Using sobriety tests to increase awareness of alcohol impairment

There is a need to investigate methods by which drinkers canbe made aware of their level of alcohol impairment prior todriving. In the current research, 195 students at various bloodalcohol concentration (BAC) levels participated in an evaluationof three simple sobriety tests: a ruler drop/reaction time task,a balance test and a verbal task. Although self-reported measuresof impairment were the best predictors of BAC, both the rulerdrop and body balance tests accounted for significant portionsof BAC variance. These tasks were also perceived by the studentsas reflecting substantial driving ability. Unfortunately, asBAC increased, poor test performance was less likely to resultin a decision not to drive. These results are discussed in termsof the need to continue studying ways to educate drinkers abouttheir level of alcohol impairment so that they can make informeddrinking/driving decisions.     

Production of elastase and other exoproducts by environmental isolates of Pseudomonas aeruginosa.

Pseudomonas aeruginosa isolates from environmental sources and bacteremic patients were compared for their levels of elastolytic activity. No significant differences were found. The incidence of production of toxin A, phospholipase C, alkaline protease, and elastase among the environmental strains was also as high as that previously reported for clinical isolates.     

Carnitine deficiency associated with ornithine transcarbamylase deficiency

An infant with X-linked recessive ornithine transcarbamylase deficiency is described who also had severe deficiency of plasma and liver carnitine during normoammonemic periods. Treatment with L-carnitine (100 mg/kg/day) for 12 months decreased the frequency of hospitalizations for hyperammonemia, although it did not alter his neurologic status. This report demonstrates that persistent carnitine deficiency may be present in patients with ornithine transcarbamylase deficiency even when plasma ammonia is normal. Carnitine evaluation and supplementation may be important in the treatment of patients with this metabolic disorder.     

Pathogenesis and treatment of diabetic neuropathy]

The pathogenesis of neuropathy and other late, degenerative complications of diabetes remains largely unresolved. Metabolic derangements thought to be responsible for their development are induced by chronic hyperglycaemia. The present studies concern as follows: sorbitol accumulation due to increased polyol pathway activity, altered myoinositol metabolism in diabetic nerve, followed by diminished sodium-potassium ATPase activity, nonenzymatic glycosylation of structural proteins and rheologic changes in microcirculation. These processes impair nerve metabolism, function and structure directly or indirectly, due to primary vascular alternations and endoneural hypoxia. Partial elucidation of the mechanism involved in pathogenesis of diabetic neuropathy has provoked emergence of new therapeutic approaches. So far their results are equivocal and require further studies. At present, improved glycaemia control is undoubtedly the most important factor in prevention and treatment of neuropathy and other late complications of diabetes.