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Institution

University of Texas Health Science Center at Houston

EducationHouston, 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.


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Journal ArticleDOI
TL;DR: The effects of several cross-tumor nonsynonymous RNA editing events on cell viability are experimentally demonstrated and the evidence that RNA editing could selectively affect drug sensitivity is provided, highlighting RNA editing as an exciting theme for investigating cancer mechanisms, biomarkers, and treatments.

392 citations

Journal ArticleDOI
TL;DR: The findings reinforce the utility of major, modifiable risk factor assessment to identify individuals at risk for CHD for preventive action and suggest that routine measurement of these novel markers is not warranted for risk assessment.
Abstract: Background There has been interest in recent years in whether additional, and in particular novel, risk factors or blood markers, such as C-reactive protein, can enhance existing coronary heart disease (CHD) prediction models. Methods Using a series of case-cohort studies, the prospective Atherosclerosis Risk in Communities (ARIC) Study assessed the association of 19 novel risk markers with incident CHD in 15 792 adults followed up since 1987-1989. Novel markers included measures of inflammation, endothelial function, fibrin formation, fibrinolysis, B vitamins, and antibodies to infectious agents. Change in the area under the receiver operating characteristic curve (AUC) was used to assess the additional contribution of novel risk markers to CHD prediction beyond that of traditional risk factors. Results The basic risk factor model, which included traditional risk factors (age, race, sex, total and high-density lipoprotein cholesterol levels, systolic blood pressure, antihypertensive medication use, smoking status, and diabetes), predicted CHD well, as evidenced by an AUC of approximately 0.8. The C-reactive protein level did not add significantly to the AUC (increase in AUC of 0.003), and neither did most other novel risk factors. Of the 19 markers studied, lipoprotein-associated phospholipase A 2 , vitamin B 6 , interleukin 6, and soluble thrombomodulin added the most to the AUC (range, 0.006-0.011). Conclusions Our findings suggest that routine measurement of these novel markers is not warranted for risk assessment. On the other hand, our findings reinforce the utility of major, modifiable risk factor assessment to identify individuals at risk for CHD for preventive action.

392 citations

Journal ArticleDOI
TL;DR: Patients with resected primary solitary fibrous tumor were identified and the most common sites of occurrence were abdomen and pleura; these tumors were larger than those occurring in the extremities, head and neck or trunk, but did not demonstrate significant outcome differences.

392 citations

Journal ArticleDOI
TL;DR: Results suggest that leukocyte-fibroblast interactions in the aortic adventitia potentiate IL-6 production, inducing local monocyte recruitment and activation, thereby promoting MCP-1 secretion, vascular inflammation, ECM remodeling, and aortIC destabilization.
Abstract: Vascular inflammation contributes to cardiovascular diseases such as aortic aneurysm and dissection. However, the precise inflammatory pathways involved have not been clearly defined. We have shown here that subcutaneous infusion of Ang II, a vasopressor known to promote vascular inflammation, into older C57BL/6J mice induced aortic production of the proinflammatory cytokine IL-6 and the monocyte chemoattractant MCP-1. Production of these factors occurred predominantly in the tunica adventitia, along with macrophage recruitment, adventitial expansion, and development of thoracic and suprarenal aortic dissections. In contrast, a reduced incidence of dissections was observed after Ang II infusion into mice lacking either IL-6 or the MCP-1 receptor CCR2. Further analysis revealed that Ang II induced CCR2+CD14hiCD11bhiF4/80- macrophage accumulation selectively in aortic dissections and not in aortas from Il6-/- mice. Adoptive transfer of Ccr2+/+ monocytes into Ccr2-/- mice resulted in selective monocyte uptake into the ascending and suprarenal aorta in regions of enhanced ROS stress, with restoration of IL-6 secretion and increased incidence of dissection. In vitro, coculture of monocytes and aortic adventitial fibroblasts produced MCP-1- and IL-6-enriched conditioned medium that promoted differentiation of monocytes into macrophages, induced CD14 and CD11b upregulation, and induced MCP-1 and MMP-9 expression. These results suggest that leukocyte-fibroblast interactions in the aortic adventitia potentiate IL-6 production, inducing local monocyte recruitment and activation, thereby promoting MCP-1 secretion, vascular inflammation, ECM remodeling, and aortic destabilization.

392 citations

Journal ArticleDOI
Felix R. Day1, Deborah J. Thompson1, Hannes Helgason2, Hannes Helgason3  +241 moreInstitutions (67)
TL;DR: In this article, the authors used 1000 Genomes Project-imputed genotype data in up to ∼370,000 women to identify 389 independent signals (P < 5 × 10-8) for age at menarche, a milestone in female pubertal development.
Abstract: The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project-imputed genotype data in up to ∼370,000 women, we identify 389 independent signals (P < 5 × 10-8) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain ∼7.4% of the population variance in age at menarche, corresponding to ∼25% of the estimated heritability. We implicate ∼250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility.

392 citations


Authors

Showing all 27450 results

NameH-indexPapersCitations
Paul M. Ridker2331242245097
Eugene Braunwald2301711264576
Eric N. Olson206814144586
Hagop M. Kantarjian2043708210208
André G. Uitterlinden1991229156747
Gordon B. Mills1871273186451
Eric Boerwinkle1831321170971
Bruce M. Psaty1811205138244
Aaron R. Folsom1811118134044
Daniel R. Weinberger177879128450
Bharat B. Aggarwal175706116213
Richard A. Gibbs172889249708
Russel J. Reiter1691646121010
James F. Sallis169825144836
Steven N. Blair165879132929
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202342
2022231
20213,048
20202,807
20192,467
20182,224