Aromatizing polymerization of 1,2-diisocyanobenzene derivatives was mediated by optically active organopalladium(II) complexes bearing 1,1′-binaphth-2-yl groups to give optically active poly(quinoxaline-2,3-diyl)s with varying screw-sense selectivities, which crucially depended upon the substituents on the binaphthyl groups. The most effective catalyst, which has 7′-methoxy-1,1′-binaphthyl group, induced the formation of a single screw-sense. Isolation and structural analyses (single-crystal X-ray diffraction and 1 H NMR spectroscopy) of intermediary [oligo(quinoxalinyl)]palladium complexes revealed that the screw-sense selection in the polymerization may be decisively governed by the diastereomeric ratios of the (terquinoxalinyl)-palladium(II) complex intermediate.

Background— Many cardiac arrhythmias have their own characteristic circadian variations. Because the expression of many genes, including clock genes, is regulated variably during a day, circadian variations of ion channel gene expression, if any, could contribute to the fluctuating alterations of cardiac electrophysiological characteristics and subsequent arrhythmogenesis. Methods and Results— To examine whether cardiac K + channel gene expression shows a circadian rhythm, we analyzed the mRNA levels of 8 Kv and 6 Kir channels in rat hearts every 3 hours throughout 1 day. Among these channels, Kv1.5 and Kv4.2 genes showed significant circadian variations in their transcripts: ≈2-fold increase of Kv1.5 mRNA from trough at Zeitgeber time (ZT) 6 to peak at ZT18 and a completely reverse pattern in Kv4.2 mRNA (≈2-fold increase from trough at ZT18 to peak at ZT6). Actually, along with the variations in the immunoreactive proteins, the density of the transient outward and steady-state currents in isolated myocytes and the responses of atrial and ventricular refractoriness to 4-aminopyridine in isolated-perfused hearts showed differences between ZT6 and ZT18, a circadian pattern comparable to that of Kv1.5 and Kv4.2 gene expression. Reversal of light stimulation almost inverted these circadian rhythms, although pharmacological autonomic blockade only partially attenuated the rhythm of Kv1.5 but not of Kv4.2 transcripts. Conclusions— Among all the cardiac K + channels, Kv1.5 and 4.2 channels are unique in showing characteristic circadian patterns in their gene expression, with Kv1.5 increase during the dark period partially dependent on β-adrenergic activities and Kv4.2 increase during the light period independent of the autonomic nervous function.

Background-Atrial fibrillation (AF) is well known as one of the cardiogenic causes for thromboembolism. Although decreased flow and hypercoagulable state of the blood in the fibrillating atrium have been emphasized as the underlying mechanisms, endocardial dysfunction in maintaining the local coagulation balance could also contribute to the thrombogenesis in AF. Methods and Results-The paroxysmal AF model was created by rapid atrial pacing in anesthetized rats. To test the hypothesis that AF induces local coagulation imbalance by disturbing the atrial endocardial function, the gene expression of intrinsic anticoagulant factors, thrombomodulin (TM) and tissue factor pathway inhibitor (TFPI), were determined by means of ribonuclease protection assay, Western blotting, and immunohistochemistry. Rapid atrial pacing for 8 hours significantly decreased TM and TFPI mRNA levels in the left atrium but not in the ventricle, leading to the downregulation of their immunoreactive proteins. Immunohistochemical analysis revealed that TM and TFPI were expressed predominantly in the endocardial cells of the normal atrium, presumably preventing local blood coagulation, and that rapid atrial pacing induced the loss of TM and TFPI expression in the endocardium, leading to deficiency in anticoagulant barriers between the atria and the blood. Conclusions-Rapid

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he L-type Ca 2+ channel expressed in cardiac muscle plays an important role in determining the intracellular Ca 2+ and thus the action potential duration of cardiomyocytes. 1 Although Ca 2+ overload is a major cause of myocardial cell injury, 2 blocking this channel could be either beneficial or detrimental. In fact, the available L-type Ca 2+ channel blockers should be useful for treating several types of cardiac arrhythmias, but might cause negative inotropic effects that lead to pump failure. A T-type Ca 2+ channel blocker, mibefradil, has shown potential for preventing tachycardia-induced atrial fibrillation remodeling, 3 although its underlying mechanism of prevention remains unclear. Because the T-type Ca 2+ channel blockers are one of the "atrium specific Ca 2+ channel blockers", regional differences in the L-type Ca 2+ channel blocker, if any, would open a new paradigm for controlling regional intracellular Ca 2+ .The function of the L-type Ca 2+ channel is characterized by its main subunit, 1C (Cacna1c) (Cav1.2), and also the auxiliary subunits 2 (Cacna2d) and (Cacnb). However, there are few reports investigating regional differences in Ca 2+ channel composition. Because previous studies have focused on regional or developmental differences of a single subunit, 4,5 it would be inappropriate to discuss regional differences of the L-type Ca 2+ channel with special reference to the relative expression of the composite subunits. In the present study, to determine whether the composition of the L-type Ca 2+ channel is identical throughout the heart, we analyzed both the distribution of the mRNAs and proteins that comprise the L-type Ca 2+ channel and its electrophysiological properties in rat atria and ventricles. Methods mRNA Analysis and Ribonuclease Protection AssayHearts were harvested from 10-week-old female SpragueDawley (SD) rats. For mRNA analysis, the excised hearts were divided into the sinus-node, the right atrium, the left atrium, the intraventricular septum, the epicardial side of the left ventricular free wall, the endocardial side, the left Methods and ResultsTo determine whether the L-type Ca 2+ channel is identical throughout the heart, the distribution of the mRNAs and proteins comprising the L-type Ca 2+ channel and its electrophysiological properties were analyzed in rat atria and ventricles. The mRNA of 2 -2 (Cacna2d2) was more abundantly expressed in the atrium (~5-fold) than in the ventricle. In contrast, 1C (Cacna1c) (Cav1.2) mRNA was significantly less abundant in the atrium. The level of the 1C (Cacna1c) (Cav1.2) protein was decreased (~0.5-fold) and that of 2 -1 (Cacna2d1) was increased (~2-fold) in the atrium compared with the ventricle. Although the peak ICa,L density showed no significant differences, voltage dependence of inactivation and activation of the current showed a more depolarized shift in the atrium than in the ventricle. Conclusion These results indicate that in the rat heart the L-type Ca 2+ channel differs between the atrium and ventricle with regard to gene expre...