Exploring the Impact of Experiences with Everyday and Major Discrimination and HIV-Related Stigma on Engagement in HIV Care Among Older African Americans Living with HIV.

OBJECTIVES: The purpose of this pilot study was to explore the effect of HIV-related stigma and everyday major experiences of discrimination on medication and clinic visit adherence among older African Americans living with HIV in Ohio. METHODS: We collected data from 53 individuals who were living with HIV in Ohio, ≥ 50 years of age, and who identified as Black or African American. We conducted logistic regression models to examine the impact of HIV-related stigma and experiences of discrimination on medication and visit adherence. Each model controlled for age, time since diagnosis, and sexual orientation. RESULTS: The average age was 53.6 ± 2.1 years and 94.3% were men. Almost half (49.1%) of the participants reported poor medication adherence and almost a third (31.4%) reported poor visit adherence. HIV-related stigma (adjusted odds ratio (aOR) = 1.39; 95% confidence interval (CI) = 1.02-1.89) and major experiences of discrimination (aOR = 1.70; 95% CI = 1.11-2.60) were associated with a greater odds of poor medication adherence. Additionally, major experiences of discrimination were associated with a threefold increase in the odds of poor visit adherence (aOR = 3.24; 95% CI = 1.38-7.64). CONCLUSIONS: HIV-related stigma and major experiences of discrimination impede optimal medication and HIV clinic visit adherence for older African Americans living with HIV. To reduce the impact of stigma and discrimination on HIV care engagement, our first step must be in understanding how intersecting forms of stigma and discrimination impact engagement among older African Americans living with HIV.

Translational outcomes relevant to neurodevelopmental disorders following early life exposure of rats to chlorpyrifos.

BACKGROUND: Neurodevelopmental disorders (NDDs), including intellectual disability, attention deficit hyperactivity disorder (ADHD), and autism spectrum disorder (ASD), are pervasive, lifelong disorders for which pharmacological interventions are not readily available. Substantial increases in the prevalence of NDDs over a relatively short period may not be attributed solely to genetic factors and/or improved diagnostic criteria. There is now a consensus that multiple genetic loci combined with environmental risk factors during critical periods of neurodevelopment influence NDD susceptibility and symptom severity. Organophosphorus (OP) pesticides have been identified as potential environmental risk factors. Epidemiological studies suggest that children exposed prenatally to the OP pesticide chlorpyrifos (CPF) have significant mental and motor delays and strong positive associations for the development of a clinical diagnosis of intellectual delay or disability, ADHD, or ASD. METHODS: We tested the hypothesis that developmental CPF exposure impairs behavior relevant to NDD phenotypes (i.e., deficits in social communication and repetitive, restricted behavior). Male and female rat pups were exposed to CPF at 0.1, 0.3, or 1.0 mg/kg (s.c.) from postnatal days 1-4. RESULTS: These CPF doses did not significantly inhibit acetylcholinesterase activity in the blood or brain but significantly impaired pup ultrasonic vocalizations (USV) in both sexes. Social communication in juveniles via positive affiliative 50-kHz USV playback was absent in females exposed to CPF at 0.3 mg/kg and 1.0 mg/kg. In contrast, this CPF exposure paradigm had no significant effect on gross locomotor abilities or contextual and cued fear memory. Ex vivo magnetic resonance imaging largely found no differences between the CPF-exposed rats and the corresponding vehicle controls using strict false discovery correction; however, there were interesting trends in females in the 0.3 mg/kg dose group. CONCLUSIONS: This work generated and characterized a rat model of developmental CPF exposure that exhibits adverse behavioral phenotypes resulting from perinatal exposures at levels that did not significantly inhibit acetylcholinesterase activity in the brain or blood. These data suggest that current regulations regarding safe levels of CPF need to be reconsidered.

Neumonía grave de evolución tórpida en paciente joven con prueba molecular negativa para nuevo coronavirus / Severe Pneumonia Of Torpid Evolutión In A Young Patient With A Negative Molecular Test For A New Coronavirus

La enfermedad por coronavirus originada en el año 2019 (COVID-19), se ha diseminado rápidamente en todo el mundo produciendo estragos en el sistema de salud y la sociedad. Se reporta el caso de un varón de 26 años de edad con antecedentes de asma y obesidad, que retornó de EE.UU y acudió a emergencia con síntomas respiratorios, hipoxemia e infiltrado intersticial en la radiografía de tórax, se decide internamiento en sala de aislamiento, la prueba molecular RT-PCR de hisopado nasofaríngeo resultó negativa, por lo que fue traslado a una sala de emergencia común. El manejo inicial fue conservador, sin embargo el paciente evolucionó desfavorablemente requiriendo soporte ventilatorio, pero fallece al quinto día de internamiento. Se recibió un segundo resultado positivo para SARS-CoV-2 al día siguiente de fallecido el paciente, siendo una de las primeras víctimas jóvenes en el Perú.

The coronavirus disease originated in the year 2019 (COVID-19), has spread rapidly throughout the world, wreaking havoc on the health system and society. We report the case of a 26-year-old man with a history of asthma and obesity, who returned from the US and went to the emergency room with respiratory symptoms, hypoxemia and interstitial infiltrate on chest radiography, he was admitted to the isolation room The nasopharyngeal swab RT-PCR molecular test was negative, so he was transferred to a common emergency room. Initial management was conservative, however the patient evolved unfavorably requiring ventilatory support, but died on the fifth day of hospitalization. A second positive result for SARS-CoV-2 was received the day after the patient died, being one of the first young victims in Peru.

Developmental social communication deficits in the Shank3 rat model of phelan-mcdermid syndrome and autism spectrum disorder.

Mutations in the SHANK3 gene have been discovered in autism spectrum disorder (ASD), and the intellectual disability, Phelan-McDermid Syndrome. This study leveraged a new rat model of Shank3 deficiency to assess complex behavioral phenomena, unique to rats, which display a richer social behavior repertoire than mice. Uniquely detectable emissions of ultrasonic vocalizations (USV) in rats serve as situation-dependent affective signals and accomplish important communicative functions. We report, for the first time, a call and response acoustic playback assay of bidirectional social communication in juvenile Shank3 rats. Interestingly, we found that Shank3-deficient null males did not demonstrate the enhanced social approach behavior typically exhibited following playback of pro-social USV. Concomitantly, we discovered that emission of USV in response to playback was not genotype-dependent and emitted response calls were divergent in meaning. This is the first report of these socially relevant responses using a genetic model of ASD. A comprehensive and empirical analysis of vigorous play during juvenile reciprocal social interactions further revealed fewer bouts and reduced durations of time spent playing by multiple key parameters, including reduced anogenital sniffing and allogrooming. We further discovered that male null Shank3-deficient pups emitted fewer isolation-induced USV than Shank3 wildtype controls. Postnatal whole brain anatomical phenotyping was applied to visualize anatomical substrates that underlie developmental phenotypes. The data presented here lend support for the important role of Shank3 in social communication, the core symptom domain of ASD. By increasing the number of in vivo functional outcome measures, we improved the likelihood for identifying and moving forward with medical interventions. Autism Res 2018, 11: 587-601. © 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Clinically relevant outcomes are required to demonstrate the utility of therapeutics. We introduce findings in a rat model, and assess the impact of mutations in Shank3, an autism risk gene. We found that males with deficient expression of Shank3 did not demonstrate typical responses in a bi-directional social communication test and that social interaction was lower on key parameters. Outcome measures reported herein extend earlier results in mice and capture responses to acoustic calls, which is analogous to measuring receptive and expressive communication.