Minority Tax on Medical Students: A Review of the Literature and Mitigation Recommendations.

BACKGROUND AND OBJECTIVES: Accreditation standards for MD- and DO-granting institutions require medical schools to recruit a diverse student body and educate students about diverse groups of patients. The minority tax is a summary of responsibilities assigned to racial and ethnic underrepresented faculty to achieve diversity, equity, and inclusion in medical institutions in addition to their typical academic workload. This article provides a narrative review of medical students' experiences of the minority tax and recommendations on how medical educators can support an equitable learning environment by eliminating the minority tax. METHODS: We searched the PubMed, Web of Science, and Scopus databases, Google Scholar, and medical society websites, blogs, and fora for terms, including minority tax, medical students, and undergraduate medical education. We included publications if they discussed the underrepresented in medicine medical students' experiences of the minority tax. RESULTS: Our search yielded six peer-reviewed original research articles and six publications of commentaries, opinion pieces, or news pieces. Students who were underrepresented in medicine reported spending more hours on diversity efforts compared with students who were not underrepresented; moreover, students reported that they had to sacrifice academic excellence in order to fulfill these additional diversity duties. CONCLUSIONS: The minority tax among medical students constitutes an unequitable and unjust barrier to career advancement, and it likely represents an early cause of attrition in the pipeline of underrepresented in medicine academic faculty. Medical educators can enact specific recommendations to eliminate or mitigate the minority tax experience for medical students.

PSMA redirects cell survival signaling from the MAPK to the PI3K-AKT pathways to promote the progression of prostate cancer.

Increased abundance of the prostate-specific membrane antigen (PSMA) on prostate epithelium is a hallmark of advanced metastatic prostate cancer (PCa) and correlates negatively with prognosis. However, direct evidence that PSMA functionally contributes to PCa progression remains elusive. We generated mice bearing PSMA-positive or PSMA-negative PCa by crossing PSMA-deficient mice with transgenic PCa (TRAMP) models, enabling direct assessment of PCa incidence and progression in the presence or absence of PSMA. Compared with PSMA-positive tumors, PSMA-negative tumors were smaller, lower-grade, and more apoptotic with fewer blood vessels, consistent with the recognized proangiogenic function of PSMA. Relative to PSMA-positive tumors, tumors lacking PSMA had less than half the abundance of type 1 insulin-like growth factor receptor (IGF-1R), less activity in the survival pathway mediated by PI3K-AKT signaling, and more activity in the proliferative pathway mediated by MAPK-ERK1/2 signaling. Biochemically, PSMA interacted with the scaffolding protein RACK1, disrupting signaling between the ß1 integrin and IGF-1R complex to the MAPK pathway, enabling activation of the AKT pathway instead. Manipulation of PSMA abundance in PCa cell lines recapitulated this signaling pathway switch. Analysis of published databases indicated that IGF-1R abundance, cell proliferation, and expression of transcripts for antiapoptotic markers positively correlated with PSMA abundance in patients, suggesting that this switch may be relevant to human PCa. Our findings suggest that increase in PSMA in prostate tumors contributes to progression by altering normal signal transduction pathways to drive PCa progression and that enhanced signaling through the IGF-1R/ß1 integrin axis may occur in other tumors.

The MAO-B inhibitor deprenyl reduces the oral tremor and the dopamine depletion induced by the VMAT-2 inhibitor tetrabenazine.

Tetrabenazine (TBZ) is prescribed for the treatment of chorea associated with Huntington's disease. Via inhibition of the vesicular monoamine transporter (VMAT-2), TBZ blocks dopamine (DA) storage and depletes striatal DA; this drug also has been shown to induce Parkinsonian motor side effects in patients. Recently, TBZ was shown to induce tremulous jaw movements (TJMs) in rats and mice. TJMs are an oral tremor that has many of the characteristics of Parkinsonian tremor in humans. The present study focused upon the ability of the well-established antiparkinsonian agent deprenyl to attenuate the behavioral and neurochemical effects of 2.0mg/kg TBZ. Deprenyl is a selective and irreversible inhibitor of monoamine oxidase-B, and administration of deprenyl produced a dose-related suppression of TBZ-induced TJMs. A second experiment employed in vivo microdialysis to examine extracellular DA levels in the ventrolateral striatum, the neostriatal region most closely associated with the production of TJMs, after administration of TBZ and deprenyl. Consistent with the behavioral data, TBZ alone produced a biphasic effect on extracellular DA, with an initial increases followed by a prolonged decrease during the period in which TJMs are displayed. Co-administration of deprenyl with TBZ increased DA levels compared to rats treated with TBZ alone. These results provide support for use of TBZ as a rodent model of Parkinsonism, and future studies should utilize this model to evaluate putative anti-Parkinsonian agents.