Increased regional left atrial coagulation activity in mitral stenosis occurs in the presence of LASEC, is evident in either sinus rhythm or atrial fibrillation, and is associated with normal systemic coagulation activity.
Using silicon photodiodes with an ultrathin passivation layer, the average total energy lost to silicon target electrons (electronic stopping) by incident low energy ions and the recoil target atoms they generate is directly measured. We find that the total electronic energy deposition and the ratio of the total nuclear to electronic stopping powers for the incident ions and their recoils each follow a simple, universal representation, thus enabling systematic prediction of ion-induced effects in silicon. We also observe a velocity threshold at 0.05 a.u. for the onset of electronic stopping.
A hypothetical model for receptor binding of leukotriene D4 (LTD4) was deduced from conformational analysis of LTD4 and from the structure-activity relationships (SAR) of known LTD4 receptor antagonists. A new structural series of LTD4 receptor antagonists exemplified by 5-[4-(4-phenylbutoxy)phenyl]-2-[4-(tetrazol-5-yl)butyl]-2H-t etrazole was designed in which a phenyltetrazole moiety was incorporated as a receptor binding equivalent of the triene unit of LTD4. A number of these phenyltetrazoles were prepared and found to possess LTD4 receptor antagonist activity. The structure-activity relationship (SAR) of this series is described.
The effect of mexiletine, a new antiarrhythmic agent, on ventricular refractoriness and monophasic action potentials recorded from the right ventricle was studied in nine subjects. The effective refractory period of the right ventricle was determined by the extra stimulus technique using a pacing electrode situated at the right ventricular apex. Following this determination the right ventricular apex was paced at a constant cycle length and premature stimuli were introduced starting at a coupling interval of 2 ms greater than the ventricular refractory period and then at progressively increasing coupling intervals of 5 ms increments. Simultaneous recordings of monophasic action potentials of both the regular paced beats and the induced premature beats were made using a specially designed suction electrode catheter. The monophasic action potential durations were measured at 50% and 90% repolarisation. All these control measurements were repeated after an intravenous dose of 2 mg.kg-1 body wt. of mexiletine. The results showed that mexiletine did not significantly change the effective ventricular refractory period nor did it alter the monophasic action potential duration of the regular paced beat. The drug did, however, significantly prolong the monophasic action potential duration of the early induced premature beats and it is possible that this property of the drug may be related to its antiarrhythmic activity.
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