Institution
University of Alabama at Birmingham
Education•Birmingham, Alabama, United States•
About: University of Alabama at Birmingham is a education organization based out in Birmingham, Alabama, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 38523 authors who have published 86775 publications receiving 3930642 citations. The organization is also known as: UAB & The University of Alabama at Birmingham.
Topics: Population, Poison control, Transplantation, Health care, Immune system
Papers published on a yearly basis
Papers
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TL;DR: Exposure to violence among youth is clearly significant to their reporting of PTSD symptomatology, yet the clinical implications of this relationship remain largely unexplored.
Abstract: The objective of this study was to examine the relationship between chronic exposure to community violence and post-traumatic stress disorder (PTSD) symptoms in a nonrandom sample (N = 221) of low-income African-American youth between 7 and 18 years old. Results showed males were more likely than females to be victims of and witnesses to violent acts; there were no other significant sociodemographic differences in the degree of exposure to violence. PTSD symptom reporting was moderately high for this sample of youth; 54 youth (27.1%) met all three of the diagnostic criteria considered. Regression analyses revealed that being victimized and witnessing violence were significantly related to the reporting of PTSD symptoms. These symptoms were more extreme among victimized females and victimized youth who had no primary males living with them in the household (i.e., fathers and/or brothers). Exposure to violence among youth is clearly significant to their reporting of PTSD symptomatology, yet the clinical implications of this relationship remain largely unexplored.
708 citations
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TL;DR: It is found that exposure of mice and rats to male but not female experimenters produces pain inhibition, and experimenter sex can affect apparent baseline responses in behavioral testing.
Abstract: We found that exposure of mice and rats to male but not female experimenters produces pain inhibition. Male-related stimuli induced a robust physiological stress response that results in stress-induced analgesia. This effect could be replicated with T-shirts worn by men, bedding material from gonadally intact and unfamiliar male mammals, and presentation of compounds secreted from the human axilla. Experimenter sex can thus affect apparent baseline responses in behavioral testing.
705 citations
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TL;DR: A number of alterations, both directly and indirectly related to hepatic injury and portal hypertension, result in the production or release of mediators into the venous circulation, where they influence the pulmonary microcirculation in experimental hepatopulmonary syndrome.
Abstract: ⇓“The tantalizing problem of the connective link in cirrhotic patients between oxygen unsaturation and possible arteriovenous shunting in the lungs remains unsolved, and any relation between arterial unsaturation and pulmonary vasodilation remains obscure.”
Fig. 1.—
Working model of molecular alterations in the pulmonary microcirculation in experimental hepatopulmonary syndrome (HPS). a) In the normal microvasculature, a balance of vasoconstrictive and vasodilatory factors, including paracrine endothelin (ET)-1-mediated vasoconstriction through the ETA receptor (▪) on smooth muscle cells (SMCs) and ET-1-mediated vasodilatation mediated through the ETB receptor (□) linked to endothelial nitric oxide synthase (eNOS) in endothelial cells (ECs), maintain tone. b) During the development of HPS, a number of alterations, both directly and indirectly related to hepatic injury and portal hypertension, result in the production or release of mediators into the venous circulation, where they influence the pulmonary microcirculation. Increased expression of pulmonary endothelial ETB receptors and increased hepatic production and release of ET-1 contribute to an increase in eNOS expression and enhanced nitric oxide (NO) production in the microvascular endothelium during the initiation of HPS. Tumour necrosis factor (TNF)-α-mediated accumulation of intravascular macrophage-like cells also occurs after chronic common bile duct ligation. Haem oxygenase (HO)-1 and inducible nitric oxide synthase (iNOS) expression increase in these cells and contribute to the progression of HPS. CO: carbon monoxide.
Fig. 2.—
Algorithm for screening and therapeutic decisions in hepatopulmonary syndrome (HPS). OLT: orthotopic liver transplantation; P a,O2: arterial oxygen tension; P A–a,O2: alveolar–arterial oxygen tension difference; CEE: contrast-enhanced echocardiography; PFT: pulmonary function test; MAA: macroaggregated albumin. #: high-resolution thoracic computed tomographic scanning is highly recommended in order to exclude chronic respiratory comorbid conditions; ¶: high risk for post-operative OLT mortality. 1 mmHg=0.133 kPa.
Fig. 3.—
Plot demonstrating the relationship between cardiac output ( Q ') and transpulmonary pressure gradient (TPG; mean pulmonary arterial …
705 citations
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TL;DR: Guidelines and recommendations developed and/or endorsed by the American College of Rheumatology are intended to provide guidance for particular patterns of practice and not to dictate the care of a particular patient.
Abstract: Guidelines and recommendations developed and/or endorsed by the American College of Rheumatology (ACR) are intended to provide guidance for particular patterns of practice and not to dictate the care of a particular patient The ACR considers adherence to these guidelines and recommendations to be voluntary, with the ultimate determination regarding their application to be made by the physician in light of each patient’s individual circumstances Guidelines and recommendations are intended to promote beneficial or desirable outcomes but cannot guarantee any specific outcome Guidelines and recommendations developed or endorsed by the ACR are subject to periodic revision as warranted by the evolution of medical knowledge, technology, and practice
704 citations
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Columbia University1, University of Oxford2, Indiana University – Purdue University Indianapolis3, Harvard University4, Massachusetts Institute of Technology5, University of Zulia6, University of California, Los Angeles7, University of Texas Health Science Center at Houston8, University of South Florida9, University of Rochester10, Boston Children's Hospital11, North Shore-LIJ Health System12, University of Southern California13, Mount Sinai Hospital14, University of California, Berkeley15, New York University16, National Institutes of Health17, University of California, Irvine18, University of Alabama at Birmingham19, Thomas Jefferson University20, University of Iowa21, City University of New York22, Oregon Health & Science University23, Albany Medical College24, University of Ulm25
TL;DR: A model estimated the components of additive genetic, shared environment, and nonshared environment variances confirming that approximately 40% of the variance remaining in onset age is attributable to genes other than the HD gene and 60% is environmental.
Abstract: Huntington's disease (HD) is an autosomal dominant neurodegenerative disease caused by a triplet (CAG) expansion mutation. The length of the triplet repeat is the most important factor in determining age of onset of HD, although substantial variability remains after controlling for repeat length. The Venezuelan HD kindreds encompass 18,149 individuals spanning 10 generations, 15,409 of whom are living. Of the 4,384 immortalized lymphocyte lines collected, 3,989 DNAs were genotyped for their HD alleles, representing a subset of the population at greatest genetic risk. There are 938 heterozygotes, 80 people with variably penetrant alleles, and 18 homozygotes. Analysis of the 83 kindreds that comprise the Venezuelan HD kindreds demonstrates that residual variability in age of onset has both genetic and environmental components. We created a residual age of onset phenotype from a regression analysis of the log of age of onset on repeat length. Familial correlations (correlation ± SE) were estimated for sibling (0.40 ± 0.09), parent-offspring (0.10 ± 0.11), avuncular (0.07 ± 0.11), and cousin (0.15 ± 0.10) pairs, suggesting a familial origin for the residual variance in onset. By using a variance-components approach with all available familial relationships, the additive genetic heritability of this residual age of onset trait is 38%. A model, including shared sibling environmental effects, estimated the components of additive genetic (0.37), shared environment (0.22), and nonshared environment (0.41) variances, confirming that ≈40% of the variance remaining in onset age is attributable to genes other than the HD gene and 60% is environmental.
704 citations
Authors
Showing all 38940 results
Name | H-index | Papers | Citations |
---|---|---|---|
Rudolf Jaenisch | 206 | 606 | 178436 |
Joel Schwartz | 183 | 1149 | 109985 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Jasvinder A. Singh | 176 | 2382 | 223370 |
Gregg L. Semenza | 168 | 502 | 130316 |
David R. Jacobs | 165 | 1262 | 113892 |
Hua Zhang | 163 | 1503 | 116769 |
David R. Holmes | 161 | 1624 | 114187 |
David Cella | 156 | 1258 | 106402 |
Elaine S. Jaffe | 156 | 828 | 112412 |
Michael A. Matthay | 151 | 998 | 98687 |
Lawrence Corey | 146 | 773 | 78105 |
Barton F. Haynes | 144 | 911 | 79014 |
Douglas D. Richman | 142 | 633 | 82806 |
Kjell Fuxe | 142 | 1479 | 89846 |