Single question screening for problem drinking.

There is evidence that acquired dysfunction of neutrophils, monocytes, or macrophages is an important cause of infection in patients with diabetes mellitus, renal or hepatic failure, alcoholism, autoimmune diseases, influenza or human immunodeficiency virus infection, burns, and trauma. Distinguishable mechanisms of acquired phagocyte dysfunction include inhibitory effects of metabolic disturbances (e.g., hyperglycemia, uremia), chemical toxins (e.g., ethanol), viral proteins on phagocyte activation, and pathologic activation of phagocytes in the circulation (e.g., after hemodialysis, burns, or cardiopulmonary bypass). Although the burden of morbidity and mortality resulting from acquired phagocyte dysfunction appears to be vast, research in this area has been hampered by the complexity of the underlying illnesses and by limitations of laboratory assays and clinical study methodology. Given the advent of improved assays of phagocyte functions and treatments that can enhance these functions, there is a pressing need for more prospective studies of acquired phagocyte dysfunction.

Alcoholism↗

PubMed2001

Acute ethanol administration differentially modulates mu opioid receptors in the rat meso-accumbens and mesocortical pathways.

Biochemical and pharmacological evidence suggest that the dopaminergic mesolimbic system plays a key role in mediating the reinforcing properties of alcohol and other drugs of abuse. Alcohol reinforcement and high alcohol drinking behavior have been postulated to be partially mediated by a neurobiological mechanism involving the alcohol-induced activation of the endogenous opioid system. The aim of this work was to study the effect of the in vivo acute administration of ethanol on mu (mu) opioid receptors in the rat dopaminergic meso-accumbens and mesocortical pathways by quantitative receptor autoradiography. [(3)H]DAMGO binding was significantly decreased in the ventral tegmental area (VTA) 30 min after ethanol administration. A small ethanol-induced reduction was observed in the shell region of the nucleus accumbens 1 h after exposure. In contrast, 2 h after ethanol administration, [(3)H]DAMGO binding was significantly increased in the frontal and prefrontal cortices. The observed changes correlated well with high ethanol plasma levels. Our results suggest that the reinforcing properties of ethanol may be partially mediated by mechanisms involving the ethanol-induced down- and up-regulation of mu receptors in the dopaminergic mesolimbic system. Mu receptors in the VTA and the frontal and prefrontal cortices may be involved in the in vivo acute responses to ethanol and could play a key role in modulating the dopaminergic activity of the mesocortical pathway in response to the drug. In contrast, the contribution of both mu and delta receptors in the nucleus accumbens might be relevant in these processes.

Alcoholism↗