Evidence for an own-age bias in age estimation from voices in older persons

Previous studies have investigated the effect of ageing on age estimation from faces as well as the occurrence of an own-age bias in such age estimation from faces. To the best of our knowledge, the occurrence of an own age effect on age estimation from voices has never been examined earlier using an experimental design in which the age of participants (young vs. old) and the age of voice stimuli (young vs. old) were crossed. Results revealed an own-age bias in older adults only. In comparison with younger adults, older participants showed age estimation abilities that are preserved for voices from their own age group and impaired for younger voices. This own age bias was absent in younger participants.     

Reappraisal of the Traditional Wenckebach Phenomenon with a Modified Ladder Diagram

Understanding of the traditional Wenckebach phenomenon is enhanced by using a modified ladder diagram where AV conduction in any cycle is represented by a slanted line in the AV bar together with similar AV conduction lines of all the preceding cycles. The diagram facilitates calculation of the duration of RR intervals (equal to the basic PP or sinus interval minus the PR or AV increment applied to this particular cycle) and the duration of the pause (equal to 2 × PP or sinus interval minus the sum of all the increments applied to the AV delay). The modified Wenckebach diagram should help students understand the mysterious clustering of QRS complexes or “paradoxical” increase of the ventricular rate that occurs during a Wenckebach sequence. Ann Noninvasive Electrocardiol 2012;17(1):3–7     

Quantitation in gated perfusion SPECT imaging: the Cedars-Sinai approach.

Cedars-Sinai's approach to the automation of gated perfusion single photon emission computed tomography (SPECT) imaging is based on the identification of key procedural steps (processing, quantitation, reporting), each of which is then implemented, in completely automated fashion, by use of mathematic algorithms and logical rules combined into expert systems. Our current suite of software applications has been designed to be platform- and operating system-independent, and every algorithm is based on the same 3-dimensional sampling scheme for the myocardium. The widespread acceptance of quantitative software by the nuclear cardiology community (QGS alone is used at over 20,000 locations) has provided the opportunity for extensive validation of quantitative measurements of myocardial perfusion and function, in our opinion, helping to make nuclear cardiology the most accurate and reproducible modality available for the assessment of the human heart.     

Abnormal calcium signaling and sudden cardiac death associated with mutation of calsequestrin

Mutations in human cardiac calsequestrin (CASQ2), a high-capacity calcium-binding protein located in the sarcoplasmic reticulum (SR), have recently been linked to effort-induced ventricular arrhythmia and sudden death (catecholaminergic polymorphic ventricular tachycardia). However, the precise mechanisms through which these mutations affect SR function and lead to arrhythmia are presently unknown. In this study, we explored the effect of adenoviral-directed expression of a canine CASQ2 protein carrying the catecholaminergic polymorphic ventricular tachycardia-linked mutation D307H (CASQ2(D307H)) on Ca2+ signaling in adult rat myocytes. Total CASQ2 protein levels were consistently elevated approximately 4-fold in cells infected with adenoviruses expressing either wild-type CASQ2 (CASQ2(WT)) or CASQ2(D307H). Expression of CASQ2(D307H) reduced the Ca2+ storing capacity of the SR. In addition, the amplitude, duration, and rise time of macroscopic I(Ca)-induced Ca2+ transients and of spontaneous Ca2+ sparks were reduced significantly in myocytes expressing CASQ2(D307H). Myocytes expressing CASQ2(D307H) also displayed drastic disturbances of rhythmic oscillations in [Ca2+]i and membrane potential, with signs of delayed afterdepolarizations when undergoing periodic pacing and exposed to isoproterenol. Importantly, normal rhythmic activity was restored by loading the SR with the low-affinity Ca2+ buffer, citrate. Our data suggest that the arrhythmogenic CASQ2(D307H) mutation impairs SR Ca2+ storing and release functions and destabilizes the Ca2+-induced Ca2+ release mechanism by reducing the effective Ca2+ buffering inside the SR and/or by altering the responsiveness of the Ca2+ release channel complex to luminal Ca2+. These results establish at the cellular level the pathological link between CASQ2 mutations and the predisposition to adrenergically mediated arrhythmias observed in patients carrying CASQ2 defects.