An Equitable Electronic Scheduling System for Anesthesiology Residents: A Quality Improvement Project.

BACKGROUND: Most postgraduate medical education occurs in hospitals in an apprenticeship model with actual patients. Creating a work shift schedule must account for complex factors, including hospital needs, work-hour restrictions, trainee qualifications, and case distribution in order to fairly allocate the resident workload. In this study, we report the first successful implementation of an equitable, computer-generated scheduling system for anesthesiology residents. METHODS: A total of 24 residents at a single, urban training program were surveyed in 2015 to rank work shift difficulty. Shifts were categorized and translated into a weighted point system by program leadership based on the survey results. An automated and modifiable scheduling system was created to incorporate rule-based assignment of prerequisites and evenly distribute points throughout the academic year. Point values were retrospectively calculated in 2014, and prospectively calculated from 2015 to 2018. The equality of variance test was used to evaluate the variation of the SD of monthly average point distributions year-over-year and within each class of trainees. RESULTS: Year-over-year analysis revealed that post-point system implementation, call point distribution trended toward reduced variance in all 4 years, with significant reductions of 63% in 2016 (SD 4.9, P < .01), and 57% in 2017 (SD 5.8, P < .01). Analyzed by class, first-year trainees' SD decreased by 73% in 2016 (SD 2.5, P < .01), by 67% in 2017 (SD 3.1, P < .04), and 65% in 2018 (SD 3.3, P < .02) compared with the pre-point system year in 2014. The second year clinical anesthesia resident class SD decreased by 56% in 2015 (SD 5.9, P < .01), 41% in 2016 (SD 7.9, P < .02), and 49% in 2017 (SD 6.9, P < .01). CONCLUSION: The computerized point system improved work distribution equity year-over-year and within trainee cohort groups.

A systematic review of the Second Step program.

This article presents findings from a meta-analysis of 24 primary research studies on the Second Step social emotional learning program. Program content knowledge, outcomes related to prosociality, and outcomes related to antisociality are examined as outcome categories in randomized controlled trials, quasi-experimental studies and, separately, single-group repeated measures design studies. Students participating in Second Step demonstrated increased knowledge of program content and increased prosocial outcomes. Participation in the program was not associated with significant changes in antisocial outcomes. Evidence suggests the possibility of publication bias in studies reporting knowledge outcomes but no evidence of publication bias in studies reporting prosocial and antisocial outcomes. This study complements broader meta-analyses on SEL programs and aims to inform local decision making by providing an estimate of the overall effects of the Second Step program on a variety of student outcomes.

Corrigendum: Sex-specific transcriptional signatures in human depression.

This corrects the article DOI: 10.1038/nm.4386.

Sex-specific transcriptional signatures in human depression.

Major depressive disorder (MDD) is a leading cause of disease burden worldwide. While the incidence, symptoms and treatment of MDD all point toward major sex differences, the molecular mechanisms underlying this sexual dimorphism remain largely unknown. Here, combining differential expression and gene coexpression network analyses, we provide a comprehensive characterization of male and female transcriptional profiles associated with MDD across six brain regions. We overlap our human profiles with those from a mouse model, chronic variable stress, and capitalize on converging pathways to define molecular and physiological mechanisms underlying the expression of stress susceptibility in males and females. Our results show a major rearrangement of transcriptional patterns in MDD, with limited overlap between males and females, an effect seen in both depressed humans and stressed mice. We identify key regulators of sex-specific gene networks underlying MDD and confirm their sex-specific impact as mediators of stress susceptibility. For example, downregulation of the female-specific hub gene Dusp6 in mouse prefrontal cortex mimicked stress susceptibility in females, but not males, by increasing ERK signaling and pyramidal neuron excitability. Such Dusp6 downregulation also recapitulated the transcriptional remodeling that occurs in prefrontal cortex of depressed females. Together our findings reveal marked sexual dimorphism at the transcriptional level in MDD and highlight the importance of studying sex-specific treatments for this disorder.

Nuclear export inhibitors avert progression in preclinical models of inflammatory demyelination.

Axonal damage has been associated with aberrant protein trafficking. We examined a newly characterized class of compounds that target nucleo-cytoplasmic shuttling by binding to the catalytic groove of the nuclear export protein XPO1 (also known as CRM1, chromosome region maintenance protein 1). Oral administration of reversible CRM1 inhibitors in preclinical murine models of demyelination significantly attenuated disease progression, even when started after the onset of paralysis. Clinical efficacy was associated with decreased proliferation of immune cells, characterized by nuclear accumulation of cell cycle inhibitors, and preservation of cytoskeletal integrity even in demyelinated axons. Neuroprotection was not limited to models of demyelination, but was also observed in another mouse model of axonal damage (that is, kainic acid injection) and detected in cultured neurons after knockdown of Xpo1, the gene encoding CRM1. A proteomic screen for target molecules revealed that CRM1 inhibitors in neurons prevented nuclear export of molecules associated with axonal damage while retaining transcription factors modulating neuroprotection.

Selective chemical modulation of gene transcription favors oligodendrocyte lineage progression.

Lysine acetylation regulates gene expression through modulating protein-protein interactions in chromatin. Chemical inhibition of acetyl-lysine binding bromodomains of the major chromatin regulators BET (bromodomain and extraterminal domain) proteins has been shown to effectively block cell proliferation in cancer and inflammation. However, whether selective inhibition of individual BET bromodomains has distinctive functional consequences remains only partially understood. In this study, we show that selective chemical inhibition of the first bromodomain of BET proteins using our small-molecule inhibitor, Olinone, accelerated the progression of mouse primary oligodendrocyte progenitors toward differentiation, whereas inhibition of both bromodomains of BET proteins hindered differentiation. This effect was target specific, as it was not detected in cells treated with inactive analogs and independent of any effect on proliferation. Therefore, selective chemical modulation of individual bromodomains, rather than use of broad-based inhibitors, may enhance regenerative strategies in disorders characterized by myelin loss such as aging and neurodegeneration.

Developing school psychologists as agents of social justice: a qualitative analysis of student understanding across three years.

This study employed a cohort-sequential design with four cohorts over 3 years to investigate school psychology graduate trainees' (n=37) understanding of social justice. Using consensual qualitative research methods, participants' perspectives on social justice writ large, social justice as it applies to school psychology, and effective aspects of social justice training in their graduate training program were collected through semi-structured focus group interviews. Field-based training though service-learning in diverse communities provided trainees with exposure to experiences that were viewed as instrumental in their understanding of social justice in general and as it applies to school psychology. Trainees described aspects of the training program that were viewed as conducive to educating school psychologists as agents of social justice. Based on findings from the study, a descriptive model of school psychology training for social justice is proposed.

Caffeine prevents weight gain and cognitive impairment caused by a high-fat diet while elevating hippocampal BDNF.

Obesity, high-fat diets, and subsequent type 2 diabetes (T2DM) are associated with cognitive impairment. Moreover, T2DM increases the risk of Alzheimer's disease (AD) and leads to abnormal elevation of brain beta-amyloid levels, one of the hallmarks of AD. The psychoactive alkaloid caffeine has been shown to have therapeutic potential in AD but the central impact of caffeine has not been well-studied in the context of a high-fat diet. Here we investigated the impact of caffeine administration on metabolism and cognitive performance, both in control rats and in rats placed on a high-fat diet. The effects of caffeine were significant: caffeine both (i) prevented the weight-gain associated with the high-fat diet and (ii) prevented cognitive impairment. Caffeine did not alter hippocampal metabolism or insulin signaling, likely because the high-fat-fed animals did not develop full-blown diabetes; however, caffeine did prevent or reverse a decrease in hippocampal brain-derived neurotrophic factor (BDNF) seen in high-fat-fed animals. These data confirm that caffeine may serve as a neuroprotective agent against cognitive impairment caused by obesity and/or a high-fat diet. Increased hippocampal BDNF following caffeine administration could explain, at least in part, the effects of caffeine on cognition and metabolism.

Maternal depressive history, teen 5HTTLPR genotype, and the processing of emotional faces: Exploring mechanisms of risk.

Variations in the serotonin transporter gene (5HTTLPR) and biased processing of face-emotion displays both have been implicated in the transmission of depression risk, but little is known about developmental influences on these relationships. Within a community sample of adolescents, we examine whether 5HTTLPR genotype moderates the link between maternal depressive history and errors in face-emotion labeling. When controlling for current levels of depression and anxiety among youth, a two-way interaction between maternal depressive history and 5HTTLPR genotype was detected. Specifically, adolescents whose mothers reported a depressive history and who had a low expressing genotype made more errors in classifying emotional faces when compared with adolescents with an intermediate or high expressing genotype, with or without maternal depression history. These findings highlight the complex manner in which maternal depression and genetic risk may interact to predict individual differences in social information processing.

The immune response to pneumococcal proteins during experimental human carriage.

Colonization of the nasopharynx is the initial step in all infections caused by Streptococcus pneumoniae. The antibody response to carriage was examined in an experimental model of human colonization in healthy adults. Asymptomatic colonization was detected in 6/14 subjects and continued for up to 122 d. Susceptibility to carriage did not correlate with total serum immunoglobulin (Ig)G to the homotypic capsular polysaccharide. All of the colonized subjects, in contrast, developed a serum IgG and secretory IgA response to a 22 kD protein, whereas 7 of 8 subjects who did not become colonized had preexisting antibody to this protein. Analysis of the 22 kD protein identified it as the NH(2)-terminal region of pneumococcal surface protein A (PspA). Our findings provide evidence for the role of antibody to this protein fragment in preventing pneumococcal carriage by humans.