Innovative Wellness Models to Support Advancement and Retention Among Women Physicians.

Despite improvements in representation of women in academic medicine, the rate of promotion and career advancement remains unequal. Compared with their male colleagues, women report lower rates of personal-organizational value alignment and higher rates of burnout. Particular challenges further exist for Black women, Indigenous women, women of color, and third gender or gender nonbinary faculty. Promoting the well-being of women physicians requires innovative approaches beyond the traditional scope of physician well-being efforts and careful attention to the unique barriers women face. Three wellness-oriented models are presented to promote the professional fulfillment and well-being of women physicians: (1) redefine productivity and create innovative work models, (2) promote equity through workplace redesign and burnout reduction, and (3) promote, measure, and improve diversity, equity, and inclusion. By engaging in innovative models for equitable advancement and retention, it is anticipated that diverse groups of women faculty will be better represented at higher levels of leadership and thus contribute to the creation of more equitable work climates, fostering well-being for women physicians.

Epileptic-like convulsions associated with LIS-1 in the cytoskeletal control of neurotransmitter signaling in Caenorhabditis elegans.

Cortical malformations are a collection of disorders affecting brain development. Mutations in the LIS1 gene lead to a disorganized and smooth cerebral cortex caused by failure in neuronal migration. Among the clinical consequences of lissencephaly are mental retardation and intractable epilepsy. It remains unclear whether the seizures result from aberrant neuronal placement, disruption of intrinsic properties of neurons, or both. The nematode Caenorhabditis elegans offers an opportunity to study such convulsions in a simple animal with a defined nervous system. Here we show that convulsions mimicking epilepsy can be induced by a mutation in a C. elegans lis-1 allele (pnm-1), in combination with a chemical antagonist of gamma-aminobutyric acid (GABA) neurotransmitter signaling. Identical convulsions were obtained using C. elegans mutants defective in GABA transmission, whereas none of these mutants or the antagonist alone caused convulsions, indicating a threshold was exceeded in response to this combination. Crosses between pnm-1 and fluorescent marker strains designed to exclusively illuminate either the processes of GABAergic neurons or synaptic vesicles surprisingly showed no deviations in neuronal architecture. Instead, presynaptic defects in GABAergic vesicle distribution were clearly evident and could be phenocopied by RNAi directed against cytoplasmic dynein, a known LIS1 interactor. Furthermore, mutations in UNC-104, a neuronal-specific kinesin, and SNB-1, a synaptic vesicle-associated protein termed synaptobrevin, exhibit similar convulsion phenotypes following chemical induction. Taken together, these studies establish C. elegans as a system to investigate subtle cytoskeletal mechanisms regulating intrinsic neuronal activity and suggest that it may be possible to dissociate the epileptic consequences of lissencephaly from the more phenotypically overt cortical defects associated with neuronal migration.