Elderly vs. younger problem drinker 'treatment' and recovery experiences

To address the question of whether or not elderly problem drinkers experience any treatment contact discrimination or recovery rate disadvantages, the programmme utilization and recovery rate experiences of a representative sample of older and younger persons arrested for drinking and driving (OWI) in Iowa were compared. Subjects were interviewed by phone or mail shortly after their OWI arrest and then again approximately 12 months later. Younger persons (18–54 years old) were compared with elderly persons (55 and over and 65 and over). The elderly subjects were also dichotomized as early onset (at least one problem drinking indicator occurred prior to age 55) or late onset (all problem drinking indicators occurred at age 55 or later). The elderly were as likely as, or more likely than, their younger counterparts to make a treatment contact, to remain in treatment and to recover.     

Chronic Exposure to a Simulated Urban Profile of Ozone Alters Ventilatory Responses to Carbon Dioxide Challenge in Rats

Chronic Exposure to a Simulated Urban Profile of Ozone AltersVentilatory Responses to Carbon Dioxide Challenge in Rats. TEPPER,J. S., WIESTER, M. J., WEBER, M. F., FITZGERALD, S., AND COSTA,D. L. (1991). Fundam. Appl. Toxicol. 17, 52–60. Male Fischer344 rats were exposed to a simulated urban profile of ozone(O³) (9-hr ramped spike, integrated concentration = 0.19 ppm)for up to 78 weeks. Small, but statistically significant, changesin breathing patterns and mechanics in unanesthetized, restrainedrats were observed at Weeks 1,3, 13, 52, and 78 during postexposurechallenge with 0, 4, and 8% carbon dioxide (CO²). The data indicatethat O³ exposure caused an overall increase in expiratory resistance(R^e), but particularly at 78 weeks. This increase in R^e mostlikely accounts for the rats' reduced ability to increase ventilationduring CO² challenge compared to control rats. Reductions inCO²-induced tidal volume increases were observed in all Orexposedanimals during postexposure challenges to 4 and 8% CO². Cumulatively,over all time points, spontaneous frequency of breathing andCO²-induced hyperventilation were also reduced. The decreasein frequency was dependent on a significant increase in theinspiratory time relative to control without a change in expiratorytime. Light microscopic evaluation of the lung did not revealany lesions associated with O³ exposure at any time point. Althoughstatistically significant effects were detected, the etiologyof the above-mentioned functional changes remains speculative.The potential relevance of these data to acute and chronic O³exposure in humans is also discussed.     

VISUAL DEPRIVATION IN INFANCY AND CHILDHOOD: CLINICAL ASPECTS

The effects of visual deprivation in 75 patients (14 children and one adult) were studied. The age of onset of deprivation and the significance of final visual outcome are discussed. Results indicate that a critically sensitive period in visual development occurs between approximately four months and three years of age, A period of plasticity, when the effects of deprivation are more responsive to therapy, follows. Age of onset of deprivation was found to be most important, but in addition loss of accommodation in association with deprivation may be a significant factor in the development of amblyopia.     

The translational therapeutics of prostaglandin inhibition in atherothrombosis

Summary.  Prostaglandins, products of the cyclo-oxygenase (COX) enzymes, can both promote and restrain atherothrombosis. While non-steroidal anti-inflammatory drugs (NSAIDs) selective for inhibition of COX-2 predispose to myocardial infarction, heart failure, hypertension and stroke, suppression of products of COX-1, such as thromboxane (Tx) A₂, underlie cardioprotection from low-dose aspirin. Data from clinical pharmacology, rodent models, human genetics, observational studies and randomized trials provide insight into the implications of inhibiting COX product synthesis or function. Many lines of evidence afford a mechanistic explanation for the cardiovascular (CV) hazard from NSAIDs. Elucidation of the biology of this pathway using diversified approaches is also relevant to understanding the implications of substrate rediversion following inhibition of enzymes downstream of COXs, such as the microsomal PGE synthase (mPGES)-1 and of combining D prostanoid antagonism with niacin to attenuate facial flushing.