ABSTRACT
Background In the 1960s, less than 10% of medical school graduates were women. Today, almost half of all medical school graduates are women. Despite the significant rise in female medical school graduates, there continues to be a large gender gap in most subspecialties, particularly surgical subspecialties such as neurosurgery. Objective The purpose of our study was to assess the factors contributing to differences in the academic ranks of male and female staff in academic neurosurgery programs in Canada and the United States (US). Methods Data about women in academic neurosurgery was collected from a number of sources, including Fellowship and Residency Electronic Interactive Database (FREIDA), Accreditation Council for Graduate Medical Education (ACGME), Canadian Resident Matching Service (CaRMS) FRIEDA, ACGME, CaRMS, Pubmed, and Scopus, to create a database of all neurosurgeons in the US and Canada. The analysis included neurosurgeons in academic and leadership ranks and also the H index, citations, publications, citations per year, and publications per year. Results Women represent only 12% of neurosurgeons in the US and Canada. When gender is further analyzed by academic appointment, women represent just over 12% of neurosurgeons at the assistant and associate professor levels (15.44% and 13.27%, respectively) but significantly less at the full professor level (5.84%). Likewise, only 7.45% of women hold first-in command leadership positions while 4.69% hold second-in-command positions within their institutions. Conclusions The existing data shows that women are significantly under-represented in academic neurosurgery. Lack of role models, experience, limited scientific output, and aspirations of a controlled lifestyle could be the potential contributing factors.
ABSTRACT
OBJECTIVES: Brain imaging studies have implicated white matter dysfunction in the pathophysiology of both bipolar disorder (BD) and schizophrenia (SCZ). However, the contribution of axons to white matter pathology in these disorders is not yet understood. Maintenance of neuronal function is dependent on the active transport of biological material, including synaptic proteins, along the axon. In this study, the expression of six proteins associated with axonal transport of synaptic cargoes was quantified in postmortem samples of prefrontal white matter in subjects with BD, those with SCZ, and matched controls, as a measure of axonal dysfunction in these disorders. METHODS: Levels of the microtubule-associated proteins ß-tubulin and microtubule-associated protein 6 (MAP6), the motor and accessory proteins kinesin-1 and disrupted-in-schizophrenia 1 (DISC1), and the synaptic cargoes synaptotagmin and synaptosomal-associated protein-25 (SNAP-25) were quantified in white matter adjacent to the dorsolateral prefrontal cortex in subjects with BD (n = 34), subjects with SCZ (n = 35), and non-psychiatric controls (n = 35) using immunoblotting and an enzyme-linked immunosorbent assay (ELISA). RESULTS: Protein expression of ß-tubulin, kinesin-1, DISC1, synaptotagmin, and SNAP-25 was significantly lower in subjects with BD compared to controls. Levels of axon-associated proteins were also lower in subjects with SCZ, but failed to reach statistical significance. CONCLUSIONS: These data provide evidence for deficits in axon-associated proteins in prefrontal white matter in BD. Findings are suggestive of decreased axonal density or dysregulation of axonal function in this disorder.
