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
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TL;DR: The results indicate that depending on the stimulatory context, the activity of GSK-3 can be modulated either by growth factors that work through the phosphatidylinositol 3-kinase-protein kinase B cascade or by hormonal stimulation of G protein-coupled receptors that link to changes in intracellular cAMP levels.
Abstract: Glycogen synthase kinase 3 (GSK-3) is implicated in multiple biological processes including metabolism, gene expression, cell fate determination, proliferation, and survival. GSK-3 activity is inhibited through phosphorylation of serine 21 in GSK-3 alpha and serine 9 in GSK-3 beta. These serine residues of GSK-3 have been previously identified as targets of protein kinase B (PKB/Akt), a serine/threonine kinase located downstream of phosphatidylinositol 3-kinase. Here, we show that serine 21 in GSK-3 alpha and serine 9 in GSK-3 beta are also physiological substrates of cAMP-dependent protein kinase A. Protein kinase A physically associates with, phosphorylates, and inactivates both isoforms of GSK-3. The results indicate that depending on the stimulatory context, the activity of GSK-3 can be modulated either by growth factors that work through the phosphatidylinositol 3-kinase-protein kinase B cascade or by hormonal stimulation of G protein-coupled receptors that link to changes in intracellular cAMP levels.
779 citations
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TL;DR: Although H3K36 methylation is most commonly associated with the transcription of active euchromatin, it has also been implicated in diverse processes, including alternative splicing, dosage compensation and transcriptional repression, as well as DNA repair and recombination.
Abstract: Histone side chains are post-translationally modified at multiple sites, including at Lys36 on histone H3 (H3K36). Several enzymes from yeast and humans, including the methyltransferases SET domain-containing 2 (Set2) and nuclear receptor SET domain-containing 1 (NSD1), respectively, alter the methylation status of H3K36, and significant progress has been made in understanding how they affect chromatin structure and function. Although H3K36 methylation is most commonly associated with the transcription of active euchromatin, it has also been implicated in diverse processes, including alternative splicing, dosage compensation and transcriptional repression, as well as DNA repair and recombination. Disrupted placement of methylated H3K36 within the chromatin landscape can lead to a range of human diseases, underscoring the importance of this modification.
776 citations
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TL;DR: Findings support the protective effects of physical activity on depression for older adults and argue against excluding disabled subjects from similar studies.
Abstract: Previous studies assessing protective effects of physical activity on depression have had conflicting results; one recent study argued that excluding disabled subjects attenuated any observed effects. The authors' objective was to compare the effects of higher levels of physical activity on prevalent and incident depression with and without exclusion of disabled subjects. Participants were 1,947 community-dwelling adults from the Alameda County Study aged 50-94 years at baseline in 1994 with 5 years of follow-up. Depression was measured using criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (Washington, DC: American Psychiatric Association, 1994). Physical activity was measured with an eight-point scale; odds ratios are based upon a one-point increase on the scale. Even with adjustments for age, sex, ethnicity, financial strain, chronic conditions, disability, body mass index, alcohol consumption, smoking, and social relations, greater physical activity was protective for both prevalent depression (adjusted odds ratio (OR) = 0.90, 95% confidence interval (CI): 0.79, 1.01) and incident depression (adjusted OR = 0.83, 95% CI: 0.73, 0.96) over 5 years. Exclusion of disabled subjects did not attenuate the incidence results (adjusted OR = 0.79, 95% CI: 0.67, 0.92). Findings support the protective effects of physical activity on depression for older adults and argue against excluding disabled subjects from similar studies.
776 citations
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National Institutes of Health1, University of Queensland2, University of Edinburgh3, Columbia University4, Erasmus University Rotterdam5, King's College London6, University of Minnesota7, University of Texas Health Science Center at Houston8, Baylor College of Medicine9, Johns Hopkins University10, Harvard University11, Boston University12, University of Exeter13, Innsbruck Medical University14, University of Düsseldorf15, Stanford University16, University of California, Los Angeles17, United States Department of Veterans Affairs18, Northwestern University19, George Washington University20, University of California, San Diego21, University of Washington22, Fred Hutchinson Cancer Research Center23
TL;DR: Evidence that epigenetic age predicts all-cause mortality above and beyond chronological age and traditional risk factors is strengthened and estimates that incorporate information on blood cell counts lead to highly significant associations with all- Cause mortality are demonstrated.
Abstract: Estimates of biological age based on DNA methylation patterns, often referred to as "epigenetic age", "DNAm age", have been shown to be robust biomarkers of age in humans. We previously demonstrated that independent of chronological age, epigenetic age assessed in blood predicted all-cause mortality in four human cohorts. Here, we expanded our original observation to 13 different cohorts for a total sample size of 13,089 individuals, including three racial/ethnic groups. In addition, we examined whether incorporating information on blood cell composition into the epigenetic age metrics improves their predictive power for mortality. All considered measures of epigenetic age acceleration were predictive of mortality (p≤8.2x10-9), independent of chronological age, even after adjusting for additional risk factors (p<5.4x10-4), and within the racial/ethnic groups that we examined (non-Hispanic whites, Hispanics, African Americans). Epigenetic age estimates that incorporated information on blood cell composition led to the smallest p-values for time to death (p=7.5x10-43). Overall, this study a) strengthens the evidence that epigenetic age predicts all-cause mortality above and beyond chronological age and traditional risk factors, and b) demonstrates that epigenetic age estimates that incorporate information on blood cell counts lead to highly significant associations with all-cause mortality.
775 citations
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University of Texas MD Anderson Cancer Center1, Radiation Therapy Oncology Group2, University of Lausanne3, University of Texas Health Science Center at Houston4, Medical College of Wisconsin5, Tel Aviv Sourasky Medical Center6, Johns Hopkins University7, University of Edinburgh8, Maastricht University9, University Hospitals Bristol NHS Foundation Trust10, Rambam Health Care Campus11, Ohio State University12, Emory University13, University of Maryland, Baltimore14
TL;DR: This study did not demonstrate improved efficacy for DD temozolomide for newly diagnosed GBM, regardless of methylation status, but it did confirm the prognostic significance of MGMT methylation.
Abstract: Purpose Radiotherapy with concomitant and adjuvant temozolomide is the standard of care for newly diagnosed glioblastoma (GBM) O 6 -methylguanine-DNA methyltransferase (MGMT) methylation status may be an important determinant of treatment response Dose-dense (DD) temozolomide results in prolonged depletion of MGMT in blood mononuclear cells and possibly in tumor This trial tested whether DD temozolomide improves overall survival (OS) or progression-free survival (PFS) in patients with newly diagnosed GBM Patients and Methods This phase III trial enrolled patients older than age 18 years with a Karnofsky performance score of 60 with adequate tissue Stratification included clinical factors and tumor MGMT methylation status Patients were randomly assigned to standard temozolomide (arm 1) or DD temozolomide (arm 2) for 6 to 12 cycles The primary end point was OS Secondary analyses evaluated the impact of MGMT status
775 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 |