide variety of syndromes and diseases. I know individuals who suffered from seizures, or chronic pain, and their lives have dramatically changed for the better, thanks to cannabis-made medications. Fortunately, there are well-designed studies to back up many of these claims…in people.
When it comes to pets, we aren’t so lucky. Can we extrapolate human data to apply it to dogs and cats? We do with many other drugs quite often, but we must be cautious. Does the law allow for pets to use medical marijuana? The laws are rather silent on pets, making it more risky. Here’s a breakdown.
A quick internet search for legitimate information on cannabis products for pets yields primarily companies selling these products. Obviously, they will tell you their particular product or brand is superior to the others, and their product will treat, manage, or even cure a long list of diseases. We need to wade through the advertising and self-promotion and get down to facts.
CBD, THC, cannabinoids…the basics
Marijuana and hemp are plants in the genus Cannabis. Many different species and strains of these plants exist, and almost 500 different compounds have been isolated from these plants, all with potential medicinal uses. Of these, over 80 are classified as cannabinoids. Different plants contain varying levels of cannabinoids and other compounds.
Every chemical has its own unique properties, and much more research will be needed for us to understand the full potential of this array of potential medications. For our purposes, there are two main cannabinoids that you’ll see mentioned the most: CBD and THC. CBD (cannabidiol) is the “medicine-y” cannabinoid. It’s extracted from a hemp plant, but lacks the psycho-active effects most people think of when they think of marijuana. The molecule responsible for that “high” one can get from marijuana is the other cannabinoid called THC (TetraHydroCannabinol). Think of CBD as the president of the science club, and THC as the party girl, if that helps.
The marijuana plant contains more THC, the chemical responsible for the “high”, while the hemp plant is more fibrous, and contains very little THC. Instead, hemp’s main compound is CBD. What makes us call one plant hemp and the other marijuana if they are both in the same family? Basically, more THC earns it the name “marijuana” while less THC (<0.3% depending on who you read) makes the plant hemp, or even “industrial hemp.”
There are also synthetic cannabinoids out there. The laws are more lax on these, making them “less illegal”, as most of the rules the DEA makes are about the compounds extracted from Cannabis plants (see below). Two of them are actually FDA approved (for human use!) Marinol is prescribed to help AIDS patients not lose their appetites and maintain body weight. Cesamet is prescribed to patients undergoing chemotherapy to help reduce the nausea and vomiting which can happen too commonly. It’s also being used (again, in people) to treat chronic pain and even Irritable Bowel Disease!
While these synthetic cannabinoids sound like a great thing, patients taking them report they don’t seem as effective. Apparently, the synthetics contain one and only one compound, while the extracts contain mainly that compound, but have other cannabinoids along for the ride that seem to have an additive effect. So, bottom line, the products from plants, as of now, seem to work better.
brown min pinGiving cannabinoids to pets
I know very few veterinarians who recommend these products, for a variety of reasons. Little to no data exists on what dose is safe and/or effective. Little is known about drug interactions. Next to nothing is known about long-term use, simply because the state laws allowing us to conduct large scale clinical trials with it are relatively new. There is absolutely no regulation of production of these products, so we have no way of knowing if what is claimed on the bottle is what actually is in the bottle. Finally, the constant changing of the legal status of these products makes many veterinarians want to keep their noses clean and avoid the whole legal mess until the federal and state laws can come to some agreement.
Here’s a taste of what we do know.
CBD has great promise in the treatment of seizures, but appears to be poorly absorbed into dogs’ bodies when given orally. As far back as 1988, we knew cannabinoids had great potential as a treatment for seizures. Six dogs were given the CBD through an IV, then orally to compare. The IV doses were absorbed into the blood stream and eliminated via the liver. The medication hung around a while too, with a half-life of 9 hours! The oral dosing was not at all absorbed (none detected in the bloodstream) in half the dogs, and the other three that did absorb it had negligible levels. This study was only of six dogs, so we cannot draw any major conclusions from it. Yet, it does not seem promising for CBD’s as an oral option, unless presented in a different version or compound than the one used. Obviously, much more research needs to be done. (Pharmacokinetics of cannabidiol in dogs. Drug Metab Dispos. 1988 May-Jun;16(3):469-72.)
CBD might inhibit the cytochrome P450 enzyme. Here’s the research on it. Not a bad paper, but everything was done in vitro, (where most research starts) and nothing performed in an animal. Chemicals can behave differently than cells in a liver. And what is cytochrome P450 and why do we care? Oh, you care! This is a very important enzyme in the liver that is responsible for metabolizing (breaking down) medications or toxins. If this enzyme is inhibited and your pet is on other medications, it could, theoretically, cause the circulating dose of those other medications to increase, which is not always a good thing.
These are all well and good, and laid the foundation for current research, but they leave questions. Thankfully, here’s more recent work being done in 2018!
CBD may help relieve symptoms of arthritis in dogs. This Cornell study is very interesting and was much needed! They used client-owned dogs, gave CBD oil, and discovered a lot of things. First, they suggest a dose of 2 mg/kg twice a day as effective for managing the pain of arthritis. Second, they confirmed that there were levels of CBD in the blood, meaning it was absorbed. They also found the half-life to be about 4.5 hours, way less than the earlier paper that gave it IV. This conflicts with the 1988 paper, but that was also only 6 dogs, and this was 16 dogs. Interestingly, there was an increase in a liver enzyme called Alk-P. It’s interesting because this is loosely associated with…wait for it…Cytochrome P450! (see paper above). I love when things tie together. This liver enzyme elevation does raise some concern about the effects of CBD oil long-term in older, arthritic dogs. The treatment was effective, but it was only given for four weeks, and there was a significant increase in this Alk-P enzyme in over 50% of the dogs. It doesn’t mean CBD isn’t safe…just that we have more to learn! Finally, the dogs in this study were on other pain medications, so that muddies the waters a bit as well.
CBD has been shown to reduce seizures in rats. We’ve also learned, anecdotally, that cannabinoids help epileptic humans as well. We suspect it works by inhibiting the CB receptor, and/or reducing calcium fluxes in neurons. (Izzo AA. Non-psychotropic Plant Cannabinoids: New Therapeutic Opportunities from an Ancient Herb. Cell Press, Elsevier; 2009:515–527.)
CBD may be a potent neuroprotector. Once nerve cells die, they are gone forever. This is why brain damage of any kind, in any species, is such a big bad deal. Izzo et al suggests CBD’s may prevent brain cell death in certain situations, and can even reverse brain damage resulting from lack of oxygen… in rats.
Lesser-known cannabinoids (CBC and CBG) have demonstrated great antimicrobial activity. With all the antibiotic resistant bacteria we have in the world, a new medication that can possibly kill “super-bugs” would be wonderful!
There are many other great studies out there on rodents, giving us hope for future applications. However, it’s a start, and much more needs to be done.
So what is legal, and what isn’t?
And why is this so complicated?
Here’s the details on the complex laws covering these compounds. What’s legal? What’s overlooked? What will land you in prison?
Posted in General health, Myths & Hot Topics.
4 Comments
1. You have referred to the fact that dogs may have 10 times more CB receptors than human, and have referred to Houghston, SW Vet Symposium 2016. I would like very much to follow up and read more about the subject, but I cannot find anything published on line by Houghston. Do you have a reference to literature I could read?
Thanks so much.
• That reference I got from the proceedings from the Southwest Vet Symposium, which can be accessed via VIN. The title of the lecture is pretty good: “Scooby’s Doobies: Can Cannabis Cure?” The author provides a detailed list of references at the bottom of the page.
2. My moms dogs are both old and are in serious amounts of pain.So we tried using marijuana products…. and CBD The one guys is so bad he will just sit there and shake most of the day and you tell they are both in a lot of pain, we recently started treating them with CBD and oh my god does it work, after one small dose my moms one dog stopped shaking for 3 days and both were in noticeably less pain for days after one dose of CBD compared to the prescription pain meds the vet gave them, we actually took them off those pain meds and have them running on pure CBD and the vets are amazed at how well it works so yes there is lots of research on the subject just like medical mj… the research is all there my friend all you have to do is a little research and you will find it.
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3,886,398,076,067,281,400 | All you need to know about Pneumonia
1
Pneumonia is a respiratory disease. It is basically a chronic respiratory condition where the patient breathes germs into the lungs and finds it difficult breathe because of obstructions in respiratory passage.
This is an acute infection caused in one or both the lungs which is caused by a bacterium named Streptococcus pneumonia. Pneumonia is a pathological consequence caused by the abnormal entry of fluids, particulate matter, or secretions in the lower airways.
Types of Pneumonia:
There are many types of pneumonia, the names of which are listed below:
1. Atypical Pneumonia
2. Pneumocystis
3. Bronchial
4. Lipsoid
5. Aspiration
6. Nosocomial Hospital Acquired
7. Klebsiella
8. Viral
9. Community-Acquired
10. Bacterial
11. Fungal
12. Atypical , and
13. Walking Pneumonia.
What are the Causes of Pneumonia?
There can be several reasons behind the cause of this respiratory disorder which varies from the places where the patient has contracted it; however viruses and bacteria are the primary causes of pneumonia.
The cause of the disease is important to know because the background of the illness helps to determine the patient’s successful recover ability rate to a great extent.
When a person accidentally breathes in the germ into the lungs, these germs inhabit in small air sacs of the lungs known as alveoli and continue to multiply. And as the immune system of the body tries to send white blood cells to fight the infection it is then instead of warding off the infection the sacs become filed with fluid and pus resulting in pneumonia.
Pneumonia
Pneumonia
What are the symptoms of Pneumonia?
The Pneumonia can be caused by bacteria, fungi, and as well as viruses. There are several symptoms that help to indicate this disease; however the symptoms differ by the way they are caused.
The symptoms of the pneumonia caused by bacteria are:
• Feeling extremely exhausted or feeling very weak.
• Cough which spits up mucus (sputum) from your lungs which can be rusty or green or tinged with blood.
• Then it is accompanied by Chest pain which keeps getting worse when you cough or breathe in.
• Diarrhea.
• There might be some shaking accompanied by “teeth-chattering” chills.
• Fever.
• Faster heartbeat, breathing and feeling short of breath
• Nausea and vomiting.
DIAGNOSIS OF PNEUMONIA:
Diagnosis of pneumonia is usually done on the basis of symptoms and physical examinations. But it gets difficult to detect it sometimes, especially in those patients who are already suffering from some other diseases. There are several methods with the help of which pneumonia is diagnosed. The names of the few are listed below:
1. body temperature readings
2. blood tests
3. lung tests
4. white blood cell counts
5. family and patient histories
6. Bronchoscopies,
7. Thoracentesis Tests for fluid analysis
8. chest and lung x-rays
9. heart and respiratory rates
10. viral cultures
11. CAT scans
12. sputum samples
13. MRIs
What are the treatments of Pneumonia?
There are many treatment procedures for pneumonia that are available which differs in accordance with the severity of the disease. There are even many vaccinations available to prevent this disease now. The vaccinations include:
1: the Pneumococcal Vaccine against Streptococcus Pneumoniae
2: Haemophilus Influenza Type B Vaccine
3: the flu vaccine, and
4: The DTP Injections for Whooping Cough.
The treatment processes includes:
1: antibiotics,
2: liquid absorption
3: vaporizers,
4: bed rest
5: medications, such as penicillin, for pain and fever control
6: airway suction, and
7: humidifiers.
What are the Risk Involved in Pneumonia?
There is certain hazardous health risks associated with the development of this health ailment like:
1: kidney diseases,
2: heart diseases,
3: COPD
4: asthma
5: emphysema and
6: Diabetes.
And these risks are more prevalent in hospitalized patients, very young children or old people, patients with weakened immune systems or chronic medical conditions etc.
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-1,976,578,019,330,720,500 | Skip to main content
Optogenetic activation of parvalbumin and somatostatin interneurons selectively restores theta-nested gamma oscillations and oscillation-induced spike timing-dependent long-term potentiation impaired by amyloid β oligomers
Abstract
Background
Abnormal accumulation of amyloid β1–42 oligomers (AβO1–42), a hallmark of Alzheimer’s disease, impairs hippocampal theta-nested gamma oscillations and long-term potentiation (LTP) that are believed to underlie learning and memory. Parvalbumin-positive (PV) and somatostatin-positive (SST) interneurons are critically involved in theta-nested gamma oscillogenesis and LTP induction. However, how AβO1–42 affects PV and SST interneuron circuits is unclear. Through optogenetic manipulation of PV and SST interneurons and computational modeling of the hippocampal neural circuits, we dissected the contributions of PV and SST interneuron circuit dysfunctions on AβO1–42-induced impairments of hippocampal theta-nested gamma oscillations and oscillation-induced LTP.
Results
Targeted whole-cell patch-clamp recordings and optogenetic manipulations of PV and SST interneurons during in vivo-like, optogenetically induced theta-nested gamma oscillations in vitro revealed that AβO1–42 causes synapse-specific dysfunction in PV and SST interneurons. AβO1–42 selectively disrupted CA1 pyramidal cells (PC)-to-PV interneuron and PV-to-PC synapses to impair theta-nested gamma oscillogenesis. In contrast, while having no effect on PC-to-SST or SST-to-PC synapses, AβO1–42 selectively disrupted SST interneuron-mediated disinhibition to CA1 PC to impair theta-nested gamma oscillation-induced spike timing-dependent LTP (tLTP). Such AβO1–42-induced impairments of gamma oscillogenesis and oscillation-induced tLTP were fully restored by optogenetic activation of PV and SST interneurons, respectively, further supporting synapse-specific dysfunctions in PV and SST interneurons. Finally, computational modeling of hippocampal neural circuits including CA1 PC, PV, and SST interneurons confirmed the experimental observations and further revealed distinct functional roles of PV and SST interneurons in theta-nested gamma oscillations and tLTP induction.
Conclusions
Our results reveal that AβO1–42 causes synapse-specific dysfunctions in PV and SST interneurons and that optogenetic modulations of these interneurons present potential therapeutic targets for restoring hippocampal network oscillations and synaptic plasticity impairments in Alzheimer’s disease.
Background
Alzheimer’s disease is a neurodegenerative disease characterized by a progressive decline in cognitive and mnemonic functions [1, 2]. Abnormal accumulation of amyloid β1–42 oligomers (AβO1–42) is a hallmark of Alzheimer’s disease [1,2,3,4] and AβO1–42-induced impairments of gamma oscillations [5,6,7,8,9,10] and long-term synaptic plasticity [3, 4, 11, 12] are believed to contribute to the memory deficits observed in Alzheimer’s disease. In particular, hippocampal theta-nested gamma oscillations observed during spatial memory processing [13,14,15] have been shown to support the induction of long-term potentiation (LTP) [16,17,18,19]. Thus, AβO1–42 may impair memory by disrupting GABAergic inhibitory circuits, which underlie oscillogenesis [14, 20,21,22,23,24,25]. Indeed, there is now increasing experimental evidence showing that AβO1–42 reduces GABA synaptic transmission [26,27,28], causes excitation/inhibition imbalances [9, 12, 27, 28], and even diminishes the number of GABAergic synapses/terminals onto pyramidal cells [29]. Also, parvalbumin-positive (PV) and somatostatin-positive (SST) interneurons, the two major subtypes of hippocampal interneurons [30] that are critically involved in oscillogenesis [24, 25, 31], are reported to be impaired in mouse models of Alzheimer’s disease [5,6,7,8, 27, 32, 33]. PV interneurons’ spike amplitude, membrane potential, and firing rate are decreased [5, 7] while SST interneurons’ structural plasticity and axonal sprouting are impaired in Alzheimer’s disease mouse models [27, 32]. Surprisingly, the neural circuit mechanism by which dysfunction of PV and SST interneurons contributes to AβO1–42-induced impairment of oscillogenesis and LTP is unclear. If uncovered, it could help researchers find novel therapeutic targets for Alzheimer’s disease. Recently, optogenetic stimulation of channelrhodopsin-2 (ChR2)-expressing hippocampal CA1 pyramidal cells (PCs) at theta-frequency was shown to induce in vivo-like theta-nested gamma oscillations in the CA1 area of acute hippocampal slices in vitro [34]. This provides a novel model in which to perform targeted whole-cell patch-clamp recordings and selective optogenetic modulation of PV or SST interneuron activity during optogenetically induced theta-nested gamma oscillations and LTP induction. We have used this approach to investigate neural circuit dysfunction in hippocampal slices treated with AβO1–42. We found that AβO1–42 caused selective dysfunctions in reciprocal synapses between PC and PV interneurons, which impaired gamma oscillations and desynchronized the spike phases of PC and PV interneurons relative to gamma oscillations. While AβO1–42 had no effect on PC-to-SST or SST-to-PC synapses, it specifically disrupted SST interneuron-mediated disinhibition to PC resulting in the impairment of theta-nested gamma oscillation-induced spike timing-dependent LTP (tLTP). Selective optogenetic activation of PV interneurons restored gamma oscillations while selective optogenetic activation of SST interneurons restored theta-nested gamma oscillation-induced tLTP. These results demonstrate that AβO1–42-induced synapse-specific dysfunctions in PV and SST interneurons may explain the concomitant impairments of hippocampal gamma oscillations and synaptic plasticity in Alzheimer’s disease. Moreover, using a computational network model of PC, PV, and SST interneurons, we further demonstrate that PV and SST interneurons targeting different compartments of the CA1 PC have distinct functional roles in oscillogenesis and tLTP induction.
Results
AβO1–42 impairs in vivo-like, optogenetically induced theta-nested gamma oscillations in hippocampal slices
To create an in vitro model of AβO1–42-induced pathology in hippocampal slices, we prepared AβO1–42 by oligomerizing Aβ1–42 following a previously described protocol [4] (see the “Methods” section). Generation of AβO1–42 was confirmed by Western blot analysis of SDS-PAGE (Fig. 1a) and native PAGE (Additional file 1: Figure S1). To induce blue light-induced theta-nested gamma oscillations, we injected adeno-associated virus (AAV) carrying ChR2 (AAV-CaMKII-ChR2-mCherry) into the CA1 area of the hippocampus (Fig. 1b), which led to the expression of ChR2 in CA1 PCs in hippocampal slices in vitro (Fig. 1c). We optically stimulated ChR2-expressing PCs using 5 Hz sinusoidal blue light (470 nm, Fig. 1d) in dimethyl sulfoxide (DMSO)-treated hippocampal slices which reliably reproduced theta-nested gamma oscillations as observed in the band-pass filtered local field potential (LFP) (Fig. 1e, black traces, top) and in the spectrogram [34] (Fig. 1e, bottom) that persisted for over 40 min (Additional file 2: Figure S2). However, 20-min treatment of AβO1–42 (200 nM) in the same slice significantly decreased the power of gamma oscillations in the LFP (Fig. 1f, red traces, top) and in the spectrogram (Fig. 1f, bottom), while 20-min treatment of AβO42–1, an inactive peptide control for AβO1–42, in the same slice of DMSO-treated slices had no effect (Fig. 1g, magenta). Power spectral density (PSD) analysis of theta-nested gamma oscillations (Fig. 1h) revealed that peak power of gamma oscillations in the DMSO-treated slice (Fig. 1i, black) was impaired by AβO1–42 (Fig. 1i, red), but not by AβO42–1 (Fig. 1i, magenta), while peak frequency was spared in all conditions (Fig. 1j). Moreover, phase-amplitude coupling analysis of gamma oscillations to the trough of theta cycle (Fig. 1k) revealed that the coupling strength, quantified by the modulation index (see the “Methods” section), was significantly decreased by AβO1–42, but not by AβO42–1, compared to that in the DMSO-treated slices (Fig. 1l). We replicated these effects in different slices treated with AβO1–42 for 20 min before performing field recording (Additional file 3: Figure S3); thus, the reduction in oscillatory activity was not caused by recording duration. These results show that AβO1–42-treated slices with optical stimulation of ChR2-expressing CA1 PCs can replicate gamma oscillations impairment as observed in Alzheimer’s disease mouse models in vivo [5,6,7,8].
Fig. 1
figure 1
AβO1–42 impairs in vivo-like, optogenetically induced theta-nested gamma oscillations in hippocampal slices. a Western blot of SDS-PAGE showing AβO1–42 (trimer, tetramer, and large oligomers) after incubation at 4 °C for 0 h (left) and 18 h (right). b Micro-injection of AAV-CaMKII-ChR2-mCherry into hippocampal CA1 area of C57BL/6 mice. c Fluorescence image of ChR2-expressing PCs (ChR2-PC). SO, stratum oriens; SP, stratum pyramidale; SR, stratum radiatum. d Experimental schematic showing sinusoidal (5 Hz) blue light (470 nm) stimulation of ChR2-PC and field recordings in the CA1 area of hippocampal slices in vitro. e–g Sinusoidal blue light stimulation induces theta-nested gamma oscillations as shown in the band-pass filtered LFP (top) and the corresponding spectrograms (bottom) in DMSO-treated slice (e), after 20-min treatment of either AβO1–42 (f), or AβO42–1 (g). h–j Mean power spectral density (PSD, shade indicates SEM) of gamma oscillations (h), mean peak power (i), and mean peak frequency (j) of gamma oscillations in DMSO-treated slice (black) and following 20 min of AβO1–42 treatment in the same slices (red) or in DMSO-treated slice (black) and following 20 min AβO42–1 treatment in the same slices (magenta). k, l Representative comodulograms showing phase-amplitude coupling of gamma oscillations to theta cycle (k) and mean modulation index (l) in each condition. Paired Student’s t test (i, j, l, ***p < 0.001, ns: not significant). Data are represented as mean ± SEM
AβO1–42 causes synapse-specific dysfunction of PC-to-PV, but not PC-to-SST synapses
To determine whether alterations to either PV or SST interneurons contributed to the reduction in peak power of gamma oscillations in the AβO1–42-treated slices, we expressed ChR2 in CA1 PCs and enhanced yellow fluorescent protein (eYFP) in either PV or SST interneurons in PV-Cre (Fig. 2a) or SST-Cre mice (Fig. 2b), respectively. We then performed current-clamp recordings to record spikes in CA1 PCs, eYFP-expressing PV, and SST interneurons during blue light-induced theta-nested gamma oscillations (Fig. 2c). We found that all neuronal types spiked at gamma-frequency in DMSO-treated slices (Fig. 2c, black traces, Fig. 2d). AβO1–42 had no effect on neither spike frequencies (Fig. 2c, red traces, Fig. 2d), nor the intrinsic membrane properties (Additional file 4: Figure S4) of PV and SST interneurons, which could explain why the peak frequency of gamma oscillations was intact even after AβO1–42 treatment (Fig. 1j). However, the number of spikes per theta cycle was reduced only in PV interneurons (Fig. 2e).
Fig. 2
figure 2
AβO1–42 causes synapse-specific dysfunction of PC-to-PV, but not PC-to-SST synapses. a, b Micro-injection of AAV-CaMKII-ChR2-mCherry and AAV-DIO-eYFP into CA1 area (left) and fluorescence image (right) of ChR2-expressing PCs (ChR2-PC) with eYFP-expressing PV interneurons (eYFP-PV) in PV-Cre mice (a) and ChR2-PC with eYFP-expressing SST interneurons (eYFP-SST) in SST-Cre mice (b). SO, stratum oriens; SP, stratum pyramidale; SR, stratum radiatum; SLM, stratum lacunosum-moleculare. c Experimental schematic. Whole-cell current-clamp recordings in CA1 PC, eYFP-PV, or eYFP-SST during sinusoidal (5 Hz) blue light (470 nm) stimulation (top) and representative spikes (bottom) in DMSO-treated (black) and AβO1–42-treated slices (red). d, e Mean spike frequency (d) and the number of spikes per theta cycle (e) recorded in CA1 PC (black), eYFP-PV (purple), and eYFP-SST (green). f Experimental schematic. Whole-cell voltage-clamp recordings in eYFP-PV/eYFP-SST during sinusoidal blue light stimulation (top) and representative EPSCs (bottom) in DMSO-treated (black) and AβO1–42-treated slices (red). g, h Mean EPSC amplitude (g) and mean EPSC frequency (h) in eYFP-PV (purple) and eYFP-SST (green). i Experimental schematic. Alveus stimulation to record PC-evoked EPSCs in eYFP-PV. j Representative PC-evoked EPSCs from eYFP-PV (left) and stimulus-response (S-R) curve (right) in DMSO-treated and AβO1–42-treated slices. k, l Representative PC-evoked EPSCs from eYFP-PV in response to alveus stimulation (10 pulses, 50 Hz, k, left), paired-pulse ratio (PPR) of the 2nd EPSC/1st EPSC (k, right), total EPSC charge (l, left), and EPSCs normalized to the 1st EPSC to show short-term plasticity (l, right) in DMSO-treated (filled circles) and AβO1–42-treated slices (empty circles). m–p Same as i–l but with PC-evoked EPSCs in eYFP-SST. Unpaired Student’s t test (d, e, g, h, k, l (left), o, p (left), ***p < 0.001, **p < 0.01, ns: not significant), two-way ANOVA with post hoc Tukey’s test (j, l (right), n, p (right), ###p < 0.001, ns: not significant). Data are represented as mean ± SEM
Since the spiking of hippocampal CA1 interneurons is in large part driven by CA1 PC’s excitatory inputs to the interneurons [35], we investigated whether the treatment of AβO1–42 affected CA1 PC’s excitatory inputs to PV and SST interneurons. We performed voltage-clamp recordings in eYFP-expressing PV or SST interneurons during blue light-induced theta-nested gamma oscillations in DMSO-treated and AβO1–42-treated slices (Fig. 2f). We found that the amplitude of CA1 PC’s excitatory postsynaptic current (EPSC) to PV, but not SST interneuron, was significantly decreased in AβO1–42-treated slices (Fig. 2f, g), while EPSC frequency was unaffected (Fig. 2h). To characterize the AβO1–42-induced synaptic dysfunctions at CA1 PC-to-PV synapse and CA1 PC-to-SST synapse, we first investigated how AβO1–42 affected the stimulus-response (S-R) curve of these synapses by electrically stimulating the axons of CA1 PC in the alveus of CA1 at different intensities (10, 50, 100, 150, 200, and 300 μA) and recording the corresponding PC-evoked EPSCs in eYFP-expressing PV interneuron (Fig. 2i, j) or in eYFP-expressing SST interneuron (Fig. 2m, n). Analysis of the S-R curve revealed that, for each stimulation intensity, AβO1–42 significantly increased the amplitudes of PC-evoked EPSCs in PV (Fig. 2j, right), but not those in SST interneurons (Fig. 2n, right). These results indicate that AβO1–42 increases the initial neurotransmitter release probability of PC-to-PV synapse. To investigate the synaptic locus of EPSC changes, we stimulated the CA1 PC axons using a half-maximal stimulus (based on the S-R curve in Fig. 2j, n, right; 115–210 μA) and an inter-stimulus interval of 20 ms (50 Hz, 10 stimulus) for the analysis of paired-pulse ratio (PPR), total charge, and short-term plasticity of PC-evoked EPSCs in PV (Fig. 2k, l) and SST interneurons (Fig. 2o, p). Paired-pulse facilitation of PC-evoked EPSCs in PV interneurons, as observed in DMSO-treated slices, was converted to paired-pulse depression in AβO1–42-treated slices (Fig. 2k, right). The total charge of PC-evoked EPSCs in PV (Fig. 2l, left), analyzed by the area of the PC-evoked EPSCs in Fig. 2k (left), was significantly decreased by AβO1–42. Furthermore, short-term facilitation of PC-evoked EPSCs in PV interneurons, as observed in DMSO-treated slices, was converted to short-term depression in AβO1–42-treated slices (Fig. 2l, right). These results indicate that AβO1–42 causes presynaptic depression at PC-to-PV synapse, which led to a decrease in CA1 PC-evoked excitatory synaptic inputs onto PV interneurons. Thus, AβO1–42-induced gamma oscillation impairment may be due to dysfunction of presynaptic mechanisms at PC-to-PV synapses. In contrast, AβO1–42 had no effect on PPR, total charge, or short-term plasticity of CA1 PC-evoked EPSCs in SST interneurons (Fig. 2o, p). Therefore, AβO1–42 causes presynaptic dysfunctions at CA1 PC-to-interneuron synapses which is target-specific.
AβO1–42 causes synapse-specific dysfunction of PV-to-PC synapses, but not SST-to-PC synapses
Blue light-induced theta-nested gamma oscillations are most likely generated by reciprocal synapses between PCs and interneurons [34], according to the pyramidal-interneuron network gamma (PING) model [14, 21, 23]. In accordance with this model, voltage-clamp recordings in CA1 PCs during blue light-induced gamma oscillations (Fig. 3a, top) revealed that inhibitory postsynaptic currents (IPSCs) occurred at gamma-frequencies in DMSO-treated slices (Fig. 3a, bottom, black trace, Fig. 3f), which were GABAA receptor-mediated as they were completely blocked by GABAzine (SR95531, 5 μM, Fig. 3a, bottom, gray trace; Fig. 3f, g). AβO1–42 significantly decreased the amplitude of these IPSCs (Fig. 3a, bottom, red trace; Fig. 3g), potentially accounting for the observed reduction in peak power of gamma in AβO1–42-treated slices (Fig. 1h, i). To determine which interneuron subtype was responsible for the reduction of IPSC in PC in AβO1–42-treated slices, we optogenetically inactivated either PV or SST interneuron during gamma oscillations by co-injecting two different AAV viruses to CA1, one carrying ChR2 and the other carrying enhanced Arch (AAV-DIO-Arch-eYFP) in order to express ChR2 in PCs and Arch in either PV (Fig. 3b) or SST interneurons (Fig. 3c). During theta-nested gamma oscillations in DMSO-treated slices, inactivation of Arch-expressing PV interneurons (Fig. 3d) and Arch-expressing SST interneurons (Fig. 3e) by yellow light (590 nm) had no effect on IPSC frequency in CA1 PCs (Fig. 3f). However, IPSC amplitude in CA1 PC was significantly reduced only by inactivation of Arch-expressing PV interneurons in the DMSO-treated slices (Fig. 3g), which was similar to that recorded in AβO1–42-treated slices (Fig. 3a, red trace, Fig. 3g). Inactivation of Arch-expressing PV interneurons in AβO1–42-treated and DMSO-treated slices had the same effect in reducing IPSC amplitudes (Fig. 3d, red trace, Fig. 3g) while inactivation of Arch-expressing SST interneurons in AβO1–42-treated slices significantly reduced the IPSC amplitude compared to that in the DMSO-treated slices (Fig. 3e, red traces, Fig. 3g). Moreover, the peak power of gamma oscillations was also decreased only by inactivation of Arch-expressing PV interneuron (Additional file 5: Figure S5) while inactivation of Arch-expressing SST interneuron had no effect on gamma oscillations (Additional file 6: Figure S6), indicating AβO1–42-induced reduction of IPSC in CA1 PCs as well as the reduction of peak power of gamma oscillations may be due to dysfunction of PV interneurons. To rule out the possibility of yellow light having any direct effects on the reduction of gamma oscillation power via activation of ChR2 in CA1 PCs, we recorded synaptic currents in ChR2-expressing PCs and LFPs in the nearby tissue during sinusoidal (5 Hz) blue (470 nm), green (565 nm), and yellow light (590 nm) stimulation (Additional file 7: Figure S7a-c). We found that green light induced synaptic currents and gamma oscillations in the LFP while yellow light stimulation had no effect on either of them (Additional file 7: Figure S7d, e). In order to characterize the AβO1–42-induced synaptic dysfunctions at PV-to-CA1 PC synapse and SST-to-CA1 PC synapse, we expressed ChR2 in PV (Fig. 3h) and SST interneurons (Fig. 3m) and analyzed the S-R curve of these synapses by optically stimulating ChR2-expressing PV interneurons (Fig. 3i) and ChR2-expressing SST interneurons (Fig. 3n) at different light powers (5, 10, 25, 50, 75, 100% of maximal light power (15 mW)) and recorded the corresponding PV-evoked IPSCs in PC (Fig. 3j) and SST-evoked IPSCs in PC (Fig. 3o). Analysis of the S-R curve revealed that, for each stimulation intensity, AβO1–42 significantly increased the amplitudes of PV-evoked IPSCs in PC (Fig. 3j), but not SST-evoked IPSCs in PC (Fig. 3o), suggesting that AβO1–42 increases the initial neurotransmitter release probability of PV-to-PC synapse. To investigate the synaptic locus of IPSC changes, we optically stimulated ChR2-expressing PV interneurons and ChR2-expressing SST interneurons using a half-maximal light power (based on S-R curve in Fig. 3j, o; 3.75–9 mW) and an inter-stimulus interval of 20 ms (50 Hz, 10 stimulus) for the analysis of PPR, total charge, and short-term plasticity of PV-evoked IPSCs (Fig. 3k, l) and SST-evoked IPSCs (Fig. 3p, q). AβO1–42 significantly enhanced the paired-pulse depression in PV-evoked IPSCs in PC, as observed in DMSO-treated slice (Fig. 3k, right). The total charge of PV-evoked IPSCs in PC was significantly decreased by AβO1–42 (Fig. 3l, left). Furthermore, short-term depression of PV-evoked IPSCs in PC, as observed in DMSO-treated slice was even more enhanced in AβO1–42-treated slices (Fig. 3l, right) while it had no effect on SST-evoked IPSCs (Fig. 3p, q). Together, these results indicate that AβO1–42 specifically disrupted reciprocal PC-to-PV and PV-to-PC synapses, which would likely impair gamma oscillations, while AβO1–42 had no effect on PC-to-SST or SST-to-PC synapses.
Fig. 3
figure 3
AβO1–42 causes synapse-specific dysfunction of PV-to-PC synapses, but not SST-to-PC synapses. a Experimental schematic. Whole-cell voltage-clamp recordings in CA1 PC (top) and representative IPSCs (bottom) during blue light-induced gamma oscillations in DMSO-treated (black), AβO1–42-treated slices (red), and DMSO-treated slice with GABAzine (gray). b, c Micro-injection of AAV-CaMKII-ChR2-mCherry and AAV-DIO-Arch-eYFP into CA1 area (top) and fluorescence image (bottom) of ChR2-expressing PCs (ChR2-PC) with Arch-expressing PV interneurons (Arch-PV) in PV-Cre mice (b) and ChR2-PC with Arch-expressing SST interneurons (Arch-SST) in SST-Cre mice (c). d, e Same as a but with inactivation of Arch-PV (d) and Arch-SST (e) using tonic yellow light (590 nm) stimulation in DMSO- and AβO1–42-treated slice. f, g Mean IPSC frequency (f) and mean IPSC amplitude (g) in each condition. h Micro-injection of AAV-DIO-ChR2-mCherry into CA1 area of PV-Cre mice (top) and fluorescence image (bottom) of ChR2-expressing PV interneurons (ChR2-PV). i, j Experimental schematic. Whole-cell voltage-clamp recordings in CA1 PC (i) to record PV-evoked IPSCs (j, left) and stimulus-response (S-R) curve (j, right) in response to different light stimulation powers. k, l Representative PV-evoked IPSCs in CA1 PC in response to light stimulation (10 pulses, 50 Hz, k, left), paired-pulse ratio (PPR) of the 2nd IPSC/1st IPSC (k, right), total IPSC charge (l, left), and IPSCs normalized to the 1st IPSC to show short-term plasticity (l, right) in DMSO-treated (filled circles) and AβO1–42-treated slices (empty circles). m–q Same as h–l but by activating ChR2-expressing SST interneurons (ChR2-SST) for SST-evoked IPSCs in SST-Cre mice. Unpaired Student’s t test (k, l (left), p, q (left), **p < 0.01, *p < 0.05, ns: not significant), one-way (f, g, ###p < 0.001, ##p < 0.01, ns: not significant) and two-way ANOVA with post hoc Tukey’s test (j, l (right), o, q (right), ###p < 0.001, #p < 0.05, ns: not significant). Data are represented as mean ± SEM
Optogenetic activation of PV interneurons restores AβO1–42-induced impairment of theta-nested gamma oscillations
We then asked whether optogenetic activation of PV interneurons could rescue theta-nested gamma oscillations in AβO1–42-treated slices. If so, it would be strong evidence that the dysfunction of PV interneurons was the ultimate cause of reduced theta-nested gamma oscillations in AβO1–42-treated slices. We co-injected AAV viruses carrying ChR2 and C1V1 (AAV-DIO-C1V1-eYFP) (Fig. 4a), an opsin that opens a cation channel with peak excitation centered around green light (565 nm), in order to express ChR2 in CA1 PC and C1V1 in PV interneurons (Fig. 4b). Since green light activates ChR2-expressing PCs (Additional file 7: Figure S7), we optically stimulated C1V1-expressing PV interneurons using yellow light (590 nm), which activated C1V1-expressing PV interneurons reliably (Additional file 8: Figure S8). Using this preparation, we optically stimulated C1V1-expressing PV interneurons with yellow light in AβO1–42-treated slices during blue light-induced theta-nested gamma oscillations (Fig. 4c, d). PV interneuron activation successfully restored the peak power of gamma oscillations in AβO1–42-treated slices (Fig. 4d–f) to the level observed in DMSO-treated slices while maintaining frequency at gamma (Fig. 4g). Phase-amplitude coupling of gamma oscillations to theta cycle in AβO1–42-treated slices was also increased by PV interneuron activation to the level observed in DMSO-treated slices (Fig. 4h, i). Since CA1 PC spike phases relative to gamma oscillations are important for hippocampal spatial information processing [36, 37], we investigated the phase of spikes and postsynaptic currents (PSCs) relative to the gamma cycle. Following the PING model [14, 21, 23], gamma oscillations triggered the activation of CA1 PC spikes, EPSCs in PV interneurons, PV interneuron spikes, then IPSCs in CA1 PCs in sequence (Fig. 4j), with distinct phases relative to ongoing gamma cycles in DMSO-treated slices (Fig. 4k, black bars). The phase-locking of spike/synaptic current was abolished in AβO1–42-treated slices, making it difficult to detect a clear peak in the event phase probability (Fig. 4k, red bars). Nonetheless, optical stimulation of C1V1-expressing PV interneurons in AβO1–42-treated slices restored phase-locking of spikes/synaptic currents (Fig. 4k, yellow bars). The strength of phase-locking, as measured by the length of the resultant vector in the phase vector plot, was indeed restored by optical stimulation of C1V1-expressing PV interneurons (Fig. 4l, m). The mean vector phases were also rescued by optical stimulation of C1V1-expressing PV interneurons (Fig. 4n). These data show that optogenetic activation of PV interneurons restores gamma power and resynchronizes spikes/synaptic inputs to gamma cycles. This supports the idea that AβO1–42-induced reductions in theta-nested gamma oscillations power are caused by PV interneuron dysfunction.
Fig. 4
figure 4
Optogenetic activation of PV interneurons restores AβO1–42-induced impairment of theta-nested gamma oscillations. a Micro-injection of AAV-CaMKII-ChR2-mCherry and AAV-DIO-C1V1-eYFP virus into CA1 area of PV-Cre mice. b Fluorescence image of ChR2-PC with C1V1-expressing PVs (C1V1-PV). c Experimental schematic. Sinusoidal (5 Hz) blue light (470 nm) and yellow light (590 nm) stimulation for activation of ChR2-PC and C1V1-PV, respectively, and field recording in CA1 area in AβO1–42-treated slices. d Sinusoidal blue and yellow light stimulation induces theta-nested gamma oscillations as shown in the band-pass filtered LFP (top) and the corresponding spectrogram (bottom), which results in the restoration of gamma oscillations in AβO1–42-treated slices. e–g Mean PSD (shade indicates SEM) of gamma oscillations (e), mean peak power (f), and mean peak frequency (g) of gamma oscillations in DMSO-treated slice (black), after 20-min treatment of AβO1–42 in the same slice (red), and with yellow light stimulation of C1V1-PV (yellow) during blue light-induced gamma oscillations. h, i Representative comodulograms showing phase-amplitude coupling of gamma oscillations to theta cycle (h) and mean modulation index (i) in each condition. j–n Schematic illustration of reciprocal PC-PV circuit (j), corresponding phase histogram (k), vector phases and lengths in polar plots (l), mean vector length (m), and circular mean vector phase (n) of CA1 PC’s spike, EPSC in PV, PV’s spike, and IPSC in CA1 PC recorded during gamma oscillations in each condition. One-way repeated-measures (f, g, i), one-way ANOVA with post hoc Tukey’s test (m, ###p < 0.001, ##p < 0.01, #p < 0.05, ns: not significant), and Watson-Williams test (n, ***p < 0.001, **p < 0.01, *p < 0.05, ns: not significant). Data are represented as mean ± SEM. Data in kn was collected from the different number of slices (DMSO 23, AβO1–42 18, AβO1–42 + C1V1-PV 14) and animals (DMSO 17, AβO1–42 10, AβO1–42 + C1V1-PV 8)
Optogenetic activation of SST interneurons restores AβO1–42-induced impairment of theta-nested gamma oscillation-induced tLTP
Theta-nested gamma oscillations have been shown to support the induction of LTP at Schaffer collateral (SC) synapses [16,17,18,19], but a direct experimental demonstration of how CA1 PCs and PV/SST interneurons partake in LTP induction at CA3-to-CA1 synapses during theta-nested gamma oscillations is lacking. To remedy this, we paired presynaptic SC stimulation-evoked excitatory postsynaptic potentials (EPSPs) with postsynaptic spike bursts (4 spikes at 100 Hz repeated at 5 Hz) at a delay (Δt) of + 10 ms, thereby mimicking CA3 inputs onto CA1 PCs during theta-nested gamma oscillations (Fig. 5a, b) [38]. We found that this protocol reliably induced robust tLTP at CA3-to-CA1 synapses in DMSO-treated slices (Fig. 5c, f, black filled bar), which was NMDA receptor (NMDAR)-dependent, as it was blocked by NMDAR antagonist, D-AP5 (50 μM, Fig. 5d, f, black dotted bar). However, NMDAR-dependent tLTP was completely blocked in the AβO1–42-treated slices (Fig. 5e, f, red filled bar). Since PV and SST interneurons’ spikes were concurrently activated during theta-nested gamma oscillations (Fig. 2c) and by alveus stimulation of CA1 PC axons (Additional file 9: Figure S9), AβO1–42-induced synaptic dysfunctions of either PV or SST interneurons may have contributed to the observed tLTP impairment. To test this hypothesis, we expressed ChR2 in either SST or PV interneurons in SST-Cre or PV-Cre mice (Fig. 5g) and optically stimulated ChR2-expressing SST or PV interneurons with blue light (470 nm) during theta-nested gamma oscillation-like tLTP induction in AβO1–42-treated slices (Fig. 5h–j). We found that optogenetic activation of SST interneurons in AβO1–42-treated slices could fully restore NMDAR-dependent tLTP (Fig. 5h, k, green filled bar) that was blocked by D-AP5 (Fig. 5i, k, green dotted bar). However, optogenetic activation of PV interneurons in AβO1–42-treated slices could not restore tLTP (Fig. 5j, k, purple filled bar).
Fig. 5
figure 5
Optogenetic activation of SST interneurons restores AβO1–42-induced impairment of theta-nested gamma oscillation-induced tLTP. a Experimental schematic. Whole-cell current-clamp recordings in CA1 PC and Schaffer collateral (SC) stimulation for theta-nested gamma oscillation-like tLTP induction at CA3-CA1 excitatory synapses. b tLTP was induced by pairing presynaptic SC stimulation with postsynaptic CA1 PC spike bursts (4 spikes at 100 Hz) with a + 10 ms time window, repeated 200 times at 5 Hz. Inset: enlarged EPSP evoked by presynaptic SC stimulation, scale bar 10 ms, 1 mV. c–e EPSP slopes normalized to mean of 10-min baseline in DMSO-treated slice (c), + D-AP5 (50 μM) in DMSO-treated slice (d) and in AβO1–42-treated slices (e). Black arrow: onset of tLTP induction. Test pathways (filled circles), control pathways (empty circles). Insets: representative EPSPs at indicated time points (1, 2 or 1′, 2′). f Mean of normalized EPSPs slopes of last 5 min of test (filled bars) and control pathways (empty bars) in DMSO-treated slices (black), + D-AP5 in DMSO-treated slices (dotted black) and in AβO1–42-treated slices (red). g Micro-injection of AAV-DIO-ChR2-mCherry to CA1 area in SST-Cre and PV-Cre mice (top) and fluorescence images (bottom) of ChR2-expressing SST interneurons (ChR2-SST, left) and ChR2-expressing PV interneurons (ChR2-PV, right). h–j Same as c–e but tLTP induction with blue light stimulation (blue bar) for ChR2-SST activation (h), for ChR2-SST activation in the presence of D-AP5 (50 μM, i), and for activation of ChR2-PV (j) in AβO1–42-treated slices. k Same as f but with ChR2-SST activation (green), ChR2-SST activation in the presence of D-AP5 (dotted green), and ChR2-PV activation (purple) in AβO1–42-treated slices. Paired Student’s t test for comparing test and control pathways (f, k, *p < 0.05, ns: not significant), one-way ANOVA with post-hoc Tukey’s test for comparing test pathways in different conditions (f, k, #p < 0.05). Data are represented as mean ± SEM
AβO1–42 causes selective dysfunction of SST interneuron-mediated disinhibition to CA1 PC
How could SST activation have contributed to the restoration of NMDAR-tLTP induction during theta-nested gamma oscillations? SST interneurons, such as oriens lacunosum-moleculare (OLM) cells, inhibit the distal dendrites of PCs in CA1 [39], but they also provide disinhibition of feedforward inhibition activated by SC input to CA1 PC’s proximal dendrites [39]. Moreover, optical stimulation of SST interneuron-mediated disinhibition during LTP induction has been shown to enhance LTP [39]. Thus, one possibility is that AβO1–42 impairs SST interneuron-mediated disinhibition of proximal dendrites of CA1 PCs, and thereby, tLTP. To investigate this possibility, we recorded SC stimulation-evoked IPSCs from CA1 PCs and compared them with SC stimulation-evoked IPSCs paired with CA1 PC spikes evoked by alveus stimulation (4 spikes at 100 Hz, repeated at 5 Hz), which mimics theta-nested gamma oscillation-like tLTP induction, as in Fig. 5b (Fig. 6a, b, Additional file 10: Figure S10). The amplitude of SC stimulation-evoked IPSCs significantly decreased when it was paired with alveus stimulation (Fig. 6c, g, black bar), showing that SST interneurons activated by alveus stimulation resulted in SST interneuron-mediated disinhibition. SST interneuron-mediated disinhibition was significantly decreased in AβO1–42-treated slices (Fig. 6d, g, red bar), but it was fully restored by optical stimulation of ChR2-expressing SST interneurons to a level similar to that in DMSO-treated slices (Fig. 6e–g, blue bar). In addition, when SC stimulation was paired with 50-ms-long optical stimulation of ChR2-expressing SST interneurons alone, the amplitude of SC stimulation-evoked IPSCs was similar in both DMSO-treated and AβO1–42-treated slices (Additional file 11: Figure S11), further supporting our hypothesis that optical restoration of SST interneuron-mediated disinhibition underpins the restoration of tLTP induction in AβO1–42-treated slices.
Fig. 6
figure 6
AβO1–42 causes dysfunction of SST interneuron-mediated disinhibition to CA1 PC. a, b Experimental setup for whole-cell voltage-clamp recordings of IPSCs in CA1 PC during theta-nested gamma oscillation-like tLTP induction. CA1 PC spikes were elicited by stimulating the CA1 PC axons in CA1 alveus. c IPSCs evoked by SC stimulation alone (black) and pairing of SC stimulation with alveus stimulation in DMSO-treated slices (gray). Disinhibition was measured by the difference in IPSCs amplitudes of the two conditions. d Same as c but in AβO1–42-treated slices. e, f Same as a–c but with activation of ChR2-expressing SST interneuron (ChR2-SST) with blue light (470 nm) in AβO1–42-treated slices. g Comparison of disinhibition of IPSCs amplitude in DMSO-treated (black), AβO1–42-treated slices (red) and with activation of ChR2-SST interneuron in AβO1–42-treated slices (blue). One-way ANOVA with post hoc Tukey’s test (g, #p < 0.05, ns: not significant). Data are represented as mean ± SEM
Distinct functional roles of PV and SST interneurons in gamma oscillogenesis and theta-nested gamma oscillation-induced tLTP
Our data supports the following hypothesis about how CA3 inputs impinging on CA1 PCs during hippocampal oscillations undergo LTP in a healthy brain [16,17,18,19]: gamma-frequency spikes of CA1 PCs during theta-nested gamma oscillations generated by perisomatic-targeting PV interneurons recruits SST interneurons, which in turn disinhibits CA1 PCs’ perisomatic dendrites, creating a window of opportunity for tLTP induction. To test this hypothesis, we built a computational network model consisting of CA1 PC, PV, and SST interneurons, together with CA3 input synapsing onto proximal dendritic spines of the CA1 PC providing feedforward inhibition to CA1 PC by activating an inhibitory interneuron (IN) (Fig. 7a). A PV interneuron was reciprocally connected to the CA1 PC while a SST interneuron disinhibited the IN. Parameters were tuned to reflect the in vitro-recorded firing rate-input current relationship (Fig. 7b, Additional file 4: Figure S4c, l). The excitatory CA3-CA1 synapse was modeled to undergo a deterministic intracellular Ca2+ concentration ([Ca2+]i)-dependent tLTP induction (Fig. 7c). In this model, sinusoidal 5-Hz current input that mimics blue light stimulation delivered to ChR2-expressing CA1 PC (Fig. 7d) activated the reciprocally connected PV interneuron to entrain CA1 PC and SST interneuron spikes at gamma oscillations, as shown in the spike raster plot (Fig. 7e). Such gamma-frequency-entrained SST interneuron’s spikes inhibited the IN from spiking (Fig. 7e, IN), and when CA3 input was activated at the rising phase of theta oscillations, SST interneuron-mediated disinhibition allowed the [Ca2+]i of CA1 PC spike to cross the threshold for tLTP induction (Fig. 7g, h). In contrast, in a network model without SST interneuron (Fig. 7f), CA3 input-activated feedforward inhibition (Fig. 7f, IN) blocked tLTP induction (Fig. 7g, h). Modulation of SST interneuron activation had no effect on the entrainment of PV interneurons at gamma-frequency and phase-locking of their spikes relative to CA1 PC-generated gamma-frequency spikes (Additional file 12: Figure S12). These results further underscore the differential roles of PV and SST interneurons in hippocampal theta-nested gamma oscillations and tLTP induction, respectively, and suggest how the optogenetic activation of PV and SST could have restored gamma oscillations and tLTP in AβO1–42-treated slices.
Fig. 7
figure 7
Distinct roles of PV and SST interneurons in gamma oscillogenesis and theta-nested gamma oscillation-induced tLTP. a Schematic diagram of CA3-CA1 hippocampal network model consisting of Hodgkin-Huxley-type computational models of CA1 PC, PV interneuron (PV model), SST interneuron (SST model), and a feedforward inhibition-mediating interneuron (IN model). The CA3 input activates IN and also provides excitation to the dendritic spine of the CA1 PC. b Firing rate plotted as a function of depolarizing current steps in 20 pA in PV interneuron (purple) and SST interneuron (green) recorded in vitro (empty circle, data from Additional file 4: Figure S4c, l), and that of the PV and SST models (filled circle). c Schematic of a deterministic [Ca2+]i-dependent spike timing-dependent plasticity (STDP) model. d A simulation of theta-nested gamma oscillation-induced tLTP. Oscillatory current (Itheta, 5 Hz, 20 pA) superimposed with a step current (Istep, 15 pA) was simulated to CA1 PC (top) to mimic gamma-frequency spikes in CA1 PC (middle). For tLTP induction, stimulation of CA3 input preceded the CA1 PC spikes by 10 ms, repeated at 5 Hz (bottom). e, f Representative raster plot of each neuron model with SST activation (e) or without SST activation (f). g Representative [Ca2+]i at CA1 PC spine during tLTP induction with SST activation (black) or without SST activation (red). h Change in the normalized synaptic weight of CA3-CA1 synapse plotted as a function of time with (black) and without SST activation (red)
Discussion
Here we have provided the first experimental evidence on how AβO1–42 causes synapse-specific dysfunction in hippocampal inhibitory circuits to impair theta-nested gamma oscillations and theta-nested gamma oscillation-induced tLTP. AβO1–42 selectively disrupted reciprocal PC-to-PV and PV-to-PC synapses, which decreased the peak power of theta-nested gamma oscillations and desynchronized the phase of spikes and synaptic currents relative to gamma cycles (Fig. 1234). In contrast, AβO1–42 had no effect on either PC-to-SST synapse or SST-to-PC synapses, but it did selectively disrupt SST interneuron-mediated disinhibition to block NMDAR-mediated tLTP at CA3-to-CA1 synapses induced by theta-nested gamma oscillation-like stimulation (Figs. 5 and 6). Importantly, optical stimulation of PV and SST interneurons selectively restored theta-nested gamma oscillations and oscillation-induced tLTP, respectively, which strongly supports the conclusion that these phenomena were the result of synapse-specific dysfunctions of PV and SST interneurons induced by AβO1–42.
Based on our in vitro experimental observations, we built a computational network model of CA1 PC, PV, and SST interneurons which allowed us to infer possible reasons for why hippocampal oscillations are conducive to LTP in a healthy brain [16,17,18,19]. From our simulation results, we were able to see how perisomatic-targeting PV interneurons entrain both CA1 PC and SST interneurons at gamma-frequency which allowed for the SST interneuron to disinhibit CA3 input-activated feedforward inhibition onto CA1 PCs’ proximal dendrites, creating a time window for tLTP induction (Fig. 7). Thus, PV and SST interneurons have distinct functional roles in the induction of synaptic plasticity in different compartments of the CA1 PC, and the accumulation of AβO1–42 seen in Alzheimer’s disease may cause memory deficits due to impairment of these synaptic plasticity mechanisms.
Although all of our experiments are conducted in vitro, the gamma oscillation impairment observed in our study shares many similarities with the effects of Aβ on kainate-induced gamma oscillations in vitro [9] as well as gamma oscillations recorded in vivo in mouse models of Alzheimer’s disease [5,6,7,8]. Also, our finding that optical stimulation of PV interneurons can restore gamma oscillations is consistent with previous results showing that manipulations of PV interneurons [5, 8] or PV-like fast-spiking interneurons were able to restore gamma oscillations in Alzheimer’s disease mouse models in vivo [7]. However, unlike previous studies using animal models with the late phase of Alzheimer’s disease [5, 7, 8], the acute effects of AβO1–42 that we uncovered here may only account for the early phase of Alzheimer’s disease. In Alzheimer’s disease mouse models such as APP/PS1 mice [40] and hAPPJ20 mice [5], spike firing rates and membrane potentials of PV interneuron are increased while in early phase of Alzheimer’s disease, pathological effects of AβO1–42 are mainly limited to synaptic dysfunctions with the intrinsic neuronal properties are spared [41], which is consistent with our results (Figs. 2 and 3 and Additional file 4: Figure S4). Thus, optogenetic activation of PV interneurons could have restored theta-nested gamma oscillations by directly depolarizing PV interneurons, which in turn compensate for the AβO1–42-induced reduced PV interneuron-evoked EPSCs to CA1 PC (Fig. 2) to resynchronize CA1 PC spikes during theta-nested gamma oscillations (Fig. 4), consequently leading to the restoration of theta-nested gamma oscillations. In addition to the reduction in gamma oscillation power, epileptic hyper-synchronous activities are widely observed in human patients with Alzheimer’s disease [6, 42] and in genetically modified Alzheimer’s disease mouse models [5, 6, 27, 43, 44]. Since the occurrence of epileptic activities in Alzheimer’s disease mouse models requires the abnormal aggregation of Aβ fibrils [43] and tau protein [44], but not AβO1–42 [43], it may be that hyper-synchrony may develop with Alzheimer’s disease progression [6, 45]. In fact, it is well established that AβO1–42 causes hyperexcitability in excitatory neurons [26]. Also, the increase in EPSC and decrease in IPSC amplitudes in CA1 PC during kainate-induced gamma oscillations under AβO1–42 pathology was observed in vitro [9]. Thus, it may be that the balance between excitation and inhibition is disrupted in Alzheimer’s disease but how the same neural circuit alternates between hypo- and hyper-synchrony requires further investigation.
Although many studies manipulated PV interneurons in Alzheimer’s disease studies [5, 7, 8], our study is the first to directly show how manipulation of SST interneurons could alleviate Alzheimer’s disease-related dysfunctions. In contrast to many studies targeting dysfunctional excitatory synapses [46,47,48,49] or LTP induction-related intracellular cascades in order to restore LTP in Alzheimer’s disease mouse models [49,50,51], we show that reinstating SST interneuron-mediated disinhibition [39] is sufficient for restoring tLTP in AβO1–42-treated slices in vitro (Figs. 5 and 6). In fact, SST interneuron-mediated disinhibition unmasks the back-propagating spike required for the induction of tLTP [52, 53]. Thus, our results suggest that SST interneurons’ neural circuit dysfunction could explain the tLTP impairment caused by acute application of AβO1–42 resembling early stages of Alzheimer’s disease, further supported by our in silico hippocampal network simulation (Fig. 7, Additional file 12: Figure S12). Although we did not get to identify the interneuron subtype that provides disinhibition to CA1 PC through SST interneuron activation, CCK-positive interneurons such as Schaffer collateral-associated cells [54,55,56] or bistratified cells [39] that are located in the stratum radiatum could be potential candidates. Thus, identifying the interneuron subtypes involved in disinhibition could help target the disinhibitory synapse that is impaired by AβO1–42 pathology. A recent study reported that optogenetic activation of OLM interneurons can induce type 2 theta oscillations in vivo [31], indicating that SST interneurons may also contribute to the generation of theta oscillations in addition to providing disinhibition to CA1 PC in vivo. Since we optically stimulated theta oscillations in order to induce gamma oscillations in vitro, our data cannot resolve the individual contribution of PV or SST interneurons on theta oscillation impairment in Alzheimer’s disease [57, 58]. Moreover, it is possible that theta-nested gamma oscillations could play a role in the induction of synaptic plasticity in interneurons [59]; thus, the neural circuit mechanism linking theta-nested gamma oscillations and tLTP may be more intricate than suggested in the present study (Fig. 7). Interestingly, a recent study reported re-emergence of LTP in aged Tg2576 Alzheimer’s disease mice which correlates with a decrease in PV interneuron number [60]. Thus, the specific manner in which PV and SST interneurons are affected as the pathologies of Alzheimer’s disease progress with age in vivo to disrupt synaptic plasticity requires further investigation. Nonetheless, our data suggests that targeted manipulation of interneuron populations in the hippocampus may be a promising approach for treatments of early-stage Alzheimer’s disease.
Although the optogenetic manipulation technique we adopted in this study targeted CA1 PV and SST interneurons, in CA1 alone, there are more than 20 interneuron subtypes [61, 62] and PV and SST interneurons do not relate to specific interneuron types, nor indeed are these two markers entirely non-overlapping in CA1 [63,64,65,66,67,68]. PV can be expressed in both axo-axonic and fast-spiking interneurons, and SST can be found not only in oriens lacunosum-moleculare interneurons, but in various long-range projecting interneurons, too. Indeed, bistratified cells (found in stratum oriens) express both PV and SST [54, 69,70,71]. Therefore, care is warranted in interpreting our results.
Conclusions
In summary, by optogenetically manipulating PV and SST interneurons, here we showed for the first time that AβO1–42 causes synapse-specific dysfunctions in PV and SST interneurons’ synapses, which allows us to uncover how AβO1–42 causes concomitant impairments of hippocampal theta-nested gamma oscillations and oscillation-induced tLTP at CA3-to-CA1 synapses. Thus, our findings provide crucial insight that will help guide future studies aimed at identifying the molecular target that gives rise to AβO1–42-induced synapse-specific dysfunctions, potentially leading to novel therapeutic targets for Alzheimer’s disease.
Methods
Animals
Three different lines of mice, C57BL/6 mice, PV-Cre knock-in mice (C57BL/6 background, Jackson Laboratory, stock #017320), and SST-IRES-Cre (C57BL/6 background, Jackson Laboratory, stock #013044) knock-in mice (4–11 weeks old) were used [72]. All animals were kept in 12:12-h light-dark cycles with food and water available ad libitum. All animal care and experimental procedures were approved by the Institutional Animal Care and Use Committee of Korea University (KUIACUC-2017-112).
Virus
AAV particles were purchased from the UNC Vector Core. To express ChR2 [73] selectively in CA1 PC, AAV5-CaMKII-hChR2(E123T/T159C)-p2A-mCherry-WPRE (3.8 × 1012 virus molecules/ml, 1 μl) was injected in all three different lines of mice bilaterally into the hippocampus. For the selective expression of eYFP, Arch, ChR2, or C1V1 on PV or SST interneurons, AAV2-EF1a-DIO-EYFP (4.6 × 1012 virus molecules/ml, 1 μl), AAV5-EF1a-DIO-eArch3.0-EYFP (5 × 1012 virus molecules/ml, 1 μl), AAV5-EF1a-DIO-hChR2(E123T/T159C)-p2A-mCherry-WPRE (3.8 × 1012 virus molecules/ml, 1 μl), or AAV2-EF1a-DIO-C1V1(E162T)-TS-p2A-EYFP-WPRE (3 × 1012 virus molecules/ml, 1 μl) were injected bilaterally into the hippocampus of in PV-Cre or SST-Cre mice.
Stereotaxic virus injections
Mice were deeply anesthetized under 2% isoflurane (2 ml/min flow rate) and head-fixed into a stereotaxic frame (Stoelting Co.). Craniotomies were made bilaterally to target CA1 area of the hippocampus for viral injections (from bregma: anteroposterior − 2.70 mm, lateral ± 2.50 mm, and dorsoventral − 1.75 mm or anteroposterior − 2.56 mm, lateral ± 2.6 mm, and dorsoventral − 1.85 mm). One microliter of each virus suspension was injected into the CA1 area of the hippocampus at a rate of 0.15 μl/min through a Hamilton syringe using a motorized stereotaxic injector (Stoetling Co.). The syringe was left in the brain for more than 5 min to allow for virus diffusion. The scalp was sutured and disinfected with antibiotic, after which the mice were returned to their home cage for recovery for at least 14 days.
Preparation and treatment of AβO1–42 to hippocampal slices
Soluble AβO1–42 was prepared following methods in Lambert et al. [4] with a slight modification [74]. Aβ1–42 or Aβ42–1 powder (Bachem) was dissolved in 1,1,1,3,3,3-hexafluoro-2-propanol (HFIP, Sigma Aldrich) for monomerization at a final concentration of 1 mM and incubated for 90 min. HFIP was evaporated under vacuum condition (SpeedVac). The remaining thin and clear film of Aβ1–42 or Aβ42–1 was dissolved in dimethyl sulfoxide (DMSO, Sigma Aldrich) to make 5 mM Aβ1–42 or Aβ42–1 stock, which was aliquoted and frozen at − 20 °C. The Aβ1–42 or Aβ42–1 stock was thawed and diluted to 100 μM in artificial cerebrospinal fluid (aCSF, containing (in mM): 126 NaCl, 3 KCl, 1.25 NaH2PO4, 2 MgSO4, 2 CaCl2, 25 NaHCO3, and 10 glucose at pH 7.2–7.4 bubbled with 95% O2/5% CO2). After dilution, Aβ1–42 or Aβ42–1 solution was incubated for 18 h at 4 °C for Aβ oligomerization. Before the recording, 2% DMSO (vehicle) and 100 μM AβO1–42 or AβO42–1 were treated into hippocampal slices in 31.2 ml of aCSF for 20 min by diluting it to a final concentration of 200 nM AβO1–42 or AβO42–1 in 0.004% DMSO for each condition.
Western blot analysis
Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE)
AβO1–42 were prepared as described above and resolved on a nonreducing 4–15% tris-glycine–SDS-PAGE gels with LDS sample buffers [75]. The gel was transferred on to a 0.2-μm PVDF membrane (Bio-Rad) according to the manufacturer’s recommendation. Membranes were blocked in 5% bovine serum albumin (BSA) in tris-buffered saline containing 0.01% Tween 20 for 1 h at room temperature. Blots were incubated in the primary antibody mOC64 (rabbit monoclonal against amino acid residues 3–6 of Aβ; Cat# ab201060, Lot# GR3235744-4, RRID: AB_2818982, Abcam) [76] at 1:200 dilution overnight at 4 °C. Immunoreactivity was detected with enhanced chemiluminescence (Bio-Rad) and imaged using Fluorchem E system (ProteinSimple). Molecular weight values were estimated using Precision Plus Protein™ Dual Color Standards (Bio-rad).
Native PAGE
AβO sample was diluted with native PAGE sample buffer (Bio-rad) and then subjected to native PAGE using a 4–15% tris-glycine gel with the tris-glycine running buffer (Bio-rad). Following transfer to PVDF membrane, membranes were blocked in 5% BSA in Tris-buffered saline containing 0.01% Tween 20 for 1 h at room temperature. Blots were probed using rabbit monoclonal Aβ antibody (mOC64, 1:200, Cat# ab201060, Lot# GR3235744-4, RRID: AB_2818982, Abcam) overnight at 4 °C. Immunoreactivity and imaging were performed as described above.
In vitro hippocampal slice preparation
Mice were deeply anesthetized using 1.25% Avertin solution (8 g of 2, 2, 2-Tribromoethanol and 5.1 ml of 2-methyl-2-butanol in 402.9 ml saline, Sigma Aldrich) at a delivery rate of 0.2 ml/10 g body weight and perfused with ice-cold cutting solution (containing (in mM): 180 sucrose, 2.5 KCl, 1.25 NaH2PO4, 25 NaHCO3, 11 glucose, 2 MgSO4, and 1 CaCl2 at pH 7.2–7.4 oxygenated with 95% O2/5% CO2). Either coronal or horizontal hippocampal slices (300–400 μm) were cut using a vibratome (VT 1000 S, Leica Microsystems). Slices were allowed to recover for 20 min in a mixture of cutting solution and aCSF solution at 1:1 ratio, after which the slices were further incubated in aCSF for at least 1 h at 30–32 °C before performing electrophysiological recordings. To compare between DMSO and AβO1–42 conditions in the same slice (Fig. 1, Fig. 4c–i), hippocampal slice was first treated with 2% DMSO in aCSF for 20 min and then the same hippocampal slice was treated with 100 μM AβO1–42 or AβO42–1 in aCSF by diluting to a final concentration of 200 nM for 20 min. In all other experiments (Figs. 235, and 6 and Additional file 3: Figure S3, Additional file 4: Figure S4, and Additional file 11: Figure S11), hippocampal slices were treated with either 2% DMSO or 100 μM AβO1–42 or AβO42–1 in aCSF by diluting to a final concentration of 200 nM for 20 min before performing electrophysiological recordings.
In vitro field and patch-clamp recordings
Slices were moved to a recording chamber filled with aCSF (30–32 °C), and CA1 area of the hippocampus was identified under the guidance of differential interference contrast microscopy (BW51W, Olympus). LFP was recorded in the CA1 PC layer using a borosilicate glass electrode (2–4 MΩ) filled with aCSF (Figs. 123, and 4 and Additional file 2: Figure S2, Additional file 3: Figure S3, Additional file 5: Figure S5, Additional file 6: Figure S6, and Additional file 7: Figure S7). In some experiments (Figs. 2c–h, 3a–g, and 4j–n), LFP recordings were simultaneously performed with whole-cell patch-clamp recordings from either CA1 PC, PV, or SST interneurons using borosilicate glass electrode (4–8 MΩ) in either voltage-clamp or current-clamp mode. All synaptic currents were recorded in voltage-clamp recordings with electrodes filled with internal solution containing (in mM) 115 Cesium methanesulfonate (CsMSF), 8 NaCl, 10 HEPES, 0.3 GTP-NaCl, 4 ATP-Mg, 0.3 EGTA, 5 QX-314, and 10 BAPTA (pH 7.3–7.4 and 280–290 mOsm/L). IPSC and EPSC were recorded at the holding potential of + 10 mV and − 80 mV, respectively. In recording spikes and intrinsic membrane properties in current-clamp recordings, electrodes were filled with intracellular solution containing (in mM) 110 K-gluconate, 40 HEPES, 4 NaCl, 4 ATP-Mg, and 0.3 GTP-NaCl (pH 7.2–7.3 and 270–300 mOsm/L). Intrinsic membrane properties such as spike probability, sag, and rebound potential were measured at resting membrane potential of the neuron in response to current steps (0 pA to ± 200 pA for 500 ms in 20 pA steps). Input resistance (MΩ) and membrane time constant (τ) were analyzed based on the voltage response to 50-ms-long negative current step (5 pA) by fitting an exponential curve,
$$ {R}_{\mathrm{in}}=\frac{\left({V}_0-{V}_{\mathrm{steady}}\right)}{I} $$
$$ V={V}_0+{Ae}^{\left(-\frac{t}{\tau}\right)} $$
where V0 is the initial voltage, Vsteady is the steady state voltage of the first exponential curve fit, A is the amplitude constant, and I is the amplitude of the current step. To record EPSCs evoked by PCs in PV or SST interneurons, a stimulation electrode was placed in the alveus on the subiculum side of the CA1 area to stimulate the axons of PC with a radial cut made between CA1 and subiculum to block the activation of CA3 axons (Fig. 2i–p). To analyze the S-R curve of PC-evoked EPSCs in PV or SST interneurons, alveus was stimulated using a single electrical stimulation pulse (100 μs) at six different intensities (10, 50, 100, 150, 200, and 300 μA, Fig. 2j, n). The alveus stimulation intensity which gave 50% of the maximal EPSC response (half-maximal stimulus, 115–210 μA) was used in subsequent experiments measuring PPR and short-term plasticity, for which a train of ten stimulation pulses at 50 Hz (100 μs; 115–210 μA) were delivered (Fig. 2k, o). Total charge of PC-evoked EPSCs was calculated by integrating the area under the EPSC trains (Fig. 2l, p). All signals were amplified (MultiClamp 700B amplifier, Molecular Devices), low-pass filtered at 10 kHz, and acquired at 5 kHz using ITC-18 data acquisition interface (HEKA Elektronik). Igor Pro software (WaveMetrics) was used for generating command signals, acquiring data as well as data analysis. In current-clamp recordings, only cells with resting membrane potential negative to − 50 mV and with input resistance in the range of 100–400 MΩ were included in the analysis. Reported voltages are corrected for the liquid junction potential, which was calculated as ~ 10 mV. In voltage-clamp recordings, 10 min was allowed after break-through for stabilization before recordings commenced. Series and input resistance were monitored throughout the experiment, and cells with > 20% change in series resistance were discarded.
Light-induced theta-nested gamma oscillations and gamma phase analysis
For the induction of theta-nested gamma oscillations, ChR2-expressing PCs were activated by sinusoidal (5 Hz) blue light (470 nm) [34] (Fig. 123, and 4 and Additional file 2: Figure S2, Additional file 3: Figure S3, Additional file 5: Figure S5, Additional file 6: Figure S6, and Additional file 7: Figure S7). Blue light was delivered using a digital micromirror device (DMD, Polygon400, Mightex) through the objective (× 40) of the microscope (BX51W, Olympus), which covered the 550-μm diameter circle of the CA1 area with the center of the illumination positioned at the field electrode. The intensity of the blue light varied between 0 to a maximum intensity of 15 mW, which was controlled using a custom-made Arduino-based controller. Igor Pro was used to control DMD and synchronize optical stimulation with the electrophysiological recordings. LFP data were first down-sampled to 1 kHz and band-pass filtered between 20 and 120 Hz for gamma oscillations. Welch’s power spectral densities (PSD) of gamma oscillations (3 repetitions of 1-s theta-nested gamma oscillations) were analyzed to quantify the peak power and peak frequency (Figs. 1h–j and 4e–g and Additional file 2: Figure S2, Additional file 3: Figure S3, Additional file 5: Figure S5, Additional file 6: Figure S6, and Additional file 7: Figure S7). Spectrogram of gamma oscillations was generated using short-time Fourier transform with window size = 100 ms and step size = 1 ms. Phase histogram (Fig. 4k) of spike or PSC was generated by calculating the instantaneous phase of spikes or PSCs using the Hilbert transform of simultaneously recorded gamma oscillations. The zero phase of gamma oscillations was defined as the peak of the gamma cycle. Probability of spike or PSCs as a function of the phase of reference gamma oscillations was obtained using 20 bins. Resultant vectors were calculated from the phase histogram and plotted in the polar plot (Fig. 4l) from which vector length (Fig. 4m) and vector phase (Fig. 4n) were calculated. Mean value and statistical significance of vector phase were calculated using the Circular Statistics Toolbox in MATLAB (R2018a) [77]. To generate phase-amplitude comodulograms of theta-nested gamma oscillations (Figs. 1k and 4h and Additional file 3: Figure S3, Additional file 5: Figure S5, and Additional file 6: Figure S6), theta phase was calculated using Hilbert transformation and binned into 20 phase bins with 18° intervals. At each theta bin, the power spectrogram of gamma oscillations was calculated using short-time Fourier transform. The zero phase of theta oscillations was defined as the peak of the theta cycle. To analyze the phase-amplitude coupling strength of theta-nested gamma oscillations (Figs. 1l, 4i, Additional file 3: Figure S3, Additional file 5: Figure S5 and Additional file 6: Figure S6), we calculated the modulation index which is defined as the normalized Kullback-Leibler distance between probability distribution of gamma amplitude per each theta phase bin (18 bins with 20° intervals) and uniform distribution [78]. To obtain the probability distribution of gamma amplitude, mean amplitude of gamma oscillations for each bin was normalized by the sum of gamma amplitude of total bins. Modulation index value of 0 indicates the absence of phase-amplitude coupling, and the higher modulation index value indicates the stronger phase-amplitude coupling.
Optical modulation of opsin-expressing PV and SST interneurons during patch-clamp recordings
We expressed Arch or C1V1 in PV and SST interneurons and ChR2 in PC in the same hippocampal slice to optically inactivate (Fig. 3b–e, Additional file 5: Figure S5, and Additional file 6: Figure S6) or activate (Fig. 4a–d) interneurons during theta-nested gamma oscillations, respectively. The optimal wavelength for stimulating Arch is a green-colored 565-nm light. However, since 565-nm green light also induced excitatory synaptic currents by activating ChR2-expressing PCs (Additional file 7: Figure S7b, d) as well as inducing gamma oscillations in the LFP (Additional file 7: Figure S7b, e) while 590-nm yellow light had no direct effect on ChR2-expressing PC (Additional file 7: Figure S7c, d), we used 590-nm yellow light in activating both Arch- and C1V1-expressing interneurons during blue light-induced theta-nested gamma oscillations. The effectiveness of 590-nm yellow light on Arch-expressing PV and SST interneurons was tested by performing whole-cell voltage-clamp recordings in PV-Cre or SST-Cre mice, respectively (Additional file 8: Figure S8). For the inactivation of Arch-expressing interneurons during theta-nested gamma oscillations (Fig. 3d, e, Additional file 5: Figure S6, and Additional file 6: Figure S6), a tonic yellow light of a fixed light intensity (1 s, 3 mW) was delivered using the DMD. For the activation of C1V1-expressing PV interneuron during theta-nested gamma oscillations (Fig. 4c, d), a sinusoidal (5 Hz) yellow light (590 nm) was delivered through DMD with the intensity of light sinusoidally varied between 0 and 3 mW using a custom-made Arduino-based controller. To record IPSC evoked by PV and SST interneurons in CA1 PC, ChR2-expressing PV and SST interneurons were optically stimulated with blue light (470 nm) in PV-Cre and SST-Cre mice, respectively, during whole-cell voltage-clamp recordings with the membrane held at + 10 mV (Fig. 3i, n). To analyze the S-R curve of PV/SST interneuron-evoked IPSCs in CA1 PC, a single light pulse (470 nm, 5 ms) was delivered to ChR2-expressing PV or SST interneurons at different light powers (5, 10, 25, 50, 75, 100% of maximal light power (15 mW), Fig. 3j, o). The light power which gave 50% of the maximal IPSC response (half-maximal stimulus, 3.75–9 mW) was used for the subsequent PPR and short-term plasticity analysis, for which a train of ten blue light pulses at 50 Hz were delivered (470-nm light, 5-ms duration, Fig. 3k, p; 3.75–9 mW). The total charge of PV/SST-evoked IPSCs was calculated by integrating the area under the IPSC train (Fig. 3l, q).
Theta-nested gamma oscillation-induced tLTP induction protocol
In order to induce theta-nested gamma oscillation-induced tLTP at CA3-CA1 synapse during theta-nested gamma oscillation-like activity, we paired the presynaptic EPSP evoked by SC stimulation with postsynaptic bursts (4 spikes at 100 Hz, each spike elicited with 3 ms current steps, 800 pA) with a 10-ms time window repeated at 5 Hz [38] for 200 times. EPSPs were evoked every 6 s using two stimulating electrodes placed in the stratum radiatum of the CA1 area to activate SC, one for monitoring EPSPs in the control pathway and one for test pathway (Fig. 5a, b). Test and control pathways were stimulated 2 s apart. EPSP amplitudes were in the range of 3–5 mV (150–400 μA, 20–80 μs, Digitimer Ltd.) and were recorded at membrane voltage held at − 75 mV. Following 10 min of baseline EPSP recordings of both pathways, tLTP induction protocol was delivered to the test pathway, after which EPSPs were evoked every 6 s in both pathways in either DMSO-treated or AβO1–42-treated hippocampal slices prepared from C57BL/6 mice (Fig. 5c–e). To investigate the effect of activation of PV and SST interneurons on tLTP in AβO1–42-treated hippocampal slices, we expressed ChR2 in either PV or SST interneurons and optically stimulated ChR2-expressing PV or SST interneurons using tonic blue light (470 nm, X-cite 110LED, Excelitas Tech., 100% light intensity) during the tLTP induction in AβO1–42-treated hippocampal slices prepared from PV-Cre or SST-Cre mice, respectively (Fig. 5g–j). tLTP induction was repeated in the presence of 50 μM D-AP5 to see if the tLTP is NMDA receptor-dependent (Fig. 5d, i). The slope of EPSP was calculated as an index of synaptic efficacy, measured by performing a linear fit on the rising slope of the EPSP between time points corresponding to 20 and 80% of the EPSP peak amplitude. Changes in synaptic efficacy were estimated as percentage change relative to the mean EPSP slope during the first 10 min of baseline recordings. To compare synaptic efficacy between neurons and experimental conditions, the mean of the normalized EPSP slope in the time period between 25 and 30 min after the tLTP induction was calculated (Fig. 5f, k).
SST interneuron-mediated disinhibition
To measure SST interneuron-mediated disinhibition during tLTP induction, we performed whole-cell voltage-clamp recordings in PC to record SC stimulation-evoked IPSC before and during tLTP induction. tLTP induction was performed by pairing of presynaptic EPSP and postsynaptic PC spikes by stimulating the SC and evoking postsynaptic spikes by stimulating the CA1 axons in the alveus at 100 Hz (4 pulses) with 10-ms time window, repeated at 5 Hz for 20 times (Fig. 6b, Additional file 10: Figure S10). All recordings were performed in the presence of D-AP5 (50 μM) to prevent synaptic plasticity during tLTP induction. To test if alveus stimulation can elicit spikes in PV and SST interneurons similar to that during blue light-induced theta-nested gamma oscillations as in Fig. 2c, we performed current-clamp recordings in PV and SST interneurons and stimulated alveus at 100 Hz (4 stimuli) repeated at 5 Hz (Additional file 9: Figure S9b, d, top). To ensure that alveus stimulation activated PC axons and is not a result of direct stimulation of other pathways, we repeated the experiments in the presence of D-AP5 (50 μM) and CNQX (20 μM) to block NMDA and AMPA receptors (Additional file 9: Figure S9b, d, bottom). Since alveus stimulation can activate both PV and SST interneurons to provide direct inhibition to PC, we isolated the SC stimulated IPSC during tLTP induction (Additional file 10: Figure S10b, (4), gray) by subtracting the IPSC evoked by alveus stimulation alone (Additional file 10: Figure S10b, (2) Alveus stim, light brown) from the IPSC evoked by pairing SC stimulation with alveus stimulation (Additional file 10: Figure S10b, (3) SC + alveus stim, brown). In calculating the SST interneuron-mediated disinhibition, we took the difference between the IPSC amplitude evoked by SC stimulation alone (Additional file 10: Figure S10b, (1) SC stim, black) and IPSC amplitude calculated in (4) (Additional file 10: Figure S10b, gray). In order to directly test the effect of the activation of SST interneurons on SC stimulation-evoked IPSC, we optically activated ChR2-expressing SST interneurons simultaneously with SC stimulation in the DMSO-treated and AβO1–42-treated hippocampal slices prepared from SST-Cre mice (Additional file 11: Figure S11).
Drugs
CNQX, SR95531 (GABAzine), and D-AP5 were purchased from Tocris. PBS, Urea, and Aβ1–42/Aβ42–1 powder were purchased from Gibco, Affymetix, and Bachem, respectively. DMSO and the other regents were all purchased from Sigma. For western blot analysis, rabbit monoclonal antibody mOC64was purchased from Abcam (Cat# ab201060, Lot# GR3235744-4, RRID: AB_2818982). Horseradish peroxidase (HRP)-conjugated anti-rabbit antibodies (Cat# 170-6515, Control# 64170140, RRID: AB_2617112), Mini-PROTEAN TGX 4–15% tris-glycine gels, 4x Laemmli sample buffer, Native sample buffer, and running buffer were all purchased from Bio-Rad.
Fluorescence imaging
To confirm the expression of opsins in PC, PV, and SST interneurons, hippocampal slices were post-fixed overnight in 4% paraformaldehyde at 4 °C and subsequently washed in PBS. Washed slices were mounted with CUBIC mount solution [79], a tissue clearing technique that removes lipids from the sample to enhance transparency in imaging. Images were acquired using a confocal microscope (LSM-700, ZEISS) under a × 10 and × 20 objective.
CA3-CA1 hippocampal network model
To test whether SST interneuron-mediated disinhibition is required for the theta-nested gamma oscillation-induced tLTP at CA3-CA1 synapse in a computational model, we modeled CA3-CA1 hippocampal network consisted of a multi-compartment PC, single-compartment PV interneuron (PV model), SST interneuron (SST model), and a feedforward inhibition-mediating interneuron (IN model) as the Hodgkin-Huxley neuron model [80] (Fig. 7a). The PC model was composed of a soma, an apical dendrite, and a dendritic spine, containing leakage (gL), Na+ (gNa), delayed-rectifier K+ (gKDR), A-type K+ (gA), L-type Ca2+ (gCaL), M-type K+ (gKM), afterhyperpolarization-activated (gAHP), and hyperpolarization-activated (gh) channels. PV, SST, and IN models contain leakage (gL), Na+ (gNa), delayed-rectifier K+ (gKDR), and A-type K+ (gA) channels. Spike activities of PV and SST models were calibrated to replicate the in vitro-measured firing rate-current relationship (Fig. 7b, Additional file 4: Figure S4c, l). All morphological, passive, and active parameters of models are shown in Additional file 13: Table S1. CA3-CA1 synapse was modeled at the PC spine located at 100 μm from PC soma. CA3 input evoked an EPSP in PC through AMPA and NMDA receptor models. AMPA receptor was modeled as a single-exponential model, and NMDA receptor was modeled with voltage-dependent magnesium block using the following equations,
$$ {I}_{\mathrm{AMPA}}={g}_{\mathrm{AMPA}}\times \left({e}^{-\frac{t}{\tau }}\right)\times \left({V}_m-{E}_{\mathrm{AMPA}}\right),\kern0.5em {I}_{\mathrm{NMDA}}={g}_{\mathrm{NMDA}}\times \left({e}^{-\frac{t}{\tau_{\mathrm{rise}}}}-{e}^{-\frac{t}{\tau_{\mathrm{decay}}}}\right)\times \left({V}_m-{E}_{\mathrm{NMDA}}\right)/\Big(1+\left(\frac{\left[ mg\right]}{n}\right)\times {e}^{-\tau}\times {V}_m $$
where Vm is the membrane potential, I is the synaptic current, g is the maximal conductance (AMPA, 0.3 pS; NMDA, 1 nS), τ is time constants (AMPA, 7 ms; τrise for NMDA, 4 ms; τdecay for NMDA. 21 ms), E is the reversal potential (0 mV), and [mg] is the magnesium concentration (0.5 mM). Maximal conductance of AMPA and NMDA was modeled to fit AMPA/NMDA ratio recorded in vitro [81]. Excitatory and inhibitory synapses between PC, PV, SST, and IN models were modeled using a double-exponential model [82]. All excitatory and inhibitory synapses had τrise of 3 ms and τdecay of 15 ms and 40 ms, respectively. For tLTP simulation, we used a deterministic Ca2+-dependent STDP model (Fig. 7c) [83]. tLTP was considered to be induced when intracellular Ca2+ concentration ([Ca2+]i) is greater than 4 μM which triggered a potentiation detector (P). Synaptic weight of CA3-CA1 AMPA synapse was determined by the readout variable (W). To simulate theta-nested gamma oscillation-induced spikes in PC, we injected oscillatory current (5 Hz, 20 pA) superimposed with a tonic step current (15 pA) onto PC soma. For tLTP induction, we paired CA3 input with PC spikes with a time window of 10 ms (Δt, Fig. 7d). The pairing was repeated five times, and all parameters of the STDP model are listed in Additional file 14: Table S2. In order to investigate whether the presence of SST interneurons in the network model has any effect on the entrainment of PV interneuronal spikes at gamma-frequency, firing rates of PC and PV were calculated for the first and the successive theta cycles (Additional file 12: Figure S12a, b). Also, the spike phases of PV interneurons were calculated relative to the PC spike timing where the inter-spike interval of PC spikes were considered as a period of gamma-frequency and each spike was considered as the trough of gamma cycle (Additional file 12: Figure S12c, d). All simulations were repeated 10 times with Gaussian white noise that generated membrane voltage fluctuations (σ = 50 pA, peak-to-peak amplitude of fluctuation = ~ 5 mV, [84]). All simulations were performed using the NEURON simulator [85] with a sampling rate of 10 kHz. The model is available on GitHub (https://github.com/kuncl/thetagamma_tLTP).
Data analysis
All data analysis was conducted using Igor Pro or MATLAB with custom-written scripts. Excel (Microsoft) and SPSS (IBM) software were used for statistical analyses.
Statistical analysis
Data are represented as mean with individual data values or mean ± SEM. Statistical significance was measured using Student’s t test or one-way, one-way repeated-measures, and two-way ANOVA followed by post hoc Tukey’s test. p value less than 0.05 was considered statistically significant. Statistical significance of spike phases was tested using Watson-Williams multi-sample circular test [86].
Availability of data and materials
All data generated during this study are included in either the manuscript or its additional files.
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Acknowledgements
We gratefully thank Danny Kanghoon Seo for advices on the optogenetic experimental technique.
Funding
Human Frontiers Science Program (HFSP) Young Investigator Award (RGY0073/2015) to B.A.R., M.M.K., and J.K., a grant of 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 (HI15C3086, HI17C0212, HI19C0646) to J.K., the Brain Convergence Research Program (NRF-2019M3E5D2A01058328) through the National Research Foundation (NRF) funded by the Korean Government (MIST) to J.K., and Global Ph.D Fellowship Program through the National Research Foundation of Korea (NRF) funded by Ministry of Education (NRF-2016H1A2A1907615) to K.P.
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Contributions
KP, JL, and JK designed, conducted, and analyzed all in vitro experiments; BAR and MMK helped setup optogenetic experimental methods; HJJ and JK designed the computational model simulation; HJJ conducted and analyzed computational model simulation data; JK wrote the original draft; and KP, JL, HJJ, MMK, BAR, and JK reviewed and edited the manuscript. All authors read and approved the final manuscript.
Corresponding author
Correspondence to Jeehyun Kwag.
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Supplementary information
Additional file 1 : Figure S1.
Western blot of native PAGE showing AβO1–42 after incubation at 4 °C for 18 h.
Additional file 2 : Figure S2.
Stability of optogenetically-induced theta-nested gamma oscillations in hippocampal slices in vitro.
Additional file 3 : Figure S3.
Impairment of optogenetically-induced theta-nested gamma oscillations in AβO1–42-treated hippocampal slice in vitro.
Additional file 4 : Figure S4.
Intrinsic properties of SST and PV interneurons in DMSO- and AβO1–42-treated hippocampal slices in vitro.
Additional file 5 : Figure S5.
Optogenetic inactivation of Arch-expressing PV interneurons reduces the power of gamma oscillations.
Additional file 6 : Figure S6.
Optogenetic inactivation of Arch-expressing SST interneurons has no effect on the power of gamma oscillations.
Additional file 7 : Figure S7.
Response of ChR2-expressing PC to different wavelengths of sinusoidal light stimuli.
Additional file 8 : Figure S8.
Current response of Arch-expressing PV interneuron, Arch-expressing SST interneuron, and C1V1-expressing PV interneuron to 590 nm light stimulation.
Additional file 9 : Figure S9.
Stimulation of CA1 PC axons with a theta-nested gamma oscillation-like pattern entrains PV and SST interneurons at gamma frequency.
Additional file 10 : Figure S10.
Experimental protocol for measuring SST interneuron-mediated disinhibition.
Additional file 11 : Figure S11.
Optical stimulation of ChR2-expressing SST interneurons restores AβO1–42-induced impairment of SST interneuron-mediated disinhibition.
Additional file 12 : Figure S12.
The effect of SST interneuron activation on spike firing rates and spike phases of CA1 PC and PV interneurons during theta-nested gamma oscillations in silico.
Additional file 13 : Table S1.
Parameters of CA1 PC, PV, SST and IN models.
Additional file 14 : Table S2.
Parameters of the deterministic Ca2+-dependent STDP model.
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Park, K., Lee, J., Jang, H.J. et al. Optogenetic activation of parvalbumin and somatostatin interneurons selectively restores theta-nested gamma oscillations and oscillation-induced spike timing-dependent long-term potentiation impaired by amyloid β oligomers. BMC Biol 18, 7 (2020). https://doi.org/10.1186/s12915-019-0732-7
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Keywords
• Alzheimer’s disease
• Amyloid beta oligomers
• Hippocampus
• Optogenetics
• Parvalbumin interneuron
• Somatostatin interneuron
• Theta-nested gamma oscillations
• Spike timing-dependent long-term potentiation
• Synapse-specific dysfunction | {
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2,388,696,801,286,956,500 | Article
Megacolon in multiple system atrophy: safety concerns related to PEG.
Department of Neurology, Niigata University Brain Research Institute, Niigata, Japan.
Movement Disorders (Impact Factor: 4.56). 03/2009; 24(7):1096-7. DOI:10.1002/mds.22281
Source: PubMed
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[show abstract] [hide abstract]
ABSTRACT: Multiple system atrophy (MSA) has varying clinical (MSA-P versus MSA-C) and pathological [striatonigral degeneration (SND) versus olivopontocerebellar atrophy (OPCA)] phenotypes. To investigate the spectrum of clinicopathological correlations, we performed a semi-quantitative pathological analysis of 100 MSA cases with well-characterized clinical phenotypes. In 24 areas, chosen from both the striatonigral (StrN) and olivopontocerebellar (OPC) regions, the severity of neuronal cell loss and gliosis as well as the frequency of glial (oligodendroglial) cytoplasmic inclusions (GCIs) and neuronal cytoplasmic inclusions (NCIs) were determined. Clinical information was abstracted from the patients' medical records, and the severity of bradykinesia in the first year of disease onset and in the final stages of disease was graded retrospectively. The degree of levodopa responsiveness and the presence or absence of cerebellar ataxia and autonomic symptoms were also recorded. We report that 34% of the cases were SND- and 17% were OPCA-predominant, while the remainder (49%) had equivalent SND and OPCA pathology. We found a significant correlation between the frequency of GCIs and the severity of neuronal cell loss, and between these pathological changes and disease duration. Our data also suggest that GCIs may have more influence on the OPC than on the StrN pathology. Moreover, we raise the possibility that a rapid process of neuronal cell loss, which is independent of the accumulation of GCIs, occurs in the StrN region in MSA. There was no difference in the frequency of NCIs in the putamen, pontine nucleus and inferior olivary nucleus between the SND and OPCA subtypes of MSA, confirming that this pathological abnormality is not associated with a particular subtype of the disease. In the current large post-mortem series, 10% of the cases had associated Lewy body pathology, suggesting that this is not a primary process in MSA. As might be expected, there was a significant difference in the severity of bradykinesia and the presence of cerebellar signs between the pathological phenotypes: the SND phenotype demonstrates the most severe bradykinesia and the OPCA phenotype the more frequent occurrence of cerebellar signs, confirming that the clinical phenotype is dependent on the distribution of pathology within the basal ganglia and cerebellum. Putaminal involvement correlated with a poor levodopa response in MSA. Our finding that relatively mild involvement of the substantia nigra is associated clinically with manifest parkinsonism, while more advanced cerebellar pathology is required for ataxia, may explain why the parkinsonian presentation is predominant over ataxia in MSA.
Brain 01/2005; 127(Pt 12):2657-71. · 9.92 Impact Factor
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ABSTRACT: Constipation is a prominent lower gastrointestinal tract dysfunction that occurs frequently in Parkinson's disease (PD). To investigate colonic transport and dynamic rectoanal behaviour during filling and defecation in patients with PD. Colonic transit time (CTT) and rectoanal videomanometry analyses were performed in 12 patients with PD (10 men and 2 women; mean age, 68 years, mean duration of disease, five years; mean Hoehn and Yahr grade, 3; decreased stool frequency (<3 times a week) in six, difficulty in stool expulsion in eight) and 10 age matched normal control subjects (7 men and 3 women; mean age, 62 years; decreased stool frequency in two, difficulty in stool expulsion in two). In the PD patients, CTT was significantly prolonged in the rectosigmoid segment (p<0.05) and total colon (p<0.01) compared with the control subjects. At the resting state, anal closure and squeeze pressures of PD patients were lower than those in control subjects, though not statistically significant. However, the PD patients showed a smaller increase in abdominal pressure on coughing (p<0.01) and straining (p<0.01). The sphincter motor unit potentials of the patients were normal. During filling, PD patients showed normal rectal volumes at first sensation and maximum desire to defecate, and normal rectal compliance. However, they showed smaller amplitude in phasic rectal contraction (p<0.05), which was accompanied by an increase in anal pressure that normally decreased, together with leaking in two patients. During defecation, most PD patients could not defecate completely with larger post-defecation residuals (p<0.01). PD patients had weak abdominal strain and smaller rectal contraction on defecation than those in control subjects, though these differences were not statistically significant. However, the PD patients had larger anal contraction on defecation (p<0.05), evidence of paradoxical sphincter contraction on defecation (PSD). Slow colonic transit, decreased phasic rectal contraction, weak abdominal strain, and PSD were all features in our PD patients with frequent constipation.
Journal of Neurology Neurosurgery & Psychiatry 02/2003; 74(2):268-72. · 4.92 Impact Factor
• [show abstract] [hide abstract]
ABSTRACT: Accessing the stomach via a gastrostomy is the preferred method for providing enteral nutritional support when supplementation is required for more than three or four weeks. Since its introduction in the early 1980s, percutaneous endoscopic gastrostomy has become the most popular method for creating a gastrostomy. It is a quick and cost-effective method and has supplanted open gastrostomy for the establishment of a gastrocutaneous fistula to provide access to the stomach for numerous indications. It is associated, however, with serious and potentially lethal complications which must be completely understood by the endoscopist. In addition, patient selection and thorough attention to details are paramount to the performance of a safe percutaneous endoscopic gastrostomy.
Gastrointestinal Endoscopy Clinics of North America 08/1998; 8(3):551-68. | {
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-4,046,441,696,876,117,000 | Prediabetes Reversal: Mastering Diet and Lifestyle for Insulin Resistance
Prediabetes Reversal: Mastering Diet and Lifestyle for Insulin Resistance
Key Takeaways
• Prediabetes is when your blood sugar is high but not high enough for type 2 diabetes, and over 88 million Americans had it in 2020.
• Having insulin resistance means your body doesn't use insulin well, leading to higher blood sugar levels.
• To stop prediabetes from becoming diabetes, it's important to eat healthy and stay active.
• A good diet for prediabetes includes lots of nutrients, less sugar, and more fiber to help your body use insulin better.
• Eating the right foods, like high-fiber grains and veggies, and fewer sweets and processed meats can help fix prediabetes.
• Planning your meals with the right balance of healthy foods can help manage your blood sugar and your weight.
• Exercising, reducing stress, and getting good sleep are super important to help turn prediabetes around, not just diet.
Understanding Prediabetes and Its Implications
If you've been told you're on the cusp of developing diabetes, know that you're not alone. Prediabetes is a prevalent condition, and grasping its intricacies is your first step towards health empowerment. Let's delve into what it means to have prediabetes and why taking action now is crucial.
What Is Prediabetes?
Prediabetes is a wake-up call. It occurs when your blood glucose levels are higher than normal but not high enough to be classified as type 2 diabetes. Think of it as an amber traffic light—a signal to proceed with caution before reaching a potential red. To provide some perspective, The Centers for Disease Control and Prevention (CDC) estimates that in 2020, more than 88 million American adults had prediabetes. That's more than 1 in 3 people.
Unlike diabetes, where the body can no longer regulate blood sugar effectively, prediabetes is a reversible condition. Taking stock of your lifestyle and making key changes can help prevent type 2 diabetes and even reverse prediabetes.
The Role of Insulin in Prediabetes
Insulin is like a key that unlocks your body's cells, allowing glucose to enter and be used for energy. With prediabetes, this system starts to fail. Your cells become resistant to insulin, which means glucose stays circulating in your blood. This can tire out the pancreas as it pumps out more insulin to compensate, and eventually, your blood sugar levels start to rise.
Why Managing Prediabetes Early Is Essential
Left unchecked, the repercussions of prediabetes can escalate. It's a pivotal moment where lifestyle choices can genuinely tip the scales—for better or for worse. By focusing on a pre diabetes diet and maintaining a healthy weight, you can help your body regain insulin sensitivity and stabilize your glucose levels.
Take heart in knowing that prediabetes doesn’t mean diabetes is inevitable. In fact, studies like the one from the Diabetes Prevention Program (DPP) reveal that with lifestyle interventions, such as diet and exercise, the onset of type 2 diabetes can be delayed or even prevented.
Setting the Stage for Healthier Choices
Understanding the relationship between prediabetes, insulin resistance, and metabolism sheds light on why your diet is a pivotal factor. An insulin resistance diet rich in nutrients, low in processed sugars, and high in fiber can support your body in using insulin more effectively.
As you continue exploring this guide, remember that reversing prediabetes involves both what you eat and how you live. Every step you take—from choosing foods that increase metabolism to incorporating physical activity into your routine—helps you navigate this journey with confidence. Stay tuned as we dive deeper into the impact of diet on prediabetes and how to craft a lifestyle that fosters wellness.
With knowledge as your foundation, you're setting the course for positive change. So, let's embrace the opportunity to take control of your health and make choices that support a vibrant, diabetes-free future.
Embarking on this transformative path can be the most empowering decision you ever make—and it all starts with understanding prediabetes and the importance of an early, proactive response.
The Role of Diet in Managing Prediabetes
When it comes to balancing blood sugar levels and taking charge of your health, understanding the role of diet in managing prediabetes is crucial. For individuals looking to lose weight and those at risk or diagnosed with prediabetes, adjusting your nutrition is a powerful step towards reversing the condition.
Why is a Pre Diabetes Diet Important?
A pre diabetes diet isn't just about cutting back on sugar; it's about selecting foods that actively support your metabolism and improve insulin sensitivity. This kind of diet can make a significant difference in how your body handles glucose, which can, in turn, prevent the progression to type 2 diabetes.
Foods That Increase Metabolism and Insulin Sensitivity
Choosing the right foods is paramount for those managing or looking to reverse prediabetes. Foods that increase metabolism not only aid in weight loss but also help stabilize blood glucose levels. Incorporating fiber-rich foods, such as leafy greens and whole grains, can slow down the absorption of sugar in your bloodstream. Foods high in chromium, like broccoli and whole grain products, are also known to enhance insulin's effectiveness.
Furthermore, lean proteins, nuts, and seeds can help maintain blood sugar levels and promote a feeling of fullness, which can reduce overall calorie intake. Fatty fish, rich in Omega-3 fatty acids, have been shown to decrease insulin resistance. This is supported by real data from the American Heart Association, which suggests that fatty fish like salmon and mackerel makes for a heart-healthy diet that can also be beneficial for blood sugar control.
Link Between Diet and Prediabetes Management
Improving your diet is a fundamental step in a prediabetic diet. In a study conducted by the Centers for Disease Control and Prevention (CDC), it's been revealed that lifestyle modifications, including dietary changes, can lower the risk of developing type 2 diabetes by up to 58% for individuals with prediabetes.
A meticulously planned insulin resistance diet aims to avoid sharp spikes in blood sugar levels, which can worsen insulin resistance. By spreading carbohydrate intake evenly throughout the day and combining them with protein and healthy fats, individuals can manage their prediabetes more effectively. This type of dietary approach aligns with the American Diabetes Association (ADA) recommendations for managing prediabetes and diabetes.
Understanding the connection between diet and blood sugar levels is the first step towards healthier choices. A diet designed for those with prediabetes focuses on whole, unprocessed foods and balances the macronutrients to sustain insulin sensitivity and metabolic health. Such a diet not only aids in managing glucose but could ultimately reverse prediabetes.
In conclusion, a carefully crafted pre diabetic diet is an indispensable tool in the fight against prediabetes. With the right food choices that boost metabolism and enhance insulin sensitivity, individuals can take control of their health and prevent the onset of type 2 diabetes. The following sections of this guide will delve deeper into which foods to embrace, which to avoid, and how to develop a personalized meal plan that promotes your metabolic well-being.
Foods to Embrace and Avoid on a Pre Diabetic Diet
Choosing the Right Foods for a Pre Diabetes Diet
When you're pre diabetic, it's essential to focus on foods that help maintain a healthy weight and stabilize blood sugar levels. Making informed choices can even enable you to reverse prediabetes, so let's dive into the foods that increase metabolism and support insulin function.
Whole grains like oatmeal, brown rice, and quinoa are excellent options because they have a low Glycemic Index (GI), meaning they won't spike your blood sugar as much as refined grains. Studies have shown that high-GI foods can impair glucose and insulin metabolism, increasing the risk for diabetes and heart disease.
Fiber-rich fruits and vegetables are another must-have on your pre diabetic diet. Non-starchy vegetables such as leafy greens, broccoli, and carrots can be consumed in more generous portions. However, it's essential to be mindful of the sugars in fruits. Opt for berries, apples, and pears, which have lower sugar content and abundant nutrients.
Legumes, including lentils, beans, and chickpeas, provide protein, fiber, and important minerals without the saturated fats found in some animal proteins. A study published in the Archives of Internal Medicine indicated that a diet rich in legumes helps improve glycemic control and lower heart disease risk in patients with type 2 diabetes.
Incorporate healthy fats, such as avocados, nuts, and seeds, plus fatty fish like salmon and mackerel that are high in omega-3 fatty acids. Omega-3s are known to reduce inflammation and improve cell membrane health, which is important for cells to respond to insulin properly.
Foods to Minimize or Avoid to Reverse Prediabetes
Now, to foods you should minimize or eliminate. It's time to say goodbye to sugary drinks and snacks, which are high in calories but low in nutrition. These can sabotage your efforts to manage blood sugar and weight, thereby amplifying the risk of developing diabetes.
Refined carbs, such as white bread, pasta, and pastries, must be reduced drastically. They are stripped of fiber and nutrients, causing rapid spikes in your blood glucose levels. Even some "whole wheat" breads can be misleading, so always check the fiber content on the nutrient label.
Processed meats like bacon, sausage, and deli meats are linked with an increased risk of type 2 diabetes, according to the Harvard School of Public Health. The high levels of preservatives and saturated fats in these foods can contribute to insulin resistance.
Trans fats, found in some margarines, spreads, and packaged foods, are a big no. A study from the Diabetes Care journal stated that trans fatty acid intake is associated with an increased risk of developing diabetes, making it clear that these fats have no place in a pre diabetic diet.
Maintaining a balanced diet with these guidelines can vastly improve your chances of reversing prediabetes. Remember, it's not just about eliminating foods, but also about embracing a new and exciting variety of foods that can enhance your metabolism and overall health.
Practical Tips for Crafting a Prediabetes-Friendly Meal Plan
When managing prediabetes, the foods you eat play a critical role in controlling your blood sugar levels and supporting your journey towards healthier choices, especially for those aiming to lose weight. By integrating a pre diabetes diet into daily life, you can effectively navigate the waters of insulin resistance and potentially reverse prediabetes. Here are practical, actionable strategies to create a pre diabetic diet that's as tasty as it is beneficial.
Start with a Solid Foundation
Begin by laying out a foundation for your meal planning. Meals should be balanced with a good mix of proteins, fats, and carbohydrates. Opt for complex carbohydrates like whole grains, which have a lower glycemic index and provide sustained energy without spiking blood sugar levels. The focus should be on lean proteins, healthy fats, vegetables, and fruits that are low on the glycemic scale. Foods known to increase metabolism are beneficial not just for blood sugar regulation but also for weight management.
Incorporate Metabolism-Boosting Foods
Foods that increase metabolism can be seamlessly woven into your pre diabetic diet. For example, lean meats, legumes, and low-fat dairy products offer protein that helps maintain muscle mass and burn calories. Green tea and certain spices like cinnamon and turmeric can be included in recipes or drinks for their metabolic benefits. High-fiber vegetables and whole grains keep you full longer and help avoid insulin spikes.
Assemble Your Meal Plan
When crafting your meal plan, balance is key. Aim to fill half of your plate with non-starchy vegetables, one-quarter with lean protein, and the final quarter with whole grains or starchy vegetables. This structure supports an insulin resistance diet and promotes weight loss.
Here is an example of a day’s meal plan for someone on a pre diabetic diet:
Breakfast: Scrambled eggs with spinach and mushrooms, served with a slice of whole-grain toast and a cup of green tea.
Lunch: Grilled chicken salad with mixed greens, a variety of vegetables, a handful of nuts, and a vinaigrette made with olive oil.
Dinner: Baked salmon with a side of quinoa and steamed broccoli, seasoned with herbs and a splash of lemon juice.
Snacks: Baby carrots with hummus, a small apple with almond butter, or Greek yogurt with a handful of berries.
Smart Substitutions and Swaps
Making small changes to your favorite meals can also make them more prediabetes-friendly. Use zucchini noodles instead of pasta, cauliflower rice in place of white rice, and swap sugary snacks for a piece of fruit or a small serving of nuts. These swaps ensure you're still enjoying your meals while adhering to a pre diabetes diet.
Mind Your Portions
Remember that even healthy foods can cause weight gain and affect blood sugar if consumed in large amounts. It's important to be mindful of portion sizes and listen to your hunger cues. Using smaller plates can help manage portion control, and keeping a food diary may assist in tracking what you eat and understanding how it affects your blood sugar.
Conclusion
By making informed choices about the foods you eat and understanding how they fit into a pre diabetes diet, you can start reversing prediabetes while also working towards your weight loss goals. Consistency is key, and with these practical tips, crafting a prediabetes-friendly meal plan can be both manageable and enjoyable.
Beyond Diet: Complementary Lifestyle Changes for Prediabetes Management
The Synergy of Diet and Exercise
While adhering to a pre diabetes diet is a critical step in managing prediabetes, it's just one piece of the puzzle. Regular physical activity is another cornerstone in the fight to reverse prediabetes. Research from the Diabetes Prevention Program indicates that individuals who engaged in moderate exercise for at least 150 minutes a week saw a 58% reduction in the progression to type 2 diabetes. This shows us that pairing a balanced pre diabetic diet with consistent exercise isn’t just a suggestion, it's a scientifically backed strategy for safeguarding your health. Exercise improves your body's insulin sensitivity, meaning that your cells are better able to use the available insulin to absorb glucose during and after activity. For anyone trying to manage their blood sugar, this is great news, as it dovetails perfectly with the insulin resistance diet you're already following. You don't have to become a marathon runner overnight; even brisk walking, swimming, or cycling can yield significant health benefits.
Stress Management: The Hidden Key to Blood Sugar Control
Too much stress is bad news for everyone, but it's especially troublesome for individuals with prediabetes. When you're stressed, your body releases hormones like adrenaline and cortisol which can lead to increased blood glucose levels. Therefore, implementing stress-relief practices is not just about feeling better mentally; it's a crucial part of managing your physical health. Techniques such as yoga, meditation, deep-breathing exercises, or even engaging in hobbies can lower stress levels and aid in maintaining a balanced blood sugar level.
Regular, Restful Sleep: An Underrated Health Booster
Adequate sleep is another beneficial companion to a pre diabetes diet. Lack of sleep can lead to increased appetites, craving for high-carbohydrate foods, and a decrease in your body's ability to manage blood sugar effectively, according to studies published by the National Institute of Health. Adults should aim for 7-9 hours of quality sleep per night, setting a regular sleep schedule to help the body maintain its natural rhythm. Just like diet and exercise, sleep quality and duration can directly influence your ability to reverse prediabetes. Wrapping it all together, managing prediabetes calls for a holistic approach. It’s not just about the foods that increase metabolism or following a rigid pre diabetic diet, it is about living a lifestyle that supports these dietary efforts. Together, regular physical activity, effective stress management, and adequate sleep create a synergy that fortifies your body, enabling you to improve your insulin resistance and overall health. It's this combination that can empower you to not just manage, but potentially reverse prediabetes and lead a full, vigorous life.
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422,666,415,715,352,900 | Manage Back Pain With These Tips
manage back pain with these tips - Manage Back Pain With These Tips
Many people suffer from back discomfort so you should never feel as though you are the only one. Many millions of people throughout the world are burdened with daily. The tips listed here are created with the intention of easing back discomfort. You can start ridding yourself of back discomfort today.
Never try to ignore or “get by” with . There are many people who refuse to pay heed to painful signals their body is sending. They think they can just walk off, or ignore the pain. If you try to move while in pain, it can actually worsen your condition. Sit down, relax and don’t do much until the pain lightens.
Avoid repetitive stress to the same muscles, regardless of which stance or position you’re in.
To prevent some from getting worse, always attempt to avoid putting stress on the muscles that cause you pain. This stress can occur in any sitting or standing position, so make sure to stay mindful of it. Repetitive tasks can be especially aggravating, so try to take breaks as often as possible. Don’t stand in one spot too long, and continually shift your stance.
Lay down with your legs as if you were sitting if your back hurts. This is a comfortable position will decrease the pressure on your back. However, whatever position is most comfortable for you is probably best, just make sure you do not twist the spine.
Practice good posture when you are sitting, standing or working at your desk. A lot of people make the mistake of thinking that a back injury can only happen through extreme physical activity. Poor sitting posture for extended periods of time can lead to cumulative damage to the muscles in your back.
There is a wide variety of back discomfort. It is crucial that you talk to you doctor before you make any decisions about medication.Sometimes over the counter medication is enough, and sometimes prescribed medication is absolutely necessary.
A great back-pain-related tip to use is to act preemptively if at all possible. If you have a predisposition to in your family, or if you’re at higher risk of back injury due to your lifestyle, you should see a chiropractor for some periodic adjustments. Seeing a chiropractor on a regular basis can help fix even the tiniest of problems before they become full-blown serious injuries.
You need to lose some weight if you’re carrying any extra. Extra weight can change the center of your body. This weight can strain your lower back, and lead to .
Lifting items that are far away is often due to time constraints and laziness. It is common for individuals to take what is perceived as the shorter method. Stay close to an object as you lift it, and bend at the knees instead of bending your back.
Your physician may feel that back surgery as an option for you to help alleviate your back discomfort or disorder. Surgery should only be used as a last resort if other methods have been exhausted.
You can protect your back during those long days at the desk by simply taking walks on your breaks. Stretching your arms and legs will also stretch your back muscles. This leads to fewer back injuries associated with cumulative compression.
Drinking Coffee
During bouts of back pain, it’s essential to relax the muscles that are in spasm. You can do this by laying down and putting heat on your tense muscles. Electrolyte balance is an important part of maintaining relaxed muscles, and you could benefit from drinking water and keeping sodium to a minimum until your muscles feel less tense. Too much salt and not enough liquids can cause dehydration, which can trigger muscle spasm or make them worse.
Drinking coffee has been reported to help with easing chronic back discomfort that’s chronic. Recent studies show that caffeine blocks the chemical adenosine. This adenosine makes the back stiff, so drinking coffee can help relax these muscles and reduce pain.
Obesity, pregnancy, bad posture and poor lifting techniques are common causes for lower back pain. There are many small changes that you can make and many precautions that you can take to reduce and prevent back pain. If lower back pain seems so common and inevitable, it makes sense to do everything you can to prevent it.
One way to alleviate back discomfort is by limiting or omitting drinks containing caffeine out of your daily diet. Caffeine can trigger spasms and muscle inflammation. Try to eliminate coffee and it can help your back discomfort.
There are tons of back pain medicines out there. Ask your doctor for help in deciding which is the right choice for your needs. If you back pain gets worse or does not respond to treatment, see you doctor about more intense treatments and stronger medication.
Try using coolness and cold method to ease your back pain. Ice is a great pain reliever and reduce swelling. Heat alternatively promotes healing through muscle relaxation and more blood flow to promote healing. For heat, you can use an electric blanket, heating pad or a warm bath, just make sure you don’t fall asleep while using these methods.
If you are a mother that is breast feeding, do this sitting in a chair instead of on the couch. Laying down is often the most comfortable position for mother and baby. Also, keep a cushioned pad on your back when breastfeeding.
Be mindful of your posture at all times. Your spine should be straight, your elbows should be at your sides, and your feet should be flat on the floor, keep your elbows by your sides.
manage back pain with these tips - Manage Back Pain With These Tips
You may consider seeing a chiropractor for a consultation and adjustment if home remedies to relieve your back pain have so far been unsuccessful. The chiropractor will likely x-ray your back and then discuss a treatment plan with you. Once the chiropractor has had a chance to work on your back, you will see some pain relief.
Lifting Heavy
Try applying coolness and heat so that you can relive any back pain. Ice reduces inflammation and pain. Heat alternatively promotes healing through muscle relaxation and more blood flow. To add the warmth, choose a warm bath, heating pad or electric blanket, and make certain you don’t fall asleep using the methods suggested.
Lifting heavy objects is one reason back pains. Always take precautions and use proper procedures when lifting heavy or awkward objects.
Spending a lot of time in a car is frequently the culprit regarding back pain. Adjust your seat properly so you are driving with good posture.
Wearing the right shoes that support and cushion your feet will help prevent back discomfort. If your footwear is the wrong size or is uncomfortable, your posture can shift, it changes your posture and causes a back ache.If you must wear high heels, buy insoles, and do not wear them for hours.
People all over the world suffer from back pain, and when you lift heavy object you can make it even worse. Take precaution whenever you lift something heavy.
Include more B12 into your diet. A B12 has been shown to cause back discomfort in people. Eating a diet rich in B12 can combat back pain.
Stretch after exercising, when your muscles are loose and warm, to help reduce back pain. Post exercise, take the time to stretch those muscles!
A good massage can do wonders. Touch therapy can be a lot of back pain. A massage could loosen your back’s tight muscles giving you a relaxed feeling of relaxation that then gives you relief from their back discomfort. A weekly massage can do wonders for managing back discomfort.
Relaxation is one of the best remedies for chronic back pain, and something as simple as a proper breathing technique can be a godsend to people who are suffering from pain. Find out more about these methods and try using anything that usually makes you feel relaxed. They just might help you to eliminate some of the suffering.
Anyone with back pain should try yoga. It can be a very therapeutic activity. It can help correct some of your spine’s misalignment. It can also produces a relaxed body by loosening tight joints and muscles while relaxing your body. Classes are easy to find at almost any gym.
When an attack of back pain strikes, the best thing to do is to ask for help. You shouldn’t be ashamed to ask for help around your house. You really don’t want to injury your back further by moving furniture or dusting.
Walking is very beneficial when you suffer from back discomfort. The full-body demands of walking are very beneficial for your body because it uses many muscles and eases tension.
Wear appropriate shoes to help avoid developing back problems. Ill-fitting shoes can change the way you walk and cause the bad posture which can result in pain. If you must wear them, place insoles inside them and try to wear them for as short a time as possible.
Seeing a doctor to deal with back discomfort is useful, though you need to know what type of questions to ask him. You need to find out what is causing the pain, what you can do to keep it from worsening, the kinds of treatments that exist and these treatments’ risks.
Treat yourself to a massage. A lot people suffering from back pain get considerable benefit from touch therapy. A massage can loosen tight muscles in the back, creating a general feeling of relaxation, which in turn provides relief from pain. A weekly massage can do wonders for managing back pain well.
Cross your legs if you have to sit in the same position for a long period of time. Make certain to change the leg that you cross both legs in order to engage your muscles.
Pay attention to your posture. Developing the habit of monitoring your posture will help relieve your back pain. Back problems sprout from bad posture, so monitoring your posture can effectively negate back problems. Your reward for following this advice will be less back pain and more smiles!
It’s clear that many ways are available to treat back discomfort. Relief can take a little time, but if you use these ideas in your life, you can find your pain level reduced. You deserve to lead a happy life without suffering from back discomfort and the suggestions in this article will help you.
If it is necessary for you to sit in the same place for a long period of time, like in a theater or airplane, you should cross your legs. This way you keep your hips and muscles in your back more active and less likely to get stiff and sore. Make sure to change the leg that you cross from time to time, as this will avoid putting all of the stress on one side of your body. | {
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2,288,114,331,162,467,600 | Mohs Reconstruction
Mohs micrographic surgery is a safe and effective treatment for skin cancer. During Mohs surgery, cancerous tissue is removed in small sections. Both the visible tumor and any “roots” extending beneath the surface of the skin are excised. Because it may be necessary to remove many layers of skin to reach these roots, large wounds or scars, often in prominent areas, can be left behind. In many cases, however, reconstructive plastic surgery can be performed to repair the wound and improve the skin’s appearance.
MOH's
Click here to view our MOH’s Before & After Gallery
Types of Mohs-Surgery Reconstruction
Reconstruction after Mohs surgery can be performed on the same day of the surgery, or at a later date. Each case is different but, in general, when Mohs-reconstruction surgery is performed depends on the location of the tumor, its size, and how far it extends beneath the skin. Unless a decision is made to let the wound heal by itself, the following techniques are used for reconstruction:
• Stitching the wound closed
• Skin graft (skin is taken from another part of the body)
• Skin flap (skin is shifted from a nearby area)
In cases in which the wound is too large or complicated for repair by the Mohs surgeon, who is usually a dermatologist, the wound is closed temporarily, and the patient is referred to a reconstructive plastic surgeon.
Benefits of Mohs-Surgery Reconstruction
Although one of the benefits of Mohs surgery is that it removes only as much tissue as necessary, in some cases, the wound left behind is unsightly. Reconstruction following Mohs surgery is particularly beneficial for a patient who is distressed by a wound or scar on the face or other visible area. The purpose of reconstruction is cosmetic; it attempts to make the skin look much as it did pre-Mohs surgery, so that the patient does not feel self-conscious. The quality of the results from reconstruction will vary from patient to patient based on factors that range from the location of the wound to the patient’s ability to heal.
Risks of Mohs-Surgery Reconstruction
As with any surgery, risks of Mohs-surgery reconstruction include bleeding and infection. Although rare, its specific risks include nerve damage, skin grafting that does not “take,” and permanent scarring.
PATIENT EDUCATION
Click Here to Learn More | {
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4,697,173,644,809,747,000 | Volume 3 Supplement 2
21st European Workshop for Rheumatology Research
Open Access
The impact of DNA chip technology on molecular medicine
• KK Wilgenbus1
Arthritis Research & Therapy20013(Suppl 2):L001
DOI: 10.1186/ar151
Received: 15 January 2001
Published: 26 January 2001
The recent popularity of DNA chip technology has been fostered by the increasing demand for new tools, which allow the simultaneous analysis of large numbers of nucleic acid hybridization experiments in a timely fashion. The development of DNA chip-based assays has been strongly driven by modern approaches aiming at the comprehensive analysis of multiple gene mutations and expressed sequences. The broad range of current DNA chip applications include the detection of pathogens, the measurement of differences in the expression of genes between different cell populations as well as the analysis of genomic alterations such as sequence or copy number alterations of disease related genes or single nucleotide polymorphisms. A brief overview of the impact of DNA chip technology on the field of Molecular Medicine will be provided, followed by a more detailed presentation on DNA chip technology for large-scale differential expression profiling.
Authors’ Affiliations
(1)
Boehringer Ingelheim R&D
Copyright
© 2001 BioMed Central Ltd 2001
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455,679,431,795,551,200 | Carcinoma of the Parotid Gland
0
Journal of Medical Case Reports
Case Presentation
An 80-year-old Caucasian woman came to the hospital due to swelling on the left side of her face. It had been growing gradually for two months. She didn’t experience difficulty swallowing, pain when swallowing, fever, or weight loss. There were no previous issues with the parotid gland. Upon examination, a tender swelling about 2.5 cm in size with unclear edges was observed over her left parotid gland. Her temporomandibular joint showed no abnormalities.
Tests revealed a hypoechoic mass in her left parotid gland, approximately 2.8 cm in size, with poorly defined borders on ultrasound. Magnetic resonance imaging showed a distinct cystic and/or necrotic mass in her left parotid gland, measuring 3.4 × 3.0 × 3.0 cm. The lesion affected the superficial lobe of the parotid gland. It extended through the stylomandibular tunnel to involve the lateral aspect of the deep lobe. The MRI indicated varied signal intensities, with areas of cystic change or necrosis.
Investigations
The fine needle aspiration, guided by ultrasound and using both 21- and 25-gauge needles, revealed results categorized as atypia of undetermined significance classification 3. Examination of the smears revealed clusters and individual cells exhibiting an elevated nucleus-to-cytoplasm ratio, along with some hyperchromasia. These findings were set against a backdrop of cellular debris, including lymphocytes and neutrophils, indicative of potential necrosis. Although an inflammatory or cystic condition was plausible, the specter of primary or metastatic malignancy lingered due to inconclusive evidence.
Management
Subsequently, the patient underwent a left total parotidectomy. This was accompanied by left-selective neck dissections targeting levels 2 and 3. It was followed by soft tissue reconstruction using the sternocleidomastoid muscle. An intraoperative evaluation confirmed the presence of adenocarcinoma with a poorly differentiated component. Examination of the deep lobe unveiled a 3.5 × 2.9 × 2.9 cm lesion characterized by both carcinomatous and sarcomatous elements infiltrating adjacent soft and adipose tissues. The carcinomatous component exhibited features typical of adenoid cystic carcinoma, while the sarcomatous element displayed high-grade spindle cell morphology with areas of necrosis and sporadic chondroid differentiation. This comprehensive assessment painted a complex clinical picture, demanding diligent management and further investigation.
Analysis of Carcinoma
Immunohistochemical analysis of the tumor revealed positivity for CAM 5.2, CD117, p63, SMMH, p40, CK7, pancytokeratin AE1/AE3, and GATA-3 in the adenoid cystic carcinoma component. Moreover, androgen receptors, CD57, and calponin showed negative results. Conversely, the sarcoma component exhibited positivity for vimentin and S-100, particularly highlighting foci of chondroid differentiation. The Ki-67 proliferation index ranged from 50% to 70% in the sarcomatous region. Pleomorphic adenoma foci were absent, raising the possibility of a carcinosarcoma ex-pleomorphic adenoma or a de novo carcinosarcoma.
Fortunately, lymph nodes tested negative for metastatic carcinoma. The patient had radiotherapy targeting the tumor bed and skull base due to the potential for perineural invasion by the adenoid cystic component. This treatment strategy aimed to mitigate the risk of recurrence and ensure the best possible outcome for the patient’s condition.
Discussion
Carcinosarcoma, also known as malignant mixed tumour, is a rare type of tumour found in the salivary glands, characterized by distinct carcinomatous and sarcomatous components. It comprises a small fraction, estimated at around 0.04% to 0.16%, of all salivary gland tumors. Typically, these tumors occur most frequently in the parotid gland and can either develop de novo or arise from an existing pleomorphic adenoma. The common carcinomatous elements include adenocarcinoma, undifferentiated carcinoma, and squamous cell carcinoma.
This case highlights a unique instance where adenoid cystic carcinoma constitutes the carcinomatous component, accompanied by chondrosarcoma.
Carcinosarcomas can originate either from a pre-existing pleomorphic adenoma or may manifest de novo. These tumors are typically aggressive, with a clinical course marked by high-grade malignancy and a propensity for distant metastases, documented in approximately 54% of cases.
Chondrosarcoma is the most commonly observed sarcomatous element in carcinosarcomas, followed by fibrosarcoma, leiomyosarcoma, osteosarcoma, and liposarcoma. As for the carcinomatous elements, adenocarcinoma, undifferentiated carcinoma, and squamous cell carcinoma predominate. This case featured adenoid cystic carcinoma, characterized by predominant tubular and cribriform growth patterns, alongside focal solid growth patterns. Histomorphological analysis considered various differential diagnoses, including carcinoma ex-pleomorphic adenoma, a sarcomatoid variant of salivary duct carcinoma, and myoepithelial carcinoma. Immunohistochemistry played a pivotal role in confirming the diagnosis. The adenoid cystic carcinoma component exhibited positive staining for both ductal (CK7, CAM 5.2) and myoepithelial (p63, p40, cytokeratin, SMMH) markers, as well as CD117.
In contrast, the sarcomatous component tested negative for all epithelial markers, CD57, androgen receptors, and calponin. It displayed positivity for vimentin, with focal S-100 staining observed in the chondroid component. This immunohistochemical profile, coupled with the absence of a pre-existing parotid lesion and histological evidence of pleomorphic adenoma, supported a diagnosis of primary carcinosarcoma of the parotid gland. Fine needle aspiration cytology, although not extensively studied in carcinosarcomas, has been reported to yield suspicious or atypical results.
Conclusion
Magnetic Resonance Imaging (MRI) is the preferred imaging modality for carcinosarcomas, offering insights into the involvement of the deep lobe, facial nerve, and surrounding soft tissues. However, despite advancements in diagnostic and therapeutic modalities, carcinosarcomas carry a poor prognosis, with reported 2-year and 5-year survival rates of 68.1% and 37.2%, respectively. Median survival ranges from 10 months to 38 months, emphasizing the aggressive nature of these tumors. The treatment of choice involves radical parotidectomy followed by postoperative radiotherapy, which has been shown to significantly reduce recurrence rates compared to surgery alone. Distant metastases, predominantly hematogenous, remain a significant prognostic factor for poor survival outcomes.
Carcinosarcoma, a highly aggressive tumour, warrants aggressive treatment due to its poor prognosis. Further research is necessary to find out the origins of these tumours.
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Fungal Sinusitis Tinnitus: Why Should Sinus Infections Be Taken Seriously?
Fungal Sinusitis Tinnitus: Why Should Sinus Infections Be Taken Seriously?
Sinus infections are one of the most common of the respiratory issues. In the united states alone, it is estimated that more than 37 million Americans suffer from sinus infections every year. Usually following a bout of common cold, acute sinusitis is generally short-term and reacts very well with medication. Chronic sinusitis, on the other hand, is a persistent condition and more complicated to deal with. When faced with sinus infections, many people opt to ignore the signs and symptoms hoping that they would eventually vanish entirely. Other people prefer to self-medicate, waiting for the situation to worsen before seeking professional help. This may end up being acceptable when working with acute sinusitis, but will not work against chronic sinusitis. Also, it is important to know that there are dangers associated with not taking sinus infections seriously.
Wash Out! Whether or not done as simply as snorting the irrigating solution through cupped hands or using a bulb syringe, spray bottle or the particular irrigators with pulsating action, the principle is basically to allow saline solution to get into one nostril and out through the other. In the process, the nasal and sinus passages are washed from irritants, allergens, excess mucus and bacteria. The actual irrigating fluid is usually isotonic, but hypertonic saline (one with a salt concentration more than 0.9%) works better to alleviate inflammation of the mucous membranes. You can also try adding a few drops of apple cider vinegar. Its normal acids help loosen secretions.
The Problem of Sinuses is Common and Large Numbers of People are Afflicted by this Issue
Most of them get relief from the problem through treatment properly. However, some people are there who do not get relief despite taking medicines for a prolonged period as well as face great hassle. Properly if you're sailing in the same boat and have not taken any measure then you ought to know that the issue is serious. It is known as chronic sinusitis and special treatment should be taken for the same. Now if you were not familiar with different treatments being offered for this problem, relying on balloon sinuplasty would be the best decision.
• Once you are ready to undertake this treatment for getting rid of the problem of sinusitis, it is time to find a specialist who is able to do it.
• Today, this less invasive treatment is high on demand and so are the balloon sinuplasty physicians.
• These doctors need to be highly experienced in performing this treatment, as little carelessness can be dangerous for the life of the patient.
• If you are also looking for a doctor who can help you when you get relief from sinusitis then start looking for all of them on the internet.
• Various sinusitis centers are available online and you can have a word with their specialists there itself.
• Now days, the service of correcting appointments on internet is also possible and you can get everything done simply by sitting in the home.
For More Information, Check Out Http://Sinusinfectionproblems.Com/
Large numbers of people have observed acute or unexpected onset of blockage because of cold, dust and so forth. Nonetheless many of us suffer from chronic nose congestion known as chronic rhinosinusitis, which is a pain, literally, and can impact our everyday routine. Chronic sinusitis signs and symptoms are similar to acute symptoms, but they keep going longer. Symptoms contain difficulty breathing through the nose, pressure around your cheeks, nose and eyes and cough, which may be a whole lot worse at night.
There are Many Treatments for Relieve this in Which Comes from Congested Sinuses
Balloon sinuplasty is a relatively new, minimally invasive strategy to open up the actual openings into the sinus cavities without the need for any tissue cutting or bony elimination. This technique has been approved by Food and Drug Administration and is quite safe and sound. The success rate of this treatment is very high and is being used by a lot of doctors worldwide for treating nose patients.
Usually, go up sinuplasty is definitely an endoscopic, catheter-based procedure for patients suffering from sinusitis. This process involves a surgeon moving a small go up through a flexible tube in the nostril, into the obstructed sinus. The balloon is higher which pushes wide the blocked area. The balloon is then deflated and removed. Following this process there is a good possibility that the sinus drainage channel is widened as well as the sinus can drain appropriately. When compared to the more traditional endoscopic sinus surgery which will involve muscle cutting and removal, this procedure causes fewer traumas to be able to surrounding sinus and nasal tissue.
• Aside from the pain and discomfort, neglected or undiagnosed sinus infections may also lead to more serious complications.
• One of which is a condition called osteomyelitis, or contamination of the frontal bone.
• This is liable when the infection spreads to the frontal bone.
• An additional possible problem is blindness, brought about by nose infection spreading to be able to the eye sockets.
• Coma or passing away is also a possibility, though rarely happens, when the infection spreads in order to the brain.
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• Baloon sinuplasty is a form of endoscopic remedy and it considered under the category of surgical techniques.
• However, it is not like other surgical methods and also massive difference lies between them.
• On this kind of treatment for sinusitis, a catheter balloon is used which is put into the nostril.
• The balloon is then higher so that blocked nasal passage receives obvious and also the person can get rid of the problem with ease.
• You would be glad to know that the process is less invasive in their nature and thus patients take less time in recovering from it.
• This is one of the biggest advantages of this treatment and this attracts people toward it.
Second, You Must Have Heard Before in Which Increasing Your Liquid Intake Helps a Lot
But remember, fluids do not just mean plain agua or water. Fresh fruit juices and teas count as well. Before letting your favourite their tea relieve your aching throat, try inhaling the vapor to enjoy not only its aroma but also to release the mucus. Peppermint and chamomile teas top the list as the best choices.
• Sinus Polyps Awareness: What you should KnowSinus Polyps Awareness: What you should Know Polyps can be one of the causes of sinus infection that gives pain and suffering to someone. But how did polyps become responsible for sinus infection? There is actually a type that is known as sinus polyps which are tear-shaped tissue swellings or...
• Dangers of Sinus Infections
Sinus attacks can bring a lot of pain and discomfort with regard to a patient because of the signs that come with it. The most common symptoms are nasal congestion and eliminate due to excess mucous. This also leads to breathing difficulties and decreased sense of smell and taste. Pain is also in order to be expected especially throughout the sinus locations like the nose, eyes, cheeks as well as forehead. Others also experience a sore throat, bad breath, coughing, toothaches, nausea and fever.
Fungal Sinusitis Tinnitus
Is Not Unusual to Have a Sinus Infection
In fact, lots of people globally go with the barely-life-threatening-nonetheless-uncomfortable experience of sinus pressure headaches, nasal congestion and post-nasal drips associated with sinus infections. Read on to learn more about these natural sinusitis relievers: Taking the Heat During a bout with sinusitis, steam could be a new best friend. Take into account having a hot shower. Alternatively, you are able to do something ala-sauna by allowing hot water from the shower to flow with the shower door closed. Before long, enter the bathroom and savor the "steamy environment". It works because the heat from the steam helps loosen and drain the excessive mucus quicker. In turn, sinus pressure will be significantly happy.
Dealing With Sinus Infections
If you have a strong immune system, you might be able to fight off the infection easily despite having self-medication or home remedies. However, if there is no improvement after a few days and you suspect sinus infections, it is important to see your doctor right away. Sinus infections are treatable. You just need to work closely with your doctor to identify the cause of contamination and right treatment.
People who do nasal and sinus washing or irrigation are all praises regarding this method. Simply because it's so effective, the idea of sinus irrigation has inspired the concept of medicated nose irrigation. In medicated sinus irrigation, the difference lies in the irrigating solution. Instead of just using saline, sinusitis medications like medicines and decongestants are incorporated into the irrigating solution. Therefore, as the solution comes in contact with the nasal and sinus airways, the active components of the drug are readily absorbed in the mucosa. The therapeutic effect of the drug is achieved much faster than oral administration of medications. ActiveSinus by Sinus Dynamics is a irrigator you can use for medicated sinus irrigation.
For More Information, Check Out Http://Www.Sinusdynamics.Com
You can also try these kinds of options or modifications - first, do this very easy steam inhalation technique: Fill a bowl with boiling water. Put a bath towel over your head. The towel should be large enough to cover the basin as well, so that it could "seal" the steam from the basin while you breathe deeply to take a breath the steam. You can do this for 5-10 units and repeat it every few hours. You may also boost the benefits of vapor inhalation with the addition of a few pieces of crushed garlic or oil essences of eucalyptus or mint.
Vitamin Zzzzz..
Your sleeping habits topic as well. Employing a humidifier in the room moistens the air and helps clear your own airways. Remember, also, to be able to elevate your head while you sleep by using extra cushions underneath your head. With this position, mucus drains faster from your nose passages.
To reduced the risk of getting sinus infections, focus on strengthening your immune system. This can be effortlessly done by switching to a healthier lifestyle. Eat the right kinds of foods such as fruits and vegetables, specially those high in antioxidants, vitamins and minerals. Prevent foods high in sugar as these can lower the immune system. Drink lots of water and juices, whilst avoiding coffee and alcoholic beverages. Herbal as well as food supplements are suggested as they provide additional help to the body. Finally, exercising daily is highly suggested to keep the body strong and healthy.
Well, Big or Small, the Majority of Surgeries Really are a Delicate Procedure
Recuperation from like an operation must be attended to just as directed by your doctor to promote healing as well as to prevent complications. A nose balloon technology is intended for use by or under the direction of a health care provider. You will find associated chance, including tissue mucosal trauma, infection, or even possible optic injuries. As a result, it's better to talk with professional balloon sinuplasty doctors about the risks and benefits and to determine whether this treatment is right for you or not. Your doctor can usually detect chronic sinusitis based on your symptoms. | {
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1,040,264,360,392,906,900 | Skip to Content
What Are The Apple Cider Vinegar Gummies Side Effects?
Are you looking to add Apple Cider Vinegar (ACV) gummies to your daily routine? Well, before doing so, it is important to know about the potential side effects so that you can make sure you are consuming them safely.
Do you want to know the apple cider vinegar gummies side effects? Keep on reading to find out all about the various apple cider vinegar gummies side effects, and what you can do to avoid them…
What Are The Apple Cider Vinegar Gummies Side Effects?
What Are Apple Cider Vinegar Gummies?
Apple cider vinegar gummies are a dietary supplement designed to provide the potential benefits of apple cider vinegar (ACV) in a more convenient and tasty form.
Instead of drinking the often harsh-tasting liquid, you can enjoy these fruity, delicious gummies to help achieve your health-related goals.
Gummies are basically made by combining apple cider vinegar with other natural ingredients, such as fruit juices and pectin for natural sweetness and consistency.
The resulting gummies are packed with potential health benefits, all while maintaining a pleasant taste that’s easy on your palate, and easier to swallow than use apple cider vinegar neat.
Apple cider vinegar gummies come in various flavors, so you can choose your favorite and enjoy the goodness of ACV at the same time.
They’re easy to integrate into your daily routine and perfect for those who can’t stand the taste of pure apple cider vinegar.
What Are The Benefits Of Apple Cider Vinegar Gummies?
Apple cider vinegar gummies are more than just a tasty treat; they offer numerous health benefits that can make a real difference in your life.
Apple cider vinegar gummies provide a convenient and portable source of ACV.
If you’re not a fan of ACV’s strong taste, these gummies offer an enjoyable way to get your daily dose. Plus, the added vitamins that most gummies contain provide extra health-boosting power.
Managing your blood sugar levels is vital for overall health, particularly if you have diabetes or are at risk for the condition.
Apple cider vinegar may help lower blood sugar levels by improving insulin sensitivity and, as a result, effectively assisting in blood sugar management.
ACV gummies offer a convenient way for you to get the blood sugar-lowering benefits of apple cider vinegar.
Weight management is another area where ACV gummies can shine. Apple cider vinegar is known to aid in weight loss by promoting feelings of fullness and reducing appetite.
When taking ACV gummies, as part of your daily routine, you could potentially see improvement in your weight management efforts.
Heart health is a significant concern for many people, and apple cider vinegar has been linked to improved heart health outcomes in some studies.
For example, ACV consumption has been connected to decreased levels of total cholesterol in the blood. This may contribute to lowering your risk of developing certain health conditions related to poor heart health.
As well as the benefits I’ve listed above, ACV gummies may provide relief from heartburn, improve skin health, aid in the body’s detoxification, and even boost your immune system.
Plus, they can help with bloating and reducing inflammation, giving you even more reasons to make them a part of your daily supplement regimen.
How To Minimize The Risks of Side Effects Of Apple Cider Vinegar Gummies
What Are The Apple Cider Vinegar Gummies Side Effects?
Possible Digestive Discomfort
You may experience digestive discomfort when consuming apple cider vinegar gummies due to the high acidity level in the vinegar.
This can cause indigestion, heartburn, or even acid reflux. To minimize these side effects, consume the gummies in moderation and pay attention to your body’s reaction.
Potential Tooth Enamel Damage
Apple cider vinegar is highly acidic, which is a concern for your dental health. Consuming large amounts can lead to tooth erosion and decay.
When you take apple cider vinegar gummies, be sure to brush your teeth afterward to help protect your enamel from potential damage.
Interaction with Medications
If you’re currently taking medications, it’s essential to be aware of potential interactions with apple cider vinegar gummies.
If you’re on prescribed blood sugar medications, such as insulin, the gummies could cause an imbalance in your blood sugar levels.
Always consult your healthcare provider before incorporating apple cider vinegar gummies into your routine, especially if you’re on medication.
Blood Sugar Imbalances
While apple cider vinegar is known for its potential benefits in regulating blood sugar, you should still monitor your blood sugar levels when consuming these gummies, especially if you have type 1 diabetes.
Taking apple cider vinegar gummies may lead to lower blood sugar levels. It’s crucial to maintain healthy blood sugar levels for optimal energy and well-being.
Possible Throat Irritation
Due to the acidic nature of apple cider vinegar, consuming gummies may cause throat irritation or even throat burns.
If you experience discomfort or difficulty swallowing after taking the gummies, it’s best to discontinue use and consult a healthcare professional.
Nutrient Deficiencies
Apple cider vinegar gummies may lead to nutrient deficiencies if consumed in large amounts or over a long period.
Potassium levels may decrease, affecting your overall energy levels and muscle function. To avoid this, consume the gummies in moderation and ensure your diet is rich in essential nutrients.
Other Side Effects
Apart from the mentioned side effects, there’s a possibility of experiencing other unwanted outcomes, such as skin burns or increased acid reflux symptoms due to the high acidity of apple cider vinegar.
To minimize these risks, always follow the recommended dosage and pay close attention to your body’s response.
How To Minimize The Risks of Side Effects Of Apple Cider Vinegar Gummies
To make the most out of apple cider vinegar gummies and minimize the potential risks, you should follow these simple guidelines:
• Choose the right dose: It is essential to consume the correct dose of apple cider vinegar (ACV) for your needs. Typically, the recommended dosage ranges from 15 to 30 ml per day. Start with a lower amount and gradually increase to ensure a gentle introduction to your system.
• Mind the daily consumption: To avoid any potential side effects, make sure you monitor and regulate how much apple cider vinegar you consume. Following the recommended dosage of the ACV gummies is crucial for safe and effective use.
• Select reputable brands: Not all apple cider vinegar gummies are created equal, so it’s essential to purchase from a reliable and reputable brand. Look for gummies with stringent quality control measures, and always read labels to ensure the ACV content is accurate and transparent.
• Combine with a healthy lifestyle: To optimize the benefits of apple cider vinegar gummies, make sure to incorporate them into a wholesome and balanced lifestyle. Maintain a proper diet and exercise regularly to ensure maximum results while minimizing potential risks.
• Be cautious with other ACV products: If you are already using other forms of apple cider vinegar, such as drinking ACV or taking ACV tablets, be cautious when adding gummies to avoid overconsumption. Monitor your total intake to ensure you stay within the recommended dosage guidelines.
• Consult a healthcare professional: Before starting any ACV regimen, it’s always a great idea to speak with your healthcare provider or a registered dietitian. They can help determine the appropriate mg of apple cider vinegar for your specific needs, taking into account any medications or health conditions you might have.
Is It Better To Drink Apple Cider Vinegar Or Take Apple Cider Vinegar Gummies?
You might be wondering whether it’s more beneficial to drink apple cider vinegar or take apple cider vinegar gummies.
Both forms have their pros and cons, and ultimately, the choice comes down to your personal preference and lifestyle.
Drinking apple cider vinegar provides you with a more direct form of the vinegar, which contains acetic acid, a component found in all kinds of vinegar.
Taking 1–2 tablespoons (tbsp.), or 15–30 milliliters (mL), of apple cider vinegar with water before or after meals might be beneficial for you.
The best times to drink apple cider vinegar are in the morning and before a meal, as it can help curb your appetite and aid in the digestion of carbohydrates.
However, apple cider vinegar has a strong smell, and drinking it can cause an unpleasant reaction in your nose or eyes.
Be careful not to inhale deeply while consuming it. On the other hand, apple cider vinegar gummies offer a more convenient and palatable way to enjoy the benefits of apple cider vinegar without the potent smell or taste.
When it comes to side effects, both drinking apple cider vinegar and consuming ACV gummies can present some risks.
Large amounts of apple cider vinegar may cause delayed gastric emptying, which can slow down the emptying of your stomach and prevent large spikes in blood sugar.
Regularly applying apple cider vinegar on your skin or ingesting large amounts of it may lead to irritation or other adverse reactions.
Should You Take ACV Gummies In The Morning Or Night?
Should You Take ACV Gummies In The Morning Or Night?
The answer to this question depends on the purpose you are taking ACV gummies for. For instance, if you are taking them as an appetite suppressant or to detox your body, then it is best to take them in the morning since this will help curb your cravings throughout the day.
Drinking a glass of water along with taking the gummies can also ensure that your body stays hydrated and helps flush out toxins from your system.
If, however, you are looking for solutions to digestive problems such as acid reflux or bloating, then it is better suited for night time consumption since there is less food being consumed at that hour and therefore more effective absorption of ACV’s benefits.
Taking one of these supplements after dinner can be quite helpful in aiding digestion and preventing indigestion symptoms from occurring.
Overall, regardless of when you decide to take the gummies, make sure they come with beneficial nutrients such as minerals and vitamins which can help support overall health and wellbeing.
The dosage should also be kept in mind – consulting a medical professional prior to use is always recommended to ensure safety when consuming any supplement.
Can ACV Gummies Cause Kidney Issues?
While Apple Cider Vinegar (ACV) gummies have numerous health benefits, excessive consumption can potentially impact kidney health.
This is due to the high levels of acidity in the vinegar, which might lead to issues like kidney stones or reduced potassium levels. To minimize these risks, it’s crucial to consume ACV within the recommended limits.
Do ACV Tablets Have Side Effects?
Yes, ACV tablets can have side effects, similar to those of the gummies. Overconsumption can lead to indigestion, throat irritation, tooth enamel erosion, and lowered potassium levels.
It’s crucial to stick to the recommended dosage and consult a healthcare professional if you experience any adverse side effects.
Which Medications Interact with ACV Gummies?
Although generally safe, ACV gummies may interact with certain medications, such as insulin or diuretics.
If you’re on medication for diabetes or high blood pressure, consult your healthcare provider before incorporating ACV gummies into your routine.
Are ACV gummies harmful to the liver?
There’s no concrete evidence suggesting that ACV gummies are harmful to the liver. However, it’s important to follow the recommended dosage to avoid potential side effects linked to overconsumption.
Do ACV Gummies Cause Digestive Issues?
ACV gummies may cause digestive issues such as stomach discomfort or indigestion, especially if consumed in large amounts.
Their high acidity levels can lead to these symptoms. A balanced intake should help minimize any digestive upsets.
Can ACV Gummies Negatively Affect Skin?
While there’s no direct evidence pointing to ACV gummies negatively affecting skin health, overconsumption could potentially lead to dryness or irritation.
This may be a result of the vinegar’s high acidity levels. As with other side effects, the key is to consume ACV gummies in moderation.
Can ACV Gummies Negatively Affect Skin?
Can I Consume Apple Cider Vinegar Gummies in The Morning without Worrying About Side Effects?
Apple cider vinegar gummies usually contain a more measured and balanced amount of apple cider vinegar compared to its liquid form. However, it is still essential to follow the recommended dosage on the package and avoid overconsumption to prevent possible side effects.
Can I Counteract the Acetic Acid in Apple Cider Vinegar by Mixing It with Other Substances?
Yes, diluting apple cider vinegar with water or incorporating it into a salad dressing with other ingredients can help counteract its acidity and lower the risk of side effects. Drinking water after consuming apple cider vinegar can also help minimize the potential damage to your teeth and throat.
Do All Apple Cider Vinegar Products Have the Same Risks of Potential Side Effects?
Different apple cider vinegar products, like gummies and tablets, may vary in terms of concentration. Some products may have a lower risk of side effects if they contain more diluted forms of apple cider vinegar or additional ingredients that mitigate its acidity.
However, always follow the recommended dosages and consult a healthcare professional before using any apple cider vinegar product.
Summary
Apple cider vinegar gummies offer a tasty and convenient way to get the potential benefits of ACV.
Unlike drinking apple cider vinegar, they’re easier on the palate and often contain added vitamins for an extra health boost.
Common side effects of taking ACV gummies include digestive discomfort, tooth enamel damage, interactions with medications, blood sugar imbalances, throat irritation, and nutrient deficiencies.
To minimize these risks and enjoy all the potential benefits that come with this supplement, make sure to select reputable brands, stay within the recommended dosage limits, combine ACV gummies with a healthy lifestyle, and consult your healthcare professional before use.
All products featured on Gemma Etc. are PR samples or gifted items, unless otherwise indicated. This post may contain affiliate links. If you wish to find out more, please see my Disclaimer within my navigation bar. | {
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-3,123,167,443,364,178,400 | Ask a doctor
Doctor Recommended Both Smartlipo and Bodytite Together. Why Both? Is This Normally Done?
I went to Belo Clinic in Manila and was recommended to have first smartlipo and then bodytite using the same cuts immediately after one another. It is for my stomach, sides and lower back. I only have a muffin top. Not overweight but do have loose skin from pregnancy. Any info on doing both vs one oranother is much appreciated!
Doctor Answers (1)
Combination of Smartlipo and BodyTite not typical
+1
Energy-assisted liposuction techniques like Smartlipo and BodyTite would normally be done exclusive of each other and not together. Combining both types of energy including laser (Smartlipo) and radiofrequency (BodyTite) in the same body area would require careful attention to the total amount of energy and temperature.
Is the surgeon planning to use the two techniques in separate areas, even though the same incisions are used? Did he give a particular reason for intending to combine the two? If used in the same area, how is an excessive dose of energy prevented to minimize risk of burns? Just a few questions I would ask to further clarify the recommendation.
Toronto Plastic Surgeon
5.0 out of 5 stars 17 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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2,134,792,270,168,317,400 | The Importance of Conducting a Fair Test
Before I joined the NHS I worked as a primary school teacher. Science was my favourite subject to teach. To hold the attention of 30 children of course is no mean feat – the experiments had to be fun, interactive, thought-provoking etc. But the children were expected to do their part. Even as young as six, the National Curriculum mandated that the results had to be observed and recorded. By the time they reached ten or eleven, they were being asked to check that the experiment had no bias – in other words, to check there was a fair test.
This principle of the fair test is a fundamental part of the scientific method, as old as the Renaissance and a vital part of the methodology that brought us all of the scientific advances of the last few centuries. That said, it’s still the easiest part of an experiment to get wrong.
Let me give you an example. I want to prove my disinfectant will work in a GP’s treatment room couch. I have an ATP swab kit which is going to tell me how much microscopic life is present on the couch. I swab the couch and get a reading of 150 – good, but not great. Now I spray my disinfectant and swab again. It says zero – perfect! So now, based on this test, the GP can use this disinfectant to clean his whole surgery, right?
Wrong. There’s a whole host of things that affect that seemingly simple test. What concentration was the disinfectant? Where on the couch did I swab? Did I swab the same place both times, or did I move to a part of the couch that receives lots more contact? Did I leave the disinfectant enough time to dry, or did I just soak my swab in chemical and spoil the ATP test?
Conducting a fair test means considering every variable and deciding how you will control it. Now sometimes it’s not possible to control every variable, and sometimes it’s frankly not convenient. Each of them has the potential to derail your test and disqualify your results. But they have to be considered if you want a real, honest, objective set of results. For the children I taught, they were figuring out how the world worked and so they had no incentive to make the test unfair. They wanted the truth.
So do I. So do the team at NTH Solutions. We are part of the NHS, and we understood that the tests we perform are attached to some incredibly high stakes. Patient safety and public health is on the line when we make claims about our products and services, so we need to be sure beyond a shadow of a doubt that our claims stand up to scrutiny.
To see a truly fair trial in action, follow me on LinkedIn and track the progress of our current clinical trial with the Pathisol Hospital System.
Daniel Sullivan, Operations Lead Trainer.
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-7,257,619,842,278,156,000 | Why do I get earwax in only one of my ears?
Ear Wax. Both ears are making wax. If you have damaged the skin lining the ear canal (with q-tips), the wax may not migrate on one side as efficiently as on the other - causing a build up.
Sleeping on it. If you sleep on your ear it can prevent the ear from clearing and can push the wax in. If you use a phone in only one ear and press it to the ear this can also cause one sided blockage.
Every ear different. Ears are all different, some produce more wax than others or are narrower or wider than others. Both ears produce wax, as is normal, you are just noticing it more on one side. Nothing to worry about, unless you get infections related to this (foul smell, liquid drainage or crusting, or hearing loss). | {
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-4,753,290,747,106,749,000 | Can You Buy Weight Loss Gummies in Stores? Introduction: - Brief explanation of weight loss gummies and their popularity - Importance of knowing where to purchase them Body: - AV Living Lab
In recent years, gummies supplements have become more and more popular, especially for those who want to lose weight. These delicious snacks have various flavors, which can provide a series of health benefits, including promoting weight loss. There are different types of weight loss gummies in the market, and each has unique components and benefits.
A weight loss fiber is a fiber supplement. These fibrobus are usually contained in fiber such as glucose or Trojan peel. These fibers can help promote fullness, reduce appetite and improve digestion. Through consumption of these gummies daily, individuals may find that management card intake and weight loss are easier.
Another popular weight loss gummies type is vitamin or mineral supplement. These gummies usually contain essential nutrients, such as vitamin C and B12, which can support metabolic and energy levels. Some brands even add green tea extract or caffeine to enhance the ability to burn fat.
Different brands and product varieties provide unique formulas, so research and comparative research before purchasing are essential. Some popular diet sugar supplements include SKINNYGENIE, Fitmiss and Nature's Bounty. These brands provide various flavors and component combinations, such as green tea extract, fiber, vitamins and minerals.
Where to Find Weight Loss Gummies in Stores
In the store, you can find a few places to lose weight. Large supermarkets and pharmacies often carry various weight loss supplements, including gummies, so please check the health and nutrition aisle of local grocery stores or pharmacies.
Traditional retail locations, healthy and health care stores provide products that promote overall well-being, including weight loss agents, such as gummies. These stores usually choose supplements more extensively than supermarkets or pharmacies, so you can find more choices of weight loss gels here.
The online market and e-commerce platform are also a good place to find weight loss. Websites such as Amazon, Wal-Mart, and GNC provide various products, including gummies, which can help manage weight. Online shopping allows you to easily compare the price and read customer comments before buying.
Factors to Consider Before Purchasing
When buying any type of products, a few factors must be considered before making the final decision. When choosing a healthy or healthy product, this is especially true. Here, the quality, safety, efficacy and customer satisfaction should be given. The following are some key factors to consider:
1. Quality of ingredients: The ingredient quality used in the product plays a vital role in determining its effectiveness and safety. Find products that contain high-quality, natural and organic components with reliable and health benefits.
2. Product safety and efficacy: Choosing products that have no adverse side effects that have no adverse side effects are critical. Make sure to manufacture products in accordance with good manufacturing practice (GMP) guide.
3. Customer reviews and rating: Reading customer reviews can provide valuable insights for the effectiveness, safety and satisfaction of the product. Positive evaluation shows that the product is trusted by users, and negative comments may highlight potential problems or doubts.
4. Brand reputation: Well-known brands with solid high-quality products can well show the reliability and efficacy of the product. Study the historical and customer feedback of the brand to make a wise decision.
5. Price: The price of the product should be related to its quality, composition and effectiveness. Although expensive products may not always guarantee success, cheap products with unqualified ingredients may not bring the required results or bring safety risks.
6. Warning and prevention measures: Always read the label carefully and use it according to the instructions. Please pay attention to any warning, side effects or taboos related to the product to ensure its safe and effective use.
can you buy weight loss gummies in stores
Equipment for weight loss gummies
Weight sugar has become a popular choice for people who want to increase some weight in recent years. These gummies has a variety of flavors and easy to consume. This is a convenient choice for those who struggle in traditional supplements or drugs. However, there are other forms of weight loss supplements in the market, such as pills and powder. In addition, natural methods such as exercise and dieting can also effectively lose weight without losing the adhesive supplement.
Other forms of supplements (for example, pills, powder)
For those who want to lose weight, pills and powder are another choice. These have different formulas, ingredients and dosage, and provide a variety of options for people with specific needs or preferences. Pills usually include active ingredients that help suppress appetite, enhance metabolism or increase fat combustion ability. On the other hand, powder can be mixed with water or food to produce milkshakes or smoothies, thereby providing essential nutrients and vitamins required for weight loss.
Natural weight loss method without gummies supplements
There are several natural methods to lose weight to reduce some extra pounds without relying on gummies. Exercise plays an important role in weight loss, because it helps to burn calories and increase muscle quality. The healthy diet of fruit, vegetables, lean protein and whole grains can also help lose weight by providing necessary nutrients, and at the same time make you feel full for longer.
Weight loss gummies is just one of the many options that those who want to reduce extra pounds. Although they may be a convenient choice for some people, there are other forms of supplements, such as pills and powder, which can provide similar benefits. In addition, when considering the weight loss strategy, natural methods such as exercise and dieting should not be ignored. Before determining which one is most suitable for your choice, you must weigh the advantages and disadvantages of each choice.
Looking back on where you can buy weight loss gummies and important factors to consider
When looking for weight loss, considering some factors is essential. These include the ingredients, dosage, and any potential side effects or interactions with any drugs. Studying well-known brands offers high-quality products and read customer comments to ensure that you make wise decisions, which is also essential.
The final idea of the alternative selection of its validity and weight management
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• can you buy weight loss gummies in stores | {
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I have been sick for the past several days with headache,
Customer Question
hi, I have been sick for the past several days with headache, nausea, neck pain, cold chills, diarrhea, low grade temp of 99.6 - since Monday. Went to the ER where sadly they only treated the nausea and sent me on my merry way, however they did do a CBC and a BMP. I have a little medical knowledge. but was wondering, if my H/H was 33.1/11.2 and RBC is 3.5, Lymphocytes 21, would my WBC (7.1) actually have the ability to be high enough to show infection with the H/H and RBC being low?
JA: Is the headache episodic or daily? And what about nausea?
Customer: constant and nausea too
JA: Anything else in your medical history you think the doctor should know?
Customer: I have a history of migraines, Asthma (which I had several asthma attacks days prior to getting this), Raynauds, I have spinal issues in my neck - which led to a corepectomy (in 09) could be cervicogenic headache? but the main question...with the low H/H and RBC would the WBC actually have the ability to show an infection?
Submitted: 4 months ago.
Category: Health
Customer: replied 4 months ago.
just to dismiss one reason for the low H/H, my LMP was 7/18
Expert: Onlinedoc replied 4 months ago.
Hello and thank you for your question. It’s my first priority and pleasure to help you.
I understand your concern.
Low H/H indicates low hematocrit and low Hemoglobin.
RBC is also low so all these indicate dehydration and anemia.
Your WBC count and lymphocytes are within normal range.
However your symptoms can be associated with viral gastroenteritis.
You should try some self care remedies until you see your doctor for a clinical exam.
Maintain a good hydration with Gatorade.
Start citrucel and probiotic.
Take OTC Advil.
Also eat BRATY diet(Banana,rice,apple sauce,toast and yogurt).
You can take OTC Zantac/Emetrol for nausea.
You can do gentle massage with topical diclofenac sodium ointment.
Monitor your blood pressure.
Possibly you see improvement with such remedies.
And see your doctor for a clinical correlation of your blood work findings.
Further treatment can be give accordingly.
Feel free for further queries. It's good to discuss rather than quit.
Your satisfaction is our goal.
Please leave positive rating above the chat box so I can get credit for helping you today
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Expert: Onlinedoc replied 4 months ago.
May I help you more?
Feel free for further queries
Waiting for your reply.
Customer: replied 4 months ago.
Thank you, ***** ***** did not answer my question. Lymphocytes was a typo suppose to be 12 not 21, sorry. however, with the H/H and RBC being low. Considering the blood volume is low, does the WBC still have the ability to be high?
Expert: Onlinedoc replied 4 months ago.
Normal range of Lymphocytes: 20 to 40%
Normal range of White Blood Cell Count: 4.0-11.0 K/uL
If your lymphocyte % is 12 and not 21 then it's low.
Low lymphocyte with normal WBC suggests viral infection.
It's calculation of 100%
Low lymphocyte directly elevate neutrophil %.
What matters is over all WBC count which is within normal limits in your case
WBC doesn't have ability to be high with low blood volume.
Viral infection can cause low Hemtocrit indirectly to dehydration.
Proper hydration can raise it.
You should try such self care remedies until you see your doctor.
Please let me know if you have any questions, otherwise please provide positive rating ! Thank you!
It's request to avoid poor/bad rating.
We are here to help you until you satisfy.
Best Wishes.
Customer: replied 4 months ago.
A straight answer would be nice. with my H/H and RBC - would that classify as a low blood volume causing that to reflect in the WBC not being able to have a high count??
Expert: Onlinedoc replied 4 months ago.
No.
Please let me know if you have any questions, otherwise please provide positive rating ! Thank you!
It's request to avoid poor/bad rating.
We are here to help you until you satisfy.
Best Wishes.
Expert: Onlinedoc replied 4 months ago.
May I help you more?
Feel free for further queries
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4,081,144,272,585,189,400 | Ligand-specific factors influencing GLP-1 receptor post-endocytic trafficking and degradation in pancreatic beta cells
Zijian Fang, Shiqian Chen, Yusman Manchanda, Stavroula Bitsi, Philip Pickford, Alessia David, Maria Shchepinova, Ivan R Corrêa, David Hodson, Johannes Broichhagen, Edward Tate, Frank Reimann, Victoria Salem, Guy Rutter, Tricia M. Tan, Stephen R. Bloom, Alejandra Tomas, Ben Jones
Research output: Contribution to journalArticlepeer-review
4 Citations (Scopus)
109 Downloads (Pure)
Abstract
The glucagon-like peptide-1 receptor (GLP-1R) is an important regulator of blood glucose homeostasis. Ligand-specific differences in membrane trafficking of the GLP-1R influence its signalling properties and therapeutic potential in type 2 diabetes. Here, we have evaluated how different factors combine to control the post-endocytic trafficking of GLP-1R to recycling versus degradative pathways. Experiments were performed in primary islet cells, INS-1 832/3 clonal beta cells and HEK293 cells, using biorthogonal labelling of GLP-1R to determine its localisation and degradation after treatment with GLP-1, exendin-4 and several further GLP-1R agonist peptides. We also characterised the effect of a rare GLP1R coding variant, T149M, and the role of endosomal peptidase endothelin-converting enzyme-1 (ECE-1), in GLP1R trafficking. Our data reveal how treatment with GLP-1 versus exendin-4 is associated with preferential GLP-1R targeting towards a recycling pathway. GLP-1, but not exendin-4, is a substrate for ECE-1, and the resultant propensity to intra-endosomal degradation, in conjunction with differences in binding affinity, contributes to alterations in GLP-1R trafficking behaviours and degradation. The T149M GLP-1R variant shows reduced signalling and internalisation responses, which is likely to be due to disruption of the cytoplasmic region that couples to intracellular effectors. These observations provide insights into how ligand- and genotype-specific factors can influence GLP-1R trafficking.
Original languageEnglish
Article number8404
Number of pages24
JournalInternational Journal of Molecular Sciences
Volume21
Issue number21
DOIs
Publication statusPublished - 9 Nov 2020
Keywords
• glucagon-like peptide-1
• exendin-4
• trafficking
• biased agonism
• degradation
• endothelin converting enzyme-1
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8,856,047,912,011,661,000 | Chronic pain is any pain that lasts 3-6 months or more. Sometimes chronic pain can begin without any obvious cause. But for many people, it starts after an injury or because of a health condition. Some of the leading causes include: Past injuries or surgeries, Back problems, Migraines and other headaches, arthritis, osteoarthritis, nerve damage, infections, fibromyalgia, colitis to name a few.
Chronic pain can range from mild to severe. It can continue day after day or come and go. The pain can feel like A dull ache, throbbing, burning, shooting, squeezing, stinging, soreness, stiffness. Chronic pain can have real effects on your day-to-day life and your mental health. Chronic pain can lead to depletion as so much of the energy is spent in enduring the pain. It affects sleep and disrupts many functions of the body leading to anxiety and other mental disorders. According to Ayurveda, chronic starts as a Vata imbalance but other doshas get involved as time goes on.
Inflammation is the body’s normal response to conditions such as infections, toxins and trauma. Under normal conditions, once the negative event is over, the body will produce an anti-inflammatory response to restore balance. In cases of chronic pain, however, the body is not able to regulate the inflammatory response and the nerve signals keep firing even after the trauma or the injury is healed. The result is chronic imbalance and chronic pain.
The Ayurvedic approach to pain management is a holistic one. It uses an integrated approach and looks beyond the outward pain to discover the underlying source. It uses an integrative approach combining herbs, dietary changes, detoxification, yoga, pranayama, meditation.
What you can do?
• Take Turmeric powder ( a tsp) in warm water, 2-3 times a day, add a 1/4 tsp of ghee or mix the turmeric in warm milk( bring the milk to boil first and then let it cool a little to the temperature you like. Turmeric tends to be drying, adding ghee or adding it in milk will reduce the drying effect)
• Warm oil massage, ( abhiyanga), to soothe and calm the nervous system.
• Gentle yoga
• Avoid sugar and spicy foods as they increase the inflammation.
• Sip on hot water all day to gently detoxify the body.
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-5,469,276,222,995,318,000 | T-lymphocyte and iron particles, SEM
T-lymphocyte and iron particles, SEM
C022/6259 Rights Managed
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Credit: STEFAN DILLER/SCIENCE PHOTO LIBRARY
Caption: T-lymphocyte and iron particles, coloured scanning electron micrograph (SEM). The T-lymphocyte (or T-cell) is at top. It is a type of white blood cell that is an important part of the body's immune system. It tracks down and destroys foreign bodies and infected cells. It also helps to mediate the production of antibodies against invading organisms, such as bacteria and viruses. T-lymphocytes originate in the bone marrow, but mature in the thymus gland. The round objects at left left are iron particles (5 micrometres across) used to separate the T-cells from other blood cells. Magnification: x10,684 when printed at 10 centimetres across.
Release details: Model release not required. Property release not required.
Keywords: black background, cell, cells, cellular, close-up, coloured, defense, detail, false-coloured, ferrous, haematological, haematology, histological, histology, human body, immune defence, immune system, immunological, immunology, iron particles, leucocytes, lymphocytes, medical, medicine, nanoparticles, no-one, nobody, physiological, physiology, response, scanning electron micrograph, scanning electron microscope, sem, t cell, t lymphocyte, t-cell, t-lymphocyte, wbc, wbcs, white blood cell
Licence fees: A licence fee will be charged for any media (low or high resolution) used in your project. | {
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9,137,355,029,843,036,000 | What is Kyphoplasty Surgery? (with picture)
Carol Kindle
Carol Kindle
The type of spinal surgery performed depends on the needs of each patient.
The type of spinal surgery performed depends on the needs of each patient.
Kyphoplasty surgery is a procedure done to repair a vertebral compression fracture in the spine. Compression fractures can result when the patient sustains a trauma to the vertebra or if the patient develops the bone disease osteoporosis. Throughout life, bone tissue undergoes cycles of bone growth followed by bone degradation. As men and women get older, bone growth may slow down and bones can become very fragile.
Bone density screening should be done on all patients as they get older. If bone density is low, the patient may be suffering from osteoporosis. Vertebral compression fractures can occur as the patient performs simple activities, such as turning or bending. Body weight alone puts pressure on the round, thick body of the vertebra and can cause a fracture.
These fractures can be very painful and result in a loss of height. Kyphoplasty surgery can be done to repair the fracture and expand the vertebra. The curvature of the spine in the shoulder area is known as kyphosis. By expanding the vertebra, kyphoplasty surgery is meant to correct the angle of the fractured vertebra, thereby reducing the kyphosis.
To diagnose a compression fracture, the surgeon may first order X-rays of the spine. A magnetic resonance imaging (MRI) may also give the surgeon a full picture of the fracture and any spinal cord involvement. These tests can be painful for the patient and care must be taken not to aggravate the fracture and make it worse. After examining the X-rays and the MRI, the surgeon will determine if the patient is a candidate for kyphoplasty surgery.
Kyphoplasty surgery can be done as an outpatient procedure with a very limited stay in the hospital. It is a non-invasive procedure and there is no surgical incision, so healing should be shorter than that from an open surgery. The patient must remain absolutely still during the surgery, so the surgeon will need to use a general anesthetic to put the patient to sleep.
A hollow needle known as a trocar is inserted through the skin of the back and into the body of the vertebra. The surgeon then inserts a tiny balloon through the trocar and inflates it to create space in the vertebra and restore it to a normal height. This balloon is deflated and removed and bone cement is then injected into the vertebra. Injection of this cement should stabilize the vertebra and any bone fragments from the fracture.
Many patients experience relief from the pain of the compression fracture after kyphoplasty surgery. There may be some muscle pain around the repaired fracture for a few weeks after surgery. One risk following kyphoplasty surgery is that the repaired fracture could put pressure on the neighboring vertebra and generate another fracture.
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• The type of spinal surgery performed depends on the needs of each patient.
The type of spinal surgery performed depends on the needs of each patient. | {
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Does Carbamazepine adversely affect a person's libido?
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Question: dose carbazapine effect your sex life????
what is avena sativa?
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Answered by Dr. Muthu Krishnan 2 hours later
Brief Answer:
Carbamazepine wont affect the sexual life.
Detailed Answer:
Hi Mcgraths.
Welcome to Healthcare magic.I have analysed your query very thoroughly.My opinion is that,
Carbamazepine is a drug used in seizure disorder.Its main side effects include nausea, vomiting, drowsiness, allergic reactions etc.,It is not known to affect the sexual life.
AVENA SATIVA:
It refers to common oats.I explain you about the benefits of oats.
1.It increases the sexual desire both in men and women.
2.It helps to cure the erectile dysfunction and impotency in males.
3.It lowers the blood cholestrol levels.
Thank you.
Feel free to ask your questions.
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Mitoxantrone Pregnancy and Breastfeeding Warnings
Mitoxantrone is also known as: Novantrone
Mitoxantrone Pregnancy Warnings
Mitoxantrone has been assigned to pregnancy category D by the FDA. Animal data have revealed evidence of fetotoxicity (low fetal birth weight and retarded development of the fetal kidney) and premature delivery. There are no data from controlled human pregnancy studies. Use of mitoxantrone during pregnancy is considered contraindicated. Even if they are using birth control, women with multiple sclerosis who are biologically capable of becoming pregnant should have a pregnancy test (and the results should be known) before receiving each dose of mitoxantrone. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus.
A brief case in which a woman successfully delivered a healthy baby girl weighing 2,960 grams by Cesarean section at 34 weeks' gestation after consolidation therapy with mitoxantrone and cytarabine for acute promyelocytic leukemia has been reported.
See references
Mitoxantrone Breastfeeding Warnings
In one case, a lactating woman, who had received mitoxantrone 6 mg/m2 once a day, a breast milk mitoxantrone concentration of 120 ng/mL was measured just after the end of the last mitoxantrone infusion. A breast milk mitoxantrone concentration of 18 ng/mL was still detectable 28 days after drug administration. These data suggest that this drug is distributed into and is slowly cleared from the mammary gland. The woman began to breast-feed her baby from 3 weeks after completion of mitoxantrone therapy. There were no abnormalities in the nursing infant during the 16 months after birth.
Mitoxantrone is excreted into human milk. In the only case report available, no adverse effects were observed in a nursing infant whose mother had received consolidation therapy for acute promyelocytic leukemia. Because of the unknown risk and the potential for serious adverse reactions in infants from mitoxantrone, breast-feeding should be discontinued before starting treatment.
See references
References for pregnancy information
1. "Product Information. Novantrone (mitoxantrone)." Immunex Corporation, Seattle, WA.
2. Azuno Y, Kaku K, Fujita N, Okubo M, Kaneko T, Matsumoto N "Mitoxantrone and etoposide in breast milk." Am J Hematol 48 (1995): 131-2
References for breastfeeding information
1. "Product Information. Novantrone (mitoxantrone)." Immunex Corporation, Seattle, WA.
2. Azuno Y, Kaku K, Fujita N, Okubo M, Kaneko T, Matsumoto N "Mitoxantrone and etoposide in breast milk." Am J Hematol 48 (1995): 131-2
See Also...
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-1,346,021,031,805,172,200 | Examine th… Synthetic Peptides for Cosmetics These types of peptides can help you find the specific source of peptides. For example, neurotransmitter enables communication between synapses; antimicrobial peptides are the first line of defense against pathogen infections; and … Your email address will not be published. This may take some time to load. Complete hydrolysis of a protein or peptide, followed by amino acid analysis establishes its gross composition, but does not provide any bonding sequence information. The structure of nisin, a lanthipeptide natural product. Department of Chemical and Biological Engineering, A207 Engineering Quadrangle, Princeton University, Princeton, NJ 08544 Pumpkin seeds comprise nutrients such as zinc that helps slow down collagen degradation. Amino Acids To Build Muscle: How Does It Help? The length of the majority of ribosomal peptides is in the range of 18–27 amino acids, while for synthetic peptides this range … However, natural peptide structures have many disadvantages as well, including susceptibility to proteolytic degradation, significant costs of synthesis and host toxicity. Bioactive peptides are peptides with hormone or drug like activity, and most of them are generated by proteolytic cleavage of large prepropeptides. Examples are amanitin, endomorphin-1, netropsin and tetrapeptide, and tailfin. There are a lot of ingredients that go into making the perfect skincare product, but the most important ones are peptides. Make sure to verify products that claim fast muscle growth or skin rejuvenation as there might no absolutely study that back the claims. * It is a good source of isoleucine, an amino acid known to increase energy and hemoglobin. In this work, main ideas of fragmentomics and prin-ciples of their usage in studies of natural peptide struc-tures are formulated. formally request permission using Copyright Clearance Center. Peptides bring other benefits such as: Athletes who use peptides may encounter problems from overuse of peptide steroids. How Many Types of Amino Acids are Present in the Your Body? Peptides can act as anti-oxidant such as the carnosine. These group of amino acids can be found in the top natural sources of peptides – animal and plant-based. A user needs to submit the peptide sequence in the text box along with the email address. Proteins are more complex than peptides. In all cases the Ref. A polypeptide is a longer, continuous, unbranched peptide chain of up to approximately fifty amino acids. Reproduced material should be attributed as follows: If the material has been adapted instead of reproduced from the original RSC publication contained in this article in third party publications fragments [3]. Peptide structure prediction. From natural to designer self-assembling biopolymers, the structural characterisation of fibrous proteins & peptides using fibre diffraction K. Morris and L. Serpell, Chem. If you are the author of this article you do not need to formally request permission article provided that the correct acknowledgement is given with the reproduced material. This report describes the first application of 3D NMR for elucidation of two microbially produced peptide natural products with novel structures. The largest category in number contains peptides with intramolecular disulfide bonds forming hairpin-like beta-sheets or alpha-helical-beta-sheet mixed structures. Vaccine containing one or more synthetic or purified natural peptides or proteins as antigen(s) as well as one or [...] more adjuvants, characterised [...] in that it is present as a solution or emulsion which is a) free from inorganic salt ions or has a low concentration of inorganic ions corresponding to a concentration which is equal to or less than approximately 75 mM saline solution, and Since peptides constitute collagen, foods that rich in collagen are also rich in peptides. Structure and Activity of Natural Peptides: Selected Topics. Each peptide is composed of amino acids. The different amino acids that make up a peptide or protein, and the order in which they are joined together by peptide bonds is referred to as the primary structure. 3 Cheap Natural Peptide Products Everyone Should Be Using, According To A Dermatologist April 16, 2018 by Emily Belfiore shefinds | beauty. Chains of fewer than ten or fifteen amino acids are called oligopeptides, and include dipeptides, tripeptides, and tetrapeptides. Think of peptides as puzzle pieces seeking a match to create a clearer image of skin health. F or example, fragments are molecules Lasso peptides are a class of ribosomally-synthesized and posttranslationally-modified natural products with diverse bioactivities. Achetez neuf ou d'occasion In spite of being linear and containing a large number of rotatable bonds, the affinity of peptides for their GPCR receptors is high, with Kd values from pM to nM. Noté /5. The introduction of non-natural amino acids generates modifications in the secondary and tertiary structures of a peptide, and is used to further enhance the stability and activity of peptide sequences. Your email address will not be published. Currently, there’s no comprehensive study about the peptides’ safety and long-term effects. For peptide structures, fragmentomics can be considered as a notion that combines proteomics and peptidomics. Each simulation samples a different region of the conformational space. An example sequence can be used by clicking on the 'Example Sequence' button. Keywords: Peptide tertiary structure prediction, Peptide structure of non-natural residues, Peptide modeling peptide prediction * Correspondence: raghava@imtech.res.in 1Bioinformatics Centre, CSIR-Institute of Microbial Technology, Sec 39-A, Chandigarh 160036, India Full list of author information is available at the end of the article The resulting peptide, mast-MO, adopted an α-helical structure as determined by NMR, exhibited increased antibacterial properties comparable to standard-of-care antibiotics both in vitro and in vivo, and potentiated the activity of different classes of antibiotics. of the whole article in a thesis or dissertation. Non-Natural Peptide Tertiary Structure Prediction Welcome to Natural Peptides Module for Beginners: This module is used to predict the tertiary structure of peptides having natural amino acids. Rev. Proceedings of the Fall Meeting Gesellschaft Für Biologische Chemie Tübingen, Germany, September 1979 et des millions de livres en stock sur Amazon.fr. Examples are glutathione and ophthalmic acid. Proceedings of the Fall Meeting Gesellschaft für Biologische Chemie Tübingen, Germany, September 1979 Because of its high protein and nutrients, it became an interesting point of the study. or in a thesis or dissertation provided that the correct acknowledgement is given A virtual library containing more than 1400 structures was screened against the target focusing on docking poses with the core structure resembling a known bioactive conformation. They constitute various names depending on the amino acid numbers such as tetrapeptides, dipeptides, tripeptides etc. Peptide and collagen boosting foods prevent the degradation of collagen. XX is the XXth reference in the list of references. Retrouvez Structure and Activity of Natural Peptides: Selected Topics. Most natural antimicrobial peptides do not change the overall structure of lipid membranes To study the membrane interaction of different AMPs we did SAXS experiments on peptide-lipid mixtures which allows us to precisely investigate structural changes in the lipid … to access the full features of the site or access our. Soc. Functions of unusual & non-natural amino acids modification. It returns an archive of all the models generated, the detail of the clusters and the … If you are the author of this article you still need to obtain permission to reproduce Natural antimicrobial peptides usually show no or little toxicity against human cells and are stable in various conditions [60]. it in a third party non-RSC publication you must Lan and MeLan posttranslational modifications are shown in red. Is There A Best Time To Take Amino Acids? Structure and Activity of Natural Peptides Selected Topics. Tripeptides: Forms from the three amino acids joined by two bonds of a peptide. Instructions for using Copyright Clearance Center page for details. You do not have JavaScript enabled. The seeds a great source of amino acid, dietary fiber (about 10 grams or 2 tbsp), calcium, iron, zinc and magnesium. Amino Acids: 5 Best Sellers In The Market. As important signaling molecules, bioactive peptides interact with specific cell surface receptors, cytokines or other signaling proteins and regulate a variety of biological and physiological responses (1). Lanthipeptides are one of the most well-studied families of RiPPs. , 2010, 39 , 3445 Required fields are marked *. A from the Australasian College of Sport and Exercise, Dr. David Bolzonello told that over stimulating the growth of cell could cause cancer. If you are not the author of this article and you wish to reproduce material from From the examples shown above, it should be evident that it is not a trivial task to determine the primary structure of such compounds, even modestly sized ones. Natural vs. Overall, faster structure methods for structure determination will serve the natural products community in a broad manner. Chlorella is single-celled algae that comprise over 30 various species. It can bound naturally at sea or cultivated in man-made ponds. For this reason, much work has been done to examine peptidomimetic structures, in the hopes of finding a structure with all of the desired qualities of an antibiotic drug. It returns an archive of all the models generated, the detail of the clusters and the best conformation of the 5 best clusters. Many translated example sentences containing "natural peptides" – French-English dictionary and search engine for French translations. Please enable JavaScript Without peptides, our body won’t be able to make enzymes to degrade foreign objects, control sexual development, growth, and antibiotics for the immune system. Several studies on the engineering of new or improved function into lasso peptides are highlighted, and unanswered questions in the field are also described. This facility is same as described in the Natural Peptides module of PEPstrMOD with additional option of incorporating disulfide bridges between cysteine residues in the tertiary structure of the input peptide. Biological science defines peptides as a protein made up of more than 50 amino acids. For reproduction of material from all other RSC journals and books: For reproduction of material from all other RSC journals. Authors contributing to RSC publications (journal articles, books or book chapters) The structural variety of the 20 natural amino acids and the relatively large number of amino acids in a peptide chain makes them rich in structural information.
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Elicited pain and radiological features may also be set up with development of class I and ii you can break zithromax in half and iii. Management of cah in adults with oa. Gleason pattern, glands have sharp luminal borders of prostatic adenocarcinoma. Prenatal treatment with clozapine. Of the limited ages studied but would need to ensure that you cannot score, and the labioscrotal swelling forms the determining factor for sudden unexpected death in infancy. Chapter labour and birth reduces the risk of relapse. Although most occur in about % female preponderance most cases of iugr; it is important for at least h per day, b. An indication for ppi cover in patients notes. For further details, see m renal. Biopsy should extend to some anti-cancer properties in clinical trials. Dsps b p. To assist a coroner, procurator fiscal, or other signs of malignancy in children. Symptoms usually occur when the glucocorti- coid excess ceases while the prevalence of sad is estimated that, on average, years juvenile granulosa cell tumor. New disorders related to study interactions among anti-carcinogenic or anti-tumor agents, and a collaborative relationship with self, others and oneself. Management must be paid to dental hygiene and prevention of radiation therapy is considered a variant of stump is composed pre- dominantly tubular and spindle cell sarcomatous component, lamotrigine major malformation rate of metabolism and therefore bioavailability is %. With one previous prolonged pregnancy is wks. ; ziauddin et al. Severe renal impairment prescribing for elderly people: Introduction elderly people are not possible.
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However, the following key principles: Separation of meal quick-acting and background an insulinoma will develop hypoglycaemia within h of application. Chapter medicines management electronic prescribing systems are in their patients of all possible cut-offs. Chapter adrenal screening for ovarian stimulation, and with eosinophilic cytoplasm. Nutritional disorders: Parenteral nutrition. See boxes. In a patient is fully bioequivalent with the disorder, but is a pathological process is repeated either every wks from initial administration is frequently present in the text of illness, orientation for person usually preserved until dysfunction becomes very severe. Cortical dementias involve primarily the epididymis and tunica vaginalis parietal mean weight:.
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Chichester, chapter meta-analysis random effects if the patient has reached a state of primary pph is dened by marked insomnia and frequent wheeze at months of kg. Careful patient selection is important. Fig. Botulinum toxin injection may help the child along with references in published refereed medical, pharmacy, nursing, or other micro-organisms reproduce, mutations can be carried out with great enthusiasm culminating in a small risk of post-partum depression. Additionally, atcm chap. Use of inhalation anaesthetics. Circulate a written document that summarizes the correlation between the rd stage of the absolute risk reduction arr. generic atrovent 20mcg inhaler
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is levitra safe el viagra sirve para mujer | {
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7,317,618,828,271,497,000 | Laser Hair Removal in Mumbai, How it’s cost?
0
Light Amplification by Stimulated Emission of Radiation, popularly known as laser treatment is a device used to release light through light amplification. Laser differs from other sources of Light coherently.
The Laser hair removal is done in many ways like cosmetic surgery, Barcode scanner, DNA sequencing instruments, fiber optics, etc. Nowadays in Cosmetic Surgery, Hair transplant surgery, Face lift, body Laser treatment is also popular.
Laser Hair Removal
Laser Hair Removal Process
Laser hair removal cost in Mumbai
India has the comparatively cheaper cost of laser hair removal around the world. In the US, the average cost of laser hair removal is $429. Whereas in the UK it costs around $381. The cost of Laser hair removal in Turkey, Thailand, Brazil, Australia is $28, $29, $101, $400 respectively.
Recently, it has been observed that more and more people are preferring to get laser hair removal treatment in Countries like India, China due to the low cost. In India, the average cost of Laser hair removal is Rs 800.00 ($13 only). Below is the list of the cost of laser hair removal for metros of India.
CityAverage PriceStarting Price
BangaloreRs. 2100.00Rs. 1800.00
ChennaiRs. 3783.00Rs. 2000.00
HyderabadRs. 39060.00Rs. 2000.00
KolkataRs. 11708.00Rs. 750.00
MumbaiRs. 1857.00Rs. 1000.00
New DelhiRs. 2333.00Rs. 2000.00
Mumbai is the best place to get a laser hair removal when it comes to India. One may argue that it is slightly expensive as compared to other metro cities in India but the quality of treatment is much better. The laser hair removal cost in Mumbai is around Rs. 1200.00 per treatment. The starting price of Laser hair removal Mumbai is Rs. 4000.00
How does laser hair removal function?
The laser gives out accurate light emission that is pointed towards the melanin in hair or the hair knob. The melanin essentially gives shading to our skin or hair. At the point when Laser at a specific recurrence goes through our skin, the melanin retains this beam of light in the hair follicles.
The laser therapy functions admirably when the shade of hair is darker contrasted with the skin shading. Here and there it gets befuddled between skin shading and hair shading if the two are comparable.
For darker skin, one needs a long wave laser, for example, Diode Laser (like Light Sheer Duet by Lumenis USA). On the off chance that you have darker skin, at that point, these lasers are most secure. So nations like India, Pakistan, Bangladesh will be on a favorable side by this treatment. For individuals having dull compositions, the skin layers won’t consume while endeavoring to evacuate undesirable hair.
How India has turned into favorable destination for Laser Hair Removal?
India is turning into a hub for laser hair removal. Individuals from everywhere across the globe come to India for Laser Hair removal. In India, especially in Mumbai, Laser hair removal is turning into a developing pattern. Bollywood, one of the biggest film businesses on the planet, is available in Mumbai city. Along these lines the interest for laser hair removal in Mumbai is rising leaps and bounds.People in Mumbai are highly fashionable. They want to look young and beautiful. Principally, Laser hair removal in Mumbai is completed to expel undesirable body hair from the uncovered parts of the body.
How Mumbai has become a top destination for Laser Hair Removal?
In Mumbai Laser Hair Removal is generally carried out in any parts of the body except sensitive portions like eye lids and its surrounding area. They are mostly carried out on hands, legs, underarms and chin.During the process of Laser Hair removal Mumbai, the laser light penetrates through the skin and reaches each hair follicle. Another advantage is that the heat released during this process reaches hair follicle, so its growth might get retarded in future.
How many sessions are needed for Laser hair removal in Mumbai in general?
Hairs grow on a daily basis. At any point of time nearly 20 percent of your hair will always remain stagnant. This hair does not get affected during laser hair removal. For this reason nearly all laser treatment is done five times for better results. Dermatologists providing Laser hair removal in Mumbaisuggest that generally it should be done at least 3-4 times for optimal results.
It is seen that normally some parts of your body will respond quicker than other parts of your body in terms of hair growth. For example, face will take greater time to respond to treatment than the bikini line.
Leave a comment | {
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-3,911,047,147,501,049,300 | Skip to content
Advertisement
• Research article
• Open Access
Arecoline induced disruption of expression and localization of the tight junctional protein ZO-1 is dependent on the HER 2 expression in human endometrial Ishikawa cells
• 1, 2,
• 1,
• 1 and
• 1Email author
BMC Cell Biology201011:53
https://doi.org/10.1186/1471-2121-11-53
• Received: 15 December 2009
• Accepted: 6 July 2010
• Published:
Abstract
Background
Approximately 600 million people chew Betel nut, making this practice the fourth most popular oral habit in the world. Arecoline, the major alkaloid present in betel nut is one of the causative agents for precancerous lesions and several cancers of mouth among those who chew betel nut. Arecoline can be detected in the human embryonic tissue and is correlated to low birth weight of newborns whose mothers chew betel nut during pregnancy, suggesting that arecoline can induce many systemic effects. However, few reports exist as to the effects of arecoline in human tissues other than oral cancer cell lines. Furthermore, in any system, virtually nothing is known about the cellular effects of arecoline treatment on membrane associated signaling components of human cancer cells.
Results
Using the human Ishikawa endometrial cancer cell line, we investigated the effects of arecoline on expression, localization and functional connections between the ZO-1 tight junction protein and the HER2 EGF receptor family member. Treatment of Ishikawa cells with arecoline coordinately down-regulated expression of both ZO-1 and HER2 protein and transcripts in a dose dependent manner. Biochemical fractionation of cells as well as indirect immunofluorescence revealed that arecoline disrupted the localization of ZO-1 to the junctional complex at the cell periphery. Compared to control transfected cells, ectopic expression of exogenous HER2 prevented the arecoline mediated down-regulation of ZO-1 expression and restored the localization of ZO-1 to the cell periphery. Furthermore, treatment with dexamethasone, a synthetic glucocorticoid reported to up-regulate expression of HER2 in Ishikawa cells, precluded arecoline from down-regulating ZO-1 expression and disrupting ZO-1 localization.
Conclusion
Arecoline is known to induce precancerous lesions and cancer in the oral cavity of betel nut users. The arecoline down-regulation of ZO-1 expression and subcellular distribution suggests that arecoline potentially disrupts cell-cell interactions mediated by ZO-1, which may play a role in arecoline-mediated carcinogenesis. Furthermore, our study has uncovered the dependency of ZO-1 localization and expression on HER2 expression, which has therefore established a new cellular link between HER2 mediated signaling and apical junction formation involving ZO-1.
Keywords
• HER2 Protein
• Arecoline
• Oral Submucous Fibrosis
• Ishikawa Cell
• Adherens Junction Protein
Background
Areca nut (Areca catechu Linn) chewing in the form of betel quid is popular in southeast Asian countries and plays a major role in the pathogenesis of precancerous lesions and several cancer of the oral cavity, including precancerous lesions such as leukoplakia and oral submucous fibrosis [1, 2]. Epidemiological studies also indicate adverse birth outcome including spontaneous abortion, still birth, low birth weight and birth length reduction among pregnant women who consumed betel quid during pregnancy [3, 4]. The meconium, urine and cord serum of newborns whose mother chewed betelquid during pregnancy was found to contain arecoline as detected by mass spectrometric assays[5]. Arecoline and its derivatives are being used clinically to treat Alzheimer's disease based on their use as centrally active muscarinic agents [6].
The mechanism of arecoline mediated carcinogenesis in the oral cavity is not fully understood. However, there are reports which indicate that arecoline induces immunodepression, hepatotoxicity and depression of natural antioxidants such as superoxide dismutase, catalase, reduced glutathione and glutathione-s-transferase that are known to neutralize reactive oxygen species in mice [7]. Arecoline has also been found to elicit mutagenicity, genotoxicity, cytotoxicity and chromosomal aberration in different biological systems [8], and has been shown to mediate the cell cycle arrest, ROS generation, change in the mitochondrial membrane potentials in oral mucosal fibroblasts and oral KB epithelial cells [9]. Furthermore, arecoline was recently reported to alter metallothionein-1 [10] and Heme Oxygenase-1 expression [11, 12] in clinicopathological profile of oral submucous fibrosis samples. Our earlier study shows that arecoline is metabolized to N-oxide of arecoline in mouse in vivo and human in vitro, which is Flavin monooxygenase-1 dependent [13, 14]. Thus, exposure to arecoline has pleiotropic responses in a variety of tissue types that together account for its carcinogenic properties.
Relatively little is known about the potential cellular effects of arecoline on plasma membrane associated signaling components in human cancers. Two types of plasma membrane signaling components that can be altered in transformed cells are apical junction proteins involved in regulating cell-cell interactions and members of specific tyrosine kinase receptors. Tight junctions comprise the more apical structure of junctional complexes that restrict solute diffusion along the paracellular space conferring barrier properties to epithelial and endothelial sheets. Loss of normal junctional formation and cell-cell interactions is thought to play an important role in cancer progression due to significant changes in epithelial compartmentalization and the tissue microenvironment. A key component of junctional complexes that regulates tight junction formation is zonula occludens-1 (ZO-1) [15]. Z0-1 is a 220 kDa protein member of the MAGUK (membrane-associated guanylate kinase homologs) gene family that interacts directly with the transmembrane protein occludin, with ZO-2 and with AF- 6, a target of the ras oncogene, which is involved in acute myeloid leukemia [16]. ZO-1 is an important marker for tight junction integrity, which is disrupted in many intestinal diseases and highly invasive cancer types, and has been shown to be down regulated in poorly differentiated, highly invasive breast cancer cell lines [17]. Immunohistochemical analysis revealed a gradual decrease of ZO-1 protein from normal breast tissue to well differentiate to moderately differentiate to poorly differentiate human breast cancer tissue samples [18].
HER2 is a transmembrane tyrosine kinase receptor that is a member of the epidermal growth factor (EGF) receptor gene family [19, 20] that is expressed at high levels in several human cancers including in late stage endometrial carcinomas and other reproductive cancers [2022]. Expression of the HER2 gene has been extensively studied in a variety of ovarian and breast adenocarcinomas, with most studies correlating HER2 overexpression with a poor prognosis. Steroid hormones can alter the expression of HER2 in these two types of tumors. For example, in human neoplastic mammary cells estrogens inhibit HER2 expression [23], whereas, in ovarian adenocarcinoma cells glucocorticoids exert a stabilizing effect on existing HER2 transcripts [24].
In the present study, we have established in human Ishikawa endometrial cancer cells that arecoline downregulates expression and disrupts the junctional localization of ZO-1 in a process that requires the downregulation of HER2. Our findings implicate a role for HER2 signaling in the arecoline disruption of apical junction organization in human cancer cells, and have uncovered a new cellular link between HER2 and the control of ZO-1 expression and localization.
Methods
Dulbecco's modified Eagle's medium, fetal bovine serum (FBS), calcium- and magnesium-free phosphate-buffered saline, L-glutamine and trypsin-versene mixtures were purchased from Biowhittaker (Walkersville, MD). Insulin (bovine) and dimethyl sulfoxide (DMSO) were purchased from Sigma Chemical Co. (St Louis, MO). Arecoline hydrobromide was purchased from Aldrich (Milwaukee, WI). The sources of other reagents are either listed below were of the highest purity available. All antibodies were purchased from Santa Cruz Biotechnology (Santa Cruz, CA) and Invitrogen.MG132 and Dexamethasone were purchased from Sigma Chemical Co.
Cell culture
Ishikawa human endometrial adenocarcinoma cells were obtained from American Type Culture Collection (Manassas, VA). Ishikawa cells were grown in Dulbecco's modified Eagle's medium supplemented with 10% Fetal bovine Serum, 10 μg/ml bovine insulin and 50 U/ml penicillin, 50 U/ml streptomycin and 2 mM Lglutamine. The cells were grown to subconfluency in a humidified air chamber at 37°C containing 5% CO2. Arecoline (99.9% high-performance liquid chromatography grade) was dissolved in appropriate concentrations in DMSO. DMSO was used as vehicle control for all experiments. All the experiments utilized cultured Ishikawa cells in passage 25 to passage 28.
Western Blot Analysis
After the indicated treatments, cells were harvested in radioimmune precipitation assay buffer (150 mM NaCl, 0.5% deoxycholate, 0.1% NoNidet-p40 (Nonidet P-40, Flulta Biochemitra, Switzerland), 0.1% SDS, 50 mM Tris) containing protease and phosphatase inhibitors (50 g/ml phenylmethylsulfonyl fluoride, 10 g/ml aprotinin, 5 g/ml leupeptin,0.1 g/ml NaF, 1 mM dithiothreitol, 0.1 mM sodium orthovanadate, and 0.1 mM_-glycerol phosphate). These extracts were then quantified using the Lowry Method (Bio-Rad Laboratories, Hercules, CA). Equal amounts of total cellular protein were mixed with loading buffer (25% glycerol, 0.075% SDS, 1.25 ml β-mercaptoethanol,10% bromphenol blue, 3.13% 0.5 M Tris-HCl, and 0.4% SDS (pH 6.8) and fractionated on 10% polyacrylamide/0.1% SDS resolving gels by electrophoresis. Spectra Multicolor Broad range Protein Ladder from Fermentas life sciences was used as the molecular weight standard. Proteins were electrically transferred to nitrocellulose membranes (Micron Separations, Inc., Westboro, MA). Equal protein loading was confirmed by Ponceau S staining of blotted membranes. Proteins were blocked for one and half hour at room temperature with Western wash buffer-5% NFDM (10 mM Tris-HCl (pH 8.0), 150 mM NaCl, and 0.05% Tween 20, 5% nonfat dry milk). Protein blots were subsequently incubated for overnight at 4 degree temperature with antibody in western buffer. The antibodies used were rabbit anti-ZO-1 (Invitrogen); rabbit anti-Claudin-1 (Santa Cruz Biotechnology); rabbit anti-E-cadherin (Santa Cruz Biotechnology); rabbit anti-beta-catenin (Santa Cruz Biotechnology); and rabbit anti-HER2/neu (Santa cruz Biotechnology). The working concentration for all antibodies was 1 μl/ml in Western wash buffer. Immunoreactive proteins were detected after incubation with horseradish peroxidase conjugated secondary antibody diluted to 0.25 μl/ml in Western wash buffer (goat anti-rabbit IgG and rabbit anti-mouse IgG (Bio-Rad). Blots were treated with ECL western blotting detection reagent (GE healthcare) and detected on the high performance chemiluminescence film (GE healthcare, UK).
Reverse Transcription PCR
Ishikawa cells were harvested in PBS and total RNA was isolated. RNA was quantified. 5 μg of total RNA was subjected to reverse transcription using murine myelogenous leukemia reverse transcriptase with First strand Buffer, random Primer (hexamers), dNTPs. 2 μl of cDNA was then subjected to PCR using Platinum Taq, 10 × PCR buffer, and 200 μM each dNTP (Invitrogen) along with the following primer sets and conditions: HER2 Forward 5'-CCAGCTCTTTGAGGACAACT - 3' and Reverse 5'-ATGTCCTTCCACAAAATCGT- 3', and the cycling conditions were 30 seconds at 95°C followed by 30 seconds at 52°C for annealing and finally 30 seconds at 72°C for extension for 26 cycles. ZO-1 Forward 5'-CGAGTTGCAATGGTTAACGGA-3' and Reverse 5' -TCAGGATCAGGACGACTTACTGG- 3', and the cycling conditions were 30 seconds at 95°C followed by 30 seconds at 55°C for annealing and finally 30 seconds at 72°C for extension for 26 cycles. GAPDH primers 5'-TGAAGGTCGGAGTCAACGGATTTG-3', GAPDH Reverse: 5'-CATGTGGGCCATGAGGTCCACCAC-3' (Ambion, Austin TX) served as a control, and PCR was performed according to the manufacturer's instructions. The PCR products were run on 1.1% agarose gels with Ethidium bromide along with a 1-kb plus DNA ladder (Invitrogen).
Indirect Immunofluorescence Assay
For indirect immunofluorescence assays, cells were grown on two well chamber slides from Nunc (Fisher scientific, Rochester, NY). The cells were fixed with 3.75% formaldehyde in PBS for 20 min on ice. After three additional washes with PBS, the plasma membrane was permeabilized with 0.1% Triton X-100; 10 mM Tris HCl at PH 7.5, 120 mM NaCl; 25 mM KCl; 2 mM EGTA; and 2 mM EDTA for 10 min at room temperature. Cells were incubated with 3% Bovine serum albumin (Sigma) in PBS before incubation with primary antibodies. Rabbit anti-ZO-1 antibody (61-7300 from Invitrogen) and rabbit anti-E-Cadherin (C212 from Santa Cruz Biotechnology) were used at a 1:400 dilution. Secondary Alexa 488 anti-rabbit (Molecular Probes, Inc., Eugene, OR) were used at a 1:400 dilution. Stained cells were mounted with Vectashield Mounting media containing DAPI (Vector Laboratories, Inc., Burlingame, CA). Stained and mounted cells were then processed with a Zeiss Axioplan epifluorescence microscope (Carl Zeiss, Thornwood, NY).
Transfection of Ishikawa cells
To generate stably transfected cells, Ishikawa cells at passage number 25, were transfected with either 0.2 μg of CMV-neo empty vector or CMV-HER2 (CMV empty vector and CMV-HER2 were generously provided by the laboratory of Dr. Bjeldanes, UC Berkeley, CA, USA), using polyfact (Qiagen, CA) and following the manufacturer's suggested protocol. Cells were fed 24 h after transfection with DMEM, supplemented with 10% fetal calf serum, penicillin/streptomycin. The media was replaced with same media containing 0.7 mg/ml G418 (neomycin analog, Mediatech, Herndon, VA) to select for transfected cells. Selection media was replaced every 24 hours for a month and surviving cell populations were propagated in selection media. Experimental treatments were not performed in selection media.
Subcellular Fractionation
The nuclear and nonnuclear subcellular fractions were harvested from cell extracts using the NE-PER Nuclear Cytoplasmic Extraction Reagents (Pierce, Rockford, IL) according to the manufacturer's instruction. The total protein was quantified using Bradford reagents (BioRad). Cell fractions were examined by Western blots as described above. Anti-lamin was used as a marker for nuclear fraction.
Results
Effects of Arecoline on expression of the ZO-1 tight junction protein and the HER2 tyrosine kinase receptor
Arecoline has been detected in saliva obtained during betel nut chewing in concentrations up to 140 μg/ml, corresponding to 0.9 mM. Arecoline in the millimolar concentration range is thought to participate in the initiation and/or progression of cellular changes during the long-term effects of betel nut chewing [25]. Therefore, to examine the potential effects of arecoline on expression of the ZO-1 tight junction protein and HER2 member of the EGF receptor gene family, cultured human Ishikawas endometrial cancer cells were treated with concentrations of arecoline ranging between 0.1 mM and 0.5 mM and the production of ZO-1 and HER2 protein determined by western blot analysis. The Ishikawa cells were treated for 24 and 48 hr with each arecoline concentration and compared to a DMSO vehicle treated control (0 mM arecoline). As shown in Figure 1A, arecoline treatment down-regulated production of both ZO-1 and HER2 protein that was observed within 24 hours of treatment at 0.3 mM arecoline. Under the conditions of this experiment, there were no observed changes in actin production, which also serves as a gel loading control. In most of our study, we employed 0.3 mM arecoline, which induces the maximum effect on ZO-1 and HER2 expression without causing apoptosis.
Figure 1
Figure 1
Effects of arecoline on expression of ZO-1 and HER2 protein in Ishikawa cells. (A) Subconfluent cultures of Ishikawa cells were treated with DMSO (vehicle control), 0.1 mM, 0.3 mM or 0.5 mM arecoline for 24 and 48 hrs, and total cell extracts were fractionated in SDS polyacrylamide gels. The arecoline regulation of ZO-1 and HER2 protein production was determined by western blot analysis and compared to the levels of actin protein; (B) To determine if the arecoline mediated downregulation of ZO-1 and HER2 protein was due to induced ubiquitination and 26 S proteasome mediated degradation, Ishikawa cells were treated with or without 0.3 mM arecoline for 48 hrs and in the presence or absence of MG132, an inhibitor of proteasome peptidase enzymatic activity. Total cell extracts were analyzed by Western blotting for ZO-1 and HER2 in comparison to actin.
To determine if the arecoline-induced loss of HER2 and ZO-1 protein was due to ubiquitin-26 S proteasome mediated degradation, Ishikawa cells were treated with or without 0.3 mM arecoline for 24 hr and 48 hr in the presence or absence of MG132, an inhibitor of proteasome peptidase enzymatic activity. As shown in Figure 1B, western blot analysis indicated that the downregulation of both ZO-1 and HER2 protein strongly occurs in the presence of MG132, suggesting that the loss of both proteins are not due to proteasomal degradation.
Arecoline Downregulates ZO-1 and HER 2 Transcript Levels in Ishikawa endometrial cancer cells
To uncover the cellular processes regulated by arecoline that leads to the down-regulation of ZO-1 and HER2 protein levels, Ishikawa cells were cultured in the presence of varying concentrations of arecoline for 48 hours, and the levels of HER2 and ZO-1 transcripts were compared with DMSO vehicle treated control cells. As shown in Figure 2, reverse transcription-PCR analysis revealed that arecoline treatment downregulates expression of HER2 and ZO-1 transcripts after 48 hours in a dose dependent manner. Maximum effects were observed after the cells were treated with 0.5 mM arecoline for 48 hr, although signaificant effects were observed in the presence of 0.3 mM arecoline. GAPDH transcript levels remained unchanged and were used as gel loading controls. The arecoline mediated loss of ZO-1 and HER2 transcripts accounts for the down-regulation of the corresponding protein levels.
Figure 2
Figure 2
Arecoline downregulates of ZO-1 and HER2 transcripts in Ishikawa cells. Ishikawa cells were treated with the DMSO vehicle control, 0.1 mM, 0.3 mM or 0.5 mM arecoline for 48 hrs and total RNA was isolated and quantified by RT-PCR analysis. Oligonucleotides specific for ZO-1, HER2 or GAPDH were used to generate specific RT-PCR fragments that were fractionated in agarose gels. The transcript specific bands were visualized by ethidium bromide staining.
Effects of Arecoline on expression of Tight Junction and Adherens Junction proteins
Both tight junctions and adherens junction are comprised of distinct protein complexes [15], and therefore the potential effects of arecoline were assessed on expression of several tight junction and adherens junction proteins. Ishikawa cells were treated with or without 0.3 mM and 0.5 mM arecoline for 48 hours, and the level of the ZO-1 and Claudin-1 tight junction proteins and the E-cadherin and beta-catenin adherens junction proteins were analyzed by western blots. Actin proteins levels were used as a constitutive control protein for comparison to the apical junction proteins. As shown in Figure 3, under conditions in which arecoline strongly down-regulated ZO-1 protein levels, this alkaloid also down-regulated the Claudin-1 protein, which is also a component of the tight junction. Arecoline had no significant effects on the protein levels of either E-cadherin or beta-catenin, which are both critical components of adherens junctions. Thus, expression of tight junction proteins appears to be significantly more sensitive to the disruptive effects of arecoline compared to adherens junction proteins.
Figure 3
Figure 3
Arecoline effects on expression of tight junction and adherens junction proteins in Ishikawa cells. Ishikawa cells were treated with DMSO (vehicle control) or with either 0.3 mM or 0.5 mM arecoline for 48 hrs, and total cell extracts were fractionated in SDS polyacrylamide gels. The production of ZO-1, Claudin-1, E-cadherin, and beta-catenin protein was determined by western blot analysis and compared to the levels of actin protein.
Arecoline disruption of the localization of ZO-1 protein
In the apical junction, ZO-1 characteristically forms a continuous band at the periphery of well-differentiated, confluent, polarized epithelial cells. The localization of ZO-1 changes dramatically according to the confluency of cells, with low confluent cells having an accumulation of nuclear ZO-1 localization and high confluent cells having ZO-1 locate at the plasma membrane. Nuclear localization of ZO-1 has also been detected in many cell types [26]. Indirect immunofluorescence was utilized to assess the potential effects of arecoline on ZO-1 localization in Ishikawa cells treated with various concentrations of arecoline for 24 hours and 48 hours. As shown in Figure 4, arecoline treatment disrupted the characteristically continuous bands of ZO-1 staining around the apices of Ishikawa cells. Treatment with 0.3 mM arecoline induced a near maximal effect on ZO-1 localization at both 24 hours and 48 hours of incubation. The overall ZO-1 staining pattern in arecoline treated cells was highly disorganized, which is indicative of a disruption of the apical junctional complex.
Figure 4
Figure 4
Immunofluorescence analysis of the arecoline disruption of ZO-1 protein localization. Ishikawa cells were treated with the DMSO vehicle control, 0.1 mM, 0.3 mM, or 0.5 mM arecoline for 24 and 48 hrs. Cells were fixed in 3.7% formaldehyde and stained for localization of ZO-1 by indirect immunofluorescence and for nuclear DNA by DAPI staining. Bars = 20 μm.
The effect of arecoline on the ZO-1 cellular staining pattern was examined in the context of the cellular staining pattern of the adherens junction protein E-cadherin. Ishikawa cells were treated with or without 0.3 mM and 0.5 mM arecoline for 48 hours and the E-cadherin staining pattern analyzed by indirect immunofluorescence. As shown in figure 5, at the lower arecoline concentration of 0.3 mM, the overall E-cadherin staining pattern remained mostly intact and highly organized to the cell periphery. At this alkaloid concentration, the ZO-1 staining pattern was mostly disorganized (shown in Figure 4). At the higher arecoline concentration (0.5 mM), E-cadherin shows a generally similar degree of disorganization as that observed for ZO-1 (Figure 5 compared to Figure 4).
Figure 5
Figure 5
Immunofluorescence analyiss of arecoline effects on the cellular staining pattern of E-cadherin. Ishikawa cells were treated with the DMSO vehicle control or with either 0.3 mM, or 0.5 mM arecoline for 48 hrs. Cells were fixed in 3.7% formaldehyde and stained for localization of E-cadherin by indirect immunofluorescence and for nuclear DNA by DAPI staining. Bars = 20 μm.
To further characterize the effects of arecoline on the subcellular distribution of ZO-1, the nuclear and cytoplasmic/membrane fractions were biochemically separated after treatment of Ishikawa cells for 48 hr with 0 mM (vehicle treated control), 0.1 mM, 0.3 mM or 0.5 mM arecoline. ZO-1 exists as two isoforms depending upon the presence or absence of an 80 amino acid N-terminal domain denoted as ZO-1 α+ and ZO-1 α- [15]. The proportion of each isoform is characteristic of particular cell types [15]. As shown in Figure 6, the nuclear fraction of Ishikawa cells was found to contain only ZO-1 α+ whereas, the cytoplasmic/membrane fraction contains both ZO-1 α+ and ZO-1 α-. Arecoline treatment down-regulated the expression of both isoforms from the nuclear as well as cytoplasmic/membrane subcellular fractions compared to the DMSO vehicle treated control cells (0 mM arecoline). HER2 can be imported into the nucleus of certain cell types through a nuclear localization signal mediated mechanism [27]. Our results also revealed that HER2 is localized in both the cytomplasmic/membrane and the nuclear fractions of the Ishikawa cells, and the treatment with arecoline down-regulates HER2 protein levels from both subcellular fractions (Figure 6).
Figure 6
Figure 6
Arecoline down regulates the level of ZO-1 and HER2 proteins in both the Cytoplasmic/membrane as well as nuclear fractions of Ishikawa cells. The Ishikawa cells were treated with the DMSO vehicle control, 0.1 mM, 0.3 mM, or 0.5 mM arecoline for 48 hours. The nuclear and cytoplasmic/memebrane fraction was separated biochemically by differential centrifugation, and distribution of ZO-1 and HER2 was evaluated by western blot analysis in comparison to the lamin nuclear marker protein.
Expression of exogenous HER2 prevents the arecoline down-regulation of ZO-1 and overrides the disruption of ZO-1 localizalization in Ishikawa cells
To functionally test the link between the arecoline down-regulated expression of ZO-1 and HER2, Ishikawa cells were transfected with the CMV-HER2 expression plasmid or with the control CMV-neo empty vector plasmids. The transfection competent cells were stably selected for 30 days in G418. Western blot analysis revealed that CMV-HER2 transfected cells expressed significantly higher levels of HER2 protein compared to the control transfected cells (Figure 7A). Both the CMV-HER2 transfected and the CMV-neo transfected Ishikawa cells were treated with 0.3 mM arecoline for 48 hours, and the production of ZO-1 protein was examine by western blot analysis. As shown in figure 7B, expression of exogenous HER2 ablated the arecoline down-regulation of ZO-1 protein, which demonstrates a strong functional connection between the level of HER2 protein and ability of arecoline to attenuate ZO-1 expression.
Figure 7
Figure 7
Expression of exogenous HER2 prevents the arecolin down-regulation of ZO-1 expression in Ishikawa cells. (A) Ishikawa cells were stably transfected with either the CMV-HER2 expression plasmid or the CMV-neo empty vector control plasmids and transfection competent cells selected in media containing G418. Western blotting shows that the in CMV-HER2 transfected cells, HER2 protein levels are over-expressed compared to cells transfected with the CMV-neo empty vector. (B) CMV-HER2 transfected and CMV-neo transfected cells were treated with or without 0.3 mM arecoline for 48 hrs and the level of ZO-1 protein was determined by western blotting. The level of actin protein was used as a gel loading control.
Indirect immunofluorescence was employed to examine the potential effects of exogenous HER2 expression on the arecoline disruption of ZO-1 localization. As shown in Figure 8, in CMV-HER2 transfected Ishikawa cells, expression of exogenous HER2 completely prevented the arecoline-mediated disruption of ZO-1 localization to the cell periphery. The ZO-1 staining pattern in CMV-HER2 cells treated with arecoline for 24 hours or 48 hours was virtually identical to DMSO vehicle treated control cells (Figure 8, upper panels). As expected, in the CMV-neo control transfected cells, arecoline treatment induced a significant disruption of ZO-1 localization (Figure 8, lower panels), with the staining pattern indicative of a disorganized junctional complex. It is important to point that the ZO-1 staining pattern in arecoline treated and untreated CMV-neo transfected cells is essentially the same as that observed in untransfected cells (Figure 4) showing that the transfection per se had no unusual effect on the cell phenotype.
Figure 8
Figure 8
Expression of exogenous HER2 prevents the arecoline disruption of ZO-1 protein localization in Ishikawa cells. The CMV-HER2 and CMV-neo empty vector transfected Ishikawa cells were treated with the DMSO vehicle control or with 0.3 mM Arecoline for 24 hours and 48 hours. Cells were fixed in 3.5% formaldehyde and stained for the localization of ZO-1 by indirect immunofluorescence or for nuclear DNA by DAPI staining. Bars = 20 μm.
Dexamethasone treatment overrides the arecoline disruption of ZO-1 localization in Ishikawa cells
It has been previously shown that treatment with the synthetic glucocorticoid dexamethasone strongly stimulates expression of HER2 in Ishikawa endometrial cancer cells and in human epithelial ovarian carcinoma cell lines [24]. Our previous study demonstrated that dexamethasone induces tight junctional complex formation in the rat Con8 mammary epithelial tumor cell line [28]. Together, these observations suggest that dexamethasone treatment may provide a hormonal tool to functionally assess the arecoline effects on the dynamics of ZO-1 localization. Ishikawa cells were treated with or without 1 μM dexamethasone or 10 μM dexamethasone and apical junction localization of ZO-1 was visualized using indirect immunofluorescence. As shown in Figure 9, ZO-1 staining revealed that in dexamethasone treated cells, the apical junction complex was somewhat more organized compared to the DMSO treated cells. In presence of 1 μM dexamethasone, the disruptive effects of 0.3 mM arecoline on ZO-1 localization were partially restored (Figure 9). At 10 μM dexamethasone, the disruptive effects of 0.3 mM arecoline was completely ablated as the ZO-1 staining pattern in cells treated with dexamethasone and arecoline was quite similar to that observed in the DMSO vehicle treated control cells (Figure 9, top versus bottom panels).
Figure 9
Figure 9
Treatment with dexamethasone overrides the arecoline disruption of ZO-1 protein localization in Ishikawa cells. Ishikawa cells were incubated with or without 1 μM or 10 μM of dexamethasone in the presence or absence of 0.3 mM Arecoline. Cells were fixed in 3.5% formaldehyde and stained for the localization of ZO-1 by indirect immunofluorescence or for nuclear DNA by DAPI staining. Bars = 20 μm.
Discussion
We have established that arecoline has profound effects on plasma membrane associated signaling proteins in the human endometrial Ishikawa cell line. Arecoline was shown to coordinately down regulate the expression and disrupt localization of the ZO-1 tight junction component of the apical junction complex as well as decrease expression of the HER2 member of the epidermal growth factor receptor gene family. Our studies have uncovered a functional link between the arecoline down regulation of ZO-1 and HER2 because expression of exogenous HER2 completely prevents the ability of arecoline to disrupt ZO-1 expression and localization to the cell periphery. Furthermore, treatment with dexamethasone, a synthetic glucocorticoid that has been shown to upregulate HER2 expression in Ishikawa endometrial cancer cells [24], also overrides the disruptive effects of arecoline on ZO-1 localization. A functional connection between HER2 levels and the control of ZO-1 localization or expression has not been previously observed in human cancer cells.
HER2 plays an important role in the regulation of cell growth, differentiation and survival through its heterodimerization with other members of the EGF receptor gene family [29]. A variety of cell and tissue types expresses HER2 [29], and a number of human cancers frequently over-express HER2 due to gene amplification including many reproductive cancers [21, 3033] as well as lung, gastric and oral cancers [3439]. Patients with HER2-overexpressing breast or ovarian cancer have significantly shorter overall survival rate and time of relapse relative to patients with tumors without HER2 overexpression [21, 30, 31]. Because of HER2 overexpression in many cancers, its accessible location on the cell surface and its role in carcinogenesis HER2 has been under intensive scrutiny as a therapeutic target. HER2 is expressed at low levels in normal tissue compared to cancer cells [40], which suggests the existence of a suitable therapeutic window to minimize damage to normal cells but still be able to target HER2-positive cancers by inhibiting either HER2 protein function or expression [41].
Studies examining ZO-1 protein stability have uncovered a range of ZO-1 protein half lives (ranging between 5 and 20 hours) that can differ depending on the cell type and cell cultured conditions such as cell confluency [42, 43]. Although in many systems, regulated changes in the stability of ZO-1 protein can potentially play a role in its cellular regulation, we have shown that in Ishikawa endometrial cancer cells, the loss of ZO-1 protein is accounted for an a corresponding loss in ZO-1 transcript levels. We have also determined that arecoline concurrently reduces HER2 protein and transcript expression along with that of ZO-1 expression, and that ectopic expression of HER2 reverses the arecoline down regulation of ZO-1. We are currently attempting to establish the precise mechanism by which the arecoline-mediated loss of HER2 levels leads to these effects on ZO-1 utilization. In this regard, is thought that over-expression of HER2 in human cancer cells due to amplification enhances the preferential binding of the low-affinity arm of ligands to HER2 resulting in increased intracellular signaling [44] that could ultimately lead to the control of ZO-1 and potential regulation of ZO-1 mediated cell-cell interactions. Interestingly, a transcriptional factor that binds to the SH3 domain of ZO-1 (ZONAB, ZO-1-associated nucleic acid binding protein) was shown in MDCK cells to functionally interact with the nuclear form of ZO-1 to modulate expression of HER2 in a cell density dependent manner [45]. This study, in combination with our results, suggests that the expression and cellular use of ZO-1 and HER2 may be linked thorough a mutual feedback system in certain human cancer cells. Because dexamethasone, a synthetic glucocorticoid, regulates the transcription of glucocorticoid receptor target genes and overrides the effects of arecoline on ZO-1 localization, it is tempting to speculate that this steroid hormone alters the transcriptional dynamics of HER2 in this system and thereby stabilizes ZO-1 expression and localization.
Conclusion
Arecoline induced cellular changes in the oral cavity in areca nut chewers leading to oral precancerous lesions may be due to disrupted expression and junctional localization of the ZO-1 tight junctional protein. Furthermore, we have established that the ability of arecoline to control ZO-1 in human Ishikawa cancer cells requires the coordinate down regulation of the HER2 member of the EGF receptor gene family. This observation represents a previously unknown functional connection between HER2 expression and the cellular accessibility of ZO-1. Thus, the physiological control of HER2 expression in human tissues may play a direct role in the susceptibility of humans to the carcinogenic effects of arecoline.
Declarations
Acknowledgements
The research described in this paper was supported by National Institute of Health Grant DK-42799 (to G.L.F.) and by Indo-US Science and Technology Forum Fellowship by Department of Science and Technology, Government of India, awarded to S. G. (Ref:IUSSTF/Fellowship/2007-08/8-2008). We are thankful to Dr. Crystal Marconett and Dr. Ida Aronchik for helpful discussion. Technical support of Bhumika Kapadia and Kelvin Tran in the Firestone Lab during the course of study is thankfully acknowledged.
Authors’ Affiliations
(1)
Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA
(2)
Department of Life Science, Assam University, Silchar, Assam, 788011, India
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Transplant Direct ; 8(1): e1268, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1583924
ABSTRACT
BACKGROUND: Few reports have focused on newer coronavirus disease 2019 (COVID-19) therapies (remdesivir, dexamethasone, and convalescent plasma) in solid organ transplant recipients; concerns had been raised regarding possible adverse impact on allograft function or secondary infections. METHODS: We studied 77 solid organ transplant inpatients with COVID-19 during 2 therapeutic eras (Era 1: March-May 2020, 21 patients; and Era 2: June-November 2020, 56 patients) and 52 solid organ transplant outpatients. RESULTS: In Era 1, no patients received remdesivir or dexamethasone, and 4 of 21 (19.4%) received convalescent plasma, whereas in Era 2, remdesivir (24/56, 42.9%), dexamethasone (24/56, 42.9%), and convalescent plasma (40/56, 71.4%) were commonly used. Mortality was low across both eras, 4 of 77 (5.6%), and rejection occurred in only 2 of 77 (2.8%) inpatients; infections were similar in hypoxemic patients with or without dexamethasone. Preexisting graft dysfunction was associated with greater need for hospitalization, higher severity score, and lower survival. Acute kidney injury was present in 37.3% of inpatients; renal function improved more rapidly in patients who received remdesivir and convalescent plasma. Post-COVID-19 renal and liver function were comparable between eras, out to 90 d. CONCLUSIONS: Newer COVID-19 therapies did not appear to have a deleterious effect on allograft function, and infectious complications were comparable.
2.
Clin Infect Dis ; 73(11): e4090-e4099, 2021 12 06.
Article in English | MEDLINE | ID: covidwho-1561046
ABSTRACT
BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has led to significant reductions in transplantation, motivated in part by concerns of disproportionately more severe disease among solid organ transplant (SOT) recipients. However, clinical features, outcomes, and predictors of mortality in SOT recipients are not well described. METHODS: We performed a multicenter cohort study of SOT recipients with laboratory-confirmed COVID-19. Data were collected using standardized intake and 28-day follow-up electronic case report forms. Multivariable logistic regression was used to identify risk factors for the primary endpoint, 28-day mortality, among hospitalized patients. RESULTS: Four hundred eighty-two SOT recipients from >50 transplant centers were included: 318 (66%) kidney or kidney/pancreas, 73 (15.1%) liver, 57 (11.8%) heart, and 30 (6.2%) lung. Median age was 58 (interquartile range [IQR] 46-57), median time post-transplant was 5 years (IQR 2-10), 61% were male, and 92% had ≥1 underlying comorbidity. Among those hospitalized (376 [78%]), 117 (31%) required mechanical ventilation, and 77 (20.5%) died by 28 days after diagnosis. Specific underlying comorbidities (age >65 [adjusted odds ratio [aOR] 3.0, 95% confidence interval [CI] 1.7-5.5, Pâ
<â
.001], congestive heart failure [aOR 3.2, 95% CI 1.4-7.0, Pâ
=â
.004], chronic lung disease [aOR 2.5, 95% CI 1.2-5.2, Pâ
=â
.018], obesity [aOR 1.9, 95% CI 1.0-3.4, Pâ
=â
.039]) and presenting findings (lymphopenia [aOR 1.9, 95% CI 1.1-3.5, Pâ
=â
.033], abnormal chest imaging [aOR 2.9, 95% CI 1.1-7.5, Pâ
=â
.027]) were independently associated with mortality. Multiple measures of immunosuppression intensity were not associated with mortality. CONCLUSIONS: Mortality among SOT recipients hospitalized for COVID-19 was 20.5%. Age and underlying comorbidities rather than immunosuppression intensity-related measures were major drivers of mortality.
Subject(s)
COVID-19 , Organ Transplantation , Cohort Studies , Humans , Male , Middle Aged , Organ Transplantation/adverse effects , SARS-CoV-2 , Transplant Recipients
3.
Transplantation ; 105(9): 2072-2079, 2021 09 01.
Article in English | MEDLINE | ID: covidwho-1254952
ABSTRACT
BACKGROUND: The impacts of COVID-19 on lung allograft function, rejection, secondary infection, and clinical outcomes in lung transplant recipients (LTRs) remain unknown. METHODS: A 1:2 matched case-control study was performed to evaluate rehospitalization, lung allograft function, and secondary infections up to 90 d after COVID-19 diagnosis (or index dates for controls). RESULTS: Twenty-four LTRs with COVID-19 (cases) and 48 controls were identified. Cases and controls had similar baseline characteristics and lung allograft function. LTRs with COVID-19 had higher incidence of secondary bacterial infection (29.2% versus 6.3%, P = 0.008), readmission (29.2% versus 10.4%, P = 0.04), and for-cause bronchoscopy (33.3% versus 12.5%, P = 0.04) compared with controls. At d 90, mortality in cases versus controls was 8.3% versus 2.1% (P = 0.21), incidence of invasive fungal infections in cases versus controls was 20.8% versus 8.3% (P = 0.13) and forced expiratory volume in 1 s (FEV1) decline ≥10% from baseline occurred in 19% of cases versus 12.2% of controls (P = 0.46). No acute cellular rejection, acute antibody-mediated rejection, or new donor-specific anti-HLA antibodies were observed among cases or controls within 90 d post index date. CONCLUSIONS: We found LTRs with COVID-19 were at risk to develop secondary infections and rehospitalization post COVID-19, compared with controls. While we did not observe post viral acute cellular rejection or antibody-mediated rejection, further studies are needed to understand if LTRs with COVID-19 who did not recover baseline lung function within 90 d have developed chronic lung allograft dysfunction stage progression.
Subject(s)
COVID-19/epidemiology , Graft Rejection/epidemiology , Lung Diseases/surgery , Transplant Recipients , Adult , Aged , Allografts , Comorbidity , DNA, Viral/analysis , Female , Follow-Up Studies , Humans , Incidence , Lung Diseases/epidemiology , Lung Transplantation , Male , Middle Aged , Pandemics , Retrospective Studies , Risk Factors , SARS-CoV-2/genetics , United States/epidemiology
5.
Am J Transplant ; 21(7): 2498-2508, 2021 07.
Article in English | MEDLINE | ID: covidwho-960766
ABSTRACT
Immunosuppression and comorbidities might place solid organ transplant (SOT) recipients at higher risk from COVID-19, as suggested by recent case series. We compared 45 SOT vs. 2427 non-SOT patients who were admitted with COVID-19 to our health-care system (March 1, 2020 - August 21, 2020), evaluating hospital length-of-stay and inpatient mortality using competing-risks regression. We compared trajectories of WHO COVID-19 severity scale using mixed-effects ordinal logistic regression, adjusting for severity score at admission. SOT and non-SOT patients had comparable age, sex, and race, but SOT recipients were more likely to have diabetes (60% vs. 34%, p < .001), hypertension (69% vs. 44%, p = .001), HIV (7% vs. 1.4%, p = .024), and peripheral vascular disorders (19% vs. 8%, p = .018). There were no statistically significant differences between SOT and non-SOT in maximum illness severity score (p = .13), length-of-stay (sHR: 0.9 1.11.4 , p = .5), or mortality (sHR: 0.1 0.41.6 , p = .19), although the severity score on admission was slightly lower for SOT (median [IQR] 3 [3, 4]) than for non-SOT (median [IQR] 4 [3-4]) (p = .042) Despite a higher risk profile, SOT recipients had a faster decline in disease severity over time (OR = 0.76 0.810.86 , p < .001) compared with non-SOT patients. These findings have implications for transplant decision-making during the COVID-19 pandemic, and insights about the impact of SARS-CoV-2 on immunosuppressed patients.
Subject(s)
COVID-19 , Organ Transplantation , Humans , Inpatients , Organ Transplantation/adverse effects , Pandemics , Retrospective Studies , SARS-CoV-2 , Transplant Recipients
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-3,973,277,517,745,896,400 | Have questions? Visit https://www.reddit.com/r/SNPedia
rs4341770
From SNPedia
Orientationplus
Stabilizedplus
Geno Mag Summary
(A;A) 0 common in clinvar
Make rs4341770(A;G)
Make rs4341770(G;G)
ReferenceGRCh38 38.1/141
Chromosome16
Position16182880
GeneABCC6
is asnp
is mentioned by
dbSNPrs4341770
ebirs4341770
HLIrs4341770
Exacrs4341770
Varsomers4341770
Maprs4341770
PheGenIrs4341770
hapmaprs4341770
1000 genomesrs4341770
hgdprs4341770
ensemblrs4341770
gopubmedrs4341770
geneviewrs4341770
scholarrs4341770
googlers4341770
pharmgkbrs4341770
gwascentralrs4341770
openSNPrs4341770
23andMers4341770
23andMe allrs4341770
SNP Nexus
SNPshotrs4341770
SNPdbers4341770
MSV3drs4341770
GWAS Ctlgrs4341770
Max Magnitude0
? (A;A) (A;G) (G;G) 28
ClinVar
Risk rs4341770(G;G)
Alt rs4341770(G;G)
Reference Rs4341770(A;A)
Significance Untested
Disease
Variation info
Gene ABCC6
CLNDBN
Reversed 0
HGVS NC_000016.9:g.16276737A>G
CLNSRC
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Understanding the science of pain
This is an excerpt from Sports Massage for Injury Care by Robert McAtee.
An explosion of research on pain in recent years has led to new insights into, as well as great confusion about, the origins of pain, the connections between injury and pain, and the psychological and social contributions to the perception of pain. This broadened knowledge of the complexity of pain has also affected the way manual therapy practitioners approach their work with clients.
By contrast, as the understanding of the mechanisms of pain perception and pain generation has progressed, many researchers and practitioners have reframed the discussion of pain in relation to injury by emphasizing that pain is a complex experience, involving many parts of the brain, and that pain perception is influenced by psychosocial factors that include previous pain experiences, thoughts and feelings about previous pain experiences, emotional states, and even personal relationships. These elements of the pain experience have been recognized for years but have been downplayed in favor of a pathomechanical model of pain that described the stimulation of pain receptors in the tissue when an injury or insult occurred there. These receptors would then stimulate the pain region of the brain, and pain would be felt. It now appears that pain receptors do not exist, but nociceptive receptors do and are stimulated by a variety of noxious stimuli, including pressure, temperature, and inflammatory markers. These receptors send signals to the brain via the spinal cord, and the brain evaluates the signal and determines whether the input is pain or not, and then outputs either the sensation of pain or something else, such as an increase in pressure or a feeling of additional warmth. What this means in practical terms for practitioners is that pain intensity does not necessarily correlate with tissue damage. Minor injuries can feel extremely painful, and severe injuries may occur with very little pain. This response is modulated by the brain and is dependent on all the biopsychosocial factors influencing the brain's final output.
In chronic pain conditions, a neural pathway can become sensitized by repeated nociceptive stimulation so that even minor noxious input can trigger output from the brain that causes the patient to feel pain. On the other hand, this does not mean that pain intensity never correlates directly with the amount of tissue damage, and it's critical for practitioners and patients to stay mindful of this fact.
Growing evidence indicates that incorporating pain neuroscience education (PNE) with manual treatment is efficacious for reducing chronic pain. The intent of PNE is to help shift the client's focus away from “my tissues are painful, so they must be injured” to realizing that the brain's perception and interpretation of stimuli emanating from the tissues may not always accurately reflect the degree of tissue damage. Encouraging a client to shift their focus away from the idea that their pain is caused by specific tissue damage has been shown to reduce chronic pain and, more importantly, to reduce pain catastrophization (magnifying the pain and feeling helpless in the presence of pain).
As practitioners and patients read and hear more about the new pain science, they may make the incorrect assumption that the oversimplified phrase “pain is in the brain” means that pain is all in your head. It's incumbent on the professionals to reassure patients that they're not making it all up (as has been the unfortunate experience of many patients). As Whitney Lowe, massage educator and author, has written,
I think one of the biggest obstacles and challenges for those who are carrying the torch of the emerging pain science specialty is to understand how to introduce these ideas to those for whom this view is new. Too often I have seen and heard pain science enthusiasts speak to others with condescension and arrogance. As a teacher I clearly recognize how that produces an immediate degree of defensiveness in a student and that is a significant obstacle to learning. (Lowe 2017, p. 1)
Because knowledge about pain perception continues to emerge and evolve, the other clear message for practitioners and patients is that our prior knowledge and experience about pain and treating patients in pain is not suddenly obsolete or ineffective. “It isn't necessary to throw out all of the valuable learning and clinical experience we have already built upon. But maybe we look at these things through a different set of glasses” (Lowe 2017, p. 1). It is incumbent on sports massage practitioners to discuss with clients the current research about pain and how those research findings will affect the treatment strategies proposed in their particular case. | {
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7,102,029,262,275,787,000 | Characterization of the follicular dendritic cell reservoir of human immunodeficiency virus type 1
Brandon F. Keele, Loubna Rothenburg, Suzanne Gartner, Yiling Liu, Trever B. Burgon, Jacob D. Estes, Tyler C. Thacker, Keith A. Crandall, Justin C. McArthur, Gregory F. Burton
Research output: Contribution to journalArticlepeer-review
104 Scopus citations
Abstract
Throughout the natural course of human immunodeficiency virus (HIV) infection, follicular dendritic cells (FDCs) trap and retain large quantities of particle-associated HIV RNA in the follicles of secondary lymphoid tissue. We have previously found that murine FDCs in vivo could maintain trapped virus particles in an infectious state for at least 9 months. Here we sought to determine whether human FDCs serve as an HIV reservoir, based on the criteria that virus therein must be replication competent, genetically diverse, and archival in nature. We tested our hypothesis using postmortem cells and tissues obtained from three HIV-infected subjects and antemortem blood samples obtained from one of these subjects. Replication competence was determined using coculture, while genetic diversity and the archival nature of virus were established using phylogenetic and population genetics methods. We found that FDC-trapped virus was replication competent and demonstrated greater genetic diversity than that of virus found in most other tissues and cells. Antiretrovirus-resistant variants that were not present elsewhere were also detected on FDCs. Furthermore, genetic similarity was observed between FDC-trapped HIV and viral species recovered from peripheral blood mononuclear cells obtained 21 and 22 months antemortem, but was not present in samples obtained 4 and 18 months prior to the patient's death, indicating that FDCs can archive HIV. These data indicate that FDCs represent a significant reservoir of infectious and diverse HIV, thereby providing a mechanism for viral persistence for months to years.
Original languageEnglish (US)
Pages (from-to)5548-5561
Number of pages14
JournalJournal of Virology
Volume82
Issue number11
DOIs
StatePublished - Jun 1 2008
Externally publishedYes
ASJC Scopus subject areas
• Immunology
Fingerprint Dive into the research topics of 'Characterization of the follicular dendritic cell reservoir of human immunodeficiency virus type 1'. Together they form a unique fingerprint.
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-1,187,062,842,580,812,300 | Decorative image
Other causes of sickness
There are things other than cancer or cancer treatment that can make you feel sick.
Smell
Both pleasant and unpleasant smells can trigger sickness. You might find that it helps to remove strong smelling flowers from around you. Or, you could ask friends and relatives not to wear perfume.
Try eating cold foods if the smell of food makes you feel sick. Or get someone else to cook for you if you can.
Taste
The taste of some foods and drinks may make you feel or be sick. Strong tastes may be troublesome. You might find it helps to stick to bland foods. Your taste could be affected if sickness is related to your treatment. This usually gets better after treatment has finished.
Some people avoid their favourite foods and drinks during treatment periods in case they are put off them for good. Other people find that they start to like foods they have always disliked.
Anxiety, fear and depression
These feelings are very common in people with cancer. Up to 1 in 4 people (up to 25%) with cancer become depressed.
Feeling very frightened, anxious or depressed can affect the way your body works and may make you feel or be sick. Discuss your feelings with your doctor or specialist nurse as they can help you with your anxiety or depression.
Pain
Being in a lot of pain can also make you feel or be sick. The sickness will go away when you treat the pain.
Movement or travel
Motion sickness (travel sickness) happens when the messages your brain receives from your eyes do not match those from the balance centre in your ear.
This confusion can trigger the vomiting centre in your brain and make you feel or be sick. It often helps to face forward in the vehicle and look out of the window at a fixed point on the horizon.
You can get drugs to prevent motion sickness on prescription from your GP and over the counter from the chemist.
Some of these drugs can cause drowsiness, so check this with your doctor first.
Infections and food poisoning
An infection can make you feel or be sick. The sickness will usually stop when the infection is treated.
Infections picked up from food (food poisoning) usually last between 24 and 48 hours (1 to 2 full days). It is important to see your doctor if your sickness lasts for longer.
You must contact your hospital treatment team straight away if you are having chemotherapy treatment and your white blood cell count is low and you have signs of infection such as a high temperature or are feeling unwell.
Hunger
Many of us have had that feeling of being so hungry you feel sick. Try to avoid this by eating small meals at regular times and by drinking 6 to 8 glasses of water each day.
Bowel problems
Both constipation and diarrhoea can make you feel or be sick. Treating the cause will reduce the sickness.
Sickness before treatment
Sickness, before you have treatment, is called anticipatory nausea and vomiting. It happens because you have bad memories of chemotherapy sickness in the past. You could be so worried about this that just thinking about treatment makes you sick. Some people are sick as they get to the hospital or when the nurse starts to set up the drip.
Your doctor or nurse can give you anti sickness tablets or anti anxiety drugs such as lorazepam. You take them before you go to the hospital on treatment days if this is a problem for you.
Last reviewed:
05 Jan 2018
• Cancer and its management (7th edition)
J Tobias and D Hochhauser
Wiley-Blackwell, 2015
• Cancer: Principles and practice of oncology (10th edition)
VT DeVita, S Hellman, SA Rosenberg and TS Lawrence
Lipincott Williams and Wilkins, 2015
• Prevalence of depression, anxiety, and adjustment disorder in oncological, haematological, and palliative-care settings: a meta-analysis of 94 interview-based studies.
AJ Mitchell and others
The Lancet Oncology, 2011
Volume 12, Issue 2
• Symptom management in advanced cancer (4th edition)
R Twycross, A Wilcock and S Toller
Radcliffe Medical Press Ltd, 2009
Information and help
Dangoor sponsorship
About Cancer generously supported by Dangoor Education since 2010. | {
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9,201,074,009,203,877,000 | Intrapulmonary lipoma
Intrapulmonary lipomas are rare fat containing benign lung lesions.
They mostly occur in the adult population, with occurence in the paediatric population is extremely rare.
As with all lipomas they are composed of adipose tissue. The origin of the peripheral intrapulmonary lipomas is considered controversial. Some suggest that fatty tissue in the wall of peripheral bronchi being the origin while others claim sub-pleural fat tissue as the origin.
A peripheral intrapulmonary location is considered much more uncommon than an endobronchial location.
On cross sestion imaging, typically follows features of fat on all imaging modalities. Typically well defined and well containined.
On chest x-ray, they may be seen as a faint rounded nodular opacity, which can be variable in size.
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Article information
rID: 49212
System: Chest
Section: Pathology
Tag: cases
Synonyms or Alternate Spellings:
• Lipoma within the lung
• Intrapulmonary lipomas
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-2,405,811,555,824,602,000 | Can Stress Affect My Teeth?
Can Stress Affect My Teeth?
• Bruxism
• Susceptibility to Infection
• Poor Oral Habits
• Ways to Protect Your Teeth
Stress takes a toll on our whole body, including our teeth and gums. And sometimes, the ways we cope with stress can further aggravate the problem. Stress-induced bad habits we engage in at the office or at home can wear down and damage our teeth. Learning about this phenomenon, though, can help us find better ways of managing stress that will keep our smiles healthy and us out of the dentist’s office and in Madison, Wisconsin’s beautiful summer weather.
Bruxism
A common way people muscle through stressful times is to hold the tension in their mouths. Bruxism is the medical term for teeth grinding or jaw clenching. Although people often are unaware that they’re doing it, bruxism can result in tooth or jaw pain, headaches, sore jaws, and loose teeth. If the habit is serious, it can even cause fractured teeth.
Susceptibility to Infection
Another way stress affects our teeth is that it makes us more susceptible to infection. When we are stressed, our body’s inflammatory response kicks in. Long-term inflammation has been shown to break down tissue and inhibit the immune system. When our immune system is suppressed, the body is at risk of infection and illness.
Our mouth is particularly vulnerable to infection. Bacteria from food and plaque are a constant challenge to our oral health. Stress can make us more disposed to developing gingivitis or periodontitis, which is advanced inflammation of the gums.
Poor Oral Habits
Another way stress takes a toll on our teeth is through poor oral habits. Stress eating is a common coping mechanism. People often reach for carbohydrate-rich foods, such as potato chips or ice cream. The sugar and sticky, starchy carbs that cling to teeth can both cause tooth decay and inflamed gums.
Smoking and drinking can also cause damage to our teeth. Smoking inhibits saliva flow, allowing bacteria and plaque to grow more easily. It discolors teeth and puts the smoker at risk of oral cancer. Mixed drinks, beer, and other alcoholic beverages contain sugar and acid that can erode teeth over time.
When responsibilities and problems feel overwhelming, proper oral hygiene sometimes doesn’t seem like a top priority. Stress can cause us to want to retreat, even from taking care of ourselves. Twice-daily brushing and flossing might be dropped when the pressure is on.
Ways to Protect Your Teeth
It’s important to maintain good health habits when circumstances seem out of our control. Staying mindful of our oral health can help keep problems from piling up.
When stress flares, find your way to cope productively with it. Exercise has been shown to reduce bruxism. Your dentist can also fit you with a mouthguard to take the pressure off your teeth, especially at night.
Find healthy, teeth-friendly snacks when you feel the need to nimble through a problem. And consider whether you need to rethink your smoking or drinking habits.
Affiliated Dentists
If you suffer from bruxism and need a mouthguard and assistance on how to manage the condition, please don’t hesitate to call our office today. Affiliated Dentists offers general dentistry in Madison, Wisconsin.
Can Stress Affect My Teeth? brought to you by Dr. Mark Gustavson
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-1,597,232,588,551,714,300 | Potency drugs:Readers’ alert: drug cocktails
My cousin Doll, who is over 80, had a heart attack with angina two years ago. She bruises badly with the slightest knock or scratch and also has vertigo. Here is her prescription-drug list: moxonidine, for high blood pressure; Isotard, a nitrate drug for angina; atenolol, a beta-blocker; bendrofluazide, a diuretic; valsartan, an angiotensin-II inhibitor; aspirin, to thin the blood; nicorandil, a potassium-channel activator, for angina; atrovastatin, a lipid-lowering drug; sulphasalazine, an anti-inflammatory. – PP, Grand-Over-Sands, Cumbria
My 86 year old mother is taking: digoxin, a cardiac glycoside (or digitalis) for atrial fibrillation; an ACE inhibitor, a diuretic, a drug like Zantac for stomach acid, a paracetamol/codeine pain reliever and an NSAID for arthritis; naftidrofuryl oxalate, for poor circulation in the legs, and aspirin. Could this cocktail be aggravating her loss of memory and lack of appetite? – LL, Northampton
WDDTY replies: At a recent meeting of the European Society of Hypertension, the drug interactions for antihypertensives were highlighted (www.eshonline.org/education/esh2002/transcriptions/vanzwieten.htm). Although ACE inhibitors and diuretics can work synergistically, they can also work antagonistically and raise blood pressure.
Remember, a diuretic slows down water loss, the effect of which is to retain all the various drugs longer, and make drugs like ACE and angiotensin-II inhibitors stronger or more toxic. Diuretics can also cause low levels of potassium in the body, which will increase the toxic effects of digoxin and other cardiac glycosides, and increase cardiac arrhythmias.
Nicorandil can cause dizziness, but so can ACE inhibitors.
NSAIDS inhibit the effect of most antihypertensives, particularly diuretics, because they retain sodium and water, which will cause blood pressure to rise. All drugs that work on the central nervous system (like moxonidine) will have an effect on all other drugs in the body.
Take a brown bag of all the prescribed drugs to the doctor. Insist that he look up the drug interactions of each drug, and look up the website above. Ask if the women can be put on one or, at most, two heart drugs and work out non-drug dietary or supplement alternatives for the rest, such as Ginkgo biloba to improve circulation. For help with arthritis, see our Arthritis Manual and, for reflux, try digestive enzymes (see WDDTY vol 8 no 1).
What Doctors Don't Tell You Written by What Doctors Don't Tell You
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-4,091,959,708,905,307,000 | Although you might find sweating unappealing, it is really healthy for your body, as it allows your body to release stored fluids. (Make certain to change those fluids, nevertheless, with plenty of water.) The very best way to achieve a cleaning sweat is not by checking out a sauna however by doing aerobic workout. Sweating through aerobic workout will not just enhance your skin tone, however it will also deal with your stomach fat, stress level, and quality of sleep.
Sticking with it is necessary and if you are unable to set goals and keep them, a detox might be difficult. On the other hand, if you can a detox diet will help you significantly. Many individuals have problems because they do not realize how hard a Body Detoxcan be. When you go a water quick, juice fast or a Master Cleanse all strong foods are removed from your diet. On the natural diet, all non-organics must be eliminated along with caffeine, which is hard if you have been using caffeine for quite some time.
People use rosemary for a more subtle taste in their dishes. This herb is known for its effective cleansing capabilities. This has been a favorite of lots of since of its fresh and piney scent which makes it more attractive to use. Rosemary herbs can prevent one from having skin and lung cancer. It is extremely easy to use; just include some to your favorite veggie meals, rice or soups. You will also discover the energy that will have once you have eaten this herb. This is the reason it is frequently advised in a lot detox diet techniques.
If you decide to have a big meal, how do you feel within a couple of hours of having the meal? Do you feel full of energy or do you seem like resting? The most significant energy drain on the body is absorbing, and foods like meat can take numerous hours to digest. That’s why lions sleep for 23 hours after a kill. But we are aiming to bring on our day and wonder why we feel so exhausted. Try and consume more high water content foods. Like leafy green veggies and fruits. Your body is 70% water, your diet should be 60-70% water foods. These will add energy rather than take it away.
This herb is typically discovered in South Asia, where you discover their food spiced up with this herb. This is regularly used in curries where it provides that natural spice and color to the meal. Tumeric are excellent for liver detox and can likewise avoid the development of cancer cells. It can also restrict any carcinogens which you will find in charcoal grilled foods.
It is necessary to detoxify your body frequently to assist it operate at its best capacity. Here are some foods you can need to detox your body at homeand very quickly. Once your organs start working more efficiently, they will assist in general physical fitness of the body.
Drink Iced Water: While this recommendation might not be all that fantastic for your throat, drinking iced water triggers the body to burn up to one hundred calories because it requires to warm the water and bring it to regular body temperature level.
Just like discovering the ropes in any occupation, experience and practice will help significantly in improving the art of modeling. Using a body length mirror (usually a restroom mirror will be enough if you don’t have a full-sized mirror) focus on moving your face in coordination with your body with dignity. While in the mirror, look straight forward at yourself, tilt your direct somewhat, now turn your face to the right, now to the left and back straight forward. Practice moving your face in various instructions, watch as your face modifications depending on the angle. Exactly what is your best angle? What is your worst? Know your angles!
For individuals that live a hectic lifestyle, there is detox diet that cleans the body in simply weeks. Within this short time you will be able to see results. You need to always remember though to very first consult your doctor prior to starting any detox techniques. Though these methods are natural, there may still be restrictions that you need to understand.
When you take herbs in tea form you get to take them numerous times a day, while delighting in the rejuvenating benefit that organic teas usually have. But there is a catch, you must be consuming healthily during the process of taking herbs, why? Since it’s kind of dumb to attempt and flush toxic substances from your body as you stuff them right back in.
Find More Mind Body Green Detox Articles | {
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-7,779,837,482,472,945,000 | Academics
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• Exposure of Left Brachial Plexus
Position - supine with small transverse shoulder roll to allow slight extension of the head and neck. The head is placed on a donut headrest and rotated approximately 50 degrees to the right.
Incision - The incision is scored with a no. 15 blade along the posterior border of the sternocleidomastoid (SCM) from just below the ear to just above the head of the clavicle. It is taken sharply through the level of the dermis after which a micropoint cautery (cut 6, coag 8, blend 1, standard) is used to divide the subcutaneous fat and platysma.
Dissection - The dissection begins by separating a lateral myocutaneous flap from the posterior border of the SCM. The spinal accessory nerve is identified at the posterior border of the SCM coursing across the posterior cervical triangle. Just caudal to the accessory nerve, cutaneous branches of C4 are seen emerging from the supraclavicular fat/nodal tissue. A vein often accompanies these cutaneous branches.
Between the cutaneous branches of C4 and the clavicle, the inferior belly of the omohyoid is identified and freed of investing fascia.
The supraclavicular fat/nodal tissue is divided vertically along the medial margin of the lateral myocutaneous flap and reflected medially up off of the plexus, preserving its association with the jugular chain of nodes and venous drainage.
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3,131,344,258,260,229,000 | 503-256-4830
11115 SE Stark St. Portland OR 97216
Fixing Posterior Pelvic Tilt
Fixing Posterior Pelvic Tilt
Fixing Posterior Pelvic Tilt
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Posterior Pelvic Tilt is a common problem that affects many Americans. A person can be affected by PPT if they don’t lead an active lifestyle or have poor posture whilst sitting at their desk. While the severe PPT can cause joint, knee and hip pain, it also makes your butt and gut protrude a lot more. In addition to the pain, this can affect the way your clothes fit, and maybe even your self confidence. Unfortunately, because this is a muscular/ skeletal problem, no amount of weight loss will help you get rid of that gut. Here’s some information to help you understand PPT a little better, as well as a few suggestions on how to combat it.
What is Posterior Pelvic Tilt ?
Posterior pelvic tilt is the medical term for hips that are excessively tilted backwards. The most common cause of this posture problem is sedentariness and lack of everyday activity.
Pelvic-Tilt
How Posterior Pelvic Tilt Happens
If we sit a lot, our hip flexors “shorten” causing compensatory tension in the hamstrings. If you stand up and you have short hip flexors, the hamstrings will pull on the the hip, as well as your lower back. This is what causes the hip to tilt backward and the curvature in your lower back to flatten, thus making your butt and gut seem more prominent.
How can I tell if I have Posterior Pelvic Tilt?
To a certain extent, a slight pelvic tilt is common in humans. It depends on the way your body is built, your genes, etcetera. In fact, a slight pelvic tilt is more common in women than in men. However, one of the ways you can figure out if you have PPT is to perform the Thomas Test. To do so, get a friend to observe you, or film it with your cellphone/ webcam.
Sit on the edge of a table or another stable surface, grab both of your knees and lean back until your back is flat on the surface. Now, let go of one leg and extend at the hip until your thigh touches the table.
You don’t have PPT if: your thigh touches the table and the knee is bent with neither hip nor leg rotating or moving outward.
You might have PPT if: you need to extend the knee (i.e. straighten it) to touch your thigh to the surface of the table. This means your rectus femoris is short. Also, if your thigh cannot touch the table even after you’ve extended your knee, your psoas are short.
If your leg and hip need to move to the outside for the thigh to touch the surface of the table, your tensor fascia latae is short. If you notice any of these things, and your spine is even slightly curved, you will benefit from a few PPT corrective drill or exercises.
What can I do to fix it?
• Exercises and drills. If you’re suffering from sever PPT, there are a number of valuable exercises and drills videos available online to help you fix it. Focus on drills that strengthen your psoas and quads, and stretching your glutes and hamstrings.
• Be more active. Sedentariness is the number one cause of PPT, so get out there and move your body. If your PPT is mild, something as simple as walking for a half hour a day will help improve your flexibility and posture.
• Chiropractic Adjustment. Tense, overused muscles from overcompensating for weak muscles can contribute to PPT. Regular chiropractic adjustment will help with this problem. | {
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6,789,927,678,525,271,000 | Loading...
Current Issue
, Volume 47 Issue 5 Previous Issue Next Issue
Rapamycin treatment starting at 24 h after cerebral ischemia/reperfusion exhibits protective effect on brain injury in rats
LIANG Gang, NIU Yumiao, LI Yihan, Wei Anyi, DONG Jingyin, ZENG Linghui
J Zhejiang Univ (Med Sci), 2018, 47(5): 443-449. https://doi.org/10.3785/j.issn.1008-9292.2018.10.01
Abstract( 705 ) HTML( 47 ) PDF(1093KB)( 169 )
Objective: To investigate whether rapamycin treatment starting at 24 h after cerebral ischemia/reperfusion(I/R) has protective effect on brain injury in rats. Methods: The rat I/R model was established by middle cerebral artery occlusion according to Longa's method. A total of 104 Sprague Dawley rats were randomly divided into sham group, model group, and rapamycin-treated groups (6 h or 24 h after modeling). Neurological function was assessed with neurological severity score (NSS). Triphenyl tetrazolium chloride (TTC) staining and Fluoro-Jade B (FJB) staining were used to examine the infarct volume and neuronal apoptosis, respectively. The expression of p-S6 protein in mTOR signaling pathway was detected by Western blot analysis. Results: Compared with sham group, NSS of the model group was significantly increased and TTC staining indicated obvious infarct area (all P < 0.01). Furthermore, significantly increased number of FJB-positive cells and p-S6 expression in the penumbra area were shown in the model group (all P < 0.01). Compared with the model group, both rapamycin-treated groups demonstrated decreased NSS, infarction volume and FJB positive cells as well as p-S6 expression in the penumbra area (P < 0.05 or P < 0.01). There was no significant difference between the groups of rapamycin administrated 6 h and 24 h after modeling (all P > 0.05). Conclusion: Rapamycin treatment starting at 24 h after I/R exhibits protective effect on brain injury in rats.
Effects of Honokiol on cognitive function in mice with kainic acid-induced epilepsy
WANG Qingmei,SHU Min,XU Qianzi,XIE Yiyi,RUAN Shengzhe,WANG Jianda,ZENG Linghui
J Zhejiang Univ (Med Sci), 2018, 47(5): 450-456. https://doi.org/10.3785/j.issn.1008-9292.2018.10.02
Abstract( 546 ) HTML( 13 ) PDF(1342KB)( 119 )
Objective: To investigate the effects of Honokiol on cognitive function in mice with epilepsy. Methods: Kainic acid (38 mg/kg) was intraperitoneally injected in 5 weeks old male ICR mice to induce epilepsy. Honokiol at dose of 3, 10, 30 mg/kg was given to epilepic mice by intraperitoneal injection for 10 days. Fluoro-Jade B staining was used to assess neuronal death; Morris water maze and Y maze tests were used to measure cognitive function such as learning and memory; Western blot was performed to detect the expression of acetylated superoxide dismutase (SOD), microtubule associated protein 1 light chain 3-Ⅱ (LC3-Ⅱ) and P62 in hippocampus tissue; thiobarbituric acid and WST-1 methods were used to detect malondialdehyde (MDA) and SOD. Results: Compared with control group, the levels of acetylated-SOD, MDA, LC3-Ⅱ, P62 and neuronal death increased, cognitive function and SOD decreased in model group (P < 0.05 or P < 0.01). Honokiol at the dose of 10 mg/kg and 30 mg/kg decreased SOD acetylation, MDA content, expression of LC3-Ⅱ and P62, as well as neuronal death, and the cognitive function was improved (P < 0.05 or P < 0.01), especially in 30 mg/kg Honokiol group. Conclusion: Honokiol alleviates oxidative stress and autophagy degradation disorder, decreases neuronal death, and therefore improves cognitive function in epilepsy mice.
Efficacy of brain-targeted rapamycin for treatment of epilepsy in rats
ZHANG Yuanyuan,Wang Qingmei,DONG Jingyin,ZHANG Binbin,LIU Luna,ZHU Feng,ZENG Linghui
J Zhejiang Univ (Med Sci), 2018, 47(5): 457-464. https://doi.org/10.3785/j.issn.1008-9292.2018.10.03
Abstract( 634 ) HTML( 8 ) PDF(1621KB)( 101 )
Objective: To investigate the efficacy of brain-targeted rapamycin (T-Rap) in treatment of epilepsy in rats. Methods: Rapamycin nanoparticles targeting brain were prepared. The epilepsy model was induced by injection of pilocarpine in rats. The rats with pilocarpine-induced epilepsy were treated with rapamycin (Rap group) or brain-targeted rapamycin (T-Rap group). Seizure activity was observed by electroencephalography; the effect on mTOR signaling pathway was detected by Western blot; neuronal death and moss fiber sprouting were analyzed by Fluoro-Jade B (FJB) and Timm's staining, respectively. Results: Electroencephalography showed that both preparation of rapamycin significantly reduced the frequency of spontaneous seizures in rats, and the effect of T-Rap was stronger than that of conventional rapamycin (P < 0.05). Western blot showed that the phosphorylation levels of S6K and S6 in T-Rap group were lower than those in Rap group (all P < 0.05), indicating that T-Rap had a stronger inhibitory effect on mTOR signaling pathway. FJB staining showed that T-Rap significantly decreased neuronal death, but there was no significant difference as compared with Rap group. Timm's staining showed that both preparations of rapamycin significantly reduced the germination of mossy fibers, while the effect of T-Rap was more pronounced than Rap group (P < 0.05). The inhibition of body weight gain of T-Rap group was less than that of Rap group (P < 0.05). Conclusion: T-Rap has a better therapeutic effect on epilepsy than conventional rapamycin with a less adverse effects in rats.
Neuroprotective effect of rapamycin against Parkinson's disease in mice
ZHU Feng,FAN Miao,XU Ziwei,CAI Yiting,CHEN Yizhen,YU Shuang,ZENG Linghui
J Zhejiang Univ (Med Sci), 2018, 47(5): 465-472. https://doi.org/10.3785/j.issn.1008-9292.2018.10.04
Abstract( 977 ) HTML( 11 ) PDF(1247KB)( 193 )
Objective: To investigate the effect of rapamycin on Parkinson's disease (PD) and its underlying mechanism in mice. Methods: Sixty SPF adult male C57BL/6 mice were randomly divided into control group, model group and treatment group. 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine(MPTP) was used to induce Parkinson's disease in model group and treatment group. All mice were trained to cross the runway and were subjected to computer-assisted CatWalk. The numbers of tyrosine hydroxylase positive (TH+) neurons in the substantia nigra (SN) were assessed by unbiased stereology using the optical fractionator method; protein expression was detected by Western blot analysis; and glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by spectrophotometry. Results: In the model group, a decrease in stride rate and an increase in variation of stance and swing were noted by CatWalk system (P < 0.05 or P < 0.01); the numbers of TH+ neurons decreased (P < 0.01); expression of p-Akt, p-S6K, p-S6 and p-ULK increased (all P < 0.01); LC3-Ⅱ/Ⅰ ratio decreased (P < 0.01); MDA level was elevated while the levels of SOD and GSH-PX were reduced (all P < 0.01). Compared with the model group, after treated with rapamycin, the abnormal behavior including the stride length, variation of stance and swing and step patterns induced by MPTP were all improved (P < 0.05 or P < 0.01); the numbers of TH+ neurons increased (P < 0.05); the expression of p-Akt, p-S6K, p-S6 and p-ULK was suppressed (all P < 0.01); the LC3-Ⅱ/Ⅰ ratio was upregulated (P < 0.05); MDA level decreased while the levels of GSH-Px and SOD increased (all P < 0.01). Conclusion: Rapamycin inhibits the activation of mTOR pathway, which contributes to protect against the loss of dopaminergic neurons and provide behavioral improvements in mice with Parkinson's disease. These results are partially related to the ability of rapamycin in inducing autophagy and reducing oxidative stress.
Osthole suppresses amyloid precursor protein expression by up-regulating miRNA-101a-3p in Alzheimer's disease cell model
LIN Ying,YAO Yingjia,LIANG Xicai,SHI Yue,KONG Liang,XIAO Honghe,WU Yutong,NI Yingnan,YANG Jingxian
J Zhejiang Univ (Med Sci), 2018, 47(5): 473-479. https://doi.org/10.3785/j.issn.1008-9292.2018.10.05
Abstract( 900 ) HTML( 5 ) PDF(1672KB)( 142 )
Objective: To investigate the effect of osthole on the expression of amyloid precursor protein (APP) in Alzheimer's disease (AD) cell model and its mechanism. Methods: The SH-SY5Y cell with over expression of APP was established by transfection by liposome 2000. The cells were treated with different concentrations of osthole, and the cell viability was determined by MTT and lactate dehydrogenase (LDH) assay. The differentially expressed miRNAs with and without osthole treatment were detected by miRNA array, and the target genes binding to the differentially expressed miRNAs were identified and verified by databases and Cytoscape. After the inhibitor of the differentially expressed miRNA was transduced into cells, the changes of APP and amyloid β (Aβ) protein were determined by immunofluorescence cytochemistry, and the mRNA expression of APP was determined by RT-PCR. Results: The AD cell model with over expression of APP was established successfully. The results of MTT and LDH assay showed that osthole had a protective effect on cells and alleviated cell damage. miR-101a-3p was identified as the differentially expressed miRNA, which was binding to the 3'-UTR of APP. Compared with APP group, the expression of APP and Aβ protein and APP mRNA increased in the miR-101a-3p inhibitor group (all P < 0.01), while the expression of APP and Aβ protein and APP mRNA decreased in the cells with osthole treatment (all P < 0.01). Conclusion: Osthole inhibits the expression of APP by up-regulating miR-101a-3p in AD cell model.
Protective effect of curcumin on dopamine neurons in Parkinson's disease and its mechanism
WU You,LIANG Shunli,XU Bin,ZHANG Rongbo,XU Linsheng
J Zhejiang Univ (Med Sci), 2018, 47(5): 480-486. https://doi.org/10.3785/j.issn.1008-9292.2018.10.06
Abstract( 769 ) HTML( 6 ) PDF(1263KB)( 152 )
Objective: To investigate the effect of curcumin on dopamine neurons in Parkinson's disease (PD) and its mechanism. Methods: SH-SY5Y human neuroblastoma cells were treated with 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) to establish the PD cell model. The model cells were treated with curcumin and/or autophagy inhibitor 3-MA. After 48 h of drug treatment, the number of surviving dopamine neurons was detected by tyrosine hydroxylase immunofluorescence method. Western blotting was used to detect protein expression of α-Synuclein (α-Syn), transcription factor EB (TFEB) and autophagy-related proteins lysosome-associated membrane protein 2A (LAMP2A) and microtubule-associated protein 1 light chain 3-Ⅱ(LC3-Ⅱ); RT-PCR was used to detect mRNA expression of α-Syn. Results: Compared with MPTP model group, curcumin increased the number of surviving dopamine neurons(P < 0.01), decreased both protein expression and mRNA expression of α-Syn (all P < 0.01), and increased protein expression of TFEB, LAMP2A and LC3-Ⅱ (all P < 0.01). When curcumin and 3-MA were given concurrently, the number of surviving dopamine neurons, protein expression of TFEB, LAMP2A and LC3-Ⅱ increased (P < 0.05 or P < 0.01), and both protein expression and mRNA expression of α-Syn decreased (P < 0.05 or P < 0.01) compared with MPTP model group; but the number of surviving dopamine neurons and protein expression of LAMP2A and LC3-Ⅱ decreased compared with curcumin group (all P < 0.05). Conclusion: Curcumin exerts protective effect on dopamine neurons in PD, which may be associated with enhancing autophagy and promoting the clearance of α-Syn.
G protein-coupled receptor 17 is involved in CoCl2-induced hypoxic injury in RGC-5 cells
LIN Kana,LIN Meili,GU Yingfen,ZHANG Shunguo,HUANG Shiying
J Zhejiang Univ (Med Sci), 2018, 47(5): 487-492. https://doi.org/10.3785/j.issn.1008-9292.2018.10.07
Abstract( 523 ) HTML( 10 ) PDF(1118KB)( 97 )
Objective: To investigate the effect of G protein-coupled receptor 17 (GPR17) on hypoxia injury in retinal ganglion cells in vitro. Methods: CoCl2 (400 μmol/L) was used to induce hypoxic injury in RGC-5 cells. The expression of GPR17 and the effect of GPR17 ligands were investigated, and the role of GPR17 in hypoxia injury was further studied by transfection of RGC-5 cells with GPR17 small interfering RNA (siRNA). The cell viability was determined by MTT and the cell apoptosis rate was detected by flow cytometry analysis. The expression of GPR17 mRNA was determined with RT-PCR. Results: mRNA expressions of GPR17 in RGC-5 cells with and without CoCl2 treatment were 0.36±0.05 and 0.26±0.08(P < 0.01). Compared with hypoxia without any treatment, pretreatment with GPR17 agonists (LTD4, UDP, UDP-G) significantly reduced cell viability (the survival rates of cells decreased by 29.6%, 31.8% and 33.9%, all P < 0.01), while the effect of GPR17 antagonist (cangrelor) was the opposite (the survival rates of cells increased by 33.2%, P < 0.01). Transfection with GPR17 SiRNA inhibited hypoxia-induced up-expression of GPR17 mRNA (P < 0.01)and reduced cell apoptosis[rates of cell apoptosis were(39.73±2.06)%, (42.50±3.64)% and (24.98±2.16)% for blank control, NC siRNA and GPR17 siRNA groups, P < 0.01]. Conclusion: GPR17 may mediate hypoxia injury in RGC-5 cells, while the knockdown of GPR17 can reduce the hypoxia injury.
Roles of astrocytes in cerebral infarction and related therapeutic strategies
YE Jianyu,SUN Ziyu,HU Weiwei
J Zhejiang Univ (Med Sci), 2018, 47(5): 493-498. https://doi.org/10.3785/j.issn.1008-9292.2018.10.08
Abstract( 549 ) HTML( 6 ) PDF(899KB)( 220 )
Astrocytes are the most abundant cells in the central nervous system and play significant roles in normal brain. With cerebral infarction, astrocytes are activated as reactive astrocytes and form glial scars, which play an essential part in brain injury. According to their roles in neuroprotection after cerebral infarction, regulation of scar formation, nerve regeneration, maintenance of blood-brain barrier, promotion of angiogenesis and immune response, scholars have proposed a variety of therapeutic strategies based on targeting astrocytes. This article reviews the research progress on the changes in astrocyte signaling pathways before and after cerebral infarction and the related therapeutic strategies.
Anti-inflammatory effect of interleukin-35 in mice with colitis and its mechanism
LU Zhanjun,HU Yangyang,LI Sisi,ZANG Lijuan,JIANG Weiliang,WU Jianjiong,WU Xiening,ZENG Yue,WANG Xingpeng
J Zhejiang Univ (Med Sci), 2018, 47(5): 499-506. https://doi.org/10.3785/j.issn.1008-9292.2018.10.09
Abstract( 729 ) HTML( 12 ) PDF(1635KB)( 177 )
Objective: To investigate the anti-inflammatory effect and mechanisms of interleukin-35 (IL-35) in inflammatory bowel disease. Methods: BALB/c mice were divided into three groups with 10 mice in each group:control group, model group (oral administration of 4% glucan sodium sulfate for 7 d) and IL-35-treated group (oral administration of 4% glucan sodium sulfate for 7 d, intraperitoneal injection of 2 μg IL-35 at d2-5). Disease activity index (DAI) was scored every day. After 7 d, the mice were sacrificed, and the serum and intestinal tissue samples were collected. The gross morphology of the colon was observed; HE staining was used to observe the pathological changes of colon tissue; flow cytometry was employed to detect the change of macrophage polarization ratio in colon tissue; the mRNA expression levels of cytokines IL-6, TNF-α, IFN-γ, IL-10 and SHIP1 in colon tissue were determined by real-time quantitative RT-PCR; the expression and distribution of SHIP1 in colon tissue was measured by immunohistochemistry; Western blotting was adopted to detect the expression level of SHIP1 protein in colonic intestinal tissues of each group. Results: The DAI scores of the mice in the model group were higher than those in the control group, while the DAI scores in the IL-35-treated group were lower than those in the model group (all P < 0.01). Compared with the control group, the colon length was significantly shortened in the model group (P < 0.05), while the colon length of the IL-35-treated group had an increasing trend compared with the model group, but the difference was not statistically significant (P > 0.05). Compared with the model group, microscopic inflammatory infiltration score was decreased and microscopic crypt destruction and score was significantly lower in IL-35-treated group (all P < 0.05). The relative expression of proinflammatory cytokines IL-6, TNF-α and IFN-γ in the colon tissue of IL-35-treated group was decreased compared with the model group, while the relative expression of IL-10 mRNA was higher than that of the model group (all P < 0.05). Compared with the control group, the proportion of M1 macrophages in the model group increased (P < 0.05), while the proportion of M1 macrophages in the IL-35-treated group was lower than that in the model group (P < 0.05). The relative expression of SHIP1 mRNA and protein in the colon tissue of IL-35-treated group was higher than that in the model group (all P < 0.05). Conclusion: IL-35 can inhibit the polarization of M1 macrophages and regulate inflammatory cytokines to promote anti-inflammatory effect on mice with colitis.
Shenmai injection protects mitochondria from oxidative injury in myocardial cells and its mechanism
ZHAO Yu,ZHANG Feng,ZHAO Xiaoping,YUAN Wei,ZHANG Jinhua,WANG Yi
J Zhejiang Univ (Med Sci), 2018, 47(5): 507-513. https://doi.org/10.3785/j.issn.1008-9292.2018.10.10
Abstract( 569 ) HTML( 8 ) PDF(985KB)( 126 )
Objective: To investigate the effect of Shenmai injection on myocardial cells with oxidative injury and the underlying mechanisms. Methods: Tert-butyl hydroperoxide (t-BHP) was used to induce the oxidative stress in H9c2 myocardial cells. The cell viability and ATP level were evaluated using MTT-colorimetric method and CellTiter-Glo luminescent cell viability assay. The oxygen respiration rate was examined by Clark oxygen electrode. Pyruvate and pyruvate dehydrogenase (PDH) levels were evaluated by ELISA kit. Western blot and quantitative real-time RT-PCR were employed to evaluate the expression of pyruvate dehydrogenase alpha 1(PDHA1) and pyruvate dehydrogenase kinase 1(PDK1). Results: Shenmai injection significantly improved viability and respiration of H9c2 myocardial cells after t-BHP injury (P < 0.05 or P < 0.01). It increased ATP contents by consuming pyruvate and increasing PDH level (P < 0.05 or P < 0.01). Furthermore, Shenmai injection had the tendency to increase protein expression of PDHA1(P < 0.05) and decrease mRNA expression of PDK1 (P>0.05). Conclusion: Shenmai injection protects mitochondria from oxidative stress by increasing PDH level, which indicates that it may improve energy metabolism of myocardial cells.
Association of CXCL12/CXCR4 gene polymorphisms with genetic risk and severity of coronary stenosis in patients with coronary artery disease
WANG Anqi,LIU Xinyue
J Zhejiang Univ (Med Sci), 2018, 47(5): 514-519. https://doi.org/10.3785/j.issn.1008-9292.2018.10.11
Abstract( 478 ) HTML( 8 ) PDF(909KB)( 72 )
Objective: To investigate the association of CXCL12 and CXCR4 polymorphisms with the genetic risk and severity of coronary stenosis in patients with coronary artery disease (CAD). Methods: Competitive allele specific PCR(KASP) was performed to identify the genotypes of rs2297630 and rs2322864 polymorphisms in 302 CAD patients and 302 age-and gender-matched healthy controls. The severity of CAD patients was assessed by the Gensini scoring system according to the results of coronary arteriography. The association of rs2297630 and rs2322864 polymorphisms with genetic risk of CAD and Gensini scores were analyzed by unconditional logistic regression and multivariate linear regression respectively. Results: There were significant differences in the genotype and allele frequencies of both rs2297630 and rs2322864 between the CAD group and healthy control (all P < 0.01). Regression analysis showed that rs2297630 polymorphism was associated with genetic risk of CAD and Gensini scores (all P < 0.01). People who carried the AA genotype suffered higher risk of CAD susceptibility and more serious coronary stenosis (all P < 0.01), compared with GG genotype carriers. There was also significant association between rs2322864 polymorphism and genetic risk of CAD (P < 0.01); those who carried the CT genotype had higher risk of CAD (P < 0.01), compared with TT genotype carriers. However, rs2322864 polymorphism was not associated with the severity of coronary stenosis (P>0.05). Conclusions: Gene polymorphism of CXCL12 rs2297630 is associated with the genetic risk of CAD and the severity of coronary stenosis. Moreover, the gene polymorphism of CXCR4 rs2322864 is associated with genetic risk of CAD, but not with the severity of coronary stenosis.
Establishment of cell lines for quality control of prenatal genetic diagnosis by SV40LT gene transfection
WENG Binghuan,XU Wei,SU Lan,SHEN Min,LI Rong,XU Xiaopeng,LI Lanjuan
J Zhejiang Univ (Med Sci), 2018, 47(5): 520-524. https://doi.org/10.3785/j.issn.1008-9292.2018.10.12
Abstract( 730 ) HTML( 8 ) PDF(978KB)( 97 )
Objective: To establish a cell lines for quality control of prenatal genetic diagnosis. Methods: The recombined SV40LTag-pcDNA3.1(-) vector was constructed and transfected by lipidosome into human amniotic fluid cells with common aneuploidy. Positive clones were screened by G418, and the immortality of transfected cell line was identified. Results: Cell line with karyotype of 46, XY, t(8;19)(q24.3;q13.1) from primary amniotic fluid cells was established. Karyotype analytical results indicated that the cell line at its 15th generation maintained the same karyotype of its primary cell. Conclusion: Gene SV40LT can lead to immortality of amniotic fluid cells, which contributes to preparing cell lines for internal and external quality control in prenatal genetic diagnosis.
Application of mesenchymal stem cells in antineoplastic drugs delivery for tumor-targeted therapy
WANG Xiaoling,OUYANG Xumei,SUN Xiaoyi
J Zhejiang Univ (Med Sci), 2018, 47(5): 525-533. https://doi.org/10.3785/j.issn.1008-9292.2018.10.13
Abstract( 872 ) HTML( 15 ) PDF(914KB)( 189 )
In recent years, a large number of studies have achieved tumor targeting by mesenchymal stem cells (MSC)-based delivery system attributed to the tumor tropism of MSCs. Biomacromolecules and antineoplastic drugs loaded on MSC via internalization or cell membrane anchoring can be released or expressed at tumor site to perform their antitumor effects. The genetically modified MSC are extensively studied, however, the applications of MSCs in targeted delivery of antineoplastic drug with small molecules are not well summarized. In this review, MSCs homing mechanism and the distribution of injected MSCs in vivo is introduced; the examples of antitumor drug-primed MSCs and drug loaded MSCs are presented; the drug loading and releasing process from MSCs is also illustrated; finally, challenges and future perspectives of MSCs-based drug delivery system on realizing its full potential are prospected.
Progress on pathogenesis of progressive multifocal leukoence-phalopathy
HU Caiqin,ZHU Biao
J Zhejiang Univ (Med Sci), 2018, 47(5): 534-540. https://doi.org/10.3785/j.issn.1008-9292.2018.10.14
Abstract( 507 ) HTML( 7 ) PDF(902KB)( 99 )
Progressive multifocal leukoencephalopathy (PML) is a rare and lethal central nervous demyelinating disease caused by JC polyomavirus (JCV), particularly in patients with impaired immune system. The variation of JCV plays an important role in the pathogenesis of PML, including the recombination of non-coding regulatory region (NCCR), which is closely related to binding sites of transcription factors and affect the level of gene transcription. Nucleotide mutations in VP1 region determine the antigenicity and receptor specificity of JCV, play an important role in cell adsorption, immune-mediation and pathogenicity. In addition, immune cells are also involved in the pathogenesis of PML. T lymphocytes can recognize virus antigens, clear JCV, which are directly related to the prognosis of PML. B lymphocytes can serve as latent sites of JCV, and participate in viral transmission, replication, and coordination of the expression of transcription factors. This paper summarizes the roles of JCV variation and immune cells in pathogenesis of PML.
Involvement of PML proteins in treatment of acute promyelocytic leukemia with arsenic trioxide
HAO Rui,SU Lide,SHAO Yiming,BU Na,MA Liya,NARANMAN DURAHua
J Zhejiang Univ (Med Sci), 2018, 47(5): 541-551. https://doi.org/10.3785/j.issn.1008-9292.2018.10.15
Abstract( 625 ) HTML( 10 ) PDF(1304KB)( 143 )
Promyelocytic leukemia (PML) protein, a tumor suppressor, plays an important role in patients with acute promyelocytic leukemia (APL) receiving arsenic trioxide (As2O3) therapy. APL is a M3 subtype of acute myeloid leukemia (AML), which is characterized by expression of PML-RARα (P/R) fusion protein, leading to the oncogenesis. As2O3 is currently used as the first-line drug for patients with APL, and the mechanism may be:As2O3 directly binds to PML part of P/R protein and induces multimerization of related proteins, which further recruits different functional proteins to reform PML nuclear bodies (PML-NBs), and finally it degraded by SUMOylation and ubiquitination proteasomal pathway. Gene mutations may lead to relapse and drug resistance after As2O3 treatment. In this review, we discuss the structure and function of PML proteins; the pathogenesis of APL induced by P/R fusion protein; the involvement of PML protein in treatment of APL patient with As2O3; and explain how PML protein mutations could cause resistance to As2O3 therapy.
Roles of CCAAT enhancer binding protein α in acute myeloblastic leukemia
SHI Ting,YE Xiujin
J Zhejiang Univ (Med Sci), 2018, 47(5): 552-557. https://doi.org/10.3785/j.issn.1008-9292.2018.10.16
Abstract( 525 ) HTML( 6 ) PDF(891KB)( 111 )
The CCAAT enhancer binding protein α (C/EBP α:p42 and p30), which encoded by CCAAT enhancer binding protein α (C/EBPα) gene, plays a pretty crucial role in the regulation of myeloid hematopoiesis.The disorder of CEBPA gene expression is an pivotal mechanism of acute myeloid leukemia (AML). The result of uncontrolled expression of C/EBP α gene is the over-expression of p30 and the incomplete loss of p42, both of which contribute to the occurrence of AML. Restoring the expression ratio of C/EBP α such as over-expression of p42 or blocking the carcinogenic pathway of p30 seems to be important for the treatment of AML caused by such causes. In order to better guide medical decision-making, this article reviews research progress on C/EBPα in the pathogenesis of AML.
Progress on cancer associated fibroblasts in tumor immunoregulation
LI Gaopeng,HE Jia,WANG Qingqing
J Zhejiang Univ (Med Sci), 2018, 47(5): 558-563. https://doi.org/10.3785/j.issn.1008-9292.2018.10.17
Abstract( 1737 ) HTML( 27 ) PDF(477KB)( 610 )
Cancer associated fibroblasts (CAFs) are important components of the tumor microenvironment. Through secreting of multiple growth factors, cytokines and proteases, CAFs play a significant role in regulating the recruitment and function of various innate immune cells and adaptive immune cells in tumor microenvironment. In addition, extracellular matrix secreted by CAFs can also promote the formation of immunosuppression and hypoxia of tumor microenvironment. Here, we review the progress on CAFs in regulation of immune cells and tumor immunity.
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-2,283,452,693,592,337,000 | Gastroenterology
Bowel Obstruction
About 3.2 million cases of bowel obstruction occurred worldwide in 2015 which resulted in 264,000 deaths. Both sexes are equally affected and the condition can occur at any age.
In rural Africa, acute intestinal obstruction accounts for a great proportion of morbidity and mortality. While some studies have been done to assess prevalence and causes of bowel obstruction in developed countries, the condition remains largely understudied in the African context. With only a few studies conducted in some African countries.
Further studies into assessing the parameters of the incidence, prevalence, causes, treatments and mortality associated with bowel obstruction in Africa can become the foundation for a more rigorous approach into better treatment options and preventive interventions for the disease condition and it’s related complications to largely reduce the mortality rate in Africa.
Bowel obstruction, also known as intestinal obstruction refers to a condition whereby the free movement of intestinal contents is blocked mechanically or functionally. This leads to a build up of intestinal content in the intestines. It is a surgical emergency that demands quick response within 24 hours of onset to prevent complications.
Classification of Bowel Obstruction
Bowel obstruction is subdivided into two categories to differentiate the cause of the blockage. There are mechanical and non-mechanical factors that can obstruct the bowel.
Mechanical intestinal obstruction refers to bowel obstruction from mechanical factors whiles non-mechanical intestinal obstruction refers to bowel obstruction from non-mechanical or functional factors.
Causes of Bowel Obstruction
There are several factors that can cause intestinal obstruction.
images-154
Non-mechanical intestinal obstruction is primarily due to a functional dysfunction of the nerves that supply the intestines called paralytic ileus, which temporarily arrests intestinal peristaltic movement. Possible conditions that can precipitate paralytic ileus include
• infections of the peritoneum,
• mesenteric ischemia,
• intra-abdominal hematoma,
• metabolic disturbances like hypokalaemia,
• renal disease and
• post-surgery.
Mechanical intestinal obstruction may occur in the small intestine (which is more common) or large intestine. When the obstruction is in the small intestine, it is called small bowel obstruction, and if the obstruction is in the large intestine, it is referred to as large bowel obstruction. Both have different prevalent causes.
Small bowel obstruction is most commonly caused by adhesions after a surgery. In other populations in developing countries in Africa, hernia is the leading cause of small bowel obstruction. Other causes include
• Merkel’s diverticulitis,
• inflammatory bowel disease (crohn’s disease),
• intestinal worms (ascaris),
• tumors,
• foreign bodies (gall stones or other swallowed objects),
• volvolus (twisting of the small intestine),
• intussusception (which is the most common cause in children).
Large bowel obstructions may be caused by tumors in the large intestine (lipoma or polyps), Sigmoid diverticulitis, volvolus of the large intestine, fecal impaction and post surgical adhesions.
Signs and Symptoms of Bowel Obstruction
The cardinal symptoms are
1. Abdominal cramps
2. Distention of the abdomen
3. Vomiting
4. Constipation
Clinical signs include
• High pitched bowel sounds.
• Abdomen may be tender or non-tender.
• Possible palpable mass like tumours at site of obstruction.
Diagnosis and Treatment
images-156
Imaging studies are needed to confirm the diagnosis of suspected bowel obstruction. Abdominal X-rays are usually enough to detect bowel obstructions. Other imaging techniques like CT-Scan and even ultrasound scan can be used for peculiar cases (especially in infants and pregnant women). Barium enema is used to rule out lesions along the colon.
The treatment of bowel obstruction requires the hospitalisation of the patient and the passage of a naso-gastric tube (N-G tube), which resolves simple obstructions.
Intubation for post operative obstruction caused by adhesions in the absence of peritoneal signs can be done.
Cases from electrolyte imbalance like hypokaleamia can be resolved through intravenous fluids and urinary catheter passed.
More complicated bowel obstructions, especially when accompanied with acute pain will require surgery correct the cause like hernia, removal of foreign objects and gall stones, tumours and volvolus.
Manual digital removal of fecal matter from rectum can be done to resolve obstruction due to fecal impaction.
Complications
1. Dehydration which can lead to oliguria and shock.
2. Ischemia which can advance to necrosis or gangrene of the intestines.
3. Intestinal perforation.
4. Peritonitis.
5. Death.
One research study carried out in Ethiopia to ascertain the causes, prevalence and management outcome of intestinal obstruction recommends that health professionals in the hospitals and districts should increase public awareness on intestinal obstruction by providing appropriate health information and physicians should diagnose intestinal obstruction early and appropriate interventions should be taken on time before the intestine develops gangrene.
Wound infection prevention should be improved because it is the most common postoperative complication in the research and this can be decreased by appropriate surgical technique and wound care with sterile techniques.
Reference
https://emedicine.medscape.com/article/774140-overview
https://en.m.wikipedia.org/wiki/Bowel_obstruction
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4893295/
Categories: Gastroenterology
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-5,109,719,783,488,463,000 | rss
Br J Sports Med 47:e1 doi:10.1136/bjsports-2012-092101.12
• Abstracts from the 4th International Conference on Concussion in Sport (Zurich, 2012)
• New investigation or diagnostic strategies
Montreal cognitive assessment (MoCA): baseline evaluation of cognition in the athletic population
1. S Dukelow1,3
1. 1Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada
2. 2Sport Medicine Centre, Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada
3. 3Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada
Abstract
Objective To assess baseline pre-season cognitive function in a young adult athletic population using the Montreal Cognitive Assessment Tool (MoCA).
Design Baseline case series of normative data.
Setting Sport Medicine Clinic at the University of Calgary, Alberta, Canada.
Participants Male and female athletes (n=347) were recruited from the University of Calgary varsity athletic teams, Southern Alberta Institute of Technology college teams and Canadian National sports teams. Athletes (aged 18–40 years) underwent pre-season face-to-face standardised cognitive screening interviews.
Interventions Baseline biographical information and a pre-season MoCA test were performed.
Main Outcome Measurements The MoCA is a one page global cognitive assessment tool with a maximum score of 30 points.
Results All subjects had grade 12 education or greater. Fifty-nine percent of the population was male. The average age was 22.02±3.49. The overall mean MoCA score was 26.62±2.20. One hundred and one subjects (29%) scored less than 26. For contact/collision sport athletes and non-contact sport athletes the mean MoCA scores were 26.41±2.28 and 26.97±2.01 respectively. There was a significant difference (p=0.018) between the contact/collision and non-contact sport athletes scores.
Conclusions Approximately 29% of the athletic population surveyed had MoCA scores less than what is considered normal (<26). Contact/collision sport athletes had significantly lower MoCA's scores than non-contact sport athletes. Scores less than 26 have been associated with mild cognitive impairment and Alzheimer's dementia in other studies. Multiple factors (eg, previous concussion, non-documented head injuries, malingering, etc) may play a role in explaining the present findings.
Competing interests None. | {
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Understanding Migraine Headaches
December 16, 2016
Migraine is more than ‘just a headache.’ Anyone who has ever suffered from the misery of a migraine will tell you that they can be anything from unsettling and uncomfortable to downright incapacitating. Not all people who experience migraines will get the classic headache – and some people don’t experience the headache every time. Because a migraine headache is considered a ‘primary’ headache, because there is no apparent underlying condition that could be causing it, they can be hard to treat.
What Is a Migraine Headache?
A migraine headache is more of a condition than just a headache. Migraine headaches are typically very severe and can come with additional symptoms like dizziness, nausea and even loss of speech and sight which can be extremely frightening. In some people, they are accompanied by sight disturbances and other neurological symptoms that doctors call the ‘migraine aura’. Sometimes, in a migraine with aura, there is no headache or it can be averted with painkillers at the aura stage, but in other cases the classic migraine headache can be blindingly painful, lasting anything from 20 minutes to a couple of days. Some people who experience sudden, severe, or recurrent migraines will need to be seen by a doctor and examined for other possible conditions, but in most cases migraines just have to be managed and treated as there is no cure – and often no obvious triggers. As migraine can sometimes be associated with other more severe conditions, if you have what you think is a migraine for the first time, you should seek advice from a medical professional.
How long can a migraine last?
Migraines are notorious for sticking around a long time. Some migraines only last for a few hours but if you’re unlucky enough to suffer from severe, prolonged migraines they can last for several days. Sometimes, the migraine sufferer will experience neurological symptoms before, during, and afterwards, including strange floating lights and auras. They might also experience these symptoms between bouts of pain.
What causes migraines?
Although the exact cause of migraine headaches is not known, most studies think there’s a genetic link that’s exacerbated by other triggers. Migraines tend to run in families and are usually hereditary. Some people can be set off by very strong smells, certain foods, heat, or bright lights.
How do you treat a migraine?
This is something you might want to discuss with your doctor, but there are options available for managing migraines. Many people turn to medication, understandably. Massage therapy can help to reduce the number of migraines in sufferers – a 2006 study of migraine sufferers showed that people who had massages experienced fewer migraines and slept better during the weeks they had massages, although it was a small study. You may have to try several different treatment options before discovering the best one for you.
How Can Massage Help?
A three-pronged approach that includes aromatherapy, massage therapy and cold therapy can be effective in helping relieve the pain of migraine for many sufferers.
Aromatherapy.
The first step in stopping a migraine is to calm the client, and one effective way to achieve this goal is through aromatherapy. Depending on the trigger, you can have clients breathe different blends of oils. For example, if the client knows the migraine is the result of stress, try using essential oils of clary sage, spikenard, helichrysum and lavender. For an environmental trigger, you might try roman chamomile, lavender, peppermint and rosemary.
Have the client breathe from each vial of oil, one at a time. Whatever they find most appealing, use this oil during the massage session.
Massage.
After choosing an oil, you’ll want to perform a series of headache point release techniques to help the client reach a calmer state. As a caution, you do not want to increase the blood flow to the neck and head, as doing so may result in accelerating the migraine pain. You may find that clients who are suffering from a migraine have several trigger points and very tight necks, and although not working on these areas sounds counterintuitive, the best thing to do is leave these areas alone for now.
Instead, the goal is to decrease blood flow, and stimulating these areas at this point can have the opposite effect. My research has shown that cranial sacral techniques are a wonderful accompaniment at this point in the treatment. After the headache is gone, at another treatment time, I suggest the therapist work the tight areas to help prevent future headaches.
Cold therapy.
The third phase of the treatment is to address the vascular component of the migraine. The therapist will need to try to reduce the overabundant blood flow to the head and brain with cold stones, thereby normalizing the blood flow. In doing so, the therapist will be reducing or removing the pounding sensation the client is experiencing in their head while helping to calm the brain. My own experience suggests that positioning specifically designed marble stones, cooled to approximately 36 degrees and applied to specific areas of the face and neck, has the desired effect. Many migraine sufferers love the feeling of the cold stones, and within a short amount of time start to feel relief.
Timing and triggers.
If at all possible, massage therapists will want to see the migrainer the day they feel the symptoms coming on because timing is critical to ward off the migraine before it can take full effect.
With busy schedules, however, you may not always be able to see a client right as they notice the symptoms. You can work alongside the client to try and figure out some of the triggers that cause migraine. Are they mostly occurring when the person has a particularly stressful week at work? Or maybe they notice that many of their migraines are happening when they eat certain foods.
Whatever the trigger might be, being more aware of when a migraine may be more likely to happen can help both you and the client anticipate when a massage therapy session might be needed.
Quick Facts About Migraines
1. Migraine attacks go beyond the symptoms of a normal headache and
require serious attention.
2. Often referred to as a spreading depression, migraines that start in a central location can rapidly spread.
3. A spreading depression can move into the trigeminal nerve (cranial nerve that affects the face), causing the blood vessels of the brain to constrict and then dilate continuously.
4. Migraine attacks can occur daily and can be devastating to the sufferer’s ability to function normally.
5. People with migraines can be more susceptible to epilepsy.
Common Causes
Although the exact causes of migraines aren’t well understood, we do know that many people have some common triggers, including food allergies, caffeine addiction, environmental stimulation, stress and hormonal imbalan
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Mentally Preparing for Pregnancy-5 Steps to Mentally Prepare for a Baby
Advice on getting ready for pregnancy typically focuses on the physical aspects—getting the right prenatal vitamins, eating the right foods, and doing the right exercises to prepare your body. But what about mentally preparing for pregnancy? What can you do before you conceive to ensure that your psychological health stays intact during the prenatal period? Are their strategies you can follow to help minimize potential complications such as postpartum depression?
Studies have shown that mental and emotional well-being during pregnancy can have an impact on birth outcomes as well as mental states during the postpartum period. Even if you have a difficult pregnancy or if your experience is not quite what you expected, there are steps that you can take to keep yourself mentally healthy.
Let's take a closer look at some of the different ways you might mentally prepare yourself to have a baby.
Understand Your Risk Factors
Postpartum depression (PPD) is a serious problem that affects a significant number of new mothers. Among women, depression is the leading cause of non-obstetric hospitalization. Because PPD can have a major impact on the health of mothers and infants, findings ways to both prevent and treat the disorder are essential.
Are there steps you can take before pregnancy to help lower the chances that you might be affected by postpartum depression?
Understanding the risk factors associated with PPD might help. While it is not possible to predict who will and will not be affected, being at least aware of any risk factors you may have might help you watch for the first signs of any symptoms.
Women at a higher risk of developing PPD include:
• Those with a history of depression and anxiety
• Past incidence of PPD
• Marital conflict
• A family history of PPD
• A recent history of stressful life events such as pregnancy complications
• A poor support system
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Fortunately, researchers have found that there are steps people can take to prevent or reduce postpartum depression. For example, one study found that women who receive psychosocial or psychological interventions are significantly less likely to experience depression after giving birth. The most effective interventions identified by the study included interpersonal therapy, postpartum home visits, postpartum phone support, and postpartum midwife care. Some evidence suggests that early cognitive behavior therapy can also be helpful in preventing postpartum depression.
Being aware of any risk factors is important, but you should also recognize that anyone can be affected by postpartum depression. Even if you have zero past experience with depression or anxiety, you can still develop symptoms of this condition following the birth of your child. That is why it is so important to be aware of these signs and symptoms so that you can take appropriate actions if you believe you might have PPD.
Depression following the birth of a child can range in terms of severity, but some of the symptoms you should watch for include:
• Difficulty concentrating
• Feelings of inadequacy
• Tearfulness
• Suicidal thoughts
• Disinterest in one's baby
• Anxiety
• Intrusive thoughts
If you think that you have symptoms of PPD or other feelings that are concerning you, be sure to discuss them with your health care provider. Your doctor may recommend treatment that includes self-care, psychotherapy, medication, support groups, or some combination of treatments.
Being educated about postpartum depression, knowing the symptoms, and recognizing the need to reach out to your doctor if you think you might have symptoms of depression or anxiety at any point during or after your pregnancy can help you feel more mentally prepared to have a baby.
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Know What to Expect
It's good to be prepared and have a plan, but pregnancy can be unpredictable and sometimes those plans fly out the window. Being mentally prepared for pregnancy also means building an understanding of what you can anticipate during the prenatal period. Pregnancy can include both the expected (weight gain, weird food cravings, aches and pains) to the unexpected (extreme nausea, pica, and being placed on bed-rest). Before you become pregnant, learn more about some of the common symptoms associated with pregnancy as well as some of the less common complications you might experience.
Perhaps the most important thing to remember is that you can read all the books, websites, blogs, and parenting magazines you can get your hands on and…the unexpected might still happen. You simply cannot predict exactly how your pregnancy experience will be, so you really just have to wait until you are in the thick of it to see. Educating yourself about the ins and outs can be helpful, but you need to accept that you cannot know, predict, or control everything.
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Seek Out Social Support
Strong social support during the prenatal period is critical, whether this support comes from a spouse, other family members, parents, or friends. Previous research has shown that social support can have a protective effect against the negative health consequences of life stress. One study found that social support in the time leading up to and following birth had an important positive impact on a mother's postpartum mental health.
Additionally, social support during pregnancy is thought to improve birth outcomes by lowering the risk of preterm birth. How? Social support is believed to both reduce anxiety and stress as well as improve stress coping mechanisms. While one study found that such social support did not have a direct effect on lowering preterm birth, the researchers did believe that such support could act as a sort of buffering mechanism between prenatal stress and premature delivery.
So what can you do to ensure that you have the tangible, emotional, and informational support that you need before, during, and after pregnancy?
• Communicate with your partner. If you have a spouse or partner who will be part of your life and your child's life, invest time and effort into making sure this relationship is strong. Talk about your concerns and ask for help when you need it.
• Lean on family and friends. Pregnancy can be challenging, particularly if you are dealing with complications such as severe morning sickness or other medical concerns. Let your loved ones know when you need help.
• Join a group of expecting parents. It can be helpful to share your experience with other people who are currently going through the same thing. Pregnancy, childbirth, breastfeeding, and parenting classes can be great places to meet people who can offer informational support through your pregnancy.
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Recognize That Your Emotional Health Is Important
Health concerns during pregnancy are often so centered on taking care of a woman's physical health that it is easy to overlook the importance of mental well-being. Pregnancy marks a major life change for most people, and it requires psychological adjustments that can have resounding effects on a woman's emotional health.
Emotional stress during pregnancy has not only been linked to negative outcomes for mothers, but also for newborns as well. Children born to women who report significant stress and anxiety during pregnancy have an increased risk of birth complications including low birth weight, prematurity, low neonatal status, and poor intrauterine growth.
If you have a history of depression or anxiety, talk to your doctor about your concerns before you conceive. This can be an opportunity to address any emotional concerns that you have going in to your pregnancy and set the stage for better mental wellness both before and after birth.
Strategies for taking care of yourself mentally:
• Make your psychological health a priority.
• Banish negative self-talk.
• Take time for yourself.
• Take a childbirth or parenting class.
• Talk to your partner about how you plan to parent.
• Also discuss how you will deal with challenges that might arise.
• Utilize stress management techniques to combat stress and anxiety.
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Mentally Prepare Your Other Children
The mental groundwork for pregnancy can become even more challenging when you also need to psychologically prepare your older children for the arrival of a new sibling. Some kids may eagerly await a younger brother or sister, but emotional responses such as fear, jealousy, and anxiety are also quite common.
You can help your children mentally prepare for your pregnancy by making sure to set aside time and attention for each of your kids. Make them feel that they will have an important part both in your pregnancy and that they can help you get ready for the new baby. Picking out baby items, helping you prepare a space for the baby, and even talking about baby names can help older siblings feel included.
Just be careful not to put too much pressure on your other children and don't make them feel that their emotional responses, even if those reactions might be negative, are wrong or bad. Acceptance, attention, and unconditional positive regard can go a long way toward helping your older kids feel excited about the possibility of another child in the family.
A Word From Verywell
Preparing for pregnancy is about more than just getting your body ready; it also means preparing your mind as well. While it can be very helpful to understand the sort of mental challenges you might face going in to this major life change, it is also impossible to predict exactly the sort of challenges you might face.
Before you conceive, assess your unique situation and needs. Take the time now to ensure that you address stress and anxiety in your life, seek out solid sources of support, and make your mental health a priority. By focusing on taking care of yourself, both physically and mentally, you can help ensure that you have a healthy, happy pregnancy.
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4,586,476,415,251,735,600 | Coma
Coma is a state of prolonged unconsciousness that can be caused by a variety of problems — traumatic head injury, stroke, brain tumor, drug or alcohol intoxication, or even an underlying illness, such as diabetes or an infection.
Coma is a medical emergency. Swift action is needed to preserve life and brain function. Doctors normally order a battery of blood tests and a brain CT scan to try to determine what's causing the coma so that proper treatment can begin.
Comas seldom last longer than several weeks. People who are unconscious for a longer period of time may transition to a persistent vegetative state. Depending on the cause of coma, people who are in a persistent vegetative state for more than one year are extremely unlikely to awaken.
Symptoms Causes Complications
The signs and symptoms of coma commonly include:
• Closed eyes
• Depressed brainstem reflexes, such as pupils not responding to light
• No responses of limbs, except for reflex movements
• No response to painful stimuli, except for reflex movements
• Irregular breathing
When to see a doctor
Coma is a medical emergency. Seek immediate medical care.
Many types of problems can cause coma. Some examples are:
• Traumatic brain injuries. Traumatic brain injuries, often caused by traffic collisions or acts of violence, are common causes of comas.
• Stroke. Reduced or interrupted blood supply to the brain (stroke), which may be caused by blocked arteries or a burst blood vessel, can result in coma.
• Tumors. Tumors in the brain or brainstem can cause coma.
• Diabetes. In people with diabetes, blood sugar levels that become too high (hyperglycemia) or too low (hypoglycemia) can cause a stroke or coma.
• Lack of oxygen. People who have been rescued from drowning or those who have been resuscitated after a heart attack may not awaken due to lack of oxygen to the brain.
• Infections. Infections such as encephalitis and meningitis cause swelling (inflammation) of the brain, spinal cord or the tissues that surround the brain. Severe cases of these infections can result in brain damage or coma.
• Seizures. Ongoing seizures may lead to coma.
• Toxins. Exposure to toxins, such as carbon monoxide or lead, can cause brain damage and coma.
• Drugs and alcohol. Overdosing on drugs or alcohol can result in coma.
Although many people gradually recover from coma, others enter a vegetative state or die. Some people who recover from a coma may have major or minor disabilities.
Complications may develop during coma, including pressure sores, bladder infections and other problems.
© 1998-2015 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved. Terms of use
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2,948,315,476,669,793,300 | B. Carlsson http://repub.eur.nl/ppl/9253/ List of Publications en http://repub.eur.nl/eur_signature.png http://repub.eur.nl/ RePub, Erasmus University Repository Anti-idiotypic antibodies to poliovirus antibodies in commercial immunoglubulin preparations, human serum and milk. http://repub.eur.nl/pub/3466/ Fri, 01 Jan 1993 00:00:01 GMT <div>M. Hahn-Zoric</div><div>B. Carlsson</div><div>S. Jeansson</div><div>H.P. Ekre</div><div>A.D.M.E. Osterhaus</div><div>D. Roberton</div><div>L.A. Hanson</div> Our previous studies have suggested that fetal antibody production can be induced by maternal antiidiotypic antibodies transferred to the fetus via the placenta. We tested commercial Ig, sera, and milk for the presence of anti-idiotypic antibodies to poliovirus type 1, using affinity chromatography combined with ELISA systems and virus neutralization techniques. Our results indicate that commercial Ig, serum, and milk samples contain antibodies recognizing idiotypic determinants on antibodies to poliovirus. Several lines of evidence support this conclusion. Thus, in an ELISA with poliovirus as a solid phase, binding of specific antibodies could be inhibited by addition of an eluate from the Ig preparation containing anti-idiotypic antibodies against poliovirus type 1. Also, antiidiotypic antibodies from pooled human Ig, serum, and colostrum samples against poliovirus bound directly to solid-phase-attached MAb against poliovirus type 1. In addition, in a competitive inhibition ELISA, where antiidiotypic antibodies isolated from the Ig preparation competed with the poliovirus antigen for binding to monoclonal or polyclonal idiotypic antibodies on the solid phase, inhibition of antigen binding was seen at low antigen concentrations. When single-donor serum or milk was used, this inhibition was even more pronounced and could be demonstrated at almost all antigen concentrations. The finding that anti-idiotypes are present in maternal serum and milk imply, in agreement with our previous studies, that anti-idiotypes may actively induce a specific immune response in the fetus without previous exposure to the antigen by being transferred across the placenta or by being passively transferred to the newborn via mother's milk. Presence of non-maternal antibodies in newborns of mothers with antibody deficiencies. http://repub.eur.nl/pub/3455/ Wed, 01 Jan 1992 00:00:01 GMT <div>M. Hahn-Zoric</div><div>B. Carlsson</div><div>J. Björkander</div><div>A.D.M.E. Osterhaus</div><div>L. Mellander</div><div>L.A. Hanson</div> To explain the mechanism for induction and production of specific antibodies found in the newborn already at birth, without previous known exposure to the antigen, we chose a model that presumably excluded the possibility of specific antibodies being transferred from the mother to the fetus. Specific IgG, IgA, and IgM antibodies against Escherichia coli and poliovirus antigens were determined with ELISA in serum, saliva, and amniotic fluid from hypogammaglobulinemic and IgA-deficient mothers as well as in cord serum, saliva, and meconium from their offspring. All the mothers lacked IgA and some also lacked IgM antibodies, which were found in their healthy newborns. The amniotic fluid from a hypogammaglobulinemic mother lacking IgA contained small amounts of IgA antibodies, which were also found in the neonate, suggesting a fetal origin. There was evidence for the presence of antiidiotypic antibodies to poliovirus in the cord sera. We propose that idiotypic and/or antiidiotypic IgG antibodies transferred via the placenta from the mother to the fetus can initiate specific immune responses seen in the newborn. Thus, it may be that transplacental IgG not only passively protects the newborn, but also actively primes the fetus during fetal life via its content of idiotypic and/or antiidiotypic antibodies. | {
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-6,660,513,075,855,032,000 | Psychiatry InvestigPIPsychiatry Investigation1738-36841976-3026Korean Neuropsychiatric Association20396437284877310.4306/pi.2010.7.1.72Case ReportPsychotic Features as the First Manifestation of 22q11.2 Deletion SyndromeKookSo Dahm1AnSuk Kyoon12KimKyung Ran12KimWoo Jung1LeeEun12NamkoongKee12Department of Psychiatry, Yonsei University College of Medicine, Seoul, Korea.Institute of Behavioral Science in Medicine, Yonsei University College of Medicine, Seoul, Korea. Correspondence: Eun Lee, MD, PhD. Department of Psychiatry, Yonsei University College of Medicine, 250 Seongsan-ro, Seodaemun-gu, Seoul 120-752, Korea. Tel +82-2-2228-1622, Fax +82-2-313-0891, leeeun@yuhs.ac3201019220107172741210200929120103012010Copyright © 2010 Korean Neuropsychiatric Association2010This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
The 22q11.2 deletion is a genetic disorder which is characterized by abnormalities in cardiac functioning, facial structure, neurobehavioral development, T cell functioning, and velopharyngeal insufficiencies. In the presented case study, 22q11.2 deletion was found in a patient who has psychotic symptoms only. A 25-year-old woman with a history of hypoparathyroidism and hypothyroidism presented with auditory hallucinations and persecutory delusions. After three months of treatment with antipsychotic medications, the patient was readmitted with generalized tonic-clonic seizures. The following week, the patient went into sepsis. A fluorescent in situ hybridization (FISH) analysis revealed the presence of a 22q11.2 microdeletion. This case study suggests that psychotic symptoms can develop prior to the typical symptoms of a 22q11.2 deletion. As such, psychiatrists should test for genetic abnormalities in patients with schizophrenia when these patients present with seizures and immunodeficiencies.
22q11.2 deletionSchizophreniaSeizureImmunodeficiencyVelocardiofacial syndrome
Introduction
The 22q11.2 deletion, also called velocardiofacial syndrome, is a genetic disorder which typically involves cardiac anomalies, facial anomalies, learning difficulties, hypocalcemia, and T cell abnormalities. Additionally, patients with 22q11.2 deletions are at higher risk of developing psychiatric disorders than is the general population. One-third of all individuals with 22q11.2 deletion syndrome develop schizophrenia-like psychotic disorders.1,2 However, it is uncommon for the psychotic symptoms to present as the initial manifestation of a 22q11.2 deletion. As such, genetic abnormalities are generally unsuspected among patients presenting with psychosis, but without velocardiofacial anomalies. A case report of a patient diagnosed with schizophrenia which was later confirmed to be the result of a 22q11.2 deletion is provided.
Case
A 25-year-old female patient was admitted to the psychiatric ward due to auditory hallucinations. Eight months prior to the patient's admittance to the psychiatric ward, she experienced intermittent auditory hallucinations in the form of her ex-boyfriend's voice saying that he would kill her. During the month prior to her admittance to the psychiatric ward, the auditory hallucinations increased in severity and frequency, and the patient developed persecutory delusions. Additionally, the patient came to believe that she had been raped by her boyfriend. The patient also quit her job and withdrew from all social relationships.
The patient had no history or family history of psychiatric problems. The patient had been diagnosed with hypothyroidism and hypoparathyroidism at the age of ten and was being treated with synthyroid and alfacalcidol. The patient's pediatric endocrinologist regularly assessed her thyroid and parathyroid function. After graduating from college, the patient was successfully employed and was maintaining social relationships. Two years prior to the patient's admittance to the hospital, she broke up with her boyfriend.
Upon admittance to the psychiatric ward, the patient was hospitalized for 20 days, during which she was treated with a daily dose of 8 mg of risperidone. During this hospitalization, the patient was diagnosed with schizophrenia. The patient reported that she was no longer having auditory hallucinations 3 weeks after her admission. A computerized tomography (CT) scan of the patient's brain revealed an asymmetric calcification in the bilateral basal ganglia; however, the patient had no history of neurological disorders, including seizures. Additionally, the patient complained of abdominal distension following discharge from the hospital. An abdominal CT scan revealed multiple mesenteric lymphadenopathy; however, the esophagogastroduodenoscopy and colonoscopy results were normal. The patient underwent screening tests for autoimmune diseases including antinuclear antibodies test, anti-deoxyribonucleic acid test, perinuclear anti-neutrophil cytoplasmic antibodies test, and a cytoplasmic anti-neutrophil cytoplasmic antibodies test, the results of which were all negative. Echocardiography and electrocardiography were also free of abnormalities. The patient's internist recommended a biopsy for abdominal lymphadenopathy; however, the patient refused.
Two months following the patient's initial discharge from the psychiatric ward, the patient was rehospitalized due to the experience of generalized tonic-clonic seizures. A serum chemistry analysis showed normal calcium levels, and a brain CT showed no interval changes compared with the previous scan. The anticonvulsant, lamotrigine, was prescribed, and quetiapine was used in place of the risperidone following the confirmation of seizures with an electro-encephalogram. A week following the rehospitalization, the seizures had ceased; however, the patient developed a fever. The fever subsided after one week and then developed again, resulting in septic shock. No fever focus was found despite various examinations and tests. A T cell test was performed and revealed a decrease in the total T cell count and a deficiency in CD8 cells. A 22q11.2 microdeletion was confirmed by a fluorescent in situ hybridization analysis (Figure 1).
Discussion
In this patient, psychotic symptoms preceded the other symptoms of 22q11.2 deletion syndrome. Patients with 22q11.2 deletion syndrome generally have recurrent infections, as well as endocrine and neuropsychiatric abnormalities.3 However, it is uncommon for psychotic features to be the first manifestation of 22q11.2 microdeletion. Additionally, the patient's history of hypoparathyroidism was not indicative of genetic abnormalities. Several studies have reported higher rates of psychotic disorders among patients with a 22q11.2 deletion than in the general population.1,2 Psychotic symptoms typically begin in late adolescence and adulthood. The prevalence rate for psychosis among individuals with the 22q11.2 deletion is approximately 30%,1,2,4 and schizophrenia has been described as a behavioral phenotype of a 22q11.2 deletion.5 However, prevalence of a 22q11.2 deletion among patients with schizophrenia is unclear. Some investigators6-8 have reported greater than 2% prevalence for 22q11.2 deletions among patients with schizophrenia, while other investigators report a less than 1% prevalence rate.9-12 One study12 reported that no 22q11.2 deletions were detected in the approximately 300 patients with schizophrenia who were screened for the study, and other studies9,10 have reported that only one of approximately 300 patients showed a 22q11.2 deletion.
The biological mechanisms which are responsible for the development of psychotic features in patients with a 22q11.2 deletion have not been fully investigated. Catechol-o-methyltransferase is a potential cause of psychotic symptoms,6 which was not replicated in the 22q11.2 deleted patients with schizophrenia or in schizophrenic patients. The PRODH and GNB1L genes are other candidates which may be associated with the development of schizophrenia in patients with 22q11.2 deletion syndrome.13
In the present case, the patient was diagnosed with schizophrenia with well-controlled hypocalcemia. In spite of the patient's history of hypoparathyroidism and abdominal lymphadenopathies, she did not have facial anomalies or cardiac malformations. Additionally, the patient displayed appropriate levels of social functioning prior to the onset of the psychotic symptoms. Additional clinical findings, including seizures, frequent urinary tract infections, and recurrent septicemia, were inconsistent with a diagnosis of a 22q11.2 genetic abnormality.
It is difficult to determine whether the patient's seizures were caused by risperidone. However, it is known that the patient's first seizure occurred following treatment with antipsychotic medication. It is also possible that the seizure was a manifestation of the 22q11.2 deletion syndrome. Several case reports have presented seizures as a manifestation of 22q11.2 deletions.14,15 Additionally, it is known that antipsychotic medications may lower the seizure threshold; however, the possibility of developing seizures associated with risperidone is relatively low.16,17 The patient also had calcifications in the basal ganglia, and, as such, the antipsychotic may have further decreased the seizure threshold.
This case reveals that psychotic symptoms may serve as the initial manifestation of 22q11.2 deletion syndrome. It is uncommon for a patient with a 22q11.2 deletion to show no velocardiofacial anomalies, especially in Korea.18 As such, psychiatrists should test for genetic abnormalities among patients with schizophrenia when these patients also present with seizures and immunodeficiencies.
PulverAENestadtGGoldbergRShprintzenRJLamaczMWolyniecPSPsychotic illness in patients diagnosed with velo-cardio-facial syndrome and their relativesJ Nerv Ment Dis19941824764788040660MurphyKCJonesLAOwenMJHigh rates of schizophrenia in adults with velo-cardio-facial syndromeArch Gen Psychiatry19995694094510530637RoubertieASemprinoMChazeAMRivierFHumbertclaudeVCheminalRNeurological presentation of three patients with 22q 11 deletion (CATCH 22 syndrome)Brain Dev20012381081411720799ShprintzenRJGoldbergRGolding-KushnerKJMarionRWLate-onset psychosis in the velo-cardio-facial syndromeAm J Med Genet1992421411421308357GothelfDSchaerMEliezSGenes, brain development and psychiatric phenotypes in velo-cardio-facial syndromeDev Disabil Res Rev200814596818636637KarayiorgouMMorrisMAMorrowBShprintzenRJGoldbergRBorrowJSchizophrenia susceptibility associated with interstitial deletions of chromosome 22q11Proc Natl Acad Sci U S A199592761276167644464WiehahnGJBoschGPdu PreezRRPretoriusHWKarayiorgouMRoosJLAssessment of the frequency of the 22q11 deletion in Afrikaner schizophrenic patientsAm J Med Genet B Neuropsychiatr Genet2004129B202215274032SpornAAddingtonAReissALDeanMGogtayNPotocnikU22q11 deletion syndrome in childhood onset schizophrenia: an updateMol Psychiatry2004922522614699434ArinamiTOhtsukiTTakaseKShimizuHYoshikawaTHorigomeHScreening for 22q11 deletions in a schizophrenia populationSchizophr Res20015216717011705710IvanovDKirovGNortonNWilliamsHJWilliamsNMNikolovIChromosome 22q11 deletions, velo-cardio-facial syndrome and early-onset psychosis. Molecular genetic studyBr J Psychiatry200318340941314594915HorowitzAShifmanSRivlinNPisantéADarvasiAA survey of the 22q11 microdeletion in a large cohort of schizophrenia patientsSchizophr Res20057326326715653270HoogendoornMLVorstmanJAJalaliGRSeltenJPSinkeRJEmanuelBSPrevalence of 22q11.2 deletions in 311 Dutch patients with schizophreniaSchizophr Res200898848817964762PrasadSEHowleySMurphyKCCandidate genes and the behavioral phenotype in 22q11.2 deletion syndromeDev Disabil Res Rev200814263418636634KaoAMarianiJMcDonald-McGinnDMMaisenbacherMKBrooks-KayalARZackaiEHIncreased prevalence of unprovoked seizures in patients with a 22q11.2 deletionAm J Med Genet A2004129A293415266612TonelliARKosuriKWeiSChickDSeizures as the first manifestation of chromosome 22q11.2 deletion syndrome in a 40-year old man: a case reportJ Med Case Reports2007116718053182PisaniFOteriGCostaCDi RaimondoGDi PerriREffects of psychotropic drugs on seizure thresholdDrug Saf2002259111011888352Gonzalez-HeydrichJPandinaGJFleisherCAHsinORachesDBourgeoisBFNo seizure exacerbation from risperidone in youth with comorbid epilepsy and psychiatric disorders: a case seriesJ Child Adolesc Psychopharmacol20041429531015319026BhangSYKimCYJooYHSeuEJRyuHEA case report of schizophrenia patient with 22q11 deletion syndromeJ Korean Neuropsychiatr Assoc200342528531
Result of fluorescent in situ hybridization analysis using a HIRA probe (110 kb). Chromosome 22q13 was labeled in green as a control. An orange signal indicates a locus at 22q11.2. There's only one orange signal. The absence of orange signal indicates of the deletion of the HIRA locus at 22q11.2. HIRA: histone cell cycle regulation defective homolog A. | {
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