Institution
University of Texas Medical Branch
Education•Galveston, Texas, United States•
About: University of Texas Medical Branch is a education organization based out in Galveston, Texas, United States. It is known for research contribution in the topics: Population & Virus. The organization has 22033 authors who have published 38268 publications receiving 1517502 citations. The organization is also known as: The University of Texas Medical Branch at Galveston & UTMB.
Topics: Population, Virus, Immune system, Receptor, Poison control
Papers published on a yearly basis
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TL;DR: In this paper, the abdominal withdrawal reflex and responses of viscerosensitive neurons were recorded during colon distention in a rat with either mechanical or chemical colonic irritation between postnatal days 8 and 21 and were tested when they became adults.
668 citations
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TL;DR: The report that follows defines wound, acute wound, chronic wound, healing and forms of healing, wound assessment, wound extent, wound burden, and wound severity, broadly applicable to all wounds.
Abstract: Background: Chronic wounds represent a worldwide problem. For laboratory and clinical research to adequately address this problem, a common language needs to exist. Observation: This language should include a system of wound classification, a lexicon of wound descriptors, and a description of the processes that are likely to affect wound healing and wound healing end points. Conclusions: The report that follows defines wound, acute wound, chronic wound, healing and forms of healing, wound assessment, wound extent, wound burden, and wound severity. The utility of these definitions is demonstrated as they relate to the healing of a skin wound, but these definitions are broadly applicable to all wounds. (Arch Dermatol. 1994;130:489-493)
660 citations
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TL;DR: An important role of microglia and NLRP3 inflammasome activation in the pathogenesis of tauopathies is identified and the amyloid-cascade hypothesis in Alzheimer’s disease is supported, demonstrating that neurofibrillary tangles develop downstream of amyloids-beta-induced microglial activation.
Abstract: Alzheimer's disease is characterized by the accumulation of amyloid-beta in plaques, aggregation of hyperphosphorylated tau in neurofibrillary tangles and neuroinflammation, together resulting in neurodegeneration and cognitive decline1. The NLRP3 inflammasome assembles inside of microglia on activation, leading to increased cleavage and activity of caspase-1 and downstream interleukin-1β release2. Although the NLRP3 inflammasome has been shown to be essential for the development and progression of amyloid-beta pathology in mice3, the precise effect on tau pathology remains unknown. Here we show that loss of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation by regulating tau kinases and phosphatases. Tau activated the NLRP3 inflammasome and intracerebral injection of fibrillar amyloid-beta-containing brain homogenates induced tau pathology in an NLRP3-dependent manner. These data identify an important role of microglia and NLRP3 inflammasome activation in the pathogenesis of tauopathies and support the amyloid-cascade hypothesis in Alzheimer's disease, demonstrating that neurofibrillary tangles develop downstream of amyloid-beta-induced microglial activation.
659 citations
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TL;DR: This work has shown that highly populated states are located within the global free energy minimum region of a relatively rough free energy hypersurface, and the structure and dynamics of lowly populated, higher free energy states which cannot be modeled.
Abstract: Understanding the function of biological macromolecules and their complexes at the physicochemical level requires knowledge of both their structure and dynamics. Conventional biophysical techniques, such as crystallography and NMR, have yielded incredibly detailed structural information at the atomic level on highly populated static states.1 In the context of the energy landscape representation of macromolecules, highly populated states are located within the global free energy minimum region of a relatively rough free energy hypersurface.2-5 Much less is known, however, about lowly populated, higher free energy states which cannot be * E-mail: G.M.C., mariusc@mail.nih.gov; J.I., j.iwahara@utmb.edu. † National Institutes of Health. ‡ University of Texas Medical Branch. Chem. Rev. 2009, 109, 4108–4139 4108
658 citations
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University of Pennsylvania1, University of Florida2, Primary Children's Hospital3, Washington University in St. Louis4, National Institutes of Health5, Mayo Clinic6, University of Texas Medical Branch7, Marshfield Clinic8, University of California, San Francisco9, Henry Ford Health System10, University of Maryland, Baltimore11, University of Alabama at Birmingham12, Vanderbilt University13, Tulane University14, Icahn School of Medicine at Mount Sinai15, Duke University16, Yeshiva University17, University of Utah18, Harvard University19
TL;DR: Genotype-guided dosing of warfarin did not improve anticoagulation control during the first 4 weeks of therapy and there was a significant interaction between dosing strategy and race.
Abstract: Background The clinical utility of genotype-guided (pharmacogenetically based) dosing of warfarin has been tested only in small clinical trials or observational studies, with equivocal results. Methods We randomly assigned 1015 patients to receive doses of warfarin during the first 5 days of therapy that were determined according to a dosing algorithm that included both clinical variables and genotype data or to one that included clinical variables only. All patients and clinicians were unaware of the dose of warfarin during the first 4 weeks of therapy. The primary outcome was the percentage of time that the international normalized ratio (INR) was in the therapeutic range from day 4 or 5 through day 28 of therapy. Results At 4 weeks, the mean percentage of time in the therapeutic range was 45.2% in the genotype-guided group and 45.4% in the clinically guided group (adjusted mean difference, [genotype-guided group minus clinically guided group], −0.2; 95% confidence interval, −3.4 to 3.1; P=0.91). There ...
656 citations
Authors
Showing all 22143 results
Name | H-index | Papers | Citations |
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Stuart H. Orkin | 186 | 715 | 112182 |
Eric R. Kandel | 184 | 603 | 113560 |
John C. Morris | 183 | 1441 | 168413 |
Joseph Biederman | 179 | 1012 | 117440 |
Richard A. Gibbs | 172 | 889 | 249708 |
Timothy A. Springer | 167 | 669 | 122421 |
Gabriel N. Hortobagyi | 166 | 1374 | 104845 |
Roberto Romero | 151 | 1516 | 108321 |
Charles B. Nemeroff | 149 | 979 | 90426 |
Peter J. Schwartz | 147 | 647 | 107695 |
Clifford J. Woolf | 141 | 509 | 86164 |
Thomas J. Smith | 140 | 1775 | 113919 |
Edward C. Holmes | 138 | 824 | 85748 |
Jun Lu | 135 | 1526 | 99767 |
Henry T. Lynch | 133 | 925 | 86270 |