The adolescent brain is particularly vulnerable to the effects of alcohol, with intoxications at this developmental age often producing long-lasting effects. The present study addresses the effects of a single acute ethanol exposure on GAP-43 and BDNF gene expression in neurons in the cerebellum and hippocampus of adolescent rats. Male postnatal day 23 (P23) Sprague-Dawley rats were exposed to ethanol vapors for two hours and after a recovery period of two hours, the cerebellum and hippocampus were harvested and samples were taken for blood alcohol concentration (BAC) determinations. We found that this exposure resulted in a mean BAC of 174 mg/dl, which resembles levels in human adolescents after binge drinking. Analyses of total RNA and protein by qRT-PCR and western blotting, respectively, revealed that this single ethanol exposure significantly decreased the levels of GAP-43 mRNA and protein in the cerebellum but increased the levels of mRNA and protein in the hippocampus. BDNF mRNA and protein levels were also increased in the hippocampus but not in the cerebellum of these animals. In situ hybridizations revealed that GAP-43 and BDNF mRNA levels were primarily increased by alcohol exposure in hippocampal dentate granule cells and CA3 neurons. Overall, the reported alterations in the expression of the plasticity-associated genes GAP-43 and BDNF in juvenile rats are consistent with the known deleterious effects of binge drinking on motor coordination and cognitive function.

Disclaimer In an effort to expedite the publication of articles, AJHP is posting manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. Purpose People with HIV (PWH) are at increased risk for developing atherosclerotic cardiovascular disease (ASCVD). The primary objective of this study was to evaluate adherence to guideline recommendations on statin use in PWH for both primary and secondary ASCVD prevention in a single healthcare institution. Methods A retrospective chart review was performed to evaluate statin use for cardiovascular risk reduction in PWH 40 to 75 years of age at an HIV clinic over a 1-year evaluation period. The study included patients who met one of the 4 criteria for statin therapy defined in the “ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults.” Patient demographics were collected and a 10-year ASCVD risk score was calculated. Results A total of 432 PWH were evaluated for statin therapy; 205 patients (47.5%) met criteria for statin therapy. The majority of patients were male, the average age was 58 years, and the average time since HIV diagnosis was 19 years. The mean ASCVD risk score was 14.2%. Only 79 patients (38.5%) who met criteria were prescribed statin therapy, and only 45 (56.9%) were prescribed statin therapy of appropriate intensity. Use of ART pharmacokinetic enhancer was low and did not affect statin prescribing. Multivariable analysis found that age, diabetes, clinical ASCVD, and an appointment with a pharmacist clinician prescriber predicted statin utilization. A high ASCVD risk score (>20%) did not predict statin treatment. Conclusion Statin prescribing is low in PWH, who are at increased risk for ASCVD. Future research in PWH should focus on improving ASCVD risk assessment and exploring causes for statin underprescribing.