Institution
University of Arkansas for Medical Sciences
Education•Little Rock, Arkansas, United States•
About: University of Arkansas for Medical Sciences is a education organization based out in Little Rock, Arkansas, United States. It is known for research contribution in the topics: Population & Health care. The organization has 14077 authors who have published 26012 publications receiving 973592 citations. The organization is also known as: UAMS.
Topics: Population, Health care, Medicine, Poison control, Multiple myeloma
Papers published on a yearly basis
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TL;DR: The development and testing of an instrument to measure sleep in critically ill patients and the data provide support for the reliability and validity of the Richards-Campbell Sleep Questionnaire.
Abstract: Research to evaluate interventions to promote sleep in critically ill patients has been restricted by the lack of brief, inexpensive outcome measures. This article describes the development and testing of an instrument to measure sleep in critically ill patients. A convenience sample of 70 alert, oriented, critically ill males was studied using polysomnography (PSG), the gold standard for sleep measurement, for one night. In the morning the patients completed the Richards-Campbell Sleep Questionnaire (RCSQ), a five-item visual analog scale. Internal consistency reliability of the RCSQ was .90 and principal components factor analysis revealed a single factor (Eigenvalue = 3.61, percent variance = 72.2). The RCSQ total score accounted for approximately 33% of the variance in the PSG indicator sleep efficiency index (p < .001). The data provide support for the reliability and validity of the RCSQ.
301 citations
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TL;DR: The results of this study suggest that a highly varied diet in elderly nursing home residents is associated with better nutritional status as assessed by nutrient intake, biochemical measures, and body composition measures.
Abstract: Objective A narrow range of food choices may lead to dietary inadequacies, a particular concern in elderly people. We hypothesized that consumption of a more diverse diet would predict better nutritional status in frail elderly persons. Subjects Subjects included 98 frail nursing home residents (36 men, 62 women), mean age 87.1±5.5 (72 to 98) years. Methods 3-day dietary variety scores ranging from 23 to 48 and fruit and vegetable variety scores ranging from 5 to 20 were calculated from weighed 3-day food records as the number of different food or fruit and vegetable choices consumed. A higher score indicates a more varied diet. Nutritional status was assessed by weight, height, body mass index (BMI), skinfold thickness, circumference measures, calculated mean arm muscle area, total body water, computerized tomography of the thigh, and total body potassium, as well as nutritional analysis, biochemical measures, and subject medical history. Statistical methods Univariate regression analyses were performed to investigate the relationship between clinical and nutrition variables. Multiple linear regressions were used to develop models relating dietary variety scores to possible etiologic factors as well as indicators of nutritional status. Models were controlled for age, BMI, and energy intake when appropriate. Results Mean dietary variety score was 35.2±4.5, and mean fruit and vegetable variety score was 11.3±3.0. Higher dietary variety score was associated with higher energy intake (β=20.5, P P ≤.05). High dietary variety score was related to high fruit and vegetable variety score and total intake of fruits and vegetables. In men, higher dietary variety score and fruit and vegetable variety score were associated with higher high-density lipoprotein (β=1.02), lower very-low-density lipoprotein (β=−3.58) and triglycerol (β=−3.51), and higher blood folate (β=4.72) concentrations in women ( P ≤.05). In women, high dietary variety score was associated with higher BMI (β=0.34, P P =.02); high fruit and vegetable variety score was associated with higher BMI (β=0.41), mid-arm circumference (β=0.34), and mid-arm muscle area (β=2.94) ( P ≤.03). Dietary variety score was higher (mean 37.6±5.38 vs 34.6±4.14) in those who received assistance with feeding (β=2.67, P =.01). History of cancer (β=−2.04) and gastrointenstinal cancer (β=−3.54) were associated with low dietary variety score ( P ≤.05). Conclusions The results of this study suggest that a highly varied diet in elderly nursing home residents is associated with better nutritional status as assessed by nutrient intake, biochemical measures, and body composition measures. Dietary variety score is a straightforward tool for screening and identifying people at nutritional risk, as well as a mechanism for monitoring response to nutritional, medical, and environmental interventions. Preventive measures to improve dietary variety, as measured by the dietary variety score, should be evaluated and introduced before nutrition and health complications arise. J Am Diet Assoc. 2002;102:1096–1104.
301 citations
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TL;DR: Evidence is provided for a direct role of the JNK pathway in apoptotic regulation through Bcl-2/Bcl-XL phosphorylation through antisense oligonucleotides in KB-3 cells treated with vinblastine.
300 citations
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TL;DR: There were significant age-dependent increases in both cortical width and cancellous bone volume, the latter being due to an increase in trabecular thickness, and the lowest coefficients of variation were found for structural measures, as well as mineral apposition rate and wall thickness.
299 citations
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Centre Hospitalier Universitaire Sainte-Justine1, University of Washington2, Université de Montréal3, Montreal Neurological Institute and Hospital4, McGill University5, Children's Mercy Hospital6, GeneDx7, Baylor College of Medicine8, University of Toronto9, Toronto Western Hospital10, University of Melbourne11, Western General Hospital12, University Hospitals Bristol NHS Foundation Trust13, London North West Healthcare NHS Trust14, Nuffield Orthopaedic Centre15, Central Manchester University Hospitals NHS Foundation Trust16, University Hospital of Wales17, Cardiff University18, Great Ormond Street Hospital19, Leeds Teaching Hospitals NHS Trust20, State University of New York Upstate Medical University21, University Medical Center Groningen22, University of South Dakota23, Columbia University Medical Center24, Baptist Memorial Hospital-Memphis25, Boston Children's Hospital26, Washington University in St. Louis27, Radboud University Nijmegen28, University of Burgundy29, Tartu University Hospital30, Broad Institute31, Nationwide Children's Hospital32, Children's Hospital of Eastern Ontario33, University of Tasmania34, Walter and Eliza Hall Institute of Medical Research35, Children's Hospital at Westmead36, Sapienza University of Rome37, Istituto Superiore di Sanità38, Wolfson Medical Center39, University of Oklahoma Health Sciences Center40, University of British Columbia41, Pierre-and-Marie-Curie University42, Paris Diderot University43, Joint Genome Institute44, University of Alabama at Birmingham45, University of Arkansas for Medical Sciences46, Centre Hospitalier Universitaire de Sherbrooke47, University of Otago48, Université du Québec à Chicoutimi49, Florey Institute of Neuroscience and Mental Health50, Royal Children's Hospital51, University of Texas Southwestern Medical Center52
TL;DR: De novo missense variants explained a larger proportion of individuals in the series than in other series that were primarily ascertained because of ID, indicating that the genetic landscape of DEE might be different from that of ID without epilepsy.
Abstract: Developmental and epileptic encephalopathy (DEE) is a group of conditions characterized by the co-occurrence of epilepsy and intellectual disability (ID), typically with developmental plateauing or regression associated with frequent epileptiform activity. The cause of DEE remains unknown in the majority of cases. We performed whole-genome sequencing (WGS) in 197 individuals with unexplained DEE and pharmaco-resistant seizures and in their unaffected parents. We focused our attention on de novo mutations (DNMs) and identified candidate genes containing such variants. We sought to identify additional subjects with DNMs in these genes by performing targeted sequencing in another series of individuals with DEE and by mining various sequencing datasets. We also performed meta-analyses to document enrichment of DNMs in candidate genes by leveraging our WGS dataset with those of several DEE and ID series. By combining these strategies, we were able to provide a causal link between DEE and the following genes: NTRK2, GABRB2, CLTC, DHDDS, NUS1, RAB11A, GABBR2, and SNAP25. Overall, we established a molecular diagnosis in 63/197 (32%) individuals in our WGS series. The main cause of DEE in these individuals was de novo point mutations (53/63 solved cases), followed by inherited mutations (6/63 solved cases) and de novo CNVs (4/63 solved cases). De novo missense variants explained a larger proportion of individuals in our series than in other series that were primarily ascertained because of ID. Moreover, these DNMs were more frequently recurrent than those identified in ID series. These observations indicate that the genetic landscape of DEE might be different from that of ID without epilepsy.
299 citations
Authors
Showing all 14187 results
Name | H-index | Papers | Citations |
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Hagop M. Kantarjian | 204 | 3708 | 210208 |
Yusuke Nakamura | 179 | 2076 | 160313 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
David R. Williams | 178 | 2034 | 138789 |
Yang Yang | 171 | 2644 | 153049 |
John E. Morley | 154 | 1377 | 97021 |
Jeffrey L. Cummings | 148 | 833 | 116067 |
Hugh A. Sampson | 147 | 816 | 76492 |
Michael J. Keating | 140 | 1169 | 76353 |
Kristine Yaffe | 136 | 794 | 72250 |
Nancy J. Cox | 135 | 778 | 109195 |
Stephen W. Scherer | 135 | 685 | 85752 |
Nikhil C. Munshi | 134 | 906 | 67349 |
Siamon Gordon | 131 | 420 | 77948 |
Jian-Guo Bian | 128 | 1219 | 80964 |