Institution
University of Texas Medical Branch
Education•Galveston, Texas, United States•
About: University of Texas Medical Branch is a education organization based out in Galveston, Texas, United States. It is known for research contribution in the topics: Population & Virus. The organization has 22033 authors who have published 38268 publications receiving 1517502 citations. The organization is also known as: The University of Texas Medical Branch at Galveston & UTMB.
Topics: Population, Virus, Immune system, Receptor, Poison control
Papers published on a yearly basis
Papers
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University of Paris1, Cedars-Sinai Medical Center2, Imperial College London3, Katholieke Universiteit Leuven4, University of Alberta5, University of Texas Medical Branch6, Yeshiva University7, Johns Hopkins University8, Mayo Clinic9, Erasmus University Rotterdam10, University of Pittsburgh11, Charité12, Emory University13, Vanderbilt University14, University of Manitoba15, Medical University of Vienna16, Washington University in St. Louis17, University of Alabama at Birmingham18, New York University19, Westmead Hospital20, University of North Carolina at Chapel Hill21, Harvard University22, McGill University23, Autonomous University of Barcelona24
TL;DR: This report on kidney transplant pathology details clarifications and refinements to the criteria for chronic active (CA) T cell–mediated rejection, borderline, and antibody‐mediated rejection (ABMR).
368 citations
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TL;DR: Pituitary hormone deficiencies were identified in a substantial proportion of patients with previous brain injury, and GH deficiency, found in 15% by glucagon stimulation testing, may compound the physical and psychological complications of traumatic brain injury and interfere with rehabilitation.
Abstract: Although hypopituitarism is a known complication of head injury, it may be underrecognized due to its subtle clinical manifestations. The nonspecific symptoms may be masked by and may contribute to the physical and psychological sequelae of brain trauma. This study examines the prevalence of neuroendocrine abnormalities in patients rehabilitating from traumatic brain injury. Seventy adults (mean age, 31.5 +/- 1.1 yr; range, 18--58; 46 men and 24 women) with traumatic brain injury an average of 49 +/- 8 months before the study (median, 13 months) underwent a series of standard endocrine tests, including serum levels of TSH, free T(4), insulin-like growth factor I, PRL, testosterone (males), and cosyntropin stimulation. Abnormal results of these tests were followed by dynamic tests of gonadotropin, TSH, and GH secretion. Glucagon stimulation testing in 48 subjects revealed GH deficiency (peak, <3 microg/L) in 14.6%. Free T(4) (n = 6; 8.6%), TSH (n = 7; 10%), or both (n = 2; 2.9%) were low in 21.7%, whereas 87% had both TSH and free T(4) below the midnormal level. Basal morning cortisol was below normal in 45.7% of subjects, whereas cosyntropin-stimulated levels were insufficient (peak, <500 nmol/L) in 7.1%. Hypogonadism and hyperprolactinemia were uncommon. In summary, pituitary hormone deficiencies were identified in a substantial proportion of patients with previous brain injury. GH deficiency, found in 15% by glucagon stimulation testing, may compound the physical and psychological complications of traumatic brain injury and interfere with rehabilitation.
367 citations
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TL;DR: Sertraline treatment was generally well tolerated by patients as discussed by the authors, with a 40% decrease in the adjusted CDRS-R (Best Description of Child total score and reported adverse events.
Abstract: ContextThe efficacy, safety, and tolerability of selective serotonin reuptake
inhibitors (SSRIs) in the treatment of adults with major depressive disorder
(MDD) are well established. Comparatively few data are available on the effects
of SSRIs in depressed children and adolescents.ObjectiveTo evaluate the efficacy and safety of sertraline compared with placebo
in treatment of pediatric patients with MDD.Design and SettingTwo multicenter randomized, double-blind, placebo-controlled trials
were conducted at 53 hospital, general practice, and academic centers in the
United States, India, Canada, Costa Rica, and Mexico between December 1999
and May 2001 and were pooled a priori.ParticipantsThree hundred seventy-six children and adolescents aged 6 to 17 years
with Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition–defined MDD of at least moderate severity.InterventionPatients were randomly assigned to receive a flexible dosage (50-200
mg/d) of sertraline (n = 189) or matching placebo tablets (n = 187) for 10
weeks.Main Outcome MeasuresChange from baseline in the Children's Depression Rating Scale–Revised
(CDRS-R) Best Description of Child total score and reported adverse events.ResultsSertraline-treated patients experienced statistically significantly
greater improvement than placebo patients on the CDRS-R total score (mean
change at week 10, –30.24 vs –25.83, respectively; P = .001; overall mean change, –22.84 vs –20.19, respectively; P = .007). Based on a 40% decrease in the adjusted CDRS-R
total score at study end point, 69% of sertraline-treated patients compared
with 59% of placebo patients were considered responders (P = .05). Sertraline treatment was generally well tolerated. Seventeen
sertraline-treated patients (9%) and 5 placebo patients (3%) prematurely discontinued
the study because of adverse events. Adverse events that occurred in at least
5% of sertraline-treated patients and with an incidence of at least twice
that in placebo patients included diarrhea, vomiting, anorexia, and agitation.ConclusionThe results of this pooled analysis demonstrate that sertraline is an
effective and well-tolerated short-term treatment for children and adolescents
with MDD.
366 citations
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TL;DR: Tree topologies indicated that the mosquito-borne alphaviruses could have arisen in either the Old or the New World, with at least two transoceanic introductions to account for their current distribution.
Abstract: Partial E1 envelope glycoprotein gene sequences and complete structural polyprotein sequences were used to compare divergence and construct phylogenetic trees for the genus Alphavirus. Tree topologies indicated that the mosquito-borne alphaviruses could have arisen in either the Old or the New World, with at least two transoceanic introductions to account for their current distribution. The time frame for alphavirus diversification could not be estimated because maximum-likelihood analyses indicated that the nucleotide substitution rate varies considerably across sites within the genome. While most trees showed evolutionary relationships consistent with current antigenic complexes and species, several changes to the current classification are proposed. The recently identified fish alphaviruses salmon pancreas disease virus and sleeping disease virus appear to be variants or subtypes of a new alphavirus species. Southern elephant seal virus is also a new alphavirus distantly related to all of the others analyzed. Tonate virus and Venezuelan equine encephalitis virus strain 78V3531 also appear to be distinct alphavirus species based on genetic, antigenic, and ecological criteria. Trocara virus, isolated from mosquitoes in Brazil and Peru, also represents a new species and probably a new alphavirus complex.
366 citations
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TL;DR: Investigation of the effects of E2 versus several XEs on the pituitary tumor cell subline GH3/B6/F10 indicates that at very low concentrations, XEs mediate membrane-initiated intracellular Ca2+ increases resulting in PRL secretion via a mechanism similar to that for E2, but with distinct patterns and potencies that could explain their abilities to disrupt endocrine functions.
Abstract: Xenoestrogens (XEs) are widespread in our environment and are known to have deleterious effects in animal (and perhaps human) populations. Acting as inappropriate estrogens, XEs are thought to interfere with endogenous estrogens such as estradiol (E2) to disrupt normal estrogenic signaling. We investigated the effects of E2 versus several XEs representing organochlorine pesticides (dieldrin, endosulfan, o′p′-dichlorodiphenylethylene), plastics manufacturing by-products/detergents (nonylphenol, bisphenol A), a phytoestrogen (coumestrol), and a synthetic estrogen (diethylstilbestrol) on the pituitary tumor cell subline GH3/B6/F10, previously selected for expression of high levels of membrane estrogen receptor-α. Picomolar to nanomolar concentrations of both E2 and XEs caused intracellular Ca2+ changes within 30 sec of administration. Each XE produced a unique temporal pattern of Ca2+ elevation. Removing Ca2+ from the extracellular solution abolished both spontaneous and XE-induced intracellular Ca2+ changes, as did 10 μM nifedipine. This suggests that XEs mediate their actions via voltage-dependent L-type Ca2+ channels in the plasma membrane. None of the Ca2+ fluxes came from intracellular Ca2+ stores. E2 and each XE also caused unique time- and concentration-dependent patterns of prolactin (PRL) secretion that were largely complete within 3 min of administration. PRL secretion was also blocked by nifedipine, demonstrating a correlation between Ca2+ influx and PRL secretion. These data indicate that at very low concentrations, XEs mediate membrane-initiated intracellular Ca2+ increases resulting in PRL secretion via a mechanism similar to that for E2, but with distinct patterns and potencies that could explain their abilities to disrupt endocrine functions.
366 citations
Authors
Showing all 22143 results
Name | H-index | Papers | Citations |
---|---|---|---|
Stuart H. Orkin | 186 | 715 | 112182 |
Eric R. Kandel | 184 | 603 | 113560 |
John C. Morris | 183 | 1441 | 168413 |
Joseph Biederman | 179 | 1012 | 117440 |
Richard A. Gibbs | 172 | 889 | 249708 |
Timothy A. Springer | 167 | 669 | 122421 |
Gabriel N. Hortobagyi | 166 | 1374 | 104845 |
Roberto Romero | 151 | 1516 | 108321 |
Charles B. Nemeroff | 149 | 979 | 90426 |
Peter J. Schwartz | 147 | 647 | 107695 |
Clifford J. Woolf | 141 | 509 | 86164 |
Thomas J. Smith | 140 | 1775 | 113919 |
Edward C. Holmes | 138 | 824 | 85748 |
Jun Lu | 135 | 1526 | 99767 |
Henry T. Lynch | 133 | 925 | 86270 |