A Trauma-Informed Approach to Peer Physical Examination.

Introduction: The majority of medical schools utilize peer physical examination (PPE) as a teaching tool. In recent years, trauma-informed care (TIC) has been applied as a framework for physical examination to prevent patient retraumatization. Although medical students experience rates of trauma comparable to those of the general population, trauma-informed principles have not been integrated into PPE curricula. Methods: We created a novel trauma-informed PPE (TIPPE) curriculum grounded in core principles of TIC for first-year medical students. Perceptions of safety, trust, and autonomy in PPE practice were compared between the 152 students participating in the TIPPE curriculum and a control group from the prior year. Results: Twenty-nine percent of the 42 first-year medical student respondents in our sample endorsed a prior diagnosis with a mental health condition, and 33% endorsed a trauma history. Approximately 5% of student respondents (n = 5) in the interventional and control groups reported that PPE triggered recall of a prior traumatic event. Following participation in the TIPPE curriculum, familiarity with TIC principles rose significantly, although overall rating of the experience did not change. Thematic analysis of qualitative data highlighted students' desire for earlier and increased inclusion of TIC principles in the curriculum. Discussion: Our results demonstrate the necessity of adapting the standard PPE model in medical education in response to the real risk of student retraumatization. In sharing our curriculum, associated resources, and student-derived suggestions for further improvement, we provide a blueprint for other institutions seeking to train trauma-informed clinicians.

Downsizing the molecular spring of the giant protein titin reveals that skeletal muscle titin determines passive stiffness and drives longitudinal hypertrophy.

Titin, the largest protein known, forms an elastic myofilament in the striated muscle sarcomere. To establish titin's contribution to skeletal muscle passive stiffness, relative to that of the extracellular matrix, a mouse model was created in which titin's molecular spring region was shortened by deleting 47 exons, the TtnΔ112-158 model. RNA sequencing and super-resolution microscopy predicts a much stiffer titin molecule. Mechanical studies with this novel mouse model support that titin is the main determinant of skeletal muscle passive stiffness. Unexpectedly, the in vivo sarcomere length working range was shifted to shorter lengths in TtnΔ112-158 mice, due to a ~ 30% increase in the number of sarcomeres in series (longitudinal hypertrophy). The expected effect of this shift on active force generation was minimized through a shortening of thin filaments that was discovered in TtnΔ112-158 mice. Thus, skeletal muscle titin is the dominant determinant of physiological passive stiffness and drives longitudinal hypertrophy. Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (see decision letter).

Thin filament length in the cardiac sarcomere varies with sarcomere length but is independent of titin and nebulin.

Thin filament length (TFL) is an important determinant of the force-sarcomere length (SL) relation of cardiac muscle. However, the various mechanisms that control TFL are not well understood. Here we tested the previously proposed hypothesis that the actin-binding protein nebulin contributes to TFL regulation in the heart by using a cardiac-specific nebulin cKO mouse model (αMHC Cre Neb cKO). Atrial myocytes were studied because nebulin expression has been reported to be most prominent in this cell type. TFL was measured in right and left atrial myocytes using deconvolution optical microscopy and staining for filamentous actin with phalloidin and for the thin filament pointed-end with an antibody to the capping protein Tropomodulin-1 (Tmod1). Results showed that TFLs in Neb cKO and littermate control mice were not different. Thus, deletion of nebulin in the heart does not alter TFL. However, TFL was found to be ~0.05µm longer in the right than in the left atrium and Tmod1 expression was increased in the right atrium. We also tested the hypothesis that the length of titin's spring region is a factor controlling TFL by studying the Rbm20(ΔRRM) mouse which expresses titins that are ~500kDa (heterozygous mice) and ~1000kDa (homozygous mice) longer than in control mice. Results revealed that TFL was not different in Rbm20(ΔRRM) mice. An unexpected finding in all genotypes studied was that TFL increased as sarcomeres were stretched (~0.1µm per 0.35µm of SL increase). This apparent increase in TFL reached a maximum at a SL of ~3.0µm where TFL was ~1.05µm. The SL dependence of TFL was independent of chemical fixation or the presence of cardiac myosin-binding protein C (cMyBP-C). In summary, we found that in cardiac myocytes TFL varies with SL in a manner that is independent of the size of titin or the presence of nebulin.