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phospholipase/diarrea
L'enllaç es desa al porta-retalls
Pàgina 1 des de 58 resultats
Intestinal Candida phospholipase is not elevated in patients with antibiotic-associated diarrhea.
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In order to assess the role of Candida-secreted phospholipase in antibiotic-associated diarrhea (AAD), 43 fecal Candida isolates from patients with AAD and from controls were tested on egg yolk agar for production of phospholipase. Phospholipase zones did not differ between the isolates from
Darapladib, a lipoprotein-associated phospholipase A2 inhibitor, in diabetic macular edema: a 3-month placebo-controlled study.
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OBJECTIVE
To investigate the potential of lipoprotein-associated phospholipase A2 inhibition as a novel mechanism to reduce edema and improve vision in center-involved diabetic macular edema (DME).
METHODS
Prospective, multicenter, randomized, double-masked, placebo-controlled phase IIa
A 50 kDa membrane protein from bovine kidney cells is a putative receptor for bovine viral diarrhea virus (BVDV).
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A 50 kDa cell surface protein from MDBK cells has been identified as a putative receptor for bovine viral diarrhea virus (BVDV) by using a BVDV specific anti-idiotypic antibody (Anti-D89). This study delineates further characterization of the receptor protein. Protease treatment of cultured MDBK
Characterization of a putative receptor protein for bovine viral diarrhea virus.
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In a previous communication, we reported a 50-kDa cell surface protein from Madin-Darby bovine kidney (MDBK) cells as a putative receptor for bovine viral diarrhea virus (BVDV). The present study delineates further characterization of the receptor protein. Protease treatment of cultured MDBK cells
How do the rotavirus NSP4 and bacterial enterotoxins lead differently to diarrhea?
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Rotavirus is the major cause of infantile gastroenteritis and each year causes 611,000 deaths worldwide. The virus infects the mature enterocytes of the villus tip of the small intestine and induces a watery diarrhea. Diarrhea can occur with no visible tissue damage and, conversely, the histological
[Involvement of nitric oxide, which was synthesized by constitutive nitric oxide synthase, and prostaglandin on diarrhea induced by castor oil in rats].
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To clarify the mechanism of castor oil-induced diarrhea, this study was performed by using rats in relation to nitric oxide (NO) and prostaglandin (PG). Castor oil induced diarrhea in all rats within 3 hr in the control group. The pretreatment of NG-nitro-L-arginine methyl ester prevented the
PCR detection and prevalence of enterotoxin (cpe) gene in Clostridium perfringens isolated from diarrhea patients.
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Clostridium perfringens isolated from patients with diarrhea (n=233) were analysed by a duplex PCR assay, in order to determine the prevalence of enterotoxin (cpe) gene and various factors involved in patients with cpe-positive isolates. This duplex PCR uses two sets of primers which amplify in the
Role of phospholipase A2 and tyrosine kinase in Clostridium difficile toxin A-induced disruption of epithelial integrity, histologic inflammatory damage and intestinal secretion.
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Clostridium difficile-associated disease causes diarrhea to fulminant colitis and death. We investigated the role of phospholipase A2 (PLA2) inhibitors, aristolochic acid (AA), bromophenacyl bromide (BPB) and quinacrine (QUIN) on the C. difficile toxin A-induced disruption of epithelial integrity,
Pyridopyrimidine derivatives as inhibitors of cyclic nucleotide synthesis: Application for treatment of diarrhea.
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Acute secretory diarrhea induced by infection with enterotoxigenic strains of Escherichia coli involves binding of stable toxin (STa) to its receptor on the intestinal brush border, guanylyl cyclase type C (GC-C). Intracellular cGMP is elevated, inducing increase in chloride efflux and subsequent
The Epac1 signaling pathway regulates Cl- secretion via modulation of apical KCNN4c channels in diarrhea.
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The apical membrane of intestinal epithelia expresses intermediate conductance K(+) channel (KCNN4), which provides the driving force for Cl(-) secretion. However, its role in diarrhea and regulation by Epac1 is unknown. Previously we have established that Epac1 upon binding of cAMP activates a
The B subunits of Shiga-like toxins induce regulated VWF secretion in a phospholipase D1-dependent manner.
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Shiga toxin (Stx) causes diarrhea-associated hemolytic uremic syndrome by damaging renal microvascular endothelium. The pentameric B subunits of Stx types 1 and 2 (Stx1B and Stx2B) are sufficient to stimulate acute VWF secretion from endothelial cells, but Stx1B and Stx2B exert distinct effects on
The rotavirus enterotoxin NSP4 mobilizes intracellular calcium in human intestinal cells by stimulating phospholipase C-mediated inositol 1,4,5-trisphosphate production.
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Rotavirus infection is the leading cause of severe diarrhea in infants and young children worldwide. The rotavirus nonstructural protein NSP4 acts as a viral enterotoxin to induce diarrhea and causes Ca2+-dependent transepithelial Cl- secretion in young mice. The cellular basis of this phenomenon
Phospholipases and cationic peptides inhibit Cryptosporidium parvum sporozoite infectivity by parasiticidal and non-parasiticidal mechanisms.
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The apicomplexan parasite Cryptosporidium parvum is an important cause of diarrhea in humans and cattle, and it can persistently infect immunocompromised hosts. No consistently effective parasite-specific pharmaceuticals or immunotherapies for control of cryptosporidiosis are presently available.
Pathogenesis of Shigella diarrhea. VII. Evidence for a cell membrane toxin receptor involving beta1 leads to 4-linked N-acetyl-D-glucosamine oligomers.
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The binding of ShigeUa dysenteriae 1 cytotoxin to HeLa cells in culture and to isolated rat liver cell membranes was studied by means of an indirect consumption assay of toxicity from the medium, or by determination of cytotoxicity to the HeLa cell monolayer. Both liver cell membranes and HeLa cells
Surface expression, polarization, and functional significance of CD73 in human intestinal epithelia.
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During active intestinal inflammation polymorphonuclear leukocytes (PMN) transmigrate into the lumen and release 5'-AMP (J. Clin. Invest. 1993. 91:2320-2325). 5'-AMP is converted to adenosine by the apical epithelial surface with subsequent activation of electrogenic Cl- secretion (the basis of
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