A calcium sensor in the sodium channel modulates cardiac excitability.

Sodium channels are principal molecular determinants responsible for myocardial conduction and maintenance of the cardiac rhythm. Calcium ions (Ca2+) have a fundamental role in the coupling of cardiac myocyte excitation and contraction, yet mechanisms whereby intracellular Ca2+ may directly modulate Na channel function have yet to be identified. Here we show that calmodulin (CaM), a ubiquitous Ca2+-sensing protein, binds to the carboxy-terminal 'IQ' domain of the human cardiac Na channel (hH1) in a Ca2+-dependent manner. This binding interaction significantly enhances slow inactivation-a channel-gating process linked to life-threatening idiopathic ventricular arrhythmias. Mutations targeted to the IQ domain disrupted CaM binding and eliminated Ca2+/CaM-dependent slow inactivation, whereas the gating effects of Ca2+/CaM were restored by intracellular application of a peptide modelled after the IQ domain. A naturally occurring mutation (A1924T) in the IQ domain altered hH1 function in a manner characteristic of the Brugada arrhythmia syndrome, but at the same time inhibited slow inactivation induced by Ca2+/CaM, yielding a clinically benign (arrhythmia free) phenotype.     

关于Sauer引理的一个推广

Sauer引理是统计学习理论中的基本结论．在许多实际问题中，需要研究N类模式识别问题．本文将Sauer引理推广到N类分类问题．     

乙醇三维内微肋热管的传热性能

采用实验研究的方法对三维内微肋热管的强化传热特性进行研究，首次报道了以乙醇为工质的三维内微肋热管的传热性能。在实验范围内，与光管相比，竖直放置时，沸腾换热系数可以提高98％—190％，凝结换热系数可以提高76％—178％。三维内微肋结构能够同时明显地强化热管的沸腾换热与凝结换热，可以有效地减小热管的内热阻。