Institution
Saint Louis University
Education•St Louis, Missouri, United States•
About: Saint Louis University is a education organization based out in St Louis, Missouri, United States. It is known for research contribution in the topics: Population & Health care. The organization has 18927 authors who have published 34895 publications receiving 1267475 citations. The organization is also known as: SLU & St. Louis University.
Topics: Population, Health care, Poison control, Transplantation, Medicine
Papers published on a yearly basis
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University of Iowa1, Cleveland Clinic2, University of Texas Southwestern Medical Center3, Duke University4, Washington University in St. Louis5, University of Alabama at Birmingham6, Boston University7, Maine Medical Center8, University of Utah9, Vanderbilt University10, Tufts University11, Baylor University Medical Center12, Saint Louis University13, Charleston Area Medical Center14, National Institutes of Health15, University of Pennsylvania16
TL;DR: Treatment with dipyridamole plus aspirin had a significant but modest effect in reducing the risk of stenosis and improving the duration of primary unassisted patency of newly created grafts.
Abstract: Background Arteriovenous graft stenosis leading to thrombosis is a major cause of complications in patients undergoing hemodialysis. Procedural interventions may restore patency but are costly. Although there is no proven pharmacologic therapy, dipyridamole may be promising because of its known vascular antiproliferative activity. Methods We conducted a randomized, double-blind, placebo-controlled trial of extended-release dipyridamole, at a dose of 200 mg, and aspirin, at a dose of 25 mg, given twice daily after the placement of a new arteriovenous graft until the primary outcome, loss of primary unassisted patency (i.e., patency without thrombosis or requirement for intervention), was reached. Secondary outcomes were cumulative graft failure and death. Primary and secondary outcomes were analyzed with the use of a Cox proportional-hazards regression with adjustment for prespecified covariates. Results At 13 centers in the United States, 649 patients were randomly assigned to receive dipyridamole plus as...
239 citations
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TL;DR: Neurons with somatic sensory receptive fields were examined electrophysiologically in the thalamic reticular nucleus of the cat and processes immunoreactive for glutamic acid decarboxylase and identifiable as both collateral axon terminals and presynaptic dendrites of GABAergic retic nucleus cells were revealed.
Abstract: Neurons with somatic sensory receptive fields were examined electrophysiologically in the thalamic reticular nucleus of the cat. All cells had receptive fields much larger than those of neurons in the ventral posterior nucleus and were driven by less readily defined somesthetic stimuli. Response latencies to peripheral or medial lemniscal stimulation were, on average, longer than in the ventral posterior nucleus and suggested activation of the reticular nucleus cells by collaterals of thalamocortical relay cell axons arising in the ventral posterior nucleus. When injected intracellularly with horseradish peroxidase, reticular nucleus cells displayed thin axons with intrareticular collaterals and diffuse branches through much of the ventral posterior and posterior thalamic nuclei. Dendrites ended in processes resembling synaptic terminals. Electron microscopic immunocytochemistry of the same part of the reticular nucleus revealed processes immunoreactive for glutamic acid decarboxylase and identifiable as both collateral axon terminals and presynaptic dendrites of GABAergic reticular nucleus cells. These synaptically linked reticular nucleus cells and, in addition, immunoreactive somata and presynaptic dendrites received synapses from at least three varieties of nonimmunoreactive profiles.
239 citations
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TL;DR: Amitriptyline, but not escitalopram, appears to benefit some patients with FD, particularly those with ulcer-like (painful) FD, and both antidepressants improved overall quality of life.
239 citations
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TL;DR: Since TF-induced coagulation is thought to play a significant role in many disease states, including disseminated intravascular clotting, sepsis, acute lung injury and cancer, recombinant TFPI may be a beneficial therapeutic agent in these disease states to attenuate pathologic clotting.
Abstract: Human tissue factor pathway inhibitor (TFPI) is a modular protein comprised of three Kunitz type domains flanked by peptide segments that are less structured. The sequential order of the elements are: an N-terminal acidic region followed by the first Kunitz domain (K1), a linker region, a second Kunitz domain (K2), a second linker region, the third Kunitz domain (K3), and the C-terminal basic region. The K1 domain inhibits factor VIIa complexed to tissue factor (TF) while the K2 domain inhibits factor Xa. No direct protease inhibiting functions have been demonstrated for the K3 domain. Importantly, the Xa-TFPI complex is a much more potent inhibitor of the VIIa-TF than TFPI by itself. Furthermore, the C-terminal basic region of TFPI is required for rapid physiologic inhibition of coagulation and is needed for the inhibition of smooth muscle cell proliferation. Although a number of additional targets for attachment have been reported, the C-terminal basic region appears to play an important role in binding of TFPI to cell surfaces. A primary site of TFPI synthesis is endothelium and the endothelium- bound TFPI contributes to the antithrombotic potential of the vascular endothelium. Further, increased levels of plasma TFPI under septic conditions may represent endothelial dysfunction. We have proposed that the extravascular cells that synthesize TF also synthesize TFPI providing dual components necessary for the regulation of clotting in their microenvironment. Like the TF synthesis in these cells is augmented by serum, so is the case with the TFPI gene expression. TFPI gene knock out mice reveal embryonic lethality suggesting a possible role of this protein in early development. Since TF-induced coagulation is thought to play a significant role in many disease states, including disseminated intravascular clotting, sepsis, acute lung injury and cancer, recombinant TFPI may be a beneficial therapeutic agent in these disease states to attenuate pathologic clotting. The purpose of this review is to outline recent developments in the field related to the structural specificity and biology of TFPI.
239 citations
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TL;DR: Varying concentrations of CSA were incubated with EC resulting in ET present in the supernatants in a dose-dependent manner peaking at 75% above basal activity, which may help in the understanding of C SA-induced hypertension and vasculopathy.
Abstract: Endothelin (ET), a peptide synthesized by endothelial cells (EC), causes a decreased renal blood flow and glomerular filtration rate and an increased mean arterial pressure when infused in animals. In tissue culture, ET causes smooth muscle cell (SMC) proliferation and contraction by influx of extracellular calcium, which is inhibited by calcium channel antagonists. Infusion of cyclosporine (CSA) hemodynamically parallels ET action, and knowing that CSA effects EC, we hypothesize that the vasoconstrictive effects of CSA are a result of ET synthesis by EC. Varying concentrations of CSA were incubated with EC resulting in ET present in the supernatants in a dose-dependent manner peaking at 75% above basal activity. Coincubation of either cremophor alone or cycloheximide with CSA resulted in minimal ET present in the EC supernatants (P less than 0.01 each). Incubation of conditioned media from CSA-treated EC with SMC caused proliferation at 114% above basal activity, which did not occur in the presence of CSA alone (P less than 0.01). This activity is specifically inhibited in the presence of an anti-ET antibody or nonspecifically in the presence of calcium channel antagonists (P less than 0.01 each). Therefore, CSA stimulates EC synthesis of ET which in turn causes SMC proliferation. This action is inhibited by the coincubation of a specific antibody to ET or a calcium channel antagonist. These findings may help in the understanding of CSA-induced hypertension and vasculopathy.
239 citations
Authors
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Name | H-index | Papers | Citations |
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Douglas G. Altman | 253 | 1001 | 680344 |
John E. Morley | 154 | 1377 | 97021 |
Roberto Romero | 151 | 1516 | 108321 |
Daniel S. Berman | 141 | 1363 | 86136 |
Gregory J. Gores | 141 | 686 | 66269 |
Thomas J. Smith | 140 | 1775 | 113919 |
Richard T. Lee | 131 | 810 | 62164 |
George K. Aghajanian | 121 | 277 | 48203 |
Reza Malekzadeh | 118 | 900 | 139272 |
Robert N. Weinreb | 117 | 1124 | 59101 |
Leslee J. Shaw | 116 | 808 | 61598 |
Thomas J. Ryan | 116 | 675 | 67462 |
Josep M. Llovet | 116 | 399 | 83871 |
Robert V. Farese | 115 | 473 | 48754 |
Michael Horowitz | 112 | 982 | 46952 |