Direct replication of task‐dependent neural activation patterns during sadness introspection in two independent adolescent samples

Functional neuroimaging results need to replicate to inform sound models of human social cognition and its neural correlates. Introspection, the capacity to reflect on one's thoughts and feelings, is one process required for normative social cognition and emotional functioning. Engaging in introspection draws on a network of brain regions including medial prefrontal cortex (mPFC), posterior cingulate cortex (PCC), middle temporal gyri (MTG), and temporoparietal junction (TPJ). Maturation of these regions during adolescence mirrors the behavioral advances seen in adolescent social cognition, but the neural correlates of introspection in adolescence need to replicate to confirm their generalizability and role as a possible mechanism. The current study investigated whether reflecting upon one's own feelings of sadness would activate and replicate similar brain regions in two independent samples of adolescents. Participants included 156 adolescents (50% female) from the California Families Project and 119 adolescent girls from the Pittsburgh Girls Study of Emotion. All participants completed the Emotion Regulation Questionnaire (ERQ) and underwent a functional magnetic resonance imaging scan while completing the same facial emotion‐processing task at age 16–17 years. Both samples showed similar whole‐brain activation patterns when engaged in sadness introspection and when judging a nonemotional facial feature. Whole‐brain activation was unrelated to ERQ scores in both samples. Neural responsivity to task manipulations replicated in regions recruited for socio‐emotional (mPFC, PCC, MTG, TPJ) and attention (dorsolateral PFC, precentral gyri, superior occipital gyrus, superior parietal lobule) processing. These findings demonstrate robust replication of neural engagement during sadness introspection in two independent adolescent samples.     

Internists’ Attitudes About Assessing and Maintaining Clinical Competence

BACKGROUND

Important changes are occurring in how the medical profession approaches assessing and maintaining competence. Physician support for such changes will be essential for their success.

OBJECTIVE

To describe physician attitudes towards assessing and maintaining competence.

DESIGN

Cross-sectional internet survey.

PARTICIPANTS

Random sample of 1,000 American College of Physicians members who were eligible to participate in the American Board of Internal Medicine Maintenance of Certification program.

MAIN MEASURES

Questions assessed physicians’ attitudes and experiences regarding: 1) self-regulation, 2) feedback on knowledge and clinical care, 3) demonstrating knowledge and clinical competence, 4) frequency of use and effectiveness of methods to assess or improve clinical care, and 5) transparency.

KEY RESULTS

Surveys were completed by 446 of 943 eligible respondents (47 %). Eighty percent reported it was important (somewhat/very) to receive feedback on their knowledge, and 94 % considered it important (somewhat/very) to get feedback on their quality of care. However, only 24 % reported that they receive useful feedback on their knowledge most/all of the time, and 27 % reported receiving useful feedback on their clinical care most/all of the time. Seventy-five percent agreed that participating in programs to assess their knowledge is important to staying up-to-date, yet only 52 % reported participating in such programs within the last 3 years. The majority (58 %) believed physicians should be required to demonstrate their knowledge via a secure examination every 9–10 years. Support was low for Specialty Certification Boards making information about physician competence publically available, with respondents expressing concern about patients misinterpreting information about their Board Certification activities.

CONCLUSIONS

A gap exists between physicians’ interest in feedback on their competence and existing programs’ ability to provide such feedback. Educating physicians about the importance of regularly assessing their knowledge and quality of care, coupled with enhanced systems to provide such feedback, is needed to close this gap.     

Telomere shortening accompanies increased cell cycle activity during serial transplantation of hematopoietic stem cells

Reactivation of telomerase and maintenance of telomere length can lead to the prevention of replicative senescence in some human somatic cells grown in vitro. To investigate whether telomere shortening might also play a role in the limitation of hematopoietic stem cell (HSC) division capacity in vivo, we analyzed telomere length during serial transplantation of murine HSCs. Southern blot analysis of telomere length in donor bone marrow cells revealed extensive shortening ( approximately 7 kb) after just two rounds of HSC transplantation. The number of cycling HSCs increased after transplantation and remained elevated for at least 4 mo, while the frequency of HSCs in the bone marrow was completely regenerated by 2 mo after transplantation. Direct analysis of telomeres in HSCs by fluorescent in situ hybridization during serial transplantation also revealed a reduction in telomere size. Together, these data show that telomeres shorten during division of HSCs in vivo, and are consistent with the hypothesis that telomere shortening may limit the replicative capacity of HSCs.     

Neuropeptide Y Attenuates Stress‐Induced Bone Loss Through Suppression of Noradrenaline Circuits

Chronic stress and depression have adverse consequences on many organ systems, including the skeleton, but the mechanisms underlying stress‐induced bone loss remain unclear. Here we demonstrate that neuropeptide Y (NPY), centrally and peripherally, plays a critical role in protecting against stress‐induced bone loss. Mice lacking the anxiolytic factor NPY exhibit more anxious behavior and elevated corticosterone levels. Additionally, following a 6‐week restraint, or cold‐stress protocol, Npy‐null mice exhibit three‐fold greater bone loss compared to wild‐type mice, owing to suppression of osteoblast activity. This stress‐protective NPY pathway acts specifically through Y2 receptors. Centrally, Y2 receptors suppress corticotropin‐releasing factor expression and inhibit activation of noradrenergic neurons in the paraventricular nucleus. In the periphery, they act to control noradrenaline release from sympathetic neurons. Specific deletion of arcuate Y2 receptors recapitulates the Npy‐null stress response, coincident with elevated serum noradrenaline. Importantly, specific reintroduction of NPY solely in noradrenergic neurons of otherwise Npy‐null mice blocks the increase in circulating noradrenaline and the stress‐induced bone loss. Thus, NPY protects against excessive stress‐induced bone loss, through Y2 receptor‐mediated modulation of central and peripheral noradrenergic neurons. © 2014 American Society for Bone and Mineral Research.