Predicting risk of underconfidence following maternity leave.

OBJECTIVE: To determine what factors affect paediatric trainee confidence on return to work after maternity leave. DESIGN: Information was collected anonymously via an online survey from trainees who had taken maternity leave. SETTING: The survey was distributed centrally to each UK deanery. MAIN OUTCOME MEASURES: Trainee confidence was rated retrospectively using self-assessment. RESULTS: 146 paediatric trainees from 12 out of 13 deaneries completed the survey. 96% of trainees experienced an initial lack of confidence, with 36% requiring 3 months or longer for their confidence to return. Prolonged lack of confidence was associated with longer time out of training, training stage, returning part-time, less frequent engagement with educational activities and lack of recognition by supervising consultant. CONCLUSION: We propose a scoring system using the above risk factors, the MoTHER score (Months out, Training stage, Hours worked on return, Educational activities, Recognition by consultant), which can be used to identify trainees who are at higher probability of experiencing reduced confidence on return to work.

Transgenic overexpression of the Ca2+-binding protein S100A1 in the heart leads to increased in vivo myocardial contractile performance.

S100A1, a Ca2+-sensing protein of the EF-hand family, is most highly expressed in myocardial tissue, and cardiac S100A1 overexpression in vitro has been shown to enhance myocyte contractile properties. To study the physiological consequences of S100A1 in vivo, transgenic mice were developed with cardiac-restricted overexpression of S100A1. Characterization of two independent transgenic mouse lines with approximately 4-fold overexpression of S100A1 in the myocardium revealed a marked augmentation of in vivo basal cardiac function that remained elevated after beta-adrenergic receptor stimulation. Contractile function and Ca2+ handling properties were increased in ventricular cardiomyocytes isolated from S100A1 transgenic mice. Enhanced cellular Ca2+ cycling by S100A1 was associated both with increased sarcoplasmic reticulum Ca2+ content and enhanced sarcoplasmic reticulum Ca2+-induced Ca2+ release, and S100A1 was shown to associate with the cardiac ryanodine receptor. No alterations in beta-adrenergic signal transduction or major cardiac Ca2+-cycling proteins occurred, and there were no signs of hypertrophy with chronic cardiac S100A1 overexpression. Our findings suggest that S100A1 plays an important in vivo role in the regulation of cardiac function perhaps through interacting with the ryanodine receptor. Because S100A1 protein expression is down-regulated in heart failure, increasing S100A1 expression in the heart may represent a novel means to augment contractility.