The impact on students of adverse experiences during medical school.

This study aimed to determine the consequences for, and coping method used by, medical students who experienced adverse experiences during their training. A nationwide questionnaire based census of all current medical students in New Zealand. The response rate was 83% (1384/1660). Two-thirds of students had at least one adverse experience, with humiliation being the most common and having the greatest adverse impact. Unwanted sexual advances, unfair treatment on the basis of gender or race had a lesser impact for most students. Most students took several hours or several days to get over an adverse episode and most commonly they then avoided that person or department. Around one half sought help. Only one-quarter felt it motivated their learning while one-sixth felt it made them consider leaving medical school. The most common perpetrators were senior doctors or nurses. Unwanted sexual advances were most common from other students or from patients. Humiliation is the experience that affected students the most and had a significant adverse effect on learning. There is a disturbing rate of unacceptable practice within medical schools, not all of which is from doctors.

Hippocalcin functions as a calcium sensor in hippocampal LTD.

It is not fully understood how NMDAR-dependent LTD causes Ca(2+)-dependent endocytosis of AMPARs. Here we show that the neuronal Ca(2+) sensor hippocalcin binds the beta2-adaptin subunit of the AP2 adaptor complex and that along with GluR2 these coimmunoprecipitate in a Ca(2+)-sensitive manner. Infusion of a truncated mutant of hippocalcin (HIP(2-72)) that lacks the Ca(2+) binding domains prevents synaptically evoked LTD but has no effect on LTP. These data indicate that the AP2-hippocalcin complex acts as a Ca(2+) sensor that couples NMDAR-dependent activation to regulated endocytosis of AMPARs during LTD.

Endurance training adherence in elite junior netball athletes: a test of the theory of planned behaviour and a revised theory of planned behaviour.

This study examined the utility of Ajzen's (1985) theory of planned behaviour and Maddux's (1993) revised theory of planned behaviour to predict endurance training intentions and adherence of elite junior netball athletes. One hundred and fifteen athletes from the England Netball World Class Start Programme were assessed on constructs central to the predictions of the two theories. Adherence to a recommended endurance training programme was recorded in self-report diaries across a 9-week period. Validity for the diaries was supported by significant correlations (P < 0.001) with recalls across 7 days and 9 weeks. Adherence was moderate and variable between athletes (mean = 66.05, s = 25.75%). Two separate path analyses were conducted to examine the predictions of the theories. Goodness-of-fit indices suggested acceptable fit of the data to the models. Analyses showed that attitude towards the new behaviour, subjective norms and perceived behavioural control predicted training intentions. The relationship between intention and adherence was weak. The present results suggest that the constructs of the theory of planned behaviour offer some insight into the explanation of intentions to follow an endurance training programme. Constructs unique to the revised theory of planned behaviour did not significantly predict training intentions or behaviour. Implications for practitioners working with team sport performers are provided.

The molecular pharmacology and cell biology of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors.

Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs) are of fundamental importance in the brain. They are responsible for the majority of fast excitatory synaptic transmission, and their overactivation is potently excitotoxic. Recent findings have implicated AMPARs in synapse formation and stabilization, and regulation of functional AMPARs is the principal mechanism underlying synaptic plasticity. Changes in AMPAR activity have been described in the pathology of numerous diseases, such as Alzheimer's disease, stroke, and epilepsy. Unsurprisingly, the developmental and activity-dependent changes in the functional synaptic expression of these receptors are under tight cellular regulation. The molecular and cellular mechanisms that control the postsynaptic insertion, arrangement, and lifetime of surface-expressed AMPARs are the subject of intense and widespread investigation. For example, there has been an explosion of information about proteins that interact with AMPAR subunits, and these interactors are beginning to provide real insight into the molecular and cellular mechanisms underlying the cell biology of AMPARs. As a result, there has been considerable progress in this field, and the aim of this review is to provide an account of the current state of knowledge.