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 & Cancer. 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, Cancer, Poison control, Medicine, Health care
Papers published on a yearly basis
Papers
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TL;DR: The generation of Dspp-null mice that develop tooth defects similar to human dentinogenesis imperfecta III with enlarged pulp chambers, increased width of predentin zone, hypomineralization, and pulp exposure are reported.
372 citations
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TL;DR: It is suggested that the DASS may be used with older adults in lieu of multiple scales designed to measure similar constructs, thereby reducing participant burden and facilitating assessment in settings with limited assessment resources.
372 citations
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TL;DR: The PHD-Bromo of TRIM24 provides a structural rationale for chromatin activation through a non-canonical histone signature, establishing a new route by which chromatin readers may influence cancer pathogenesis.
Abstract: Recognition of modified histone species by distinct structural domains within 'reader' proteins plays a critical role in the regulation of gene expression. Readers that simultaneously recognize histones with multiple marks allow transduction of complex chromatin modification patterns into specific biological outcomes. Here we report that chromatin regulator tripartite motif-containing 24 (TRIM24) functions in humans as a reader of dual histone marks by means of tandem plant homeodomain (PHD) and bromodomain (Bromo) regions. The three-dimensional structure of the PHD-Bromo region of TRIM24 revealed a single functional unit for combinatorial recognition of unmodified H3K4 (that is, histone H3 unmodified at lysine 4, H3K4me0) and acetylated H3K23 (histone H3 acetylated at lysine 23, H3K23ac) within the same histone tail. TRIM24 binds chromatin and oestrogen receptor to activate oestrogen-dependent genes associated with cellular proliferation and tumour development. Aberrant expression of TRIM24 negatively correlates with survival of breast cancer patients. The PHD-Bromo of TRIM24 provides a structural rationale for chromatin activation through a non-canonical histone signature, establishing a new route by which chromatin readers may influence cancer pathogenesis.
372 citations
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TL;DR: Aliment Pharmacol Ther 2011; 34: 1269–1281.
Abstract: Aliment Pharmacol Ther 2011; 34: 1269–1281
Summary
Background The use of proton pump inhibitors (PPIs) is increasing worldwide. Suppression of gastric acid alters the susceptibility to enteric bacterial pathogens.
Aim This systematic review was undertaken to examine the relationship between PPI use and susceptibility to enteric infections by a specific pathogen based on published literature and to discuss the potential mechanisms of PPI enhanced pathogenesis of enteric infections.
Methods PubMed, OVID Medline Databases were searched. Search terms included proton pump inhibitors and mechanisms of, actions of, gastric acid, enteric infections, diarrhoea, Clostridium difficile, Salmonella, Shigella and Campylobacter.
Results The use of PPIs increases gastric pH, encourages growth of the gut microflora, increases bacterial translocation and alters various immunomodulatory and anti-inflammatory effects. Enteric pathogens show variable gastric acid pH susceptibility and acid tolerance levels. By multiple mechanisms, PPIs appear to increase susceptibility to the following bacterial enteropathogens: Salmonella, Campylobacter jejuni, invasive strains of Escherichia coli, vegetative cells of Clostridium difficile, Vibrio cholerae and Listeria. We describe the available evidence for enhanced susceptibility to enteric infection caused by Salmonella, Campylobacter and C. difficile by PPI use, with adjusted relative risk ranges of 4.2–8.3 (two studies); 3.5–11.7 (four studies); and 1.2–5.0 (17 of 27 studies) for the three respective organisms.
Conclusions Severe hypochlorhydria generated by PPI use leads to bacterial colonisation and increased susceptibility to enteric bacterial infection. The clinical implication of chronic PPI use among hospitalized patients placed on antibiotics and travellers departing for areas with high incidence of diarrhoea should be considered by their physicians.
371 citations
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TL;DR: It is found that whereas alerting improves overall response speed, it exerts negative influence on executive control under certain conditions, and the hypothesis of functional integration and interaction of these brain networks is supported.
371 citations
Authors
Showing all 27450 results
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 |