Bridget Freisthler

Objective. The ability to determine the geographic locations of illicit drug markets is central to the development of preventive interventions that address access to drugs and associated problems, ...

Background:This paper examines neighborhood, outlet, and server characteristics related to successful purchases of alcohol by intoxicated patrons and underage drinkers at alcohol establishments. It is hypothesized that outlets in commercial areas near to other premises, with poor exterior maintenance, much advertising, and inexperienced youthful servers will be more likely to sell alcohol to intoxicated and underage patrons.Methods:Data were collected using pseudo‐intoxicated patron and apparent minor surveys of randomly selected alcohol establishments in a metropolitan area of northern California. Data collection operations included independent surveillance of these drinking places to establish neighborhood and premise characteristics and pseudo‐intoxicated patron and apparent minor stings to assess rates of these forms of illegal alcohol sales. Male actors feigning intoxication and female of‐age youth identified as appearing to be 20 years or younger attempted to purchase alcohol at on‐ and off‐premise establishments, respectively. Rates of sales (off‐premise) and service (on‐premise) were the primary outcomes.Results:Apparent minors purchased alcohol in 39% of attempts (95% CI, 34–45%) while pseudo‐intoxicated patrons were served alcohol in 58% of attempts (95% CI, 50–67%). Sales to apparent minors were significantly related to percentage of Hispanic residents and areas with greater population density. Sales to pseudo‐intoxicated patrons were more frequent when the server was male and appeared to be under the age of 30. These sales were also more frequent in Hispanic neighborhoods with high population density and high numbers of on‐premise outlets but were less frequent in African American neighborhoods.Conclusion:The findings suggest that underage and intoxicated patron sales differ by areas. Both forms of illegal sales of alcohol are more likely in highly populated areas of communities. The findings also suggest that server characteristics are strongly related to sales to intoxicated patrons, suggesting some leverage for responsible beverage service programs in these environments.

Background: The purpose of the present study was to determine whether acute alcohol (EtOH) intoxication impairs the signal transduction pathway used to coordinate insulin‐like growth factor (IGF)‐I stimulation of myocardial protein synthesis.Methods: Rats were injected intraperitoneally with EtOH or saline. After 2.5 h, IGF‐I or saline was injected intravenously and the heart was excised at 2 min or 20 min. Additional rats were pretreated with RU486 or tumor necrosis factor (TNF) binding protein (BP) to assess the importance of elevations in glucocorticoids or TNF, respectively, as endogenous modulators of IGF‐I signal transduction.Results: EtOH did not alter the total amount or tyrosine phosphorylation of the IGF‐I receptor, IRS‐1 or PKB under basal or IGF‐stimulated conditions. However, EtOH attenuated the ability of IGF‐I to phosphorylate ribosomal S6 kinase (S6K)‐1 on residues T389 (∼62%) and T421/S424 (∼40%), and also reduced ribosomal protein S6 phosphorylation. Under basal conditions, EtOH altered the distribution of eukaryotic initiation factor (eIF) 4E, as evidenced by a decreased amount of the active eIF4E·eIF4G complex (53%), an increased amount of inactive eIF4E·4E‐BP1 complex (∼3‐fold), and decreased phosphorylation of 4E‐BP1 (56%). EtOH also impaired the ability of IGF‐I to reverse the above‐mentioned changes in the eIF4E system. Pretreatment of rats with RU486 or TNFBP was unable to attenuate the EtOH‐induced changes in either eIF4E distribution or the phosphorylation state of 4E‐BP1, S6K1 or S6.Conclusions: These data indicate that acute EtOH intoxication alters selected aspects of translational control in the heart under basal conditions. Furthermore, despite appropriate stimulation of IGF‐I receptor, IRS‐1 and PKB, EtOH impairs IGF‐I signaling via S6K1 and 4E‐BP1 pathways, and this defect is regulated in a glucocorticoid‐ and TNF‐independent manner. This IGF‐I resistance may represent a participating mechanism by which alcohol limits protein synthesis in heart.