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Minorities, particularly non-White minorities, often encounter implicit biases from healthcare professionals that may impact their standard of care and quality of life. The study of dermatology has long been based on Whites, unintentionally affecting the treatment of non-White patients. Melanoma, although mostly curable, can become fatal in those presenting with advanced stages at diagnosis. Despite being rare in racial minorities, melanoma is associated with a worse prognosis among them compared to White populations. In light of this, the objective of this study was to determine the role of education in preventing biases and improving the diagnosis and treatment of melanoma in minority groups to improve patient outcomes. This study was designed as a scoping review to gather evidence on the impact of implicit bias and lack of education on the treatment of melanoma in people of color. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we searched for peer-reviewed studies involving melanoma, education, and treatment bias in people of color on the databases PubMed, Medline EBSCO, CINAHL, and Cochrane. The data were extracted pertaining to the following main aspects: (1) risk factors, (2) surveys of current knowledge, and 3) educational interventions. This scoping review identified socioeconomic factors, bias, and lack of education in minority populations as causes of increased mortality rates in melanoma. Moreover, because preventative dermatology is largely based on White skin types, incorporating darker skin tones into education will help dispel implicit bias. Additionally, there is evidence to indicate that current patient knowledge and understanding of skin cancer is inaccurate among many and can be significantly improved through educational interventions, such as brochures and videos. Further educational interventions may be beneficial to increase understanding of melanoma in populations of color to address health disparities in dermatological care., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2022, Rizvi et al.)

The tricarboxylic acid (TCA) cycle converts the end products of glycolysis and fatty acid β-oxidation into the reducing equivalents NADH and FADH 2 Although mitochondrial matrix uptake of Ca 2+ enhances ATP production, it remains unclear whether deprivation of mitochondrial TCA substrates alters mitochondrial Ca 2+ flux. We investigated the effect of TCA cycle substrates on MCU-mediated mitochondrial matrix uptake of Ca 2+ , mitochondrial bioenergetics, and autophagic flux. Inhibition of glycolysis, mitochondrial pyruvate transport, or mitochondrial fatty acid transport triggered expression of the MCU gatekeeper MICU1 but not the MCU core subunit. Knockdown of mitochondrial pyruvate carrier (MPC) isoforms or expression of the dominant negative mutant MPC1 R97W resulted in increased MICU1 protein abundance and inhibition of MCU-mediated mitochondrial matrix uptake of Ca 2+ We also found that genetic ablation of MPC1 in hepatocytes and mouse embryonic fibroblasts resulted in reduced resting matrix Ca 2+ , likely because of increased MICU1 expression, but resulted in changes in mitochondrial morphology. TCA cycle substrate-dependent MICU1 expression was mediated by the transcription factor early growth response 1 (EGR1). Blocking mitochondrial pyruvate or fatty acid flux was linked to increased autophagy marker abundance. These studies reveal a mechanism that controls the MCU-mediated Ca 2+ flux machinery and that depends on TCA cycle substrate availability. This mechanism generates a metabolic homeostatic circuit that protects cells from bioenergetic crisis and mitochondrial Ca 2+ overload during periods of nutrient stress., (Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)