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Graphics, survey research, and multivariate statistical techniques were applied at a private liberal arts college to help development professionals better understand and predict alumni giving behavior, both on an aggregate and individual basis.

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SUMMARY PARAGRAPHPhysiological systems require feedback to maintain normal function. In the heart, electrical excitation causes mechanical contraction1, with feedback of mechanics to electrics occurring through ‘mechano-electric coupling’ processes2. In diseases that affect cardiac mechanics, this feedback can result in deadly mechanically-induced arrythmias (‘mechano-arrhythmogenicity’)3. However, the molecular identity of the specific factor(s) driving mechano-arrhythmogenicity are unknown4. Here we show that mechano-sensitive5–10 transient receptor potential kinase ankyrin 1 (TRPA1) channels11 are a source of cardiac mechano-arrhythmogenicity through a calcium (Ca2+)-driven mechanism. Using a cell-level approach involving stretch of single ventricular myocytes combined with simultaneous voltage-Ca2+ imaging, we found that activation of TRPA1 channels resulted in an increase in diastolic Ca2+ load and the appearance of stretch-induced arrhythmias, which were driven by trans-sarcolemmal fluxes and intracellular oscillations of Ca2+, and prevented by pharmacological TRPA1 channel block or Ca2+ buffering. Our results demonstrate that TRPA1 channels act as a trigger for stretch-induced excitation (via Ca2+-influx) and create a substrate for complex arrhythmic activity (via Ca2+-overload), and thus may represent a novel anti-arrhythmic target in cardiac diseases in which TRPA1 channel expression and activity are augmented12–16.