Female victims and female perpetrators: medical students' narratives of gender dynamics and professionalism dilemmas.

Medicine is a gendered discipline, in which women, both as patients and practitioners, have often held subordinate positions. The reproduction of dominant gender biases in the medical setting can negatively impact the professional development of medical students and the wellbeing of patients. In this analysis of medical students' narratives of professionalism dilemmas, we explore students' experiences of gender bias in hospital settings. Seventy-one students participated in 12 group interviews, where they discussed witnessing or participating in various activities that they thought were professionalism lapses. Within the dataset, 21 narratives had a distinctly gendered component broadly pertaining to patient dignity and safety dilemmas, informed consent issues, and female student abuse. Interestingly, perpetrators of such acts were commonly female healthcare professionals and educators. Although students recognized such acts as professionalism lapses and often expressed concern for patient wellbeing, students did not intervene or report such acts due to hierarchical cultural contexts, and at times even reproduced the discriminatory behavior they were criticizing. This raises concerns about medical students' professionalism development and the extent to which gender bias is ingrained within particular medical systems. The normalization of disrespectful and abusive treatment of female patients poses immediate and future consequences to the wellbeing and safety of women. Furthermore, the same socio-cultural values that sustain these acts may account for perpetrators often being women themselves as they strive to overcome their subordinate position within medicine.

Silencing of Fem1cR3 gene expression in the DBA/2J mouse precedes retinal ganglion cell death and is associated with histone deacetylase activity.

PURPOSE: Downregulation of normal gene expression in dying retinal ganglion cells has been documented in both acute and chronic models of optic nerve disease. The authors examined the mechanism and timing of this phenomenon in DBA/2J mice, using genetically modified substrains of this inbred line. METHODS: DBA/2J mice, doubly congenic for the Bax mutant allele and the ganglion cell reporter gene Fem1c(Rosa3) (R3), were evaluated to elucidate the timing of loss of normal gene expression during the apoptotic process. The localization of histone deacetylase 3 (HDAC3) and nuclear histone H4 acetylation were examined by immunofluorescence in dying cells. The role of HDACs in gene silencing during glaucoma was interrogated using the global HDAC inhibitor trichostatin A (TSA). RESULTS: Silencing of the R3 allele occurred in Bax(-/-) ganglion cells, indicating that this process preceded the committed step of the intrinsic apoptotic pathway. Weekly TSA treatment, between the ages of 6 and 10 months, was able to attenuate the loss of R3 expression in the retina, but had no effect on optic nerve degeneration. Dying cells in aging DBA/2J mice exhibited nuclear localization of HDAC3 and a decrease in the level of H4 acetylation. CONCLUSIONS: Retinal ganglion cells exhibit a loss of normal gene expression as an early (pre-BAX involvement) part of their apoptotic program during glaucomatous degeneration. This process can be ameliorated, but not completely blocked, using HDAC inhibitors. Epigenetic changes to active chromatin, such as deacetylation, may be mediated by HDAC3 in dying neurons.