Crack Schemaplic V 3.0
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Drug-induced leukopenia, lymphopenia, and thrombocytopenia in a renal transplant patient: Case report and literature review.
Drug-induced leukopenia, lymphopenia, and thrombocytopenia are well documented but only rarely reported complications in the context of solid organ transplantation. The other complications of solid organ transplantation are well known. In this study, the authors present a renal transplant patient who was treated for leukopenia, lymphopenia, and thrombocytopenia due to paracetamol (acetaminophen). Paracetamol has been associated with a few cases of immunosuppression-associated leukopenia, lymphopenia, and thrombocytopenia in patients without renal transplants. To the best of the authors‘ knowledge, this is the first case of drug-induced leukopenia, lymphopenia, and thrombocytopenia after a kidney transplant, documented by the authors. The literature review shows that this is the most common drug-induced complication in solid organ transplantation, with the lowest described prevalence of only 0.13%. When indicated, kidney transplant patients should be monitored for drug-induced complications because of associated hemorrhagic and thrombotic complications.Q:
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for (i=0;i
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Acetylcholine-stimulated phosphoinositide hydrolysis in response to stimulation of muscarinic receptors in rat cortical slices.
Rats were anesthetized with urethane. The muscarinic receptor subtype(s) coupled to phosphoinositide hydrolysis was studied in slices of rat cortical tissue containing the somatosensory and temporal cortex. The concentration of inositol phosphates (IPs) was measured in the presence of lithium. The muscarinic receptor antagonist atropine reversibly decreased the stimulation of IP accumulation that was produced by carbachol, an agonist at M1 and M2 muscarinic receptors. In contrast, the muscarinic receptor agonist oxotremorine-M, an M4 agonist, increased phosphoinositide hydrolysis. Phencyclidine, a non-competitive receptor antagonist at NMDA receptors, reversibly reduced the elevation in IP accumulation caused by carbachol and oxotremorine-M. The results of this study provide evidence that phosphoinositide hydrolysis in neurons is a possible mechanism for enhancing calcium influx that is mediated by M1 and M2 muscarinic receptors. In addition, the stimulation of phosphoinositide hydrolysis by oxotremorine-M in the somatosensory and temporal cortex suggests a novel pathway for acetylcholine that involves the activation of M4 receptors./* -*- Mode: C++; tab-width: 2; indent-tabs-mode: nil; c-basic-offset: 2 -*- */
/* ***** BEGIN LICENSE BLOCK *****
* Version: MPL 1.1/GPL 2.0/LGPL 2.1
*
* The contents of this file are subject to the Mozilla Public License Version
* 1.1 (the „License“); you may not use this file except in compliance with
* the License. You may obtain a copy of the
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