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Institution

University of Texas Medical Branch

EducationGalveston, 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.


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Journal ArticleDOI
TL;DR: The low fidelity of hPolη may derive from a flexible active site that renders the enzyme more tolerant of geometric distortions in DNA and enables it to synthesize DNA past a T-T dimer.

388 citations

Journal ArticleDOI
TL;DR: The need for novel treatments is paramount, and future efforts to improve outcomes and quality of life should include optimisation of wound healing to attenuate or prevent hypertrophic scarring, well-designed trials to confirm treatment efficacy, and further elucidation of molecular mechanisms to allow development of new preventive and therapeutic strategies.

386 citations

Journal ArticleDOI
16 Jul 2003-JAMA
TL;DR: Both cTnT and CRP remained independent predictors of death after adjusting for a number of potential confounders, and among stable patients with ESRD, increasing levels of cTNT andCRP are associated with increased risk of death.
Abstract: Context Cardiac troponin T (cTnT) and C-reactive protein (CRP) are prognostic markers in acute coronary syndromes. However, for patients with end-stage renal disease (ESRD) the ability of combinations of these markers to predict outcomes, and their association with cardiac pathology, are unclear. Objective To investigate the association between levels of cTnT and CRP and longterm risk of cardiac pathology and death in patients with ESRD. Design, Setting, and Participants A prospective cohort study initiated February through June 1998 and enrolling 224 patients with ESRD from 5 hemodialysis centers in the Houston-Galveston region of Texas. Levels of cTnT and CRP were analyzed at study entry in patients without ischemic symptoms. MainOutcomeMeasures All-causemortalityduringameanfollow-upof827(range, 29-1327) days. Secondary outcomes in predefined substudies were coronary artery disease (CAD), decreased (40%) left ventricular ejection fraction (LVEF), and presence of left ventricular hypertrophy (LVH). Results One hundred seventeen (52%) patients died during follow-up. For levels of cTnT and CRP, progressively higher levels predicted increased risk of death compared with the lowest quartile (for cTnT quartile 2: unadjusted hazard ratio [HR], 2.2; 95% confidence interval [CI], 1.2-4.1; quartile 3: HR, 2.7; 95% CI, 1.5-4.9; quartile 4: HR, 3.0; 95% CI, 1.6-5.3. For CRP quartile 2: HR, 0.9; 95% CI, 0.5-1.6; quartile 3: HR, 1.8; 95% CI, 1.1-3.1; quartile 4: HR, 1.8; 95% CI, 1.1-3.2). Both cTnT and CRP remained independent predictors of death after adjusting for a number of potential confounders. The combination of cTnT and CRP results provided prognostic information when patients were divided into groups at or above and below the biomarker medians (high cTnT/high CRP levels vs low cTnT/low CRP levels for risk of death: HR, 2.5; 95% CI, 1.5-4.0). Elevated levels of cTnT, but not CRP, were strongly associated with diffuse CAD (n=67; 0%, 25%, 50%, and 62% prevalence of multivessel CAD across progressive cTnT quartiles, P.001). An LVEF of 40% or less was identified in 4 (9%), 3 (8%), 10 (27%), and 7 (19%) of patients across cTnT quartiles (P=.07). No trend for cTnT levels was found among patients with LVH (P=.45); similarly, no trend for CRP was found among patients with LVH (P=.65) or an LVEF of 40% or less (P=.75). Conclusions Among stable patients with ESRD, increasing levels of cTnT and CRP are associated with increased risk of death. Furthermore, higher levels of cTnT may identify patients with severe angiographic coronary disease.

385 citations

Journal ArticleDOI
TL;DR: The presence of a functional IL-6 homologue encoded by HHV-8 may provide a mechanistic model for the hypothesized role of HHV -8 in KS, MCD and BCBL that involves the mitogenic effects of vlL-6 on surrounding cells.
Abstract: Human herpesvirus-8 (HHV-8) has been detected in Kaposi's sarcoma (KS) lesions of all types (AIDS-related, classical and endemic), in body-cavity-based B-cell lymphomas (BCBLs) and in le-sions of multicentric Castleman's disease (MCD). We have identified a major gamma-herpesvirus-divergent locus (DL-B) in HHV-8 DNA encoding several HHV-8 unique open reading frames (ORFs), including a homologue of interleukin-6 (IL-6) and two homologues of macrophage inflammatory protein MIP-1. We show that the HHV-8-encoded IL-6 homologue (vlL-6) shares functional properties with endogenous IL-6 proteins and that both vlL-6 and vMIP-1 transcripts are present at high levels following butyrate induction of an HHV-8+ BCBL cell line. Low amounts of constitutive vlL-6, but not vMIP-1, mRNA were also detected. The presence of a functional IL-6 homologue encoded by HHV-8 may provide a mechanistic model for the hypothesized role of HHV-8 in KS, MCD and BCBL that involves the mitogenic effects of vlL-6 on surrounding cells. MIP-1 proteins may enhance these effects through the chemotactic recruitment of endogenous cy-tokine-producing cells into affected tissues and could potentially influence HIV disease progression in coinfected individuals through interactions with the HIV co-receptor CCR-5.

385 citations

Journal ArticleDOI
24 Nov 1983-Nature
TL;DR: It is suggested that each population discharge is followed by a period of relative population refractoriness, and activity elicited in one neurone spreads to other neurones through multisynaptic excitatory pathways and leads eventually to the participation of the whole population in a synchronous burst.
Abstract: The synchronized firing of neuronal populations is frequently observed in the mammalian central nervous system. The generation of motor activities such as locomotion and respiration requires the simultaneous activation of many neurones and synchronous firing also underlies the cortical alpha rhythm and the hippocampal theta rhythm. However the influence that single neurones may have on such neuronal population discharges is not clear. We have examined this question using small isolated segments of the CA3 region of the guinea pig hippocampus. We report here that in the presence of picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, these segments spontaneously generate synchronized rhythmic bursts comparable with the interictal epileptiform discharges observed in the hippocampus and neocortex in the presence of penicillin. The activation of some individual neurones by intracellular current injection can partially entrain and reset the rhythm. The probability that a synchronized burst will follow stimulation of a single cell increases with time after a spontaneous synchronized discharge, suggesting that each population discharge is followed by a period of relative population refractoriness. A delay of 40-200 ms elapses between the activation of a single neurone and the synchronized discharge. We suggest that during this time activity elicited in one neurone spreads to other neurones through multisynaptic excitatory pathways and leads eventually to the participation of the whole population in a synchronous burst.

385 citations


Authors

Showing all 22143 results

NameH-indexPapersCitations
Stuart H. Orkin186715112182
Eric R. Kandel184603113560
John C. Morris1831441168413
Joseph Biederman1791012117440
Richard A. Gibbs172889249708
Timothy A. Springer167669122421
Gabriel N. Hortobagyi1661374104845
Roberto Romero1511516108321
Charles B. Nemeroff14997990426
Peter J. Schwartz147647107695
Clifford J. Woolf14150986164
Thomas J. Smith1401775113919
Edward C. Holmes13882485748
Jun Lu135152699767
Henry T. Lynch13392586270
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202330
2022196
20211,617
20201,487
20191,298
20181,152