University of Texas Health Science Center at Houston

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.

Biological clocks and shift work: circadian dysregulation and potential long-term effects.

Abstract: Long-term epidemiologic studies on large numbers of night and rotating shift workers have suggested an increase in the incidence of breast and colon cancer in these populations These studies suffer from poor definition and quantification of the work schedules of the exposed subjects Against this background, the pathophysiology of phase shift and phase adaptation is reviewed A phase shift as experienced in night and rotating shift work involves desynchronization at the molecular level in the circadian oscillators in the central nervous tissue and in most peripheral tissues of the body There is a change in the coordination between oscillators with transient loss of control by the master-oscillator (the Suprachiasmatic Nucleus, SCN) in the hypothalamus The implications of the pathophysiology of phase shift are discussed for long-term health effects and for the design of ergonomic work schedules minimizing the adverse health effects upon the worker

Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure.

Abstract: Background: Primary (1°) abdominal compartment syndrome (ACS) is a known complication of damage control. Recently secondary (2°) ACS has been reported in patients without abdominal injury who require aggressive resuscitation. The purpose of this study was to compare the epidemiology of 1° and 2° ACS and develop early prediction models in a high-risk cohort who were treated in a similar fashion. Methods: Major torso trauma patients underwent standardized resuscitation and had prospective data collected including occurrence of ACS, demographics, ISS, urinary bladder pressure, gastric tonometry (GAP CO2 = gastric regional CO 2 minus end tidal CO 2 ), laboratory, respiratory, and hemodynamic data. With 1° and 2° ACS as endpoints, variables were tested by uni- and multivariate logistic analysis (MLA). Results: From 188 study patients during the 44-month period, 26 (14%) developed ACS-11 (6%) were 1° ACS and IS (8%) 2° ACS. 1° and 2° ACS had similar demographics, shock, and injury severity. Significant univariate differences included: time to decompression from ICU admit (600 ± 112 vs. 360 ± 48 min), Emergency Department (ED) crystalloid (4 ± 1 vs. 7 ± 1 L), preICU crystalloid (8 ± 1 vs. 12 ± 1L), ED blood administration (2 ± 1 vs. 6 ± 1 U), GAP CO2 (24 ± 3 vs. 36 ± 3 mmHg), requiring pelvic embolization (9 vs. 47%), and emergency operation (82% vs. 40%). Early predictors identified by MLA of 1° ACS included hemoglobin concentration, GAP CO2 , temperature, and base deficit; and for 2° ACS they included crystalloid, urinary output, and GAP CO2 . The areas under the receiver-operator characteristic curves calculated upon ICU admission are 1° = 0.977 and 2° = 0.983. 1° and 2° ACS patients had similar poor outcomes compared with nonACS patients including ventilator days (1° = 13 ± 3 vs. 2° = 14 ± 3 vs. nonACS = 8 ± 2), multiple organ failure (55% vs. 53% vs. 12%), and mortality (64% vs. 53% vs. 17%). Conclusion: 1° and 2° ACS have similar demographics, injury severity, time to decompression from hospital admit, and bad outcome. 2° ACS is an earlier ICU event preceded by more crystalloid administration. With appropriate monitoring both could be accurately predicted upon ICU admission.

Weight Gain Following Initiation of Antiretroviral Therapy: Risk Factors in Randomized Comparative Clinical Trials

Abstract: Background Initiation of antiretroviral therapy (ART) often leads to weight gain. While some of this weight gain may be an appropriate return-to-health effect, excessive increases in weight may lead to obesity. We sought to explore factors associated with weight gain in several randomized comparative clinical trials of ART initiation. Methods We performed a pooled analysis of weight gain in 8 randomized controlled clinical trials of treatment-naive people living with human immunodeficiency virus (HIV) initiating ART between 2003 and 2015, comprising >5000 participants and 10 000 person-years of follow-up. We used multivariate modeling to explore relationships between demographic factors, HIV disease characteristics, and ART components and weight change following ART initiation. Results Weight gain was greater in more recent trials and with the use of newer ART regimens. Pooled analysis revealed baseline demographic factors associated with weight gain including lower CD4 cell count, higher HIV type 1 RNA, no injection drug use, female sex, and black race. Integrase strand transfer inhibitor use was associated with more weight gain than were protease inhibitors or nonnucleoside reverse transcriptase inhibitors (NNRTIs), with dolutegravir and bictegravir associated with more weight gain than elvitegravir/cobicistat. Among the NNRTIs, rilpivirine was associated with more weight gain than efavirenz. Among nucleoside/nucleotide reverse transcriptase inhibitors, tenofovir alafenamide was associated with more weight gain than tenofovir disoproxil fumarate, abacavir, or zidovudine. Conclusions Weight gain is ubiquitous in clinical trials of ART initiation and is multifactorial in nature, with demographic factors, HIV-related factors, and the composition of ART regimens as contributors. The mechanisms by which certain ART agents differentially contribute to weight gain are unknown.

Genome-wide association study of systemic sclerosis identifies CD247 as a new susceptibility locus

Abstract: Systemic sclerosis (SSc) is an autoimmune disease characterized by fibrosis of the skin and internal organs that leads to profound disability and premature death. To identify new SSc susceptibility loci, we conducted the first genome-wide association study in a population of European ancestry including a total of 2,296 individuals with SSc and 5,171 controls. Analysis of 279,621 autosomal SNPs followed by replication testing in an independent case-control set of European ancestry (2,753 individuals with SSc (cases) and 4,569 controls) identified a new susceptibility locus for systemic sclerosis at CD247 (1q22-23, rs2056626, P = 2.09 x 10(-7) in the discovery samples, P = 3.39 x 10(-9) in the combined analysis). Additionally, we confirm and firmly establish the role of the MHC (P = 2.31 x 10(-18)), IRF5 (P = 1.86 x 10(-13)) and STAT4 (P = 3.37 x 10(-9)) gene regions as SSc genetic risk factors.