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[DCTN4] as a modifier of [chronic Pseudomonas aeruginosa infection] in [cystic fibrosis]
[Pseudomonas aeruginosa (Pa) infection] in [cystic fibrosis] ([CF]) patients is associated with worse long-term [pulmonary disease] and shorter survival, and [chronic Pa infection] ([CPA]) is associated with reduced lung function, [faster rate of lung decline], increased rates of [exacerbations] and shorter survival. By using [exome sequencing] and extreme phenotype design, it was recently shown that [isoforms] of [dynactin 4] ([DCTN4]) may influence [Pa infection] in [CF], leading to worse [respiratory disease]. The purpose of this [study] was to investigate the role of [DCTN4] missense [variants] on [Pa infection] incidence, age at first [Pa infection] and [chronic Pa infection] incidence in a [cohort] of adult [CF] patients from a single [centre]. [Polymerase chain reaction] and [direct sequencing] were used to screen [DNA samples] for [DCTN4] [variants]. A total of 121 adult [CF] patients from the [Cochin Hospital CF centre] have been included, all of them carrying two [CFTR] defects: 103 developed at least 1 [pulmonary infection] with [Pa], and 68 patients of them had [CPA]. [DCTN4] [variants] were identified in 24% (29/121) [CF] patients with [Pa infection] and in only 17% (3/18) [CF] patients with no [Pa infection]. Of the patients with [CPA], 29% (20/68) had [DCTN4] missense [variants] vs 23% (8/35) in patients without [CPA]. Interestingly, [p.Tyr263Cys] tend to be more frequently observed in [CF] patients with [CPA] than in patients without [CPA] (4/68 vs 0/35), and [DCTN4] missense [variants] tend to be more frequent in male [CF] patients with [CPA] bearing two [class II mutations] than in male [CF] patients without [CPA] bearing two [class II mutations] (P = 0.06). Our observations reinforce that [DCTN4] missense [variants], especially [p.Tyr263Cys], may be involved in the [pathogenesis] of [CPA] in male [CF].
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[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[chronic Pseudomonas aeruginosa infection]{Disorders} is Infection Pseudomonas aeruginosa
[cystic fibrosis]{Disorders} is Cystic Fibrosis
[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[Pseudomonas aeruginosa (Pa) infection]{Disorders} is Infection Pseudomonas aeruginosa
[chronic Pseudomonas aeruginosa infection]{Disorders} is Infection Pseudomonas aeruginosa
[cystic fibrosis]{Disorders} is Cystic Fibrosis
[CF]{Disorders} is Cystic Fibrosis
[cystic fibrosis]{Disorders} is Cystic Fibrosis
[pulmonary disease]{Disorders} is Pulmonary disease
[chronic Pa infection]{Disorders} is Infection Pseudomonas aeruginosa
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[faster rate of lung decline]{Disorders} is LUNG FUNCTION, ACCELERATED RATE OF DECLINE IN, SMOKING-RELATED
[exacerbations]{Disorders} is Exacerbation
[exome sequencing]{Procedures} is Exome Sequencing
[isoforms]{Chemicals & Drugs} is Isoforms
[dynactin 4]{Chemicals & Drugs} is DCTN4 protein, human
[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[Pa infection]{Disorders} is Infection Pseudomonas aeruginosa
[CF]{Disorders} is Cystic Fibrosis
[respiratory disease]{Disorders} is Respiratory disease
[study]{Procedures} is Study
[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[variants]{Chemicals & Drugs} is Isoforms
[Pa infection]{Disorders} is Infection Pseudomonas aeruginosa
[Pa infection]{Disorders} is Infection Pseudomonas aeruginosa
[chronic Pa infection]{Disorders} is Infection Pseudomonas aeruginosa
[cohort]{Living Beings} is Cohort
[CF]{Disorders} is Cystic Fibrosis
[centre]{Organizations} is Health centre
[Polymerase chain reaction]{Procedures} is Polymerase Chain Reaction
[direct sequencing]{Procedures} is Direct Sequencing
[DNA samples]{Anatomy} is DNA - Deoxyribonucleic acid sample
[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[variants]{Chemicals & Drugs} is Isoforms
[CF]{Disorders} is Cystic Fibrosis
[Cochin Hospital CF centre]{Organizations} is Hospital
[CFTR]{Genes & Molecular Sequences} is CFTR
[pulmonary infection]{Disorders} is Pulmonary infection
[Pa]{Living Beings} is Bacillus aeruginosus
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[variants]{Chemicals & Drugs} is Isoforms
[CF]{Disorders} is Cystic Fibrosis
[Pa infection]{Disorders} is Infection Pseudomonas aeruginosa
[CF]{Disorders} is Cystic Fibrosis
[Pa infection]{Disorders} is Infection Pseudomonas aeruginosa
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[variants]{Chemicals & Drugs} is Isoforms
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[p.Tyr263Cys]{Chemicals & Drugs} is Isoforms
[CF]{Disorders} is Cystic Fibrosis
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[variants]{Chemicals & Drugs} is Isoforms
[CF]{Disorders} is Cystic Fibrosis
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[class II mutations]{Physiology} is Mutations
[CF]{Disorders} is Cystic Fibrosis
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[class II mutations]{Physiology} is Mutations
[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human
[variants]{Chemicals & Drugs} is Isoforms
[p.Tyr263Cys]{Chemicals & Drugs} is Isoforms
[pathogenesis]{Disorders} is Pathogenesis
[CPA]{Disorders} is Infection Pseudomonas aeruginosa
[CF]{Disorders} is Cystic Fibrosis
|
Prevascularized [silicon] membranes for the enhancement of transport to [implanted medical devices]
Recent advances in [drug delivery] and sensing devices for [in situ] [applications] are limited by the diffusion -limiting [foreign body response] of fibrous encapsulation. In this study, we fabricated prevascularized synthetic device ports to help mitigate this limitation. Membranes with rectilinear arrays of [square] pores with widths ranging from 40 to 200 μm were created using materials (50 μm thick double-sided [polished silicon]) and processes (photolithography and directed reactive ion etching) common in the manufacturing of microfabricated sensors. [Vascular endothelial cells] responded to membrane geometry by either forming [vascular tubes] that [extended] through the pore or completely filling membrane pores after 4 days in culture. Although tube formation began to predominate [overgrowth] around 75 μm and continued to increase at even larger pore sizes, tubes formed at these large pore sizes were not completely [round] and had relatively thin [walls]. Thus, the optimum range of pore size for prevascularization of these membranes was estimated to be 75-100 μm. This [study] lays the foundation for creating a prevascularized port that can be used to reduce fibrous encapsulation and thus enhance diffusion to [implanted medical devices] and sensors. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1602-1609, 2016.
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[silicon]{Chemicals & Drugs} is Silicones
[implanted medical devices]{Disorders} is Implanted Medical Device
[silicon]{Chemicals & Drugs} is Silicones
[drug delivery]{Devices} is Drug Delivery
[in situ]{Concepts & Ideas} is In Situ
[applications]{Procedures} is Application
[implanted medical devices]{Disorders} is Implanted Medical Device
[foreign body response]{Disorders} is Host Tissue Response To Foreign Body
[square]{Concepts & Ideas} is Square
[polished silicon]{Chemicals & Drugs} is Silicones
[Vascular endothelial cells]{Anatomy} is Vascular Endothelial Cells
[vascular tubes]{Anatomy} is Vascular structure
[extended]{Concepts & Ideas} is Extended
[overgrowth]{Disorders} is Overgrowth
[round]{Concepts & Ideas} is Round
[walls]{Concepts & Ideas} is Wall structure
[study]{Procedures} is Study
[implanted medical devices]{Disorders} is Implanted Medical Device
|
[Seated] maximum [flexion]: An alternative to [standing] maximum [flexion] for determining presence of [flexion] - relaxation?
The [flexion] - relaxation phenomenon (FRP) in [standing] is a specific and sensitive [diagnostic tool] for [low back pain]. [Seated flexion] as an alternative could be beneficial for certain [populations], yet the behavior of the [trunk extensors] during [seated] maximum [flexion] compared to [standing] [flexion] remains unclear. Compare FRP occurrences and [spine] [angles] between [seated] and [standing] [flexion] postures in three levels of the [erector spinae muscles]. Thirty-one [participants] free of [back pain] performed [seated] and [standing] maximum [trunk] [flexion]. Electromyographical signals were recorded from the [bilateral lumbar (L3)], [lower-thoracic (T9)], and [upper-thoracic (T4)] [erector spinae] and assessed for the occurrence of FRP. [Spine angles] corresponding to FRP onset and cessation were determined, and FRP occurrences and [angles] were compared between posture and [muscle]. FRP occurrence was similar in [standing] and [seated] maximum [flexion] across all [muscles], with the [lumbar muscles] showing the greatest consistency. [Standing] FRP onset and cessation angles were consistently greater than the corresponding [seated] FRP angles. Considering the similar number of FRP occurrences, [seated] maximum [flexion] may constitute an objective criterion for [low back pain] [diagnosis]. Future work should seek to confirm the utility of this test in [individuals] with [low back pain].
|
[Seated]{Disorders} is Seated
[flexion]{Physiology} is Flexion
[standing]{Concepts & Ideas} is Standing
[flexion]{Physiology} is Flexion
[flexion]{Physiology} is Flexion
[Seated]{Disorders} is Seated
[flexion]{Physiology} is Flexion
[flexion]{Physiology} is Flexion
[standing]{Concepts & Ideas} is Standing
[standing]{Concepts & Ideas} is Standing
[flexion]{Physiology} is Flexion
[diagnostic tool]{Procedures} is Diagnostic Method
[flexion]{Physiology} is Flexion
[low back pain]{Disorders} is Low back pain
[Seated flexion]{Physiology} is Flexion
[populations]{Living Beings} is Population
[trunk extensors]{Anatomy} is Muscle tissue (body structure)
[seated]{Disorders} is Seated
[flexion]{Physiology} is Flexion
[standing]{Concepts & Ideas} is Standing
[flexion]{Physiology} is Flexion
[spine]{Anatomy} is Dorsal spine
[angles]{Concepts & Ideas} is Angle
[seated]{Disorders} is Seated
[standing]{Concepts & Ideas} is Standing
[flexion]{Physiology} is Flexion
[erector spinae muscles]{Anatomy} is Erector spinae muscle
[participants]{Living Beings} is Participant
[back pain]{Disorders} is Pain back
[seated]{Disorders} is Seated
[standing]{Concepts & Ideas} is Standing
[trunk]{Anatomy} is TRUNK
[flexion]{Physiology} is Flexion
[bilateral lumbar (L3)]{Anatomy} is Third lumbar vertebra
[lower-thoracic (T9)]{Anatomy} is Ninth thoracic vertebra
[upper-thoracic (T4)]{Anatomy} is T4 part of thoracic duct
[erector spinae]{Anatomy} is Erector spinae muscle
[Spine angles]{Concepts & Ideas} is Angle
[angles]{Concepts & Ideas} is Angle
[muscle]{Anatomy} is Muscle tissue (body structure)
[standing]{Concepts & Ideas} is Standing
[seated]{Disorders} is Seated
[flexion]{Physiology} is Flexion
[muscles]{Anatomy} is Muscle tissue (body structure)
[lumbar muscles]{Anatomy} is Muscle tissue (body structure)
[Standing]{Concepts & Ideas} is Standing
[seated]{Disorders} is Seated
[seated]{Disorders} is Seated
[flexion]{Physiology} is Flexion
[low back pain]{Disorders} is Low back pain
[diagnosis]{Disorders} is Diagnosis
[individuals]{Living Beings} is Persons
[low back pain]{Disorders} is Low back pain
|
The Relationship Between Distance and [Post-operative] Visit Attendance Following Medical [Male Circumcision] in [Nyanza Province], [Kenya]
To date, there is no [research] on voluntary medical [male circumcision] ([VMMC]) [catchment areas] or the relationship between distance to a [VMMC] [facility] and attendance at a [post-operative] [follow-up visit]. We [analyzed] data from a randomly selected [subset] of [males] [self-seeking circumcision] at one of 16 participating [facilities] in [Nyanza Province], [Kenya] between 2008 and 2010. Among 1437 [participants], 46.7 % attended [follow-up]. The [median] distance from [residence] to utilized [facility] was 2.98 km (IQR 1.31-5.38). Nearly all [participants] (98.8 %) lived within 5 km from a [facility], however, 26.3 % visited a [facility] more than 5 km away. Stratified results demonstrated that among those utilizing fixed [facilities], greater distance was associated with higher odds of [follow-up] non-attendance (OR 5.01-10km vs. 0-1km = 1.71, 95 % CI 1.08, 2.70, p = 0.02; OR >10km vs. 0-1 km = 2.80, 95 % CI 1.26, 6.21, p = 0.01), adjusting for age and district of [residence]. We found 5 km marked the threshold distance beyond which [follow-up] attendance significantly dropped. These results demonstrate distance is an important predictor of attending [follow-up], and this relationship appears to be modified by [facility] type.
|
[Post-operative]{Disorders} is Post operative (finding)
[Male Circumcision]{Procedures} is Male Circumcision
[Nyanza Province]{Geographic Areas} is Province
[Kenya]{Geographic Areas} is Kenya
[research]{Procedures} is Research
[Post-operative]{Disorders} is Post operative (finding)
[male circumcision]{Procedures} is Male Circumcision
[VMMC]{Procedures} is Male Circumcision
[catchment areas]{Geographic Areas} is Catchment Area
[Male Circumcision]{Procedures} is Male Circumcision
[Nyanza Province]{Geographic Areas} is Province
[Kenya]{Geographic Areas} is Kenya
[VMMC]{Procedures} is Male Circumcision
[facility]{Organizations} is Health Facility
[post-operative]{Disorders} is Post operative (finding)
[follow-up visit]{Procedures} is Follow-up visit
[analyzed]{Procedures} is Analyzed
[subset]{Concepts & Ideas} is Subset
[males]{Living Beings} is Human, Male
[self-seeking circumcision]{Procedures} is Male Circumcision
[facilities]{Organizations} is Health Facility
[Nyanza Province]{Geographic Areas} is Province
[Kenya]{Geographic Areas} is Kenya
[participants]{Living Beings} is Participant
[follow-up]{Procedures} is Follow-up
[median]{Concepts & Ideas} is Median
[residence]{Concepts & Ideas} is Residence
[facility]{Organizations} is Health Facility
[participants]{Living Beings} is Participant
[facility]{Organizations} is Health Facility
[facility]{Organizations} is Health Facility
[facilities]{Organizations} is Health Facility
[follow-up]{Procedures} is Follow-up
[residence]{Concepts & Ideas} is Residence
[follow-up]{Procedures} is Follow-up
[follow-up]{Procedures} is Follow-up
[facility]{Organizations} is Health Facility
|
Promoting lifestyle behaviour change and [well-being] in hospital patients: a [pilot study] of an evidence-based psychological [intervention]
Lifestyle risk behaviours show an inverse social gradient, clustering in [vulnerable groups]. We designed and piloted an [intervention] to address barriers to lifestyle behaviour change among hospital patients. We designed our [intervention] using effective components of behaviour change [interventions] informed by [psychological theory]. Delivered by a [health psychologist] based at the Royal Free London NHS Foundation Trust, the 4-week [intervention] included detailed [baseline assessment], personalized [goal setting], psychological skills development, [motivation support] and [referral to] [community services]. Primary outcomes were feasibility and patient acceptability. We also evaluated changes to health and [well-being]. From 1 July 2013 to 31 September 2014, 686 patients were referred, 338 (49.3%) attended a first appointment and 172 (25.1%) completed [follow-up]. Furthermore, 72.1% of attenders were female with the median age 55 years and poor self-reported baseline health. After 4 weeks, [self-efficacy], health and well-being scores [significantly improved]: 63% of lifestyle goals and 89% of health management [goals] were fully [achieved]; 58% of [referrals to] [community] lifestyle behaviour change services and 79% of referrals to other [services] (e.g. [Citizen's Advice Bureau]) were accepted; 99% were [satisfied] / very satisfied with the [service]. Our [hospital-based intervention] was feasible, acceptable and showed [preliminary health and well-being gains].
|
[well-being]{Disorders} is Mental well-being
[pilot study]{Procedures} is Pilot Study
[intervention]{Procedures} is Interventional
[well-being]{Disorders} is Mental well-being
[vulnerable groups]{Living Beings} is Population Groups
[pilot study]{Procedures} is Pilot Study
[intervention]{Procedures} is Interventional
[intervention]{Procedures} is Interventional
[intervention]{Procedures} is Interventional
[interventions]{Procedures} is Interventional
[psychological theory]{Concepts & Ideas} is Psychological Theory
[health psychologist]{Living Beings} is Health psychologist
[intervention]{Procedures} is Interventional
[baseline assessment]{Procedures} is Baseline behavioral assessment
[goal setting]{Procedures} is Goal setting
[motivation support]{Procedures} is Emotional support
[referral to]{Procedures} is Referral to
[community services]{Organizations} is Community Services
[well-being]{Disorders} is Mental well-being
[follow-up]{Procedures} is Follow-up
[self-efficacy]{Physiology} is Self-Efficacy
[significantly improved]{Disorders} is Improved
[goals]{Concepts & Ideas} is Goals
[achieved]{Disorders} is Goal achieved
[referrals to]{Procedures} is Referral to
[community]{Organizations} is Community Services
[services]{Procedures} is Health Services
[Citizen's Advice Bureau]{Living Beings} is Organizational
[satisfied]{Concepts & Ideas} is Satisfied
[service]{Procedures} is Health Services
[hospital-based intervention]{Procedures} is Interventional
[preliminary health and well-being gains]{Disorders} is Finding (finding)
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Combining electrostatic powder with an [insecticide]: effect on stored - product [beetles] and on the [commodity]
The opportunity to reduce the amount of [pirimiphos-methyl] applied to [grain] by formulating it in an electrostatic powder was investigated. The [insecticidal] efficacy of [pirimiphos-methyl] in [EC formulation] or formulated using electrostatic powder (EP) as an inert carrier was investigated against [Sitophilus oryzae] (L.), [Oryzaephilus surinamensis] (L.), [Rhyzopertha dominica] (F.) and [Tribolium confusum Jacquelin du Val]. Furthermore, the adhesive properties of EP to [rice], [corn] and [wheat], together with the effect on bulk density and [bread] - and [pasta] - making properties, were investigated. The results showed that [pirimiphos-methyl] formulated with EP provided better efficacy against [adults] when compared with [EC formulation] for [O. surinamensis] and [T. confusum], but there was no difference for [R. dominica]. Progeny production was consistently lower in [grain] [treated with] the EP formulation than in [grain] [treated with] the [EC]. Tests showed that EP adhered to the [kernels] for longer on hard [wheat] than on [maize] or [rice]. In most [commodities], EP did not alter the bulk density. Finally, the addition of EP did not affect [flour] - and [bread] - making properties, nor the [pasta] -making properties. The results of the present study suggest that an EP could be used to reduce the amount of [pirimiphos-methyl] applied to [grain] for effective pest control, with no detrimental effects on [grain] quality. © 2016 Society of Chemical Industry.
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[insecticide]{Chemicals & Drugs} is Insecticide
[beetles]{Living Beings} is Beetles
[commodity]{Objects} is Uncooked Foods
[insecticide]{Chemicals & Drugs} is Insecticide
[pirimiphos-methyl]{Chemicals & Drugs} is Pirimiphosmethyl
[grain]{Objects} is Cereal Grain
[beetles]{Living Beings} is Beetles
[commodity]{Objects} is Uncooked Foods
[insecticidal]{Chemicals & Drugs} is Insecticide
[pirimiphos-methyl]{Chemicals & Drugs} is Pirimiphosmethyl
[EC formulation]{Chemicals & Drugs} is Insecticide
[Sitophilus oryzae]{Living Beings} is Sitophilus oryzae
[Oryzaephilus surinamensis]{Living Beings} is Oryzaephilus surinamensis
[Rhyzopertha dominica]{Living Beings} is Rhyzopertha dominica
[Tribolium confusum Jacquelin du Val]{Living Beings} is Tribolium confusum
[rice]{Objects} is Rice
[corn]{Objects} is Corn
[wheat]{Objects} is Wheat
[bread]{Objects} is Bread
[pasta]{Objects} is Pasta
[pirimiphos-methyl]{Chemicals & Drugs} is Pirimiphosmethyl
[adults]{Living Beings} is Adult insect
[EC formulation]{Chemicals & Drugs} is Insecticide
[O. surinamensis]{Living Beings} is Oryzaephilus surinamensis
[T. confusum]{Living Beings} is Tribolium confusum
[R. dominica]{Living Beings} is Rhyzopertha dominica
[grain]{Objects} is Cereal Grain
[treated with]{Procedures} is Treated with
[grain]{Objects} is Cereal Grain
[treated with]{Procedures} is Treated with
[EC]{Chemicals & Drugs} is Insecticide
[kernels]{Objects} is Food or Food Substance
[wheat]{Objects} is Wheat
[maize]{Objects} is Corn
[rice]{Objects} is Rice
[commodities]{Objects} is Uncooked Foods
[flour]{Objects} is Flour
[bread]{Objects} is Bread
[pasta]{Objects} is Pasta
[pirimiphos-methyl]{Chemicals & Drugs} is Pirimiphosmethyl
[grain]{Objects} is Cereal Grain
[grain]{Objects} is Cereal Grain
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[Radiofrequency ablation] of [posteroseptal accessory pathways] associated with [coronary sinus diverticula]
[Posteroseptal accessory pathways] may be associated with a [coronary sinus (CS) diverticulum]. Our purpose was to describe the clinical characteristics, mapping and [ablation of these pathways]. This was a [retrospective study] of all patients who underwent [ablation] of [posteroseptal accessory pathways] in a [single centre]. Patients with a [diverticulum of the CS] or one of its tributaries were included in group I, while the other patients formed group II. Clinical presentation, [ablation procedure] and outcome were compared between the two groups. A total of 51 patients were included, 16 in group I and 35 in group II. There were no significant differences in age or sex distribution. [Atrial fibrillation] ([AF]) and previous unsuccessful [ablation] were more common in group I. A [negative] [delta wave] in lead II was the [ECG] [finding] with best sensitivity and specificity for the presence of a [diverticulum]. A [pathway] potential was common at the successful [site] in group I, and the interval between local ventricular electrogram and [delta wave] onset was shorter (19.5 ± 8 vs 33.1 ± 7.6 ms, p < 0.001). There was a trend toward lower procedural success rate and higher recurrence rate in group I, although this was not significant. [CS diverticula] should be suspected in patients with manifest [posteroseptal accessory pathways] who have a previous failed [ablation], documented [AF] or typical [electrocardiographic signs]. A discrete potential is frequently seen at the successful site, but the local ventricular electrogram is not as early as in other [accessory pathways].
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[Radiofrequency ablation]{Procedures} is Radiofrequency ablation
[posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway
[coronary sinus diverticula]{Disorders} is Coronary sinus diverticulum
[Radiofrequency ablation]{Procedures} is Radiofrequency ablation
[Posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway
[posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway
[coronary sinus (CS) diverticulum]{Disorders} is Coronary sinus diverticulum
[coronary sinus diverticula]{Disorders} is Coronary sinus diverticulum
[ablation of these pathways]{Procedures} is ABLATION, ACCESSORY PATHWAYS
[retrospective study]{Procedures} is Retrospective Study
[ablation]{Procedures} is Ablation
[posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway
[single centre]{Concepts & Ideas} is Centre
[diverticulum of the CS]{Disorders} is Coronary sinus diverticulum
[ablation procedure]{Procedures} is Ablation
[Atrial fibrillation]{Disorders} is Fibrillation atrial
[AF]{Disorders} is Fibrillation atrial
[ablation]{Procedures} is Ablation
[negative]{Disorders} is Negative for
[delta wave]{Disorders} is Delta Wave
[ECG]{Procedures} is Electrocardiography NOS (procedure)
[finding]{Disorders} is Finding (finding)
[diverticulum]{Disorders} is Diverticulum
[pathway]{Anatomy} is Posteroseptal accessory pathway
[site]{Concepts & Ideas} is Sites
[delta wave]{Disorders} is Delta Wave
[CS diverticula]{Disorders} is Coronary sinus diverticulum
[posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway
[ablation]{Procedures} is Ablation
[AF]{Disorders} is Fibrillation atrial
[electrocardiographic signs]{Disorders} is Electrocardiographic Finding
[accessory pathways]{Anatomy} is Accessory pathway
|
Association of [RBP4] levels with increased [arterial stiffness] in adolescents with [family history of type 2 diabetes]
The aim of this [study] was to explore the impact of [family history of type 2 diabetes] ([FH2D]) on [arterial stiffness] in young [people] and its relationship to [adipocytokines]. This [case-control study] included 52 adolescents (male / female 28/24) with [FH2D] ([FH2D+]) and 40 adolescents (male / female 21/19) without [FH2D] ([FH2D-]). Anthropometric measurements, including height, weight, [waist circumference] ([WC]), and [blood pressure], were obtained. [Blood samples] were collected, [fasting plasma glucose] ([FPG]), [serum lipids], [Retinol Binding Protein 4] ([RBP4]), [C reactive protein] ([CRP]), [adiponectin] and [visfatin] were examined. Brachial-ankle pulse wave velocity (baPWV) was used to evaluate [arterial stiffness]. Visceral fat area (VFA) was measured by [computerized tomography]. Compared with [FH2D-] [group], [FH2D+] [group] had a significantly higher oral glucose tolerance test (OGTT) 2-hour insulin, [RBP4] and baPWV levels, a lower [adiponectin] and glucose infusing rate (GIR) (P<0.05). BaPWV was positively correlated with age, [systolic blood pressure] ([SBP]), [diastolic blood pressure] ([DBP]), 2-hour (OGTT) insulin, [RBP4], and VFA, and negatively correlated with GIR in [FH2D+] [group]. After multivariate analysis, age, [SBP], [RBP4] and VFA maintained an independent association with baPWV in [FH2D+] [group] (P<0.05), while only age, [SBP], and VFA were independent predictors of baPWV in [FH2D-] [group] (P<0.05). These [findings] led to the conclusion that [RBP4] level was associated with increased [arterial stiffness] in young [subjects] with [family history of type 2 diabetes].
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[RBP4]{Chemicals & Drugs} is RBP4 protein, human
[arterial stiffness]{Physiology} is Arterial Stiffness
[family history of type 2 diabetes]{Disorders} is Family history of diabetes mellitus type 2
[RBP4]{Chemicals & Drugs} is RBP4 protein, human
[study]{Procedures} is Study
[arterial stiffness]{Physiology} is Arterial Stiffness
[family history of type 2 diabetes]{Disorders} is Family history of diabetes mellitus type 2
[family history of type 2 diabetes]{Disorders} is Family history of diabetes mellitus type 2
[FH2D]{Disorders} is Family history of diabetes mellitus type 2
[arterial stiffness]{Physiology} is Arterial Stiffness
[people]{Living Beings} is People
[adipocytokines]{Chemicals & Drugs} is Adipocytokine
[case-control study]{Procedures} is Case-control study
[FH2D]{Disorders} is Family history of diabetes mellitus type 2
[FH2D+]{Disorders} is Family history of diabetes mellitus type 2
[FH2D]{Disorders} is Family history of diabetes mellitus type 2
[FH2D-]{Disorders} is NEGATIVE
[waist circumference]{Physiology} is Waist Circumference
[WC]{Physiology} is Waist Circumference
[blood pressure]{Physiology} is Blood pressure
[Blood samples]{Anatomy} is Blood sample
[fasting plasma glucose]{Procedures} is Plasma fasting glucose level
[FPG]{Procedures} is Plasma fasting glucose level
[serum lipids]{Procedures} is Serum lipids
[Retinol Binding Protein 4]{Chemicals & Drugs} is RBP4 protein, human
[RBP4]{Chemicals & Drugs} is RBP4 protein, human
[C reactive protein]{Procedures} is C Reactive Protein
[CRP]{Procedures} is C Reactive Protein
[adiponectin]{Procedures} is Adiponectin
[visfatin]{Chemicals & Drugs} is NAMPT Protein
[arterial stiffness]{Physiology} is Arterial Stiffness
[computerized tomography]{Procedures} is Computerized tomography
[FH2D-]{Disorders} is NEGATIVE
[group]{Living Beings} is Population Group
[FH2D+]{Disorders} is Family history of diabetes mellitus type 2
[group]{Living Beings} is Population Group
[RBP4]{Chemicals & Drugs} is RBP4 protein, human
[adiponectin]{Procedures} is Adiponectin
[systolic blood pressure]{Physiology} is Systolic Blood Pressure
[SBP]{Physiology} is Systolic Blood Pressure
[diastolic blood pressure]{Physiology} is Diastolic Blood Pressure
[DBP]{Physiology} is Diastolic Blood Pressure
[RBP4]{Chemicals & Drugs} is RBP4 protein, human
[FH2D+]{Disorders} is Family history of diabetes mellitus type 2
[group]{Living Beings} is Population Group
[SBP]{Physiology} is Systolic Blood Pressure
[RBP4]{Chemicals & Drugs} is RBP4 protein, human
[FH2D+]{Disorders} is Family history of diabetes mellitus type 2
[group]{Living Beings} is Population Group
[SBP]{Physiology} is Systolic Blood Pressure
[FH2D-]{Disorders} is NEGATIVE
[group]{Living Beings} is Population Group
[findings]{Disorders} is Finding (finding)
[RBP4]{Chemicals & Drugs} is RBP4 protein, human
[arterial stiffness]{Physiology} is Arterial Stiffness
[subjects]{Living Beings} is Research Subjects
[family history of type 2 diabetes]{Disorders} is Family history of diabetes mellitus type 2
|
The effect of [total hip arthroplasty] on [sagittal] [spinal] - [pelvic-leg] alignment and [low back pain] in patients with severe [hip osteoarthritis]
[Sagittal] [spinopelvic] [malalignment] has been reported in [spinal disorders] such as [low back pain] ([LBP]), and restoration of normal alignment is targeted when [treating] these [disorders]. [Abnormal] [sagittal] [spinal] - [pelvic-leg] alignment has been reported in patients with severe [hip osteoarthritis] ([OA]), who have a high prevalence of associated [LBP]. This [prospective longitudinal study] aimed to investigate changes in [sagittal] [spinal] - [pelvic-leg] alignment after [total hip arthroplasty] ([THA]) in patients with severe [hip OA], and whether these changes contribute to [LBP] [relief]. Patients undergoing primary [THA] due to severe unilateral [hip OA] were recruited. [Physical examination] and [X-ray films] were taken to rule out any [spinal disorder]. [Sagittal] alignment of [pelvis], [hip], and [spine] was analyzed on lateral radiographs taken before (baseline) and 1 year after ([follow-up]) [THA]. [Functional instruments] were completed by patients including: [visual analog scale] ([VAS]) for [LBP], [Roland-Morris Disability Questionnaire] ([RMDQ]), and [Harris Hip Score] ([HHS]). Comparisons were carried out at baseline and [follow-up], and between patients with and without [LBP]. The recruited 69 patients showed significantly reduced hip flexion and improved [global spinal balance] at [follow-up] compared with baseline. [LBP] was reported by 39 patients (56.5 %) before surgery; at [follow-up], 17 reported complete resolution, while 22 reported significant [relief]. Significant decreases in [VAS] and [RMDQ] scores in [lumbar spine] and increase in [hip] [HHS] were observed. [THA] in patients with severe [hip OA] could help correct abnormal [sagittal] [spinal] - [pelvic-leg] alignment and relieve [comorbid] [LBP]. Improvements in hip flexion and global [spinal] [balance] might be involved in the mechanism of [LBP] [relief].
|
[total hip arthroplasty]{Procedures} is Prosthetic total arthroplasty of the hip
[sagittal]{Anatomy} is Sagittal
[spinal]{Concepts & Ideas} is Spinal
[pelvic-leg]{Anatomy} is Body part
[low back pain]{Disorders} is Low back pain
[hip osteoarthritis]{Disorders} is Hip Osteoarthritis
[Sagittal]{Anatomy} is Sagittal
[spinopelvic]{Anatomy} is Body part
[total hip arthroplasty]{Procedures} is Prosthetic total arthroplasty of the hip
[malalignment]{Disorders} is Bone Malalignment
[sagittal]{Anatomy} is Sagittal
[spinal]{Concepts & Ideas} is Spinal
[spinal disorders]{Disorders} is Spinal Cord Disorders
[pelvic-leg]{Anatomy} is Body part
[low back pain]{Disorders} is Low back pain
[low back pain]{Disorders} is Low back pain
[LBP]{Disorders} is Low back pain
[hip osteoarthritis]{Disorders} is Hip Osteoarthritis
[treating]{Procedures} is TREAT
[disorders]{Disorders} is Spinal Cord Disorders
[Abnormal]{Disorders} is Abnormal
[sagittal]{Anatomy} is Sagittal
[spinal]{Concepts & Ideas} is Spinal
[pelvic-leg]{Anatomy} is Body part
[hip osteoarthritis]{Disorders} is Hip Osteoarthritis
[OA]{Disorders} is Hip Osteoarthritis
[LBP]{Disorders} is Low back pain
[prospective longitudinal study]{Procedures} is Study, Prospective
[sagittal]{Anatomy} is Sagittal
[spinal]{Concepts & Ideas} is Spinal
[pelvic-leg]{Anatomy} is Body part
[total hip arthroplasty]{Procedures} is Prosthetic total arthroplasty of the hip
[THA]{Procedures} is Prosthetic total arthroplasty of the hip
[hip OA]{Disorders} is Hip Osteoarthritis
[LBP]{Disorders} is Low back pain
[relief]{Disorders} is Relief
[THA]{Procedures} is Prosthetic total arthroplasty of the hip
[hip OA]{Disorders} is Hip Osteoarthritis
[Physical examination]{Procedures} is Physical Examination
[X-ray films]{Devices} is X-Ray Films
[spinal disorder]{Disorders} is Spinal Cord Disorders
[Sagittal]{Anatomy} is Sagittal
[pelvis]{Anatomy} is PELVIS
[hip]{Anatomy} is HIP
[spine]{Anatomy} is Dorsal spine
[follow-up]{Procedures} is Follow-up
[THA]{Procedures} is Prosthetic total arthroplasty of the hip
[Functional instruments]{Devices} is Instruments
[visual analog scale]{Procedures} is Visual Analog Scale
[VAS]{Procedures} is Visual Analog Scale
[LBP]{Disorders} is Low back pain
[Roland-Morris Disability Questionnaire]{Concepts & Ideas} is Roland Morris Disability Questionnaire
[RMDQ]{Concepts & Ideas} is Roland Morris Disability Questionnaire
[Harris Hip Score]{Disorders} is Harris hip score
[HHS]{Disorders} is Harris hip score
[follow-up]{Procedures} is Follow-up
[LBP]{Disorders} is Low back pain
[global spinal balance]{Disorders} is Finding (finding)
[follow-up]{Procedures} is Follow-up
[LBP]{Disorders} is Low back pain
[follow-up]{Procedures} is Follow-up
[relief]{Disorders} is Relief
[VAS]{Physiology} is Visual analogue scale score
[RMDQ]{Concepts & Ideas} is Roland Morris Disability Questionnaire
[lumbar spine]{Anatomy} is Lumbar Spine
[hip]{Anatomy} is HIP
[HHS]{Disorders} is Harris hip score
[THA]{Procedures} is Prosthetic total arthroplasty of the hip
[hip OA]{Disorders} is Hip Osteoarthritis
[sagittal]{Anatomy} is Sagittal
[spinal]{Concepts & Ideas} is Spinal
[pelvic-leg]{Anatomy} is Body part
[comorbid]{Disorders} is Comorbid conditions
[LBP]{Disorders} is Low back pain
[spinal]{Concepts & Ideas} is Spinal
[balance]{Physiology} is Balance
[LBP]{Disorders} is Low back pain
[relief]{Disorders} is Relief
|
Impact of totally [laparoscopic] combined management of [colorectal cancer] with synchronous [hepatic metastases] on severity of complications: a propensity-score -based analysis
Thanks to widespread diffusion of [minimally invasive approach] in the setting of both [colorectal] and [hepatic surgeries], the interest in combined resections for [colorectal cancer] and synchronous [liver metastases] ([SCLM]) by [totally laparoscopic approach] ([TLA]) has increased. Aim of this study was to compare outcome of combined resections for [SCLM] performed by [TLA] or by open approach, in a propensity-score-based study. All 25 patients undergoing combined [TLA] for [SCLM] at [San Raffaele Hospital] in Milano were compared in a [case-matched analysis] with 25 out of 91 patients undergoing [totally open approach] ([TOA group]). [Groups] were matched with 1:2 ratio using propensity scores based on covariates representing disease severity. Main endpoints were postoperative morbidity and long-term outcome. The [Modified Accordion Severity Grading System] was used to quantify complications. The groups resulted comparable in terms of patients and disease characteristics. The [TLA group], as compared to the [TOA group], had lower [blood loss] (350 vs 600 mL), shorter postoperative stay (9 vs 12 days), lower [postoperative morbidity index] (0.14 vs 0.20) and severity score for complicated patients (0.60 vs 0.85). [Colonic anastomosis] [leakage] had the highest fractional complication burden in both [groups]. In spite of comparable long-term overall survival, the [[TLA] group] had better [recurrence-free survival]. [TLA] for combined resections is feasible, and its indications can be widened to encompass a larger population of patients, provided its benefits in terms of reduced overall risk and severity of complications, rapid [functional recovery] and favorable long-term outcomes.
|
[laparoscopic]{Procedures} is Laparoscopic
[colorectal cancer]{Disorders} is COLORECTAL CANCER
[hepatic metastases]{Disorders} is Hepatic metastases
[laparoscopic]{Procedures} is Laparoscopic
[minimally invasive approach]{Procedures} is Minimally Invasive Surgery
[colorectal cancer]{Disorders} is COLORECTAL CANCER
[colorectal]{Procedures} is Colorectal surgery
[hepatic metastases]{Disorders} is Hepatic metastases
[hepatic surgeries]{Procedures} is Hepatic operation
[colorectal cancer]{Disorders} is COLORECTAL CANCER
[liver metastases]{Disorders} is Hepatic metastases
[SCLM]{Disorders} is Hepatic metastases
[totally laparoscopic approach]{Procedures} is Laparoscopic
[TLA]{Procedures} is Laparoscopic
[SCLM]{Disorders} is Hepatic metastases
[TLA]{Procedures} is Laparoscopic
[TLA]{Procedures} is Laparoscopic
[SCLM]{Disorders} is Hepatic metastases
[San Raffaele Hospital]{Organizations} is Hospital
[case-matched analysis]{Procedures} is Matched Case-Control Study
[totally open approach]{Procedures} is Open Surgery
[TOA group]{Living Beings} is Population Group
[Groups]{Living Beings} is Population Group
[Modified Accordion Severity Grading System]{Procedures} is Grading system used
[TLA group]{Living Beings} is Population Group
[TOA group]{Living Beings} is Population Group
[blood loss]{Disorders} is SURG BLOOD LOSS
[postoperative morbidity index]{Concepts & Ideas} is Morbidity index
[Colonic anastomosis]{Procedures} is Colonic anastomosis
[leakage]{Disorders} is Extravasation (morphologic abnormality)
[groups]{Living Beings} is Population Group
[TLA]{Procedures} is Laparoscopic
[TLA group]{Living Beings} is Population Group
[recurrence-free survival]{Disorders} is Recurrence free survival
[TLA]{Procedures} is Laparoscopic
[functional recovery]{Disorders} is Function Recovery
|
Application of an Analytical Solution as a [Screening] [Tool] for Sea Water Intrusion
Sea water intrusion into aquifers is [problematic] in many [coastal areas]. The physics and chemistry of this issue are complex, and sea water intrusion remains challenging to quantify. Simple [assessment tools] like [analytical models] offer advantages of rapid application, but their applicability to field situations is unclear. This [study] examines the reliability of a popular sharp-interface analytical approach for estimating the extent of sea water in a homogeneous [coastal] aquifer subjected to pumping and regional flow effects and under steady-state conditions. The [analytical model] is tested against observations from [Canada], the [United States], and [Australia] to assess its utility as an initial [approximation] of sea water extent for the purposes of rapid [groundwater] management [decision making]. The occurrence of sea water intrusion resulting in increased [salinity] at pumping wells was correctly predicted in approximately 60% of cases. Application of a correction to account for [dispersion] did not markedly [improve] the results. Failure of the [analytical model] to provide correct predictions can be attributed to mismatches between its simplifying assumptions and more complex field settings. The best results occurred where the toe of the [salt water] [wedge] is expected to be the closest to the [coast] under predevelopment conditions. Predictions were the poorest for aquifers where the [salt water] [wedge] was expected to extend further [inland] under predevelopment conditions and was therefore more dispersive prior to pumping. Sharp-interface solutions remain useful [tools] to [screen] for the vulnerability of [coastal] aquifers to sea water intrusion, although the significant sources of uncertainty identified in this [study] require careful consideration to avoid misinterpreting sharp-interface results.
|
[Screening]{Procedures} is Screenings
[Tool]{Concepts & Ideas} is Method (attribute)
[problematic]{Disorders} is Problem
[Screening]{Procedures} is Screenings
[Tool]{Concepts & Ideas} is Method (attribute)
[coastal areas]{Concepts & Ideas} is Coastal environment
[assessment tools]{Concepts & Ideas} is Intellectual Product
[analytical models]{Concepts & Ideas} is Theoretical Models
[study]{Procedures} is Study
[coastal]{Concepts & Ideas} is Coastal environment
[analytical model]{Concepts & Ideas} is Theoretical Models
[Canada]{Geographic Areas} is Canada
[United States]{Geographic Areas} is United States
[Australia]{Geographic Areas} is Australia
[approximation]{Procedures} is Approximation - action
[groundwater]{Concepts & Ideas} is Groundwater
[decision making]{Physiology} is Decision making
[salinity]{Phenomena} is Salinity
[dispersion]{Concepts & Ideas} is Dispersion
[improve]{Disorders} is Improved
[analytical model]{Concepts & Ideas} is Theoretical Models
[salt water]{Chemicals & Drugs} is Salt water
[wedge]{Concepts & Ideas} is Wedge
[coast]{Geographic Areas} is Area
[salt water]{Chemicals & Drugs} is Salt water
[wedge]{Concepts & Ideas} is Wedge
[inland]{Geographic Areas} is Inland water
[tools]{Concepts & Ideas} is Method (attribute)
[screen]{Procedures} is Screenings
[coastal]{Concepts & Ideas} is Coastal environment
[study]{Procedures} is Study
|
The Role of [TRAF4] and [B3GAT1] [Gene Expression] in the [Food Hypersensitivity] and [Insect Venom Allergy] in [Mastocytosis]
[Mastocytosis] is an uncommon [disease] classified as a [myeloproliferative neoplasm], however, its [symptoms] are broad and place patients at crossroads between [dermatology], [hematology] and allergology. Patients with [mastocytosis] often suffer from [symptoms] resulting from the activation and release of mediators from the [mast cells], such as generalized [itching], [redness], [headache], [abdominal cramps], [diarrhea], [bone pain] or [arthritis], [hypotension] and [shock]. The possible severe, fatal or near fatal reactions caused by [food hypersensitivity] are reasons for the research focused on [marker] identification. The aim of the [study] was to analyse the [gene expression] differences in [mastocytosis] patients with and without [food] and [drug hypersensitivity] and [insect venom allergy] ([IVA]). A total of 57 [Caucasian] patients with [mastocytosis] were studied (median age 41.8; range 18-77 years; 15 (26.3 %) males and 42 (73.7 %) females). [Quantitative RT-PCRs] of 11 [genes] plus [ribosomal 18S RNA] were run. [Symptoms] of [food hypersensitivity] were found in 12 patients (21 %), including 3 patients (13 %) with [cutaneous mastocytosis] ([CM]), and 9 (28 %) with [indolent systemic mastocytosis] ([ISM]). [IVA] was confirmed in 13 patients (22.8 %) including 6 patients (10.5 %) with [CM], and 7 patients (12.3 %) with [ISM]. [Drug hypersensitivity] was [diagnosed] in 10 patients (17.5 %). Significant differences in the [gene expression] were found for [TRAF4] (p = 0.008) in the comparison of the [mastocytosis] patients with and without concomitant [food hypersensitivity]. Furthermore significant differences were found in [gene expression] for [B3GAT1] (p = 0.003) in patients with [IVA] compared to patients without [insect sting] [anaphylaxis] in the medical history. The [expression] of studied [genes] did not differ according to the presence of [drug hypersensitivity]. The [TRAF4] [expression] was higher in [mastocytosis] patients with [food hypersensitivity] in their [medical history], the [B3GAT1] [expression] was lower in [mastocytosis] patients with [IVA] in history.
|
[TRAF4]{Genes & Molecular Sequences} is TRAF4
[B3GAT1]{Genes & Molecular Sequences} is B3GAT1
[Gene Expression]{Physiology} is Gene Expression
[Food Hypersensitivity]{Disorders} is Food Hypersensitivity
[Insect Venom Allergy]{Disorders} is Allergy disorder
[Mastocytosis]{Disorders} is Mastocytosis
[Mastocytosis]{Disorders} is Mastocytosis
[TRAF4]{Genes & Molecular Sequences} is TRAF4
[B3GAT1]{Genes & Molecular Sequences} is B3GAT1
[disease]{Disorders} is Disease
[Gene Expression]{Physiology} is Gene Expression
[Food Hypersensitivity]{Disorders} is Food Hypersensitivity
[myeloproliferative neoplasm]{Disorders} is Myeloproliferative neoplasms
[Insect Venom Allergy]{Disorders} is Allergy disorder
[symptoms]{Disorders} is Symptoms
[Mastocytosis]{Disorders} is Mastocytosis
[dermatology]{Occupations} is Dermatology
[hematology]{Occupations} is Hematology
[mastocytosis]{Disorders} is Mastocytosis
[symptoms]{Disorders} is Symptoms
[mast cells]{Anatomy} is Mast Cells
[itching]{Disorders} is Itching
[redness]{Disorders} is Skin red
[headache]{Disorders} is Headache
[abdominal cramps]{Disorders} is Abdominal Cramps
[diarrhea]{Disorders} is D - Diarrhea
[bone pain]{Disorders} is Pain bone
[arthritis]{Disorders} is Arthritis
[hypotension]{Disorders} is Vascular Hypotension
[shock]{Disorders} is Shock
[food hypersensitivity]{Disorders} is Food Hypersensitivity
[marker]{Physiology} is Marker
[study]{Procedures} is Study
[gene expression]{Physiology} is Gene Expression
[mastocytosis]{Disorders} is Mastocytosis
[food]{Disorders} is Food Hypersensitivity
[drug hypersensitivity]{Disorders} is Drug hypersensitivity
[insect venom allergy]{Disorders} is Allergy disorder
[IVA]{Disorders} is Allergy disorder
[Caucasian]{Living Beings} is Caucasian (ethnic group)
[mastocytosis]{Disorders} is Mastocytosis
[Quantitative RT-PCRs]{Procedures} is Quantitative Real-Time PCRs
[genes]{Genes & Molecular Sequences} is Genes
[ribosomal 18S RNA]{Chemicals & Drugs} is RIBOSOMAL RNA 18S
[Symptoms]{Disorders} is Symptoms
[food hypersensitivity]{Disorders} is Food Hypersensitivity
[cutaneous mastocytosis]{Disorders} is Cutaneous mastocytosis
[CM]{Disorders} is Cutaneous mastocytosis
[indolent systemic mastocytosis]{Disorders} is Indolent systemic mastocytosis
[ISM]{Disorders} is Indolent systemic mastocytosis
[IVA]{Disorders} is Allergy disorder
[CM]{Disorders} is Cutaneous mastocytosis
[ISM]{Disorders} is Indolent systemic mastocytosis
[Drug hypersensitivity]{Disorders} is Drug hypersensitivity
[diagnosed]{Disorders} is Diagnosed
[gene expression]{Physiology} is Gene Expression
[TRAF4]{Genes & Molecular Sequences} is TRAF4
[mastocytosis]{Disorders} is Mastocytosis
[food hypersensitivity]{Disorders} is Food Hypersensitivity
[gene expression]{Physiology} is Gene Expression
[B3GAT1]{Genes & Molecular Sequences} is B3GAT1
[IVA]{Disorders} is Allergy disorder
[insect sting]{Disorders} is Insect Sting
[anaphylaxis]{Disorders} is Obsolete anaphylaxis
[expression]{Physiology} is Gene Expression
[genes]{Genes & Molecular Sequences} is Genes
[drug hypersensitivity]{Disorders} is Drug hypersensitivity
[TRAF4]{Genes & Molecular Sequences} is TRAF4
[expression]{Physiology} is Gene Expression
[mastocytosis]{Disorders} is Mastocytosis
[food hypersensitivity]{Disorders} is Food Hypersensitivity
[medical history]{Disorders} is Medical History
[B3GAT1]{Genes & Molecular Sequences} is B3GAT1
[expression]{Physiology} is Gene Expression
[mastocytosis]{Disorders} is Mastocytosis
[IVA]{Disorders} is Allergy disorder
|
[Generalized Weakness] in a [Transplant] Patient: A [Case Presentation]
[Generalized weakness] in [transplant] patients is a major complaint in tertiary [rehabilitation hospitals]. The [diagnosis] and [management] of [generalized weakness] in this [population] pose challenges for [physicians]. We present the case of a [transplant] patient with [generalized weakness] who was eventually [diagnosed] with [calciphylaxis] using a [multidisciplinary diagnostic approach] of [electrodiagnostics], [vascular] [study], and [skin biopsy]. [Calciphylaxis] is a rare [cutaneous disorder] that mimics other [collagen vascular diseases] in its presentation and fulminant course. [Physiatrists] should be cognizant of [calciphylaxis], as it signals a [poor prognosis] if not correctly diagnosed and treated in a timely manner, with high incidence of [sepsis], [wound pain], and [disability]. V.
|
[Generalized Weakness]{Disorders} is Weakness generalized
[Transplant]{Disorders} is Transplant
[Case Presentation]{Concepts & Ideas} is CASE ONLY
[Generalized weakness]{Disorders} is Weakness generalized
[transplant]{Disorders} is Transplant
[Transplant]{Disorders} is Transplant
[Case Presentation]{Concepts & Ideas} is CASE ONLY
[rehabilitation hospitals]{Organizations} is Rehabilitation hospital
[diagnosis]{Disorders} is Diagnosis
[management]{Procedures} is Symptom management
[generalized weakness]{Disorders} is Weakness generalized
[population]{Living Beings} is Population
[physicians]{Living Beings} is Physicians
[transplant]{Disorders} is Transplant
[generalized weakness]{Disorders} is Weakness generalized
[diagnosed]{Disorders} is Diagnosis
[calciphylaxis]{Disorders} is Calciphylaxis
[multidisciplinary diagnostic approach]{Procedures} is Multidisciplinary assessment
[electrodiagnostics]{Procedures} is Electrodiagnoses
[vascular]{Anatomy} is Vascular structure
[study]{Procedures} is TESTS DIAG
[skin biopsy]{Procedures} is Skin Biopsy
[Calciphylaxis]{Disorders} is Calciphylaxis
[cutaneous disorder]{Disorders} is Cutaneous Disorder
[collagen vascular diseases]{Disorders} is Collagen-vascular disease
[Physiatrists]{Living Beings} is Physiatrists
[calciphylaxis]{Disorders} is Calciphylaxis
[poor prognosis]{Disorders} is Poor prognosis
[sepsis]{Disorders} is Sepsis (disorder)
[wound pain]{Disorders} is Wound pain
[disability]{Disorders} is Disability
|
Use of ecoacoustics to determine biodiversity [patterns] across [ecological] gradients
The variety of [local] [animal] sounds characterizes a [landscape]. We used ecoacoustics to noninvasively assess the [species] richness of various [biotopes] typical of an ecofriendly forest plantation with diverse [ecological] gradients and both nonnative and indigenous [vegetation]. The reference [area] was an [adjacent] large [World Heritage Site protected area] ([PA]). All [sites] were in a [global biodiversity hotspot]. Our results showed how taxa segregated into various [biotopes]. We identified 65 singing [species], including [birds], [frogs], [crickets], and [katydids]. Large, natural, protected [grassland sites] in the [PA] had the highest mean acoustic diversity (14.1 [species] / [site]). [Areas] covered in [nonnative timber] or [grass] [species] were devoid of [acoustic species]. [Sites] grazed by native and domestic [megaherbivores] were fairly rich (5.1) in [acoustic species] but none were unique to this [habitat type], where acoustic diversity was greater than in intensively managed [grassland] [sites] (0.04). Natural vegetation patches inside the plantation mosaic supported high mean acoustic diversity (indigenous forests 7.6, [grasslands] 8.0, wetlands 9.1), which increased as [plant] heterogeneity and [patch size] increased. Indigenous forest patches within the plantation mosaic contained a highly characteristic [acoustic species] assemblage, emphasizing their complementary contribution to [local] biodiversity. Overall, acoustic signals determined spatial biodiversity [patterns] and can be a useful tool for guiding conservation.
|
[patterns]{Concepts & Ideas} is Patterns
[ecological]{Concepts & Ideas} is Ecological environment
[local]{Concepts & Ideas} is Local (qualifier value)
[animal]{Living Beings} is Animal
[patterns]{Concepts & Ideas} is Patterns
[landscape]{Concepts & Ideas} is Landscapes
[ecological]{Concepts & Ideas} is Ecological environment
[species]{Concepts & Ideas} is Species
[biotopes]{Geographic Areas} is Area
[ecological]{Concepts & Ideas} is Ecological environment
[vegetation]{Living Beings} is Chlorobionta Bremer, 1985
[area]{Geographic Areas} is Area
[adjacent]{Concepts & Ideas} is Adjacent
[World Heritage Site protected area]{Geographic Areas} is Area
[PA]{Geographic Areas} is Area
[sites]{Concepts & Ideas} is Sites
[global biodiversity hotspot]{Geographic Areas} is Area
[biotopes]{Geographic Areas} is Area
[species]{Concepts & Ideas} is Species
[birds]{Living Beings} is Birds
[frogs]{Living Beings} is Frogs
[crickets]{Living Beings} is Crickets
[katydids]{Living Beings} is Eucaryotae
[grassland sites]{Concepts & Ideas} is Grassland
[PA]{Geographic Areas} is Area
[species]{Concepts & Ideas} is Species
[site]{Concepts & Ideas} is Sites
[Areas]{Concepts & Ideas} is Area
[nonnative timber]{Living Beings} is Chlorobionta Bremer, 1985
[grass]{Living Beings} is Grass
[species]{Concepts & Ideas} is Species
[acoustic species]{Concepts & Ideas} is Species
[Sites]{Concepts & Ideas} is Sites
[megaherbivores]{Living Beings} is Herbivores
[acoustic species]{Concepts & Ideas} is Species
[habitat type]{Concepts & Ideas} is Habitats
[grassland]{Concepts & Ideas} is Grassland
[sites]{Concepts & Ideas} is Sites
[grasslands]{Concepts & Ideas} is Grassland
[plant]{Living Beings} is Chlorobionta Bremer, 1985
[patch size]{Concepts & Ideas} is Size of patch
[acoustic species]{Concepts & Ideas} is Species
[local]{Concepts & Ideas} is Local (qualifier value)
[patterns]{Concepts & Ideas} is Patterns
|
Relationship between [XspI] [Site Polymorphisms] of [LDL-R Gene] and [Serum IL-2] and [IL-10] in Patients with [Hypercholesterolemia]
Relationship has been identified in [sporadic reports] between polymorphisms and [hypercholesterolemia]. However, the relationship between inflammatory [cytokines] and polymorphism of [low-density lipoprotein receptor (LDL-R) gene] in [hypercholesterolemia] is unclear. This [study] aimed to explore the relationship and significance between polymorphisms of [LDL-R gene] and [serum Interleukin-2] ([IL-2]), [IL-10] in patients with [hypercholesterolemia]. [PCR-RFLP] and [direct DNA sequencing assay] were [employed] to determine polymorphism of [LDL-R gene] in 900 patients with [hypercholesterolemia] and 400 healthy cases. [ELISA] was applied to assay serum concentration of [IL-2] and [IL-10]. Blood lipid [indexes] were tested in all cases. Compared with the healthy controls, level of [IL-2] increased significantly, while [IL-10] decreased significantly (P < 0.05). [Correlation analysis] showed that [IL-2] was positively correlated with [total cholesterol] ([TC]), [LDL-c], and genotype (r = 0.542, 0.410, 0.598, P < 0.05) and [negatively] correlated with [HDL-c] (r = -0.352, P < 0.05). [Negative] relationship also was found between [TC], [LDL-c], genotype, and [IL-10] (r = -0.452, -0.390, -0.613, P < 0.05), and [positive] correlation between [HDL-c] and [IL-10] (r = 0.398, P < 0.05). Multiple linear regression showed that genotypes and [TC] were independent factors affecting the [levels of [IL-2]] and [IL-10] (P < 0.05). [IL-2] and [IL-10] were related to gene polymorphisms of [LDL-R], which might be involved in the development and progress of [hypercholesterolemia].
|
[XspI]{Chemicals & Drugs} is Endodeoxyribonuclease XspI
[Site Polymorphisms]{Disorders} is Restriction Site Polymorphism
[LDL-R Gene]{Genes & Molecular Sequences} is LDLR Gene
[Serum IL-2]{Chemicals & Drugs} is IL 002
[IL-10]{Chemicals & Drugs} is IL 010
[Hypercholesterolemia]{Disorders} is Hypercholesterolemias
[XspI]{Chemicals & Drugs} is Endodeoxyribonuclease XspI
[Site Polymorphisms]{Disorders} is Restriction Site Polymorphism
[sporadic reports]{Disorders} is Finding (finding)
[LDL-R Gene]{Genes & Molecular Sequences} is LDLR Gene
[Serum IL-2]{Chemicals & Drugs} is IL 002
[IL-10]{Chemicals & Drugs} is IL 010
[hypercholesterolemia]{Disorders} is Hypercholesterolemias
[Hypercholesterolemia]{Disorders} is Hypercholesterolemias
[cytokines]{Chemicals & Drugs} is Cytokine
[low-density lipoprotein receptor (LDL-R) gene]{Genes & Molecular Sequences} is LDLR Gene
[hypercholesterolemia]{Disorders} is Hypercholesterolemias
[study]{Procedures} is Study
[LDL-R gene]{Genes & Molecular Sequences} is LDLR Gene
[serum Interleukin-2]{Chemicals & Drugs} is IL 002
[IL-2]{Chemicals & Drugs} is IL 002
[IL-10]{Chemicals & Drugs} is IL 010
[hypercholesterolemia]{Disorders} is Hypercholesterolemias
[PCR-RFLP]{Procedures} is RFLP analysis
[direct DNA sequencing assay]{Procedures} is DNA Sequencing
[employed]{Disorders} is Employed
[LDL-R gene]{Genes & Molecular Sequences} is LDLR Gene
[hypercholesterolemia]{Disorders} is Hypercholesterolemias
[ELISA]{Procedures} is ELISA
[IL-2]{Chemicals & Drugs} is IL 002
[IL-10]{Chemicals & Drugs} is IL 010
[indexes]{Concepts & Ideas} is Indexes
[IL-2]{Chemicals & Drugs} is IL 002
[IL-10]{Chemicals & Drugs} is IL 010
[Correlation analysis]{Procedures} is Correlation Study
[IL-2]{Chemicals & Drugs} is IL 002
[total cholesterol]{Chemicals & Drugs} is Total cholesterol
[TC]{Chemicals & Drugs} is Total cholesterol
[LDL-c]{Chemicals & Drugs} is LDL Cholesterol
[negatively]{Disorders} is Finding (finding)
[HDL-c]{Chemicals & Drugs} is HDL Cholesterol
[Negative]{Disorders} is Negative for
[TC]{Chemicals & Drugs} is Total cholesterol
[LDL-c]{Chemicals & Drugs} is LDL Cholesterol
[IL-10]{Chemicals & Drugs} is IL 010
[positive]{Disorders} is Positive for
[HDL-c]{Chemicals & Drugs} is HDL Cholesterol
[IL-10]{Chemicals & Drugs} is IL 010
[TC]{Chemicals & Drugs} is Total cholesterol
[levels of IL-2]{Procedures} is Laboratory procedure (procedure)
[IL-2]{Chemicals & Drugs} is IL 002
[IL-10]{Procedures} is Laboratory procedure (procedure)
[IL-2]{Chemicals & Drugs} is IL 002
[IL-10]{Chemicals & Drugs} is IL 010
[LDL-R]{Genes & Molecular Sequences} is LDLR Gene
[hypercholesterolemia]{Disorders} is Hypercholesterolemias
|
Low [serum] [vitamin D] is associated with higher [cortical] porosity in [elderly] [men]
[Bone loss] at [peripheral] [sites] in the [elderly] is mainly [cortical] and involves increased [cortical] porosity. However, an association between [bone loss] at these [sites] and [25-hydroxyvitamin D] has not been reported. To investigate the association between [serum] [levels of 25-hydroxyvitamin D], [bone microstructure] and [areal bone mineral density] ([BMD]) in [elderly] [men]. A [population] -based [cohort] of 444 [elderly] [men] (mean ± SD age 80.2 ± 3.5 years) was investigated. [Bone microstructure] was measured by [high-resolution peripheral quantitative computed tomography], [areal BMD] by [dual-energy X-ray absorptiometry] and [serum] [25-hydroxyvitamin D] and [parathyroid hormone levels] by [immunoassay]. Mean [cortical] porosity at the [distal tibia] was 14.7% higher (12.5 ± 4.3% vs. 10.9 ± 4.1%, P < 0.05) whilst [cortical] [volumetric BMD], [area], [trabecular bone] volume fraction and [femoral neck] [areal BMD] were lower in [men] in the lowest quartile of [vitamin D levels] compared to the highest. In [men] with [vitamin D deficiency] (<25 nmol L(-1)) or insufficiency (25-49 nmol L(-1), in combination with an elevated [serum] [level of parathyroid hormone] (>6.8 pmol L(-1))), [cortical] porosity was 17.2% higher than in [vitamin D] - sufficient [men] (P < 0.01). A linear regression [model] including age, weight, height, daily calcium intake, physical activity, smoking [vitamin D] [supplementation] and [parathyroid hormone] showed that [25-hydroxyvitamin D] independently predicted [cortical] porosity (standardized β = -0.110, R(2) = 1.1%, P = 0.024), [area] (β = 0.123, R(2) = 1.4%, P = 0.007) and [cortical] [volumetric BMD] (β = 0.125, R(2) = 1.4%, P = 0.007) of the [tibia] as well as [areal BMD] of the [femoral neck] (β = 0.102, R(2) = 0.9%, P = 0.04). [Serum] [vitamin D] is associated with [cortical] porosity, [area] and [density], indicating that [bone] [fragility] as a result of low [vitamin D] could be due to changes in [cortical] [bone microstructure] and [geometry].
|
[serum]{Anatomy} is Serum
[vitamin D]{Chemicals & Drugs} is Vitamin D product
[cortical]{Anatomy} is Cortex of bone
[elderly]{Living Beings} is ELDERLY
[men]{Living Beings} is Men
[Bone loss]{Disorders} is Bone Loss
[serum]{Anatomy} is Serum
[vitamin D]{Chemicals & Drugs} is Vitamin D product
[peripheral]{Concepts & Ideas} is Peripheral
[sites]{Anatomy} is Site
[elderly]{Living Beings} is ELDERLY
[cortical]{Anatomy} is Cortex of bone
[cortical]{Anatomy} is Cortex of bone
[elderly]{Living Beings} is ELDERLY
[men]{Living Beings} is Men
[cortical]{Anatomy} is Cortex of bone
[bone loss]{Disorders} is Bone Loss
[sites]{Anatomy} is Site
[25-hydroxyvitamin D]{Chemicals & Drugs} is 25-hydroxyvitamin D
[serum]{Anatomy} is Serum
[levels of 25-hydroxyvitamin D]{Procedures} is 25-Hydroxyvitamin D
[bone microstructure]{Anatomy} is Bone structure
[areal bone mineral density]{Physiology} is Bone Mineral Density
[BMD]{Physiology} is Bone Mineral Density
[elderly]{Living Beings} is ELDERLY
[men]{Living Beings} is Men
[population]{Living Beings} is Population
[cohort]{Living Beings} is Cohort
[elderly]{Living Beings} is ELDERLY
[men]{Living Beings} is Men
[Bone microstructure]{Anatomy} is Bone structure
[high-resolution peripheral quantitative computed tomography]{Procedures} is Computed Tomography
[areal BMD]{Physiology} is Bone Mineral Density
[dual-energy X-ray absorptiometry]{Procedures} is Dual-Energy X-Ray Absorptiometry
[serum]{Anatomy} is Serum
[25-hydroxyvitamin D]{Procedures} is 25-Hydroxyvitamin D
[parathyroid hormone levels]{Procedures} is Parathyroid hormone
[immunoassay]{Procedures} is Immunoassay
[cortical]{Anatomy} is Cortex of bone
[distal tibia]{Anatomy} is Distal tibia
[cortical]{Anatomy} is Cortex of bone
[volumetric BMD]{Physiology} is Bone Mineral Density
[area]{Concepts & Ideas} is Area
[trabecular bone]{Anatomy} is Trabecular bone
[femoral neck]{Anatomy} is Femoral neck
[areal BMD]{Physiology} is Bone Mineral Density
[men]{Living Beings} is Men
[vitamin D levels]{Procedures} is Vitamin D
[men]{Living Beings} is Men
[vitamin D deficiency]{Disorders} is Vitamin D Deficiency
[serum]{Anatomy} is Serum
[level of parathyroid hormone]{Procedures} is Parathyroid hormone
[cortical]{Anatomy} is Cortex of bone
[vitamin D]{Chemicals & Drugs} is Vitamin D product
[men]{Living Beings} is Men
[model]{Concepts & Ideas} is Model
[vitamin D]{Chemicals & Drugs} is Vitamin D product
[supplementation]{Chemicals & Drugs} is Vitamin supplementation
[parathyroid hormone]{Chemicals & Drugs} is Hormone, Parathyroid
[25-hydroxyvitamin D]{Chemicals & Drugs} is 25-hydroxyvitamin D
[cortical]{Anatomy} is Cortex of bone
[area]{Concepts & Ideas} is Area
[cortical]{Anatomy} is Cortex of bone
[volumetric BMD]{Physiology} is Bone Mineral Density
[tibia]{Anatomy} is TIBIA
[areal BMD]{Physiology} is Bone Mineral Density
[femoral neck]{Anatomy} is Femoral neck
[Serum]{Anatomy} is Serum
[vitamin D]{Chemicals & Drugs} is Vitamin D product
[cortical]{Anatomy} is Cortex of bone
[area]{Concepts & Ideas} is Area
[density]{Physiology} is Bone Mineral Density
[bone]{Anatomy} is Bone structure
[fragility]{Disorders} is Fragility
[vitamin D]{Chemicals & Drugs} is Vitamin D product
[cortical]{Anatomy} is Cortex of bone
[bone microstructure]{Anatomy} is Bone structure
[geometry]{Concepts & Ideas} is Structural
|
Rapid Fabrication of a [Cell] - [Seeded] [Collagen] [Gel] -Based [Tubular Construct] that Withstands [Arterial Pressure]: Rapid Fabrication of a [Gel] -Based Media Equivalent
Based on plastically compressed [cell] - [seeded] [collagen] [gels], we fabricated a small-diameter [tubular construct] that withstands [arterial pressure] without prolonged [culture] in vitro. Specifically, to mimic the [microstructure] of [vascular media], the [cell] - [seeded] [collagen] [gel] was uniaxially stretched prior to plastic compression to align [collagen fibers] and hence [cells] in the [gel]. The resulting [gel] [sheet] was then wrapped around a custom-made multi-layered braided tube to form aligned [tubular constructs] whereas the [gel] [sheet] prepared similarly but without uniaxial stretching formed control [constructs]. With the braided tube, fluid in the [gel] [construct] was further removed by [vacuum suction] aiming to consolidate the concentric layers of the [construct]. The [construct] was finally treated with [transglutaminase]. Both [SEM] and [histology] confirmed the absence of gaps in the wall of the [construct]. Particularly, [cells] in the wall of the aligned [tubular construct] were circumferentially aligned. The [enzyme] -mediated crosslinking increased burst pressure of both the [constructs] significantly; the extent of the increase of burst pressure for the aligned [tubular construct] was greater than that for the control counterpart. Increasing crosslinking left the compliance of the aligned [tubular construct] unchanged but reduced that of the control [construct]. [Cells] remained viable in [transglutaminase] -treated plastically compressed [gels] after 6 days in culture. This [study] demonstrated that by combining stretch-induced [fiber] alignment, plastic compression, and [enzyme] -mediated crosslinking, a [cell] - [seeded] [collagen] [gel] -based [tubular construct] with potential to be used as [vascular media] can be made within 3 days.
|
[Cell]{Anatomy} is Cell Type
[Seeded]{Procedures} is Scaffold Seeding
[Collagen]{Chemicals & Drugs} is Collagen
[Gel]{Chemicals & Drugs} is Drug gel
[Tubular Construct]{Devices} is Tube, device
[Arterial Pressure]{Physiology} is Arterial pulse pressure
[Gel]{Chemicals & Drugs} is Drug gel
[Cell]{Anatomy} is Cell Type
[Seeded]{Procedures} is Scaffold Seeding
[cell]{Anatomy} is Cell Type
[Collagen]{Chemicals & Drugs} is Collagen
[seeded]{Procedures} is Scaffold Seeding
[Gel]{Chemicals & Drugs} is Drug gel
[collagen]{Chemicals & Drugs} is Collagen
[gels]{Chemicals & Drugs} is Drug gel
[Tubular Construct]{Devices} is Tube, device
[Arterial Pressure]{Physiology} is Arterial pulse pressure
[tubular construct]{Devices} is Tube, device
[arterial pressure]{Physiology} is Arterial pulse pressure
[Gel]{Chemicals & Drugs} is Drug gel
[culture]{Procedures} is Culture - general
[microstructure]{Concepts & Ideas} is Structure
[vascular media]{Anatomy} is Vascular Media
[cell]{Anatomy} is Cell Type
[seeded]{Procedures} is Scaffold Seeding
[collagen]{Chemicals & Drugs} is Collagen
[gel]{Chemicals & Drugs} is Drug gel
[collagen fibers]{Anatomy} is Collagen fiber
[cells]{Anatomy} is Cell Type
[gel]{Chemicals & Drugs} is Drug gel
[gel]{Chemicals & Drugs} is Drug gel
[sheet]{Chemicals & Drugs} is Biocompatible Materials (Chemical/Ingredient)
[tubular constructs]{Devices} is Tube, device
[gel]{Chemicals & Drugs} is Drug gel
[sheet]{Chemicals & Drugs} is Biocompatible Materials (Chemical/Ingredient)
[constructs]{Devices} is Tube, device
[gel]{Chemicals & Drugs} is Drug gel
[construct]{Devices} is Tube, device
[vacuum suction]{Devices} is Suction regulator
[construct]{Devices} is Tube, device
[construct]{Devices} is Tube, device
[transglutaminase]{Chemicals & Drugs} is Transglutaminase
[SEM]{Procedures} is Scanning Electron Microscopies
[histology]{Procedures} is Histology
[construct]{Devices} is Tube, device
[cells]{Anatomy} is Cell Type
[tubular construct]{Devices} is Tube, device
[enzyme]{Chemicals & Drugs} is Enzyme
[constructs]{Devices} is Tube, device
[tubular construct]{Devices} is Tube, device
[tubular construct]{Devices} is Tube, device
[construct]{Devices} is Tube, device
[Cells]{Anatomy} is Cell Type
[transglutaminase]{Chemicals & Drugs} is Transglutaminase
[gels]{Chemicals & Drugs} is Drug gel
[study]{Procedures} is Study
[fiber]{Anatomy} is Collagen fiber
[enzyme]{Chemicals & Drugs} is Enzyme
[cell]{Anatomy} is Cell Type
[seeded]{Procedures} is Scaffold Seeding
[collagen]{Chemicals & Drugs} is Collagen
[gel]{Chemicals & Drugs} is Drug gel
[tubular construct]{Devices} is Tube, device
[vascular media]{Anatomy} is Vascular Media
|
[Expression] and [Purification] of [E2 Glycoprotein] from [Insect] [Cells] ([Sf9]) for Use in [Serology]
[Chikungunya virus] ([CHIKV]) is a [mosquito] - [borne] [arbovirus] which poses a major threat to global [public health]. Definitive [CHIKV] [diagnosis] is crucial, especially in distinguishing the [disease] from [dengue virus], which co-circulates in endemic [areas] and shares the same [mosquito vectors]. [Laboratory diagnosis] is mainly based on serological or molecular approaches. The [E2 glycoprotein] is a good candidate for [serological diagnosis] since it is the [immunodominant antigen] during the course of [infection], and reacts with seropositive [CHIKV] [sera]. In this chapter, we describe the generation of stable [clone] [Sf9] ([Spodoptera frugiperda]) [cells] [expressing] [secreted], [soluble], and native recombinant [CHIKV] [E2 glycoprotein]. We use direct [plasmid] [expression] in [insect] [cells], rather than the traditional technique of generating recombinant baculovirus. This [recombinant protein] is useful for [serological diagnosis] of [CHIKV] [infection].
|
[Expression]{Physiology} is Protein expression
[Purification]{Procedures} is Protein Purification
[E2 Glycoprotein]{Chemicals & Drugs} is Glycoprotein
[Insect]{Living Beings} is Insect
[Cells]{Anatomy} is Cells set
[Sf9]{Anatomy} is Sf9 Cell
[Serology]{Procedures} is Serology
[Expression]{Physiology} is Protein expression
[Chikungunya virus]{Living Beings} is Chikungunya Virus
[Purification]{Procedures} is Protein Purification
[CHIKV]{Living Beings} is Chikungunya Virus
[mosquito]{Living Beings} is Mosquito
[E2 Glycoprotein]{Chemicals & Drugs} is Glycoprotein
[borne]{Disorders} is Does carry
[arbovirus]{Living Beings} is Arboviruses
[Insect]{Living Beings} is Insect
[Cells]{Anatomy} is Cells set
[Sf9]{Anatomy} is Sf9 Cell
[Serology]{Procedures} is Serology
[public health]{Procedures} is Public health service
[CHIKV]{Living Beings} is Chikungunya Virus
[diagnosis]{Disorders} is Diagnosis
[disease]{Disorders} is Disease
[dengue virus]{Living Beings} is Dengue Virus
[areas]{Concepts & Ideas} is Area
[mosquito vectors]{Living Beings} is Mosquito Vectors
[Laboratory diagnosis]{Procedures} is Laboratory Diagnosis
[E2 glycoprotein]{Chemicals & Drugs} is Glycoprotein
[serological diagnosis]{Procedures} is Serology
[immunodominant antigen]{Chemicals & Drugs} is Immunodominant Antigens
[infection]{Disorders} is Infections
[CHIKV]{Living Beings} is Chikungunya Virus
[sera]{Anatomy} is Sera
[clone]{Anatomy} is Clone Cell
[Sf9]{Anatomy} is Sf9 Cell
[Spodoptera frugiperda]{Living Beings} is Spodoptera frugiperdas
[cells]{Anatomy} is Clone Cell
[expressing]{Physiology} is Protein expression
[secreted]{Physiology} is Secreted
[soluble]{Anatomy} is Soluble
[CHIKV]{Living Beings} is Chikungunya Virus
[E2 glycoprotein]{Chemicals & Drugs} is Glycoprotein
[plasmid]{Chemicals & Drugs} is Plasmid
[expression]{Procedures} is Expression
[insect]{Living Beings} is Insect
[cells]{Anatomy} is Cells set
[recombinant protein]{Chemicals & Drugs} is Recombinant protein
[serological diagnosis]{Procedures} is Serology
[CHIKV]{Living Beings} is Chikungunya Virus
[infection]{Disorders} is Infections
|
Acute [risk factors] for [suicide attempts] and [death]: [prospective findings] from the STEP - [BD] [study]
[Suicide] is unfortunately common in [psychiatric] [practice], but difficult to predict. The present [study] sought to assess which clinical [symptoms] increase in the months before [suicidal behavior] in a sample of [psychiatric] outpatients with [bipolar disorder]. Data from the Systematic Treatment Enhancement Program for [Bipolar Disorder] (STEP - [BD]) [trial] were used. A total of 103 [participants] who [attempted suicide] or died by [suicide] during the [trial] were included; a 15% random sample of the remaining [participants] (n = 427) was used as a comparison sample. Linear mixed models in the six months before [suicidal behavior] were conducted for each of five proposed acute [risk factors] for [suicidal behavior]. [Participants] were assessed using the [Clinical Monitoring Form] ([CMF]) at each [visit] for the following potential acute [risk factors] for [suicidal behavior]: [suicidal ideation], [loss of interest], [anxiety], [psychomotor agitation], and high-risk behavior. Each of the five [symptoms] was elevated overall in [individuals] who engaged in [suicidal behavior] (p < 0.05). The severity of both [suicidal ideation] and [loss of interest] significantly increased in the months before [suicidal behavior] (p < 0.001). [Anxiety] demonstrated comparable effect [sizes] across [multiple models]. [Psychomotor agitation] and high-risk behavior were not significantly elevated before [suicidal behavior]. [Suicidal ideation], [loss of interest] and, to a lesser [extent], [anxiety] may represent acute [suicide] [risk factors] up to four months before [suicidal behavior] in outpatients with [bipolar disorder]. Further [investigation] of these potential acute [risk factors] in [prospective analyses] is warranted.
|
[risk factors]{Disorders} is Risk Factors
[suicide attempts]{Disorders} is Suicide Attempt
[death]{Disorders} is Death (finding)
[prospective findings]{Procedures} is Study, Prospective
[BD]{Disorders} is Psychoses, Bipolar Affective
[study]{Procedures} is Study
[Suicide]{Disorders} is Suicides
[risk factors]{Disorders} is Risk Factors
[suicide attempts]{Disorders} is Suicide Attempt
[psychiatric]{Occupations} is Psychiatric
[death]{Disorders} is Death (finding)
[practice]{Physiology} is Practice Experience
[prospective findings]{Procedures} is Study, Prospective
[BD]{Disorders} is Psychoses, Bipolar Affective
[study]{Procedures} is Study
[study]{Procedures} is Study
[symptoms]{Disorders} is Symptoms
[suicidal behavior]{Disorders} is Suicidal behavior
[psychiatric]{Occupations} is Psychiatric
[bipolar disorder]{Disorders} is Psychoses, Bipolar Affective
[Bipolar Disorder]{Disorders} is Psychoses, Bipolar Affective
[BD]{Disorders} is Psychoses, Bipolar Affective
[trial]{Procedures} is Trial
[participants]{Living Beings} is Participant
[attempted suicide]{Disorders} is Suicide Attempt
[suicide]{Disorders} is Suicides
[trial]{Procedures} is Trial
[participants]{Living Beings} is Participant
[suicidal behavior]{Disorders} is Suicidal behavior
[risk factors]{Disorders} is Risk Factors
[suicidal behavior]{Disorders} is Suicidal behavior
[Participants]{Living Beings} is Participant
[Clinical Monitoring Form]{Procedures} is Clinical Trials, Monitoring
[CMF]{Procedures} is Clinical Trials, Monitoring
[visit]{Procedures} is Visit
[risk factors]{Disorders} is Risk Factors
[suicidal behavior]{Disorders} is Suicidal behavior
[suicidal ideation]{Disorders} is Suicidal Ideation
[loss of interest]{Disorders} is Loss of interest
[anxiety]{Disorders} is ANXIETY
[psychomotor agitation]{Disorders} is Psychomotor agitation
[symptoms]{Disorders} is Symptoms
[individuals]{Living Beings} is Individual (person)
[suicidal behavior]{Disorders} is Suicidal behavior
[suicidal ideation]{Disorders} is Suicidal Ideation
[loss of interest]{Disorders} is Loss of interest
[suicidal behavior]{Disorders} is Suicidal behavior
[Anxiety]{Disorders} is ANXIETY
[sizes]{Concepts & Ideas} is Size
[multiple models]{Concepts & Ideas} is Models
[Psychomotor agitation]{Disorders} is Psychomotor agitation
[suicidal behavior]{Disorders} is Suicidal behavior
[Suicidal ideation]{Disorders} is Suicidal Ideation
[loss of interest]{Disorders} is Loss of interest
[extent]{Concepts & Ideas} is Extent
[anxiety]{Disorders} is ANXIETY
[suicide]{Disorders} is Suicides
[risk factors]{Disorders} is Risk Factors
[suicidal behavior]{Disorders} is Suicidal behavior
[bipolar disorder]{Disorders} is Psychoses, Bipolar Affective
[investigation]{Procedures} is Evaluation Procedure
[risk factors]{Disorders} is Risk Factors
[prospective analyses]{Procedures} is Study, Prospective
|
Measurement of Outcomes of Upper Limb Reconstructive Surgery for [Tetraplegia]
Reconstructive arm/hand surgery for [tetraplegia] is performed to [improve] [arm/hand function] and therefore personal well-being for [individuals] who accept such [elective surgeries]. However, changes at an impairment level do not always translate into functional or quality of life changes. Therefore, multiple outcome tools should be used that incorporate sufficient responsiveness to [detect] changes in [arm/hand function], activity and participation, and quality of life of the [individuals] involved. This narrative review aims to [assist] [clinicians] to choose the most appropriate tools to assess the need for reconstructive surgery and to [evaluate] its outcomes. Our specific [objectives] are (1) to describe aspects to consider when choosing a measure and (2) to describe the measures advised by an international therapist consensus group established in 2007. All advised measures are appraised in terms of the underlying [construct], [administration], and clinical relevance to [arm/hand reconstructions]. Essentially there are currently no criterion standard measures to [evaluate] the consequences of reconstructive arm/hand surgery. However, with judicious use of available measures it is possible to ensure the [questions asked] or tasks completed are relevant to the [surgical reconstruction] (s) undertaken. Further work in this field is required. This would be best met by immediate collaboration between 2 outcome's tool developers and by analysis of pre - and postoperative data already held in various international sites, which would allow further [evaluation] of the measures already in use, or components thereof.
|
[Tetraplegia]{Disorders} is Tetraplegia
[tetraplegia]{Disorders} is Tetraplegia
[improve]{Disorders} is Improved
[Tetraplegia]{Disorders} is Tetraplegia
[arm/hand function]{Physiology} is Hand functions
[individuals]{Living Beings} is Individual (person)
[elective surgeries]{Procedures} is Elective surgery
[detect]{Disorders} is Detected
[arm/hand function]{Physiology} is Hand functions
[individuals]{Living Beings} is Individual (person)
[assist]{Procedures} is Assisting
[clinicians]{Living Beings} is Clinician
[evaluate]{Procedures} is Evaluate
[objectives]{Concepts & Ideas} is Objective
[construct]{Concepts & Ideas} is Construct
[administration]{Procedures} is Administration
[arm/hand reconstructions]{Procedures} is Hand reconstruction
[evaluate]{Procedures} is Evaluate
[questions asked]{Disorders} is Asks questions
[surgical reconstruction]{Procedures} is Surgical reconstruction
[evaluation]{Procedures} is Evaluate
|
Factors preventing [kneeling] in a group of pre-educated patients post [total knee arthroplasty]
[Difficulties in kneeling], one of the [poorest scoring functional outcomes] post [total knee arthroplasty] ([TKA]),have been attributed to a lack of patient education. This is the first study to investigate specific factors affecting a patient's [perceived] ability to kneel post [TKA], following exposure to a preoperative [kneeling] education session. A [cross-sectional study] was conducted following [TKA] with patients who had been educated about [kneeling] prior to the [operation]. Patients completed [kneeling] [questionnaires] at 6 (n = 115) and 12 (n = 82) months post [TKA]. In addition to the 12-month [kneeling] [questionnaire], patients also completed the [Oxford knee score] ([OKS]) survey. Seventy-two percent of patients [perceived] they could [kneel] at 12 months post [TKA]. Overall, [pain] and [discomfort] were the most common factors deterring patients from [kneeling]. [Perceived] [kneeling] ability was the poorest scored outcome on the [OKS] with patients reporting mild to moderate [difficulty] with this task. [Kneeling] scores were strongly correlated with overall [knee function scores] (R = 0.70), strongly correlated with [pain scores] (R = 0.45) and weakly correlated with [knee stability scores] (R = 0.29). When asked about other factors preventing [kneeling] other than [pain] or [discomfor] t, 75 % had reasons [unrelated] to the [knee] or [TKA]. The most common reason was 'problems with the other [knee] ' (n = 19). Patients in this study were provided with education regarding their [kneeling] ability post [TKA], yet still experienced limitations in [perceived] [kneeling] ability post operatively. Contrary to previous research, our study suggests that factors other than patient education [affect] a patient's [perceived] [kneeling] ability post [TKA].
|
[kneeling]{Physiology} is Kneeling function
[total knee arthroplasty]{Procedures} is Total Knee Arthroplasty
[Difficulties in kneeling]{Disorders} is Difficulty kneeling
[kneeling]{Physiology} is Kneeling function
[poorest scoring functional outcomes]{Disorders} is Investigation Finding
[total knee arthroplasty]{Procedures} is Total Knee Arthroplasty
[total knee arthroplasty]{Procedures} is Total Knee Arthroplasty
[TKA]{Procedures} is Total Knee Arthroplasty
[perceived]{Physiology} is Perceived
[TKA]{Procedures} is Total Knee Arthroplasty
[kneeling]{Physiology} is Kneeling function
[cross-sectional study]{Procedures} is Cross-Sectional Study
[TKA]{Procedures} is Total Knee Arthroplasty
[kneeling]{Physiology} is Kneeling function
[operation]{Procedures} is Operation
[kneeling]{Physiology} is Kneeling function
[questionnaires]{Concepts & Ideas} is Questionnaire
[TKA]{Procedures} is Total Knee Arthroplasty
[kneeling]{Physiology} is Kneeling function
[questionnaire]{Concepts & Ideas} is Questionnaire
[Oxford knee score]{Physiology} is Oxford knee score
[OKS]{Physiology} is Oxford knee score
[perceived]{Physiology} is Perceived
[kneel]{Physiology} is Kneeling function
[TKA]{Procedures} is Total Knee Arthroplasty
[pain]{Disorders} is Pain finding
[discomfort]{Disorders} is Actual Discomfort
[kneeling]{Physiology} is Kneeling function
[Perceived]{Physiology} is Perceived
[kneeling]{Physiology} is Kneeling function
[OKS]{Physiology} is Oxford knee score
[difficulty]{Disorders} is Difficulty kneeling
[Kneeling]{Physiology} is Kneeling function
[knee function scores]{Disorders} is Investigation Finding
[pain scores]{Disorders} is Pain score
[knee stability scores]{Disorders} is Investigation Finding
[kneeling]{Physiology} is Kneeling function
[pain]{Disorders} is Pain finding
[discomfor]{Disorders} is Actual Discomfort
[unrelated]{Disorders} is Unrelated
[knee]{Anatomy} is Bone structure of knee
[TKA]{Procedures} is Total Knee Arthroplasty
[knee]{Anatomy} is Bone structure of knee
[kneeling]{Physiology} is Kneeling function
[TKA]{Procedures} is Total Knee Arthroplasty
[perceived]{Physiology} is Perceived
[kneeling]{Physiology} is Kneeling function
[affect]{Procedures} is Assessment of affect
[perceived]{Physiology} is Perceived
[kneeling]{Physiology} is Kneeling function
[TKA]{Procedures} is Total Knee Arthroplasty
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[Improved] diagnostic yield of [neuromuscular disorders] applying clinical [exome sequencing] in patients arising from a consanguineous [population]
[Neuromuscular diseases] ([NMDs]) include a broad range of [disorders] affecting [muscles], [nerves] and [neuromuscular junctions]. Their overlapping phenotypes and heterogeneous genetic nature have created challenges in [diagnosis] which calls for the implementation of [massive parallel sequencing] as a candidate strategy to increase the diagnostic yield. In this [study], total of 45 patients, mostly offspring of consanguineous marriages were examined using [whole exome sequencing]. Data analysis was performed to identify the most probable [pathogenic] [rare variants] in known [NMD] [genes] which led to identification of causal variants for 33 out of 45 patients (73.3%) in the following known [genes]: [CAPN3], [Col6A1], [Col6A3], [DMD], [DYSF], [FHL1], [GJB1], [ISPD], [LAMA2], [LMNA], [PLEC1], [RYR1], [SGCA], [SGCB], [SYNE1], [TNNT1] and 22 novel [pathogenic] [variants] were [detected]. Today, the advantage of [whole exome sequencing] in [clinical diagnostic] strategies of [heterogeneous disorders] is clear. In this [cohort], a diagnostic yield of 73.3% was achieved which is quite high compared to the overall reported diagnostic yield of 25% to 50%. This could be explained by the consanguineous background of these patients and is another strong advantage of offering clinical [exome sequencing] in diagnostic [laboratories], especially in [populations] with high rate of [consanguinity].
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[Improved]{Disorders} is Improved
[neuromuscular disorders]{Disorders} is Neuromuscular disorders
[exome sequencing]{Procedures} is Exome Sequencing
[population]{Living Beings} is Population
[Improved]{Disorders} is Improved
[Neuromuscular diseases]{Disorders} is Neuromuscular disorders
[NMDs]{Disorders} is Neuromuscular disorders
[neuromuscular disorders]{Disorders} is Neuromuscular disorders
[disorders]{Disorders} is Disorders
[exome sequencing]{Procedures} is Exome Sequencing
[muscles]{Anatomy} is Muscle
[nerves]{Anatomy} is Nervus
[neuromuscular junctions]{Anatomy} is Neuromuscular Junctions
[population]{Living Beings} is Population
[diagnosis]{Disorders} is Diagnosis
[massive parallel sequencing]{Procedures} is Massively Parallel Sequencing
[study]{Procedures} is Study
[whole exome sequencing]{Procedures} is Exome Sequencing
[pathogenic]{Disorders} is Pathogenic
[rare variants]{Genes & Molecular Sequences} is Gene Variant
[NMD]{Disorders} is Neuromuscular disorders
[genes]{Genes & Molecular Sequences} is Genes
[genes]{Genes & Molecular Sequences} is Genes
[CAPN3]{Genes & Molecular Sequences} is CAPN3
[Col6A1]{Genes & Molecular Sequences} is COL6A1
[Col6A3]{Genes & Molecular Sequences} is COL6A3
[DMD]{Genes & Molecular Sequences} is DMD
[DYSF]{Genes & Molecular Sequences} is DYSF
[FHL1]{Genes & Molecular Sequences} is FHL1 gene
[GJB1]{Genes & Molecular Sequences} is GJB1
[ISPD]{Genes & Molecular Sequences} is IspD
[LAMA2]{Genes & Molecular Sequences} is LAMA2
[LMNA]{Genes & Molecular Sequences} is LMNA
[PLEC1]{Genes & Molecular Sequences} is PLEC
[RYR1]{Genes & Molecular Sequences} is RYR1
[SGCA]{Genes & Molecular Sequences} is SGCA
[SGCB]{Genes & Molecular Sequences} is SGCB
[SYNE1]{Genes & Molecular Sequences} is SYNE1
[TNNT1]{Genes & Molecular Sequences} is TNNT1
[pathogenic]{Disorders} is Pathogenic
[variants]{Genes & Molecular Sequences} is Gene Variant
[detected]{Disorders} is Detected
[whole exome sequencing]{Procedures} is Exome Sequencing
[clinical diagnostic]{Procedures} is Clinical diagnosis
[heterogeneous disorders]{Disorders} is Heterogeneous disorder
[cohort]{Living Beings} is Cohort
[exome sequencing]{Procedures} is Exome Sequencing
[laboratories]{Organizations} is Laboratories
[populations]{Living Beings} is Population
[consanguinity]{Disorders} is Consanguinities
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Laser -facilitated [epicutaneous] [immunotherapy] to [IgE-mediated allergy]
[Allergen specific immunotherapy] has been shown to be the only effective [treatment] for long-lasting clinical benefit to [IgE-mediated allergic diseases], but a fewer than 5% of patients choose the [treatment] because of inconvenience and a [high risk of] [anaphylaxis]. Recently, [epicutaneous allergen-specific immunotherapy] ([EPIT]) has proven effective, yet with limitations owing to [strong skin reactions]. We demonstrate here safer and faster [EPIT], named [μEPIT], by delivering [powdered allergen] and [adjuvants] into many [micropores] in the [epidermis]. We fabricated a microarray [patch] fractionally coated with a [powder mixture of ovalbumin] ([OVA]) model [allergen], [CpG], and [1,25-dihydroxyvitamin D3] ([VD3]). Topical application of the [patch] onto [laser-microperforated] [skin] resulted in a high level of [epidermal] delivery while greatly minimizing [allergen] [leakage] into [circulation system] as compared to current [subcutaneous immunotherapy] ([SCIT]). Moreover, only three times of [μEPIT] over two weeks could sufficiently inhibit [allergen-specific IgE] responses in [mice] suffering [OVA] -induced [airway hyperresponsivness] ([AHR]), which was unattainable by eight times of [SCIT] over three weeks. Mechanistically, [μEPIT] preferably enhanced [IgG2a] [production] suggesting [TH1-biased] [immune responses] and induced a high level of [T-regulatory] ([Treg]) [cells] against repeated [allergen sensitization]. The [immune tolerance] was confirmed by marked [reduction] in [airway wall] [thickness] as well as [eosinophil] and [neutrophil infiltration] into the [respiratory airway]. The [μEPIT] represents a novel and painless technology to [treat] [IgE-mediated allergic diseases] with little [local skin reaction] and a minimal risk of [anaphylaxis].
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[epicutaneous]{Procedures} is ADMIN CUTANEOUS
[immunotherapy]{Procedures} is Immunotherapy
[IgE-mediated allergy]{Disorders} is Atopic IgE-mediated allergic disorder
[Allergen specific immunotherapy]{Procedures} is Allergen immunotherapy
[epicutaneous]{Procedures} is ADMIN CUTANEOUS
[immunotherapy]{Procedures} is Immunotherapy
[IgE-mediated allergy]{Disorders} is Atopic IgE-mediated allergic disorder
[treatment]{Procedures} is Treatments
[IgE-mediated allergic diseases]{Disorders} is Atopic IgE-mediated allergic disorder
[treatment]{Procedures} is Treatments
[high risk of]{Disorders} is High risk of
[anaphylaxis]{Disorders} is Obsolete anaphylaxis
[epicutaneous allergen-specific immunotherapy]{Procedures} is Allergen immunotherapy
[EPIT]{Procedures} is Allergen immunotherapy
[strong skin reactions]{Physiology} is Reaction skin
[EPIT]{Procedures} is Allergen immunotherapy
[μEPIT]{Procedures} is Allergen immunotherapy
[powdered allergen]{Chemicals & Drugs} is ALLERGEN
[adjuvants]{Chemicals & Drugs} is ADJUVANTS IMMUNOL
[micropores]{Anatomy} is Pore
[epidermis]{Anatomy} is Epidermis structure
[patch]{Devices} is Skin patch
[powder mixture of ovalbumin]{Chemicals & Drugs} is Ovalbumin
[OVA]{Chemicals & Drugs} is Ovalbumin
[allergen]{Chemicals & Drugs} is ALLERGEN
[CpG]{Chemicals & Drugs} is CpG
[1,25-dihydroxyvitamin D3]{Chemicals & Drugs} is 1,25-Dihydroxyvitamin D3
[VD3]{Chemicals & Drugs} is 1,25-Dihydroxyvitamin D3
[patch]{Devices} is Skin patch
[laser-microperforated]{Disorders} is Microperforation
[skin]{Anatomy} is Skin of body
[epidermal]{Anatomy} is Epidermis structure
[allergen]{Chemicals & Drugs} is ALLERGEN
[leakage]{Disorders} is Leakage
[circulation system]{Anatomy} is Circulatory system
[subcutaneous immunotherapy]{Procedures} is Subcutaneous immunotherapy
[SCIT]{Procedures} is Subcutaneous immunotherapy
[μEPIT]{Procedures} is Allergen immunotherapy
[allergen-specific IgE]{Chemicals & Drugs} is Allergen specific IgE
[mice]{Living Beings} is Laboratory Mice
[OVA]{Chemicals & Drugs} is Ovalbumin
[airway hyperresponsivness]{Disorders} is Airway Hyper Responsiveness
[AHR]{Disorders} is Airway Hyper Responsiveness
[SCIT]{Procedures} is Subcutaneous immunotherapy
[μEPIT]{Procedures} is Allergen immunotherapy
[IgG2a]{Chemicals & Drugs} is IgG2A
[production]{Phenomena} is Antibody Production
[TH1-biased]{Anatomy} is Th1 cell
[immune responses]{Physiology} is Immune Response
[T-regulatory]{Anatomy} is Regulatory T-Cells
[Treg]{Anatomy} is Regulatory T-Cells
[cells]{Anatomy} is Cells set
[allergen sensitization]{Disorders} is Food allergen sensitization
[immune tolerance]{Disorders} is Immune Tolerance
[reduction]{Procedures} is Reduction
[airway wall]{Anatomy} is Airway
[thickness]{Disorders} is Increased thickness
[eosinophil]{Anatomy} is Eosinophil
[neutrophil infiltration]{Physiology} is Neutrophil Infiltration
[respiratory airway]{Anatomy} is Respiratory Tract
[μEPIT]{Procedures} is Allergen immunotherapy
[treat]{Procedures} is Treatments
[IgE-mediated allergic diseases]{Disorders} is Atopic IgE-mediated allergic disorder
[local skin reaction]{Physiology} is Reaction skin
[anaphylaxis]{Disorders} is Obsolete anaphylaxis
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Predicting real - [world] functional milestones in [schizophrenia]
[Schizophrenia] is a [severe disorder] that often causes impairments in major areas of functioning, and most patients do not achieve expected real - [world] functional milestones. The aim of this [study] was to identify which variables of demography, [illness] activity, and [functional capacity] predict patients ' ability to attain real - [world] functional milestones. [Participants] were 235 outpatients, 149 [men] and 86 [women], [diagnosed] with [schizophrenia] [spectrum disorder]. Our results showed that younger patients managed to achieve a higher level of functioning in [educational level], marital status, and [social contacts]. Patients ' [functional capacity] was primarily associated with [educational level] and housing situation. We also found that [women] needed less support regarding housing and obtained a higher level of marital status as compared with [men]. Our [findings] demonstrate the importance of considering current [symptoms], especially [negative] [symptoms], and [remission] stability over time, together with age, duration of illness, gender, [educational level], and current [functional capacity], when predicting patients ' future real - [world] functioning. We also conclude that there is an advantage in exploring [symptoms] divided into [positive], [negative], and general domains considering their probable impact on functional achievements.
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[world]{Living Beings} is World
[schizophrenia]{Disorders} is Schizophrenia
[Schizophrenia]{Disorders} is Schizophrenia
[world]{Living Beings} is World
[severe disorder]{Disorders} is Severe disorder
[schizophrenia]{Disorders} is Schizophrenia
[world]{Living Beings} is World
[study]{Procedures} is Study
[illness]{Disorders} is Illness
[functional capacity]{Disorders} is Functional capacity
[world]{Living Beings} is World
[Participants]{Living Beings} is Participant
[men]{Living Beings} is Men
[women]{Living Beings} is Women
[diagnosed]{Disorders} is Diagnosed
[schizophrenia]{Disorders} is Schizophrenia
[spectrum disorder]{Disorders} is Mental disorder (disorder)
[educational level]{Disorders} is Educational Level
[social contacts]{Disorders} is Finding (finding)
[functional capacity]{Disorders} is Functional capacity
[educational level]{Disorders} is Educational Level
[women]{Living Beings} is Women
[men]{Living Beings} is Men
[findings]{Disorders} is Finding (finding)
[symptoms]{Disorders} is Symptoms
[negative]{Disorders} is Negative for
[symptoms]{Disorders} is Symptoms
[remission]{Disorders} is Remission
[educational level]{Disorders} is Educational Level
[functional capacity]{Disorders} is Functional capacity
[world]{Living Beings} is World
[symptoms]{Disorders} is Symptoms
[positive]{Disorders} is Positive for
[negative]{Disorders} is Negative for
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[LDLR], [ApoB] and [ApoE genes] polymorphisms and classical [risk factors] in [premature coronary artery disease]
[Lipoproteins] play a central role in the development of [atherosclerotic disease]. So, with their ability to affect [lipid levels], the [LDLR], [ApoB] and [ApoE] polymorphisms could be one of the factors influencing development of [atherosclerosis]. This hypothesis has been [tested] in different populations with conflicting results. The purpose of the present study was to investigate the association between the [LDLR], [ApoB] and [ApoE genes] polymorphisms with [premature CAD] ([PCAD]) in [Egyptians]. One hundred thirty-five patients of [PCAD] and one hundred thirty-two ages and sex matched control subjects were included in the study. [LDLR] and [ApoB genes] polymorphisms were [analyzed] by [polymerase chain reaction] ([PCR]). The [ApoE] genotypes were identified by [multiplex amplification refractory mutation system] ([multi-AMRS]). We found that [LDLR A(+)A(+)] genotype, [ApoB X(+)] [allele] and [ApoE E4] [allele] increased the risk of [PCAD] by 1.8, 2.1 and 12.1 respectively. The present study proved that smoking, [metabolic syndrome], [ApoB X(+)X(+)] genotype and [ApoE E4] [allele] were independent [risk factors] for the development of [PCAD]. This is the first study investigate the association between [low density lipoprotein receptor], [apolipoprotein B] and [apolipoprotein E genes] polymorphisms with [PCAD] and [lipid levels] in [Egyptians] and we concluded that the [LDLR A(+)A(+)] genotype, [ApoB X(+)] [allele] and [ApoE E4] [allele] may be associated with an increased risk for development of [PCAD] by elevated [levels of total cholesterol (TC)] and [low density lipoprotein] ([LDLc]). The coexistence of [CAD] [risk factors] with [LDLR A(+)A(+)] genotype, [ApoB X(+)] [allele] and [ApoE E4] [allele] may increase the risk of the development of [PCAD] in [Egyptian] patients.
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[LDLR]{Genes & Molecular Sequences} is LDLR Gene
[ApoB]{Genes & Molecular Sequences} is APOB
[ApoE genes]{Genes & Molecular Sequences} is APOE gene
[risk factors]{Disorders} is Risk Factors
[premature coronary artery disease]{Disorders} is Premature coronary artery disease
[LDLR]{Genes & Molecular Sequences} is LDLR Gene
[Lipoproteins]{Chemicals & Drugs} is Lipoproteins
[ApoB]{Genes & Molecular Sequences} is APOB
[ApoE genes]{Genes & Molecular Sequences} is APOE gene
[risk factors]{Disorders} is Risk Factors
[atherosclerotic disease]{Disorders} is Atherosclerotic cardiovascular disease
[premature coronary artery disease]{Disorders} is Premature coronary artery disease
[lipid levels]{Phenomena} is Lipid level
[LDLR]{Genes & Molecular Sequences} is LDLR Gene
[ApoB]{Genes & Molecular Sequences} is APOB
[ApoE]{Genes & Molecular Sequences} is APOE gene
[atherosclerosis]{Disorders} is Atherosclerotic cardiovascular disease
[tested]{Concepts & Ideas} is Tests
[LDLR]{Genes & Molecular Sequences} is LDLR Gene
[ApoB]{Genes & Molecular Sequences} is APOB
[ApoE genes]{Genes & Molecular Sequences} is APOE gene
[premature CAD]{Disorders} is Premature coronary artery disease
[PCAD]{Disorders} is Premature coronary artery disease
[Egyptians]{Living Beings} is Egyptians
[PCAD]{Disorders} is Premature coronary artery disease
[LDLR]{Genes & Molecular Sequences} is LDLR Gene
[ApoB genes]{Genes & Molecular Sequences} is APOB
[analyzed]{Procedures} is Analyzed
[polymerase chain reaction]{Procedures} is Polymerase Chain Reaction
[PCR]{Procedures} is Polymerase Chain Reaction
[ApoE]{Genes & Molecular Sequences} is APOE gene
[multiplex amplification refractory mutation system]{Procedures} is Analysis using amplification refractory mutation system PCR
[multi-AMRS]{Procedures} is Analysis using amplification refractory mutation system PCR
[LDLR A(+)A(+)]{Genes & Molecular Sequences} is LDLR Gene
[ApoB X(+)]{Genes & Molecular Sequences} is APOB
[allele]{Genes & Molecular Sequences} is Allele
[ApoE E4]{Genes & Molecular Sequences} is APOE gene
[allele]{Genes & Molecular Sequences} is Allele
[PCAD]{Disorders} is Premature coronary artery disease
[metabolic syndrome]{Disorders} is Metabolic syndrome
[ApoB X(+)X(+)]{Genes & Molecular Sequences} is APOB
[ApoE E4]{Genes & Molecular Sequences} is APOE gene
[allele]{Genes & Molecular Sequences} is Allele
[risk factors]{Disorders} is Risk Factors
[PCAD]{Disorders} is Premature coronary artery disease
[low density lipoprotein receptor]{Genes & Molecular Sequences} is LDLR Gene
[apolipoprotein B]{Genes & Molecular Sequences} is APOB
[apolipoprotein E genes]{Genes & Molecular Sequences} is APOE gene
[PCAD]{Disorders} is Premature coronary artery disease
[lipid levels]{Phenomena} is Lipid level
[Egyptians]{Living Beings} is Egyptians
[LDLR A(+)A(+)]{Genes & Molecular Sequences} is LDLR Gene
[ApoB X(+)]{Genes & Molecular Sequences} is APOB
[allele]{Genes & Molecular Sequences} is Allele
[ApoE E4]{Genes & Molecular Sequences} is APOE gene
[allele]{Genes & Molecular Sequences} is Allele
[PCAD]{Disorders} is Premature coronary artery disease
[levels of total cholesterol (TC)]{Procedures} is Cholesterol level
[low density lipoprotein]{Procedures} is Low density lipoprotein measurement
[LDLc]{Procedures} is Low density lipoprotein measurement
[CAD]{Disorders} is Premature coronary artery disease
[risk factors]{Disorders} is Risk Factors
[LDLR A(+)A(+)]{Genes & Molecular Sequences} is LDLR Gene
[ApoB X(+)]{Genes & Molecular Sequences} is APOB
[allele]{Genes & Molecular Sequences} is Allele
[ApoE E4]{Genes & Molecular Sequences} is APOE gene
[allele]{Genes & Molecular Sequences} is Allele
[PCAD]{Disorders} is Premature coronary artery disease
[Egyptian]{Living Beings} is Egyptians
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[Mandibular] [kinesiographic pattern] of [women] with chronic [TMD] after [management] with [educational] and [self-care therapies]: A [double-blind], [randomized clinical trial]
[Limited mandibular movements] are one of the most important [signs] of [temporomandibular disorders] ([TMDs]) and may cause functional difficulties. The purpose of this [double-blind], [randomized clinical trial] was to [evaluate] the effect of [treatment] with only [educational] or [education] associated with [self-care therapies] on the [pattern] of [mandibular] [movements] of [women] with [chronic painful] [TMDs]. Forty-two [women] were selected and randomly divided into 3 groups, control group (CG, n=13), education group (EG, n=16), and education and self-care group (ESG, n=13), according to the sequence of [treatment] they received. A [kinesiograph device] recorded [mandibular] [movements] during maximum [mouth] [opening] and [mastication] at baseline (T0) and at 30-day (T1) and 60-day (T2) [follow-up]. [Kinesiographic data] were statistically analyzed using 1-way ANOVA, followed by the Bonferroni test for multiple comparisons of means (α=.05). The ESG group demonstrated an improvement in the [maximum vertical opening] ([MVO] = 5.1 ±3.4 mm; P=.012) and [anteroposterior mandibular movement] ([MAM]) during maximum [opening] (7.4 ±9.5; P=.019), significantly higher than that of the EG ([MVO] =1.8 ±3.5 mm; [MAM] =0.8 ±5.0 mm) and the CG ([MVO] =0.9 ±3.8 mm; [MAM] =0.8 ±4.4 mm) after 30 days of [follow-up]. Moreover, at T1, [vertical] [mandibular] [movement] during [mastication] was significantly higher in the ESG group (17.4 ±1.7 mm) than in the EG group (15.0 ±2.8, P=.027). [No significant] differences were [found] between the [women] who received [treatment] with [educational] and [self-care therapies] for 60 days and the [women] who received this [treatment] for 30 days. In the short-term, [education] and [self-care treatment] [positively] influenced the [mandibular] [movement] [pattern] of [women] with [chronic painful] [TMDs].
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[Mandibular]{Anatomy} is Mandibular
[kinesiographic pattern]{Concepts & Ideas} is Intellectual Product
[women]{Living Beings} is Women
[TMD]{Disorders} is TMJ DIS
[management]{Procedures} is DIS MANAGEMENT
[educational]{Concepts & Ideas} is Education
[self-care therapies]{Procedures} is Self-care practice (regime/therapy)
[double-blind]{Procedures} is Double-Blinded
[randomized clinical trial]{Procedures} is Randomized clinical trial
[Mandibular]{Anatomy} is Mandibular
[Limited mandibular movements]{Disorders} is Limited mandibular mobility
[kinesiographic pattern]{Concepts & Ideas} is Intellectual Product
[women]{Living Beings} is Women
[TMD]{Disorders} is TMJ DIS
[signs]{Disorders} is SIGNS SYMPTOMS
[management]{Procedures} is DIS MANAGEMENT
[temporomandibular disorders]{Disorders} is TMJ DIS
[educational]{Concepts & Ideas} is Education
[TMDs]{Disorders} is TMJ DIS
[self-care therapies]{Procedures} is Self-care practice (regime/therapy)
[double-blind]{Procedures} is Double-Blinded
[randomized clinical trial]{Procedures} is Randomized clinical trial
[double-blind]{Procedures} is Double-Blinded
[randomized clinical trial]{Procedures} is Randomized clinical trial
[evaluate]{Procedures} is Evaluate
[treatment]{Procedures} is Treatments
[educational]{Concepts & Ideas} is Education
[education]{Concepts & Ideas} is Education
[self-care therapies]{Procedures} is Self-care practice (regime/therapy)
[pattern]{Concepts & Ideas} is Intellectual Product
[mandibular]{Anatomy} is Mandibular
[movements]{Physiology} is Movements
[women]{Living Beings} is Women
[chronic painful]{Disorders} is Chronic Pain
[TMDs]{Disorders} is TMJ DIS
[women]{Living Beings} is Women
[treatment]{Procedures} is Treatments
[kinesiograph device]{Devices} is Device
[mandibular]{Anatomy} is Mandibular
[movements]{Physiology} is Movements
[mouth]{Anatomy} is Cavity of mouth
[opening]{Physiology} is Movements
[mastication]{Physiology} is Mastication (function)
[follow-up]{Procedures} is Follow-up
[Kinesiographic data]{Concepts & Ideas} is Clinical Data
[maximum vertical opening]{Physiology} is Movements
[MVO]{Physiology} is Movements
[anteroposterior mandibular movement]{Physiology} is Movements
[MAM]{Physiology} is Movements
[opening]{Physiology} is Movements
[MVO]{Physiology} is Movements
[MAM]{Physiology} is Movements
[MVO]{Physiology} is Movements
[MAM]{Physiology} is Movements
[follow-up]{Procedures} is Follow-up
[vertical]{Concepts & Ideas} is Vertical
[mandibular]{Anatomy} is Mandibular
[movement]{Physiology} is Movements
[mastication]{Physiology} is Mastication (function)
[No significant]{Disorders} is Not significant
[found]{Disorders} is Found
[women]{Living Beings} is Women
[treatment]{Procedures} is Treatments
[educational]{Concepts & Ideas} is Education
[self-care therapies]{Procedures} is Self-care practice (regime/therapy)
[women]{Living Beings} is Women
[treatment]{Procedures} is Treatments
[education]{Concepts & Ideas} is Education
[self-care treatment]{Procedures} is Self-care practice (regime/therapy)
[positively]{Disorders} is Positive for
[mandibular]{Anatomy} is Mandibular
[movement]{Physiology} is Movements
[pattern]{Concepts & Ideas} is Intellectual Product
[women]{Living Beings} is Women
[chronic painful]{Disorders} is Chronic Pain
[TMDs]{Disorders} is TMJ DIS
|
[MiR-211] is [epigenetically regulated] by [DNMT1] mediated [methylation] and inhibits [EMT] of [melanoma cells] by [targeting] [RAB22A]
[MiR-211] has strong inhibitive effects on [melanoma] [cell growth], [invasion] and [metastasis]. However, how it is [downregulated] and whether other [genes] are involved its [downstream] [regulation] in [melanoma] are not clear. In this study, we firstly verified the [expression] of [miR-211] in [melanoma cell lines] and observed that its [downregulation] is associated with increased [DNMT1] [expression]. By performing [qRT-PCR] and [MSP analysis], we confirmed that [DNMT1] is [negatively] correlated with [miR-211] [expression] and can [modulate] [DNA methylation] in the [promoter region] of [miR-211]. By performing [bioinformatics analysis], we found that [RAB22A] is a possible target of [miR-211], which has two broadly [conversed] [binding sites] with [miR-211] in the [3'UTR]. Following dual [luciferase] [assay], [qRT-PCR] and [western blot analysis] confirmed the direct [binding] between [miR-211] and [RAB22A] and the [suppressive effect] of [miR-211] on [RAB22A] [expression]. [Knockdown] of [RAB22A] increased epithelial properties and impaired mesenchymal properties of the [melanoma cells], suggesting that [miR-211] [modulates] [epithelial mesenchymal transition] ([EMT]) of [melanoma cells] via [downregulating] [RAB22A]. In summary, the present study firstly demonstrated that [DNMT1] mediated [promoter] [methylation] is a mechanism of [miRNA] [suppression] in [melanoma] and revealed a new [tumor suppressor] role of the [miR-211] by [targeting] [RAB22A] in [melanoma]. The [DNMT1] / [miR-211] / [RAB22A] axis provides a novel insight into the [pathogenesis] of [melanoma], particularly in the [EMT process].
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[MiR-211]{Genes & Molecular Sequences} is MIR211
[epigenetically regulated]{Physiology} is Regulation of gene expression, epigenetic
[DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene
[methylation]{Physiology} is Methylations
[EMT]{Physiology} is EMT
[melanoma cells]{Anatomy} is Melanoma Cell
[targeting]{Procedures} is Gene Targeting
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[MiR-211]{Genes & Molecular Sequences} is MIR211
[epigenetically regulated]{Physiology} is Regulation of gene expression, epigenetic
[DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene
[melanoma]{Disorders} is Melanoma
[cell growth]{Physiology} is Cell Growth
[methylation]{Physiology} is Methylations
[invasion]{Disorders} is Cell Invasion
[metastasis]{Disorders} is Metastasis
[EMT]{Physiology} is EMT
[melanoma cells]{Anatomy} is Melanoma Cell
[targeting]{Procedures} is Gene Targeting
[downregulated]{Physiology} is Downregulation
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[genes]{Genes & Molecular Sequences} is Genes
[downstream]{Concepts & Ideas} is Downstream
[regulation]{Physiology} is Downregulation
[melanoma]{Disorders} is Melanoma
[expression]{Physiology} is Expression
[miR-211]{Genes & Molecular Sequences} is MIR211
[melanoma cell lines]{Anatomy} is Melanoma Cell
[downregulation]{Physiology} is Downregulation
[DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene
[expression]{Physiology} is Expression
[qRT-PCR]{Procedures} is QRT-PCR
[MSP analysis]{Procedures} is Microspectrophotometries
[DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene
[negatively]{Disorders} is NEGATIVE
[miR-211]{Genes & Molecular Sequences} is MIR211
[expression]{Physiology} is Expression
[modulate]{Concepts & Ideas} is Modulate
[DNA methylation]{Physiology} is DNA methylation
[promoter region]{Chemicals & Drugs} is Promoter Region
[miR-211]{Genes & Molecular Sequences} is MIR211
[bioinformatics analysis]{Occupations} is Bioinformatics
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[miR-211]{Genes & Molecular Sequences} is MIR211
[conversed]{Genes & Molecular Sequences} is CONSERVED SEQ
[binding sites]{Chemicals & Drugs} is Binding Sites
[miR-211]{Genes & Molecular Sequences} is MIR211
[3'UTR]{Genes & Molecular Sequences} is 3'UTR
[luciferase]{Chemicals & Drugs} is Luciferase
[assay]{Procedures} is BIOL ASSAY
[qRT-PCR]{Procedures} is QRT-PCR
[western blot analysis]{Procedures} is Blot, Western
[binding]{Physiology} is Binding
[miR-211]{Genes & Molecular Sequences} is MIR211
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[suppressive effect]{Physiology} is SUPPRESSION GENET
[miR-211]{Genes & Molecular Sequences} is MIR211
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[expression]{Physiology} is Expression
[Knockdown]{Procedures} is Gene Knockdown
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[melanoma cells]{Anatomy} is Melanoma Cell
[miR-211]{Genes & Molecular Sequences} is MIR211
[modulates]{Concepts & Ideas} is Modulate
[epithelial mesenchymal transition]{Physiology} is EMT
[EMT]{Physiology} is EMT
[melanoma cells]{Anatomy} is Melanoma Cell
[downregulating]{Physiology} is Downregulation
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene
[promoter]{Chemicals & Drugs} is Promoter Region
[methylation]{Physiology} is Methylations
[miRNA]{Chemicals & Drugs} is MiRNA
[suppression]{Physiology} is SUPPRESSION GENET
[melanoma]{Disorders} is Melanoma
[tumor suppressor]{Genes & Molecular Sequences} is Tumor Suppressor
[miR-211]{Genes & Molecular Sequences} is MIR211
[targeting]{Procedures} is Gene Targeting
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[melanoma]{Disorders} is Melanoma
[DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene
[miR-211]{Genes & Molecular Sequences} is MIR211
[RAB22A]{Genes & Molecular Sequences} is RAB22A
[pathogenesis]{Disorders} is Pathogenesis
[melanoma]{Disorders} is Melanoma
[EMT process]{Physiology} is EMT
|
[Body mass index] and [suicide] methods
[Overweight] and [obesity] is associated with lower rates of [suicide]. However, little is known about the association with different [suicide] methods. We studied the association between groups of [body mass index] and [suicide] methods. We identified all [medicolegal] [autopsy] cases with a [cause of death] due to external causes in [Sweden] during 1999-2013 (N = 39,368) and included 11,715 [suicides] and 13,316 accidents or homicides as controls. We applied multinomial [regression models] adjusted for age, sex, year and season of [death]. [Obesity] was associated with [suicidal] [intoxication], OR 1.15 (95% confidence interval (CI) 1.02, 1.30) and [negatively] associated with all other [suicide] methods studied. [Underweight] showed a [negative] association with [suicidal] [drowning] and there was an indication towards a [negative] association with [hanging] in [men] OR 0.81 (95% CI 0.65, 1.01). We conclude that [body mass index] ([BMI]) is associated with the choice of [suicide] method. This may be of importance in a [public health perspective], e.g. potential for [prevention] of [intoxications]. In the practice of [forensic medicine], the [physician's] level of [suspicion] may rise if the apparent [suicidal] method is less common for the individual characteristics of the [deceased], such as [BMI].
|
[Body mass index]{Physiology} is Body Mass Index
[suicide]{Disorders} is Suicides
[Overweight]{Disorders} is Overweight
[Body mass index]{Physiology} is Body Mass Index
[obesity]{Disorders} is Obesity (disorder)
[suicide]{Disorders} is Suicides
[suicide]{Disorders} is Suicides
[suicide]{Disorders} is Suicides
[body mass index]{Physiology} is Body Mass Index
[suicide]{Disorders} is Suicides
[medicolegal]{Concepts & Ideas} is Medicolegal aspects
[autopsy]{Procedures} is Autopsy
[cause of death]{Disorders} is Cause of Death
[Sweden]{Geographic Areas} is Sweden
[suicides]{Disorders} is Suicides
[regression models]{Concepts & Ideas} is REGRESSION ANAL
[death]{Disorders} is Death (finding)
[Obesity]{Disorders} is Obesity (disorder)
[suicidal]{Disorders} is Suicidal
[intoxication]{Disorders} is Intoxication
[negatively]{Disorders} is Negative for
[suicide]{Disorders} is Suicides
[Underweight]{Disorders} is Underweight
[negative]{Disorders} is Negative for
[suicidal]{Disorders} is Suicidal
[drowning]{Disorders} is Drowning
[negative]{Disorders} is Negative for
[hanging]{Disorders} is Hanging
[men]{Living Beings} is Men
[body mass index]{Physiology} is Body Mass Index
[BMI]{Physiology} is Body Mass Index
[suicide]{Disorders} is Suicides
[public health perspective]{Procedures} is Public health service
[prevention]{Procedures} is Suicide prevention
[intoxications]{Disorders} is Intoxication
[forensic medicine]{Occupations} is Forensic Medicine
[physician's]{Living Beings} is Physician
[suspicion]{Physiology} is Suspicion
[suicidal]{Disorders} is Suicidal
[deceased]{Physiology} is Deceased
[BMI]{Physiology} is Body Mass Index
|
[Cognitive impairment] in [HIV] and [HCV] [co-infected] patients: a systematic [review] and [meta-analysis]
[Cognitive impairment] has been well documented in [human immunodeficiency virus] ([HIV]) and [hepatitis C virus] ([HCV]) [mono-infections]. However, in the context of [HIV] / [HCV] [co-infection] the research is more limited. The aim of this systematic [review] was to describe the characteristics of [cognitive impairment] in [HIV] / [HCV] [co-infection] and to [examine] the differences in [cognitive performance] between [HIV] / [HCV] and [HIV] and [HCV] [mono-infected] patients. Of the 437 records initially [screened], 24 papers met the inclusion criteria and were included in the systematic [review]. Four [studies] were included in the [meta-analysis]. Most [studies] indicated that [HIV] / [HCV] [co-infected] patients had a higher level of [cognitive impairment] than [HIV] [mono-infected] patients. [Meta-analysis] also indicated that [HIV] [mono-infected] patients had a significantly lower global deficit score than [co-infected] patients. The results also indicated that [co-infected] patients were more likely to be [impaired] in information processing speed than [HIV] [mono-infected] patients. These [findings] can be challenged by biasing factors such as the small number of included [studies], heterogeneity of the samples and a large diversity of methodological procedures. Future research with consistent and comprehensive [neuropsychological batteries] and covering a greater diversity of [risk factors] is needed, in order to clarify the effects of both [viruses] on [cognitive function] and the mechanisms that underlie these effects. Because [cognitive impairments] may pose significant [challenges] to [medication adherence], quality of life and overall functioning, such knowledge may have important implications to the [planning] and [implementation] of effective interventions aimed at optimising the [clinical management] of these [infections].
|
[Cognitive impairment]{Disorders} is Cognitive impairment
[HIV]{Living Beings} is HIV
[HCV]{Living Beings} is HCV
[co-infected]{Disorders} is Co-infections
[review]{Concepts & Ideas} is Review
[meta-analysis]{Procedures} is Meta-analysis
[Cognitive impairment]{Disorders} is Cognitive impairment
[HIV]{Living Beings} is HIV
[HCV]{Living Beings} is HCV
[co-infected]{Disorders} is Co-infections
[human immunodeficiency virus]{Living Beings} is HIV
[review]{Concepts & Ideas} is Review
[HIV]{Living Beings} is HIV
[meta-analysis]{Procedures} is Meta-analysis
[hepatitis C virus]{Living Beings} is HCV
[HCV]{Living Beings} is HCV
[mono-infections]{Disorders} is Infections
[HIV]{Living Beings} is HIV
[HCV]{Living Beings} is HCV
[co-infection]{Disorders} is Co-infections
[review]{Concepts & Ideas} is Review
[cognitive impairment]{Disorders} is Cognitive impairment
[HIV]{Living Beings} is HIV
[HCV]{Living Beings} is HCV
[co-infection]{Disorders} is Co-infections
[examine]{Disorders} is Examined
[cognitive performance]{Physiology} is Cognitive functions
[HIV]{Living Beings} is HIV
[HCV]{Living Beings} is HCV
[HIV]{Living Beings} is HIV
[HCV]{Living Beings} is HCV
[mono-infected]{Disorders} is Infections
[screened]{Procedures} is Screenings
[review]{Concepts & Ideas} is Review
[studies]{Procedures} is Study
[meta-analysis]{Procedures} is Meta-analysis
[studies]{Procedures} is Study
[HIV]{Living Beings} is HIV
[HCV]{Living Beings} is HCV
[co-infected]{Disorders} is Co-infections
[cognitive impairment]{Disorders} is Cognitive impairment
[HIV]{Living Beings} is HIV
[mono-infected]{Disorders} is Infections
[Meta-analysis]{Procedures} is Meta-analysis
[HIV]{Living Beings} is HIV
[mono-infected]{Disorders} is Infections
[co-infected]{Disorders} is Co-infections
[co-infected]{Disorders} is Co-infections
[impaired]{Disorders} is Cognitive impairment
[HIV]{Living Beings} is HIV
[mono-infected]{Disorders} is Infections
[findings]{Disorders} is Finding (finding)
[studies]{Procedures} is Study
[neuropsychological batteries]{Concepts & Ideas} is Neuropsychological battery
[risk factors]{Disorders} is Risk Factors
[viruses]{Living Beings} is Virus
[cognitive function]{Physiology} is Cognitive functions
[cognitive impairments]{Disorders} is Cognitive impairment
[challenges]{Procedures} is Challenge
[medication adherence]{Disorders} is Medication adherence
[planning]{Procedures} is Health Planning
[implementation]{Procedures} is Health Plan Implementation
[clinical management]{Procedures} is Clinical Management
[infections]{Disorders} is Infections
|
Usefulness of [Embolization] for [Iatrogenic] [Dural Arteriovenous Fistula] Associated with Recurrent [Chronic Subdural Hematoma]: A [Case Report] and [Literature Review]
Refractory [chronic subdural hematomas] due to [iatrogenic] [dural arteriovenous fistulas] ([dAVFs]) are difficult to treat. We report our experience and propose a guideline on basis of a [literature review] for the usefulness of [embolization] of [middle meningeal artery] ([MMA]) for the [treatment] of the same. We report a case with [right hemiparesis] and [aphasia] 1 month after a [fall] from a bicycle. [Computed tomography scan] of the [head] showed [left] [chronic subdural hematoma], which was evacuated by burr-hole drainage. The postoperative course was complicated by [reaccumulation] within short period of time. On [superselective digital subtraction angiography] of [MMA], [iatrogenic] [dAVF] was found on [left side]. We [embolized] successfully it using [n-butyl cyanoacrylate] after a third [irrigation]. No [reaccumulation] found in the postoperative period or at last [follow-up]. We propose [treatment protocol] based on our experience and [literature review]. Refractory [chronic subdural hematoma] with [reaccumulation] within a short interval should be subjected to [digital subtraction angiography] of the [MMA]. [Embolization] of [ipsilateral] [MMA] is safe, effective, and a useful option for the [treatment] of [iatrogenic] [dAVF] and resolution of [hematoma].
|
[Embolization]{Procedures} is Embolization
[Iatrogenic]{Disorders} is Iatrogenesis
[Dural Arteriovenous Fistula]{Disorders} is Dural arteriovenous fistula
[Chronic Subdural Hematoma]{Disorders} is Chronic subdural hematoma
[Case Report]{Concepts & Ideas} is Case report
[Literature Review]{Concepts & Ideas} is Review Literature
[chronic subdural hematomas]{Disorders} is Chronic subdural hematoma
[Embolization]{Procedures} is Embolization
[Iatrogenic]{Disorders} is Iatrogenesis
[Dural Arteriovenous Fistula]{Disorders} is Dural arteriovenous fistula
[iatrogenic]{Disorders} is Iatrogenesis
[dural arteriovenous fistulas]{Disorders} is Dural arteriovenous fistula
[dAVFs]{Disorders} is Dural arteriovenous fistula
[Chronic Subdural Hematoma]{Disorders} is Chronic subdural hematoma
[Case Report]{Concepts & Ideas} is Case report
[Literature Review]{Concepts & Ideas} is Review Literature
[literature review]{Concepts & Ideas} is Review Literature
[embolization]{Procedures} is Embolization
[middle meningeal artery]{Anatomy} is Structure of middle meningeal artery
[MMA]{Anatomy} is Structure of middle meningeal artery
[treatment]{Procedures} is Treatments
[right hemiparesis]{Disorders} is Right hemiparesis
[aphasia]{Disorders} is Aphasia
[fall]{Disorders} is Fall
[Computed tomography scan]{Procedures} is Computed tomography scan -
[head]{Anatomy} is Heads
[left]{Concepts & Ideas} is Left sided
[chronic subdural hematoma]{Disorders} is Chronic subdural hematoma
[reaccumulation]{Disorders} is Accumulation
[superselective digital subtraction angiography]{Procedures} is Digital Subtraction Angiography
[MMA]{Anatomy} is Structure of middle meningeal artery
[iatrogenic]{Disorders} is Iatrogenesis
[dAVF]{Disorders} is Dural arteriovenous fistula
[left side]{Concepts & Ideas} is Left side
[embolized]{Procedures} is Embolization
[n-butyl cyanoacrylate]{Chemicals & Drugs} is N-butyl-cyanoacrylate
[irrigation]{Procedures} is Therapeutic Irrigation
[reaccumulation]{Disorders} is Accumulation
[follow-up]{Procedures} is Follow-up
[treatment protocol]{Procedures} is Treatment Protocol
[literature review]{Concepts & Ideas} is Review Literature
[chronic subdural hematoma]{Disorders} is Chronic subdural hematoma
[reaccumulation]{Disorders} is Accumulation
[digital subtraction angiography]{Procedures} is Digital Subtraction Angiography
[MMA]{Anatomy} is Structure of middle meningeal artery
[Embolization]{Procedures} is Embolization
[ipsilateral]{Concepts & Ideas} is Ipsilateral
[MMA]{Anatomy} is Structure of middle meningeal artery
[treatment]{Procedures} is Treatments
[iatrogenic]{Disorders} is Iatrogenesis
[dAVF]{Disorders} is Dural arteriovenous fistula
[hematoma]{Disorders} is Hematoma subdural
|
Incidence of [crown fracture] and [risk factors] in the [primary dentition]: a [prospective longitudinal study]
Few studies have assessed the incidence and [risk factors] to [crown fractures] in preschool children. The aim of this study was to estimate the incidence of [crown fracture] in the [primary dentition] over a 1-year [follow-up] period, identify [risk factors], and test the hypothesis that children with previous [crown fracture] are more prone to experience further cases of [crown fracture] independently of other [risk factors]. This study was developed in two phases: [cross-sectional] and [prospective longitudinal study]. The [cross-sectional study] was carried out 261 preschool children. The [prospective longitudinal study] was carried out 194 children allocated to two groups: [exposed group] (children with prior exposure to [crown fracture]) and [non] - [exposed group] (children without prior exposure). On both occasions, children were examined for the [diagnosis] of [crown fracture] and evaluation of [lip] coverage and [overjet]. The parents were interviewed with regard to the socioeconomic indicators. New cases of [crown fracture] were identified based on the comparison of the two examinations. Data analysis involved [Pearson's chi-square test], [McNemar's test], and [Poisson regression] with robust variance. Among the 261 children who participated in the [cross-sectional study], 194 were re-examined (65 in the [exposed group] and 129 in the [non] - [exposed group]). The overall incidence of [crown fracture] was 55.7% (n = 108). The difference in percentage of [increased risk of] [crown fracture] in exposed and [non] - [exposed groups] was 13.4%. A greater incidence of [crown fracture] was found in the exposed group (64.6%; P < 0,001). The children exposed (RR: 1.30; 95% CI: 1.01-1.67) had a [greater risk of] developing new cases of [crown fracture] in comparison with the [non] - [exposed group]. The incidence of [crown fracture] was high and children with previous [crown fracture] had a [greater risk of] suffering new cases of [crown fracture] during the 1-year [follow-up] period.
|
[crown fracture]{Disorders} is Tooth crown fracture
[risk factors]{Disorders} is Risk Factors
[primary dentition]{Anatomy} is Primary dentition
[prospective longitudinal study]{Procedures} is Longitudinal Study
[crown fracture]{Disorders} is Tooth crown fracture
[risk factors]{Disorders} is Risk Factors
[risk factors]{Disorders} is Risk Factors
[primary dentition]{Anatomy} is Primary dentition
[crown fractures]{Disorders} is Tooth crown fracture
[prospective longitudinal study]{Procedures} is Longitudinal Study
[crown fracture]{Disorders} is Tooth crown fracture
[primary dentition]{Anatomy} is Primary dentition
[follow-up]{Procedures} is Follow-up
[risk factors]{Disorders} is Risk Factors
[crown fracture]{Disorders} is Tooth crown fracture
[crown fracture]{Disorders} is Tooth crown fracture
[risk factors]{Disorders} is Risk Factors
[cross-sectional]{Procedures} is Cross-Sectional Study
[prospective longitudinal study]{Procedures} is Longitudinal Study
[cross-sectional study]{Procedures} is Cross-Sectional Study
[prospective longitudinal study]{Procedures} is Longitudinal Study
[exposed group]{Living Beings} is Exposed Group
[crown fracture]{Disorders} is Tooth crown fracture
[non]{Disorders} is NEGATIVE
[exposed group]{Living Beings} is Exposed Group
[diagnosis]{Disorders} is Diagnosis
[crown fracture]{Disorders} is Tooth crown fracture
[lip]{Anatomy} is LIP
[overjet]{Disorders} is Overjet
[crown fracture]{Disorders} is Tooth crown fracture
[Pearson's chi-square test]{Concepts & Ideas} is Hypothesis Test
[McNemar's test]{Concepts & Ideas} is Hypothesis Test
[Poisson regression]{Concepts & Ideas} is REGRESSION ANAL
[cross-sectional study]{Procedures} is Cross-Sectional Study
[exposed group]{Living Beings} is Exposed Group
[non]{Disorders} is NEGATIVE
[exposed group]{Living Beings} is Exposed Group
[crown fracture]{Disorders} is Tooth crown fracture
[increased risk of]{Disorders} is High risk of
[crown fracture]{Disorders} is Tooth crown fracture
[non]{Disorders} is NEGATIVE
[exposed groups]{Living Beings} is Exposed Group
[crown fracture]{Disorders} is Tooth crown fracture
[greater risk of]{Disorders} is High risk of
[crown fracture]{Disorders} is Tooth crown fracture
[non]{Disorders} is NEGATIVE
[exposed group]{Living Beings} is Exposed Group
[crown fracture]{Disorders} is Tooth crown fracture
[crown fracture]{Disorders} is Tooth crown fracture
[greater risk of]{Disorders} is High risk of
[crown fracture]{Disorders} is Tooth crown fracture
[follow-up]{Procedures} is Follow-up
|
An Efficient and Reliable [Statistical Method] for Estimating Functional [Connectivity] in Large Scale [Brain] [Networks] Using Partial Correlation
Currently, [network-oriented] [analysis] of [fMRI] data has become an important tool for understanding [brain] [organization] and [brain] [networks]. Among the range of [network] modeling methods, partial correlation has shown great promises in accurately [detecting] true [brain] [network] [connections]. However, the application of partial correlation in investigating [brain] [connectivity], especially in large-scale [brain] [networks], has been limited so far due to the technical challenges in its estimation. In this paper, we propose an efficient and reliable [statistical method] for estimating partial correlation in large-scale [brain] [network] [modeling]. Our [method] derives partial correlation based on the precision matrix estimated via [Constrained L1-minimization Approach] ([CLIME]), which is a recently developed [statistical method] that is more efficient and demonstrates better performance than the existing [methods]. To help select an appropriate tuning parameter for sparsity control in the [network] estimation, we propose a new [Dens-based selection method] that provides a more informative and flexible [tool] to allow the users to select the tuning parameter based on the desired sparsity level. Another appealing feature of the [Dens-based method] is that it is much faster than the existing [methods], which provides an important advantage in [neuroimaging applications]. [Simulation studies] show that the [Dens-based method] demonstrates comparable or better performance with respect to the existing [methods] in [network] estimation. We applied the proposed partial correlation [method] to investigate [resting state functional connectivity using rs-fMRI data] from the Philadelphia Neurodevelopmental Cohort (PNC) study. Our results show that partial correlation [analysis] removed considerable between-module [marginal connections] identified by full [correlation analysis], suggesting these [connections] were likely caused by global effects or common [connection] to other [nodes]. Based on partial correlation, we find that the most significant direct [connections] are between homologous [brain] [locations] in the [left] and [right hemisphere]. When comparing partial correlation derived under different sparse tuning parameters, an important finding is that the sparse regularization has more shrinkage effects on [negative] functional [connections] than on [positive] [connections], which supports previous findings that many of the [negative] [brain] [connections] are due to [non-neurophysiological effects]. An [R package "DensParcorr"] can be downloaded from [CRAN] for implementing the proposed [statistical methods].
|
[Statistical Method]{Procedures} is Statistical Method
[Connectivity]{Concepts & Ideas} is Connection
[Brain]{Anatomy} is Brains
[Networks]{Physiology} is Nerve network
[network-oriented]{Physiology} is Nerve network
[Statistical Method]{Procedures} is Statistical Method
[analysis]{Procedures} is Analyzed
[fMRI]{Procedures} is FMRI
[Connectivity]{Concepts & Ideas} is Connection
[brain]{Anatomy} is Brains
[Brain]{Anatomy} is Brains
[organization]{Physiology} is Organization
[Networks]{Physiology} is Nerve network
[brain]{Anatomy} is Brains
[networks]{Physiology} is Nerve network
[network]{Physiology} is Nerve network
[detecting]{Disorders} is Detected
[brain]{Anatomy} is Brains
[network]{Physiology} is Nerve network
[connections]{Concepts & Ideas} is Connection
[brain]{Anatomy} is Brains
[connectivity]{Concepts & Ideas} is Connection
[brain]{Anatomy} is Brains
[networks]{Physiology} is Nerve network
[statistical method]{Procedures} is Statistical Method
[brain]{Anatomy} is Brains
[network]{Physiology} is Nerve network
[modeling]{Procedures} is Modeling
[method]{Concepts & Ideas} is Methods
[Constrained L1-minimization Approach]{Procedures} is Statistical Method
[CLIME]{Procedures} is Statistical Method
[statistical method]{Procedures} is Statistical Method
[methods]{Concepts & Ideas} is Methods
[network]{Physiology} is Nerve network
[Dens-based selection method]{Procedures} is Statistical Method
[tool]{Concepts & Ideas} is Software Tool
[Dens-based method]{Procedures} is Statistical Method
[methods]{Concepts & Ideas} is Methods
[neuroimaging applications]{Procedures} is Neuroimaging
[Simulation studies]{Procedures} is Simulation
[Dens-based method]{Procedures} is Statistical Method
[methods]{Concepts & Ideas} is Methods
[network]{Physiology} is Nerve network
[method]{Concepts & Ideas} is Methods
[resting state functional connectivity using rs-fMRI data]{Procedures} is Resting State Functional Connectivity MRI
[analysis]{Procedures} is Analyzed
[marginal connections]{Concepts & Ideas} is Connection
[correlation analysis]{Procedures} is Correlation Study
[connections]{Concepts & Ideas} is Connection
[connection]{Concepts & Ideas} is Connection
[nodes]{Anatomy} is Node
[connections]{Concepts & Ideas} is Connection
[brain]{Anatomy} is Brains
[locations]{Anatomy} is Location
[left]{Anatomy} is Left Brain Hemisphere
[right hemisphere]{Anatomy} is Right Brain Hemisphere
[negative]{Disorders} is Negative for
[connections]{Concepts & Ideas} is Connection
[positive]{Disorders} is Positive for
[connections]{Concepts & Ideas} is Connection
[negative]{Disorders} is Negative for
[brain]{Anatomy} is Brains
[connections]{Concepts & Ideas} is Connection
[non-neurophysiological effects]{Physiology} is Unknown Physiological Effect
[R package "DensParcorr"]{Concepts & Ideas} is Software Tool
[CRAN]{Concepts & Ideas} is Intellectual Product
[statistical methods]{Procedures} is Statistical Method
|
[Metabolite] Profiling of [Italian] [Tomato] Landraces with Different [Fruit] Types
Increased interest toward traditional [tomato] varieties is fueled by the need to rescue desirable organoleptic traits and to [improve] the quality of fresh and processed [tomatoes] in the [market]. In addition, the phenotypic and genetic variation preserved in [tomato] landraces represents a means to understand the genetic basis of traits related to health and organoleptic aspects and improve them in modern varieties. To establish a framework for this approach, we [studied] the content of several [metabolites] in a panel of [Italian] [tomato] landraces categorized into three broad [fruit] type classes (flattened / ribbed, [pear] / [oxheart], [round] / elongate). Three modern hybrids, corresponding to the three [fruit] [shape] [typologies], were included as reference. [Red ripe fruits] were [morphologically] characterized and biochemically analyzed for their content in [glycoalkaloids], [phenols], [amino acids], and [Amadori products]. The [round] / elongate types showed a higher content in [glycoalkaloids], whereas flattened types had higher levels of [phenolic compounds]. Flattened [tomatoes] were also rich in total [amino acids] and in particular in [glutamic acid]. Multivariate analysis of [amino acid content] clearly separated the three classes of [fruit] types. Making allowance of the very low number of genotypes, phenotype-marker relationships were [analyzed] after retrieving [single nucleotide polymorphisms] ([SNPs]) among the landraces available in the [literature]. Sixty-six [markers] were significantly associated with the [studied] traits. The positions of several of these [SNPs] showed correspondence with already described genomic regions and [QTLs] supporting the reliability of the association. Overall the data indicated that significant changes in quality -related [metabolites] occur depending on the genetic background in traditional [tomato] [germplasm], frequently according to specific [fruit] [shape] categories. Such a variability is suitable to harness association mapping for metabolic quality traits using this [germplasm] as an experimental population, paving the way for investigating their genetic / molecular basis, and facilitating [breeding] for quality-related [compounds] in [tomato] [fruits].
|
[Metabolite]{Chemicals & Drugs} is Metabolite
[Italian]{Geographic Areas} is Italy
[Tomato]{Objects} is Tomato
[Fruit]{Objects} is Fruit
[Metabolite]{Chemicals & Drugs} is Metabolite
[Italian]{Geographic Areas} is Italy
[Tomato]{Objects} is Tomato
[tomato]{Objects} is Tomato
[Fruit]{Objects} is Fruit
[improve]{Disorders} is Improved
[tomatoes]{Objects} is Tomato
[market]{Geographic Areas} is Market
[tomato]{Objects} is Tomato
[studied]{Procedures} is Study
[metabolites]{Chemicals & Drugs} is Metabolite
[Italian]{Geographic Areas} is Italy
[tomato]{Objects} is Tomato
[fruit]{Objects} is Fruit
[pear]{Objects} is Pear
[oxheart]{Objects} is Fruit
[round]{Concepts & Ideas} is Round
[fruit]{Objects} is Fruit
[shape]{Concepts & Ideas} is SHAPE
[typologies]{Concepts & Ideas} is General Typologies
[Red ripe fruits]{Objects} is Fruit
[morphologically]{Concepts & Ideas} is Morphological
[glycoalkaloids]{Chemicals & Drugs} is Alkaloids
[phenols]{Chemicals & Drugs} is Phenols
[amino acids]{Chemicals & Drugs} is Amino Acids
[Amadori products]{Chemicals & Drugs} is Organic Chemical
[round]{Concepts & Ideas} is Round
[glycoalkaloids]{Chemicals & Drugs} is Alkaloids
[phenolic compounds]{Chemicals & Drugs} is Phenols
[tomatoes]{Objects} is Tomato
[amino acids]{Chemicals & Drugs} is Amino Acids
[glutamic acid]{Chemicals & Drugs} is Glutamic acid
[amino acid content]{Procedures} is Amino acid level
[fruit]{Objects} is Fruit
[analyzed]{Procedures} is Analyzed
[single nucleotide polymorphisms]{Genes & Molecular Sequences} is Single Nucleotide Polymorphisms
[SNPs]{Genes & Molecular Sequences} is Single Nucleotide Polymorphisms
[literature]{Concepts & Ideas} is Literature
[markers]{Genes & Molecular Sequences} is DNA Markers
[studied]{Procedures} is Study
[SNPs]{Genes & Molecular Sequences} is Single Nucleotide Polymorphisms
[QTLs]{Genes & Molecular Sequences} is QTL
[metabolites]{Chemicals & Drugs} is Metabolite
[tomato]{Objects} is Tomato
[germplasm]{Anatomy} is Germ plasm
[fruit]{Objects} is Fruit
[shape]{Concepts & Ideas} is SHAPE
[germplasm]{Anatomy} is Germ plasm
[breeding]{Physiology} is Breeding
[compounds]{Chemicals & Drugs} is Compound
[tomato]{Objects} is Tomato
[fruits]{Objects} is Fruit
|
[Cross-reactivity] features of [deoxynivalenol] ([DON])-targeted [immunoaffinity] columns aiming to achieve simultaneous [analysis] of [DON] and major [conjugates] in [cereal] samples
[Immunoaffinity] columns (IACs) are a well-established tool in the determination of regulated [mycotoxins] in [food] and [feed commodities]. However, they also have the potential to become attractive pre-concentration and clean-up materials for the determination of masked (also called modified) [mycotoxins], which have been recognised as important contributors to the [toxicological] hazard deriving from fungal spoilage of [goods]. However, the information available in the literature concerning the [cross-reactivity] of [DON] - IACs against the major [conjugates] ([DON-3-G], [15-AcDON] and [3-AcDON]) is incomplete and often contradictory. We have carried out a detailed characterisation of the [cross-reactivity] of the four main IACs brands against [DON] and its [conjugates] as well as an assessment of the competition among the [analytes]. Only one IAC enabled the simultaneous [analysis] of all relevant [DON] forms while two missed [15-AcDON] and the fourth one missed [DON-3-G] and [3-AcDON]. In the case of the multivalent IAC, the [analytes] modified at the C-3 position compete for the [antibody binding] with preference for [3-AcDON] (less spatially hindered) while [DON-3-G] has the more-hindered access to the [active sites]. Taking into consideration the levels of [DON] [conjugates] existing in real samples, the [cross-reactivity] of one [DON] - IAC allows a quantitative analysis of all of these [analytes]. Important but rather neglected aspects such as the continuous supply of IACs with identical characteristics, and of columns which are strictly blank, are also addressed in this paper.
|
[Cross-reactivity]{Physiology} is Cross Reactivity
[deoxynivalenol]{Chemicals & Drugs} is Deoxynivalenol
[DON]{Chemicals & Drugs} is Deoxynivalenol
[immunoaffinity]{Procedures} is Immunoaffinity Chromatography
[analysis]{Procedures} is Analysis of substances
[DON]{Chemicals & Drugs} is Deoxynivalenol
[conjugates]{Chemicals & Drugs} is Derivatives
[cereal]{Objects} is Cereal
[Immunoaffinity]{Procedures} is Immunoaffinity Chromatography
[Cross-reactivity]{Physiology} is Cross Reactivity
[deoxynivalenol]{Chemicals & Drugs} is Deoxynivalenol
[DON]{Chemicals & Drugs} is Deoxynivalenol
[immunoaffinity]{Procedures} is Immunoaffinity Chromatography
[mycotoxins]{Chemicals & Drugs} is Mycotoxins
[food]{Objects} is Food
[analysis]{Procedures} is Analysis of substances
[feed commodities]{Objects} is Food
[DON]{Chemicals & Drugs} is Deoxynivalenol
[conjugates]{Chemicals & Drugs} is Derivatives
[cereal]{Objects} is Cereal
[mycotoxins]{Chemicals & Drugs} is Mycotoxins
[toxicological]{Phenomena} is Toxicological Concept
[goods]{Objects} is Food
[cross-reactivity]{Physiology} is Cross Reactivity
[DON]{Chemicals & Drugs} is Deoxynivalenol
[conjugates]{Chemicals & Drugs} is Derivatives
[DON-3-G]{Chemicals & Drugs} is DON-3-Glc
[15-AcDON]{Chemicals & Drugs} is Deoxynivalenol
[3-AcDON]{Chemicals & Drugs} is Deoxynivalenol
[cross-reactivity]{Physiology} is Cross Reactivity
[DON]{Chemicals & Drugs} is Deoxynivalenol
[conjugates]{Chemicals & Drugs} is Derivatives
[analytes]{Chemicals & Drugs} is Deoxynivalenol
[analysis]{Procedures} is Analysis of substances
[DON]{Chemicals & Drugs} is Deoxynivalenol
[15-AcDON]{Chemicals & Drugs} is Deoxynivalenol
[DON-3-G]{Chemicals & Drugs} is DON-3-Glc
[3-AcDON]{Chemicals & Drugs} is Deoxynivalenol
[analytes]{Chemicals & Drugs} is Deoxynivalenol
[antibody binding]{Chemicals & Drugs} is Antibody binding site
[3-AcDON]{Chemicals & Drugs} is Deoxynivalenol
[DON-3-G]{Chemicals & Drugs} is DON-3-Glc
[active sites]{Chemicals & Drugs} is Antibody binding site
[DON]{Chemicals & Drugs} is Deoxynivalenol
[conjugates]{Chemicals & Drugs} is Derivatives
[cross-reactivity]{Physiology} is Cross Reactivity
[DON]{Chemicals & Drugs} is Deoxynivalenol
[analytes]{Chemicals & Drugs} is Deoxynivalenol
|
Improving Early Identification and Ongoing Care of Children With [Autism Spectrum Disorder]
Poor adherence to recommended [screening] for [autism spectrum disorder] ([ASD]) and [pediatricians] ' [lack of confidence] in providing care for children with [ASD] reflect quality gaps in [primary care]. This [study] aimed to increase the proportion of toddlers screened for [ASD] and [improve] [physicians] ' [self-efficacy] in providing care to children with [ASD]. Twenty-six Utah [primary care practices] participated in a 3 to 6 month [learning collaborative] ([LC]) to [improve] [identification] and ongoing care of children with [ASD]. Monthly chart audits assessed whether an [ASD] [screening tool] was administered at 18- and 24- month [visits]. [Physicians] completed pre-LC and post-LC [surveys] to assess changes in [self-efficacy] in providing care and changes in [perceived] barriers to implementation of [screening] and caring for children with [ASD]. Before the [LC], 15% of 18- and 24- month [visits] had [documented] [ASD] [screening], compared with 91% during the last month of the [LC] (P < .001). This rate of [ASD] [screening] was sustained 4 years after the [LC] by most practices. Compared with [survey] responses before the [LC], [physicians] reported significant improvement in their ability to care for children with [ASD] and decreases in their [perceived] barriers to [screening] and caring for children with [ASD]. The [LC] was effective in increasing and sustaining recommended [ASD] [screening] of toddlers and improving [physicians] ' perceived [self-efficacy] in caring for children with [ASD]. Improving [primary care] [screening], skills, and knowledge may [improve] the timing of [diagnosis], initiation of [treatment], [quality of care], and outcomes for children with [ASD].
|
[Autism Spectrum Disorder]{Disorders} is Autism or autism spectrum disorder
[screening]{Procedures} is Screening Generic
[autism spectrum disorder]{Disorders} is Autism or autism spectrum disorder
[Autism Spectrum Disorder]{Disorders} is Autism or autism spectrum disorder
[ASD]{Disorders} is Autism or autism spectrum disorder
[pediatricians]{Living Beings} is Pediatricians
[lack of confidence]{Disorders} is Lacks confidence
[ASD]{Disorders} is Autism or autism spectrum disorder
[primary care]{Procedures} is Primary Care
[study]{Procedures} is Study
[ASD]{Disorders} is Autism or autism spectrum disorder
[improve]{Disorders} is Improved
[physicians]{Living Beings} is Physicians
[self-efficacy]{Physiology} is Self-Efficacy
[ASD]{Disorders} is Autism or autism spectrum disorder
[primary care practices]{Procedures} is Primary Care
[learning collaborative]{Organizations} is Entity - organization
[LC]{Organizations} is Entity - organization
[improve]{Disorders} is Improved
[identification]{Physiology} is Identification
[ASD]{Disorders} is Autism or autism spectrum disorder
[ASD]{Disorders} is Autism or autism spectrum disorder
[screening tool]{Procedures} is Screening Generic
[visits]{Procedures} is Visit
[Physicians]{Living Beings} is Physicians
[surveys]{Concepts & Ideas} is Surveys
[self-efficacy]{Physiology} is Self-Efficacy
[perceived]{Physiology} is Perceived
[screening]{Procedures} is Screening Generic
[ASD]{Disorders} is Autism or autism spectrum disorder
[LC]{Organizations} is Entity - organization
[visits]{Procedures} is Visit
[documented]{Procedures} is Documented
[ASD]{Disorders} is Autism or autism spectrum disorder
[screening]{Procedures} is Screening Generic
[LC]{Organizations} is Entity - organization
[ASD]{Disorders} is Autism or autism spectrum disorder
[screening]{Procedures} is Screening Generic
[LC]{Organizations} is Entity - organization
[survey]{Procedures} is Health Survey
[LC]{Organizations} is Entity - organization
[physicians]{Living Beings} is Physicians
[ASD]{Disorders} is Autism or autism spectrum disorder
[perceived]{Physiology} is Perceived
[screening]{Procedures} is Screening Generic
[ASD]{Disorders} is Autism or autism spectrum disorder
[LC]{Organizations} is Entity - organization
[ASD]{Disorders} is Autism or autism spectrum disorder
[screening]{Procedures} is Screening Generic
[physicians]{Living Beings} is Physicians
[self-efficacy]{Physiology} is Self-Efficacy
[ASD]{Disorders} is Autism or autism spectrum disorder
[primary care]{Procedures} is Primary Care
[screening]{Procedures} is Screening Generic
[improve]{Disorders} is Improved
[diagnosis]{Procedures} is DIAGNOSIS
[treatment]{Procedures} is Treatments
[quality of care]{Procedures} is Quality of Care
[ASD]{Disorders} is Autism or autism spectrum disorder
|
Describing Self-Care [Self-Efficacy]: [Definition], Measurement, Outcomes, and Implications
The [pragmatic utility method] of concept [analysis] was used to explore the usefulness of the concept self-care [self-efficacy]. Empirical studies across disciplines published between 1996 and 2015 were used as data. A data matrix was developed. Analytical questions and [responses] were derived from the data to understand patterns, develop new [knowledge] and achieve synthesis. Usefulness of the concept is contingent on how it is defined and measured. Self-care [self-efficacy] is associated with performance of self-care activities and [positive] health outcomes in diverse [populations]. [Research] can guide development of targeted [interventions] to increase patients ' self-care [self-efficacy], thus reducing costs, and [assisting] [people] to achieve optimal health.
|
[Self-Efficacy]{Physiology} is Self-Efficacy
[Definition]{Concepts & Ideas} is Definition
[pragmatic utility method]{Procedures} is Pragmatic Clinical Trial
[Self-Efficacy]{Physiology} is Self-Efficacy
[Definition]{Concepts & Ideas} is Definition
[analysis]{Procedures} is Analyzed
[self-efficacy]{Physiology} is Self-Efficacy
[responses]{Concepts & Ideas} is Response
[knowledge]{Concepts & Ideas} is Knowledge
[self-efficacy]{Physiology} is Self-Efficacy
[positive]{Disorders} is Positive for
[populations]{Living Beings} is Population
[Research]{Procedures} is Research
[interventions]{Procedures} is Nursing interventions
[self-efficacy]{Physiology} is Self-Efficacy
[assisting]{Procedures} is Assisting - action
[people]{Living Beings} is People
|
Dynamics of [intestinal] [metabolites] and morphology in response to [necrotic enteritis] [challenge] in [broiler chickens]
Despite the relatively small contribution to metabolizable energy that [volatile fatty acids] ([VFAs]) provide in [chickens], these [organic acids] have been [reported] to play beneficial roles in the [gastrointestinal tract] ([GIT]) of [birds], for example, [inhibition of the growth] of some pathogenic [bacteria]. However, information regarding the dynamics of these [metabolites] in the [GIT] of [chickens] is still scarce, especially under [disease conditions] such as [necrotic enteritis] ([NE]). Here, we investigated the dynamics of [VFAs] and [lactic acid], and [intestinal] morphology in response to [NE] predisposing factors, that is, excessive [dietary] fishmeal and [Eimeria] [inoculation], and [causative agent] [Clostridium perfringens] producing [NetB toxin]. The [experiment] was [designed] in a 2 × 2 × 2 factorial [arrangement] of [treatments] with or without: fishmeal feeding, [Eimeria] [inoculation] and [C. perfringens] [challenge]. The results showed that these factors significantly influenced [composition] and concentration of [VFAs] and [lactic acids], pH and histomorphometry in one way or another. These changes may be important for the onset of [NE] or only the synergetic responses to micro environmental [stress]. [Eimeria] appeared to be more important than fishmeal in predisposing [birds] to [NE], thus the application of [Eimeria] in [NE] [challenge] provides more consistent success in inducing the [disease]. The metabolic responses to various [adverse] factors such as excessive [dietary] fishmeal and [Eimeria] [infection] are complex. Thus, intensive [efforts] are required to better [understand] [NE] so as to achieve the [control of the disease] in the absence of [antibiotics].
|
[intestinal]{Anatomy} is Intestinal
[metabolites]{Chemicals & Drugs} is Metabolite
[necrotic enteritis]{Disorders} is Necrotic enteritis
[challenge]{Procedures} is Challenge
[broiler chickens]{Living Beings} is Broiler Chicken
[intestinal]{Anatomy} is Intestinal
[metabolites]{Chemicals & Drugs} is Metabolite
[necrotic enteritis]{Disorders} is Necrotic enteritis
[volatile fatty acids]{Chemicals & Drugs} is Volatile Fatty Acids
[challenge]{Procedures} is Challenge
[VFAs]{Chemicals & Drugs} is Volatile Fatty Acids
[broiler chickens]{Living Beings} is Broiler Chicken
[chickens]{Living Beings} is Broiler Chicken
[organic acids]{Chemicals & Drugs} is Organic acid
[reported]{Procedures} is Reporting
[gastrointestinal tract]{Anatomy} is Gastrointestinal Tract
[GIT]{Anatomy} is Gastrointestinal Tract
[birds]{Living Beings} is Birds
[inhibition of the growth]{Physiology} is Inhibition of growth
[bacteria]{Living Beings} is BACTERIA
[metabolites]{Chemicals & Drugs} is Metabolite
[GIT]{Anatomy} is Gastrointestinal Tract
[chickens]{Living Beings} is Broiler Chicken
[disease conditions]{Disorders} is Disease condition finding
[necrotic enteritis]{Disorders} is Necrotic enteritis
[NE]{Disorders} is Necrotic enteritis
[VFAs]{Chemicals & Drugs} is Volatile Fatty Acids
[lactic acid]{Chemicals & Drugs} is Lactic Acid
[intestinal]{Anatomy} is Intestinal
[NE]{Disorders} is Necrotic enteritis
[dietary]{Objects} is Dietary
[Eimeria]{Living Beings} is Eimerias
[inoculation]{Procedures} is Inoculate
[causative agent]{Disorders} is Causative agent
[Clostridium perfringens]{Living Beings} is Clostridium perfringens
[NetB toxin]{Chemicals & Drugs} is NetB toxin, Clostridium perfringes
[experiment]{Procedures} is Animal Experiment
[designed]{Procedures} is EXPER DESIGN
[arrangement]{Procedures} is Arrangement of care
[treatments]{Procedures} is Treatments
[Eimeria]{Living Beings} is Eimerias
[inoculation]{Procedures} is Inoculate
[C. perfringens]{Living Beings} is Clostridium perfringens
[challenge]{Procedures} is Challenge
[composition]{Physiology} is Composition
[VFAs]{Chemicals & Drugs} is Volatile Fatty Acids
[lactic acids]{Chemicals & Drugs} is Lactic Acid
[NE]{Disorders} is Necrotic enteritis
[stress]{Disorders} is State of stress
[Eimeria]{Living Beings} is Eimerias
[birds]{Living Beings} is Birds
[NE]{Disorders} is Necrotic enteritis
[Eimeria]{Living Beings} is Eimerias
[NE]{Disorders} is Necrotic enteritis
[challenge]{Procedures} is Challenge
[disease]{Disorders} is Disease
[adverse]{Disorders} is Adverse effects
[dietary]{Objects} is Dietary
[Eimeria]{Living Beings} is Eimerias
[infection]{Disorders} is Infections
[efforts]{Physiology} is Effort
[understand]{Physiology} is Understanding
[NE]{Disorders} is Necrotic enteritis
[control of the disease]{Procedures} is Infectious disease prevention / control
[antibiotics]{Chemicals & Drugs} is Antibiotics
|
[Ehlers-Danlos syndrome]
The [Ehlers-Danlos syndromes] ([EDSs]) were originally [described] by [Ehlers] in [Denmark] and [Danlos] in [Paris] in 1898 and 1908, respectively. They had both published individual [case studies] in which the common factor was [laxity of ligaments] leading to [joint hypermobility] and [hyperextensibility of the skin]. The choice of the [name] of this [eponymous disease] had been made by [Dr Parkes Weber], an eminent [London] [physician] in the 1930s, who had a penchant for [eponymous diseases], having had no less than seven attributed to himself, at least in part. Unfortunately, this was before the age of a [computerised literature] search, and [Parkes Weber] had inadvertently overlooked the very first [description] of [EDS] which had been made by [Tchernabogov], a [Russian] [dermatologist], whose [description] was published in 1891 and remains one of the best [descriptions] of [EDS] in the [literature].
|
[Ehlers-Danlos syndrome]{Disorders} is Ehlers-danlos syndrome
[Ehlers-Danlos syndrome]{Disorders} is Ehlers-danlos syndrome
[Ehlers-Danlos syndromes]{Disorders} is Ehlers-danlos syndrome
[EDSs]{Disorders} is Ehlers-danlos syndrome
[described]{Concepts & Ideas} is DESCR
[Ehlers]{Living Beings} is Homo sapiens (organism)
[Denmark]{Geographic Areas} is Denmark
[Danlos]{Living Beings} is Homo sapiens (organism)
[Paris]{Geographic Areas} is Paris, France
[case studies]{Concepts & Ideas} is Case Studies
[laxity of ligaments]{Disorders} is Laxity of ligaments
[joint hypermobility]{Disorders} is Joint Hypermobility
[hyperextensibility of the skin]{Disorders} is Hyperextensibility of the skin
[name]{Concepts & Ideas} is Names
[eponymous disease]{Concepts & Ideas} is Intellectual Product
[Dr Parkes Weber]{Living Beings} is Homo sapiens (organism)
[London]{Geographic Areas} is London
[physician]{Living Beings} is Physician
[eponymous diseases]{Concepts & Ideas} is Intellectual Product
[computerised literature]{Concepts & Ideas} is Literature
[Parkes Weber]{Living Beings} is Homo sapiens (organism)
[description]{Concepts & Ideas} is DESCR
[EDS]{Disorders} is Ehlers-danlos syndrome
[Tchernabogov]{Living Beings} is Homo sapiens (organism)
[Russian]{Living Beings} is Russian
[dermatologist]{Living Beings} is Dermatologist
[description]{Concepts & Ideas} is DESCR
[descriptions]{Concepts & Ideas} is DESCR
[EDS]{Disorders} is Ehlers-danlos syndrome
[literature]{Concepts & Ideas} is Literature
|
[Assessment] of [laparoscopic stomach preserving surgery] with [sentinel basin dissection] versus standard [gastrectomy] with [lymphadenectomy] in [early gastric cancer] -A [multicenter randomized phase III clinical trial (SENORITA trial) protocol]
Along with the marked increase in [early gastric cancer] ([EGC]) in the [Eastern countries], there has been an effort to adopt the [sentinel node] concept in [EGC] to preserve [gastric function] and reduce the occurrence of [postoperative complications]. Based on promising results from a [previous quality control study], this [prospective multicenter randomized controlled phase III clinical trial] aims to elucidate the [oncologic] [safety] of [laparoscopic stomach-preserving surgery] with [sentinel basin dissection] ([SBD]) compared to a standard [laparoscopic] [gastrectomy]. This trial is an investigator-initiated, open-label, [multicenter randomized controlled phase III trial] with a [non-inferiority design]. Patients diagnosed with a [single lesion] of clinical stage T1N0M0 [gastric adenocarcinoma], with a diameter of 3 cm or less are eligible for the present study. A total of 580 patients (290 per group) will be [randomized] to either [laparoscopic stomach-preserving surgery] with [SBD] or [standard surgery]. The primary end-point is 3-year disease-free survival (DFS) and the secondary endpoints include postoperative morbidity and mortality, quality of life, 5-year DFS, and overall survival. [Qualified investigators] who completed the prior quality control study are exclusively allowed to participate in this [phase III clinical trial]. The proposed trial is expected to verify whether [laparoscopic stomach-preserving surgery] with [SBD] achieves similar [oncologic outcomes] and improved quality of life compared to a [standard gastrectomy] in [EGC] patients. This study was registered at the NIH ClinicalTrial.gov database (NCT01804998) on March 4th, 2013.
|
[Assessment]{Procedures} is Assessment - action
[laparoscopic stomach preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach
[sentinel basin dissection]{Procedures} is Node Dissection, Lymph
[gastrectomy]{Procedures} is Gastrectomy
[lymphadenectomy]{Procedures} is Lymphadenectomy
[early gastric cancer]{Disorders} is Early Gastric Cancer
[multicenter randomized phase III clinical trial (SENORITA trial) protocol]{Procedures} is Phase III Clinical Trial
[Assessment]{Procedures} is Assessment - action
[laparoscopic stomach preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach
[early gastric cancer]{Disorders} is Early Gastric Cancer
[EGC]{Disorders} is Early Gastric Cancer
[sentinel basin dissection]{Procedures} is Node Dissection, Lymph
[Eastern countries]{Geographic Areas} is Area
[gastrectomy]{Procedures} is Gastrectomy
[lymphadenectomy]{Procedures} is Lymphadenectomy
[sentinel node]{Anatomy} is Sentinel Node
[early gastric cancer]{Disorders} is Early Gastric Cancer
[EGC]{Disorders} is Early Gastric Cancer
[multicenter randomized phase III clinical trial (SENORITA trial) protocol]{Procedures} is Phase III Clinical Trial
[gastric function]{Physiology} is Gastric function
[postoperative complications]{Disorders} is Postoperative Complications
[previous quality control study]{Procedures} is Historical Control Study
[prospective multicenter randomized controlled phase III clinical trial]{Procedures} is Phase III Clinical Trial
[oncologic]{Occupations} is Oncologic (qualifier value)
[safety]{Procedures} is SAFETY
[laparoscopic stomach-preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach
[sentinel basin dissection]{Procedures} is Node Dissection, Lymph
[SBD]{Procedures} is Node Dissection, Lymph
[laparoscopic]{Concepts & Ideas} is Laparoscopic
[gastrectomy]{Procedures} is Gastrectomy
[multicenter randomized controlled phase III trial]{Procedures} is Phase III Clinical Trial
[non-inferiority design]{Procedures} is EXPER DESIGN
[single lesion]{Disorders} is Single lesion
[gastric adenocarcinoma]{Disorders} is Gastric adenocarcinoma
[randomized]{Disorders} is RANDOMIZED
[laparoscopic stomach-preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach
[SBD]{Procedures} is Node Dissection, Lymph
[standard surgery]{Procedures} is Gastrectomy
[Qualified investigators]{Living Beings} is CLIN INVESTIGATORS
[phase III clinical trial]{Procedures} is Phase III Clinical Trial
[laparoscopic stomach-preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach
[SBD]{Procedures} is Node Dissection, Lymph
[oncologic outcomes]{Disorders} is Disease Outcome
[standard gastrectomy]{Procedures} is Gastrectomy
[EGC]{Disorders} is Early Gastric Cancer
|
Association of [Metabolites] with [Obesity] and [Type 2 Diabetes] Based on [FTO] Genotype
The [single nucleotide polymorphism] [rs9939609 of the gene FTO], which encodes fat mass and [obesity] -associated [protein], is strongly associated with [obesity] and [type 2 diabetes] ([T2D]) in multiple [populations]; however, the underlying mechanism of this association is unclear. The present [study] aimed to investigate [FTO] genotype -dependent [metabolic] changes in [obesity] and [T2D]. To elucidate metabolic dysregulation associated with [disease risk] genotype, [genomic] and [metabolomic datasets] were recruited from 2,577 [participants] of the [Korean Association REsource (KARE) cohort], including 40 homozygous [carriers] of the [FTO] risk [allele (AA)], 570 heterozygous [carriers] (AT), and 1,967 [participants] carrying no risk [allele (TT)]. A total of 134 [serum] [metabolites] were quantified using a targeted [metabolomics] approach. Through comparison of various [statistical methods], seven [metabolites] were identified that are significantly altered in [obesity] and [T2D] based on the [FTO] risk [allele] (adjusted p < 0.05). These identified [metabolites] are relevant to [phosphatidylcholine] metabolic pathway, and previously reported to be [metabolic markers] of [obesity] and [T2D]. In conclusion, using [metabolomics] with the information from [genome-wide association studies] revealed significantly altered [metabolites] depending on the [FTO] genotype in complex disorders. This [study] may contribute to a better understanding of the biological mechanisms linking [obesity] and [T2D].
|
[Metabolites]{Chemicals & Drugs} is Metabolite
[Obesity]{Disorders} is Obesity (disorder)
[Type 2 Diabetes]{Disorders} is Type 2 Diabetes
[FTO]{Genes & Molecular Sequences} is FTO
[single nucleotide polymorphism]{Genes & Molecular Sequences} is Single nucleotide polymorphism
[Metabolites]{Chemicals & Drugs} is Metabolite
[Obesity]{Disorders} is Obesity (disorder)
[rs9939609 of the gene FTO]{Genes & Molecular Sequences} is FTO
[Type 2 Diabetes]{Disorders} is Type 2 Diabetes
[FTO]{Genes & Molecular Sequences} is FTO
[obesity]{Disorders} is Obesity (disorder)
[protein]{Chemicals & Drugs} is Protein
[obesity]{Disorders} is Obesity (disorder)
[type 2 diabetes]{Disorders} is Type 2 Diabetes
[T2D]{Disorders} is Type 2 Diabetes
[populations]{Living Beings} is Population
[study]{Procedures} is Study
[FTO]{Genes & Molecular Sequences} is FTO
[metabolic]{Physiology} is Metabolic process
[obesity]{Disorders} is Obesity (disorder)
[T2D]{Disorders} is Type 2 Diabetes
[disease risk]{Physiology} is Disease Susceptibility (Disease/Finding)
[genomic]{Concepts & Ideas} is Data Set
[metabolomic datasets]{Concepts & Ideas} is Data Set
[participants]{Living Beings} is Participant
[Korean Association REsource (KARE) cohort]{Living Beings} is Cohort
[carriers]{Disorders} is GENET CARRIERS
[FTO]{Genes & Molecular Sequences} is FTO
[allele (AA)]{Genes & Molecular Sequences} is Allele
[carriers]{Disorders} is GENET CARRIERS
[participants]{Living Beings} is Participant
[allele (TT)]{Genes & Molecular Sequences} is Allele
[serum]{Anatomy} is Serum
[metabolites]{Chemicals & Drugs} is Metabolite
[metabolomics]{Occupations} is Metabolomics
[statistical methods]{Procedures} is Statistical Method
[metabolites]{Chemicals & Drugs} is Metabolite
[obesity]{Disorders} is Obesity (disorder)
[T2D]{Disorders} is Type 2 Diabetes
[FTO]{Genes & Molecular Sequences} is FTO
[allele]{Genes & Molecular Sequences} is Allele
[metabolites]{Chemicals & Drugs} is Metabolite
[phosphatidylcholine]{Chemicals & Drugs} is Phosphatidylcholine
[metabolic markers]{Chemicals & Drugs} is Metabolic Marker
[obesity]{Disorders} is Obesity (disorder)
[T2D]{Disorders} is Type 2 Diabetes
[metabolomics]{Occupations} is Metabolomics
[genome-wide association studies]{Procedures} is Genome-Wide Association Studies
[metabolites]{Chemicals & Drugs} is Metabolite
[FTO]{Genes & Molecular Sequences} is FTO
[study]{Procedures} is Study
[obesity]{Disorders} is Obesity (disorder)
[T2D]{Disorders} is Type 2 Diabetes
|
[Anthology] of Venezuelan [psychiatry]
Reception of [Psychiatry] in [Venezuela] since the 19th Century to the late 20th Century merits a historical approach. The following work proposes to [research] some of the very origins of Venezuelan [psychiatry] and its possible influence on contemporary [mental health practice]. Through documental research, the early works of [local authors] from the 19th Century through 20th Century finals: [Carlos Arvelo], [Lisandro Alvarado], [Francisco Herrera Luque], [Jose Luis Vethencourt] and [Jose Solanes], are subjected to study. This journey illustrates a descriptive panoramic view which allows to better comprenhend the current state of our [psychiatry]. In a brief introduction the most important events are described, since the arrival of [Pinel's] ideas, followed by the early research paperworks published and the beginnings of the academic teachings of this specialty in [Venezuela] and displaying the main contemporary research groups [thorough the country].
|
[Anthology]{Concepts & Ideas} is Collections (publication)
[psychiatry]{Occupations} is Psychiatry
[Anthology]{Concepts & Ideas} is Collections (publication)
[Psychiatry]{Occupations} is Psychiatry
[psychiatry]{Occupations} is Psychiatry
[Venezuela]{Geographic Areas} is Venezuela
[research]{Procedures} is Research
[psychiatry]{Occupations} is Psychiatry
[mental health practice]{Procedures} is Health Care
[local authors]{Living Beings} is Authors
[Carlos Arvelo]{Living Beings} is Homo sapiens (organism)
[Lisandro Alvarado]{Living Beings} is Homo sapiens (organism)
[Francisco Herrera Luque]{Living Beings} is Homo sapiens (organism)
[Jose Luis Vethencourt]{Living Beings} is Homo sapiens (organism)
[Jose Solanes]{Living Beings} is Homo sapiens (organism)
[psychiatry]{Occupations} is Psychiatry
[Pinel's]{Living Beings} is Homo sapiens (organism)
[Venezuela]{Geographic Areas} is Venezuela
[thorough the country]{Geographic Areas} is Venezuela
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How variation [between] [individuals] affects [species] coexistence
Although the effects of variation [between] [individuals] within [species] are traditionally ignored in [studies] of [species] coexistence, the magnitude of intraspecific variation in nature is forcing [ecologists] to reconsider. Compelling intuitive arguments suggest that [individual] variation may provide a previously unrecognised [route] to diversity maintenance by blurring [species] - level competitive differences or substituting for [species] - level niche differences. These arguments, which are [motivating] a large [body] of empirical work, have rarely been evaluated with quantitative theory. Here we incorporate intraspecific variation into a common [model] of competition and identify three pathways by which this variation affects coexistence: (1) changes in competitive [dynamics] because of nonlinear averaging, (2) changes in [species] ' mean interaction strengths because of variation in underlying traits (also via nonlinear averaging) and (3) effects on stochastic demography. As a consequence of the first two mechanisms, we [find] that intraspecific variation in competitive ability increases the dominance of superior [competitors], and intraspecific niche variation reduces [species] - level niche differentiation, both of which make coexistence more difficult. In addition, [individual] variation can exacerbate the effects of demographic stochasticity, and this further destabilises coexistence. Our work provides a [theoretical foundation] for emerging empirical [interests] in the effects of intraspecific variation on [species] diversity.
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[between]{Concepts & Ideas} is Between
[individuals]{Living Beings} is Individual (person)
[species]{Concepts & Ideas} is Species
[between]{Concepts & Ideas} is Between
[individuals]{Living Beings} is Individual (person)
[between]{Concepts & Ideas} is Between
[species]{Concepts & Ideas} is Species
[individuals]{Living Beings} is Individual (person)
[species]{Concepts & Ideas} is Species
[studies]{Procedures} is Study
[species]{Concepts & Ideas} is Species
[ecologists]{Living Beings} is Ecologist
[individual]{Living Beings} is Individual (person)
[route]{Concepts & Ideas} is Route
[species]{Concepts & Ideas} is Species
[species]{Concepts & Ideas} is Species
[motivating]{Physiology} is Motivation finding
[body]{Concepts & Ideas} is Structural
[model]{Concepts & Ideas} is Model
[dynamics]{Concepts & Ideas} is Nonlinear Dynamics
[species]{Concepts & Ideas} is Species
[find]{Disorders} is Finding (finding)
[competitors]{Living Beings} is Group (social concept)
[species]{Concepts & Ideas} is Species
[individual]{Living Beings} is Individual (person)
[theoretical foundation]{Procedures} is Theoretical Study
[interests]{Physiology} is Interest
[species]{Concepts & Ideas} is Species
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[Intracellular Metabolism] of α,β-Unsaturated Carbonyl Compounds, [Acrolein], [Crotonaldehyde] and [Methyl Vinyl Ketone], Active Toxicants in [Cigarette Smoke]: Participation of [Glutathione] [Conjugation] Ability and [Aldehyde-Ketone Sensitive Reductase Activity]
The major toxicants in [cigarette smoke], [α,β-unsaturated aldehydes], such as [acrolein] ([ACR]) and [crotonaldehyde] ([CA]), and [α,β-unsaturated ketone], [methyl vinyl ketone] ([MVK]), are known to form Michael-type adducts with [glutathione] ([GSH]) and consequently cause [intracellular] [GSH] depletion, which is involved in [cigarette smoke] - induced [cytotoxicity]. We have previously clarified that exposure to [cigarette smoke extract] ([CSE]) of a [mouse] [melanoma cell] [culture medium] causes rapid reduction of [intracellular] [GSH] levels, and that the [GSH] - [MVK] adduct can be [detected] by [LC/MS analysis] while the [GSH] - [CA] adduct is hardly [detected]. In the present [study], to clarify why the [GSH] - [CA] adduct is difficult to [detect] in the [cell] [medium], we conducted detailed investigation of the [structures] of the reaction products of [ACR], [CA], [MVK] and [CSE] in the [GSH] solution or the [cell] [culture medium]. The [mass spectra] indicated that in the presence of the [cells], the [GSH] - [CA] and [GSH] - [ACR] adducts were almost not [detected] while their [corresponding alcohols] were [detected]. On the other hand, both the [GSH] - [MVK] adducts and their reduced products were [detected]. In the absence of the [cells], the reaction of [GSH] with all α,β-unsaturated carbonyls produced only their corresponding adducts. These results show that the [GSH] adducts of [α,β-unsaturated aldehydes], [CA] and [ACR], are quickly reduced by certain [intracellular] [carbonyl reductase(s)] and excreted from the [cells], unlike the [GSH] adduct of [α,β-unsaturated ketone], [MVK]. Such a difference in reactivity to the [carbonyl reductase] might be related to differences in the [cytotoxicity] of [α,β-unsaturated aldehydes] and [ketones].
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[Intracellular Metabolism]{Physiology} is Cellular metabolism
[Acrolein]{Chemicals & Drugs} is Acrolein
[Crotonaldehyde]{Chemicals & Drugs} is Crotonaldehyde
[Methyl Vinyl Ketone]{Chemicals & Drugs} is Methyl vinyl ketone
[Cigarette Smoke]{Chemicals & Drugs} is Cigarette smoke
[Glutathione]{Chemicals & Drugs} is Glutathione
[Conjugation]{Physiology} is Molecular function
[Aldehyde-Ketone Sensitive Reductase Activity]{Physiology} is Aldehyde reductase 1
[Intracellular Metabolism]{Physiology} is Cellular metabolism
[cigarette smoke]{Chemicals & Drugs} is Cigarette smoke
[α,β-unsaturated aldehydes]{Chemicals & Drugs} is Aldehydes
[Acrolein]{Chemicals & Drugs} is Acrolein
[Crotonaldehyde]{Chemicals & Drugs} is Crotonaldehyde
[acrolein]{Chemicals & Drugs} is Acrolein
[ACR]{Chemicals & Drugs} is Acrolein
[Methyl Vinyl Ketone]{Chemicals & Drugs} is Methyl vinyl ketone
[crotonaldehyde]{Chemicals & Drugs} is Crotonaldehyde
[CA]{Chemicals & Drugs} is Crotonaldehyde
[α,β-unsaturated ketone]{Chemicals & Drugs} is Ketone
[Cigarette Smoke]{Chemicals & Drugs} is Cigarette smoke
[methyl vinyl ketone]{Chemicals & Drugs} is Methyl vinyl ketone
[MVK]{Chemicals & Drugs} is Methyl vinyl ketone
[Glutathione]{Chemicals & Drugs} is Glutathione
[Conjugation]{Physiology} is Molecular function
[Aldehyde-Ketone Sensitive Reductase Activity]{Physiology} is Aldehyde reductase 1
[glutathione]{Chemicals & Drugs} is Glutathione
[GSH]{Chemicals & Drugs} is Glutathione
[intracellular]{Concepts & Ideas} is Intracellular
[GSH]{Chemicals & Drugs} is Glutathione
[cigarette smoke]{Chemicals & Drugs} is Cigarette smoke
[cytotoxicity]{Disorders} is Cytotoxicity
[cigarette smoke extract]{Chemicals & Drugs} is Cigarette smoke
[CSE]{Chemicals & Drugs} is Cigarette smoke
[mouse]{Living Beings} is Laboratory Mouse
[melanoma cell]{Anatomy} is Melanoma Cell
[culture medium]{Chemicals & Drugs} is Culture medium
[intracellular]{Concepts & Ideas} is Intracellular
[GSH]{Chemicals & Drugs} is Glutathione
[GSH]{Chemicals & Drugs} is Glutathione
[MVK]{Chemicals & Drugs} is Methyl vinyl ketone
[detected]{Disorders} is Detected
[LC/MS analysis]{Procedures} is LC/MS
[GSH]{Chemicals & Drugs} is Glutathione
[CA]{Chemicals & Drugs} is Crotonaldehyde
[detected]{Disorders} is Detected
[study]{Procedures} is Study
[GSH]{Chemicals & Drugs} is Glutathione
[CA]{Chemicals & Drugs} is Crotonaldehyde
[detect]{Disorders} is Detected
[cell]{Anatomy} is Melanoma Cell
[medium]{Chemicals & Drugs} is Culture medium
[structures]{Concepts & Ideas} is 3D Molecular Structures
[ACR]{Chemicals & Drugs} is Acrolein
[CA]{Chemicals & Drugs} is Crotonaldehyde
[MVK]{Chemicals & Drugs} is Methyl vinyl ketone
[CSE]{Chemicals & Drugs} is Cigarette smoke
[GSH]{Chemicals & Drugs} is Glutathione
[cell]{Anatomy} is Melanoma Cell
[culture medium]{Chemicals & Drugs} is Culture medium
[mass spectra]{Procedures} is Mass Spectrum
[cells]{Anatomy} is Melanoma Cell
[GSH]{Chemicals & Drugs} is Glutathione
[CA]{Chemicals & Drugs} is Crotonaldehyde
[GSH]{Chemicals & Drugs} is Glutathione
[ACR]{Chemicals & Drugs} is Acrolein
[detected]{Disorders} is Detected
[corresponding alcohols]{Chemicals & Drugs} is Alcohols
[detected]{Disorders} is Detected
[GSH]{Chemicals & Drugs} is Glutathione
[MVK]{Chemicals & Drugs} is Methyl vinyl ketone
[detected]{Disorders} is Detected
[cells]{Anatomy} is Melanoma Cell
[GSH]{Chemicals & Drugs} is Glutathione
[GSH]{Chemicals & Drugs} is Glutathione
[α,β-unsaturated aldehydes]{Chemicals & Drugs} is Aldehydes
[CA]{Chemicals & Drugs} is Crotonaldehyde
[ACR]{Chemicals & Drugs} is Acrolein
[intracellular]{Concepts & Ideas} is Intracellular
[carbonyl reductase(s)]{Chemicals & Drugs} is Carbonyl reductase (NADPH)
[cells]{Anatomy} is Melanoma Cell
[GSH]{Chemicals & Drugs} is Glutathione
[α,β-unsaturated ketone]{Chemicals & Drugs} is Ketone
[MVK]{Chemicals & Drugs} is Methyl vinyl ketone
[carbonyl reductase]{Physiology} is Aldehyde reductase 1
[cytotoxicity]{Disorders} is Cytotoxicity
[α,β-unsaturated aldehydes]{Chemicals & Drugs} is Aldehydes
[ketones]{Chemicals & Drugs} is Ketone
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[Strategies] for [Assaying] [Lysosomal Membrane] [Permeabilization]
[Late endosomal] [organelles] have an acidic pH and contain [hydrolytic enzymes] to degrade cargo delivered either from the [extracellular] [environment] by [endocytosis] or from within the [cell] itself by [autophagy]. In the event of [lysosomal membrane] [permeabilization] ([LMP]), the contents of [late endosomes] and [lysosomes] can be released into the [cytosol] and then initiate [apoptosis]. Compounds that can trigger [LMP] are therefore candidates for the induction of [apoptosis], in particular in [anticancer therapy]. Alternatively, [drug-delivery systems], such as nanoparticles, can have side effects that can include [LMP], which has [toxic consequences] for the [cells]. To determine when, to what extent, and with what consequences [LMP] occurs is therefore of paramount importance for the [evaluation] of new potentially [LMP] - inducing compounds. In this introduction, we provide an overview of some [basic assays] for assessing [LMP], such as staining with [lysosomotropic dyes] and measurement of [cysteine] [cathepsin] [activity], and discuss additional [strategies] for the [detection] of the release of endogenous [lysosomal] molecules or preloaded exogenous [tracers] into the [cytosol].
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[Strategies]{Procedures} is Intervention Strategies
[Assaying]{Procedures} is Assay technique
[Lysosomal Membrane]{Anatomy} is Lysosomal membrane
[Permeabilization]{Physiology} is Cell Function
[Strategies]{Procedures} is Intervention Strategies
[Late endosomal]{Anatomy} is Late Endosome
[Assaying]{Procedures} is Assay technique
[organelles]{Anatomy} is Organelles
[Lysosomal Membrane]{Anatomy} is Lysosomal membrane
[Permeabilization]{Physiology} is Cell Function
[hydrolytic enzymes]{Chemicals & Drugs} is Hydrolase
[extracellular]{Anatomy} is Extracellular
[environment]{Concepts & Ideas} is Environment
[endocytosis]{Physiology} is Endocytosis
[cell]{Anatomy} is Cell Type
[autophagy]{Physiology} is Autophagy
[lysosomal membrane]{Anatomy} is Lysosomal membrane
[permeabilization]{Physiology} is Cell Function
[LMP]{Physiology} is Cell Function
[late endosomes]{Anatomy} is Late Endosome
[lysosomes]{Anatomy} is Lysosomes
[cytosol]{Anatomy} is Cytosols
[apoptosis]{Physiology} is Apoptosis
[LMP]{Physiology} is Cell Function
[apoptosis]{Physiology} is Apoptosis
[anticancer therapy]{Procedures} is Anticancer therapy
[drug-delivery systems]{Devices} is Drug Delivery Systems
[LMP]{Physiology} is Cell Function
[toxic consequences]{Disorders} is Toxic effect
[cells]{Anatomy} is Cell Type
[LMP]{Physiology} is Cell Function
[evaluation]{Procedures} is Evaluations
[LMP]{Physiology} is Cell Function
[basic assays]{Procedures} is Assay technique
[LMP]{Physiology} is Cell Function
[lysosomotropic dyes]{Chemicals & Drugs} is Dyes
[cysteine]{Chemicals & Drugs} is Cysteine
[cathepsin]{Chemicals & Drugs} is Cathepsin
[activity]{Physiology} is Enzyme activity
[strategies]{Procedures} is Intervention Strategies
[detection]{Procedures} is Detection
[lysosomal]{Anatomy} is Lysosomes
[tracers]{Chemicals & Drugs} is Tracer
[cytosol]{Anatomy} is Cytosols
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Stimulation of [cell proliferation] by [glutathione monoethyl ester] in [aged bone marrow stromal cells] is associated with the assistance of [TERT] [gene expression] and [telomerase activity]
The [proliferation] and [differentiation] potential of [aged bone marrow stromal cells] ([BMSCs]) are significantly reduced. In order to [improve] the performance of the aged [BMSCs], these [cells] were treated with 2 mM [glutathione monoethyl ester] ([GSH-MEE]) for 24 h. [Proliferation] rate, [telomerase activity], [telomere] length, and [differentiation] to [cholinergic neuron-like cells] ([CNLCs]) were observed to increase. Though, the expression level of [telomerase reverse transcriptase gene] increased, but [CTC1] and [TEN1 genes] from [Ctc1-Stn1-Ten1 complex] encoding [proteins] with [regulatory function] significantly decreased. [Trypan blue exclusion assay] was used to analyze the [proliferation] and, while [telomere] length, its several related [gene expressions], and [telomerase activity] were measured using the [real time reverse transcription-polymerase chain reaction] and [polymerase chain reaction] [enzyme-linked immunosorbent assay techniques], respectively. [CNLCs] [differentiation] potential was evaluated by estimating the percentage of [choline acetyltransferase] [immunereactive cells] .The results suggested that [GSH-MEE] could [improve] aged [rat] [BMSC] properties and would be of potential benefit for enhancing the performance of [aged people's] [BMSCs].
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[cell proliferation]{Physiology} is Cell proliferation
[glutathione monoethyl ester]{Chemicals & Drugs} is Glutathione monoethyl ester
[aged bone marrow stromal cells]{Anatomy} is Bone Marrow Stromal Cells
[TERT]{Genes & Molecular Sequences} is TERT Gene
[gene expression]{Physiology} is Gene Expression
[telomerase activity]{Physiology} is Telomerase activity
[proliferation]{Physiology} is Cell proliferation
[cell proliferation]{Physiology} is Cell proliferation
[differentiation]{Physiology} is Cell Differentiation
[glutathione monoethyl ester]{Chemicals & Drugs} is Glutathione monoethyl ester
[aged bone marrow stromal cells]{Anatomy} is Bone Marrow Stromal Cells
[aged bone marrow stromal cells]{Anatomy} is Bone Marrow Stromal Cells
[BMSCs]{Anatomy} is Bone Marrow Stromal Cells
[improve]{Disorders} is Improved
[TERT]{Genes & Molecular Sequences} is TERT Gene
[gene expression]{Physiology} is Gene Expression
[telomerase activity]{Physiology} is Telomerase activity
[BMSCs]{Anatomy} is Bone Marrow Stromal Cells
[cells]{Anatomy} is Cells set
[glutathione monoethyl ester]{Chemicals & Drugs} is Glutathione monoethyl ester
[GSH-MEE]{Chemicals & Drugs} is Glutathione monoethyl ester
[Proliferation]{Physiology} is Cell proliferation
[telomerase activity]{Physiology} is Telomerase activity
[telomere]{Anatomy} is Telomere
[differentiation]{Physiology} is Cell Differentiation
[cholinergic neuron-like cells]{Anatomy} is Cholinergic Neuron
[CNLCs]{Anatomy} is Cholinergic Neuron
[telomerase reverse transcriptase gene]{Genes & Molecular Sequences} is TERT Gene
[CTC1]{Genes & Molecular Sequences} is CTC1
[TEN1 genes]{Genes & Molecular Sequences} is TEN1 gene
[Ctc1-Stn1-Ten1 complex]{Anatomy} is Cell component
[proteins]{Chemicals & Drugs} is Proteins
[regulatory function]{Physiology} is Gene Action Regulation
[Trypan blue exclusion assay]{Procedures} is BIOL ASSAY
[proliferation]{Physiology} is Cell proliferation
[telomere]{Anatomy} is Telomere
[gene expressions]{Physiology} is Gene Expression
[telomerase activity]{Physiology} is Telomerase activity
[real time reverse transcription-polymerase chain reaction]{Procedures} is Reverse Transcription Polymerase Chain Reaction
[polymerase chain reaction]{Procedures} is Polymerase Chain Reaction
[enzyme-linked immunosorbent assay techniques]{Procedures} is Enzyme-linked immunosorbent assay
[CNLCs]{Anatomy} is Cholinergic Neuron
[differentiation]{Physiology} is Cell Differentiation
[choline acetyltransferase]{Genes & Molecular Sequences} is CHOLINE ACETYLTRANSFERASE
[immunereactive cells]{Anatomy} is Cells set
[GSH-MEE]{Chemicals & Drugs} is Glutathione monoethyl ester
[improve]{Disorders} is Improved
[rat]{Living Beings} is Rat (organism)
[BMSC]{Anatomy} is Bone Marrow Stromal Cells
[aged people's]{Living Beings} is People
[BMSCs]{Anatomy} is Bone Marrow Stromal Cells
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[Wild food plants] and [fungi] used in the [mycophilous] [Tibetan] community of [Zhagana] ([Tewo County], [Gansu], [China])
The aim of the [study] was to investigate [knowledge] and use of [wild food plants] and [fungi] in a highland [valley] in the [Gannan Tibetan Autonomous Region] on the north-eastern edges of the [Tibetan Plateau]. Field research was carried out in four neighbouring [villages] in a [mountain] [valley] of the [Diebu (Tewo) county], surrounded by spruce forests. The [study] consisted of 30 interviews with single informants, or [group interviews] (altogether 63 informants). Apart from collecting voucher specimens, we also identified [fungi] using [DNA barcoding]. We recorded the use of 54 [species] of [vascular plants]. We also recorded the use of 22 [mushroom taxa], which made up the largest category of [wild foods]. [Fruits] formed the largest category of [food plants], with 21 [species], larger than the [wild greens] category, which consisted of 20 [species] [eaten] after boiling or frying and 7 as raw [snacks]. We also recorded the alimentary use of 10 [species] of [edible flowers] and 3 [species] with underground [edible organs]. On average, 20.8 [edible taxa] were listed per interview (median - 21). The most listed category of [wild foods] was [green vegetables] (mean - 7.5 [species], median - 8 [species]), but [fruits] and [mushrooms] were listed nearly as frequently (mean - 6.3, median - 6 and mean - 5.8, - median 6 respectively). Other category lists were very short, e.g., [flowers] (mean - 1.3, median - 1) and underground [edible parts] (mean - 0.7, median - 1). [Wild vegetables] are usually boiled and/or fried and served as side-dishes, or their [green parts] are [eaten] as [snacks] during [mountain] treks (e.g., [peeled rhubarb shoots]). [Wild fruits] are mainly collected by children and [eaten] raw, they are not stored for further use. The most widely used [wild staple foods] are [Potetilla anserina] [roots], an important [ceremonial food] served on such occasions as New Year or at funerals. They are boiled and served with [sugar] and [butter]. The most important famine [plants] remembered by [people] are the [aerial bulbils] of [Persicaria vivipara]. [Flowers] are used as children's [snacks] - their [nectar] is sucked. The number of [wild taxa] [eaten] in the studied [valley] is similar to that of other [Tibetan areas]. The structure of [wild food plant] taxa is also very typical for Tibetan speaking [areas] (e.g., the use of [rhubarb shoots], [Potentilla anserina], [Persicaria vivipara]). The studied community show a high level of [mycophilia].
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[Wild food plants]{Objects} is Food Plants
[fungi]{Living Beings} is Fungi
[mycophilous]{Objects} is Mushroom - dietary
[Tibetan]{Geographic Areas} is Tibet
[Zhagana]{Geographic Areas} is Area
[Tewo County]{Geographic Areas} is Area
[Gansu]{Geographic Areas} is Area
[China]{Geographic Areas} is China
[Wild food plants]{Objects} is Food Plants
[study]{Procedures} is Study
[fungi]{Living Beings} is Fungi
[mycophilous]{Objects} is Mushroom - dietary
[knowledge]{Concepts & Ideas} is Knowledge
[Tibetan]{Geographic Areas} is Tibet
[wild food plants]{Objects} is Food Plants
[Zhagana]{Geographic Areas} is Area
[Tewo County]{Geographic Areas} is Area
[fungi]{Living Beings} is Fungi
[Gansu]{Geographic Areas} is Area
[China]{Geographic Areas} is China
[valley]{Concepts & Ideas} is Valley
[Gannan Tibetan Autonomous Region]{Geographic Areas} is Area
[Tibetan Plateau]{Geographic Areas} is Tibet
[villages]{Geographic Areas} is Village
[mountain]{Geographic Areas} is Mountain
[valley]{Concepts & Ideas} is Valley
[Diebu (Tewo) county]{Geographic Areas} is Area
[study]{Procedures} is Study
[group interviews]{Procedures} is Group Interviews
[fungi]{Living Beings} is Fungi
[DNA barcoding]{Procedures} is Taxonomic DNA Barcoding
[species]{Concepts & Ideas} is Species
[vascular plants]{Living Beings} is Vascular plants
[mushroom taxa]{Objects} is Mushroom - dietary
[wild foods]{Objects} is Foods
[Fruits]{Objects} is Fruits
[food plants]{Objects} is Food Plants
[species]{Concepts & Ideas} is Species
[wild greens]{Living Beings} is Wild plant
[species]{Concepts & Ideas} is Species
[eaten]{Physiology} is Eat
[snacks]{Objects} is Snacks
[species]{Concepts & Ideas} is Species
[edible flowers]{Living Beings} is Flowers
[species]{Concepts & Ideas} is Species
[edible organs]{Objects} is Food Plants
[edible taxa]{Objects} is Food Plants
[wild foods]{Objects} is Foods
[green vegetables]{Objects} is Green Vegetable
[species]{Concepts & Ideas} is Species
[species]{Concepts & Ideas} is Species
[fruits]{Objects} is Fruits
[mushrooms]{Objects} is Mushroom - dietary
[flowers]{Living Beings} is Flowers
[edible parts]{Objects} is Food Plants
[Wild vegetables]{Objects} is Vegetables
[green parts]{Living Beings} is Green plants
[eaten]{Physiology} is Eat
[snacks]{Objects} is Snacks
[mountain]{Geographic Areas} is Mountain
[peeled rhubarb shoots]{Living Beings} is Shoot
[Wild fruits]{Objects} is Fruits
[eaten]{Physiology} is Eat
[wild staple foods]{Objects} is Foods
[Potetilla anserina]{Living Beings} is Potentilla anserina
[roots]{Living Beings} is Plant Roots
[ceremonial food]{Objects} is Foods
[sugar]{Chemicals & Drugs} is SUGAR
[butter]{Objects} is Butter
[plants]{Living Beings} is Green plants
[people]{Living Beings} is People
[aerial bulbils]{Living Beings} is Green plants
[Persicaria vivipara]{Living Beings} is Persicaria vivipara
[Flowers]{Living Beings} is Flowers
[snacks]{Objects} is Snacks
[nectar]{Chemicals & Drugs} is Nectars
[wild taxa]{Living Beings} is Wild plant
[eaten]{Physiology} is Eat
[valley]{Concepts & Ideas} is Valley
[Tibetan areas]{Geographic Areas} is Tibet
[wild food plant]{Objects} is Food Plants
[areas]{Geographic Areas} is Area
[rhubarb shoots]{Living Beings} is Shoot
[Potentilla anserina]{Living Beings} is Potentilla anserina
[Persicaria vivipara]{Living Beings} is Persicaria vivipara
[mycophilia]{Objects} is Mushroom - dietary
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Comparison of [Head] [Elevation Protocols] Following [Femoral Artery Sheath] [Removal] After [Coronary Angiography]
To compare 2 standard [protocols] for [head] [elevation] following removal of a [femoral artery sheath] after [coronary angiography] and their effects on [bleeding] [complications] and reported levels of [back pain]. One [protocol] involved flat [supine] [bed rest]; the other allowed progressive [head] [elevation]. A prospective [comparative study] of 80 adult patients undergoing [coronary angiography] via the [femoral] [approach]. The [Numeric Rating Scale] was used as the measure of reported [pain]. No [bleeding] [complications] occurred in either group. Both groups had very low mean [pain scores]. Repeated- measures [analysis] demonstrated that the experience of [pain] differed significantly over time by [location] (F5,70 = 3.864, P = .004), with a notable decrease in [pain scores] more than 1 hour after [sheath] [removal] at the [location] that used the progressive [head] [elevation protocol]. Patients ' satisfaction scores after discharge did not differ significantly between the 2 groups. Patients with a [history] of chronic [back pain] had consistently higher [pain scores], but those [pain scores] did not differ significantly by [location] (or [protocol]). It appears that using a progressive [head] - [elevation protocol] within the first 3 hours after diagnostic [angiography] is not associated with an increased risk of [bleeding] [complications] at the [access site] and warrants further exploration in the mitigation of [back pain] associated with prolonged [supine] [bed rest].
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[Head]{Anatomy} is Heads
[Elevation Protocols]{Procedures} is Elevation
[Femoral Artery Sheath]{Anatomy} is Femoral Artery
[Removal]{Procedures} is Removal - action
[Coronary Angiography]{Procedures} is Coronary angiography
[Head]{Anatomy} is Heads
[Elevation Protocols]{Procedures} is Elevation
[protocols]{Procedures} is CLIN PROTOCOLS
[head]{Anatomy} is Heads
[elevation]{Procedures} is Elevation
[Femoral Artery Sheath]{Anatomy} is Femoral Artery
[Removal]{Procedures} is Removal - action
[femoral artery sheath]{Anatomy} is Femoral Artery
[Coronary Angiography]{Procedures} is Coronary angiography
[coronary angiography]{Procedures} is Coronary angiography
[bleeding]{Disorders} is Bleeding
[complications]{Disorders} is Complication
[back pain]{Disorders} is Pain back
[protocol]{Procedures} is CLIN PROTOCOLS
[supine]{Concepts & Ideas} is Supine
[bed rest]{Procedures} is Bed rest
[head]{Anatomy} is Heads
[elevation]{Procedures} is Elevation
[comparative study]{Procedures} is Comparative study research
[coronary angiography]{Procedures} is Coronary angiography
[femoral]{Anatomy} is Femoral
[approach]{Concepts & Ideas} is Approach
[Numeric Rating Scale]{Concepts & Ideas} is Numeric Rating Scale
[pain]{Disorders} is Pain finding
[bleeding]{Disorders} is Bleeding
[complications]{Disorders} is Complication
[pain scores]{Disorders} is Pain score
[analysis]{Procedures} is Analyzed
[pain]{Disorders} is Pain finding
[location]{Anatomy} is Location
[pain scores]{Disorders} is Pain score
[sheath]{Anatomy} is Femoral Artery
[removal]{Procedures} is Removal - action
[location]{Anatomy} is Location
[head]{Anatomy} is Heads
[elevation protocol]{Procedures} is Elevation
[history]{Disorders} is Medical History
[back pain]{Disorders} is Pain back
[pain scores]{Disorders} is Pain score
[pain scores]{Disorders} is Pain score
[location]{Anatomy} is Location
[protocol]{Procedures} is CLIN PROTOCOLS
[head]{Anatomy} is Heads
[elevation protocol]{Procedures} is Elevation
[angiography]{Procedures} is Angiography
[bleeding]{Disorders} is Bleeding
[complications]{Disorders} is Complication
[access site]{Concepts & Ideas} is Site of access
[back pain]{Disorders} is Pain back
[supine]{Concepts & Ideas} is Supine
[bed rest]{Procedures} is Bed rest
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Heterogeneous Mechanisms of [Primary and Acquired Resistance] to [Third-Generation EGFR Inhibitors]
To identify novel mechanisms of [resistance] to [third-generation EGFR inhibitors] in patients with [lung adenocarcinoma] that progressed under [therapy] with either [AZD9291] or [rociletinib] ([CO-1686]). We [analyzed] [tumor biopsies] from seven patients obtained before, during, and/or after [treatment] with [AZD9291] or [rociletinib] ([CO-1686]). [Targeted sequencing] and [FISH analyses] were performed, and the relevance of [candidate genes] was functionally assessed in [in vitro models]. We found [recurrent amplification] of either [MET] or [ERBB2] in [tumors] that were [resistant] or [developed resistance] to [third-generation EGFR inhibitors] and show that [ERBB2] and [MET activation] can confer [resistance] to [these compounds]. Furthermore, we identified a [KRAS(G12S) mutation] in a patient with [acquired resistance] to [AZD9291] as a potential driver of [acquired resistance]. Finally, we show that dual inhibition of [[EGFR] /MEK] might be a viable strategy to overcome [resistance] in [EGFR-mutant cells] expressing [mutant KRAS] CONCLUSIONS: Our data suggest that heterogeneous mechanisms of [resistance] can drive [primary and acquired resistance] to [third-generation EGFR inhibitors] and provide a rationale for potential [combination strategies]. Clin Cancer Res; 1-11. ©2016 AACR.
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[Primary and Acquired Resistance]{Phenomena} is Drug Resistance
[Third-Generation EGFR Inhibitors]{Chemicals & Drugs} is EGFR Inhibitor
[Primary and Acquired Resistance]{Phenomena} is Drug Resistance
[resistance]{Phenomena} is Drug Resistance
[third-generation EGFR inhibitors]{Chemicals & Drugs} is EGFR Inhibitor
[Third-Generation EGFR Inhibitors]{Chemicals & Drugs} is EGFR Inhibitor
[lung adenocarcinoma]{Disorders} is Lung adenocarcinoma
[therapy]{Procedures} is Therapy
[AZD9291]{Chemicals & Drugs} is AZD9291
[rociletinib]{Chemicals & Drugs} is Rociletinib
[CO-1686]{Chemicals & Drugs} is CO-1686
[analyzed]{Procedures} is Analyzed
[tumor biopsies]{Procedures} is Biopsies
[treatment]{Procedures} is Therapy
[AZD9291]{Chemicals & Drugs} is AZD9291
[rociletinib]{Chemicals & Drugs} is Rociletinib
[CO-1686]{Chemicals & Drugs} is CO-1686
[Targeted sequencing]{Procedures} is Gene Sequencing
[FISH analyses]{Procedures} is FISH
[candidate genes]{Genes & Molecular Sequences} is Candidate Genes
[in vitro models]{Procedures} is In Vitro Model
[recurrent amplification]{Physiology} is Gene amplification
[MET]{Genes & Molecular Sequences} is MET gene
[ERBB2]{Genes & Molecular Sequences} is ERBB2 gene
[tumors]{Disorders} is Tumors
[resistant]{Phenomena} is Drug Resistance
[developed resistance]{Phenomena} is Drug Resistance
[third-generation EGFR inhibitors]{Chemicals & Drugs} is EGFR Inhibitor
[ERBB2]{Physiology} is Activation, Gene
[MET activation]{Physiology} is Activation, Gene
[resistance]{Phenomena} is Drug Resistance
[these compounds]{Chemicals & Drugs} is EGFR Inhibitor
[KRAS(G12S) mutation]{Disorders} is KRAS G12S
[acquired resistance]{Phenomena} is Drug Resistance
[AZD9291]{Chemicals & Drugs} is AZD9291
[acquired resistance]{Phenomena} is Drug Resistance
[EGFR]{Chemicals & Drugs} is RECEPT EGF
[EGFR /MEK]{Chemicals & Drugs} is MEK
[resistance]{Phenomena} is Drug Resistance
[EGFR-mutant cells]{Anatomy} is Cells set
[mutant KRAS]{Disorders} is KRAS mutation
[resistance]{Phenomena} is Drug Resistance
[primary and acquired resistance]{Phenomena} is Drug Resistance
[third-generation EGFR inhibitors]{Chemicals & Drugs} is EGFR Inhibitor
[combination strategies]{Procedures} is Combination Drug Therapies
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[Nax] [signaling] evoked by an increase in ([Na+]) in [CSF] induces [water intake] via [EET] -mediated [TRPV4] activation
[Water-intake] behavior is under the control of [brain systems] that sense [body-fluid] conditions at [sensory circumventricular organs] ([sCVOs]); however, the underlying mechanisms have not yet been elucidated in detail. [Nax] is a [sodium] ([Na(+)]) level [sensor] in the [brain], and the [transient receptor potential vanilloid (TRPV) channels], [TRPV1] and [TRPV4], have been proposed to function as [osmosensors]. We herein investigated voluntary [water intake] immediately induced after an [intracerebroventricular] ([icv]) [administration] of a [hypertonic NaCl solution] in [TRPV1-], [TRPV4-], [Nax-], and their [double-gene knockout (KO) mice]. The induction of [water intake] by [TRPV1] - [KO mice] was normal, whereas that by [TRPV4] - [KO] and [Nax] - [KO mice] was significantly less than that by [WT mice]. [Water intake] by [Nax] / [TRPV4] - [double KO mice] was similar to that by the respective single [KO mice]. When [TRPV4] activity was blocked with a [specific antagonist] [HC-067047], [water intake] by [WT mice] was significantly reduced, whereas that by [TRPV4] - [KO] and [Nax] - [KO mice] was not. Similar results were obtained with the [administration] of [miconazole], which inhibits the biosynthesis of [epoxyeicosatrienoic acids] ([EETs]), endogenous [agonists] for [TRPV4], from [arachidonic acid] ([AA]). [Icv] [injection] of [hypertonic NaCl] with [AA] or [5,6-EET] restored [water intake] by [Nax] - [KO mice] to the [WT] level, but not that by [TRPV4] - [KO mice]. These results suggest that the [Na(+)] signal generated in [Nax] - [positive] [glial cells] leads to the activation of [TRPV4] - [positive] [neurons] in [sCVOs] in order to [stimulate] [water intake] by using [EETs] as [gliotransmitters].
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[Nax]{Chemicals & Drugs} is Nax sodium channel, mouse
[signaling]{Physiology} is Signaling
[Na+]{Chemicals & Drugs} is Na+
[CSF]{Anatomy} is CSF
[water intake]{Physiology} is Water intake
[EET]{Chemicals & Drugs} is EET
[TRPV4]{Chemicals & Drugs} is TRPV4 protein, human
[Nax]{Chemicals & Drugs} is Nax sodium channel, mouse
[Water-intake]{Physiology} is Water intake
[signaling]{Physiology} is Signaling
[Na+]{Chemicals & Drugs} is Na+
[brain systems]{Anatomy} is Nervous System, Brain
[CSF]{Anatomy} is CSF
[water intake]{Physiology} is Water intake
[body-fluid]{Anatomy} is Body Fluid
[EET]{Chemicals & Drugs} is EET
[TRPV4]{Chemicals & Drugs} is TRPV4 protein, human
[sensory circumventricular organs]{Anatomy} is Sensory Circumventricular Organs
[sCVOs]{Anatomy} is Sensory Circumventricular Organs
[Nax]{Chemicals & Drugs} is Nax sodium channel, mouse
[sodium]{Chemicals & Drugs} is Na+
[Na(+)]{Chemicals & Drugs} is Na+
[sensor]{Physiology} is Osmosensor activity
[brain]{Anatomy} is Nervous System, Brain
[transient receptor potential vanilloid (TRPV) channels]{Chemicals & Drugs} is Vanilloid Receptors
[TRPV1]{Chemicals & Drugs} is TRPV1 protein, human
[TRPV4]{Chemicals & Drugs} is TRPV4 protein, human
[osmosensors]{Physiology} is Osmosensor activity
[water intake]{Physiology} is Water intake
[intracerebroventricular]{Concepts & Ideas} is Intracerebroventricular
[icv]{Concepts & Ideas} is Intracerebroventricular
[administration]{Procedures} is Administration
[hypertonic NaCl solution]{Chemicals & Drugs} is Hypertonic Saline Solution
[TRPV1-]{Genes & Molecular Sequences} is TRPV1
[TRPV4-]{Genes & Molecular Sequences} is TRPV4
[Nax-]{Genes & Molecular Sequences} is NaG
[double-gene knockout (KO) mice]{Living Beings} is Knockout Mice
[water intake]{Physiology} is Water intake
[TRPV1]{Genes & Molecular Sequences} is TRPV1
[KO mice]{Living Beings} is Knockout Mice
[TRPV4]{Genes & Molecular Sequences} is TRPV4
[KO]{Living Beings} is Knockout Mice
[Nax]{Genes & Molecular Sequences} is NaG
[KO mice]{Living Beings} is Knockout Mice
[WT mice]{Living Beings} is Wild Type Mouse
[Water intake]{Physiology} is Water intake
[Nax]{Genes & Molecular Sequences} is NaG
[TRPV4]{Genes & Molecular Sequences} is TRPV4
[double KO mice]{Living Beings} is Knockout Mice
[KO mice]{Living Beings} is Knockout Mice
[TRPV4]{Chemicals & Drugs} is Trpv4 protein, mouse
[specific antagonist]{Chemicals & Drugs} is Antagonists & inhibitors
[HC-067047]{Chemicals & Drugs} is HC-067047
[water intake]{Physiology} is Water intake
[WT mice]{Living Beings} is Wild Type Mouse
[TRPV4]{Genes & Molecular Sequences} is TRPV4
[KO]{Living Beings} is Knockout Mice
[Nax]{Genes & Molecular Sequences} is NaG
[KO mice]{Living Beings} is Knockout Mice
[administration]{Procedures} is Administration
[miconazole]{Chemicals & Drugs} is Miconazole product
[epoxyeicosatrienoic acids]{Chemicals & Drugs} is EET
[EETs]{Chemicals & Drugs} is EET
[agonists]{Chemicals & Drugs} is Agonist
[TRPV4]{Chemicals & Drugs} is Trpv4 protein, mouse
[arachidonic acid]{Chemicals & Drugs} is Arachidonic Acid
[AA]{Chemicals & Drugs} is Arachidonic Acid
[Icv]{Concepts & Ideas} is Intracerebroventricular
[injection]{Procedures} is Injection - action
[hypertonic NaCl]{Chemicals & Drugs} is Hypertonic Saline Solution
[AA]{Chemicals & Drugs} is Arachidonic Acid
[5,6-EET]{Chemicals & Drugs} is 5,6-EET
[water intake]{Physiology} is Water intake
[Nax]{Genes & Molecular Sequences} is NaG
[KO mice]{Living Beings} is Knockout Mice
[WT]{Genes & Molecular Sequences} is Wild Type
[TRPV4]{Genes & Molecular Sequences} is TRPV4
[KO mice]{Living Beings} is Knockout Mice
[Na(+)]{Chemicals & Drugs} is Na+
[Nax]{Chemicals & Drugs} is Nax sodium channel, mouse
[positive]{Disorders} is Positive for
[glial cells]{Anatomy} is Glial Cells
[TRPV4]{Chemicals & Drugs} is Trpv4 protein, mouse
[positive]{Disorders} is Positive for
[neurons]{Anatomy} is Neurons
[sCVOs]{Anatomy} is Sensory Circumventricular Organs
[stimulate]{Procedures} is Stimulation
[water intake]{Physiology} is Water intake
[EETs]{Chemicals & Drugs} is EET
[gliotransmitters]{Chemicals & Drugs} is Neurotransmitters
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An Accessible and [Pragmatic Experimental Model] of [Nonalcoholic Fatty Liver Disease]
BACKGROUND There is no convenient cheap [pragmatic experimental model] for [Nonalcoholic Fatty Liver Disease] ([NAFLD])/ [Nonalcoholic Steatohepatitis] ([NASH]). Our objective was to create a [pragmatic model] of [NAFLD] / [NASH]. METHODS [Sprague-Dawley rats] were fed a [high-fat], [high sugar homemade diet] ad libitum for seven weeks. The [high-fat], [high sugar diet] included 59% of energy derived from [fat], 30% from [carbohydrates], and 11% from [protein]. [Serum levels of fasting glucose], [triglyceride], [cholesterol], [liver enzymes], [insulin], and [hepatic] [tumor necrosis factor-alpha] ([TNF-α]) [gene expression] were determined. [Hepatic] [histology] was examined by [H&E stain]. RESULTS [Rats] fed the [high-fat], [high sugar diet] developed [hepatic steatosis], and a [moderate inflammation], which was associated with [increased serum levels of liver enzymes], [glucose], [insulin], [triglyceride], [cholesterol], and [hepatic] [TNF-α] [gene expression]. CONCLUSION This [rat] [model] resembles the key features of [human] [NAFLD] / [NASH] and provides a simple [pragmatic experimental model] for elucidating the disease prevention and [treatment].
|
[Pragmatic Experimental Model]{Living Beings} is Experimental Animal Model
[Nonalcoholic Fatty Liver Disease]{Disorders} is Nonalcoholic Fatty Liver Disease
[Pragmatic Experimental Model]{Living Beings} is Experimental Animal Model
[pragmatic experimental model]{Living Beings} is Experimental Animal Model
[Nonalcoholic Fatty Liver Disease]{Disorders} is Nonalcoholic Fatty Liver Disease
[Nonalcoholic Fatty Liver Disease]{Disorders} is Nonalcoholic Fatty Liver Disease
[NAFLD]{Disorders} is Nonalcoholic Fatty Liver Disease
[Nonalcoholic Steatohepatitis]{Disorders} is Nonalcoholic Steatohepatitis
[NASH]{Disorders} is Nonalcoholic Steatohepatitis
[pragmatic model]{Living Beings} is Experimental Animal Model
[NAFLD]{Disorders} is Nonalcoholic Fatty Liver Disease
[NASH]{Disorders} is Nonalcoholic Steatohepatitis
[Sprague-Dawley rats]{Living Beings} is Sprague-Dawley Rats
[high-fat]{Procedures} is High-Fat Diet
[high sugar homemade diet]{Procedures} is High sugar diet
[high-fat]{Procedures} is High-Fat Diet
[high sugar diet]{Procedures} is High sugar diet
[fat]{Chemicals & Drugs} is Dietary Fat
[carbohydrates]{Objects} is Carbohydrate food
[protein]{Objects} is Protein food
[Serum levels of fasting glucose]{Procedures} is Serum fasting glucose level
[triglyceride]{Procedures} is Serum triglycerides
[cholesterol]{Procedures} is Cholesterol total
[liver enzymes]{Procedures} is Liver enzymes
[insulin]{Procedures} is Serum insulin
[hepatic]{Anatomy} is Hepatic
[tumor necrosis factor-alpha]{Chemicals & Drugs} is Tumor Necrosis Factor-alpha
[TNF-α]{Chemicals & Drugs} is Tumor Necrosis Factor-alpha
[gene expression]{Physiology} is Gene Expression
[Hepatic]{Anatomy} is Hepatic
[histology]{Procedures} is Histology
[H&E stain]{Procedures} is H&E Stain
[Rats]{Living Beings} is Rattus
[high-fat]{Procedures} is High-Fat Diet
[high sugar diet]{Procedures} is High sugar diet
[hepatic steatosis]{Disorders} is Hepatic lipidosis
[moderate inflammation]{Disorders} is Moderate inflammation
[increased serum levels of liver enzymes]{Disorders} is Elevated liver enzymes level
[glucose]{Phenomena} is Serum glucose level
[insulin]{Phenomena} is Serum insulin result
[triglyceride]{Phenomena} is Serum triglyceride levels
[cholesterol]{Phenomena} is Serum cholesterol level
[hepatic]{Anatomy} is Hepatic
[TNF-α]{Chemicals & Drugs} is Tumor Necrosis Factor-alpha
[gene expression]{Physiology} is Gene Expression
[rat]{Living Beings} is Rattus
[model]{Living Beings} is Experimental Animal Model
[human]{Living Beings} is Human
[NAFLD]{Disorders} is Nonalcoholic Fatty Liver Disease
[NASH]{Disorders} is Nonalcoholic Steatohepatitis
[pragmatic experimental model]{Living Beings} is Experimental Animal Model
[treatment]{Procedures} is Treatments
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Comparison of the Effects of [Subcutaneous] Versus [Continuous Infusion] of [Heparin] on Key Inflammatory Parameters Following [Sepsis]
[Sepsis] is the result of the interaction between [inflammatory mediators] and [coagulation pathway]. [Unfractionated heparin] may play a role as an [anti-inflammatory agent] beyond its anticoagulatory effect in [sepsis]. As a result, it may cause reduction in [organ failure] rate in patients with [sepsis] due to its impact on both inflammatory and [coagulation process]. The aim of this [study] was to evaluate the anti-inflammatory effects of [heparin] in [sepsis]. [Plasma] [plasminogen activator inhibitor-1] ([PAI-1]) as an [inflammatory mediator] and urinary [necoutrophil gelatinase-associated lipocalin] ([NGAL]) as a [marker] of [kidney injury] were investigated. This [prospective], [randomized controlled trial] was conducted in a 32- [bed] [intensive care unit]. Thirty patients with [sepsis] were [randomized] to receive [heparin] infusion of 500 units/hour or 5000 units of [heparin] three times a day, [subcutaneously]. The [plasma] level of [PAI-1] and urinary level of [NGAL] were determined at [day 0], 2 and 7. The infusion group had a [lower] [plasma] [PAI-1] level compared to the subcutaneous group at day 7 (11.3 ± 1.6 vs. 16.5 ± 4.2; P = 0.003). The urinary [NGAL] level was [lower] in the infusion group at day 2 (131.3 ± 11.9 vs. 151.2 ± 20.6; P = 0.014); however, at day 7 the [NGAL] level was decreased in the subcutaneous group as much as the infusion group and there was no significant difference between the two groups. There was no significant difference in the [acute physiology and chronic health evaluation (APACHE) II] and [sequential organ failure assessment (SOFA) scores] between the two groups at [day 0], 2 and 7. Low-dose [heparin] infusion compared to [subcutaneous] [heparin] can decrease the [plasma] [PAI-1] and urinary [NGAL] levels more rapidly. It can be related to anti-inflammatory effects of [heparin], which may be more prominent in infusion route.
|
[Subcutaneous]{Procedures} is Subcutaneous infusion
[Continuous Infusion]{Procedures} is Continuous infusion
[Heparin]{Chemicals & Drugs} is Heparin
[Sepsis]{Disorders} is Sepsis (disorder)
[Sepsis]{Disorders} is Sepsis (disorder)
[Subcutaneous]{Procedures} is Subcutaneous infusion
[inflammatory mediators]{Chemicals & Drugs} is MEDIATORS INFLAMM
[Continuous Infusion]{Procedures} is Continuous infusion
[Heparin]{Chemicals & Drugs} is Heparin
[coagulation pathway]{Physiology} is Pathway
[Unfractionated heparin]{Chemicals & Drugs} is Unfractionated Heparin (EPC)
[Sepsis]{Disorders} is Sepsis (disorder)
[anti-inflammatory agent]{Chemicals & Drugs} is Anti-inflammatory agent
[sepsis]{Disorders} is Sepsis (disorder)
[organ failure]{Disorders} is Multi organ failure
[sepsis]{Disorders} is Sepsis (disorder)
[coagulation process]{Physiology} is Coagulation process
[study]{Procedures} is Research study
[heparin]{Chemicals & Drugs} is Heparin
[sepsis]{Disorders} is Sepsis (disorder)
[Plasma]{Anatomy} is Plasma
[plasminogen activator inhibitor-1]{Chemicals & Drugs} is Plasminogen activator inhibitor-1
[PAI-1]{Chemicals & Drugs} is Plasminogen activator inhibitor-1
[inflammatory mediator]{Chemicals & Drugs} is MEDIATORS INFLAMM
[necoutrophil gelatinase-associated lipocalin]{Chemicals & Drugs} is Neutrophil Gelatinase Associated Lipocalin
[NGAL]{Chemicals & Drugs} is Neutrophil Gelatinase Associated Lipocalin
[marker]{Physiology} is Marker
[kidney injury]{Disorders} is Injury to kidney
[prospective]{Procedures} is Study, Prospective
[randomized controlled trial]{Procedures} is Randomized Controlled Clinical Trial
[bed]{Concepts & Ideas} is Patient Location - Bed
[intensive care unit]{Organizations} is Intensive Care Unit
[sepsis]{Disorders} is Sepsis (disorder)
[randomized]{Procedures} is Randomized
[heparin]{Chemicals & Drugs} is Heparin
[heparin]{Chemicals & Drugs} is Heparin
[subcutaneously]{Disorders} is Administered subcutaneously
[plasma]{Anatomy} is Plasma
[PAI-1]{Chemicals & Drugs} is Plasminogen activator inhibitor-1
[NGAL]{Chemicals & Drugs} is Neutrophil Gelatinase Associated Lipocalin
[day 0]{Disorders} is Finding (finding)
[lower]{Concepts & Ideas} is Lower
[plasma]{Anatomy} is Plasma
[PAI-1]{Chemicals & Drugs} is Plasminogen activator inhibitor-1
[NGAL]{Chemicals & Drugs} is Neutrophil Gelatinase Associated Lipocalin
[lower]{Concepts & Ideas} is Lower
[NGAL]{Chemicals & Drugs} is Neutrophil Gelatinase Associated Lipocalin
[acute physiology and chronic health evaluation (APACHE) II]{Procedures} is APACHE II score
[sequential organ failure assessment (SOFA) scores]{Disorders} is Sequential Organ Failure Assessment Scores
[day 0]{Disorders} is Finding (finding)
[heparin]{Chemicals & Drugs} is Heparin
[subcutaneous]{Concepts & Ideas} is Subcutaneous
[heparin]{Chemicals & Drugs} is Heparin
[plasma]{Anatomy} is Plasma
[PAI-1]{Chemicals & Drugs} is Plasminogen activator inhibitor-1
[NGAL]{Chemicals & Drugs} is Neutrophil Gelatinase Associated Lipocalin
[heparin]{Chemicals & Drugs} is Heparin
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The Spreading of Social Energy: How Exposure to [Positive] and [Negative] Social [News] Affects Behavior
Social [news], unlike video games or TV programs, conveys real-life [interactions]. Theoretically, social [news] in which [people] help or harm each other and violate [rules] should influence both prosocial and violation behaviors. In two experiments, we demonstrated the spreading effects of social [news] in a [social interaction] context emphasizing social conventions and a [nonsocial interaction] context emphasizing moral norms. Across the two [studies], the results showed that [positive] social [news] increased cooperation (decreased defection) but had [no] effect on cheating, whereas [negative] social [news] increased cheating but with [no] change in cooperation (or defection). We conclude that there is a spreading impact of [positive] social [news] in the conventional norm domain and of [negative] social [news] in the moral norm domain.
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[Positive]{Disorders} is Positive for
[Negative]{Disorders} is Negative for
[News]{Concepts & Ideas} is News
[news]{Concepts & Ideas} is News
[Positive]{Disorders} is Positive for
[Negative]{Disorders} is Negative for
[interactions]{Disorders} is Social Interactions
[News]{Concepts & Ideas} is News
[news]{Concepts & Ideas} is News
[people]{Living Beings} is People
[rules]{Concepts & Ideas} is Rules of conduct
[news]{Concepts & Ideas} is News
[social interaction]{Disorders} is Social Interactions
[nonsocial interaction]{Disorders} is NEGATIVE
[studies]{Procedures} is Study
[positive]{Disorders} is Positive for
[news]{Concepts & Ideas} is News
[no]{Disorders} is NEGATIVE
[negative]{Disorders} is Negative for
[news]{Concepts & Ideas} is News
[no]{Disorders} is NEGATIVE
[positive]{Disorders} is Positive for
[news]{Concepts & Ideas} is News
[negative]{Disorders} is Negative for
[news]{Concepts & Ideas} is News
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Using [Evolutionary Theory] to Guide [Mental Health] [Research]
[Evolutionary approaches] to [medicine] can shed light on the origins and etiology of disease. Such an [approach] may be especially useful in [psychiatry], which frequently addresses conditions with heterogeneous presentation and unknown causes. We review several previous applications of [evolutionary theory] that highlight the ways in which psychiatric conditions may persist despite and because of natural selection. One lesson from the [evolutionary approach] is that some conditions currently [classified] as [disorders] (because they cause [distress] and [impairment]) may actually be caused by functioning [adaptations] operating " normally " (as designed by natural selection). Such conditions suggest an alternative [illness model] that may generate alternative [intervention strategies]. Thus, the [evolutionary approach] suggests that [psychiatry] should sometimes think differently about [distress] and [impairment]. The complexity of the [human] [brain], including normal functioning and potential for [dysfunctions], has developed over evolutionary time and has been shaped by natural selection. Understanding the evolutionary origins of psychiatric conditions is therefore a crucial component to a complete understanding of etiology.
|
[Evolutionary Theory]{Concepts & Ideas} is Theory of Evolution
[Mental Health]{Physiology} is Mental Health
[Research]{Procedures} is Research
[Evolutionary approaches]{Concepts & Ideas} is Approaches
[Evolutionary Theory]{Concepts & Ideas} is Theory of Evolution
[medicine]{Occupations} is Medicine
[Mental Health]{Physiology} is Mental Health
[Research]{Procedures} is Research
[approach]{Concepts & Ideas} is Approaches
[psychiatry]{Procedures} is Psychiatric service
[evolutionary theory]{Concepts & Ideas} is Theory of Evolution
[evolutionary approach]{Concepts & Ideas} is Approaches
[classified]{Concepts & Ideas} is Classified
[disorders]{Disorders} is Mental disorders NOS (disorder)
[distress]{Disorders} is Distress
[impairment]{Disorders} is Impairment
[adaptations]{Phenomena} is Adaptation
[illness model]{Disorders} is Disease model
[intervention strategies]{Procedures} is Intervention Strategies
[evolutionary approach]{Concepts & Ideas} is Approaches
[psychiatry]{Procedures} is Psychiatric service
[distress]{Disorders} is Distress
[impairment]{Disorders} is Impairment
[human]{Living Beings} is Human
[brain]{Anatomy} is Brains
[dysfunctions]{Disorders} is Cerebral dysfunction
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[Transcriptomic] and [Physiological Responses] of the [Green Microalga] [Chlamydomonas reinhardtii] during Short-Term Exposure to Subnanomolar [Methylmercury] Concentrations
The effects of short-term exposure to subnanomolar [methyl-mercury] ([MeHg]) concentrations, representative of contaminated [environments], on the [microalga] [Chlamydomonas reinhardtii] were assessed using both [physiological end points] and [gene expression analysis]. [MeHg] [bioaccumulated] and induced significant increase of the photosynthesis efficiency, while the algal growth, [oxidative stress], and [chlorophyll fluorescence] were unaffected. At the molecular level, [MeHg] significantly [dysregulated] the [expression of genes] involved in [motility], [energy metabolism], [lipid metabolism], [metal transport], and [antioxidant] [enzymes]. Data suggest that the [cells] were [able to cope] with subnanomolar [MeHg] exposure, but this tolerance resulted in a significant cost to the [cell energy and reserve metabolism] as well as ample changes in the [nutrition] and [motility] of [C. reinhardtii]. The present results allowed gaining new insights on the effects and [uptake mechanisms] of [MeHg] at subnanomolar concentrations in [aquatic primary producers].
|
[Transcriptomic]{Physiology} is Expression, Gene
[Physiological Responses]{Physiology} is Physiological aspects
[Green Microalga]{Living Beings} is Microalgae
[Chlamydomonas reinhardtii]{Living Beings} is Reinhardtii, Chlamydomonas
[Methylmercury]{Chemicals & Drugs} is METHYLMERCURY CPDS
[Transcriptomic]{Physiology} is Expression, Gene
[Physiological Responses]{Physiology} is Physiological aspects
[Green Microalga]{Living Beings} is Microalgae
[methyl-mercury]{Chemicals & Drugs} is METHYLMERCURY CPDS
[Chlamydomonas reinhardtii]{Living Beings} is Reinhardtii, Chlamydomonas
[MeHg]{Chemicals & Drugs} is METHYLMERCURY CPDS
[environments]{Concepts & Ideas} is Environments
[Methylmercury]{Chemicals & Drugs} is METHYLMERCURY CPDS
[microalga]{Living Beings} is Microalgae
[Chlamydomonas reinhardtii]{Living Beings} is Reinhardtii, Chlamydomonas
[physiological end points]{Physiology} is Physiological aspects
[gene expression analysis]{Procedures} is Gene Expression Analysis
[MeHg]{Chemicals & Drugs} is METHYLMERCURY CPDS
[bioaccumulated]{Physiology} is Bioaccumulation
[oxidative stress]{Disorders} is Oxidative stress
[chlorophyll fluorescence]{Physiology} is Chlorophyll fluorescence
[MeHg]{Chemicals & Drugs} is METHYLMERCURY CPDS
[dysregulated]{Physiology} is Gene Regulation
[expression of genes]{Physiology} is Expression, Gene
[motility]{Physiology} is Motility (observable entity)
[energy metabolism]{Physiology} is Energy Metabolism
[lipid metabolism]{Physiology} is Lipid metabolism
[metal transport]{Physiology} is Metal ion transport
[antioxidant]{Chemicals & Drugs} is Antioxidant
[enzymes]{Chemicals & Drugs} is Enzymes
[cells]{Anatomy} is Cells set
[able to cope]{Disorders} is Able to cope
[MeHg]{Chemicals & Drugs} is METHYLMERCURY CPDS
[cell energy and reserve metabolism]{Physiology} is Energy reserve metabolism
[nutrition]{Physiology} is Nutrition
[motility]{Physiology} is Motility (observable entity)
[C. reinhardtii]{Living Beings} is Reinhardtii, Chlamydomonas
[uptake mechanisms]{Physiology} is Uptake
[MeHg]{Chemicals & Drugs} is METHYLMERCURY CPDS
[aquatic primary producers]{Living Beings} is Microalgae
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Hierarchical Targeting [Strategy] for Enhanced [Tumor Tissue] Accumulation / Retention and [Cellular Internalization]
Targeted delivery of [therapeutic agents] is an important way to improve the therapeutic index and reduce [side effects]. To design nanoparticles for targeted delivery, both enhanced [tumor tissue] accumulation / retention and enhanced [cellular internalization] should be considered simultaneously. So far, there have been very few nanoparticles with immutable [structures] that can achieve this goal efficiently. Hierarchical targeting, a novel targeting [strategy] based on stimuli responsiveness, shows good potential to enhance both [tumor tissue] accumulation / retention and [cellular internalization]. Here, the recent design and development of hierarchical targeting nanoplatforms, based on changeable particle sizes, switchable surface charges and activatable [surface] [ligands], will be introduced. In general, the targeting moieties in these nanoplatforms are not activated during [blood circulation] for efficient [tumor tissue] accumulation, but re-activated by certain [internal] or [external] stimuli in the tumor microenvironment for enhanced [cellular internalization].
|
[Strategy]{Procedures} is STYPE
[Tumor Tissue]{Anatomy} is Tumor tissue
[Cellular Internalization]{Physiology} is Plasma membrane invagination
[therapeutic agents]{Chemicals & Drugs} is Therapeutic agent
[Strategy]{Procedures} is STYPE
[Tumor Tissue]{Anatomy} is Tumor tissue
[Cellular Internalization]{Physiology} is Plasma membrane invagination
[side effects]{Disorders} is Drug Side Effects
[tumor tissue]{Anatomy} is Tumor tissue
[cellular internalization]{Physiology} is Plasma membrane invagination
[structures]{Concepts & Ideas} is Structure
[strategy]{Procedures} is STYPE
[tumor tissue]{Anatomy} is Tumor tissue
[cellular internalization]{Physiology} is Plasma membrane invagination
[surface]{Concepts & Ideas} is Surface
[ligands]{Chemicals & Drugs} is Ligands
[blood circulation]{Physiology} is Blood Circulation
[tumor tissue]{Anatomy} is Tumor tissue
[internal]{Concepts & Ideas} is Internal
[external]{Concepts & Ideas} is External
[cellular internalization]{Physiology} is Plasma membrane invagination
|
[Subsolid pulmonary nodule] morphology and associated patient characteristics in a routine clinical [population]
To determine the presence and morphology of [subsolid pulmonary nodules] ([SSNs]) in a non-screening setting and relate them to clinical and patient characteristics. A total of 16,890 [reports] of clinically obtained [chest CT] (06/2011 to 11/2014, single-centre) were searched describing an [SSN]. [Subjects] with a visually confirmed [SSN] and at least two [thin-slice CTs] were included. [Nodule] volumes were measured. Progression was defined as volume increase exceeding the [software interscan] variation. [Nodule] morphology, [location], and patient characteristics were [evaluated]. Fifteen transient and 74 persistent [SSNs] were included (median [follow-up] 19.6 (8.3-36.8) months). [Subjects] with an [SSN] were slightly older than those without (62 vs. 58 years; p = 0.01), but no gender predilection was found. [SSNs] were mostly [located] in the [upper lobes]. [Women] showed significantly more often persistent [lesions] than [men] (94 % vs. 69 %; p = 0.002). [Part-solid lesions] were larger (1638 vs. 383 mm(3); p < 0.001) and more often progressive (68 % vs. 38 %; p = 0.02), compared to pure [ground-glass nodules]. Progressive [SSNs] were rare under the age of 50 years. Logistic regression analysis did not identify additional [nodule] [parameters] of future progression, apart from part-solid nature. This [study] confirms previously reported characteristics of [SSNs] and associated factors in a [European], routine clinical [population]. • [SSNs] in [women] are significantly more often persistent compared to [men]. • [SSN] persistence is not associated with age or prior [malignancy]. • The majority of (persistent) [SSNs] are located in the [upper lung lobes]. • A part-solid nature is associated with future [nodule] [growth]. • Progressive [solitary SSNs] are rare under the age of 50 years.
|
[Subsolid pulmonary nodule]{Disorders} is Pulmonary Nodule
[population]{Living Beings} is Population
[Subsolid pulmonary nodule]{Disorders} is Pulmonary Nodule
[subsolid pulmonary nodules]{Disorders} is Pulmonary Nodule
[SSNs]{Disorders} is Pulmonary Nodule
[population]{Living Beings} is Population
[reports]{Concepts & Ideas} is Reported
[chest CT]{Procedures} is Chest CT
[SSN]{Disorders} is Pulmonary Nodule
[Subjects]{Living Beings} is Research Subjects
[SSN]{Disorders} is Pulmonary Nodule
[thin-slice CTs]{Procedures} is CTT
[Nodule]{Disorders} is Nodule
[software interscan]{Procedures} is Scans
[Nodule]{Disorders} is Nodule
[location]{Anatomy} is Location
[evaluated]{Procedures} is Evaluated
[SSNs]{Disorders} is Pulmonary Nodule
[follow-up]{Procedures} is Follow-up
[Subjects]{Living Beings} is Research Subjects
[SSN]{Disorders} is Pulmonary Nodule
[SSNs]{Disorders} is Pulmonary Nodule
[located]{Concepts & Ideas} is Location
[upper lobes]{Anatomy} is Upper Lobe
[Women]{Living Beings} is Women
[lesions]{Disorders} is Lesion
[men]{Living Beings} is Men
[Part-solid lesions]{Disorders} is Part Solid Nodule
[ground-glass nodules]{Disorders} is Part Solid Nodule
[SSNs]{Disorders} is Pulmonary Nodule
[nodule]{Disorders} is Nodule
[parameters]{Disorders} is Parameters
[study]{Procedures} is Study
[SSNs]{Disorders} is Pulmonary Nodule
[European]{Living Beings} is Ethnic european
[population]{Living Beings} is Population
[SSNs]{Disorders} is Pulmonary Nodule
[women]{Living Beings} is Women
[men]{Living Beings} is Men
[SSN]{Disorders} is Pulmonary Nodule
[malignancy]{Disorders} is Malignancies
[SSNs]{Disorders} is Pulmonary Nodule
[upper lung lobes]{Anatomy} is Upper Lobe
[nodule]{Disorders} is Nodule
[growth]{Physiology} is Tissue Growth
[solitary SSNs]{Disorders} is Solitary pulmonary nodule
|
[Dynamic CT myocardial perfusion imaging] identifies early perfusion [abnormalities] in [diabetes] and [hypertension]: Insights from a [multicenter] [registry]
To identify patients with [early signs] of myocardial perfusion reduction, a reference base for perfusion measures is needed. To analyze perfusion [parameters] derived from [dynamic computed tomography perfusion imaging] ([CTPI]) in patients with suspected [coronary artery disease] ([CAD]), and relationship with [risk factors]. In this [multicenter study], [coronary CT angiography] ([cCTA]) and [dynamic CTPI] were performed by [second-generation dual-source CT] in patients suspected of [CAD]. [Risk factors] were collected from [hospital records]. Patients with visual perfusion defects on [CTPI], previous [coronary intervention], or missing [risk factor] details were excluded. This [analysis] included 98 patients (mean age ± standard deviation (SD), 59.0 ± 8.6yrs; 73 [male]). Global measures of [left ventricular] [myocardial blood flow] ([MBF]), [myocardial blood volume] ([MBV]) and volume transfer constant (K(trans)) were calculated. Mean [MBF] was 139.3 ± 31.4 mL/100 mL/min, [MBV] 19.1 ± 2.7 mL/100 mL, and Ktrans 85.0 ± 17.5 mL/100 mL/min. No significant differences in perfusion [parameters] were found by gender or age category. [Hypertension] and [diabetes mellitus] resulted in lower perfusion [parameters] ([hypertension] vs normotension: [MBV] 18.5 ± 3.0 vs 19.7 ± 2.3 mL/100 mL and K(trans) 82.0 ± 18.0 vs 89.0 ± 16.0, p < 0.05; [diabetes] vs [no diabetes]: [MBF] 128.5 ± 31.5 vs 144.0 ± 30.5 mL/100 mL/min and [MBV] 17.9 ± 2.4 vs 19.4 ± 2.8 mL/100 mL, p < 0.05). In patients with [hyperlipidemia], [MBF] was higher (146.8 ± 34.4 vs 130.7 ± 24.3 mL/100 mL/min, p < 0.05). Smoking and [family history] did not show perfusion [parameter] differences. [Dynamic CTPI] identifies early perfusion disturbances in conditions like [diabetes] and [hypertension]. With further [standardization], absolute perfusion measures may improve [CAD] risk [stratification] in patients without visual perfusion defects.
|
[Dynamic CT myocardial perfusion imaging]{Procedures} is Computed Tomography Perfusion Imaging
[abnormalities]{Disorders} is Abnormality
[diabetes]{Disorders} is Diabetes
[hypertension]{Disorders} is HT - Hypertension
[multicenter]{Procedures} is Multicenter trial
[registry]{Concepts & Ideas} is Registry
[Dynamic CT myocardial perfusion imaging]{Procedures} is Computed Tomography Perfusion Imaging
[early signs]{Disorders} is SIGNS SYMPTOMS
[abnormalities]{Disorders} is Abnormality
[diabetes]{Disorders} is Diabetes
[hypertension]{Disorders} is HT - Hypertension
[multicenter]{Procedures} is Multicenter trial
[registry]{Concepts & Ideas} is Registry
[parameters]{Disorders} is Parameters
[dynamic computed tomography perfusion imaging]{Procedures} is Computed Tomography Perfusion Imaging
[CTPI]{Procedures} is Computed Tomography Perfusion Imaging
[coronary artery disease]{Disorders} is Coronary Artery Disease
[CAD]{Disorders} is Coronary Artery Disease
[risk factors]{Disorders} is Risk Factors
[multicenter study]{Procedures} is Multicenter trial
[coronary CT angiography]{Procedures} is CT angiography of coronary arteries
[cCTA]{Procedures} is CT angiography of coronary arteries
[dynamic CTPI]{Procedures} is Computed Tomography Perfusion Imaging
[second-generation dual-source CT]{Procedures} is CT XRAY
[CAD]{Disorders} is Coronary Artery Disease
[Risk factors]{Disorders} is Risk Factors
[hospital records]{Concepts & Ideas} is Hospital Records
[CTPI]{Procedures} is Computed Tomography Perfusion Imaging
[coronary intervention]{Procedures} is Interventional
[risk factor]{Disorders} is Risk Factors
[analysis]{Procedures} is Analyzed
[male]{Living Beings} is Human, Male
[left ventricular]{Anatomy} is Left ventricular structure
[myocardial blood flow]{Physiology} is Myocardial Blood Flow
[MBF]{Physiology} is Myocardial Blood Flow
[myocardial blood volume]{Physiology} is Blood Volume
[MBV]{Physiology} is Blood Volume
[MBF]{Physiology} is Myocardial Blood Flow
[MBV]{Physiology} is Blood Volume
[parameters]{Disorders} is Parameters
[Hypertension]{Disorders} is HT - Hypertension
[diabetes mellitus]{Disorders} is Diabetes Mellitus
[parameters]{Disorders} is Parameters
[hypertension]{Disorders} is HT - Hypertension
[MBV]{Physiology} is Blood Volume
[diabetes]{Disorders} is Diabetes
[no diabetes]{Disorders} is Finding (finding)
[MBF]{Physiology} is Myocardial Blood Flow
[MBV]{Physiology} is Blood Volume
[hyperlipidemia]{Disorders} is Hyperlipidemia
[MBF]{Physiology} is Myocardial Blood Flow
[family history]{Disorders} is Family history
[parameter]{Disorders} is Parameters
[Dynamic CTPI]{Procedures} is Computed Tomography Perfusion Imaging
[diabetes]{Disorders} is Diabetes
[hypertension]{Disorders} is HT - Hypertension
[standardization]{Procedures} is Standardization
[CAD]{Disorders} is Coronary Artery Disease
[stratification]{Procedures} is Stratification
|
[Cognition] Enhancing Activity of [Sulforaphane] Against [Scopolamine] Induced [Cognitive Impairment] in [Zebra Fish] ([Danio rerio])
Several [epidemiological studies] have shown that consumption of large quantities of [vegetables] especially [cruciferous vegetables] ([Broccoli] and [Brussels sprouts]) can protect against [chronic diseases]. [Sulforaphane], an [isothiocynate] [found] in [cruciferous vegetables] has been demonstrated to have neuroprotective effects in several experimental paradigms. This [study] was undertaken to examine the effect of [sulforaphane] on [cognitive impairment] in [zebra fish] [model] using a novel [method] of [fear conditioning]. Initially, the normal behaviour of [zebra fishes] was [studied] in light-dark tank for 10 min daily for 10 days. [Fishes] were then divided into seven groups of twelve in each. Group I served as normal, group II served as [fear conditioned control], group III and group IV were [sulforaphane] (25 µM/L) and [piracetam] (200 mg/L) treated respectively. Group V served as [scopolamine] (400 µM/L) induced [memory impairment] [fishes]. Group VI and VII were [sulforaphane] (25 µM/L) and [piracetam] (200 mg/L) treated [scopolamine] induced [memory impairment] groups respectively. In normal [behavioural analysis], [fishes] preferred to stay in dark [compartment]. The average number of entries into the dark and time spent in dark were significantly more. [Fishes] in group II to VII were individually subjected to [fear conditioning] passive avoidance task and [evaluated] for [learned task memory]. It was observed that the average number of entries into dark and time spent in dark were significantly decreased. After exposure to respective treatment [fishes] in group III to VII were subjected to [cognitive] [evaluation]. There was [no significant] difference in [cognition] of group III and IV [fishes] exposed to [sulforaphane] and [piracetam] alone respectively. [Fishes] exposed to [scopolamine] showed a significant [cognitive impairment]. [Sulforaphane] exposure prior to [scopolamine] significantly retained the [memory] of [learned] task. These [findings] suggest that [sulforaphane] might be a promising [therapeutic agent] for [cognitive] enhancement in [Alzheimer's disease].
|
[Cognition]{Physiology} is Cognition
[Sulforaphane]{Chemicals & Drugs} is Sulforaphane
[Scopolamine]{Chemicals & Drugs} is Scopolamine
[Cognitive Impairment]{Disorders} is Cognitive impairment
[Zebra Fish]{Living Beings} is Zebra Fish
[Danio rerio]{Living Beings} is Zebra Fish
[Cognition]{Physiology} is Cognition
[epidemiological studies]{Procedures} is Epidemiological Studies
[Sulforaphane]{Chemicals & Drugs} is Sulforaphane
[Scopolamine]{Chemicals & Drugs} is Scopolamine
[Cognitive Impairment]{Disorders} is Cognitive impairment
[vegetables]{Objects} is Vegetables
[Zebra Fish]{Living Beings} is Zebra Fish
[cruciferous vegetables]{Objects} is Cruciferous vegetable
[Danio rerio]{Living Beings} is Zebra Fish
[Broccoli]{Objects} is Broccoli
[Brussels sprouts]{Objects} is Brussels sprouts
[chronic diseases]{Disorders} is Chronic Diseases
[Sulforaphane]{Chemicals & Drugs} is Sulforaphane
[isothiocynate]{Chemicals & Drugs} is Organic Chemical
[found]{Disorders} is Found
[cruciferous vegetables]{Objects} is Cruciferous vegetable
[study]{Procedures} is Study
[sulforaphane]{Chemicals & Drugs} is Sulforaphane
[cognitive impairment]{Disorders} is Cognitive impairment
[zebra fish]{Living Beings} is Zebra Fish
[model]{Disorders} is Animal model
[method]{Concepts & Ideas} is Methods
[fear conditioning]{Physiology} is Conditional learning
[zebra fishes]{Living Beings} is Zebra Fish
[studied]{Procedures} is Study
[Fishes]{Living Beings} is Zebra Fish
[fear conditioned control]{Physiology} is Conditional learning
[sulforaphane]{Chemicals & Drugs} is Sulforaphane
[piracetam]{Chemicals & Drugs} is Piracetam
[scopolamine]{Chemicals & Drugs} is Scopolamine
[memory impairment]{Disorders} is Memory Impairment
[fishes]{Living Beings} is Zebra Fish
[sulforaphane]{Chemicals & Drugs} is Sulforaphane
[piracetam]{Chemicals & Drugs} is Piracetam
[scopolamine]{Chemicals & Drugs} is Scopolamine
[memory impairment]{Disorders} is Memory Impairment
[behavioural analysis]{Procedures} is Behavioural analysis
[fishes]{Living Beings} is Zebra Fish
[compartment]{Concepts & Ideas} is Part
[Fishes]{Living Beings} is Zebra Fish
[fear conditioning]{Physiology} is Conditional learning
[evaluated]{Procedures} is Evaluated
[learned task memory]{Physiology} is Memory
[fishes]{Living Beings} is Zebra Fish
[cognitive]{Physiology} is Cognition
[evaluation]{Procedures} is Evaluated
[no significant]{Disorders} is Not significant
[cognition]{Physiology} is Cognition
[fishes]{Living Beings} is Zebra Fish
[sulforaphane]{Chemicals & Drugs} is Sulforaphane
[piracetam]{Chemicals & Drugs} is Piracetam
[Fishes]{Living Beings} is Zebra Fish
[scopolamine]{Chemicals & Drugs} is Scopolamine
[cognitive impairment]{Disorders} is Cognitive impairment
[Sulforaphane]{Chemicals & Drugs} is Sulforaphane
[scopolamine]{Chemicals & Drugs} is Scopolamine
[memory]{Physiology} is Memory
[learned]{Physiology} is Learning
[findings]{Disorders} is Finding (finding)
[sulforaphane]{Chemicals & Drugs} is Sulforaphane
[therapeutic agent]{Chemicals & Drugs} is Therapeutic agent
[cognitive]{Physiology} is Cognition
[Alzheimer's disease]{Disorders} is Alzheimer's disease
|
Value of [MDM2], [CDK4] and [SATB2] [immunohistochemistry] in [histologic] [diagnosis] of [low-grade] [osteosarcoma]
To investigate the value of combined application of [MDM2], [CDK4] and [SATB2] [immunohistochemistry] in pathological [diagnosis] of [low-grade] [osteosarcoma]. Forty-seven cases of [low grade] [osteosarcoma], including [low grade central osteosarcoma] (n=20) and [parosteal osteosarcoma] (n=27), were selected from [Shanghai Jiaotong University] Affiliated the [Sixth People's Hospital]. The clinical, [radiography] and [histopathology] were reviewed. The sensitivity and specificity of [MDM2], [CDK4] and [SATB2] [immunohistochemistry] in the [diagnosis] of [low-grade] [osteosarcoma] were [assessed] along with an [evaluation] of their [expressions] in [fibrous dysplasia], [desmoplastic fibroma], [low-grade] [fibrosarcoma] and other [fibrous tumors]. [Low-grade] [osteosarcoma] had [protracted clinical course], occurring mostly in elder adults and mainly involving long [bones]. Radiographic studies showed that [low-grade central osteosarcoma] had a mainly malignant lytic presentation, however about 5/18 of t [umors overlapping] with intermediate and benign [bone diseases], while [parosteal osteosarcoma] was characterized by a densely sclerotic malignant appearance. [Histologically], [low-grade] [osteosarcoma] s were characterized by well-differentiated spindle [tumor cells], various [mature] [tumor bones] and an aggressive [growth pattern]. The [positive expression] rates of [MDM2] and [CDK4] in [low-grade] [osteosarcoma] were 74.5% and 55.3%, respectively. Eighty-three percent of [low-grade] [osteosarcoma] expressed one or both markers. [Low-grade] [osteosarcoma] and [fibrous dysplasia] were both [positive] for [SATB2], while [desmoplastic fibroma], [low-grade] [fibrosacoma] and other [fibrous tumors] were [negative] for [SATB2]. Accurate [diagnosis] of [low-grade] [osteosarcoma] should be based on combination of clinical presentation, [imaging] and [histopathology], with [immunohistochemistry] as a diagnostic adjunct. [Positive immunostaining] for [CDK4] and/or [MDM2] supports the [diagnosis] of [low-grade] [osteosarcoma], but the negative one does not rule out such [lesion]. The negative [expression] of [SATB2] is helpful to exclude [fibrous tumors] originating from [bone] with the exception of [fibrous dysplasia].
|
[MDM2]{Chemicals & Drugs} is Mdm2 Protein
[CDK4]{Chemicals & Drugs} is Cdk4 Protein
[SATB2]{Chemicals & Drugs} is SATB2 protein, human
[immunohistochemistry]{Procedures} is Immunohistochemistry
[histologic]{Physiology} is Histologic Type
[diagnosis]{Disorders} is Diagnosis
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[MDM2]{Chemicals & Drugs} is Mdm2 Protein
[CDK4]{Chemicals & Drugs} is Cdk4 Protein
[SATB2]{Chemicals & Drugs} is SATB2 protein, human
[immunohistochemistry]{Procedures} is Immunohistochemistry
[MDM2]{Chemicals & Drugs} is Mdm2 Protein
[histologic]{Physiology} is Histologic Type
[CDK4]{Chemicals & Drugs} is Cdk4 Protein
[diagnosis]{Disorders} is Diagnosis
[SATB2]{Chemicals & Drugs} is SATB2 protein, human
[immunohistochemistry]{Procedures} is Immunohistochemistry
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[diagnosis]{Disorders} is Diagnosis
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[low grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[low grade central osteosarcoma]{Disorders} is Low grade central osteosarcoma
[parosteal osteosarcoma]{Disorders} is Parosteal osteosarcoma
[Shanghai Jiaotong University]{Organizations} is University
[Sixth People's Hospital]{Organizations} is Hospital
[radiography]{Procedures} is Diagnostic radiography
[histopathology]{Phenomena} is Histopathology finding
[MDM2]{Chemicals & Drugs} is Mdm2 Protein
[CDK4]{Chemicals & Drugs} is Cdk4 Protein
[SATB2]{Chemicals & Drugs} is SATB2 protein, human
[immunohistochemistry]{Procedures} is Immunohistochemistry
[diagnosis]{Disorders} is Diagnosis
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[assessed]{Procedures} is Assessment - action
[evaluation]{Procedures} is Assessment - action
[expressions]{Physiology} is Protein expression
[fibrous dysplasia]{Disorders} is Fibrous Dysplasia
[desmoplastic fibroma]{Disorders} is Desmoplastic Fibroma
[low-grade]{Disorders} is Low grade (lymphoma grade)
[fibrosarcoma]{Disorders} is Fibrosarcoma
[fibrous tumors]{Disorders} is Fibrous Tumor
[Low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[protracted clinical course]{Disorders} is Protracted course
[bones]{Anatomy} is Bones set
[low-grade central osteosarcoma]{Disorders} is Low grade central osteosarcoma
[umors overlapping]{Concepts & Ideas} is Overlapping tumor
[bone diseases]{Disorders} is Bone Diseases
[parosteal osteosarcoma]{Disorders} is Parosteal osteosarcoma
[Histologically]{Physiology} is Histologic Type
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[tumor cells]{Anatomy} is Tumor Cell
[mature]{Anatomy} is Mature Bone
[tumor bones]{Disorders} is Bone Tumor
[growth pattern]{Disorders} is Growth pattern
[positive expression]{Physiology} is Protein expression
[MDM2]{Chemicals & Drugs} is Mdm2 Protein
[CDK4]{Chemicals & Drugs} is Cdk4 Protein
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[Low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[fibrous dysplasia]{Disorders} is Fibrous Dysplasia
[positive]{Disorders} is POSITIVE
[SATB2]{Chemicals & Drugs} is SATB2 protein, human
[desmoplastic fibroma]{Disorders} is Desmoplastic Fibroma
[low-grade]{Disorders} is Low grade (lymphoma grade)
[fibrosacoma]{Disorders} is Fibrosarcoma
[fibrous tumors]{Disorders} is Fibrous Tumor
[negative]{Disorders} is NEGATIVE
[SATB2]{Chemicals & Drugs} is SATB2 protein, human
[diagnosis]{Disorders} is Diagnosis
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[imaging]{Procedures} is IMAGING DIAG
[histopathology]{Phenomena} is Histopathology finding
[immunohistochemistry]{Procedures} is Immunohistochemistry
[Positive immunostaining]{Procedures} is Staining
[CDK4]{Chemicals & Drugs} is Cdk4 Protein
[MDM2]{Chemicals & Drugs} is Mdm2 Protein
[diagnosis]{Disorders} is Diagnosis
[low-grade]{Disorders} is Low grade (lymphoma grade)
[osteosarcoma]{Disorders} is Osteosarcoma
[lesion]{Disorders} is Lesion
[expression]{Physiology} is Protein expression
[SATB2]{Chemicals & Drugs} is SATB2 protein, human
[fibrous tumors]{Disorders} is Fibrous Tumor
[bone]{Anatomy} is Bones set
[fibrous dysplasia]{Disorders} is Fibrous Dysplasia
|
Biobank and [Genomic] [Research] in [Uganda]: Are Extant Privacy and Confidentiality Regimes Adequate?
Not many [African countries] have been able to develop a robust system for regulating [health research] within their respective [jurisdictions], particularly in the realm of biobanking and [genomics]. This is not without reason. Aside from underdevelopment and all that it entails or perhaps in consequence thereof, [countries] in the [region] have been unable to make significant strides in [medical research]. But there are exceptions. Amongst the few seeming success stories is [Uganda]. Nonetheless, although the country has developed what appears to be a functional framework to govern [genomic] [research] and biobanking, the consistency of key provisions with international [standards], especially those pertaining to privacy of [research] [participants] and confidentiality of their health information, is not at all clear. Yet, making this determination - the main [objective] of this [article] - is critical in determining the adequacy of protection available to [human] [research subjects] in the [country].
|
[Genomic]{Occupations} is Genomics
[Research]{Procedures} is Research
[Uganda]{Geographic Areas} is Uganda
[African countries]{Geographic Areas} is Africa
[Genomic]{Occupations} is Genomics
[Research]{Procedures} is Research
[Uganda]{Geographic Areas} is Uganda
[health research]{Procedures} is RESEARCH HEALTH SERV
[jurisdictions]{Concepts & Ideas} is Jurisdiction
[genomics]{Occupations} is Genomics
[countries]{Geographic Areas} is Countries
[region]{Geographic Areas} is Region
[medical research]{Procedures} is Medical Research
[Uganda]{Geographic Areas} is Uganda
[genomic]{Occupations} is Genomics
[research]{Procedures} is Research
[standards]{Concepts & Ideas} is Standards
[research]{Procedures} is Research
[participants]{Living Beings} is Participant
[objective]{Concepts & Ideas} is Objective
[article]{Concepts & Ideas} is Article
[human]{Living Beings} is Human
[research subjects]{Living Beings} is Research Subjects
[country]{Geographic Areas} is Countries
|
Impact of a Casino [Opening] on Gambling Behaviors of [People] Engaged in [Methadone] Maintenance
This study examined gambling behavior in the context of a newly [opening] casino, comparing disordered gamblers to non-disordered gamblers, in a [population] of [individuals] involved in methadone maintenance treatment. Disordered gamblers (N = 50) and non-disordered gamblers (N = 50) were surveyed before and after the [opening] of a new casino on gambling behaviors, [substance use], and [psychological symptoms]. [No statistically significant changes] in gambling behaviors were observed for disordered gamblers or non-disordered gamblers across time points; however, non-disordered gamblers demonstrated [non-significant increases] in [horse] and [dog] race betting, electronic games, and casino [table games]. As expected, disordered gamblers were found to spend significantly more money on electronic games and casino [table games] (p < 0.05) and demonstrated higher rates of [drug use] and impulsivity than non-disordered gamblers. The introduction of a new casino did not appear to have a major impact on gambling behaviors of [individuals] attending methadone maintenance treatment, though the [non-significant increases] in gambling among non-disordered gamblers may indicate that this [population] is preferentially impacted by the [opening] of a new casino. Future investigation into the longer term effects of [opening] a new casino on this [population] may be warranted.
|
[Opening]{Concepts & Ideas} is Open
[People]{Living Beings} is People
[Methadone]{Chemicals & Drugs} is Methadone
[Opening]{Concepts & Ideas} is Open
[People]{Living Beings} is People
[opening]{Concepts & Ideas} is Open
[Methadone]{Chemicals & Drugs} is Methadone
[population]{Living Beings} is Population
[individuals]{Living Beings} is People
[opening]{Concepts & Ideas} is Open
[substance use]{Disorders} is Substance Use Status
[psychological symptoms]{Disorders} is Psychological symptom
[No statistically significant changes]{Disorders} is Investigation Finding
[non-significant increases]{Disorders} is Investigation Finding
[horse]{Living Beings} is HORSE
[dog]{Living Beings} is DOG
[table games]{Concepts & Ideas} is Playing Cards or Table Games
[table games]{Concepts & Ideas} is Playing Cards or Table Games
[drug use]{Disorders} is Drug usage
[individuals]{Living Beings} is People
[non-significant increases]{Disorders} is Investigation Finding
[population]{Living Beings} is Population
[opening]{Concepts & Ideas} is Open
[opening]{Concepts & Ideas} is Open
[population]{Living Beings} is Population
|
Association between [Leukoaraiosis] and [Poor Outcome] is not due to [Reperfusion] [Inefficiency] after [Intravenous Thrombolysis]
[Leukoaraiosis] ([LA]) is associated with [structural] and [functional cerebrovascular impairment], which may compromise the capacity of ischemic [tissue] to maximize [reperfusion] after [intravenous thrombolysis] ([IVT]). We aimed to determine whether severe [LA] is correlated with [reperfusion] [inefficiency], which contributes to infarct growth and [poor functional outcome]. We analyzed data from our consecutive [acute ischemic stroke] ([AIS]) patients who had acquired baseline and 24-h [follow-up] [diffusion-] and [perfusion-weighted imaging]. [Reperfusion] was defined as [reduction] of ≥70 % of [hypoperfusion] [lesion] at 24 h from baseline. Severe [LA] was defined as Fazekas score 2 or 3 on [FLAIR images]. We investigated the relationship between severity of [LA] and [reperfusion] status. Multivariate statistical analysis was carried out for [modeling] the independent predictors of [reperfusion], infarct growth, and functional outcome. Finally, 79 patients were included, among them 30 (37.97 %) had severe [LA]. [Reperfusion] was observed in 41 (51.89 %) patients, the proportion of [reperfusion] was very similar in patients with and without severe [LA] (53.33 vs 51.02 %, p = 1.000). Large [artery occlusion] was the only independent unfavorable predictor for [reperfusion] (OR = 0.202, 95 % confidence interval, 0.060-0.673; p = 0.014). [Multiple linear regression analysis] revealed that severe [LA] was independently associated with infarct growth (standardized coefficients = 0.191, p = 0.040). Severe [LA] was also an independent predictor of [poor outcome] (mRS ≥ 3) (OR = 4.004, 95 % confidence interval, 1.267-12.656, p = 0.018) after adjusting for [reperfusion] and baseline severity of [stroke]. Severe [LA] was associated with infarct growth and [poor outcome] independent of [reperfusion] status, which may expand the notion that [LA] contributes the intrinsic vulnerability of [brain tissue] to [acute ischemic insults]. The burden of [LA] may not serve as an imaging indicator of [reperfusion] [inefficiency] after [IVT] for [AIS] patients.
|
[Leukoaraiosis]{Disorders} is Leukoaraiosis
[Poor Outcome]{Disorders} is Poor outcome
[Reperfusion]{Phenomena} is Physiological reperfusion
[Inefficiency]{Disorders} is Inefficiency
[Intravenous Thrombolysis]{Procedures} is THER THROMBOLYSIS
[Leukoaraiosis]{Disorders} is Leukoaraiosis
[LA]{Disorders} is Leukoaraiosis
[Leukoaraiosis]{Disorders} is Leukoaraiosis
[structural]{Disorders} is Cerebral damage
[Poor Outcome]{Disorders} is Poor outcome
[functional cerebrovascular impairment]{Disorders} is Cerebral damage
[Reperfusion]{Phenomena} is Physiological reperfusion
[Inefficiency]{Disorders} is Inefficiency
[Intravenous Thrombolysis]{Procedures} is THER THROMBOLYSIS
[tissue]{Anatomy} is Tissue
[reperfusion]{Phenomena} is Physiological reperfusion
[intravenous thrombolysis]{Procedures} is THER THROMBOLYSIS
[IVT]{Procedures} is THER THROMBOLYSIS
[LA]{Disorders} is Leukoaraiosis
[reperfusion]{Phenomena} is Physiological reperfusion
[inefficiency]{Disorders} is Inefficiency
[poor functional outcome]{Disorders} is Poor outcome
[acute ischemic stroke]{Disorders} is Ischemic stroke
[AIS]{Disorders} is Ischemic stroke
[follow-up]{Procedures} is Follow-up
[diffusion-]{Procedures} is Diffusion-Weighted MRI
[perfusion-weighted imaging]{Procedures} is Perfusion-Weighted MR
[Reperfusion]{Phenomena} is Physiological reperfusion
[reduction]{Procedures} is Reduction
[hypoperfusion]{Disorders} is Hypoperfusion (qualifier value)
[lesion]{Disorders} is Lesion
[LA]{Disorders} is Leukoaraiosis
[FLAIR images]{Procedures} is FLAIR image
[LA]{Disorders} is Leukoaraiosis
[reperfusion]{Phenomena} is Physiological reperfusion
[modeling]{Procedures} is Modeling
[reperfusion]{Phenomena} is Physiological reperfusion
[LA]{Disorders} is Leukoaraiosis
[Reperfusion]{Phenomena} is Physiological reperfusion
[reperfusion]{Phenomena} is Physiological reperfusion
[LA]{Disorders} is Leukoaraiosis
[artery occlusion]{Disorders} is Occlusion of artery
[reperfusion]{Phenomena} is Physiological reperfusion
[Multiple linear regression analysis]{Concepts & Ideas} is Regression Analysis
[LA]{Disorders} is Leukoaraiosis
[LA]{Disorders} is Leukoaraiosis
[poor outcome]{Disorders} is Poor outcome
[reperfusion]{Phenomena} is Physiological reperfusion
[stroke]{Disorders} is Stroke
[LA]{Disorders} is Leukoaraiosis
[poor outcome]{Disorders} is Poor outcome
[reperfusion]{Phenomena} is Physiological reperfusion
[LA]{Disorders} is Leukoaraiosis
[brain tissue]{Anatomy} is Brain tissue structure
[acute ischemic insults]{Disorders} is Ischemia
[LA]{Disorders} is Leukoaraiosis
[reperfusion]{Phenomena} is Physiological reperfusion
[inefficiency]{Disorders} is Inefficiency
[IVT]{Procedures} is THER THROMBOLYSIS
[AIS]{Disorders} is Ischemic stroke
|
[RNA topoisomerase] is prevalent in all domains of life and associates with [polyribosomes] in [animals]
[DNA Topoisomerases] are essential to resolve topological problems during [DNA metabolism] in all [species]. However, the prevalence and function of [RNA topoisomerases] remain uncertain. Here, we show that [RNA topoisomerase activity] is prevalent in [Type IA topoisomerases] from [bacteria], archaea, and [eukarya]. Moreover, this [activity] always requires the [conserved Type IA core domains] and the same catalytic residue used in [DNA topoisomerase reaction]; however, it does not absolutely require the [non-conserved carboxyl-terminal domain] ([CTD]), which is necessary for [relaxation reactions] of [supercoiled DNA]. The [RNA topoisomerase activity] of [human Top3β] differs from that of [Escherichia coli] [topoisomerase I] in that the former but not the latter requires the [CTD], indicating that [topoisomerases] have developed distinct mechanisms during evolution to catalyze [RNA topoisomerase] reactions. Notably, [Top3β proteins] from several [animals] associate with [polyribosomes], which are units of [mRNA] [translation], whereas the Top3 homologs from [E. coli] and [yeast] lack the association. The [Top3β] - [polyribosome] association requires [TDRD3], which directly interacts with [Top3β] and is present in [animals] but not [bacteria] or [yeast]. We propose that [RNA topoisomerases] arose in the early [RNA] world, and that they are retained through all domains of [DNA] -based life, where they mediate [mRNA] [translation] as part of [polyribosomes] in [animals].
|
[RNA topoisomerase]{Chemicals & Drugs} is Topoisomerase
[polyribosomes]{Anatomy} is Polyribosome (body structure)
[animals]{Living Beings} is Animals
[RNA topoisomerase]{Chemicals & Drugs} is Topoisomerase
[DNA Topoisomerases]{Chemicals & Drugs} is DNA Topoisomerases
[DNA metabolism]{Physiology} is DNA metabolism
[polyribosomes]{Anatomy} is Polyribosome (body structure)
[animals]{Living Beings} is Animals
[species]{Concepts & Ideas} is Species
[RNA topoisomerases]{Chemicals & Drugs} is Topoisomerase
[RNA topoisomerase activity]{Physiology} is Topoisomerase activity
[Type IA topoisomerases]{Chemicals & Drugs} is Topoisomerase
[bacteria]{Living Beings} is BACTERIA
[eukarya]{Living Beings} is Eukarya
[activity]{Physiology} is Molecular function
[conserved Type IA core domains]{Genes & Molecular Sequences} is CONSERVED SEQ
[DNA topoisomerase reaction]{Physiology} is DNA topoisomerase activity
[non-conserved carboxyl-terminal domain]{Genes & Molecular Sequences} is Domain
[CTD]{Genes & Molecular Sequences} is Domain
[relaxation reactions]{Physiology} is Gene function (function)
[supercoiled DNA]{Chemicals & Drugs} is Supercoiled DNA
[RNA topoisomerase activity]{Physiology} is Topoisomerase activity
[human Top3β]{Chemicals & Drugs} is TOP3B protein, human
[Escherichia coli]{Living Beings} is Escherichia coli
[topoisomerase I]{Chemicals & Drugs} is DNA Topoisomerase
[CTD]{Genes & Molecular Sequences} is Domain
[topoisomerases]{Chemicals & Drugs} is Topoisomerase
[RNA topoisomerase]{Chemicals & Drugs} is Topoisomerase
[Top3β proteins]{Chemicals & Drugs} is TOP3B protein, human
[animals]{Living Beings} is Animals
[polyribosomes]{Anatomy} is Polyribosome (body structure)
[mRNA]{Chemicals & Drugs} is MRNA
[translation]{Physiology} is Translational
[E. coli]{Living Beings} is Escherichia coli
[yeast]{Living Beings} is YEAST
[Top3β]{Chemicals & Drugs} is TOP3B protein, human
[polyribosome]{Anatomy} is Polyribosome (body structure)
[TDRD3]{Chemicals & Drugs} is Tdrd3 protein, human
[Top3β]{Chemicals & Drugs} is TOP3B protein, human
[animals]{Living Beings} is Animals
[bacteria]{Living Beings} is BACTERIA
[yeast]{Living Beings} is YEAST
[RNA topoisomerases]{Chemicals & Drugs} is Topoisomerase
[RNA]{Chemicals & Drugs} is RNA
[DNA]{Chemicals & Drugs} is DNA
[mRNA]{Chemicals & Drugs} is MRNA
[translation]{Physiology} is Translational
[polyribosomes]{Anatomy} is Polyribosome (body structure)
[animals]{Living Beings} is Animals
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[First Draft] [Genome Sequence] of [Staphylococcus condimenti F-2T]
This [report] describes the [draft] [genome sequence] of [S. condimenti strain F-2(T) (DSM 11674)], a potential [starter culture]. The [genome assembly] comprised 2,616,174 [bp] with 34.6% GC content. To the best of our knowledge, this is the first [documentation] that [reports] the [whole-genome sequence] of [S. condimenti].
|
[First Draft]{Concepts & Ideas} is Draft
[Genome Sequence]{Genes & Molecular Sequences} is Genome Assembly Sequence
[Staphylococcus condimenti F-2T]{Living Beings} is Staphylococcus condimenti
[First Draft]{Concepts & Ideas} is Draft
[report]{Concepts & Ideas} is Reported
[Genome Sequence]{Genes & Molecular Sequences} is Genome Assembly Sequence
[draft]{Concepts & Ideas} is Draft
[Staphylococcus condimenti F-2T]{Living Beings} is Staphylococcus condimenti
[genome sequence]{Genes & Molecular Sequences} is Genome Assembly Sequence
[S. condimenti strain F-2(T) (DSM 11674)]{Living Beings} is Staphylococcus condimenti
[starter culture]{Procedures} is Bacterial culture
[genome assembly]{Genes & Molecular Sequences} is Genome Assembly Sequence
[bp]{Physiology} is Base pair
[documentation]{Concepts & Ideas} is Documentation
[reports]{Concepts & Ideas} is Reported
[whole-genome sequence]{Genes & Molecular Sequences} is Genome Assembly Sequence
[S. condimenti]{Living Beings} is Staphylococcus condimenti
|
Efficacy of a coaxial system with a compliant [balloon catheter] for navigation of the [Penumbra] [reperfusion] [catheter] in [tortuous arteries]: technique and case [experience]
[OBJECTIVE] The [authors] describe a [method] by which they [easily] and atraumatically navigate a [large-bore] [reperfusion] [catheter] of the [Penumbra system] to an [embolus] by using a coaxial system with a compliant [balloon catheter] in patients with [tortuous arteries]. [METHODS] A [retrospective review] of the prospective endovascular [database] was performed to identify cases in which a coaxial system with a compliant [balloon catheter] ([Scepter C], [MicroVention] / Terumo; or [TransForm C], [Stryker] [Neurovascular]) and a [large-bore] [reperfusion] [catheter] of the [Penumbra system] ([Penumbra, Inc.]) was used. The [authors] achieved a stable [guiding] [sheath] [position] and delivered the coaxial system with a compliant [balloon catheter] and a [large-bore] [reperfusion] [catheter]. Then, the [balloon] was inflated somewhat when the [distal] tip of the [balloon] was slightly advanced from the tip of the [reperfusion] [catheter], and together the coaxial system was advanced to an [embolus] over a 0.014-in guidewire, even around the corner. When the [distal] tip of the [balloon catheter] reached the [embolus], the [authors] deflated the [balloon] and navigated the [large-bore] [reperfusion] [catheter] to the [embolus]. Finally, the [aspiration] of the [embolus] with the [Penumbra] [MAX pump] was begun. RESULTS Between May 2014 and September 2015, the [authors] used this technique in 17 cases: 16 cases of [middle cerebral artery occlusion] (including 5 cases of [internal carotid artery occlusion]) and 1 case of [basilar artery occlusion] (age range 36-88 years, mean age 74.7 years, 13 [men]). For the [reperfusion] [catheter] of the [Penumbra system], the [5MAX ACE] was used in 15 cases, and the [5MAX] was used in 2 cases. As a compliant [balloon catheter], the [Scepter C] was used in 16 cases, and the [TransForm C] was used in 1 case. The technique was successful in 16 cases (94.1%). No parent [artery dissections] were noted in any cases. [Catheter] -induced [vasospasm] was noted in 1 case, but the [vasospasm] was transient. CONCLUSIONS A coaxial system with a compliant [balloon catheter] can help safely and [easily] to navigate the [large-bore] [reperfusion] [catheter] of the [Penumbra system] to an [embolus] in patients with [tortuous arteries].
|
[balloon catheter]{Devices} is Cardiac balloon catheter
[Penumbra]{Devices} is Biomedical equipment, device (physical object)
[reperfusion]{Phenomena} is Physiological reperfusion
[catheter]{Devices} is Catheters
[tortuous arteries]{Disorders} is Tortuous cerebral arteries
[experience]{Physiology} is Experience
[OBJECTIVE]{Concepts & Ideas} is Objective
[authors]{Living Beings} is Authors
[method]{Concepts & Ideas} is Methods
[balloon catheter]{Devices} is Cardiac balloon catheter
[easily]{Disorders} is Easily
[Penumbra]{Devices} is Biomedical equipment, device (physical object)
[large-bore]{Devices} is Large-bore introducer
[reperfusion]{Phenomena} is Physiological reperfusion
[reperfusion]{Phenomena} is Physiological reperfusion
[catheter]{Devices} is Catheters
[catheter]{Devices} is Catheters
[tortuous arteries]{Disorders} is Tortuous cerebral arteries
[Penumbra system]{Devices} is Biomedical equipment, device (physical object)
[embolus]{Disorders} is Embolus
[experience]{Physiology} is Experience
[balloon catheter]{Devices} is Cardiac balloon catheter
[tortuous arteries]{Disorders} is Tortuous cerebral arteries
[METHODS]{Concepts & Ideas} is Methods
[retrospective review]{Procedures} is RETROSPECTIVE
[database]{Concepts & Ideas} is Databases
[balloon catheter]{Devices} is Cardiac balloon catheter
[Scepter C]{Devices} is Biomedical equipment, device (physical object)
[MicroVention]{Devices} is Biomedical equipment, device (physical object)
[TransForm C]{Devices} is Biomedical equipment, device (physical object)
[Stryker]{Devices} is Biomedical equipment, device (physical object)
[Neurovascular]{Anatomy} is Neurovascular Bundle
[large-bore]{Devices} is Large-bore introducer
[reperfusion]{Phenomena} is Physiological reperfusion
[catheter]{Devices} is Catheters
[Penumbra system]{Devices} is Biomedical equipment, device (physical object)
[Penumbra, Inc.]{Concepts & Ideas} is Organization Name
[authors]{Living Beings} is Authors
[guiding]{Devices} is Guiding catheter
[sheath]{Anatomy} is Schwann sheath
[position]{Concepts & Ideas} is Positioning
[balloon catheter]{Devices} is Cardiac balloon catheter
[large-bore]{Devices} is Large-bore introducer
[reperfusion]{Phenomena} is Physiological reperfusion
[catheter]{Devices} is Catheters
[balloon]{Devices} is Cardiac balloon catheter
[distal]{Concepts & Ideas} is Distal
[balloon]{Devices} is Cardiac balloon catheter
[reperfusion]{Phenomena} is Physiological reperfusion
[catheter]{Devices} is Catheters
[embolus]{Disorders} is Embolus
[distal]{Concepts & Ideas} is Distal
[balloon catheter]{Devices} is Cardiac balloon catheter
[embolus]{Disorders} is Embolus
[authors]{Living Beings} is Authors
[balloon]{Devices} is Cardiac balloon catheter
[large-bore]{Devices} is Large-bore introducer
[reperfusion]{Phenomena} is Physiological reperfusion
[catheter]{Devices} is Catheters
[embolus]{Disorders} is Embolus
[aspiration]{Procedures} is Aspiration - action
[embolus]{Disorders} is Embolus
[Penumbra]{Devices} is Biomedical equipment, device (physical object)
[MAX pump]{Devices} is Biomedical equipment, device (physical object)
[authors]{Living Beings} is Authors
[middle cerebral artery occlusion]{Disorders} is Middle Cerebral Artery Occlusion
[internal carotid artery occlusion]{Disorders} is Internal carotid artery occlusion
[basilar artery occlusion]{Disorders} is Basilar artery occlusion
[men]{Living Beings} is Men
[reperfusion]{Phenomena} is Physiological reperfusion
[catheter]{Devices} is Catheters
[Penumbra system]{Devices} is Biomedical equipment, device (physical object)
[5MAX ACE]{Devices} is Biomedical equipment, device (physical object)
[5MAX]{Devices} is Biomedical equipment, device (physical object)
[balloon catheter]{Devices} is Cardiac balloon catheter
[Scepter C]{Devices} is Biomedical equipment, device (physical object)
[TransForm C]{Devices} is Biomedical equipment, device (physical object)
[artery dissections]{Disorders} is Artery dissection
[Catheter]{Devices} is Catheters
[vasospasm]{Disorders} is Vasospasm
[vasospasm]{Disorders} is Vasospasm
[balloon catheter]{Devices} is Cardiac balloon catheter
[easily]{Disorders} is Easily
[large-bore]{Devices} is Large-bore introducer
[reperfusion]{Phenomena} is Physiological reperfusion
[catheter]{Devices} is Catheters
[Penumbra system]{Devices} is Biomedical equipment, device (physical object)
[embolus]{Disorders} is Embolus
[tortuous arteries]{Disorders} is Tortuous cerebral arteries
|
[Hepatic] and [renal] toxicological [evaluations] of an industrial [ovotoxic chemical], [4-vinylcyclohexene diepoxide], in both sexes of [Wistar rats]
[4-Vinylcyclohexene diepoxide] ([VCD]) is an industrial occupational health hazard chemical because it induces [ovotoxicity] in [rodents]. The current [study] investigated the impacts of [VCD] on selected [hepatic] and [renal] [markers] of [oxidative stress] and [inflammation] in both sexes of [Wistar rats]. Thus, male and female [rats] were randomly distributed into four groups of ten [rats] per group, and dosed orally with [VCD] for 28 days. The control male and female groups of [rats] received [corn oil] only, while each of the three remaining groups of both sexes of [rats] received [VCD] (100, 250 and 500 mg/kg BW) respectively. Thereafter, [biomarkers] of [hepatic] and [renal oxidative damage], [inflammation] and [immunohistochemical expressions] of [iNOS], [COX-2], [caspase-9] and [caspase-3] were [evaluated]. The results revealed that [VCD] increased [markers] of [liver] and [kidney functions], [oxidative damage] and [inflammation], and disrupted the [antioxidant homeostasis] of the [rats] (p<0.05). Lastly, [VCD] enhanced the [immunohistochemical expressions] of [iNOS], [COX-2], [caspase-9] and [caspase-3] in the [liver] of the [rats]. Thus, our data imply that [VCD] induced [toxicity] in the [liver] and [kidney] of [rats] via the combined impacts of [oxidative damage] and [inflammation].
|
[Hepatic]{Anatomy} is Hepatic
[renal]{Anatomy} is Renal
[evaluations]{Procedures} is Evaluations
[ovotoxic chemical]{Chemicals & Drugs} is Toxic chemical
[4-vinylcyclohexene diepoxide]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[Wistar rats]{Living Beings} is Wistar Rats
[Hepatic]{Anatomy} is Hepatic
[4-Vinylcyclohexene diepoxide]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[renal]{Anatomy} is Renal
[VCD]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[evaluations]{Procedures} is Evaluations
[ovotoxic chemical]{Chemicals & Drugs} is Toxic chemical
[4-vinylcyclohexene diepoxide]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[ovotoxicity]{Disorders} is Toxicity
[rodents]{Living Beings} is Rodents
[Wistar rats]{Living Beings} is Wistar Rats
[study]{Procedures} is Study
[VCD]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[hepatic]{Anatomy} is Hepatic
[renal]{Anatomy} is Renal
[markers]{Physiology} is BIOL MARKERS
[oxidative stress]{Disorders} is Oxidative stress
[inflammation]{Disorders} is Inflammation
[Wistar rats]{Living Beings} is Wistar Rats
[rats]{Living Beings} is Wistar Rats
[rats]{Living Beings} is Wistar Rats
[VCD]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[rats]{Living Beings} is Wistar Rats
[corn oil]{Chemicals & Drugs} is Corn oil
[rats]{Living Beings} is Wistar Rats
[VCD]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[biomarkers]{Physiology} is BIOL MARKERS
[hepatic]{Disorders} is Hepatic damage
[renal oxidative damage]{Disorders} is Kidney damage
[inflammation]{Disorders} is Inflammation
[immunohistochemical expressions]{Procedures} is Laboratory procedures -general (situation)
[iNOS]{Chemicals & Drugs} is NOS Family
[COX-2]{Chemicals & Drugs} is COX-2 Prostaglandin Synthase
[caspase-9]{Chemicals & Drugs} is Caspase-9
[caspase-3]{Chemicals & Drugs} is Caspase-3
[evaluated]{Procedures} is Evaluations
[VCD]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[markers]{Physiology} is BIOL MARKERS
[liver]{Physiology} is Liver function
[kidney functions]{Physiology} is Renal function
[oxidative damage]{Disorders} is Poisoning / injury (navigational concept)
[inflammation]{Disorders} is Inflammation
[antioxidant homeostasis]{Phenomena} is Homeostasis
[rats]{Living Beings} is Wistar Rats
[VCD]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[immunohistochemical expressions]{Procedures} is Laboratory procedures -general (situation)
[iNOS]{Chemicals & Drugs} is NOS Family
[COX-2]{Chemicals & Drugs} is COX-2 Prostaglandin Synthase
[caspase-9]{Chemicals & Drugs} is Caspase-9
[caspase-3]{Chemicals & Drugs} is Caspase-3
[liver]{Anatomy} is Livers
[rats]{Living Beings} is Wistar Rats
[VCD]{Chemicals & Drugs} is 4-vinylcyclohexene diepoxide
[toxicity]{Disorders} is Toxicity
[liver]{Anatomy} is Livers
[kidney]{Anatomy} is Renal
[rats]{Living Beings} is Wistar Rats
[oxidative damage]{Disorders} is Poisoning / injury (navigational concept)
[inflammation]{Disorders} is Inflammation
|
[Combinatorial Library] Screening Coupled to [Mass Spectrometry] to Identify Valuable [Cyclic Peptides]
[Combinatorial library] screening coupled to [mass spectrometry (MS) analysis] is a practical [approach] to identify useful [peptides]. [Cyclic peptides] can have high [biological activity], selectivity, and affinity for target [proteins], and high stability against [proteolytic degradation]. Here we describe two strategies to prepare [combinatorial libraries] suitable for [MS analysis] to accelerate the [discovery] of [cyclic peptide] [structures]. Both [approaches] use [ChemMatrix resin] and the linker [4-hydroxymethylbenzoic acid]. One strategy involves the synthesis of a [one-bead-two-peptides library] in which each bead contains both the [cyclic peptide] and its linear counterpart to facilitate [MS analysis]. The other protocol is based on the synthesis of a [cyclic depsipeptide library] in which a glycolamidic ester group is incorporated by adding [glycolic acid]. After [library] screening, the ring is opened and the [peptide] is released simultaneously for subsequent [MS analysis]. © 2016 by John Wiley & Sons, Inc.
|
[Combinatorial Library]{Chemicals & Drugs} is Synthetic Peptide Combinatorial Library
[Mass Spectrometry]{Procedures} is Mass spectrometry
[Cyclic Peptides]{Chemicals & Drugs} is Cyclic Peptides
[Combinatorial library]{Chemicals & Drugs} is Synthetic Peptide Combinatorial Library
[Mass Spectrometry]{Procedures} is Mass spectrometry
[mass spectrometry (MS) analysis]{Procedures} is Mass spectrometry
[Cyclic Peptides]{Chemicals & Drugs} is Cyclic Peptides
[approach]{Concepts & Ideas} is Approach
[peptides]{Chemicals & Drugs} is Peptide
[Cyclic peptides]{Chemicals & Drugs} is Cyclic Peptides
[biological activity]{Phenomena} is Biological Function
[proteins]{Chemicals & Drugs} is Proteins
[proteolytic degradation]{Physiology} is Proteolytic
[combinatorial libraries]{Chemicals & Drugs} is Synthetic Peptide Combinatorial Library
[MS analysis]{Procedures} is Mass spectrometry
[discovery]{Procedures} is Discovery Science
[cyclic peptide]{Chemicals & Drugs} is Cyclic Peptides
[structures]{Concepts & Ideas} is Structure
[approaches]{Concepts & Ideas} is Approach
[ChemMatrix resin]{Chemicals & Drugs} is Organic Chemical
[4-hydroxymethylbenzoic acid]{Chemicals & Drugs} is Organic Chemical
[one-bead-two-peptides library]{Chemicals & Drugs} is Peptide Library
[cyclic peptide]{Chemicals & Drugs} is Cyclic Peptides
[MS analysis]{Procedures} is Mass spectrometry
[cyclic depsipeptide library]{Chemicals & Drugs} is Peptide Library
[glycolic acid]{Chemicals & Drugs} is Glycolic Acid
[library]{Chemicals & Drugs} is Peptide Library
[peptide]{Chemicals & Drugs} is Peptide
[MS analysis]{Procedures} is Mass spectrometry
|
[Women's] Sexual Issues After [Myocardial Infarction]: A [Literature Review]
Sexual activity after [myocardial infarction] ([MI]) is a concern for patients and often a challenge for [health care professionals] to address. It is widely recognized that most patients, of both sexes, report [sexual problems] or concerns after [MI]. However, there are reported differences between [men] and [women]. [Women] with sexual concerns may seek less help from [health care providers] and are more inclined to conceal them because of cultural barriers. The aim of the [current study] is to present a comprehensive [review of the literature] describing [women's] sexual issues after [MI]. A systematic search of the relevant [literature] was performed within [international databases], including [PubMed] / [Medline], [Scopus], [ScienceDirect], and [ProQuest], as well as [Google Scholar] using relevant [keywords]. Also, Persian electronic databases such as [Magiran], [Scientific Information Databases], and [Iran Medex] were searched from the inception to October 2014. [Articles] focusing on the sexual issues after [MI] only in [women], as well as [articles] on both sexes where [women's] results could be separated, were included in this [review]. A total of 8 [articles] were included in the final [dataset]. The main themes of [women's] sexual concerns after [MI] were " loss or decrease of sexual activity ," " [dissatisfaction of sexual relationship] ," " doubt about resumption time of sexual activity ," " [fear] of [reinfarction] or [sudden death] during sexual activity after [MI] ," " [knowledge deficit] regarding sexual activity after [MI] ," and " poor performance of [health care providers] in [sexual counseling] ." The results of this [review] demonstrate that [women's] post- [MI] sexual activity is affected by many concerns. The concerns may be a [knowledge deficit] related to not receiving necessary [consultation] on this topic. [Nurses], as [first-line care givers], can provide appropriate [consultation] and education for patients post- [MI]. As a result, breaking taboo imposed by cultural barriers, personal assumptions, or [lack of confidence] on giving [sexual consultation] may ultimately help patients to improve their quality of life.
|
[Women's]{Living Beings} is Women
[Myocardial Infarction]{Disorders} is Myocardial Infarction
[Literature Review]{Concepts & Ideas} is Review Literature
[Women's]{Living Beings} is Women
[myocardial infarction]{Disorders} is Myocardial Infarction
[Myocardial Infarction]{Disorders} is Myocardial Infarction
[MI]{Disorders} is Myocardial Infarction
[Literature Review]{Concepts & Ideas} is Review Literature
[health care professionals]{Living Beings} is Health Care Professional
[sexual problems]{Disorders} is Sexual problem
[MI]{Disorders} is Myocardial Infarction
[men]{Living Beings} is Men
[women]{Living Beings} is Women
[Women]{Living Beings} is Women
[health care providers]{Living Beings} is Health Care Providers
[current study]{Procedures} is Study
[review of the literature]{Concepts & Ideas} is Review Literature
[women's]{Living Beings} is Women
[MI]{Disorders} is Myocardial Infarction
[literature]{Concepts & Ideas} is Literature
[international databases]{Concepts & Ideas} is Databases
[PubMed]{Concepts & Ideas} is PubMed
[Medline]{Concepts & Ideas} is Medline
[Scopus]{Concepts & Ideas} is Intellectual Product
[ScienceDirect]{Concepts & Ideas} is Intellectual Product
[ProQuest]{Concepts & Ideas} is Intellectual Product
[Google Scholar]{Concepts & Ideas} is Intellectual Product
[keywords]{Concepts & Ideas} is Keyword
[Magiran]{Concepts & Ideas} is Intellectual Product
[Scientific Information Databases]{Concepts & Ideas} is Intellectual Product
[Iran Medex]{Concepts & Ideas} is Intellectual Product
[Articles]{Concepts & Ideas} is Article
[MI]{Disorders} is Myocardial Infarction
[women]{Living Beings} is Women
[articles]{Concepts & Ideas} is Article
[women's]{Living Beings} is Women
[review]{Procedures} is Ongoing review
[articles]{Concepts & Ideas} is Article
[dataset]{Concepts & Ideas} is Data Set
[women's]{Living Beings} is Women
[MI]{Disorders} is Myocardial Infarction
[dissatisfaction of sexual relationship]{Disorders} is Dissatisfied with sexual relationship
[fear]{Physiology} is Fear
[reinfarction]{Disorders} is Reinfarction of myocardium
[sudden death]{Disorders} is Sudden Death
[MI]{Disorders} is Myocardial Infarction
[knowledge deficit]{Disorders} is Knowledge deficit
[MI]{Disorders} is Myocardial Infarction
[health care providers]{Living Beings} is Health Care Providers
[sexual counseling]{Procedures} is Sexual counseling
[review]{Procedures} is Ongoing review
[women's]{Living Beings} is Women
[MI]{Disorders} is Myocardial Infarction
[knowledge deficit]{Disorders} is Knowledge deficit
[consultation]{Procedures} is Consultation
[Nurses]{Living Beings} is Nurses
[first-line care givers]{Living Beings} is Care Givers
[consultation]{Procedures} is Consultation
[MI]{Disorders} is Myocardial Infarction
[lack of confidence]{Disorders} is Lacks confidence
[sexual consultation]{Procedures} is Consultation
|
Effect of autohydrolysis on the wettability, absorbility and further [alkali] impregnation of [poplar] wood chips
Autohydrolysis with different severity factors was performed on [poplar] wood chips prior to pulping, and the wettability, absorbility and the following impregnation of [NaOH] solution for the [poplar] wood chips were then investigated. The results showed that after autohydrolysis pretreatment the porosity, shrinkage and [fiber saturation point] ([FSP]) of the [poplar] wood chips were increased, while the surface contact angle decreased as the severity factor was increased. The autohydrolyzed chips absorbed more [NaOH] in impregnation that resulted in a low [NaOH] concentration in the bulk impregnation liquor (i.e., the impregnation liquor outside wood chips), while the concentration in the [entrapped] liquor (i.e., the impregnation liquor inside wood chips) was increased. Autohydrolysis substantially [improved] the effectiveness of [alkali] impregnation.
|
[alkali]{Chemicals & Drugs} is Alkali
[poplar]{Living Beings} is Poplar
[poplar]{Living Beings} is Poplar
[alkali]{Chemicals & Drugs} is Alkali
[poplar]{Living Beings} is Poplar
[NaOH]{Chemicals & Drugs} is Sodium Hydroxide (Chemical/Ingredient)
[poplar]{Living Beings} is Poplar
[fiber saturation point]{Disorders} is Investigation Finding
[FSP]{Disorders} is Investigation Finding
[poplar]{Living Beings} is Poplar
[NaOH]{Chemicals & Drugs} is Sodium Hydroxide (Chemical/Ingredient)
[NaOH]{Chemicals & Drugs} is Sodium Hydroxide (Chemical/Ingredient)
[entrapped]{Disorders} is Investigation Finding
[improved]{Disorders} is Improved
[alkali]{Chemicals & Drugs} is Alkali
|
Effect of [Transcatheter Arterial Chemoembolization] Combined with [Argon-Helium Cryosurgery System] on the Changes of [NK Cells] and [T Cell Subsets] in [Peripheral Blood] of [Hepatocellular Carcinoma] Patients
[Hepatocellular carcinoma] ([HCC]) is one of the most aggressive [tumors] in [humans]. [T lymphocytes] and natural killer (NK) [cells] are the [body's] first line of [defense] to prevent [tumor cell] [growth]. [Previous studies] have demonstrated that [transcatheter arterial chemoembolization] ([TACE]) combined with [argon-helium cryosurgery system] ([[AHCS]]) can effectively [treat] [liver cancer]. However, the mechanism of the [treatment] is unclear yet. In the current [study], we investigated the effects of [TACE] combined with [AHCS] on the changes of [T cell subsets] and [NK cells] in [peripheral blood] of [HCC]. Our data show that [alpha-fetoprotein] ([AFP]) levels in [peripheral blood] were significantly [up-regulated] in [HCC] patients before [treatment] when compared with healthy [people] and reduced after [TACE] combined with [AHCS] [treatment] (P < 0.01). In addition, we found that [CD4+ cells] and [NK cells] decreased (P < 0.05) and [CD8+ cells] increased (P < 0.05) in [HCC] patients when compared with healthy [people]. After [treatment], the [CD4+ cells], [CD4+] / [CD8+] ratio, and [NK cells] were dramatically increased in [HCC] patients (P < 0.05). In contrast, [CD8+ cells] were significantly decreased (P < 0.05). [TACE] combined with [AHCS] [treatment] significantly prolonged 1- year survival rate of [HCC] patients and did not show significant [side effects]. Taken together, our data indicate that [TACE] combined with [AHCS] [treatment] [improves] patients ' [immune system]. It is a feasible and effective [therapeutic method] for [HCC] patients.
|
[Transcatheter Arterial Chemoembolization]{Procedures} is Transcatheter arterial chemoembolization
[Argon-Helium Cryosurgery System]{Procedures} is Cryosurgery
[NK Cells]{Anatomy} is NK Cells
[T Cell Subsets]{Anatomy} is T Cell Subsets
[Peripheral Blood]{Anatomy} is Peripheral Blood
[Hepatocellular Carcinoma]{Disorders} is Carcinoma hepatocellular
[Hepatocellular carcinoma]{Disorders} is Carcinoma hepatocellular
[Transcatheter Arterial Chemoembolization]{Procedures} is Transcatheter arterial chemoembolization
[HCC]{Disorders} is Carcinoma hepatocellular
[tumors]{Disorders} is Tumors
[Argon-Helium Cryosurgery System]{Procedures} is Cryosurgery
[humans]{Living Beings} is Humans
[T lymphocytes]{Anatomy} is T Lymphocytes
[NK Cells]{Anatomy} is NK Cells
[cells]{Anatomy} is Cells set
[T Cell Subsets]{Anatomy} is T Cell Subsets
[body's]{Living Beings} is Human Body
[Peripheral Blood]{Anatomy} is Peripheral Blood
[defense]{Physiology} is Host defense
[Hepatocellular Carcinoma]{Disorders} is Carcinoma hepatocellular
[tumor cell]{Anatomy} is Tumor Cell
[growth]{Physiology} is Cell Growth
[Previous studies]{Procedures} is Study
[transcatheter arterial chemoembolization]{Procedures} is Transcatheter arterial chemoembolization
[TACE]{Procedures} is Transcatheter arterial chemoembolization
[argon-helium cryosurgery system]{Procedures} is Cryosurgery
[AHCS]{Procedures} is Cryosurgery
[treat]{Procedures} is TREAT
[liver cancer]{Disorders} is LIVER CANCER
[treatment]{Procedures} is TREAT
[study]{Procedures} is Study
[TACE]{Procedures} is Transcatheter arterial chemoembolization
[AHCS]{Procedures} is Cryosurgery
[T cell subsets]{Anatomy} is T Cell Subsets
[NK cells]{Anatomy} is NK Cells
[peripheral blood]{Anatomy} is Peripheral Blood
[HCC]{Disorders} is Carcinoma hepatocellular
[alpha-fetoprotein]{Chemicals & Drugs} is Alpha-fetoprotein
[AFP]{Chemicals & Drugs} is Alpha-fetoprotein
[peripheral blood]{Anatomy} is Peripheral Blood
[up-regulated]{Physiology} is Up-Regulation (Physiology)
[HCC]{Disorders} is Carcinoma hepatocellular
[treatment]{Procedures} is TREAT
[people]{Living Beings} is People
[TACE]{Procedures} is Transcatheter arterial chemoembolization
[AHCS]{Procedures} is Cryosurgery
[treatment]{Procedures} is TREAT
[CD4+ cells]{Anatomy} is T4 Cells
[NK cells]{Anatomy} is NK Cells
[CD8+ cells]{Anatomy} is CD8+ cell
[HCC]{Disorders} is Carcinoma hepatocellular
[people]{Living Beings} is People
[treatment]{Procedures} is TREAT
[CD4+ cells]{Anatomy} is T4 Cells
[CD4+]{Anatomy} is T4 Cells
[CD8+]{Anatomy} is CD8+ cell
[NK cells]{Anatomy} is NK Cells
[HCC]{Disorders} is Carcinoma hepatocellular
[CD8+ cells]{Anatomy} is CD8+ cell
[TACE]{Procedures} is Transcatheter arterial chemoembolization
[AHCS]{Procedures} is Cryosurgery
[treatment]{Procedures} is TREAT
[HCC]{Disorders} is Carcinoma hepatocellular
[side effects]{Disorders} is Side Effect
[TACE]{Procedures} is Transcatheter arterial chemoembolization
[AHCS]{Procedures} is Cryosurgery
[treatment]{Procedures} is TREAT
[improves]{Disorders} is Improved
[immune system]{Anatomy} is Immune system
[therapeutic method]{Procedures} is TREAT
[HCC]{Disorders} is Carcinoma hepatocellular
|
The "tight orbit": Incidence and [management] of the [orbital compartment syndrome]
The [orbital compartment syndrome] ([OCS]) constitutes a severe emergency, requiring immediate [clinical diagnosis] and [surgical decompression]. The key [symptom] is [progressive visual impairment] caused by an increase in [intraorbital pressure], impairing the [perfusion] of relevant [neurovascular] and [neurosensory structures]. [Intraorbital bleeding] due to [trauma] and [surgical intervention] is known to be the main etiological factor. A retrospective [analysis] of all patients affected by an [OCS] between January 1, 2012, and May 31, 2015, was performed. Patients' [records] were reviewed with regard to etiology, initial ophthalmologic status, [fracture pattern], concomitant medication, [surgical management], and postoperative outcome. The incidence of [OCS] was calculated based on the total number of [craniomaxillofacial] ([CMF]) [emergencies]. Within 3.5 years, a total of 18,093 [CMF] [emergencies] were [registered]. In 16 patients, an [OCS] was [documented], corresponding to an incidence of 0.088%. The mean patient age was 67.31 ± 23.86 years, ranging from 22 to 102 years. The etiology varied, but [trauma] with subsequent [intraorbital bleeding] was the main [cause]. The use of [anticoagulative medication] was [documented] in 50% of the cases. In 14 patients, immediate [surgical orbital decompression] was performed: in 10 patients, [vision] could be [preserved]; in three patients, [blindness] resulted; and one patient was lost to [follow-up]. Two patients were managed without [surgery]. With regard to the total number of [CMF] [emergencies], [OCS] is a rare condition. Early [clinical diagnosis] and [surgical decompression] are required to prevent permanent [vision impairment]. [Anticoagulative medication] must be considered as a predisposing factor for an [orbital compartment syndrome] in patients affected by periorbital trauma.
|
[management]{Procedures} is DIS MANAGEMENT
[orbital compartment syndrome]{Disorders} is Compartmental syndrome
[orbital compartment syndrome]{Disorders} is Compartmental syndrome
[management]{Procedures} is DIS MANAGEMENT
[OCS]{Disorders} is Compartmental syndrome
[orbital compartment syndrome]{Disorders} is Compartmental syndrome
[clinical diagnosis]{Procedures} is Clinical diagnosis
[surgical decompression]{Procedures} is Surgical Decompression
[symptom]{Disorders} is Symptom
[progressive visual impairment]{Disorders} is Progressive visual impairment
[intraorbital pressure]{Physiology} is Intraocular pressure
[perfusion]{Procedures} is Perfusions
[neurovascular]{Anatomy} is Neurovascular network
[neurosensory structures]{Anatomy} is Sensory structure
[Intraorbital bleeding]{Disorders} is Bleeding
[trauma]{Disorders} is Trauma
[surgical intervention]{Disorders} is Surgical intervention
[analysis]{Procedures} is Analyzed
[OCS]{Disorders} is Compartmental syndrome
[records]{Concepts & Ideas} is Records
[fracture pattern]{Disorders} is Finding (finding)
[surgical management]{Procedures} is Surgical Management
[OCS]{Disorders} is Compartmental syndrome
[craniomaxillofacial]{Anatomy} is Anatomic Region
[CMF]{Anatomy} is Anatomic Region
[emergencies]{Disorders} is Emergencies
[CMF]{Anatomy} is Anatomic Region
[emergencies]{Disorders} is Emergencies
[registered]{Procedures} is Registered
[OCS]{Disorders} is Compartmental syndrome
[documented]{Procedures} is Documented
[trauma]{Disorders} is Trauma
[intraorbital bleeding]{Disorders} is Bleeding
[cause]{Disorders} is Injury cause
[anticoagulative medication]{Procedures} is Anticoagulation Therapy
[documented]{Procedures} is Documented
[surgical orbital decompression]{Procedures} is Orbital decompression
[vision]{Physiology} is Vision
[preserved]{Procedures} is Preserved
[blindness]{Disorders} is Blindness
[follow-up]{Procedures} is Follow-up
[surgery]{Procedures} is Surgery
[CMF]{Anatomy} is Anatomic Region
[emergencies]{Disorders} is Emergencies
[OCS]{Disorders} is Compartmental syndrome
[clinical diagnosis]{Procedures} is Clinical diagnosis
[surgical decompression]{Procedures} is Surgical Decompression
[vision impairment]{Disorders} is Vision impairment
[Anticoagulative medication]{Procedures} is Anticoagulation Therapy
[orbital compartment syndrome]{Disorders} is Compartmental syndrome
|
[Ammonia] as an [In Situ] Sanitizer: Influence of [Virus] [Genome Type] on Inactivation
Treatment of [human] [excreta] and [animal] manure ([HEAM]) is key in controlling the spread of persistent [enteric] pathogens, such as [viruses]. The [extent] of [virus inactivation] during [HEAM] storage and treatment appears to vary with [virus] [genome type], although the reasons for this variability are not clear. Here, we investigated the inactivation of [viruses] of different [genome types] under conditions representative of [HEAM] storage or mesophilic [digestion]. The goals were to characterize the influence of [HEAM] solution conditions on inactivation and to determine the potential mechanisms involved. Specifically, eight [viruses] representing the four [viral genome types] ([single-stranded RNA] ([ssRNA]), [double-stranded RNA] ([dsRNA]), [single-stranded DNA] ([ssDNA]), and [double-stranded DNA] ([dsDNA])) were exposed to synthetic solutions with well-controlled temperature (20 to 35°C), pH (8 to 9), and [ammonia] ([NH3]) concentrations (0 to 40 mmol liter(-1)). [DNA] and [dsRNA] [viruses] were considerably more resistant than [ssRNA viruses], resulting in up to 1,000-fold-longer treatment times to reach a 4-log inactivation. The apparently slower inactivation of [DNA viruses] was rationalized by the higher [stability] of [DNA] than that of [ssRNA] in [HEAM]. Pushing the system toward harsher pH (>9) and temperature (>35°C) conditions, such as those encountered in thermophilic [digestion] and alkaline treatments, led to more consistent inactivation kinetics among [ssRNA] and other [viruses]. This suggests that the dependence of inactivation on [genome type] disappeared in favor of [protein] -mediated inactivation mechanisms common to all [viruses]. Finally, we recommend the use of [MS2] as a conservative indicator to assess the inactivation of [ssRNA viruses] and the stable [ΦX174] or [dsDNA] [phages] as indicators for persistent [viruses]. [Viruses] are among the most [environmentally] persistent pathogens. They can be [present] in high concentrations in [human] [excreta] and [animal] manure ([HEAM]). Therefore, appropriate treatment of [HEAM] is important prior to its reuse or [discharge] into the [environment]. Here, we investigated the factors that determine the persistence of [viruses] in [HEAM], and we determined the main mechanisms that lead to their inactivation. Unlike other organisms, [viruses] can have four different [genome types] (double- or [single-stranded RNA] or [DNA]), and the [viruses] studied herein represent all four types. [Genome type] appeared to be the major determinant for persistence. [Single-stranded RNA viruses] are the most labile, because this [genome type] is susceptible to degradation in [HEAM]. In contrast, the other [genome types] are more stable; therefore, inactivation is slower and mainly driven by the degradation of [viral proteins]. Overall, this study allows us to better understand the behavior of [viruses] in [HEAM].
|
[Ammonia]{Chemicals & Drugs} is Ammonia
[In Situ]{Concepts & Ideas} is In Situ
[Virus]{Living Beings} is Virus
[Genome Type]{Genes & Molecular Sequences} is Genome
[Ammonia]{Chemicals & Drugs} is Ammonia
[human]{Living Beings} is Human
[In Situ]{Concepts & Ideas} is In Situ
[excreta]{Anatomy} is Body Excretions
[animal]{Living Beings} is Animal
[HEAM]{Anatomy} is Body Excretions
[Virus]{Living Beings} is Virus
[Genome Type]{Genes & Molecular Sequences} is Genome
[enteric]{Concepts & Ideas} is Enteral
[viruses]{Living Beings} is Virus
[extent]{Concepts & Ideas} is Extent
[virus inactivation]{Procedures} is Virus Inactivation
[HEAM]{Anatomy} is Body Excretions
[virus]{Living Beings} is Virus
[genome type]{Genes & Molecular Sequences} is Genome
[viruses]{Living Beings} is Virus
[genome types]{Genes & Molecular Sequences} is Genome
[HEAM]{Anatomy} is Body Excretions
[digestion]{Physiology} is Digestion
[HEAM]{Anatomy} is Body Excretions
[viruses]{Living Beings} is Virus
[viral genome types]{Genes & Molecular Sequences} is Viral Genome
[single-stranded RNA]{Chemicals & Drugs} is Single-Stranded RNA
[ssRNA]{Chemicals & Drugs} is Single-Stranded RNA
[double-stranded RNA]{Chemicals & Drugs} is Double-Stranded RNA
[dsRNA]{Chemicals & Drugs} is Double-Stranded RNA
[single-stranded DNA]{Chemicals & Drugs} is Single-Stranded DNA
[ssDNA]{Chemicals & Drugs} is Single-Stranded DNA
[double-stranded DNA]{Chemicals & Drugs} is Double-Stranded DNA
[dsDNA]{Chemicals & Drugs} is Double-Stranded DNA
[ammonia]{Chemicals & Drugs} is Ammonia
[NH3]{Chemicals & Drugs} is Ammonia
[DNA]{Chemicals & Drugs} is DNA
[dsRNA]{Chemicals & Drugs} is Double-Stranded RNA
[viruses]{Living Beings} is Virus
[ssRNA viruses]{Living Beings} is SsRNA viruses
[DNA viruses]{Living Beings} is DNA Viruses
[stability]{Procedures} is DNA Stability
[DNA]{Chemicals & Drugs} is DNA
[ssRNA]{Chemicals & Drugs} is Single-Stranded RNA
[HEAM]{Anatomy} is Body Excretions
[digestion]{Physiology} is Digestion
[ssRNA]{Chemicals & Drugs} is Single-Stranded RNA
[viruses]{Living Beings} is Virus
[genome type]{Genes & Molecular Sequences} is Genome
[protein]{Chemicals & Drugs} is Protein
[viruses]{Living Beings} is Virus
[MS2]{Living Beings} is MS2 Phage
[ssRNA viruses]{Living Beings} is SsRNA viruses
[ΦX174]{Living Beings} is Phi X174
[dsDNA]{Chemicals & Drugs} is Double-Stranded DNA
[phages]{Living Beings} is Phage
[viruses]{Living Beings} is Virus
[Viruses]{Living Beings} is Virus
[environmentally]{Concepts & Ideas} is Environmental
[present]{Disorders} is Present
[human]{Living Beings} is Human
[excreta]{Anatomy} is Body Excretions
[animal]{Living Beings} is Animal
[HEAM]{Anatomy} is Body Excretions
[HEAM]{Anatomy} is Body Excretions
[discharge]{Anatomy} is Body Substance Discharge
[environment]{Concepts & Ideas} is Environmental
[viruses]{Living Beings} is Virus
[HEAM]{Anatomy} is Body Excretions
[viruses]{Living Beings} is Virus
[genome types]{Genes & Molecular Sequences} is Genome
[single-stranded RNA]{Chemicals & Drugs} is Single-Stranded RNA
[DNA]{Chemicals & Drugs} is DNA
[viruses]{Living Beings} is Virus
[Genome type]{Genes & Molecular Sequences} is Genome
[Single-stranded RNA viruses]{Living Beings} is SsRNA viruses
[genome type]{Genes & Molecular Sequences} is Genome
[HEAM]{Anatomy} is Body Excretions
[genome types]{Genes & Molecular Sequences} is Genome
[viral proteins]{Chemicals & Drugs} is Viral Proteins
[viruses]{Living Beings} is Virus
[HEAM]{Anatomy} is Body Excretions
|
An [electrochemical] genosensor for [Leishmania major] [detection] based on dual effect of [immobilization] and electrocatalysis of [cobalt-zinc ferrite] quantum dots
Identification of [Leishmania] [parasites] is important in [diagnosis] and [clinical studies] of [leishmaniasis]. Although [epidemiological] and clinical [methods] are available, they are not sufficient for identification of [causative agents] of [leishmaniasis]. In the present [study], quantum dots of magnetic [cobalt-zinc ferrite] ([Co0.5Zn0.5Fe2O4]) were synthesized and characterized by physicochemical methods. The quantum dots were then employed as an [electrode] [modifier] to immobilize a 24-mer specific [single stranded] [DNA probe], and fabrication of a label-free, PCR-free and signal-on [electrochemical] genosensor for the [detection] of [Leishmania major]. [Hybridization] of the [complementary] [single stranded] [DNA sequence] with the [probe] under the selected conditions was explored using [methylene blue] as a [redox marker], utilizing the electrocatalytic effect of the quantum dots on the [methylene blue] electroreduction process. The genosensor could [detect] a [synthetic single stranded DNA target] in a range of 1.0×10(-11) to 1.0×10(-18)molL(-1) with a limit of detection of 2.0×10(-19)molL(-1), and [genomic DNA] in a range of 7.31×10(-14) to 7.31×10(-6)ngμL(-1) with a limit of detection of 1.80×10(-14)ngμL(-1) with a high selectivity and sensitivity.
|
[electrochemical]{Procedures} is Electrochemical Technic
[Leishmania major]{Living Beings} is Leishmania leishmania majors
[detection]{Procedures} is Detection
[immobilization]{Procedures} is Immobilization test
[cobalt-zinc ferrite]{Chemicals & Drugs} is Inorganic compound
[electrochemical]{Procedures} is Electrochemical Technic
[Leishmania]{Living Beings} is Leishmania sp.
[parasites]{Living Beings} is Parasites
[Leishmania major]{Living Beings} is Leishmania leishmania majors
[detection]{Procedures} is Detection
[diagnosis]{Disorders} is Diagnosis
[clinical studies]{Procedures} is Clinical Studies
[immobilization]{Procedures} is Immobilization test
[leishmaniasis]{Disorders} is Leishmaniasis
[epidemiological]{Procedures} is Epidemiological Method
[cobalt-zinc ferrite]{Chemicals & Drugs} is Inorganic compound
[methods]{Concepts & Ideas} is Methods
[causative agents]{Disorders} is Causative agent
[leishmaniasis]{Disorders} is Leishmaniasis
[study]{Procedures} is Clinical Studies
[cobalt-zinc ferrite]{Chemicals & Drugs} is Inorganic compound
[Co0.5Zn0.5Fe2O4]{Chemicals & Drugs} is Inorganic compound
[electrode]{Devices} is Electrode
[modifier]{Devices} is Transformer
[single stranded]{Chemicals & Drugs} is Single Stranded DNA
[DNA probe]{Chemicals & Drugs} is DNA Probes
[electrochemical]{Procedures} is Electrochemical Technic
[detection]{Procedures} is Detection
[Leishmania major]{Living Beings} is Leishmania leishmania majors
[Hybridization]{Procedures} is DNA hybridization
[complementary]{Chemicals & Drugs} is Complementary DNA
[single stranded]{Chemicals & Drugs} is Single Stranded DNA
[DNA sequence]{Genes & Molecular Sequences} is DNA Sequence
[probe]{Chemicals & Drugs} is DNA Probes
[methylene blue]{Chemicals & Drugs} is Methylene Blue
[redox marker]{Physiology} is Marker
[methylene blue]{Chemicals & Drugs} is Methylene Blue
[detect]{Procedures} is Detection
[synthetic single stranded DNA target]{Chemicals & Drugs} is Synthetic construct
[genomic DNA]{Chemicals & Drugs} is Genomic DNA
|
The [N-Methyl d-Aspartate Glutamate Receptor Antagonist] [Ketamine] Disrupts the Functional State of the [Corticothalamic] Pathway
The non-competitive [N-methyl d-aspartate glutamate receptor (NMDAR) antagonist] [ketamine] elicits a [brain] state resembling [high-risk] states for developing [psychosis] and early stages of [schizophrenia] characterized by [sensory] and [cognitive deficits] and aberrant ongoing [gamma oscillations] (30-80 Hz)in [cortical] and subcortical [structures], including the [thalamus]. The underlying mechanisms are unknown. The [goal] of the present [study] was to determine whether a [ketamine] - induced [psychotic] - relevant state disturbs the functional state of the [corticothalamic] ([CT]) pathway. [Multisite field recordings] were performed in the somatosensory CT system of the [sedated] [rat]. Baseline activity was challenged by activation of [vibrissa] - related [prethalamic] inputs. The sensory - [evoked thalamic response] was characterized by a short - latency (∼4 ms) [prethalamic] -mediated negative sharp [potential] and a longer latency (∼10 ms) [CT] -mediated negative [potential]. Following a single subcutaneous injection of [ketamine] (2.5 mg/kg), spontaneously occurring and sensory - [evoked thalamic gamma oscillations] increased and decreased in power, respectively. The power of the sensory -related [gamma oscillations] was [positively] correlated with both the [amplitude] and the area under the curve of the corresponding [CT] [potential] but not with the [prethalamic] [potential]. The present results show that the [layer VI] [CT] pathway significantly contributes in [thalamic] [gamma oscillations], and they support the hypothesis that reduced [NMDAR] [activation] disturbs the functional state of [CT] and [corticocortical] [networks].
|
[N-Methyl d-Aspartate Glutamate Receptor Antagonist]{Chemicals & Drugs} is N-methyl-D-aspartate receptor antagonist
[Ketamine]{Chemicals & Drugs} is Ketamine
[Corticothalamic]{Anatomy} is Corticothalamic fibers
[N-Methyl d-Aspartate Glutamate Receptor Antagonist]{Chemicals & Drugs} is N-methyl-D-aspartate receptor antagonist
[N-methyl d-aspartate glutamate receptor (NMDAR) antagonist]{Chemicals & Drugs} is N-methyl-D-aspartate receptor antagonist
[Ketamine]{Chemicals & Drugs} is Ketamine
[ketamine]{Chemicals & Drugs} is Ketamine
[brain]{Anatomy} is Brains
[Corticothalamic]{Anatomy} is Corticothalamic fibers
[high-risk]{Disorders} is HIGH RISK
[psychosis]{Disorders} is (X) Psychosis
[schizophrenia]{Disorders} is Schizophrenia
[sensory]{Disorders} is Sensory deficit
[cognitive deficits]{Disorders} is Cognitive disorder
[gamma oscillations]{Physiology} is Brain Wave
[cortical]{Anatomy} is Cortical Plate
[structures]{Concepts & Ideas} is Structure
[thalamus]{Anatomy} is THALAMUS
[goal]{Concepts & Ideas} is Goal
[study]{Procedures} is Study
[ketamine]{Chemicals & Drugs} is Ketamine
[psychotic]{Disorders} is (X) Psychosis
[corticothalamic]{Anatomy} is Corticothalamic fibers
[CT]{Anatomy} is Corticothalamic fibers
[Multisite field recordings]{Procedures} is Diagnostic procedures (procedure)
[sedated]{Disorders} is Sedated
[rat]{Living Beings} is Rat (organism)
[vibrissa]{Anatomy} is Vibrissae
[prethalamic]{Anatomy} is Subthalamic region
[evoked thalamic response]{Physiology} is Evoked potential
[prethalamic]{Anatomy} is Subthalamic region
[potential]{Physiology} is Action potential
[CT]{Anatomy} is Corticothalamic fibers
[potential]{Physiology} is Action potential
[ketamine]{Chemicals & Drugs} is Ketamine
[evoked thalamic gamma oscillations]{Physiology} is Evoked potential
[gamma oscillations]{Physiology} is Brain Wave
[positively]{Disorders} is Positive for
[amplitude]{Concepts & Ideas} is Amplitude
[CT]{Anatomy} is Corticothalamic fibers
[potential]{Physiology} is Action potential
[prethalamic]{Anatomy} is Subthalamic region
[potential]{Physiology} is Action potential
[layer VI]{Anatomy} is Type VI layer of cerebral cortex
[CT]{Anatomy} is Corticothalamic fibers
[thalamic]{Anatomy} is THALAMUS
[gamma oscillations]{Physiology} is Brain Wave
[NMDAR]{Chemicals & Drugs} is NMDAR
[activation]{Physiology} is Receptor Activation
[CT]{Anatomy} is Corticothalamic fibers
[corticocortical]{Anatomy} is Cortical Plate
[networks]{Physiology} is Nerve network
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Novel [immunotherapeutic strategies] to target [alloantibody] -producing [B] and [plasma cells] in [transplantation]
There is an unmet need for [immunotherapeutic agents] that target humoral alloimmunity in [solid organ transplantation]. This includes sensitized patients with preformed [donor] -specific [human leucocyte antigen] [antibodies] and patients who develop de-novo [donor] -specific [antibodies], both of which are associated with acute and chronic [antibody-mediated rejection] and [allograft] loss. In this [review], we discuss recent progress in the generation of [B-cell] and [plasma cell] -targeted [therapeutics], with an emphasis on novel [agents]. To deplete or inhibit [B cells], [B-cell] -specific [mAbs] have been developed, including [CD20], [CD22], [CD19] and bi-specific [antibodies] that target two [B-cell] [antigens]. In addition, inhibition of [B-cell] - [activating] [cytokines], such as [B cell-activating factor], may also reduce [allo-B-cell activation]. [Plasma cells] remain a difficult [therapeutic] target, but inhibition of [germinal centre] responses via costimulatory blockade or [IL21] neutralization, induction of [plasma cell] [apoptosis] using [proteasome inhibitors] or disruption of the [plasma cell] niche are potential avenues being explored. The ultimate aim of these [animal] and [human studies] is to develop agents that efficiently target [humoral effectors], whilst sparing [B] and [plasma cells] with a regulatory [capacity] to promote long-term [allograft] [survival], but we remain some distance away from this [goal].
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[immunotherapeutic strategies]{Procedures} is Immunotherapies
[alloantibody]{Chemicals & Drugs} is Alloantibodies
[B]{Anatomy} is B cell
[plasma cells]{Anatomy} is Plasma Cells
[transplantation]{Procedures} is Transplantation
[immunotherapeutic strategies]{Procedures} is Immunotherapies
[immunotherapeutic agents]{Chemicals & Drugs} is Immunotherapeutic agent
[alloantibody]{Chemicals & Drugs} is Alloantibodies
[B]{Anatomy} is B cell
[plasma cells]{Anatomy} is Plasma Cells
[solid organ transplantation]{Procedures} is Organ Transplantation
[transplantation]{Procedures} is Transplantation
[donor]{Living Beings} is Organ donor
[human leucocyte antigen]{Chemicals & Drugs} is Human leucocyte antigen
[antibodies]{Chemicals & Drugs} is Antibodies
[donor]{Living Beings} is Organ donor
[antibodies]{Chemicals & Drugs} is Antibodies
[antibody-mediated rejection]{Disorders} is Antibody-mediated rejection
[allograft]{Procedures} is Allograft
[review]{Concepts & Ideas} is Review
[B-cell]{Anatomy} is B cell
[plasma cell]{Anatomy} is Plasma Cells
[therapeutics]{Procedures} is Therapeutics
[agents]{Chemicals & Drugs} is Agent (attribute)
[B cells]{Anatomy} is B cell
[B-cell]{Anatomy} is B cell
[mAbs]{Chemicals & Drugs} is MAb
[CD20]{Chemicals & Drugs} is CD20 Antigens
[CD22]{Chemicals & Drugs} is CD22 antigen
[CD19]{Chemicals & Drugs} is CD19 Antigen
[antibodies]{Chemicals & Drugs} is Antibodies
[B-cell]{Anatomy} is B cell
[antigens]{Chemicals & Drugs} is Antigens
[B-cell]{Anatomy} is B cell
[activating]{Physiology} is Cell activation
[cytokines]{Chemicals & Drugs} is Cytokine
[B cell-activating factor]{Chemicals & Drugs} is B-Cell-Activating Factor
[allo-B-cell activation]{Physiology} is Activation of B cell activation
[Plasma cells]{Anatomy} is Plasma Cells
[therapeutic]{Procedures} is Therapeutics
[germinal centre]{Anatomy} is Germinal Center
[IL21]{Chemicals & Drugs} is IL21
[plasma cell]{Anatomy} is Plasma Cells
[apoptosis]{Physiology} is Apoptosis
[proteasome inhibitors]{Chemicals & Drugs} is Proteasome Inhibitors
[plasma cell]{Anatomy} is Plasma Cells
[animal]{Living Beings} is Animal
[human studies]{Procedures} is Human study
[humoral effectors]{Anatomy} is Effector Cell
[B]{Anatomy} is B cell
[plasma cells]{Anatomy} is Plasma Cells
[capacity]{Disorders} is Endurance capacity
[allograft]{Procedures} is Allograft
[survival]{Physiology} is Graft Survival
[goal]{Concepts & Ideas} is Goal
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[Survival status] and functional outcome of children who required prolonged [intensive care] after [cardiac surgery]
Children who require prolonged [intensive care] after [cardiac surgery] are at risk of high mortality. The long-term [survival] and functional outcome of these children have not been studied in detail. Children who [stayed] in [intensive care] for >28 days after [cardiac surgery] from 1997 to 2012 were studied in a single [institution]. A total of 116 patients were identified; 107 (92%) were <1 year of age and 63 (54%) had [univentricular physiology]. The incidence of children requiring prolonged [intensive care] increased from 1.01/100 undergoing [cardiac surgery] in 1997 to 2000 to 2.66/100 in 2009 to 2012 (P trend = .002). This increase coincided with an increase in the number of children with [hypoplastic left heart syndrome] having prolonged [intensive care] during the same period (0.13/100 in 1997-2000 to 1.0/100 in 2009-2012; P trend = .001). [Survival] to [pediatric intensive care unit] ([PICU]) [discharge] was 74% (95% confidence interval (CI), 65-82) and 51% (95% CI, 41-59) at 3 years. Factors associated with mortality were [univentricular repair] (hazard ratio (HR), 2.12; 95% CI, 1.21-3.70; P = .008) and [acute renal failure] (HR, 3.01; 95% CI, 1.77-5.12; P < .001), but era did not influence mortality (1997-2005 vs 2006-2012; log-rank P = .66). Among [PICU] survivors, 3- year [survival] in those who did not need early [reoperation] was 81% (95% CI, 66-90), compared with 58% (95% CI, 42-71) in those who required early [reoperation] (log-rank P = .01). Among survivors, 36% had either [moderate] or [severe disability] and 13% had poor quality of life. The incidence of children requiring prolonged [intensive care] after [cardiac surgery] has increase d in our [institution]. Our data suggest that the long-term outcome for most of these children is poor, especially after [univentricular repair].
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[Survival status]{Disorders} is Survival Status
[intensive care]{Procedures} is Intensive care
[cardiac surgery]{Procedures} is Cardiac Surgery procedures
[Survival status]{Disorders} is Survival Status
[intensive care]{Procedures} is Intensive care
[cardiac surgery]{Procedures} is Cardiac Surgery procedures
[intensive care]{Procedures} is Intensive care
[cardiac surgery]{Procedures} is Cardiac Surgery procedures
[survival]{Disorders} is Survival Status
[stayed]{Disorders} is Medicare stay
[intensive care]{Procedures} is Intensive care
[cardiac surgery]{Procedures} is Cardiac Surgery procedures
[institution]{Organizations} is Institution
[univentricular physiology]{Disorders} is Functionally univentricular heart
[intensive care]{Procedures} is Intensive care
[cardiac surgery]{Procedures} is Cardiac Surgery procedures
[hypoplastic left heart syndrome]{Disorders} is Hypoplastic left heart syndrome
[intensive care]{Procedures} is Intensive care
[Survival]{Disorders} is Survival Status
[pediatric intensive care unit]{Organizations} is Pediatric intensive care unit
[PICU]{Organizations} is Pediatric intensive care unit
[discharge]{Procedures} is Patient discharge
[univentricular repair]{Procedures} is Repair of univentricular heart
[acute renal failure]{Disorders} is Acute Renal Failure
[PICU]{Organizations} is Pediatric intensive care unit
[survival]{Disorders} is Survival Status
[reoperation]{Procedures} is Re-operation
[reoperation]{Procedures} is Re-operation
[moderate]{Disorders} is Disability - moderate
[severe disability]{Disorders} is Disability - severe
[intensive care]{Procedures} is Intensive care
[cardiac surgery]{Procedures} is Cardiac Surgery procedures
[institution]{Organizations} is Institution
[univentricular repair]{Procedures} is Repair of univentricular heart
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Haptic [feedback] helps [bipedal] [coordination]
The present [study] investigated whether special haptic or [visual feedback] would facilitate the [coordination] of in-phase, cyclical [feet] [movements] of different [amplitudes]. Seventeen [healthy participants] sat with their [feet] on sliding panels that were moved [externally] over the same or different [amplitudes]. The [participants] were asked to generate simultaneous [knee] [flexion-extension] [movements], or to let their [feet] be [dragged], resulting in reference [foot] [displacements] of 150 mm and experimental [foot] [displacements] of 150, 120, or 90 mm. Four types of [feedback] were given: (1) special haptic [feedback], involving actively following the motions of the [sliders] [manipulated] by two [confederates], (2) haptic [feedback] resulting from [passive motion], (3) veridical [visual feedback], and (4) enhanced [visual feedback]. Both with respect to [amplitude] assimilation effects, correlations and standard deviation of relative phase, the [results] showed that enhanced [visual feedback] did not facilitate [bipedal] independence, but haptic [feedback] with [active movement] did. Implications of the [findings] for [movement] [rehabilitation] contexts are discussed.
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[feedback]{Physiology} is Feedback
[bipedal]{Anatomy} is Pedal
[coordination]{Physiology} is Coordination
[feedback]{Physiology} is Feedback
[study]{Procedures} is Study
[bipedal]{Anatomy} is Pedal
[coordination]{Physiology} is Coordination
[visual feedback]{Physiology} is Visual Feedback
[coordination]{Physiology} is Coordination
[feet]{Anatomy} is Pedal
[movements]{Physiology} is Movements
[amplitudes]{Concepts & Ideas} is Amplitude
[healthy participants]{Living Beings} is Healthy Participants
[feet]{Anatomy} is Pedal
[externally]{Concepts & Ideas} is Externally
[amplitudes]{Concepts & Ideas} is Amplitude
[participants]{Living Beings} is Participant
[knee]{Anatomy} is Bone structure of knee
[flexion-extension]{Concepts & Ideas} is Flexion/extension
[movements]{Physiology} is Movements
[feet]{Anatomy} is Pedal
[dragged]{Disorders} is Finding (finding)
[foot]{Anatomy} is Pedal
[displacements]{Procedures} is Displacements
[foot]{Anatomy} is Pedal
[displacements]{Procedures} is Displacements
[feedback]{Physiology} is Feedback
[feedback]{Physiology} is Feedback
[sliders]{Devices} is Biomedical equipment, device (physical object)
[manipulated]{Procedures} is Manipulate
[confederates]{Living Beings} is Group (social concept)
[feedback]{Physiology} is Feedback
[passive motion]{Physiology} is Passive motion
[visual feedback]{Physiology} is Visual Feedback
[visual feedback]{Physiology} is Visual Feedback
[amplitude]{Concepts & Ideas} is Amplitude
[results]{Phenomena} is Clinical Test Result
[visual feedback]{Physiology} is Visual Feedback
[bipedal]{Anatomy} is Pedal
[feedback]{Physiology} is Feedback
[active movement]{Physiology} is Active movement
[findings]{Disorders} is Finding (finding)
[movement]{Physiology} is Movements
[rehabilitation]{Disorders} is Rehabilitation proc
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Synthesis and in vitro [bone cell] activity of [analogues] of the [cyclohexapeptide dianthin G]
The [cyclohexapeptide natural product dianthin G] promotes [osteoblast (bone-forming cell) proliferation] in vitro at nanomolar concentrations, and is therefore considered a promising candidate for the treatment of [osteoporosis]. An N(α)-methyl amide bond scan of [dianthin G] was performed to probe the effect of modifying amide bonds on [osteoblast proliferation]. In addition, to provide greater [structural] diversity, a series of [dicarba dianthin G analogues] was synthesised using ring closing metathesis. [Dianthin G] and one novel [dicarba analogue] increased the number of [human] [osteoblasts] and importantly they did not increase [osteoclast (bone-resorbing cell) differentiation] in [bone marrow cells].
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[bone cell]{Anatomy} is Bone cell
[analogues]{Chemicals & Drugs} is Analogues/Derivatives
[cyclohexapeptide dianthin G]{Chemicals & Drugs} is Pharmacologic Substance
[cyclohexapeptide natural product dianthin G]{Chemicals & Drugs} is Pharmacologic Substance
[bone cell]{Anatomy} is Bone cell
[analogues]{Chemicals & Drugs} is Analogues/Derivatives
[osteoblast (bone-forming cell) proliferation]{Physiology} is Osteoblast proliferation
[cyclohexapeptide dianthin G]{Chemicals & Drugs} is Pharmacologic Substance
[osteoporosis]{Disorders} is OP - Osteoporosis
[dianthin G]{Chemicals & Drugs} is Pharmacologic Substance
[osteoblast proliferation]{Physiology} is Osteoblast proliferation
[structural]{Concepts & Ideas} is Structural
[dicarba dianthin G analogues]{Chemicals & Drugs} is Analogues/Derivatives
[Dianthin G]{Chemicals & Drugs} is Pharmacologic Substance
[dicarba analogue]{Chemicals & Drugs} is Analogues/Derivatives
[human]{Living Beings} is Human
[osteoblasts]{Anatomy} is Osteoblasts
[osteoclast (bone-resorbing cell) differentiation]{Physiology} is Osteoclast cell differentiation
[bone marrow cells]{Anatomy} is Bone Marrow Cells
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Effects of [grazing cow] [diet] on [volatile compounds] as well as physicochemical and sensory characteristics of 12- month - [ripened Montasio cheese]
The aim of this [study] was to [evaluate] the effects of [pasture] type and [cow] feeding [supplementation] level on a 12- mo - [ripened Montasio] [protected designation of origin] ([PDO]) [cheese], which is one of the most important [PDO] [cheeses] produced in [northeast Italy]. [Cheeses] were characterized for [volatile compounds], color, mechanical variables, and sensory [descriptors]. [Pasture] type significantly affected most of the instrumental variables considered and, as a consequence, sensory properties were affected as well. [Cheeses] from the [pasture] characterized by a [nutrient-rich] [vegetation] type were higher in [protein] and lower in [fat] content. Furthermore, such [cheeses], [evaluated] by a [sensory panel], were more intense in color with a more pungent and less cow-like odor, in agreement with what found through instrumental [analyses]. [Supplementation] level resulted in less pronounced effects, limited to [volatile compounds] and texture properties, which were not detected by sensory [analysis]. The characterization of the 12- mo [ripened Montasio cheese] reported here is an important step for the valorization of this [PDO] product.
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[grazing cow]{Physiology} is Animal Grazing
[diet]{Objects} is Diet
[volatile compounds]{Chemicals & Drugs} is Volatile compound
[ripened Montasio cheese]{Objects} is Cheese
[grazing cow]{Physiology} is Animal Grazing
[study]{Procedures} is Study
[diet]{Objects} is Diet
[evaluate]{Procedures} is Evaluate
[volatile compounds]{Chemicals & Drugs} is Volatile compound
[pasture]{Concepts & Ideas} is Grassland
[cow]{Living Beings} is Cow (organism)
[supplementation]{Objects} is Nutrient supplementation
[ripened Montasio]{Objects} is Cheese
[ripened Montasio cheese]{Objects} is Cheese
[protected designation of origin]{Concepts & Ideas} is Scheme
[PDO]{Concepts & Ideas} is Scheme
[cheese]{Objects} is Cheese
[PDO]{Concepts & Ideas} is Scheme
[cheeses]{Objects} is Cheese
[northeast Italy]{Geographic Areas} is Italy
[Cheeses]{Objects} is Cheese
[volatile compounds]{Chemicals & Drugs} is Volatile compound
[descriptors]{Concepts & Ideas} is Descriptors
[Pasture]{Concepts & Ideas} is Grassland
[Cheeses]{Objects} is Cheese
[pasture]{Concepts & Ideas} is Grassland
[nutrient-rich]{Objects} is Nutrient
[vegetation]{Objects} is Plants, Edible
[protein]{Chemicals & Drugs} is Protein
[fat]{Chemicals & Drugs} is Dietary Fat
[cheeses]{Objects} is Cheese
[evaluated]{Procedures} is Evaluate
[sensory panel]{Living Beings} is OCCUP GROUPS
[analyses]{Procedures} is Analyzed
[Supplementation]{Objects} is Nutrient supplementation
[volatile compounds]{Chemicals & Drugs} is Volatile compound
[analysis]{Procedures} is Analyzed
[ripened Montasio cheese]{Objects} is Cheese
[PDO]{Concepts & Ideas} is Scheme
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The biological effect of [metal] [ions] on the [granulation] of aerobic granular activated sludge
As a special [biofilm] structure, microbial attachment is believed to play an important role in the [granulation] of aerobic granular activated sludge (AGAS). This experiment was to investigate the biological effect of [Ca(2+),] [Mg(2+)], [Cu(2+)], [Fe(2+)], [Zn(2+)], and [K(+)] which are the most common [ions] present in biological wastewater treatment systems, on the microbial attachment of AGAS and [flocculent] activated sludge (FAS), from which AGAS is always derived, in order to provide a new strategy for the rapid cultivation and stability control of AGAS. The result showed that attachment biomass of AGAS was about 300% higher than that of FAS without the addition of [metal] [ions]. Different [metal] [ions] had different effects on the process of microbial attachment. FAS and AGAS reacted differently to the [metal] [ions] as well, and in fact, AGAS was more sensitive to the [metal] [ions]. Specifically, [Ca(2+)], [Mg(2+)], and [K(+)] could increase the microbial attachment ability of both AGAS and FAS under appropriate concentrations, [Cu(2+)], [Fe(2+)], and [Zn(2+)] were also beneficial to the microbial attachment of FAS at low concentrations, but [Cu(2+)], [Fe(2+)], and [Zn(2+)] greatly inhibited the attachment process of AGAS even at extremely low concentrations. In addition, the [acylated homoserine lactone] ([AHL])-based [quorum sensing system], the content of [extracellular] [polymeric substances] and the relative hydrophobicity of the sludges were greatly influenced by [metal] [ions]. As all these parameters had close relationships with the microbial attachment process, the microbial attachment may be affected by changes of these parameters.
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[metal]{Chemicals & Drugs} is Metal
[ions]{Chemicals & Drugs} is Ions
[granulation]{Procedures} is Granulation
[biofilm]{Living Beings} is Biofilm
[metal]{Chemicals & Drugs} is Metal
[ions]{Chemicals & Drugs} is Ions
[granulation]{Procedures} is Granulation
[granulation]{Procedures} is Granulation
[Ca(2+),]{Chemicals & Drugs} is Calcium Cation
[Mg(2+)]{Chemicals & Drugs} is Mg(II)
[Cu(2+)]{Chemicals & Drugs} is Cu(II)
[Fe(2+)]{Chemicals & Drugs} is Iron(2+)
[Zn(2+)]{Chemicals & Drugs} is Zn(II)
[K(+)]{Chemicals & Drugs} is Potassium Cation
[ions]{Chemicals & Drugs} is Ions
[flocculent]{Physiology} is Flocculation
[metal]{Chemicals & Drugs} is Metal
[ions]{Chemicals & Drugs} is Ions
[metal]{Chemicals & Drugs} is Metal
[ions]{Chemicals & Drugs} is Ions
[metal]{Chemicals & Drugs} is Metal
[ions]{Chemicals & Drugs} is Ions
[metal]{Chemicals & Drugs} is Metal
[ions]{Chemicals & Drugs} is Ions
[Ca(2+)]{Chemicals & Drugs} is Calcium Cation
[Mg(2+)]{Chemicals & Drugs} is Mg(II)
[K(+)]{Chemicals & Drugs} is Potassium Cation
[Cu(2+)]{Chemicals & Drugs} is Cu(II)
[Fe(2+)]{Chemicals & Drugs} is Iron(2+)
[Zn(2+)]{Chemicals & Drugs} is Zn(II)
[Cu(2+)]{Chemicals & Drugs} is Cu(II)
[Fe(2+)]{Chemicals & Drugs} is Iron(2+)
[Zn(2+)]{Chemicals & Drugs} is Zn(II)
[acylated homoserine lactone]{Chemicals & Drugs} is Acylated Homoserine Lactone
[AHL]{Chemicals & Drugs} is Acylated Homoserine Lactone
[quorum sensing system]{Physiology} is Quorum sensing system
[extracellular]{Anatomy} is Extracellular
[polymeric substances]{Chemicals & Drugs} is POLYMER SUBSTANCE
[metal]{Chemicals & Drugs} is Metal
[ions]{Chemicals & Drugs} is Ions
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[Rh(III)] - Catalyzed Oxidative Annulation Leading to [Substituted Indolizines] by Cleavage of C(sp(2))-H/C(sp(3))-H Bonds
[Rhodium(III)] - catalyzed oxidative annulation reactions of [pyridinium trifluoromethanesulfonate salts] with [alkynes] leading to [substituted indolizines] by cleavage of C(sp(2))-H/C(sp(3))-H bonds are developed. The starting materials are readily available, and the reactions have a [broad] substrate scope. This reaction overcomes some drawbacks of the previous [indolizine] synthetic methods and provides a new efficient [route] to [indolizine derivatives].
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[Rh(III)]{Chemicals & Drugs} is Rhodium AND/OR rhodium compound
[Substituted Indolizines]{Chemicals & Drugs} is Indolizines
[Rh(III)]{Chemicals & Drugs} is Rhodium AND/OR rhodium compound
[Rhodium(III)]{Chemicals & Drugs} is Rhodium AND/OR rhodium compound
[Substituted Indolizines]{Chemicals & Drugs} is Indolizines
[pyridinium trifluoromethanesulfonate salts]{Chemicals & Drugs} is PYRIDINIUM CPDS
[alkynes]{Chemicals & Drugs} is Alkynes
[substituted indolizines]{Chemicals & Drugs} is Indolizines
[broad]{Concepts & Ideas} is Broad
[indolizine]{Chemicals & Drugs} is Indolizines
[route]{Concepts & Ideas} is Route
[indolizine derivatives]{Chemicals & Drugs} is Indolizines
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[Pyomyositis] in childhood - [systemic lupus erythematosus]
[Pyomyositis] is a [pyogenic infection] of [skeletal muscle] that arises from [hematogenous spread] and usually presents with [localized] [abscess]. This muscle infection has been rarely reported in [adult-onset] [systemic lupus erythematous] and, to the best of our knowledge, [has not been diagnosed] in pediatric [lupus population]. Among our [childhood-onset] [systemic lupus erythematous] [population], including 289 patients, one presented [pyomyositis]. This patient was [diagnosed] with [childhood-onset] [systemic lupus erythematous] at the age of 10 years-old. After six years, while being treated with [prednisone], [azathioprine] and [hydroxychloroquine], she was [hospitalized] due to a 30-day history of insidious pain in the [left thigh] and no apparent [trauma] or [fever] were reported. Her [physical examination] showed [muscle tenderness] and [woody induration]. [Laboratory tests] revealed [anemia], increased [acute phase reactants] and [normal muscle enzymes]. Computer tomography of the left thigh showed collection on the [middle third] of the [vastus intermedius], suggesting purulent stage of [pyomyositis]. [Treatment] with [broad-spectrum antibiotic] was initiated, leading to a complete clinical resolution. In conclusion, we described the first case of [pyomyositis] during childhood in pediatric [lupus population]. This [report] reinforces that the presence of [localized muscle pain] in [immunocompromised patients], even without elevation of [muscle enzymes], should raise the [suspicion] of [pyomyositis]. A prompt [antibiotic therapy] is strongly recommended.
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[Pyomyositis]{Disorders} is Pyomyositis (Disease/Finding)
[systemic lupus erythematosus]{Disorders} is Lupus erythematosus systemic
[Pyomyositis]{Disorders} is Pyomyositis (Disease/Finding)
[pyogenic infection]{Disorders} is Infection pyogenic
[systemic lupus erythematosus]{Disorders} is Lupus erythematosus systemic
[skeletal muscle]{Anatomy} is Skeletal Muscle
[hematogenous spread]{Disorders} is Hematogenous Spread
[localized]{Concepts & Ideas} is Localized
[abscess]{Disorders} is Abscess
[adult-onset]{Disorders} is Adult-onset
[systemic lupus erythematous]{Disorders} is Lupus erythematosus systemic
[has not been diagnosed]{Disorders} is No diagnosis
[lupus population]{Living Beings} is Population
[childhood-onset]{Disorders} is Childhood-onset
[systemic lupus erythematous]{Disorders} is Lupus erythematosus systemic
[population]{Living Beings} is Population
[pyomyositis]{Disorders} is Pyomyositis (Disease/Finding)
[diagnosed]{Disorders} is Diagnosed
[childhood-onset]{Disorders} is Childhood-onset
[systemic lupus erythematous]{Disorders} is Lupus erythematosus systemic
[prednisone]{Chemicals & Drugs} is PredniSONE
[azathioprine]{Chemicals & Drugs} is Azathioprine
[hydroxychloroquine]{Chemicals & Drugs} is Oxychloroquine
[hospitalized]{Disorders} is Patient in hospital
[left thigh]{Anatomy} is Left Thigh
[trauma]{Disorders} is Trauma
[fever]{Disorders} is Fever
[physical examination]{Procedures} is Physical Examination
[muscle tenderness]{Disorders} is Tenderness muscle
[woody induration]{Disorders} is Induration (morphologic abnormality)
[Laboratory tests]{Procedures} is Laboratory Test
[anemia]{Disorders} is Anemia
[acute phase reactants]{Chemicals & Drugs} is Acute Phase Reactants
[normal muscle enzymes]{Disorders} is Muscle enzyme increased
[middle third]{Concepts & Ideas} is Middle third
[vastus intermedius]{Anatomy} is Vastus Intermedius
[pyomyositis]{Disorders} is Pyomyositis (Disease/Finding)
[Treatment]{Procedures} is Treatments
[broad-spectrum antibiotic]{Chemicals & Drugs} is Antibiotic
[pyomyositis]{Disorders} is Pyomyositis (Disease/Finding)
[lupus population]{Living Beings} is Population
[report]{Concepts & Ideas} is Case report
[localized muscle pain]{Disorders} is Localized muscle pain
[immunocompromised patients]{Disorders} is Immunocompromised Patients
[muscle enzymes]{Procedures} is Muscle enzyme
[suspicion]{Physiology} is Suspicion
[pyomyositis]{Disorders} is Pyomyositis (Disease/Finding)
[antibiotic therapy]{Procedures} is Antibiotic Therapy
|
Quantitative fetal fibronectin and [cervical length] to predict [preterm birth] in [asymptomatic] [women] with previous cervical surgery
Quantitative fetal fibronectin testing has demonstrated accuracy for prediction of [spontaneous preterm birth] in [asymptomatic] [women] with a [history] of [preterm birth]. Predictive accuracy in [women] with previous cervical surgery (a potentially different risk mechanism) is not known. We sought to compare the predictive accuracy of [cervicovaginal fluid] quantitative fetal fibronectin and [cervical length testing] in [asymptomatic] [women] with previous cervical surgery to that in [women] with 1 previous [preterm birth]. We conducted a [prospective] [blinded] secondary [analysis] of a larger [observational study] of [cervicovaginal fluid] quantitative fetal fibronectin concentration in [asymptomatic] [women] measured with a [Hologic 10Q system] ([Hologic], [Marlborough], [MA]). Prediction of [spontaneous preterm birth] (<30, <34, and <37 weeks) with [cervicovaginal fluid] quantitative fetal fibronectin concentration in [primiparous] [women] who had undergone at least 1 invasive [cervical procedure] (n = 473) was compared with prediction in [women] who had previous [spontaneous preterm birth], [preterm prelabor rupture of membranes], or [late miscarriage] (n = 821). Relationship with [cervical] length was explored. The rate of [spontaneous preterm birth] <34 weeks in the cervical surgery group was 3% compared with 9% in previous [spontaneous preterm birth] group. Receiver operating characteristic curves comparing quantitative fetal fibronectin for prediction at all 3 gestational end points were comparable between the cervical surgery and previous [spontaneous preterm birth] groups (34 weeks: area under the curve, 0.78 (95% confidence interval 0.64-0.93) vs 0.71 (95% confidence interval 0.64-0.78); P = .39). Prediction of [spontaneous preterm birth] using [cervical length] compared with quantitative fetal fibronectin for prediction of [preterm birth] <34 weeks of [gestation] offered similar prediction (area under the curve, 0.88 (95% confidence interval 0.79-0.96) vs 0.77 (95% confidence interval 0.62-0.92), P = .12 in the cervical surgery group; and 0.77 (95% confidence interval 0.70-0.84) vs 0.74 (95% confidence interval 0.67-0.81), P = .32 in the previous [spontaneous preterm birth] group). Prediction of [spontaneous preterm birth] using [cervicovaginal fluid] quantitative fetal fibronectin in [asymptomatic] [women] with cervical surgery is valid, and has comparative accuracy to that in [women] with a [history] of [spontaneous preterm birth].
|
[cervical length]{Procedures} is Cervical Length Measurement
[preterm birth]{Disorders} is Preterm Birth
[asymptomatic]{Disorders} is Asymptomatic
[women]{Living Beings} is Women
[cervical length]{Procedures} is Cervical Length Measurement
[preterm birth]{Disorders} is Preterm Birth
[asymptomatic]{Disorders} is Asymptomatic
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[women]{Living Beings} is Women
[asymptomatic]{Disorders} is Asymptomatic
[women]{Living Beings} is Women
[history]{Disorders} is Medical History
[preterm birth]{Disorders} is Preterm Birth
[women]{Living Beings} is Women
[cervicovaginal fluid]{Anatomy} is Vaginal secretions
[cervical length testing]{Procedures} is Cervical Length Measurement
[asymptomatic]{Disorders} is Asymptomatic
[women]{Living Beings} is Women
[women]{Living Beings} is Women
[preterm birth]{Disorders} is Preterm Birth
[prospective]{Procedures} is Study, Prospective
[blinded]{Procedures} is Blinded
[analysis]{Procedures} is Analyzed
[observational study]{Procedures} is Observational study
[cervicovaginal fluid]{Anatomy} is Vaginal secretions
[asymptomatic]{Disorders} is Asymptomatic
[women]{Living Beings} is Women
[Hologic 10Q system]{Concepts & Ideas} is Intellectual Product
[Hologic]{Concepts & Ideas} is MANUF
[Marlborough]{Geographic Areas} is Area
[MA]{Geographic Areas} is Massachusetts (geographic location)
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[cervicovaginal fluid]{Anatomy} is Vaginal secretions
[primiparous]{Disorders} is Primiparous
[women]{Living Beings} is Women
[cervical procedure]{Procedures} is Cervical biopsy (procedure)
[women]{Living Beings} is Women
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[preterm prelabor rupture of membranes]{Disorders} is Prelabor Rupture of Membranes
[late miscarriage]{Disorders} is Miscarriage
[cervical]{Concepts & Ideas} is Cervical
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[cervical length]{Procedures} is Cervical Length Measurement
[preterm birth]{Disorders} is Preterm Birth
[gestation]{Physiology} is Pregnancy, function
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
[cervicovaginal fluid]{Anatomy} is Vaginal secretions
[asymptomatic]{Disorders} is Asymptomatic
[women]{Living Beings} is Women
[women]{Living Beings} is Women
[history]{Disorders} is Medical History
[spontaneous preterm birth]{Disorders} is Spontaneous Preterm Birth
|
[Proteome] changes in [rat] [serum] after a [chronic ingestion] of enriched [uranium]: Toward a [biological signature] of internal contamination and radiological effect
The civilian and [military] use of [uranium] results in an increased risk of [human] exposure. The [toxicity] of [uranium] results from both its chemical and radiological properties that vary with isotopic [composition]. Validated [biomarkers] of health effects associated with exposure to [uranium] are neither sensitive nor specific to [uranium] [radiotoxicity] and/or radiological effect. This study aimed at investigating if [serum proteins] could be useful as [biomarkers] of both uranium exposure and radiological effect. Male [Sprague-Dawley rats] were chronically exposed through drinking water to low levels (40mg/L, corresponding to 1mg of [uranium] per [animal] per day) of either 4% (235) [U-enriched uranium] ([EU]) or 12% [EU] during 6 weeks. A [proteomics] approach based on two-dimensional electrophoresis ([2D-DIGE]) and [mass spectrometry] ([MS]) was used to establish [protein expression] [profiles] that could be relevant for discriminating between groups, and to identify some differentially [expressed proteins] following [uranium] [ingestion]. It demonstrated that the [expressions] of 174 [protein spots] over 1045 quantified [spots] were altered after uranium exposure (p<0.05). Using both inferential and [non-supervised multivariate statistics], we show sets of [spots] features that lead to a clear discrimination between controls and EU exposed groups on the one hand (21 [spots]), and between 4% [EU] and 12% [EU] on the other hand (7 [spots]), showing that investigation of the [serum] [proteome] may possibly be of relevance to address both [uranium] contamination and radiological effect. Finally, using bioinformatics tools, [pathway analyses] of differentially [expressed] [MS] - identified [proteins] find that acute phase, inflammatory and [immune responses] as well as [oxidative stress] are likely involved in the response to contamination, suggesting a physiological perturbation, but that does not necessarily lead to a [toxic effect].
|
[Proteome]{Chemicals & Drugs} is Proteome
[rat]{Living Beings} is Rat (organism)
[serum]{Anatomy} is Serum
[chronic ingestion]{Phenomena} is Ingestion (function)
[uranium]{Chemicals & Drugs} is Uranium
[biological signature]{Physiology} is Biological Marker
[Proteome]{Chemicals & Drugs} is Proteome
[military]{Living Beings} is Military <retired military>
[rat]{Living Beings} is Rat (organism)
[serum]{Anatomy} is Serum
[uranium]{Chemicals & Drugs} is Uranium
[chronic ingestion]{Phenomena} is Ingestion (function)
[uranium]{Chemicals & Drugs} is Uranium
[human]{Living Beings} is Human
[biological signature]{Physiology} is Biological Marker
[toxicity]{Disorders} is Toxicity
[uranium]{Chemicals & Drugs} is Uranium
[composition]{Physiology} is Composition
[biomarkers]{Physiology} is Biological Marker
[uranium]{Chemicals & Drugs} is Uranium
[uranium]{Chemicals & Drugs} is Uranium
[radiotoxicity]{Disorders} is Radiotoxicity
[serum proteins]{Chemicals & Drugs} is Serum proteins
[biomarkers]{Physiology} is Biological Marker
[Sprague-Dawley rats]{Living Beings} is Sprague-Dawley
[uranium]{Chemicals & Drugs} is Uranium
[animal]{Living Beings} is Animal
[U-enriched uranium]{Chemicals & Drugs} is Uranium
[EU]{Chemicals & Drugs} is Uranium
[EU]{Chemicals & Drugs} is Uranium
[proteomics]{Occupations} is Proteomics
[2D-DIGE]{Procedures} is 2-Dimensional Difference Gel Electrophoresis
[mass spectrometry]{Procedures} is Mass spectrometry
[MS]{Procedures} is Mass spectrometry
[protein expression]{Physiology} is Protein expression
[profiles]{Procedures} is Profile (lab procedure)
[expressed proteins]{Physiology} is Protein expression
[uranium]{Chemicals & Drugs} is Uranium
[ingestion]{Phenomena} is Ingestion (function)
[expressions]{Physiology} is Protein expression
[protein spots]{Chemicals & Drugs} is Protein
[spots]{Chemicals & Drugs} is Protein
[non-supervised multivariate statistics]{Procedures} is Statistical Correlation
[spots]{Chemicals & Drugs} is Protein
[spots]{Chemicals & Drugs} is Protein
[EU]{Chemicals & Drugs} is Uranium
[EU]{Chemicals & Drugs} is Uranium
[spots]{Chemicals & Drugs} is Protein
[serum]{Anatomy} is Serum
[proteome]{Chemicals & Drugs} is Proteome
[uranium]{Chemicals & Drugs} is Uranium
[pathway analyses]{Concepts & Ideas} is Pathway Analysis
[expressed]{Physiology} is Protein expression
[MS]{Procedures} is Mass spectrometry
[proteins]{Chemicals & Drugs} is Protein
[immune responses]{Physiology} is Immune Response
[oxidative stress]{Disorders} is Oxidative stress
[toxic effect]{Disorders} is Toxicity
|
Prediction of [extravasation] in [pelvic fracture] using [coagulation] [biomarkers]
To evaluate the usefulness of [coagulation] [biomarkers], which are easy and quick to analyze in emergency settings, for prediction of [arterial] [extravasation] due to [pelvic fracture]. The [medical records] of [pelvic fracture] patients transferred to the emergency department of Gunma University Hospital between December 2009 and May 2015 were reviewed. Patients were divided into two groups, those with ([Extra(+)]) and without ([Extra(-)]) [arterial] [extravasation] on enhanced [CT] or [angiography]. Levels of [fibrin degradation products] ([FDP]), [D-dimer], [fibrinogen], the [ratio of FDP to fibrinogen], the [ratio of D-dimer to fibrinogen], [systolic blood pressure], [heart rate], the [Glasgow Coma Scale], pH, [base excess], [hemoglobin] and [lactate] levels, the pattern of [pelvic injury], and [injury severity score] were measured at [hospital admission], and compared between the two groups. Parameters with a significant difference between the two groups were used to construct receiver operating characteristic (ROC) curves. The study included 29 patients with [pelvic fracture]. [FDP], [D-dimer], the ratio of FDP to fibrinogen and the ratio of D-dimer to fibrinogen were the most useful parameters for predicting [arterial] [extravasation] due to [pelvic fracture]. [FDP], [D-dimer], the ratio of FDP to fibrinogen, the ratio of D-dimer to fibrinogen, and [hemoglobin] and [lactate levels] were significantly higher in the [Extra(+)] group than in the [Extra(-)] group ([FDP], 354.8μg/mL (median) versus 96.6μg/mL; [D-dimer], 122.3μg/mL versus 42.1μg/mL; the ratio of FDP to fibrinogen, 3.39 versus 0.42; the ratio of D-dimer to fibrinogen, 1.14 versus 0.18; [hemoglobin], 10.5g/dL versus 13.5g/dL; [lactate], 3.5mmol/L versus 1.7mmol/L). The area under the ROC curves for [FDP], [D-dimer], the ratio of FDP to fibrinogen, the ratio of D-dimer to fibrinogen, [hemoglobin] and [lactate levels] were 0.900, 0.882, 0.918, 0.900, 0.815 and 0.765, respectively. [Coagulation] [biomarkers], and [hemoglobin] and [lactate levels] could be useful to predict the [existence] of [arterial] [extravasation] due to [pelvic fracture]. The ratio of FDP to fibrinogen and the ratio of D-dimer to fibrinogen were the most [accurate markers]. [Coagulation] [biomarkers] may enable more rapid and specific treatment for [pelvic fracture].
|
[extravasation]{Disorders} is Extravasation
[pelvic fracture]{Disorders} is Pelvic fracture
[coagulation]{Physiology} is Coagulation process
[biomarkers]{Physiology} is Biomarkers
[extravasation]{Disorders} is Extravasation
[coagulation]{Physiology} is Coagulation process
[pelvic fracture]{Disorders} is Pelvic fracture
[biomarkers]{Physiology} is Biomarkers
[coagulation]{Physiology} is Coagulation process
[biomarkers]{Physiology} is Biomarkers
[arterial]{Anatomy} is Arterial
[extravasation]{Disorders} is Extravasation
[pelvic fracture]{Disorders} is Pelvic fracture
[medical records]{Concepts & Ideas} is Medical Records
[pelvic fracture]{Disorders} is Pelvic fracture
[Extra(+)]{Disorders} is Ruled in
[Extra(-)]{Disorders} is Negative (qualifier value)
[arterial]{Anatomy} is Arterial
[extravasation]{Disorders} is Extravasation
[CT]{Procedures} is CT XRAY
[angiography]{Procedures} is Angiography
[fibrin degradation products]{Procedures} is Fibrin Degradation Products
[FDP]{Procedures} is Fibrin Degradation Products
[D-dimer]{Procedures} is D-dimer assay
[fibrinogen]{Procedures} is Fibrinogen
[ratio of FDP to fibrinogen]{Procedures} is Ratio measurement
[ratio of D-dimer to fibrinogen]{Procedures} is Ratio measurement
[systolic blood pressure]{Physiology} is Systolic Blood Pressure
[heart rate]{Physiology} is Heart Rate
[Glasgow Coma Scale]{Concepts & Ideas} is Glasgow coma scale
[base excess]{Procedures} is Base excess
[hemoglobin]{Procedures} is Hemoglobin
[lactate]{Procedures} is Lactate
[pelvic injury]{Disorders} is Pelvic fracture
[injury severity score]{Concepts & Ideas} is Injury Severity Score
[hospital admission]{Procedures} is Hospital admission
[pelvic fracture]{Disorders} is Pelvic fracture
[FDP]{Chemicals & Drugs} is FFDP
[D-dimer]{Chemicals & Drugs} is D-dimer
[arterial]{Anatomy} is Arterial
[extravasation]{Disorders} is Extravasation
[pelvic fracture]{Disorders} is Pelvic fracture
[FDP]{Chemicals & Drugs} is FFDP
[D-dimer]{Chemicals & Drugs} is D-dimer
[hemoglobin]{Phenomena} is Hemoglobin Level
[lactate levels]{Phenomena} is Lactate level result
[Extra(+)]{Disorders} is Ruled in
[Extra(-)]{Disorders} is Negative (qualifier value)
[FDP]{Chemicals & Drugs} is FFDP
[D-dimer]{Chemicals & Drugs} is D-dimer
[hemoglobin]{Phenomena} is Hemoglobin Level
[lactate]{Phenomena} is Lactate level result
[FDP]{Chemicals & Drugs} is FFDP
[D-dimer]{Chemicals & Drugs} is D-dimer
[hemoglobin]{Phenomena} is Hemoglobin Level
[lactate levels]{Phenomena} is Lactate level result
[Coagulation]{Physiology} is Coagulation process
[biomarkers]{Physiology} is Biomarkers
[hemoglobin]{Phenomena} is Hemoglobin Level
[lactate levels]{Phenomena} is Lactate level result
[existence]{Disorders} is Presence
[arterial]{Anatomy} is Arterial
[extravasation]{Disorders} is Extravasation
[pelvic fracture]{Disorders} is Pelvic fracture
[accurate markers]{Devices} is Markers (device)
[Coagulation]{Physiology} is Coagulation process
[biomarkers]{Physiology} is Biomarkers
[pelvic fracture]{Disorders} is Pelvic fracture
|
Social security status and [mortality] in [Belgian] and [Spanish] [male] [workers]
To assess differences in mortality rates between social security statuses in two independent [samples] of [Belgian] and [Spanish] [male] [workers]. [Study of two retrospective cohorts] ([Belgium], n=23,607; [Spain], n=44,385) of 50-60 year old [male] [employees] with 4 years of [follow-up]. Mortality rate ratios (MRR) were estimated using [Poisson regression] [models]. [Mortality] for [subjects] with permanent [disability] was higher than for the [employed], for both [Belgium] (MRR =4.56 (95% CI: 2.88-7.21)) and [Spain] (MRR =7.15 (95% CI: 5.37-9.51)). For the [unemployed] / early [retirees], [mortality] was higher in [Spain] (MRR =1.64 (95% CI: 1.24-2.17)) than in [Belgium] (MRR =0.88 (95% CI: 0.46-1.71)). MRR differences between [Belgium] and [Spain] for [unemployed] [workers] could be partly explained because of differences between the two social security systems. Future [studies] should further explore [mortality] differences between [countries] with different social security systems.
|
[mortality]{Disorders} is O/E - dead - condition fatal
[Belgian]{Living Beings} is Belgians
[Spanish]{Living Beings} is Spanish
[male]{Living Beings} is Human, Male
[workers]{Living Beings} is Workers
[mortality]{Disorders} is O/E - dead - condition fatal
[Belgian]{Living Beings} is Belgians
[Spanish]{Living Beings} is Spanish
[male]{Living Beings} is Human, Male
[workers]{Living Beings} is Workers
[samples]{Living Beings} is Subpopulation
[Belgian]{Living Beings} is Belgians
[Spanish]{Living Beings} is Spanish
[male]{Living Beings} is Human, Male
[workers]{Living Beings} is Workers
[Study of two retrospective cohorts]{Procedures} is Retrospective Cohort Study
[Belgium]{Geographic Areas} is Belgium
[Spain]{Geographic Areas} is Spain
[male]{Living Beings} is Human, Male
[employees]{Living Beings} is Employee
[follow-up]{Procedures} is Follow-up
[Poisson regression]{Concepts & Ideas} is REGRESSION ANAL
[models]{Concepts & Ideas} is Models
[Mortality]{Disorders} is O/E - dead - condition fatal
[subjects]{Living Beings} is Subject
[disability]{Disorders} is Disability
[employed]{Disorders} is Employed
[Belgium]{Geographic Areas} is Belgium
[Spain]{Geographic Areas} is Spain
[unemployed]{Disorders} is Unemployed
[retirees]{Living Beings} is Retiree
[mortality]{Disorders} is O/E - dead - condition fatal
[Spain]{Geographic Areas} is Spain
[Belgium]{Geographic Areas} is Belgium
[Belgium]{Geographic Areas} is Belgium
[Spain]{Geographic Areas} is Spain
[unemployed]{Disorders} is Unemployed
[workers]{Living Beings} is Workers
[studies]{Procedures} is Study
[mortality]{Disorders} is O/E - dead - condition fatal
[countries]{Geographic Areas} is Countries
|
Evaluation of the [Prostate Imaging Reporting and Data System] for [Magnetic Resonance Imaging] [Diagnosis] of [Prostate Cancer] in Patients with [Prostate-specific Antigen] <20 ng/ml
The [European Society of Urogenital Radiology] has built the [Prostate Imaging Reporting and Data System] ([PI-RADS]) for standardizing the [diagnosis] of [prostate cancer] ([PCa]). This [study] evaluated the [PI-RADS] [diagnosis method] in patients with [prostate-specific antigen] ([PSA]) <20 ng/ml. A total of 133 patients with [PSA] <20 ng/ml were prospectively recruited. [T2-weighted] ([T2WI]) and [diffusion-weighted (DWI) magnetic resonance images] of the [prostate] were acquired before a [12-core transrectal prostate biopsy]. Each patient's [peripheral zone] was divided into six regions on the [images]; each region corresponded to two of the 12 biopsy cores. [T2WI], [DWI], and [T2WI] + [DWI] scores were computed according to [PI-RADS]. The diagnostic accuracy of the [PI-RADS] score was evaluated using [histopathology] of [prostate biopsies] as the reference standard. [PCa] was histologically diagnosed in 169 (21.2%) regions. Increased [PI-RADS] score correlated positively with increased [cancer detection] rate. The [cancer detection] rate for scores 1 to 5 was 2.8%, 15.0%, 34.6%, 52.6%, and 88.9%, respectively, using [T2WI] and 12.0%, 20.2%, 48.0%, 85.7%, and 93.3%, respectively, using [DWI]. For [T2WI] + [DWI], the [cancer detection] rate was 1.5% (score 2), 13.5% (scores 3-4), 41.3% (scores 5-6), 75.9% (scores 7-8), and 92.3% (scores 9-10). The area under the curve for [cancer detection] was 0.700 ([T2WI]), 0.735 ([DWI]) and 0.749 ([T2WI] + [DWI]). The sensitivity and specificity were 53.8% and 89.2%, respectively, when using scores 5-6 as the cutoff value for [T2WI] + [DWI]. The [PI-RADS] score correlates with the [PCa detection] rate in patients with [PSA] <20 ng/ml. The summed score of [T2WI] + [DWI] has the highest accuracy in detection of [PCa]. However, the sensitivity should be further improved.
|
[Prostate Imaging Reporting and Data System]{Concepts & Ideas} is NCI_PI-RADS
[Magnetic Resonance Imaging]{Procedures} is Magnetic resonance imaging
[Diagnosis]{Procedures} is DIAGNOSIS
[Prostate Cancer]{Disorders} is PROSTATE CANCER
[Prostate-specific Antigen]{Chemicals & Drugs} is Prostate-specific antigen
[European Society of Urogenital Radiology]{Organizations} is HCO
[Prostate Imaging Reporting and Data System]{Concepts & Ideas} is NCI_PI-RADS
[Prostate Imaging Reporting and Data System]{Concepts & Ideas} is NCI_PI-RADS
[Magnetic Resonance Imaging]{Procedures} is Magnetic resonance imaging
[Diagnosis]{Procedures} is DIAGNOSIS
[PI-RADS]{Concepts & Ideas} is NCI_PI-RADS
[Prostate Cancer]{Disorders} is PROSTATE CANCER
[diagnosis]{Procedures} is DIAGNOSIS
[Prostate-specific Antigen]{Chemicals & Drugs} is Prostate-specific antigen
[prostate cancer]{Disorders} is PROSTATE CANCER
[PCa]{Disorders} is PROSTATE CANCER
[study]{Procedures} is Study
[PI-RADS]{Concepts & Ideas} is NCI_PI-RADS
[diagnosis method]{Procedures} is Diagnostic Method
[prostate-specific antigen]{Chemicals & Drugs} is Prostate-specific antigen
[PSA]{Chemicals & Drugs} is Prostate-specific antigen
[PSA]{Chemicals & Drugs} is Prostate-specific antigen
[T2-weighted]{Procedures} is Diagnostic imaging, not elsewhere classified
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[diffusion-weighted (DWI) magnetic resonance images]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[prostate]{Anatomy} is Prostates
[12-core transrectal prostate biopsy]{Procedures} is Transrectal Prostate Biopsy
[peripheral zone]{Anatomy} is Peripheral zone of prostate
[images]{Concepts & Ideas} is Medical Image
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[DWI]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[DWI]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[PI-RADS]{Concepts & Ideas} is NCI_PI-RADS
[PI-RADS]{Concepts & Ideas} is NCI_PI-RADS
[histopathology]{Occupations} is Histopathology
[prostate biopsies]{Procedures} is Biopsy prostate
[PCa]{Disorders} is PROSTATE CANCER
[PI-RADS]{Concepts & Ideas} is NCI_PI-RADS
[cancer detection]{Procedures} is Cancer Detection
[cancer detection]{Procedures} is Cancer Detection
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[DWI]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[DWI]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[cancer detection]{Procedures} is Cancer Detection
[cancer detection]{Procedures} is Cancer Detection
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[DWI]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[DWI]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[DWI]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[PI-RADS]{Concepts & Ideas} is NCI_PI-RADS
[PCa detection]{Procedures} is Prostate cancer early detection
[PSA]{Chemicals & Drugs} is Prostate-specific antigen
[T2WI]{Procedures} is Diagnostic imaging, not elsewhere classified
[DWI]{Procedures} is Diffusion-Weighted Magnetic Resonance Imaging
[PCa]{Disorders} is PROSTATE CANCER
|
Efficacy and safety of [asenapine] in [Asian] patients with an acute exacerbation of [schizophrenia]: a [multicentre], [randomized], [double-blind], 6- week, placebo-controlled study
[Asenapine] is a second generation [anti-psychotic] approved in the [USA] in 2009 for the [treatment] of [schizophrenia], but its efficacy has not been proven in [Asian] patients. The [objectives] of this [study] are to evaluate the efficacy and tolerability of [asenapine] in [Asian] patients experiencing an acute exacerbation of [schizophrenia]. In this prospective, [double-blind study], patients in [Japan], [Korea], and [Taiwan] were [randomized] (1:1:1) to [asenapine] 5 mg twice daily (bid), 10 mg bid or [placebo] for 6 weeks after a 3- to 7- day washout / screening period. The [primary endpoint] was the mean change in the [positive and negative syndrome scale] ([PANSS]) total score from baseline to day 42/ [treatment] end. Of the 532 [participants] [randomized], 530 received [treatment]. The [primary endpoint] was significantly greater with [asenapine] 5 and 10 mg bid than with [placebo] (-12.24 and -14.17 vs. -0.95; p < 0.0001). The results of secondary endpoints including [PANSS] negative subscale scores and [PANSS] responders at the end of [treatment] supported the results of the [primary endpoint]. There were no significant differences in the incidence of [treatment] -emergent [adverse events] reported with [asenapine] 5 and 10 mg bid and [placebo] (84.6, 80.7, and 81.6 %). There was a mean (± standard deviation) change in weight of -1.76 ± 2.45 kg for [placebo], +0.42 ± 2.65 kg for [asenapine] 5 mg bid, and +0.81 ± 2.89 kg for [asenapine] 10 mg bid group. [Asenapine] was effective and generally well tolerated when used for the [treatment] of acute exacerbations of [schizophrenia] in [Asian] patients.
|
[asenapine]{Chemicals & Drugs} is Asenapine
[Asian]{Living Beings} is Asian
[schizophrenia]{Disorders} is Schizophrenia
[multicentre]{Procedures} is Multicentre Trial
[randomized]{Procedures} is TRIALS RANDOMIZED CLIN
[double-blind]{Procedures} is Double-Blinded
[Asenapine]{Chemicals & Drugs} is Asenapine
[asenapine]{Chemicals & Drugs} is Asenapine
[anti-psychotic]{Chemicals & Drugs} is Anti-psychotic agent
[Asian]{Living Beings} is Asian
[USA]{Geographic Areas} is US
[schizophrenia]{Disorders} is Schizophrenia
[treatment]{Procedures} is Treatments
[schizophrenia]{Disorders} is Schizophrenia
[multicentre]{Procedures} is Multicentre Trial
[randomized]{Procedures} is TRIALS RANDOMIZED CLIN
[double-blind]{Procedures} is Double-Blinded
[Asian]{Living Beings} is Asian
[objectives]{Concepts & Ideas} is Objective
[study]{Procedures} is Study
[asenapine]{Chemicals & Drugs} is Asenapine
[Asian]{Living Beings} is Asian
[schizophrenia]{Disorders} is Schizophrenia
[double-blind study]{Procedures} is Double-Blinded
[Japan]{Geographic Areas} is Japan
[Korea]{Geographic Areas} is Korea
[Taiwan]{Geographic Areas} is Taiwan
[randomized]{Procedures} is Randomized
[asenapine]{Chemicals & Drugs} is Asenapine
[placebo]{Procedures} is PLACEBO
[primary endpoint]{Chemicals & Drugs} is Primary Endpoint
[positive and negative syndrome scale]{Concepts & Ideas} is Positive and negative syndrome scale
[PANSS]{Concepts & Ideas} is Positive and negative syndrome scale
[treatment]{Procedures} is Treatments
[participants]{Living Beings} is Participant
[randomized]{Procedures} is Randomized
[treatment]{Procedures} is Treatments
[primary endpoint]{Chemicals & Drugs} is Primary Endpoint
[asenapine]{Chemicals & Drugs} is Asenapine
[placebo]{Procedures} is PLACEBO
[PANSS]{Concepts & Ideas} is Positive and negative syndrome scale
[PANSS]{Concepts & Ideas} is Positive and negative syndrome scale
[treatment]{Procedures} is Treatments
[primary endpoint]{Chemicals & Drugs} is Primary Endpoint
[treatment]{Procedures} is Treatments
[adverse events]{Disorders} is Adverse event
[asenapine]{Chemicals & Drugs} is Asenapine
[placebo]{Procedures} is PLACEBO
[placebo]{Procedures} is PLACEBO
[asenapine]{Chemicals & Drugs} is Asenapine
[asenapine]{Chemicals & Drugs} is Asenapine
[Asenapine]{Chemicals & Drugs} is Asenapine
[treatment]{Procedures} is Treatments
[schizophrenia]{Disorders} is Schizophrenia
[Asian]{Living Beings} is Asian
|
Effect of target animacy on [hand preference] in [Sichuan snub-nosed monkeys] ([Rhinopithecus roxellana])
Twenty-eight captive [Sichuan snub-nosed monkeys] ([Rhinopithecus roxellana]) were involved in the current [study]. Many individuals showed handedness, with a modest tendency toward [left-hand use] especially for animate targets, although no group-level handedness was [found]. There was [no significant] gender difference in the [direction] and strength of [hand preference] for both targets. Females showed a significantly higher overall rate of actions toward animate targets than inanimate targets for both [hands], whereas males displayed almost the reversed pattern. There were [no significant] interactions between [lateral] [hand use] and target animacy for either males or females. Most individuals showed rightward or leftward laterality shift trends between inanimate and animate targets. These [findings] to some extent support the existence of a potential trend concerning a categorical neural distinction between targets demanding functional [manipulation] (inanimate objects) and those demanding social [manipulation] (animate objects), even though specialized [hand preference] based on target animacy has not been fully established in this [arboreal Old World monkey species].
|
[hand preference]{Disorders} is Hand preference
[Sichuan snub-nosed monkeys]{Living Beings} is Rhinopithecus roxellana
[Rhinopithecus roxellana]{Living Beings} is Rhinopithecus roxellana
[Sichuan snub-nosed monkeys]{Living Beings} is Rhinopithecus roxellana
[hand preference]{Disorders} is Hand preference
[Sichuan snub-nosed monkeys]{Living Beings} is Rhinopithecus roxellana
[Rhinopithecus roxellana]{Living Beings} is Rhinopithecus roxellana
[Rhinopithecus roxellana]{Living Beings} is Rhinopithecus roxellana
[study]{Procedures} is Study
[left-hand use]{Disorders} is Left-handedness
[found]{Disorders} is Found
[no significant]{Disorders} is Not significant
[direction]{Concepts & Ideas} is Direction
[hand preference]{Disorders} is Hand preference
[hands]{Anatomy} is Hands
[no significant]{Disorders} is Not significant
[lateral]{Concepts & Ideas} is Lateral
[hand use]{Physiology} is Using hands
[findings]{Disorders} is Finding (finding)
[manipulation]{Disorders} is Handling
[manipulation]{Disorders} is Handling
[hand preference]{Disorders} is Hand preference
[arboreal Old World monkey species]{Living Beings} is Rhinopithecus roxellana
|
Association of [Autoimmune Encephalitis] With Combined [Immune Checkpoint Inhibitor] Treatment for [Metastatic Cancer]
[Paraneoplastic encephalitides] usually precede a [diagnosis of cancer] and are often refractory to [immunosuppressive therapy]. Conversely, [autoimmune encephalitides] are reversible conditions that can occur in the [presence] or absence of [cancer]. To report the induction of [autoimmune encephalitis] in 2 patients after treatment of [metastatic cancer] with a combination of the [immune checkpoint inhibitors] [nivolumab] and [ipilimumab]. A [retrospective case study] was conducted of the [clinical and management] course of 2 patients with progressive, treatment - [refractory metastatic cancer] who were [treated with] a single dose each (concomitantly) of the [immune checkpoint inhibitors] [nivolumab], 1 mg/kg, and [ipilimumab], 3 mg/kg. [Nivolumab] and [ipilimumab]. The [clinical response] to [immunosuppressive therapy] in suspected [autoimmune encephalitis] in the setting of [immune checkpoint inhibitor] use. [Autoantibody testing] [confirmed] identification of [anti-N-methyl-D-aspartate receptor antibodies] in the [cerebrospinal fluid] of 1 patient. Withdrawal of [immune checkpoint inhibitors] and initiation of [immunosuppressive therapy], consisting of intravenous methylprednisolone sodium succinate equivalent to 1000 mg of methylprednisolone for 5 days, 0.4 mg/kg/d of [intravenous immunoglobulin] for 5 days, and 2 doses of [rituximab], 1000 mg, in 1 patient and oral prednisone, 60 mg/d, in the other patient, resulted in [improved] [neurologic symptoms]. [Immune checkpoint inhibition] may favor the development of [immune responses] against neuronal antigens, leading to [autoimmune encephalitis]. Early recognition and treatment of [autoimmune encephalitis] in patients receiving [immune checkpoint blockade therapy] will likely be essential for maximizing clinical recovery and minimizing the effect of drug-related toxic effects. The mechanisms by which [immune checkpoint inhibition] may contribute to [autoimmune encephalitis] require further study.
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[Autoimmune Encephalitis]{Disorders} is Autoimmune encephalitis
[Immune Checkpoint Inhibitor]{Chemicals & Drugs} is Pharmacologic Agent
[Metastatic Cancer]{Disorders} is Metastasize
[Paraneoplastic encephalitides]{Disorders} is Encephalitides, Paraneoplastic Limbic
[Autoimmune Encephalitis]{Disorders} is Autoimmune encephalitis
[diagnosis of cancer]{Procedures} is Cancer Diagnosis
[Immune Checkpoint Inhibitor]{Chemicals & Drugs} is Pharmacologic Agent
[Metastatic Cancer]{Disorders} is Metastasize
[immunosuppressive therapy]{Procedures} is Immunosuppressive Therapy
[autoimmune encephalitides]{Disorders} is Autoimmune encephalitis
[presence]{Disorders} is Presence
[cancer]{Disorders} is CA - Cancer
[autoimmune encephalitis]{Disorders} is Autoimmune encephalitis
[metastatic cancer]{Disorders} is Metastasize
[immune checkpoint inhibitors]{Chemicals & Drugs} is Pharmacologic Agent
[nivolumab]{Chemicals & Drugs} is Nivolumab
[ipilimumab]{Chemicals & Drugs} is Ipilimumab
[retrospective case study]{Procedures} is Retrospective Study
[clinical and management]{Procedures} is Clinical Management
[refractory metastatic cancer]{Disorders} is Refractory Cancer
[treated with]{Procedures} is Treated with
[immune checkpoint inhibitors]{Chemicals & Drugs} is Pharmacologic Agent
[nivolumab]{Chemicals & Drugs} is Nivolumab
[ipilimumab]{Chemicals & Drugs} is Ipilimumab
[Nivolumab]{Chemicals & Drugs} is Nivolumab
[ipilimumab]{Chemicals & Drugs} is Ipilimumab
[clinical response]{Disorders} is Clinical Response
[immunosuppressive therapy]{Procedures} is Immunosuppressive Therapy
[autoimmune encephalitis]{Disorders} is Autoimmune encephalitis
[immune checkpoint inhibitor]{Chemicals & Drugs} is Pharmacologic Agent
[Autoantibody testing]{Procedures} is Autoantibody test
[confirmed]{Disorders} is Confirmed
[anti-N-methyl-D-aspartate receptor antibodies]{Chemicals & Drugs} is Anti-N-methyl-D-aspartate receptor antibody
[cerebrospinal fluid]{Anatomy} is Cerebrospinal Fluid
[immune checkpoint inhibitors]{Chemicals & Drugs} is Pharmacologic Agent
[immunosuppressive therapy]{Procedures} is Immunosuppressive Therapy
[intravenous immunoglobulin]{Chemicals & Drugs} is Intravenous immunoglobulin
[rituximab]{Chemicals & Drugs} is RiTUXimab
[improved]{Disorders} is Improved
[neurologic symptoms]{Disorders} is Neurologic Symptoms
[Immune checkpoint inhibition]{Physiology} is Inhibition of immune response
[immune responses]{Physiology} is Immune Response
[autoimmune encephalitis]{Disorders} is Autoimmune encephalitis
[autoimmune encephalitis]{Disorders} is Autoimmune encephalitis
[immune checkpoint blockade therapy]{Procedures} is Immunosuppressive Therapy
[immune checkpoint inhibition]{Physiology} is Inhibition of immune response
[autoimmune encephalitis]{Disorders} is Autoimmune encephalitis
|
[Intron] Derived [Size] [Polymorphism] in the [Mitochondrial Genomes] of Closely Related [Chrysoporthe Species]
In this study, the complete [mitochondrial (mt) genomes] of [Chrysoporthe austroafricana] (190,834 bp), [C. cubensis] (89,084 bp) and [C. deuterocubensis] (124,412 bp) were determined. Additionally, the [mitochondrial genome] of another member of the [Cryphonectriaceae], namely [Cryphonectria parasitica] (158,902 bp), was retrieved and annotated for comparative purposes. These [genomes] showed high levels of [synteny], especially in regions including [genes] involved in [oxidative phosphorylation] and [electron transfer], [unique open reading frames] [(uORFs)], [ribosomal RNAs] [(rRNAs)] and [transfer RNAs] [(tRNAs)], as well as [intron] [positions]. Comparative analyses revealed signatures of [duplication] events, [intron] number and length variation, and varying [intronic] [ORFs] which highlighted the genetic diversity of [mt genomes] among the [Cryphonectriaceae]. These [mt genomes] showed remarkable [size] [polymorphism]. The [size] [polymorphism] in the [mt genomes] of these closely related [Chrysoporthe species] was attributed to the varying number and length of [introns], [coding sequences] and to a lesser [extent], [intergenic sequences]. Compared to publicly available fungal [mt genomes], the [C. austroafricana] [mt genome] is the second largest in the [Ascomycetes] thus far.
|
[Intron]{Chemicals & Drugs} is Intron
[Size]{Concepts & Ideas} is Size
[Polymorphism]{Physiology} is Polymorphism
[Mitochondrial Genomes]{Genes & Molecular Sequences} is Mitochondrial Genomes
[Chrysoporthe Species]{Living Beings} is Chrysoporthe
[Intron]{Chemicals & Drugs} is Intron
[Size]{Concepts & Ideas} is Size
[Polymorphism]{Physiology} is Polymorphism
[mitochondrial (mt) genomes]{Genes & Molecular Sequences} is Mitochondrial Genomes
[Mitochondrial Genomes]{Genes & Molecular Sequences} is Mitochondrial Genomes
[Chrysoporthe austroafricana]{Living Beings} is Chrysoporthe austroafricana
[Chrysoporthe Species]{Living Beings} is Chrysoporthe
[C. cubensis]{Living Beings} is Chrysoporthe cubensis
[C. deuterocubensis]{Living Beings} is Chrysoporthe deuterocubensis
[mitochondrial genome]{Genes & Molecular Sequences} is Mitochondrial Genomes
[Cryphonectriaceae]{Living Beings} is Cryphonectriaceae
[Cryphonectria parasitica]{Living Beings} is Cryphonectria parasitica
[genomes]{Genes & Molecular Sequences} is Genomes
[synteny]{Physiology} is Synteny
[genes]{Genes & Molecular Sequences} is Genes
[oxidative phosphorylation]{Physiology} is Oxidative phosphorylation
[electron transfer]{Physiology} is Electron transfer (function)
[unique open reading frames]{Genes & Molecular Sequences} is Open Reading Frames
[(uORFs)]{Genes & Molecular Sequences} is Open Reading Frames
[ribosomal RNAs]{Chemicals & Drugs} is Ribosomal RNA
[(rRNAs)]{Chemicals & Drugs} is Ribosomal RNA
[transfer RNAs]{Chemicals & Drugs} is Transfer RNA
[(tRNAs)]{Chemicals & Drugs} is Transfer RNA
[intron]{Chemicals & Drugs} is Intron
[positions]{Concepts & Ideas} is Positioning
[duplication]{Physiology} is Gene Duplication
[intron]{Chemicals & Drugs} is Intron
[intronic]{Chemicals & Drugs} is Intron
[ORFs]{Genes & Molecular Sequences} is Open Reading Frames
[mt genomes]{Genes & Molecular Sequences} is Mitochondrial Genomes
[Cryphonectriaceae]{Living Beings} is Cryphonectriaceae
[mt genomes]{Genes & Molecular Sequences} is Mitochondrial Genomes
[size]{Concepts & Ideas} is Size
[polymorphism]{Physiology} is Polymorphism
[size]{Concepts & Ideas} is Size
[polymorphism]{Physiology} is Polymorphism
[mt genomes]{Genes & Molecular Sequences} is Mitochondrial Genomes
[Chrysoporthe species]{Living Beings} is Chrysoporthe
[introns]{Chemicals & Drugs} is Intron
[coding sequences]{Genes & Molecular Sequences} is Open Reading Frames
[extent]{Concepts & Ideas} is Extent
[intergenic sequences]{Chemicals & Drugs} is Intergenic Sequences
[mt genomes]{Genes & Molecular Sequences} is Mitochondrial Genomes
[C. austroafricana]{Living Beings} is Chrysoporthe austroafricana
[mt genome]{Genes & Molecular Sequences} is Mitochondrial Genomes
[Ascomycetes]{Living Beings} is Class Ascomycetes
|
The [flavivirus] [dengue] induces [hypertrophy] of [white matter] [astrocytes]
[Flaviviruses], including [Zika] and [dengue] ([DENV]), pose a serious global threat to [human] health. Of the 50+ million [humans] [infected] with [DENV] annually, approximately 1-3 % progress to severe disease manifestations, [dengue hemorrhagic fever] ([DHF]) or [dengue shock syndrome] ([DSS]). Several factors are suspected to mediate the course of [infection] and [pathogenesis] of [DENV] [infection]. [DHF] and [DSS] are associated with vascular leakage and [neurological sequelae]. Our hypothesis was that altered [astrocyte activation] and morphology would alter the dynamics of the [extracellular space] and hence, neuronal and [vascular function]. We investigated the mechanisms of [neuropathogenesis] [DENV] [infection] in [rhesus macaques]. There were [decreased numbers] of GFAP [immunopositive astrocytes] per unit area, although those that remained had increased arbor length and [complexity]. This was combined with [structural] [hypertrophy] of [white matter] [astrocytes] in the absence of increased vascular leakage. Combined, these studies show how even low-grade [infection] with [DENV] induces measurable changes within the [parenchyma] of [infected] [individuals].
|
[flavivirus]{Living Beings} is Flavivirus
[dengue]{Living Beings} is Dengue Virus
[hypertrophy]{Disorders} is Hypertrophy
[white matter]{Anatomy} is White Matter
[astrocytes]{Anatomy} is Astrocytes
[Flaviviruses]{Living Beings} is Flavivirus
[flavivirus]{Living Beings} is Flavivirus
[dengue]{Living Beings} is Dengue Virus
[Zika]{Living Beings} is Zika virus
[hypertrophy]{Disorders} is Hypertrophy
[dengue]{Living Beings} is Dengue Virus
[DENV]{Living Beings} is Dengue Virus
[white matter]{Anatomy} is White Matter
[astrocytes]{Anatomy} is Astrocytes
[human]{Living Beings} is Human
[humans]{Living Beings} is Human
[infected]{Disorders} is Infected
[DENV]{Living Beings} is Dengue Virus
[dengue hemorrhagic fever]{Disorders} is Dengue Hemorrhagic Fever
[DHF]{Disorders} is Dengue Hemorrhagic Fever
[dengue shock syndrome]{Disorders} is Dengue Shock Syndrome
[DSS]{Disorders} is Dengue Shock Syndrome
[infection]{Disorders} is Infected
[pathogenesis]{Disorders} is Pathogenesis
[DENV]{Living Beings} is Dengue Virus
[infection]{Disorders} is Infected
[DHF]{Disorders} is Dengue Hemorrhagic Fever
[DSS]{Disorders} is Dengue Shock Syndrome
[neurological sequelae]{Disorders} is Sequelae of neurological disorders
[astrocyte activation]{Physiology} is Astrocyte activation
[extracellular space]{Anatomy} is Extracellular Space
[vascular function]{Physiology} is Vascular function
[neuropathogenesis]{Disorders} is Neuropathogenesis
[DENV]{Living Beings} is Dengue Virus
[infection]{Disorders} is Infected
[rhesus macaques]{Living Beings} is Rhesus Macaques
[decreased numbers]{Disorders} is Finding (finding)
[immunopositive astrocytes]{Anatomy} is Astrocytes
[complexity]{Disorders} is Finding (finding)
[structural]{Concepts & Ideas} is Structural
[hypertrophy]{Disorders} is Hypertrophy
[white matter]{Anatomy} is White Matter
[astrocytes]{Anatomy} is Astrocytes
[infection]{Disorders} is Infected
[DENV]{Living Beings} is Dengue Virus
[parenchyma]{Anatomy} is Parenchyma
[infected]{Disorders} is Infected
[individuals]{Living Beings} is Individual (person)
|
A DANGEROUS MUDDYING OF THE WATERS? THE ' SIGNIFICANT HARM ' OF RE B AND G (CHILDREN) (CARE PROCEEDINGS)(2015) EWFC 3
The academic debate [rages] on as to whether [male circumcision] really is in the best [interests] of the child or if it constitutes an abusive practice. This [commentary] discusses the recent case of Re B and G (children) (care proceedings) (2015) EWFC 3, delivered by the current [President] of the [Family Division of the High court], Sir James Munby. Two key [issues] are raised by this [judgment]. First, that [President] Munby's obiter [comments] constitute an attack on the legally accepted act of [male circumcision] by suggesting a similar nature between the illegal act of female genital mutilation (FGM) and that of [male circumcision] as well as the suggestion that [male circumcision] can be classed as a significant harm. Second, that this case [reflects] the woefully [unprepared] condition of the [UK] medical profession in dealing with FGM.
|
[rages]{Physiology} is Rages
[male circumcision]{Procedures} is Male Circumcision
[interests]{Physiology} is Interest
[commentary]{Concepts & Ideas} is Commentary
[President]{Living Beings} is Professional occupation status
[Family Division of the High court]{Organizations} is Organization
[issues]{Disorders} is Issue
[judgment]{Disorders} is Judgement - finding
[President]{Living Beings} is Professional occupation status
[comments]{Concepts & Ideas} is Comment
[male circumcision]{Procedures} is Male Circumcision
[male circumcision]{Procedures} is Male Circumcision
[male circumcision]{Procedures} is Male Circumcision
[reflects]{Physiology} is Reflecting
[unprepared]{Concepts & Ideas} is Unprepared
[UK]{Geographic Areas} is UK
|
[Zinc transporter] [ZIP10] forms a heteromer with [ZIP6] which [regulates] [embryonic development] and [cell migration]
There is growing evidence that [zinc] and its [transporters] are involved in [cell migration] during [development] and in [cancer]. In the present [study], we show that [zinc transporter] [ZIP10] ([SLC39A10]) stimulates [cell motility] and [proliferation], both in [mammalian cells] and in the [zebrafish] [embryo]. This is associated with [inactivation] of [GSK-3α] and [-3ß] and [downregulation] of [E-cadherin] ([CDH1]). [Morpholino] -mediated [knock-down] of [zip10] causes delayed [epiboly] and deformities of the [head], [eye], [heart] and [tail]. Furthermore, [zip10] deficiency results in [overexpression] of [cdh1], [zip6] and [stat3], the latter [gene product] driving [transcription] of both [zip6] and [zip10] The non-reduntant requirement of [Zip6] and [Zip10] for [epithelial to mesenchymal transition] ([EMT]) is consistent with our [finding] that they exist as a heteromer. We postulate that a [subset] of [ZIPs] carrying [PrP-like ectodomains], including [ZIP6] and [ZIP10], are integral to [cellular] [pathways] and [plasticity] programs, such as [EMT].
|
[Zinc transporter]{Chemicals & Drugs} is Zinc transporter
[ZIP10]{Chemicals & Drugs} is ZIP10 protein, human
[ZIP6]{Chemicals & Drugs} is Zinc Transporter ZIP6
[regulates]{Phenomena} is Regulation
[embryonic development]{Physiology} is Embryonic Development
[cell migration]{Physiology} is Cell Migration
[Zinc transporter]{Chemicals & Drugs} is Zinc transporter
[ZIP10]{Chemicals & Drugs} is ZIP10 protein, human
[zinc]{Chemicals & Drugs} is Zn - Zinc
[transporters]{Chemicals & Drugs} is Zinc transporter
[ZIP6]{Chemicals & Drugs} is Zinc Transporter ZIP6
[regulates]{Phenomena} is Regulation
[embryonic development]{Physiology} is Embryonic Development
[cell migration]{Physiology} is Cell Migration
[cell migration]{Physiology} is Cell Migration
[development]{Physiology} is Developmental
[cancer]{Disorders} is CA - Cancer
[study]{Procedures} is Study
[zinc transporter]{Chemicals & Drugs} is Zinc transporter
[ZIP10]{Chemicals & Drugs} is ZIP10 protein, human
[SLC39A10]{Chemicals & Drugs} is ZIP10 protein, human
[cell motility]{Physiology} is Cell motility
[proliferation]{Physiology} is Cell proliferation
[mammalian cells]{Anatomy} is Mammalian Cell
[zebrafish]{Living Beings} is Zebrafish
[embryo]{Anatomy} is Embryos
[inactivation]{Physiology} is Molecular inactivation
[GSK-3α]{Chemicals & Drugs} is GSK-3 Alpha
[-3ß]{Chemicals & Drugs} is GSK-3 Beta
[downregulation]{Physiology} is Downregulation
[E-cadherin]{Chemicals & Drugs} is E-cadherin
[CDH1]{Chemicals & Drugs} is CDH1
[Morpholino]{Chemicals & Drugs} is Morpholino
[knock-down]{Procedures} is Gene Knock-Down
[zip10]{Genes & Molecular Sequences} is SLC39A10
[epiboly]{Physiology} is Epiboly
[head]{Anatomy} is Heads
[eye]{Anatomy} is Eyes
[heart]{Anatomy} is Hearts
[tail]{Anatomy} is Tail
[zip10]{Chemicals & Drugs} is ZIP10 protein, human
[overexpression]{Physiology} is Overexpression
[cdh1]{Chemicals & Drugs} is CDH1
[zip6]{Chemicals & Drugs} is Zinc Transporter ZIP6
[stat3]{Chemicals & Drugs} is STAT3
[gene product]{Chemicals & Drugs} is Protein
[transcription]{Physiology} is Gene Transcription
[zip6]{Chemicals & Drugs} is Zinc Transporter ZIP6
[zip10]{Chemicals & Drugs} is ZIP10 protein, human
[Zip6]{Chemicals & Drugs} is Zinc Transporter ZIP6
[Zip10]{Chemicals & Drugs} is ZIP10 protein, human
[epithelial to mesenchymal transition]{Physiology} is Mesenchymal to epithelial transition
[EMT]{Physiology} is Mesenchymal to epithelial transition
[finding]{Disorders} is Finding (finding)
[subset]{Concepts & Ideas} is Subset
[ZIPs]{Chemicals & Drugs} is ZIP protein, human
[PrP-like ectodomains]{Genes & Molecular Sequences} is Protein Domains
[ZIP6]{Chemicals & Drugs} is Zinc Transporter ZIP6
[ZIP10]{Chemicals & Drugs} is ZIP10 protein, human
[cellular]{Procedures} is Cellular
[pathways]{Physiology} is Pathways
[plasticity]{Physiology} is Cell Plasticity
[EMT]{Physiology} is Mesenchymal to epithelial transition
|
Demographics, Health, and Risk Behaviors of Young Adults Who [Drink] [Energy Drinks] and [Coffee] [Beverages]
[Objective]: The [present] [study] investigates risk behaviors, sleep habits, and mental health factors associated with caffeinated beverage use in young adults. Materials and [Methods]: [Students] from a [midsize private university] (n = 159) completed a 15- minute anonymous [questionnaire], including questions on risk behaviors, sleep habits, alcohol, and caffeine consumption. We compared behaviors between the top ∼15% ("high end") of [energy drink] [users] (≥3/ month) and [coffee] [users] (≥16/ month) to those with less frequent or no caffeine consumption. Results: Caffeine consumption was frequent among young adults. In the last month, 36% of [students] had an [energy drink], 69% had [coffee] or [espresso], and 86% reported having any [caffeine]; however, the majority of [students] were unaware of the [caffeine] content in these [beverages]. High-end [energy drink] [consumers] reported more risk-taking behaviors (increased drug and alcohol use and less frequent [seat belt use]), [sleep disturbances] (later bedtimes, [harder time falling asleep], and more all-nighters), and higher frequency of [mental illness] [diagnoses] than those who consumed fewer [energy drinks]. In contrast, the frequency of most risk behaviors, [sleep disturbances], and [mental illness] [diagnoses] was not significantly different between the [high-end and general population] of [coffee] [drinkers]. Conclusion: [Students] with delayed [sleep patterns], [mental illness], and higher frequency of [substance use] and risk behaviors were more likely to be regular [energy drink] [users] but not [regular coffee drinkers]. It is unclear whether the [psychoactive] content in [energy drinks] results in different behavioral effects than just [caffeine] in [coffee], and/or different [personality] / [health populations] are drawn to the two types of [beverages].
|
[Drink]{Objects} is Drink
[Energy Drinks]{Objects} is Energy Drinks
[Coffee]{Objects} is Coffee
[Beverages]{Objects} is Beverages
[Objective]{Concepts & Ideas} is Objective
[present]{Disorders} is Present
[study]{Procedures} is Study
[Drink]{Objects} is Drink
[Energy Drinks]{Objects} is Energy Drinks
[Coffee]{Objects} is Coffee
[Beverages]{Objects} is Beverages
[Methods]{Concepts & Ideas} is Methods
[Students]{Living Beings} is Students
[midsize private university]{Organizations} is University
[questionnaire]{Concepts & Ideas} is Questionnaire
[energy drink]{Objects} is Energy Drinks
[users]{Living Beings} is Users
[coffee]{Objects} is Coffee
[users]{Living Beings} is Users
[students]{Living Beings} is Students
[energy drink]{Objects} is Energy Drinks
[coffee]{Objects} is Coffee
[espresso]{Objects} is Food or Food Substance
[caffeine]{Chemicals & Drugs} is Caffeine
[students]{Living Beings} is Students
[caffeine]{Chemicals & Drugs} is Caffeine
[beverages]{Objects} is Beverages
[energy drink]{Objects} is Energy Drinks
[consumers]{Living Beings} is Group (social concept)
[seat belt use]{Disorders} is Wearing seat belt
[sleep disturbances]{Disorders} is Sleep disturbances
[harder time falling asleep]{Disorders} is Trouble falling asleep
[mental illness]{Disorders} is Mental illness
[diagnoses]{Disorders} is Diagnoses
[energy drinks]{Objects} is Energy Drinks
[sleep disturbances]{Disorders} is Sleep disturbances
[mental illness]{Disorders} is Mental illness
[diagnoses]{Disorders} is Diagnoses
[high-end and general population]{Living Beings} is Group (social concept)
[coffee]{Objects} is Coffee
[drinkers]{Disorders} is Drinker
[Students]{Living Beings} is Students
[sleep patterns]{Disorders} is Abnormal sleep patterns
[mental illness]{Disorders} is Mental illness
[substance use]{Disorders} is Substance use
[energy drink]{Objects} is Energy Drinks
[users]{Living Beings} is Users
[regular coffee drinkers]{Disorders} is Excessive coffee drinker
[psychoactive]{Chemicals & Drugs} is Psychoactive Drugs
[energy drinks]{Objects} is Energy Drinks
[caffeine]{Chemicals & Drugs} is Caffeine
[coffee]{Objects} is Coffee
[personality]{Physiology} is Personality
[health populations]{Living Beings} is Group (social concept)
[beverages]{Objects} is Beverages
|
[Phytoplankton] production and taxon - specific growth rates in the [Costa Rica Dome]
During summer 2010, we investigated [phytoplankton] production and growth rates at 19 stations in the eastern tropical Pacific, where winds and strong opposing currents generate the [Costa Rica Dome] ([CRD]), an [open] - [ocean] upwelling feature. Primary production ([(14)C] - incorporation) and group-specific [growth] and net growth rates (two-treatment seawater [dilution method]) were estimated from [samples] [incubated] [in situ] at eight [depths]. Our cruise coincided with a mild El Niño event, and only weak upwelling was observed in the [CRD]. Nevertheless, the highest [phytoplankton] abundances were found near the dome [center]. However, [mixed-layer] growth rates were lowest in the dome [center] (∼0.5-0.9 day(-1)), but higher on the edge of the dome (∼0.9-1.0 day(-1)) and in [adjacent] [coastal waters] (0.9-1.3 day(-1)). We found good agreement between independent methods to estimate growth rates. [Mixed-layer] growth rates of [Prochlorococcus] and [Synechococcus] were largely balanced by mortality, whereas [eukaryotic phytoplankton] showed [positive] [net growth] (∼0.5-0.6 day(-1)), that is, [growth] available to support larger ([mesozooplankton]) consumer biomass. These are the first group-specific [phytoplankton] rate estimates in this [region], and they demonstrate that integrated primary production is high, exceeding 1 g C m(-2) day(-1) on average, even during a period of reduced upwelling.
|
[Phytoplankton]{Living Beings} is Phytoplankton
[Costa Rica Dome]{Geographic Areas} is Costa Rica
[Phytoplankton]{Living Beings} is Phytoplankton
[phytoplankton]{Living Beings} is Phytoplankton
[Costa Rica Dome]{Geographic Areas} is Costa Rica
[Costa Rica Dome]{Geographic Areas} is Costa Rica
[CRD]{Geographic Areas} is Costa Rica
[open]{Concepts & Ideas} is Open
[ocean]{Geographic Areas} is Oceans
[(14)C]{Chemicals & Drugs} is Carbon-14
[growth]{Physiology} is Plant Development
[dilution method]{Procedures} is Dilution
[samples]{Living Beings} is Chlorophyte/embryophyte group
[incubated]{Procedures} is Incubated
[in situ]{Concepts & Ideas} is In Situ
[depths]{Concepts & Ideas} is Depth
[CRD]{Geographic Areas} is Costa Rica
[phytoplankton]{Living Beings} is Phytoplankton
[center]{Concepts & Ideas} is Center
[mixed-layer]{Concepts & Ideas} is Space
[center]{Concepts & Ideas} is Center
[adjacent]{Concepts & Ideas} is Adjacent
[coastal waters]{Geographic Areas} is Coastal water
[Mixed-layer]{Concepts & Ideas} is Space
[Prochlorococcus]{Living Beings} is Genus Prochlorococcus
[Synechococcus]{Living Beings} is Synechococcus
[eukaryotic phytoplankton]{Living Beings} is Phytoplankton
[positive]{Disorders} is Positive for
[net growth]{Physiology} is 'growth'
[growth]{Physiology} is Plant Development
[mesozooplankton]{Living Beings} is Zooplankton
[phytoplankton]{Living Beings} is Phytoplankton
[region]{Geographic Areas} is Region
|
Incidence and Impact of Patient - [Prosthesis] Mismatch in [Isolated Aortic Valve Surgery]
The mains topics of this work are the incidence of patient - [prosthesis] mismatch and the influence in the early results of [isolated aortic valve surgery]. In 193 patients [isolated aortic valve surgery] was performed. The [study population] was divided in three [subgroups]: 20 patients with severe, 131 patients with moderate and 42 patients without patient - [prosthesis] mismatch. The [indexed] effective orifice area was used to define the [subgroups]. Operative mortality and [perioperative complications] were considered the indicators of the early results of [aortic valve surgery]. The incidence of severe and moderate patient - [prosthesis] mismatch was respectively 10.3% and 67.8%. Hospital mortality and [perioperative complications] were: mortality 5% vs. 3.1% vs. 2.4% (p = 0.855), [low cardiac output] 5% vs. 6.9% vs. 4.8% (p = 0.861); [pulmonary complications] 5% vs. 3.1 vs. 0.0% (p = 0.430); [exploration] for [bleeding] 5% vs. 0.8% vs. 2.4% (p = 0.319); [atrial fibrillation] 30% vs. 19.8% vs. 11.9% (p = 0.225); [wound infection] 5% vs. 0.8% vs. 0.00% (p = 0.165), respectively for the group with severe, moderate and without patient - [prosthesis] mismatch. Patient - [prosthesis] mismatch is a common occurrence in [aortic valve surgery]. This phenomenon does not affect the early results of [aortic valve surgery].
|
[Prosthesis]{Devices} is Prosthesis, device
[Isolated Aortic Valve Surgery]{Procedures} is Aortic valve replacement
[Prosthesis]{Devices} is Prosthesis, device
[Isolated Aortic Valve Surgery]{Procedures} is Aortic valve replacement
[prosthesis]{Devices} is Prosthesis, device
[isolated aortic valve surgery]{Procedures} is Aortic valve replacement
[isolated aortic valve surgery]{Procedures} is Aortic valve replacement
[study population]{Living Beings} is Study Population
[subgroups]{Concepts & Ideas} is Subgroup
[prosthesis]{Devices} is Prosthesis, device
[indexed]{Concepts & Ideas} is Indexes as Topic
[subgroups]{Concepts & Ideas} is Subgroup
[perioperative complications]{Disorders} is Peroperative Complications
[aortic valve surgery]{Procedures} is Aortic valve replacement
[prosthesis]{Devices} is Prosthesis, device
[perioperative complications]{Disorders} is Peroperative Complications
[low cardiac output]{Disorders} is Low Cardiac Output
[pulmonary complications]{Disorders} is Pulmonary Complication
[exploration]{Procedures} is Exploration
[bleeding]{Disorders} is Bleeding
[atrial fibrillation]{Disorders} is Fibrillation atrial
[wound infection]{Disorders} is Wound infection
[prosthesis]{Devices} is Prosthesis, device
[prosthesis]{Devices} is Prosthesis, device
[aortic valve surgery]{Procedures} is Aortic valve replacement
[aortic valve surgery]{Procedures} is Aortic valve replacement
|
Nutrient Intakes in Early Life and Risk of [Obesity]
There is increasing evidence that environmental factors in early life predict later health. The early adiposity rebound recorded in most [obese] [subjects] suggests that factors promoting [body fat] [development] have operated in the first years of life. Birth weight, growth velocity and [body mass index] ([BMI]) trajectories seem to be highly sensitive to the [environmental] conditions [present] during [pregnancy] and in early life ("The first 1000 days "). Particularly, nutritional exposure can have a long-term effect on health in adulthood. The [high protein-low fat diet] often recorded in young children may have contributed to the rapid rise of childhood [obesity] prevalence during the last decades. Metabolic programming by early [nutrition] could explain the [development] of later [obesity] and [adult diseases].
|
[Obesity]{Disorders} is Obesity (disorder)
[Obesity]{Disorders} is Obesity (disorder)
[obese]{Disorders} is Obesity (disorder)
[subjects]{Living Beings} is Subject
[body fat]{Physiology} is Body Fat
[development]{Physiology} is Development aspects
[body mass index]{Physiology} is Body Mass Index
[BMI]{Physiology} is Body Mass Index
[environmental]{Concepts & Ideas} is Environmental
[present]{Disorders} is Present
[pregnancy]{Physiology} is Pregnancy
[high protein-low fat diet]{Objects} is Diet
[obesity]{Disorders} is Obesity (disorder)
[nutrition]{Physiology} is Nutrition
[development]{Physiology} is Development aspects
[obesity]{Disorders} is Obesity (disorder)
[adult diseases]{Disorders} is Adult disease
|
Characteristics of the fibroplasia and [collagen] [expression] in the [abdominal wall] after [implant] of the [polypropylene mesh] and [polypropylene] / [polyglecaprone mesh] in [rats]
To compare fibroplasia and the [resistance] of the [abdominal wall] when [polypropylene meshes] and [polypropylene] / [poliglecaprone] are used. Seventy-seven male [Wistar rats] were divided into three [groups]: Control Group (for [resistance]); [Group E] ([polypropylene mesh]); and [Group U] ([polypropylene] / [poliglecaprone mesh]). The [animals] in [Groups E] and [U] had a standard [muscular] and aponeurotic defect, with [integral] [peritoneum], and correction with the [mesh]. Measurements were taken 4, 7, 14, 28 and 56 days after [surgery]. The [resistance], and [collagen] density were [studied]. [Resistance] on the 56th day was similar in both [meshes]. The gain in [resistance] described an ascending [curve] for the [polypropylene mesh] and was irregular in the case of the [polypropylene] / [poliglecaprone]. Fibroplasia showed a gain in [type I] and [type III collagen] in both [groups] (p<0.001). [Collagen III] [stabilized] in the 14th day and [collagen I] continued to ascend. The gain in [resistance] of the [polypropylene mesh] is regular and ascending, whereas the [polypropylene] / [poliglecaprone] is not regular. The final [resistance] of both [meshes] is similar; the [collagen] density increases over time, and show the same inflammatory potential.
|
[collagen]{Chemicals & Drugs} is Collagen
[expression]{Physiology} is Protein expression
[abdominal wall]{Anatomy} is Abdominal Wall
[implant]{Procedures} is Implant
[polypropylene mesh]{Chemicals & Drugs} is Polypropylene mesh
[polypropylene]{Chemicals & Drugs} is Polypropylene mesh
[polyglecaprone mesh]{Chemicals & Drugs} is Polyglecaprone 25
[rats]{Living Beings} is Mammals, Rats
[resistance]{Physiology} is Resistance Process
[collagen]{Chemicals & Drugs} is Collagen
[expression]{Physiology} is Protein expression
[abdominal wall]{Anatomy} is Abdominal Wall
[abdominal wall]{Anatomy} is Abdominal Wall
[polypropylene meshes]{Chemicals & Drugs} is Polypropylene mesh
[implant]{Procedures} is Implant
[polypropylene]{Chemicals & Drugs} is Polypropylene mesh
[polypropylene mesh]{Chemicals & Drugs} is Polypropylene mesh
[poliglecaprone]{Chemicals & Drugs} is Polyglecaprone 25
[polypropylene]{Chemicals & Drugs} is Polypropylene mesh
[polyglecaprone mesh]{Chemicals & Drugs} is Polyglecaprone 25
[Wistar rats]{Living Beings} is Wistar Rats
[rats]{Living Beings} is Mammals, Rats
[groups]{Living Beings} is Study Population (group)
[resistance]{Physiology} is Resistance Process
[Group E]{Living Beings} is Study Population (group)
[polypropylene mesh]{Chemicals & Drugs} is Polypropylene mesh
[Group U]{Living Beings} is Study Population (group)
[polypropylene]{Chemicals & Drugs} is Polypropylene mesh
[poliglecaprone mesh]{Chemicals & Drugs} is Polyglecaprone 25
[animals]{Living Beings} is Animals
[Groups E]{Living Beings} is Study Population (group)
[U]{Living Beings} is Study Population (group)
[muscular]{Anatomy} is Muscular
[integral]{Concepts & Ideas} is Internal
[peritoneum]{Anatomy} is Peritoneum
[mesh]{Devices} is SURG MESH
[surgery]{Procedures} is Surgery
[resistance]{Physiology} is Resistance Process
[collagen]{Chemicals & Drugs} is Collagen
[studied]{Procedures} is Study
[Resistance]{Physiology} is Resistance Process
[meshes]{Devices} is SURG MESH
[resistance]{Physiology} is Resistance Process
[curve]{Concepts & Ideas} is Curve
[polypropylene mesh]{Chemicals & Drugs} is Polypropylene mesh
[polypropylene]{Chemicals & Drugs} is Polypropylene mesh
[poliglecaprone]{Chemicals & Drugs} is Polyglecaprone 25
[type I]{Chemicals & Drugs} is Type I Collagen
[type III collagen]{Chemicals & Drugs} is Collagen type III
[groups]{Living Beings} is Study Population (group)
[Collagen III]{Chemicals & Drugs} is Collagen type III
[stabilized]{Disorders} is Stabilized
[collagen I]{Chemicals & Drugs} is Type I Collagen
[resistance]{Physiology} is Resistance Process
[polypropylene mesh]{Chemicals & Drugs} is Polypropylene mesh
[polypropylene]{Chemicals & Drugs} is Polypropylene mesh
[poliglecaprone]{Chemicals & Drugs} is Polyglecaprone 25
[resistance]{Physiology} is Resistance Process
[meshes]{Devices} is SURG MESH
[collagen]{Chemicals & Drugs} is Collagen
|
[Clinical evaluation] of the [AutoPulse] [automated chest compression device] for [out-of-hospital cardiac arrest] in the [northern] district of [Shanghai], [China]
Whether the [AutoPulse] [automated chest compression device] is worthy of clinical use for [out-of-hospital cardiac arrest] ([OHCA]) remains controversial. A [prospective controlled study] was conducted to [evaluate] the effect of [AutoPulse] versus manual [chest] [compression] for [cardiopulmonary resuscitation] ([CPR]) of [OHCA] patients in the [northern] district of [Shanghai], [China]. A total of 133 patients with [OHCA] who were treated at the [Emergency Medical Center of the Tenth People's Hospital] Affiliated with [Tongji University] between March 2011 and March 2012 were included. The patients were randomly assigned to the Manual [CPR] (n = 64) and [AutoPulse] [CPR] groups (n = 69) in accordance with the approach of [chest] [compression] received. The primary outcome measure was return of spontaneous circulation (ROSC), and the secondary outcome measures included 24-h survival rate, hospital discharge rate, and neurological [prognosis] at [hospital discharge]. The ROSC rate of patients with [OHCA] was significantly higher in the [AutoPulse] [CPR] group than in the Manual [CPR] group (44.9% vs. 23.4%; p = 0.009). The 24-h survival rate of [OHCA] patients was significantly higher in the [AutoPulse] [CPR] group than in the Manual [CPR] group (39.1% vs. 21.9%; p = 0.03). The hospital discharge rate of the patients with [OHCA] was significantly higher in the [AutoPulse] [CPR] group than in the Manual [CPR] group (18.8% vs. 6.3%; p = 0.03). The proportion of patients with [OHCA] and a cerebral performance category score of 1 or 2 points at [hospital discharge] was higher in the [AutoPulse] [CPR] group than in the Manual [CPR] group, but the difference was not statistically significant (16.2% vs. 13.4%, p = 1.00). Use of the [AutoPulse] increases [CPR] success and survival rates in patients with [OHCA], but its ability to [improve] [cerebral] performance requires further [evaluation].
|
[Clinical evaluation]{Procedures} is Clinical Evaluation
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[automated chest compression device]{Devices} is Cardiopulmonary resuscitator
[out-of-hospital cardiac arrest]{Disorders} is Out-of-Hospital Cardiac Arrest
[northern]{Concepts & Ideas} is Northern
[Shanghai]{Geographic Areas} is Area
[China]{Geographic Areas} is China
[Clinical evaluation]{Procedures} is Clinical Evaluation
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[automated chest compression device]{Devices} is Cardiopulmonary resuscitator
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[automated chest compression device]{Devices} is Cardiopulmonary resuscitator
[out-of-hospital cardiac arrest]{Disorders} is Out-of-Hospital Cardiac Arrest
[out-of-hospital cardiac arrest]{Disorders} is Out-of-Hospital Cardiac Arrest
[northern]{Concepts & Ideas} is Northern
[OHCA]{Disorders} is Out-of-Hospital Cardiac Arrest
[Shanghai]{Geographic Areas} is Area
[China]{Geographic Areas} is China
[prospective controlled study]{Procedures} is Study, Prospective
[evaluate]{Procedures} is Evaluate
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[chest]{Anatomy} is Chest
[compression]{Procedures} is Compression
[cardiopulmonary resuscitation]{Procedures} is Cardiopulmonary Resuscitation
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[OHCA]{Disorders} is Out-of-Hospital Cardiac Arrest
[northern]{Concepts & Ideas} is Northern
[Shanghai]{Geographic Areas} is Area
[China]{Geographic Areas} is China
[OHCA]{Disorders} is Out-of-Hospital Cardiac Arrest
[Emergency Medical Center of the Tenth People's Hospital]{Organizations} is Hospital
[Tongji University]{Organizations} is University Hospitals
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[chest]{Anatomy} is Chest
[compression]{Procedures} is Compression
[prognosis]{Procedures} is Prognosis
[hospital discharge]{Procedures} is Discharge from hospital
[OHCA]{Disorders} is Out-of-Hospital Cardiac Arrest
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[OHCA]{Disorders} is Out-of-Hospital Cardiac Arrest
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[OHCA]{Disorders} is Out-of-Hospital Cardiac Arrest
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[OHCA]{Disorders} is Out-of-Hospital Cardiac Arrest
[hospital discharge]{Procedures} is Discharge from hospital
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[AutoPulse]{Devices} is Cardiopulmonary resuscitator
[CPR]{Procedures} is Cardiopulmonary Resuscitation
[OHCA]{Disorders} is Out-of-Hospital Cardiac Arrest
[improve]{Disorders} is Improved
[cerebral]{Anatomy} is Brains
[evaluation]{Procedures} is Evaluate
|
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