Considering the effects of alcohol on cardiac electrical behavior as well as the important role of the inward rectifier potassium current I K1 in arrhythmogenesis, this study was aimed at the effect of acetaldehyd e, the primary metabolite of ethanol, on I K1 in rat ventricular myocytes. Acetaldehyde induced a reversible inhibition of I K1 with IC 50 = 53.7± 7.7 μM at -110 mV; a significant inhibition was documented even at clinically -relevant concentrations (at 3 μM by 13.1 ±3.0 % ). The inhibition was voltage -independent at physiological voltages above - 90 mV. The I K1 changes under acetaldehyde may contribute to alcohol - induced alterations of cardiac electrophysiology, especially in individuals with a genetic defect of a ldehyde dehydrogenase where the acetaldehyde level may be elevated., M. Bébarová, P. Matejovič, M. Šimurdová, J. Šimurda., and Obsahuje bibliografii
Experiments were performed in C57BL/6J male mice to determine the effects of acetylcholinesterase (AChE) inhibitor pyridostigmine bromide (PB) and stress on cardiovascular function, structure, and apoptosis. Mice were studied for seven days under the following conditions: Controls (osmotic minipump with saline), PB (10 mg/kg/day, minipumps), shaker stress (45 stressors/day, minipump with saline) and PB+Stress combination. AChE activity was significantly reduced in all PB-treated mice. PB caused no changes in 24-h mean arterial pressure (MAP) or heart rate (HR). Stress
increased 24-h MAP on day 1 and 24-h HR on day 7 in both Stress and PB+Stress groups. A significant reduction in the aortic wall thickness/diameter ratio (P <0.05 vs. control) and slightly reduced relative heart weight were observed in the PB group. These effects were blunted by simultaneous stress exposure. Immunochemistry was used to stain for Bax and Bcl-2 (apoptosis markers). There was a four-fold increase in Bax/Bcl-2 ratio in the heart of PB and PB+Stress treated mice while an attenuation was observed in aortic endothelium. Results suggest that a relatively short-term continuous PB exposure may have adverse effects on the heart and blood vessels, independently of changes in MAP and HR.
Achillea asplenifolia Vent. is one of three central European diploid species (together with A. setacea Waldst. et Kit. and A. roseoalba Ehrend.) of the A. millefolium group. Its taxonomic and phytogeographic account from the central European perspective is given mainly on the basis of herbarium and field studies. The synonymy of A. asplenifolia includes A. millefolium var. crustata Rochel and A. scabra Host; both names are typified here. No variation deserving taxonomic recognition was observed. From the taxonomic point of view, A. asplenifolia is a clearly delimited species. It grows in the Czech Republic, Slovakia, Austria, Hungary, Croatia, Serbia, and Romania. From the phytogeographic point of view, it can be classified as a Pannonian geoelement with overlaps to Transylvania and to the marginal parts of the eastern Mediterranean. Within the Czech Republic, its distribution range includes only the warmest and driest part of southern Moravia, with the northernmost site situated near the town of Vyškov. In southern Moravia, A. asplenifolia was confined to extrazonal habitats, mainly to islands of halophilous vegetation such as moist saline meadows (formerly used as pastures) and lowland fens rich in mineral nutrients, but most of the sites were destroyed. Out of six or seven localities preserved up to present, only two host vital populations.
The achromatic number of a graph $G$ is the maximum number of colours in a proper vertex colouring of $G$ such that for any two distinct colours there is an edge of $G$ incident with vertices of those two colours. We determine the achromatic number of the Cartesian product of $K_5$ and $K_n$ for all $n \le 24$.