cholera/cannabis

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14 rezilta yo

Cannabis, hypochlorhydria, and cholera.

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In 90 volunteers participating in a vaccine-development programme consumption of beer more than 3 days a week was linked with high stomach acid output, and smoking of cannabis greater than 2 days a week was linked with low acid output. In 92 volunteers challenged with Vibrio cholerae or

Differential cholera-toxin sensitivity of supraspinal antinociception induced by the cannabinoid agonists delta9-THC, WIN 55,212-2 and anandamide in mice.

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Intracerebroventricular (i.c.v.) administration to mice of delta9-tetrahydrocannabinol (delta9-THC), WIN 55,212-2 or the endogenous cannabinoid anandamide induced dose-related antinociception in the 55 degrees C warm-water tail-flick test. Pretreatment (24 h, i.c.v.) with pertussis toxin

An endogenous cannabinoid tone attenuates cholera toxin-induced fluid accumulation in mice.

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OBJECTIVE Cholera toxin (CT) is the most recognizable enterotoxin causing secretory diarrhea, a major cause of infant morbidity and mortality throughout the world. In this study, we investigated the role of the endogenous cannabinoid system (i.e., the cannabinoid receptors and their endogenous

Marijuana for cholera therapy.

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Activation of large-conductance, Ca2+-activated K+ channels by cannabinoids.

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We have examined the effects of the cannabinoid anandamide (AEA) and its stable analog, methanandamide (methAEA), on large-conductance, Ca2+-activated K+ (BK) channels using human embryonic kidney (HEK)-293 cells, in which the alpha-subunit of the BK channel (BK-alpha), both alpha- and

Cannabinoid CB1 receptor elevation of intracellular calcium in neuroblastoma SH-SY5Y cells: interactions with muscarinic and delta-opioid receptors.

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Although coupled to G(i/o) proteins, cannabinoid CB(1) receptors can also activate intracellular Ca(2+) ([Ca(2+)](i)) accumulation through not fully understood mechanisms. We report that in, human neuroblastoma SH-SY5Y cells, CB(1) activation with the specific agonist arachidonoylchloroethanolamide

Biphasic modulation of voltage-dependent currents of retinal cones by cannabinoid CB1 receptor agonist WIN 55212-2.

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Endogenous cannabinoids modulate neurotransmitter action and release in the brain. The effects are exerted on membrane permeability to Ca2+ and K+ via protein kinase A (PKA). Cannabinoid CB1 receptors are present at the synaptic terminals of cones in goldfish retina. We investigated the effects of

Cannabinoid and kappa opioid receptors reduce potassium K current via activation of G(s) proteins in cultured hippocampal neurons.

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The current study showed that potassium K current (I(K)), which is evoked at depolarizing potentials between -30 and +40 mV in cultured hippocampal neurons, was significantly reduced by exposure to the CB1 cannabinoid receptor agonist WIN 55,212-2 (WIN-2). WIN-2 (20-40 nM) produced an average 45%

G-protein mediation of cannabinoid-induced phospholipase activation.

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The release of arachidonic acid from mouse peritoneal and S49 cells induced by delta 1-tetrahydrocannabinol was found to be altered by prior exposure of the cells to either pertussis toxin or cholera toxin. The stable analogs of GTP and GDP, GTP-gamma-S and GDP-beta-S, were also effective in

The central cannabinoid receptor (CB1) mediates inhibition of nitric oxide production by rat microglial cells.

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Upon activation, brain microglial cells release proinflammatory mediators, such as nitric oxide (NO), which may play an important role in the central nervous system antibacterial, antiviral, and antitumor activities. However, excessive release of NO has been postulated to elicit immune-mediated

Cannabinoids and the digestive tract.

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In the digestive tract there is evidence for the presence of high levels of endocannabinoids (anandamide and 2-arachidonoylglycerol) and enzymes involved in the synthesis and metabolism of endocannabinoids. Immunohistochemical studies have shown the presence of CB1 receptors on myenteric and

Concurrent stimulation of cannabinoid CB1 and dopamine D2 receptors augments cAMP accumulation in striatal neurons: evidence for a Gs linkage to the CB1 receptor.

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Cannabinoids act at the CB1 receptor to inhibit adenylate cyclase activity via a pertussis toxin-sensitive G-protein. Within the striatum, CB1 receptors have been shown to be localized on the same neurons as Gi-coupled dopamine D2 receptors. In this study we have examined the interactions of CB1 and

Involvement of the carboxyl terminus of the third intracellular loop of the cannabinoid CB1 receptor in constitutive activation of Gs.

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The human cannabinoid receptor CB1 functionally couples primarily to Gi-, but also to Gs-mediated pathways to modulate intracellular cyclic AMP (cAMP) levels. To probe the features of the receptor that may be involved in promoting interactions with one G protein type over another, we generated the

Sir William Brooke O'Shaughnessy (1808-1889), MD, FRS, LRCS Ed: Chemical pathologist, pharmacologist and pioneer in electric telegraphy.

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This article reviews the life and work of Sir William O'Shaughnessy Brooke (formerly Sir William Brooke O'Shaughnessy), an Edinburgh doctor of medicine and Fellow of the Royal Society who as a young doctor in London analysed the blood and excreta of cholera victims, an action which led to the first

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