Changes in self-confidence in professional, personal, and scientific skills by gender during physician-scientist training at the University of Pittsburgh.

Introduction: Persistence in physician-scientist careers has been suboptimal, particularly among women. There is a gender gap in self-confidence in medicine. We measured the impact of our physician-scientist training programs on trainee's confidence in professional, personal, and scientific competencies, using a survey measuring self-rated confidence in 36 competencies across two timepoints.

Alterations in visible light exposure modulate platelet function and regulate thrombus formation.

Background: Variations in light exposure are associated with changes in inflammation and coagulation. The impact of light spectra on venous thrombosis (VT) and arterial thrombosis is largely unexplored.

Objectives: To investigate the impact of altering light spectrum on platelet function in thrombosis.

Career trajectories of MD-PhD physician scientists: The loss of women investigators.

Advances in biomedical research require a robust physician scientist workforce. Despite being equally successful at securing early career awards from the NIH as men, women MD-PhD physician scientists are less likely to serve as principal investigators on mid- and later careers awards. Here, we discuss the causes of gender disparities in academic medicine, the implications of losing highly trained women physician scientists, and the institutional and systemic changes needed to sustain this pool of talented investigators.

MACROPHAGE SWITCHING: POLARIZATION AND MOBILIZATION AFTER TRAUMA.

Introduction: Trauma alters the immune response in numerous ways, affecting both the innate and adaptive responses. Macrophages play an important role in inflammation and wound healing following injury. We hypothesize that macrophages mobilize from the circulation to the site of injury and secondary sites after trauma, with a transition from proinflammatory (M1) shortly after trauma to anti-inflammatory (M2) at later time points.

An AGS-associated mutation in ADAR1 catalytic domain results in early-onset and MDA5-dependent encephalopathy with IFN pathway activation in the brain.

Background: Aicardi-Goutières syndrome (AGS) is a severe neurodegenerative disease with clinical features of early-onset encephalopathy and progressive loss of intellectual abilities and motor control. Gene mutations in seven protein-coding genes have been found to be associated with AGS. However, the causative role of these mutations in the early-onset neuropathogenesis has not been demonstrated in animal models, and the mechanism of neurodegeneration of AGS remains ambiguous.