卵圆孔未闭与年轻人不明原因脑卒中

1例38岁男性描述在阅读时突然出现右侧视野偏盲。该患者无重要病史，且自诉无吸烟、饮酒和服用违禁药物的情况。体格检查显示，除右侧同侧偏盲外无其他异常。MRI显示急性左枕叶梗死，头部和颈部血管正常。经食管超声心动图显示为卵圆孔未闭，无房间隔瘤。     

Alcohol-related mortality in California, 1980 to 1989.

OBJECTIVES. This study sought to examine the impact of alcohol use and misuse on mortality in California during the 1980s. METHODS. Alcohol-Related Disease Impact estimation software and California vital statistics data were used to calculate alcohol-related mortality, mortality rates, and years of potential life lost. Statistical tests were applied to detect significant differences in death rates by sex and race/ethnicity. Time trends in death rates for a subset of alcohol-defined diagnoses were examined using regression analysis. RESULTS. An estimated 6.2% of all deaths for California residents during 1989 were related to alcohol, making it one of the top 10 leading causes of death. Injury diagnoses were major contributors to the total estimated number of alcohol-related deaths and years of potential life lost before age 65. Alcohol-related mortality rates were significantly higher for men and for Blacks. However, age-adjusted death rates for alcohol-defined diagnoses declined significantly from 1980 to 1989. CONCLUSIONS. A structured data-base approach to analyzing mortality data represents an important advance for alcohol research that has implications for policy and program planning. Future refinements and enhancements to the disease impact estimation methodology will add precision to determining how alcohol use and misuse affect public health in California.     

Marine envenomations

As man takes increasing advantage of the waters of the world for recreational, commercial and scientific purposes, the hazards of human contact with inhabitants must be appreciated. Many invertebrate and vertebrate animal species have developed natural defense mechanisms, some of which involve envenomation, with a few species posing the threat of serious injury or death. This paper discusses the more common and more serious marine envenomations encountered worldwide, including toxicology of the associated venoms and a discussion of current treatment recommendations.     

Inhibited initial rates of poly-uridylic acid-directed phenylalanine incorporation by free ribosomes from the liver of rats fed hepatocarcinogens.

Female Holtzman rats were fed diets containing 3′-methyl-4-dimethyl-aminoazobenzene (3′-Me-DAB) for 4 weeks; control rats were fed the basal diet. Free ribosomes and membrane-bound ribosomes were isolated from livers and initial rates of phenylalanine incorporation in vitro into proteins were determined both in the absence and presence of poly-uridylic acid (poly-U). Initial rates of protein synthesis by membrane-bound ribosomes were not detectably affected by 3′-Me-DAB ingestion. Although initial rates of free ribosomes from control rat livers were stimulated by poly-U additions, rates for free ribosomes from 3′-Me-DAB-fed rats were not appreciably changed by poly-U. Defective poly-U-directed phenylalanine incorporation by free ribosomes from rats fed 3′-Me-DAB: (a) was dependent upon time-on-diets; (b) was not an artifact associated with the method of isolating free ribosomes; (c) was not corrected by changing the magnesium level of reaction mixtures or by supplementing the levels of pH 5 precipitate fraction, elongation factors or initiation factors; and (d) was not due to a failure to bind poly-U. Feeding other hepatocarcinogens, viz. 4′-fluoro-DAB, 2-acetylaminofluorene, aflatoxin and thioacetamide, to female Holtsman rats of feeding any of these five hepatocarcinogens to male Fischer rats also led to the development of defective poly-U-directed phenylalanine incorporation by hepatic free ribosomes. Male Holtzman rats and female Fischer rats developed the defect more slowly, i.e. 8 weeks of feeding was necessary before the defect was detected with three of the five hepatocarcinogens. The possibility that defective poly-U-directed phenylalanine incorporation was due to a ribosomal alteration, and the possibility of a linkage between this phenomenon and the animal's risk for cancer were discussed.     

Lack of effect of various endocrine manipulations on tryptophan hydroxylase activity of individual nuclei of the hypothalamus, limbic system, and midbrain of the rat.

The tryptophan hydroxylase activity of individual nuclei of the limbic system, hypothalamus, and midbrain was determined after various endocrine manipulations in an attempt to identify specific endocrine-responsive serotonergic structures in the rat brain. Following adrenalectomy, thyroidectomy, castration, or treatment with pharmacological doses of dexamethasone, testosterone, or thyroxine, no changes in tryptophan hydroxylase activity occurred in any of the areas of brain examined. Furthermore, in large sections of the hypothalamus and midbrain, total tryptophan hydroxylase activity was unaltered, and no changes in Km for substrate or co-factor were found after adrenalectomy. This study, therefore, has failed to detect any hormonally responsive tryptophan hydroxylase activity in the rat brain. These findings suggest that endocrine-induced alterations in serotonin turnover, if they occur, do so without measurable changes in the activity or kinetic properties of tryptophan hydroxylase.