RESUMEN
BACKGROUND: We surveyed HIV patients with late-stage disease in southern Vietnam to determine if barriers to access and service quality resulted in late HIV testing and delays from initial diagnosis to entry into HIV care. METHODOLOGY: 196 adult patients at public HIV clinics with CD4 counts less than 250 cells/mm3 completed a standardized questionnaire. We used multivariate analysis to determine risk factors for delayed entry into care, defined as >3 months time from diagnosis to registration. RESULTS: Common reasons for delayed testing were feeling healthy (71%), fear of stigma and discrimination in the community (43%), time conflicts with work or school (31%), did not want to know if infected (30%), and fear of lack of confidentiality (27%). Forty-five percent of participants delayed entry into care with a median CD4 count of 65 cells/mm3. The most common reasons for delayed entry were feeling healthy (51%), fear of stigma and discrimination in the community (41%), time conflicts with work or school (33%), and fear of lack of confidentiality (26%). Independent predictors for delayed entry were feeling healthy (aOR 3.7, 95% CI 1.5-9.1), first positive HIV test at other site (aOR 2.9, CI 1.2-7.1), history of injection drug use (IDU) (aOR 2.9, 95% CI 1.1-7.9), work/school conflicts (aOR 4.3, 95% CI 1.7-10.8), prior registration at another clinic (aOR 77.4, 95% CI 8.6-697), detention or imprisonment (aOR 10.3, 95% CI 1.8-58.2), and perceived distance to clinic (aOR 3.7, 95% CI 1.0-13.7). CONCLUSION: Delayed entry into HIV care in Vietnam is common and poses a significant challenge to preventing AIDS and opportunistic infections, decreasing mortality, and reducing HIV transmission. Improved linkages between testing and care are needed, particularly for patients who feel healthy, as well as incarcerated and drug-using populations who may face structural and social barriers to accessing care.
Asunto(s)
Infecciones por VIH/diagnóstico , Infecciones por VIH/epidemiología , Programas Nacionales de Salud , Aceptación de la Atención de Salud/estadística & datos numéricos , Adulto , Femenino , Infecciones por VIH/mortalidad , Infecciones por VIH/transmisión , Humanos , Masculino , Factores de Riesgo , Factores de Tiempo , Vietnam/epidemiologíaRESUMEN
Resveratrol is known to exert a cardioprotective effect against hypoxia/reoxygenation (H/R) injury. HS-1793 is a novel, more stable resveratrol analog, but its cardioprotective effects were unknown. The present study aimed to test the cardioprotective effect of HS-1793 against H/R injury and investigate the role of mitochondria in Sprague Dawley rat heart damage using an ex vivo Langendorff system. HS-1793 ameliorated H/R-induced mitochondrial dysfunction by reducing mitochondrial reactive oxygen species production, improving mitochondrial oxygen consumption and suppressing mitochondrial calcium (Ca(2+)) overload during reperfusion. Moreover, HS-1793-treated rat heart showed reduced infarct size. Our data suggest that HS-1793 can protect cardiac against mitochondrial damage following H/R, thereby suppressing injury.
Asunto(s)
Naftoles/química , Resorcinoles/química , Estilbenos/química , Animales , Calcio/metabolismo , Corazón/fisiopatología , Hipoxia , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Daño por Reperfusión Miocárdica/tratamiento farmacológico , Daño por Reperfusión Miocárdica/metabolismo , Daño por Reperfusión Miocárdica/patología , Naftoles/farmacología , Naftoles/uso terapéutico , Ratas , Ratas Sprague-Dawley , Especies Reactivas de Oxígeno/metabolismo , Resorcinoles/farmacología , Resorcinoles/uso terapéutico , ResveratrolRESUMEN
AIMS: Preservation of mitochondrial function is essential to limit myocardial damage in ischaemic heart disease. We examined the protective effects and mechanism of a new compound, NecroX-5, on rat heart mitochondria in a hypoxia/reoxygenation (HR) model. METHODS AND RESULTS: NecroX-5 reduced mitochondrial oxidative stress, prevented the collapse in mitochondrial membrane potential, improved mitochondrial oxygen consumption, and suppressed mitochondrial Ca(2+) overload during reoxygenation in an in vitro rat heart HR model. Furthermore, NecroX-5 reduced the ouabain- or histamine-induced increase in mitochondrial Ca(2+). CONCLUSION: These findings suggest that NecroX-5 may act as a mitochondrial Ca(2+) uniporter inhibitor to protect cardiac mitochondria against HR damage.