HIV treatment adherence was monitored prospectively, using unannounced pill counts. Results: Two-thirds of the sample demonstrated adherence <85% of pills taken. Multivariable analyses showed that food insufficiency and hunger predicted antiretroviral therapy nonadherence over and above depression, internalized stigma, substance
use, and HIV-related social stressors. Conclusions: Interventions for HIV treatment nonadherence with the most socially disadvantaged persons in developed countries should be reconceptualized to directly address poverty, especially food insufficiency and hunger, as both a moral and public health imperative.”
“Considerable evidence indicates that adenosine A(2A) receptors (A(2A)Rs) modulate cholinergic neurotransmission, nicotinic acetylcholine receptor (nAChR) function, and nicotine-induced behavioural effects. To explore the interaction between A(2A) and nAChRs, we examined Dactolisib manufacturer if the complete
genetic deletion of adenosine A(2A)Rs in mice induces compensatory alterations in the binding of different nAChR subtypes, and whether the long-term effects of nicotine on nAChR regulation are altered in the absence of the A(2A)R gene. Quantitative autoradiography was used to measure cytisine-sensitive [I-125]epibatidine and [I-125]alpha-bungarotoxin LOXO-101 nmr binding to alpha 4 beta 2* and alpha 7 nAChRs, respectively, in brain sections of drug-naive (n = 6) or nicotine treated (n = 5-7), wild-type and adenosine A(2A)R knockout mice. Saline or nicotine Adenosine triphosphate (7.8 mg/kg/day; free-base weight) were administered to male CD1 mice via subcutaneous osmotic minipumps for a period of 14 days. Blood plasma levels of nicotine and cotinine were measured at the end of treatment. There were no compensatory developmental alterations in nAChR subtype distribution or density in drug-naive A(2A)R knockout mice. In nicotine treated wild-type
mice, both alpha 4 beta 2* and alpha 7 nAChR binding sites were increased compared with saline treated controls. The genetic ablation of adenosine A(2A)Rs prevented nicotine-induced upregulation of alpha 7 nAChRs, without affecting alpha 4 beta 2* receptor upregulation. This selective effect was observed at plasma levels of nicotine that were within the range reported for smokers (10-50 ng ml(-1)). Our data highlight the involvement of adenosine A(2A)Rs in the mechanisms of nicotine-induced alpha 7 nAChR upregulation, and identify A(2A)Rs as novel pharmacological targets for modulating the long-term effects of nicotine on alpha 7 receptors. (C) 2013 Elsevier Ltd. All rights reserved.”
“Objective: To assess the independent association of seven psychiatric illnesses with all-cause mortality in a representative national sample of veterans, after adjustment for demographic factors, psychiatric and medical comorbidity, obesity, tobacco use, and exercise frequency.