The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The effects of calcium entry blockade on the vulnerability of infarcted canine myocardium toward ventricular fibrillation.

The effects of the calcium entry blockers diltiazem, KB-944 [diethyl 4-(benzothiazol-2-yl)benzylphosphonate] and bepridil on the vulnerability of ischemically injured myocardium toward fibrillation were determined in urethane-anesthetized dogs 4 to 7 days after anterior myocardial infarction. Diltiazem (3.0-30.0 micrograms/kg/min X 30 min), KB-944 (0.3-3.0 mg/kg) and bepridil (1.0-10.0 mg/kg) were administered i.v. to produce equivalent increases in atrioventricular nodal effective and functional refractory periods as a measure of slow calcium channel blockade. At dosages producing equivalent increases in atrioventricular nodal refractoriness, diltiazem and KB-944 failed to increase the electrical current threshold required to produce ventricular fibrillation, whereas bepridil elevated the fibrillation threshold from 4.2 +/- 0.5 mA predrug to 14.7 +/- 2.2 mA postdrug (P less than .01). Increases in atrial (128 +/- 6-185 +/- 29 msec, P less than .01) and ventricular (156 +/- 4-175 +/- 6 msec, P less than .05) refractory periods accompanied the increase in fibrillation threshold with bepridil. These findings suggest that calcium entry blockade per se does not reduce ventricular vulnerability toward fibrillation in the setting of recent myocardial infarction.[1]


WikiGenes - Universities