Self-development groups reduce medical school stress: a controlled intervention study

<p>Abstract</p> <p>Background</p> <p>High stress levels and mental health problems are common among medical students and there is a lack of studies on group interventions that aim to reduce such distress during medical school.</p> <p>Methods</p> <p>A full class of students (n = 129) participated in group sessions during their third year of medical school in Bergen, Norway. The subsequent third-year class (n = 152) acted as control group, in order to create a quasi-experimental design. Two types of group intervention sessions were offered to the first class. One option was self-development groups led by trained group psychotherapists. Alternatively, students could choose discussion groups that focused on themes of special relevance to doctors, led by experienced general practitioners. The intervention comprised of 12 weekly group sessions each lasting 90 minutes. Data were gathered before the intervention (T1), and three months post intervention (T2). Distress was measured using the Perceived Medical School Stress (PMSS) and Symptom Check List-5 (SCL-5) assessments.</p> <p>Results</p> <p>The intervention group showed a significant reduction in PMSS over the observation period. The subsequent year control group stayed on the same PMSS levels over the similar period. The intervention was a significant predictor of PMSS reduction in a multiple regression analysis adjusted for age and sex, β = -1.93 (-3.47 to -0.38), P = 0.02. When we analysed the effects of self-development and discussion groups with the control group as reference, self-development group was the only significant predictor of PMSS reduction, β = -2.18 (-4.03 to -0.33), P = 0.02. There was no interaction with gender in our analysis. This implicates no significant difference between men and women concerning the effect of the self-development group. There was no reduction in general mental distress (SCL-5) over this period.</p> <p>Conclusion</p> <p>A three-month follow-up showed that the intervention had a positive effect on perceived medical school stress among the students, and further analyses showed this was due to participation in self-development groups.</p

Modification of the L1-CAM carboxy-terminus in pancreatic adenocarcinoma cells

The neural cell adhesion molecule L1 has recently been shown to be expressed in pancreatic adenocarcinoma (PDAC) cells. In this report, we demonstrate that L1 is expressed by moderately- to poorly-differentiated PDAC cells in situ, and that L1 expression is a predictor of poor patient survival. In vitro, reduced reactivity of an anti-L1 carboxy-terminus-specific antibody was observed in the more poorly differentiated fast-growing (FG) variant of the COLO357 population, versus its well-differentiated slow-growing (SG) counterpart, even though they express equivalent total L1. The carboxy-terminus of L1 mediates binding to the MAP kinase-regulating protein RanBPM and mutation of T1247/S1248 within this region attenuates the expression of malignancy associated proteins and L1-induced tumorigenicity in mice. Therefore, we reasoned that the differential epitope exposure observed might be indicative of modifications responsible for regulating these events. However, epitope mapping demonstrated that the major determinant of binding was actually N1251; mutation of T1247 and S1248, alone or together, had little effect on C20 binding. Moreover, cluster assays using CD25 ectodomain/L1 cytoplasmic domain chimeras demonstrated the N1251-dependent, RanBPM-independent stimulation of erk phosphorylation in these cells. Reactivity of this antibody also reflects the differential exposure of extracellular epitopes in these COLO357 sublines, consistent with the previous demonstration of L1 ectodomain conformation modulation by intracellular modifications. These data further support a central role for L1 in PDAC, and define a specific role for carboxy-terminal residues including N1251 in the regulation of L1 activity in PDAC cells

The interstitium in cardiac repair: role of the immune-stromal cell interplay

Cardiac regeneration, that is, restoration of the original structure and function in a damaged heart, differs from tissue repair, in which collagen deposition and scar formation often lead to functional impairment. In both scenarios, the early-onset inflammatory response is essential to clear damaged cardiac cells and initiate organ repair, but the quality and extent of the immune response vary. Immune cells embedded in the damaged heart tissue sense and modulate inflammation through a dynamic interplay with stromal cells in the cardiac interstitium, which either leads to recapitulation of cardiac morphology by rebuilding functional scaffolds to support muscle regrowth in regenerative organisms or fails to resolve the inflammatory response and produces fibrotic scar tissue in adult mammals. Current investigation into the mechanistic basis of homeostasis and restoration of cardiac function has increasingly shifted focus away from stem cell-mediated cardiac repair towards a dynamic interplay of cells composing the less-studied interstitial compartment of the heart, offering unexpected insights into the immunoregulatory functions of cardiac interstitial components and the complex network of cell interactions that must be considered for clinical intervention in heart diseases