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Physical interaction between bovine viral diarrhea virus nonstructural protein 4A and adenosine deaminase acting on RNA (ADAR).
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Bovine viral diarrhea virus (BVDV) is a positive-sense RNA virus known to produce double-stranded RNA (dsRNA) during its replication in the cytoplasm. Extended dsRNA duplexes can be hyperedited by adenosine deaminase acting on RNA (ADAR), which catalyzes adenosine (A)-to-inosine (I) editing. A-to-I
Adenosine A2B Receptors: An Optional Target for the Management of Irritable Bowel Syndrome with Diarrhea?
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Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder, with the characteristic symptoms of chronic abdominal pain and altered bowel habits (diarrhea, constipation, or both). IBS is a highly prevalent condition, which negatively affects quality of life and is a significant burden
Zinc in the treatment of acute diarrhea: current status and assessment.
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The improved treatment of acute diarrhea in children during the past 35 years has reduced its morbidity and mortality substantially. However, better therapy still is required. This article reviews the role of oral rehydration solution in the treatment of acute diarrhea with particular attention to
The role of bacterial and non-bacterial toxins in the induction of changes in membrane transport: implications for diarrhea.
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Bacterial toxins induce changes in membrane transport which underlie the loss of electrolyte homeostasis associated with diarrhea. Bacterial- and their secreted toxin-types which have been linked with diarrhea include: (a) Vibrio cholerae (cholera toxin, E1 Tor hemolysin and accessory cholera
Impact of disrupting adenosine A₃ receptors (A₃⁻/⁻ AR) on colonic motility or progression of colitis in the mouse.
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BACKGROUND
Pharmacological studies suggest that adenosine A₃AR influences motility and colitis. Functional A₃⁻/⁻AR knockout mice were used to prove whether A₃AR activation is involved in modulating either motility or colitis.
METHODS
A₃AR was probed by polymerase chain reaction (PCR) genotyping,
Effects of the adenosine A1-receptor antagonist on defecation, small intestinal propulsion and gastric emptying in rats.
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We examined the effects of 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) and (R)-7,8-dihydro-8-ethyl-2-(3-noradamantyl)-4-propyl-1H-imidazo[2,1 -i]purin- 5(4H)-one (KF20274), selective adenosine A1-receptor antagonists, on the gastrointestinal propulsion in rats, as compared with those of the laxative
Adenosine 2b receptor (A2bR) signals through adenylate cyclase (AC) 6 isoform in the intestinal epithelial cells.
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Adenosine 2b receptor (A2bR), a G-protein coupled receptor positively coupled to adenylate cyclase, mediates key events such as chloride, IL-6 and fibronectin secretion in intestinal epithelial cells and is upregulated during intestinal inflammation. In order to gain insight into the overall
Feedback effects of host-derived adenosine on enteropathogenic Escherichia coli.
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Enteropathogenic E. coli (EPEC) is a common cause of diarrhea in children in developing countries. After adhering to intestinal cells, EPEC secretes effector proteins into host cells, causing cell damage and eventually death. We previously showed that EPEC infection triggers the release of ATP from
Alterations of adenosine A1 receptors in morphine dependence.
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The possibility that central adenosine A1 and A2a receptors mediate opiate dependence was examined in morphine-treated mice using radioligand binding methods. Mice treated with morphine for 72 h demonstrated significant increases in naloxone precipitated abstinence behaviors of jumping, wet-dog
Inhibition by adenosine analogs of opiate withdrawal effects.
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The stable derivatives of adenosine, 2-chloroadenosine and N6-cyclohexyladenosine, with high affinity for the A1 (Ri) adenosine receptor, suppress the naloxone-precipitated withdrawal contracture of the opiate-dependent guinea-pig ileum in vitro. These adenosine derivatives also inhibit
Adenosine scavenging: a novel mechanism of chloride secretory control in intestinal epithelial cells.
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BACKGROUND
Adenosine released by cells during ischemia typically serves as a feedback inhibitor of further organ work. However, in ischemic intestine, adenosine appears to act via stimulatory A2b receptors to increase work in the form of chloride ion (Cl-) secretion. This unusual response may
Severe combined immune deficiency in an adenosine deaminase-deficient patient.
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A case of adenosine deaminase (ADA) deficiency is described briefly. The clinical characteristics, pathogenesis, diagnosis, and management of this disease are discussed, followed by clinical pearls and pitfalls. ADA deficiency was identified in 1972 as a cause of severe combined immunodeficiency
5'-adenosine monophosphate is the neutrophil-derived paracrine factor that elicits chloride secretion from T84 intestinal epithelial cell monolayers.
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Neutrophil transmigration across intestinal epithelia is thought to contribute to epithelial dysfunction and characterizes many inflammatory intestinal diseases. Neutrophils activated by factors, normally present in the lumen, release a neutrophil-derived secretagogue activity to which intestinal
Production and characterization of multiple antigenic peptide antibodies to the adenosine A2b receptor.
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A polyclonal antibody to the human adenosine A2b receptor (A2bR) was produced by immunizing a chicken with a multiple antigenic peptide consisting of eight copies of a 16-amino acid peptide, corresponding to the presumed second extracellular loop of the A2bR, linked to a branched lysine core.
[Adenosine deaminase in typhoid fever and other febrile diseases].
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The contribution of serum adenosine deaminase (ADA) activity to the diagnosis of typhoid fever was assessed in 246 children and in 46 adults, by Giusti's original technique. Children included otherwise healthy patients admitted for elective surgical conditions or under follow up for epilepsy which
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