adenosine diphosphate/diarrhea

Altered platelet function has been reported in calves experimentally infected with type II bovine viral diarrhea virus (BVDV). The purpose of the present study was to further evaluate the ability of BVDV isolates to alter platelet function and to examine for the presence of a virus-platelet

OBJECTIVE To evaluate platelet aggregation responses in calves experimentally infected with a thrombocytopenia-inducing type II bovine viral diarrhea virus (BVDV) isolate (BVDV 890). METHODS 9 neonatal male Holstein calves. METHODS 5 calves were inoculated with BVDV 890, and 4 were used as controls.

Escherichia coli heat-labile enterotoxins (LT) are responsible in part for "traveler's diarrhea" and related diarrheal illnesses. The family of LTs comprises two serogroups termed LT-I and LT-II; each serogroup includes two or more antigenic variants. The effects of LTs result from ADP ribosylation

Effective antiplatelet drugs--aspirin, ticlopidine, dipyridamole, and clopidogrel--are reviewed. Aspirin has remained the pharmacologic foundation of stroke prevention, primarily because of its low cost. It has been shown to provide a 22% relative risk reduction of stroke in high-risk patients. Its

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of ticlopidine are reviewed. Ticlopidine appears to inhibit platelet aggregation induced by adenosine diphosphate. Ticlopidine hydrochloride is rapidly absorbed after oral administration, and maximum

Ticlopidine is a powerful antiplatelet activator that inhibits adenosine diphosphate (ADP)-induced platelet aggregation. Its most common side-effects are skin rashes, diarrhea and neutropenia. Aplastic anemia is rare. This paper reports a patient with severe aplastic anemia that developed after the

Cholera toxin (CT), the most commonly used mucosal adjuvant in experimental animals, is unsuitable for humans because of potent diarrhea-inducing properties. We have constructed two CT-A subunit mutants, e.g., serine-->phenylalanine at position 61 (S61F), and glutamic acid-->lysine at 112 (E112K) by

Pathogenesis of cholera diarrhea requires cholera toxin (CT)-mediated adenosine diphosphate (ADP)-ribosylation of stimulatory G protein (Gsα) in enterocytes. CT is an AB5 toxin with an inactive CTA1 domain linked via CTA2 to a pentameric receptor-binding B subunit. Allosterically activated CTA1

The antibacterial efficacy of ceftriaxone (CTRX) against group B Streptococcus and its clinical efficacy in newborns were examined, and the results obtained are summarized as follows. 1. MIC's of CTRX against 55 strains of B group Streptococcus from the pregnant vagina were 0.10 micrograms/ml or

BACKGROUND In the aftermath of a devastating earthquake in early 2011, Haiti fell victim to an outbreak of cholera that claimed thousands of lives and affected populations in nearby Dominican Republic, Venezuela, and even the United States. This was the first time cholera had been reported in Haiti

Toona microcarpa Harms is a tonic, antiperiodic, antirheumatic, and antithrombotic agent in China and India and an astringent and tonic for treating diarrhea, dysentery, and other intestinal infections in Indonesia. In this study, we prepared ethyl-acetate extract from the air-dried leaves of Toona

Secretomotor reflexes in the gastrointestinal (GI) tract are important in the lubrication and movement of digested products, absorption of nutrients, or the diarrhea that occurs in diseases to flush out unwanted microbes. Mechanical or chemical stimulation of mucosal sensory enterochromaffin (EC)

Enteropathogenic Escherichia coli (EPEC) triggers a large release of adenosine triphosphate (ATP) from host intestinal cells and the extracellular ATP is broken down to adenosine diphosphate (ADP), AMP, and adenosine. Adenosine is a potent secretagogue in the small and large intestine. We suspected

The Vibrio cholerae bacterium causes devastating diarrhea when it infects the human intestine. The key event is adenosine diphosphate (ADP)-ribosylation of the human signaling protein GSalpha, catalyzed by the cholera toxin A1 subunit (CTA1). This reaction is allosterically activated by human