Institution
University of Texas Health Science Center at Houston
Education•Houston, Texas, United States•
About: University of Texas Health Science Center at Houston is a education organization based out in Houston, Texas, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 27309 authors who have published 42520 publications receiving 2151596 citations. The organization is also known as: UTHealth & The UT Health Science Center at Houston.
Topics: Population, Poison control, Cancer, Stroke, Health care
Papers published on a yearly basis
Papers
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TL;DR: Diffuse coronary atherosclerosis without focal stenosis at angiography causes a graded, continuous pressure fall along arterial length, which contributes to myocardial ischemia and has consequences for decision-making during percutaneous coronary interventions.
Abstract: Background Coronary arteries without focal stenosis at angiography are generally considered non–flow-limiting. However, atherosclerosis is a diffuse process that often remains invisible at angiography. Accordingly, we hypothesized that in patients with coronary artery disease, nonstenotic coronary arteries induce a decrease in pressure along their length due to diffuse coronary atherosclerosis. Methods and Results Coronary pressure and fractional flow reserve (FFR), as indices of coronary conductance, were obtained from 37 arteries in 10 individuals without atherosclerosis (group I) and from 106 nonstenotic arteries in 62 patients with arteriographic stenoses in another coronary artery (group II). In group I, the pressure gradient between aorta and distal coronary artery was minimal at rest (1±1 mm Hg) and during maximal hyperemia (3±3 mm Hg). Corresponding values were significantly larger in group II (5±4 mm Hg and 10±8 mm Hg, respectively; both P<0.001). The FFR was near unity (0.97±0.02; range, 0.92 to...
465 citations
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TL;DR: It is found that beta-thalassemia trait carriers displayed lower TC and were protected from coronary artery disease (CAD), and only some mechanisms of lowering LDL-C appeared to increase risk for type 2 diabetes (T2D); and TG-lowering alleles involved in hepatic production of TG-rich lipoproteins tracked with higher liver fat, higher risk for T2D, and lower risk for CAD.
Abstract: We screened variants on an exome-focused genotyping array in >300,000 participants (replication in >280,000 participants) and identified 444 independent variants in 250 loci significantly associated with total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), low-density-lipoprotein cholesterol (LDL-C), and/or triglycerides (TG). At two loci (JAK2 and A1CF), experimental analysis in mice showed lipid changes consistent with the human data. We also found that: (i) beta-thalassemia trait carriers displayed lower TC and were protected from coronary artery disease (CAD); (ii) excluding the CETP locus, there was not a predictable relationship between plasma HDL-C and risk for age-related macular degeneration; (iii) only some mechanisms of lowering LDL-C appeared to increase risk for type 2 diabetes (T2D); and (iv) TG-lowering alleles involved in hepatic production of TG-rich lipoproteins (TM6SF2 and PNPLA3) tracked with higher liver fat, higher risk for T2D, and lower risk for CAD, whereas TG-lowering alleles involved in peripheral lipolysis (LPL and ANGPTL4) had no effect on liver fat but decreased risks for both T2D and CAD.
465 citations
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Erasmus University Rotterdam1, Boston University2, National Institutes of Health3, University of Texas Health Science Center at Houston4, University of Washington5, University of Greifswald6, Wellcome Trust Sanger Institute7, Leiden University8, University of London9, University of Edinburgh10, Harvard University11, Wake Forest University12, University of Helsinki13, VU University Amsterdam14, University of Mainz15, Baylor College of Medicine16, University of Texas at Austin17, University of Oulu18, University of Minnesota19, Imperial College London20, University of North Carolina at Chapel Hill21, Martin Luther University of Halle-Wittenberg22, German Cancer Research Center23, Leipzig University24, Guy's and St Thomas' NHS Foundation Trust25, Amgen26, University of Iceland27, Cedars-Sinai Medical Center28, University of Split29, University of Ulm30
TL;DR: A genome-wide association analysis of CRP identified 18 loci that were associated with CRP levels and highlighted immune response and metabolic regulatory pathways involved in the regulation of chronic inflammation.
Abstract: Background—C-reactive protein (CRP) is a heritable marker of chronic inflammation that is strongly associated with cardiovascular disease. We sought to identify genetic variants that are associated with CRP levels. Methods and Results—We performed a genome-wide association analysis of CRP in 66 185 participants from 15 population-based studies. We sought replication for the genome-wide significant and suggestive loci in a replication panel comprising 16 540 individuals from 10 independent studies. We found 18 genome-wide significant loci, and we provided evidence of replication for 8 of them. Our results confirm 7 previously known loci and introduce 11 novel loci that are implicated in pathways related to the metabolic syndrome (APOC1, HNF1A, LEPR, GCKR, HNF4A, and PTPN2) or the immune system (CRP, IL6R, NLRP3, IL1F10, and IRF1) or that reside in regions previously not known to play a role in chronic inflammation (PPP1R3B, SALL1, PABPC4, ASCL1, RORA, and BCL7B). We found a significant interaction of body ...
463 citations
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TL;DR: The current approaches to gene discovery and mutation detection for retinitis pigmentosa are summarized, and pitfalls and unsolved problems are indicated.
Abstract: Retinitis pigmentosa (RP) is a heterogeneous set of inherited retinopathies with many disease-causing genes, many known mutations, and highly varied clinical consequences. Progress in finding treatments is dependent on determining the genes and mutations causing these diseases, which includes both gene discovery and mutation screening in affected individuals and families. Despite the complexity, substantial progress has been made in finding RP genes and mutations. Depending on the type of RP, and the technology used, it is possible to detect mutations in 30–80% of cases. One of the most powerful approaches to genetic testing is high-throughput ‘deep sequencing’, that is, next-generation sequencing (NGS). NGS has identified several novel RP genes but a substantial fraction of previously unsolved cases have mutations in genes that are known causes of retinal disease but not necessarily RP. Apparent discrepancy between the molecular defect and clinical findings may warrant reevaluation of patients and families. In this review, we summarize the current approaches to gene discovery and mutation detection for RP, and indicate pitfalls and unsolved problems. Similar considerations apply to other forms of inherited retinal disease.
462 citations
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TL;DR: Supranormal resuscitation was associated with more lactated Ringer infusion, decreased intestinal perfusion (higher GAPCO2), and an increased incidence of IAH, ACS, multiple organ failure, and death.
Abstract: Hypothesis Normal resuscitation (oxygen delivery index [DO 2 I] ≥500 mL/min per square meter), compared with supranormal trauma resuscitation (DO 2 I ≥600 mL/min per square meter), requires less crystalloid volume, thus decreasing the incidence of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS). Design Retrospective analysis of a prospective database. Setting Twenty-bed intensive care unit (ICU) in a regional level I trauma center. Patients Patients with major trauma (injury severity score >15, initial base deficit ≥6 mEq/L, or need for ≥6 units of packed red blood cells in the first 12 hours) or age 65 years or older with any 2 of the previous criteria. Interventions Shock/trauma resuscitation protocol: pulmonary artery catheter, gastric tonometry, urinary bladder pressure measurements, lactated Ringer infusion, packed red blood cell transfusion, and moderate inotrope support, as needed, in that sequence, to attain and maintain a DO 2 I greater than or equal to 600 mL/min per m 2 (16 months, ending January 1, 2001, n = 85) or a DO 2 I greater than or equal to 500 mL/min per square meter (16 months, starting January 1, 2001, n = 71) for the first 24 hours in the ICU. Main Outcome Measures: Lactated Ringer infusion volume (liters) at ICU admission, gastric partial carbon dioxide minus end-tidal carbon dioxide(GAP CO2 ), IAH (urinary bladder pressure measurements >20 mm Hg), ACS (urinary bladder pressure measurements >25 mm Hg with organ dysfunction), multiple organ failure, and mortality. Results Demographics, injury severity, and shock severity parameters were similar in both groups. The supranormal resuscitation group required more lactated Ringer infusion volume in the first 24 hours in the ICU (mean ± SD, 13 ± 2 vs 7 ± 1 L; P CO2 (16 ± 2 vs 7 ± 1 mm Hg; P P P P P Conclusion Supranormal resuscitation, compared with normal resuscitation, was associated with more lactated Ringer infusion, decreased intestinal perfusion (higher GAP CO2 ), and an increased incidence of IAH, ACS, multiple organ failure, and death.
462 citations
Authors
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Name | H-index | Papers | Citations |
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Paul M. Ridker | 233 | 1242 | 245097 |
Eugene Braunwald | 230 | 1711 | 264576 |
Eric N. Olson | 206 | 814 | 144586 |
Hagop M. Kantarjian | 204 | 3708 | 210208 |
André G. Uitterlinden | 199 | 1229 | 156747 |
Gordon B. Mills | 187 | 1273 | 186451 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Bruce M. Psaty | 181 | 1205 | 138244 |
Aaron R. Folsom | 181 | 1118 | 134044 |
Daniel R. Weinberger | 177 | 879 | 128450 |
Bharat B. Aggarwal | 175 | 706 | 116213 |
Richard A. Gibbs | 172 | 889 | 249708 |
Russel J. Reiter | 169 | 1646 | 121010 |
James F. Sallis | 169 | 825 | 144836 |
Steven N. Blair | 165 | 879 | 132929 |