Mindfulness Training in Mitigating Implicit Bias: Improving Cultural Competency for Nurses Caring for LGBT Individuals

Background: Equitable care remains a goal of the United States healthcare system, with cultural competency training used as one intervention to mitigate disparities. Cultural competency education is primarily based on racial and ethnic differences, often omitting other marginalized groups. Implicit bias consequences are not addressed in such training programs despite the association with health outcome disparities. Research related to implicit bias has demonstrated the ability to promote malleability in implicit associations. Objectives: This project assessed a mindfulness meditation exercise intervention on nursing awareness in interacting with lesbian, gay, bisexual, and transgender (LGBT) patients. Additionally, an LGBT health education module that integrates affirmative practice and implicit bias concepts was introduced. This project served to improve awareness of implicit bias against LGBT individuals in order to begin mitigating the associations with poorer health outcomes. Methods: Using a pre-post intervention design, participant acceptance and comfort in working with LGBT individuals was measured using the Sexuality Implicit Association Test (IAT). Participants were instructed on the use of a mindfulness meditation exercise and completed a self-paced LGBT health education module. Content included LGBT terminology, health disparities, effective communication, and an overview of implicit bias awareness. Results: Participants were comprised of registered nurses and licensed practical nurses working at a non-profit healthcare organization. A total of 81 participants completed the pre-intervention IAT, and 51 completed the post-intervention IAT. In comparing pre- and post-intervention IAT scores, there was an overall increase in neutrality of bias between heterosexual and homosexual individuals. Conclusions: Mindfulness provides a promising opportunity to decrease bias in healthcare workers interacting with marginalized groups. This project provides a basis for organizational change using implicit bias awareness education. The research contributes to the paucity of available literature related to LGBT-specific healthcare, implicit bias, and cultural competence

A Sex-Specific Metabolite Identified in a Marine Invertebrate Utilizing Phosphorus-31 Nuclear Magnetic Resonance

Hormone level differences are generally accepted as the primary cause for sexual dimorphism in animal and human development. Levels of low molecular weight metabolites also differ between men and women in circulating amino acids, lipids and carbohydrates and within brain tissue. While investigating the metabolism of blue crab tissues using Phosphorus-31 Nuclear Magnetic Resonance, we discovered that only the male blue crab (Callinectes sapidus) contained a phosphorus compound with a chemical shift well separated from the expected phosphate compounds. Spectra obtained from male gills were readily differentiated from female gill spectra. Analysis from six years of data from male and female crabs documented that the sex-specificity of this metabolite was normal for this species. Microscopic analysis of male and female gills found no differences in their gill anatomy or the presence of parasites or bacteria that might produce this phosphorus compound. Analysis of a rare gynandromorph blue crab (laterally, half male and half female) proved that this sex-specificity was an intrinsic biochemical process and was not caused by any variations in the diet or habitat of male versus female crabs. The existence of a sex-specific metabolite is a previously unrecognized, but potentially significant biochemical phenomenon. An entire enzyme system has been synthesized and activated only in one sex. Unless blue crabs are a unique species, sex-specific metabolites are likely to be present in other animals. Would the presence or absence of a sex-specific metabolite affect an animal's development, anatomy and biochemistry

Host-Species Transferrin Receptor 1 Orthologs Are Cellular Receptors for Nonpathogenic New World Clade B Arenaviruses

The ability of a New World (NW) clade B arenavirus to enter cells using human transferrin receptor 1 (TfR1) strictly correlates with its ability to cause hemorrhagic fever. Amapari (AMAV) and Tacaribe (TCRV), two nonpathogenic NW clade B arenaviruses that do not use human TfR1, are closely related to the NW arenaviruses that cause hemorrhagic fevers. Here we show that pseudotyped viruses bearing the surface glycoprotein (GP) of AMAV or TCRV can infect cells using the TfR1 orthologs of several mammalian species, including those of their respective natural hosts, the small rodent Neacomys spinosus and the fruit bat Artibeus jamaicensis. Mutation of one residue in human TfR1 makes it a functional receptor for TCRV, and mutation of four residues makes it a functional receptor for AMAV. Our data support an in vivo role for TfR1 in the replication of most, if not all, NW clade B arenaviruses, and suggest that with modest changes in their GPs the nonpathogenic arenaviruses could use human TfR1 and emerge as human pathogens

The ataxia (axJ) mutation causes abnormal GABAA receptor turnover in mice

Ataxia represents a pathological coordination failure that often involves functional disturbances in cerebellar circuits. Purkinje cells (PCs) characterize the only output neurons of the cerebellar cortex and critically participate in regulating motor coordination. Although different genetic mutations are known that cause ataxia, little is known about the underlying cellular mechanisms. Here we show that a mutated ax(J) gene locus, encoding the ubiquitin-specific protease 14 (Usp14), negatively influences synaptic receptor turnover. Ax(J) mouse mutants, characterized by cerebellar ataxia, display both increased GABA(A) receptor (GABA(A)R) levels at PC surface membranes accompanied by enlarged IPSCs. Accordingly, we identify physical interaction of Usp14 and the GABA(A)R alpha1 subunit. Although other currently unknown changes might be involved, our data show that ubiquitin-dependent GABA(A)R turnover at cerebellar synapses contributes to ax(J)-mediated behavioural impairment