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ABSTRACTAs a form of racism that is both subtle and ubiquitous, racial microaggressions (RMAs) can have cumulatively deleterious physical and emotional effects on people of a specific race or ethnicity. While a significant body of knowledge about RMAs has been developed from a Black-White perspective, this study was undertaken to explore extant empirical research that specifically addresses the physical and emotional effects of racism and RMAs on people who are Latinx-American. Through the implementation of the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines, we systematically searched multiple databases (PubMed, PsycInfo, Social Services Abstract, and CINAHL) to identify studies that specifically focused on Latinxs’ well-being in response to RMA. Following a systematic search and screening process, nine studies met all of the study’s inclusion criteria. Researchers reviewed studies for content, methods, effect sizes, and risk of bias. Strengths and shortcomings of the existing studies were identified, followed by suggestions for future research.

Current therapies to limit kidney disease progression lack specificity and often have systemic toxicity. To approach this problem, we postulated that a human monoclonal antibody (F1.1), directed against the noncollagenous-1 domain (NC1) of α3(IV) collagen that localizes in glomeruli, could serve as a vehicle for targeted drug delivery. Given enhanced exposure of the NC1 domain of α3(IV) during glomerular diseases, with limited epitope expression in other organs, α3(IV)NC1 provides an ideal target for delivery of disease-modifying agents. As a potential disease-modifying agent, we initially took advantage of recent observations that PGE2promoted recovery after established injury during the course of nephrotoxic nephritis. To address the general applicability of the approach, the efficacy of glomerular delivery of dexamethasone was also examined. To achieve glomerular targeted therapy, PGE2and dexamethasone were coupled to F1.1. After confirmation of the composition and activity of the conjugates, both glomerular localization and the capacity of the conjugates to modify disease were evaluated. After injection into mice with established nephritis, resolution of disease was enhanced with both agents, with normalization of histology and improved blood urea nitrogen levels in conjugate-treated mice compared with untreated mice. The results provide a novel means of targeting glomeruli during nephritis, irrespective of cause, by providing efficient drug delivery, with the potential of limiting systemic effects.

Crotalphine, a 14 amino acid peptide first isolated from the venom of the South American rattlesnake Crotalus durissus terrificus, induces a peripheral long-lasting and opioid receptor-mediated antinociceptive effect in a rat model of neuropathic pain induced by chronic constriction of the sciatic nerve. In the present study, we further characterized the molecular mechanisms involved in this effect, determining the type of opioid receptor responsible for this effect and the involvement of the nitric oxide–cyclic GMP pathway and of Kchannels. Crotalphine (0.2 or 5 gkg, orally; 0.0006 gpaw), administered on day 14 after nerve constriction, inhibited mechanical hyperalgesia and low-threshold mechanical allodynia. The effect of the peptide was antagonized by intraplantar administration of naltrindole, an antagonist of -opioid receptors, and partially reversed by norbinaltorphimine, an antagonist of -opioid receptors. The effect of crotalphine was also blocked by 7-nitroindazole, an inhibitor of the neuronal nitric oxide synthase; by 1H-(1,2,4) oxadiazolo4,3-aquinoxaline-1-one, an inhibitor of guanylate cyclase activation; and by glibenclamide, an ATP-sensitive Kchannel blocker. The results suggest that peripheral -opioid and -opioid receptors, the nitric oxide–cyclic GMP pathway, and ATP-sensitive Kchannels are involved in the antinociceptive effect of crotalphine. The present data point to the therapeutic potential of this peptide for the treatment of chronic neuropathic pain.