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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TL;DR: The results indicate that the response of net muscleprotein synthesis to consumption of an EAC solution immediately before resistance exercise is greater than that when the solution is consumed after exercise, primarily because of an increase in muscle protein synthesis as a result of increased delivery of amino acids to the leg.
Abstract: The present study was designed to determine whether consumption of an oral essential amino acid-carbohydrate supplement (EAC) before exercise results in a greater anabolic response than supplementa...
523 citations
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Paris Descartes University1, Cedars-Sinai Medical Center2, University of Alberta3, Johns Hopkins University4, University of Paris5, Autonomous University of Barcelona6, Westmead Hospital7, Harvard University8, University of Texas Medical Branch9, Yeshiva University10, University of Cologne11, Mayo Clinic12, University of Maryland, Baltimore13, Charité14, Leiden University15, University of Manitoba16, Washington University in St. Louis17, NewYork–Presbyterian Hospital18, University of North Carolina at Chapel Hill19, University of Pittsburgh20, University of California, Los Angeles21, Hammersmith Hospital22, Cornell University23, Northwestern University24
TL;DR: Improved definitions of TCMR and ABMR in pancreas transplants with specification of vascular lesions and prospects for defining a vascularized composite allograft rejection classification are included.
522 citations
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TL;DR: The evolving understanding of muscarinic receptor functions throughout the body is explored, with particular focus on the bladder, gastrointestinal tract, eye, heart, brain and salivary glands, and the implications for drugs used to treat OAB.
Abstract: 1 The effectiveness of antimuscarinic agents in the treatment of the overactive bladder (OAB) syndrome is thought to arise through blockade of bladder muscarinic receptors located on detrusor smooth muscle cells, as well as on nondetrusor structures. 2 Muscarinic M-3 receptors are primarily responsible for detrusor contraction. Limited evidence exists to suggest that M-2 receptors may have a role in mediating indirect contractions and/or inhibition of detrusor relaxation. In addition, there is evidence that muscarinic receptors located in the urothelium/suburothelium and on afferent nerves may contribute to the pathophysiology of OAB. Blockade of these receptors may also contribute to the clinical efficacy of antimuscarinic agents. 3 Although the role of muscarinic receptors in the bladder, other than M3 receptors, remains unclear, their role in other body systems is becoming increasingly well established, with emerging evidence supporting a wide range of diverse functions. Blockade of these functions by muscarinic receptor antagonists can lead to similarly diverse adverse effects associated with antimuscarinic treatment, with the range of effects observed varying according to the different receptor subtypes affected. 4 This review explores the evolving understanding of muscarinic receptor functions throughout the body, with particular focus on the bladder, gastrointestinal tract, eye, heart, brain and salivary glands, and the implications for drugs used to treat OAB. The key factors that might determine the ideal antimuscarinic drug for treatment of OAB are also discussed. Further research is needed to show whether the M-3 selective receptor antagonists have any advantage over less selective drugs, in leading to fewer adverse events. (Less)
520 citations
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TL;DR: The results support the notion that agonist is required to induce GppNHp binding and/or activation of the G proteins, and suggest that the muscarinic receptor and the IAch channel are separate molecular structures.
Abstract: Guanine nucleotide binding proteins, interchangeably called N or G proteins, seem to be the primary signal-transducing components of various agonist-induced cell membrane functions. In the heart, G proteins have been implicated in beta-adrenergic modulation of the slow inward Ca2+ current. We have investigated the role of G proteins in muscarinic activation of an inwardly rectifying, acetylcholine (ACh)-induced K+ current (IACh), and beta-adrenergic activation of an (isoprenaline)-induced Ca2+ current (Isi). Here we report that intracellular application of the non-hydrolysable GTP analogue 5'-guanylylimidodiphosphate (GppNHp) brought about an agonist-induced, antagonist-resistant, persistent activation of IACh and Isi. This functional uncoupling of channel from receptor suggests that the muscarinic receptor and the IACh channel are separate molecular structures. Membrane conductance responses to sequential activation of muscarinic and beta-adrenergic receptors demonstrate that in contrast to the muscarinic inhibition of Isi, muscarinic stimulation of IACh is mediated by a G protein via a pathway that does not involve adenylate cyclase. Taken together, the results support the notion that agonist is required to induce GppNHp binding and/or activation of the G proteins. Once triggered by agonist, the control system remains maximally activated, thereby transforming the cell so that it no longer responds to subsequent homologous receptor-mediated signals.
520 citations
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TL;DR: All 12 patients have been infected with a granulocytic Ehrlichia species, reflecting a recently described new disease entity, and early detection and treatment with tetracycline drugs appear to offer the best chance for complete recovery.
Abstract: Objective. —To characterize the clinical presentation and course, laboratory findings, and treatment outcome of 12 patients with human granulocytic ehrlichiosis. Setting. —The 12 patients were male, ranged in age from 29 to 91 years, and contracted their illness in Wisconsin or Minnesota. Methods. —Cases were recognized by the presence of intracytoplasmic inclusions (morulae) in peripheral neutrophils of patients presenting with temperature of 38.5°C or higher, chills, severe headache, and myalgias. All patients had a complete blood cell count and blood chemistry profile. Blood smears were examined by light microscopy. All available paired serum samples were analyzed for presence of indirect fluorescent antibodies againstEhrlichia chaffeensis, Ehrlichia phagocytophila, andEhrlichia equi. Blood samples from 12 patients were subjected to polymerase chain reaction analysis using primers specific for theE phagocytophila/E equigroup, primers that include the agent identified in our patients, as well asE chaffeensis. Results. —Varying combinations of leukopenia, anemia, and thrombocytopenia were found in all but one patient. All 12 patients demonstrated morulae in the cytoplasm of neutrophils, but not in mononuclear white blood cells. Serum assays failed to detect antibodies againstE chaffeensis, but eight of 10 patients and seven of 10 patients tested had antibody titers of 1:80 or more forE phagocytophilaandE equi, respectively. Polymerase chain reaction products obtained with primers forE phagocytophila, E equi, and the granulocytotropicEhrlichiarevealed that seven patients were infected with the same agent. The results of serological assays or polymerase chain reaction strongly suggest that all 12 patients were infected byE phagocytophila, E equi, or a closely relatedEhrlichiaspecies. Two of the 12 patients died. The other 10 patients improved rapidly with oral doxycycline treatment. Conclusions. —We believe that all 12 patients have been infected with a granulocyticEhrlichiaspecies, reflecting a recently described new disease entity. The infective organism appears to be closely related toE phagocytophilaandE equi. The geographic domain of human granulocytic ehrlichiosis is currently unknown. This novel granulocyticEhrlichiaspecies is capable of causing fatal infections in humans. Early detection and treatment with tetracycline drugs appear to offer the best chance for complete recovery. (JAMA. 1994;272:212-218)
519 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 |