Examining interviewer bias in medical school admissions: The interplay between applicant and interviewer gender and its effects on interview outcomes.

Selection interviews have long been integral to medical school admissions, yet their limited predictive validity and susceptibility to bias raise concerns. This study delves into potential interviewer bias within the dynamics of interviewee and interviewer gender. We analyze a dataset of 5,200 applicants and over 370 selection committees engaged in semi-structured interviews from 2006 to 2019 at a large German medical school with multiple linear and non-linear regression analyses. Our findings reveal that all-female committees tended to award male candidates, on average, one point more than their female counterparts, significantly enhancing the chances of submission for male applicants despite lower academic grades, which constituted 51% of the selection process points. All-male and mixed-gender committees exhibited similar ratings for both genders. The role of valuing voluntary services emerged prominently: all-male and mixed committees acknowledged women's volunteer work but not men's, while all-female committees demonstrated the opposite pattern. Our results attribute variations in interview outcomes to the absence of standardization, such as insufficient interviewer training, divergent rating strategies, variations in interviewer experience, and imbalances in candidate allocation to selection committees, rather than to a "gender bias", for example by favoritism of males because of their gender.

Alpha-synuclein fibrils amplified from multiple system atrophy and Parkinson's disease patient brain spread after intracerebral injection into mouse brain.

Parkinson's disease (PD), multiple system atrophy (MSA), and dementia with Lewy bodies (DLB) are neurodegenerative disorders with alpha-synuclein (α-syn) aggregation pathology. Different strains of α-syn with unique properties are suggested to cause distinct clinical and pathological manifestations resulting in PD, MSA, or DLB. To study individual α-syn spreading patterns, we injected α-syn fibrils amplified from brain homogenates of two MSA patients and two PD patients into the brains of C57BI6/J mice. Antibody staining against pS129-α-syn showed that α-syn fibrils amplified from the brain homogenates of the four different patients caused different levels of α-syn spreading. The strongest α-syn pathology was triggered by α-syn fibrils of one of the two MSA patients, followed by comparable pS129-α-syn induction by the second MSA and one PD patient material. Histological analysis using an antibody against Iba1 further showed that the formation of pS129-α-syn is associated with increased microglia activation. In contrast, no differences in dopaminergic neuron numbers or co-localization of α-syn in oligodendrocytes were observed between the different groups. Our data support the spreading of α-syn pathology in MSA, while at the same time pointing to spreading heterogeneity between different patients potentially driven by individual patient immanent factors.