Effects of alcohol exposure during early life on neuron numbers in the rat hippocampus. I. Hilus neurons and granule cells

We previously showed that 16-day-old rats exposed to a relatively high dose of ethanol at 10-15 postnatal days of age have fewer neurons in the hilus region of the hippocampus compared with controls. Dentate gyrus granule cell numbers, however, showed no statistically significant changes attributable to the ethanol treatment. It is possible that some of the changes in brain morphology, brought about as a result of the exposure to ethanol during early life, may not be manifested until later in life. This question has been further addressed in an extension to our previous study. Wistar rats were exposed to a relatively high daily dose of ethanol on postnatal days 10-15 by placement in a chamber containing ethanol vapour, for 3 h/day. The blood ethanol concentration was found to be similar to430 mg/dl at the end of the period of exposure. Groups of ethanol-treated (ET), separation control (SC), and mother-reared control (MRC) rats were anaesthetised and killed either at 16 or 30 days of age by perfusion with phosphate-buffered 2.5% glutaraldehyde. The Cavalieri principle and the physical disector methods were used to estimate, respectively, the regional volumes and neuron cell numerical densities in the hilus and granule cell regions of the dentate gyrus. The total numbers of neurons in the hilus region and granule cell layer were computed from these estimates. It was found that 16-day-old animals had 398,000-441,000 granule cells, irrespective of group. The numbers of granule cells increased such that by 30 days of age, rats had 487,000-525,500 granule cells. However, there were no significant differences between ethanol-treated rats and their age-matched controls in granule cell numbers. In contrast, ethanol-treated rats had slightly but significantly fewer neurons in the hilus region than did control animals at 16 days of age, but not at 30 days of age. Therefore, it appears that a short period of ethanol exposure during early life can have effects on neuron numbers of some hippocampal neurons, but not others. The effects on hilar neuron numbers, observed as a result of such short periods of ethanol treatment, appeared to be transitory. (C) 2003 Wiley-Liss, Inc.

Triggers of subarachnoid hemorrhage - Role of physical exertion, smoking, and alcohol in the Australasian Cooperative Research on Subarachnoid Hemorrhage Study (ACROSS)

Background and Purpose - Unaccustomed strenuous physical exertion can trigger myocardial infarction, but little is known about the mechanisms precipitating subarachnoid hemorrhage (SAH). Methods - We identified all cases of first-ever SAH among the combined populations (2.8 million) of 4 urban centers in Australia and New Zealand. Information on the type, time, and intensity of exposures in the 26 hours before the onset of SAH was ascertained by structured interviews. We used the case-crossover technique to assess the risk of SAH associated with transient exposures of moderate to extreme physical exertion, heavy cigarette smoking, and binge alcohol consumption. Results - We registered 432 first-ever cases of SAH (62% women; mean age, 56.5 years). A definite time of onset of SAH was established for 393 patients (91%), and information on the levels of physical activity in the preceding 26 hours was obtained in 338 ( 78%). Of these patients, 19% engaged in moderate to extreme exertion (greater than or equal to5 metabolic equivalents) in the 2 hours before SAH, which was associated with a tripling in the risk of SAH (odds ratio [OR], 2.7; 95% CI, 1.6 to 4.6). There was no evidence of any association between heavy cigarette smoking or binge drinking and risk of SAH in the subsequent 2 hours ( OR, 1.1; 95% CI, 0.4 to 3.7; and OR, 0.41; 95% CI, -infinity to 5.3). Habitual exercise did not appear to alter the risk of SAH associated with moderate to extreme exertion. Conclusions - Moderate to extreme physical exertion tripled the risk of SAH, but there was no association between transient heavy smoking or binge drinking and risk of SAH. These data suggest that heavy physical activity may trigger SAH.

Does the tendency to act impulsively underlie binge eating and alcohol use problems? An empirical investigation

The co-occurrence of problem drinking and binge eating and purging has been well documented. However, there has been relatively little investigation of etiological models that may influence the development of this co-occurrence. This study tests the hypotheses that impulsivity is heightened in eating disordered women compared with controls, and that women with comorbid bulimia and alcohol use disorders show higher impulsivity than bulimic-only women. The Impulsivity scale, BIS/BAS scales, State Anxiety Inventory, and a behavioural measure of reward responsiveness (CARROT) were administered to 22 women with bulimia, 23 women with comorbid bulimia and alcohol abuse/dependence, and 21 control women. As hypothesised, eating disordered women scored higher than controls on several self-report measures of impulsivity and sorted cards faster during a financially rewarded trial on the behavioural task. Also, as predicted, comorbid women scored higher than bulimic women on the Impulsivity scale. These findings suggest that individual differences in impulsiveness and a tendency to approach rewarding stimuli may contribute to developing these disorders. (C) 2003 Elsevier Ltd. All rights reserved.

Effects of age and alcohol exposure during early life on pyramidal cell numbers in the CA1-CA3 region of the rat hippocampus

We have previously shown that exposing rats to a relatively high dose of ethanol during early postnatal life can result in an alteration in spatial learning ability. The hippocampal formation is known to be involved in the control of this ability. The purpose of the present study was to determine whether exposure of rats to ethanol during early postnatal life had either immediate or delayed effects on the numbers of pyramidal cells in the CA1-CA3 subregion of the hippocampus. Wistar rats were exposed to a relatively high daily dose of ethanol at postnatal day 10-15 by placing them for 3 h/day in a chamber containing ethanol vapor. Groups of ethanol-treated (ET), separation control (SC), and mother-reared control (MRC) rats were anesthetized and killed at 16 and 30 days of age by perfusion with phosphate-buffered 2.5% glutaraldehyde. The Cavalieri principle was used to determine the volumes of the CA1 and CA2+CA3 regions. The physical disector method was used to estimate the numerical density of neurons in each of the subdivisions. The total number of pyramidal cells was calculated by multiplying the appropriate estimates of the numerical density by the volume. There were significant age-related reductions in the total numbers of pyramidal cells at 16-30 days of age irrespective of the groups examined. Ethanol treated rats were found to have slightly but significantly fewer pyramidal cell neurons than either the MRC or SC groups. These observations indicate that pyramidal cells in the hippocampus may be vulnerable to a relatively high dose of ethanol exposure during this short period of early postnatal life. (C) 2003 Wiley-Liss, Inc.

Fuel stagnation temperature effects on mixing with supersonic combustion flows

An experimental study of the effect of fuel stagnation temperature on mixing in a supersonic hydrogen-air flame is described, The combustor consisted of a constant-area rectangular duct with a centrally located fuel-injection strut that spanned the width. A high-enthalpy stream of air was supplied by a free-piston shock tunnel, and heated hydrogen fuel, supplied by a gun-tunnel, was injected into the freestream as a coflowing planar jet. The freestream total enthalpies were 5.6, 6.5, and 9 MJ/kg, and fuel stagnation temperatures were 300, 450, and 700 K, Raising the fuel stagnation temperature increased the fuel velocity to be near that of the airstream and resulted in a decrease in the mixing rate, Even as the fuel and air velocities became equal, significant mixing still occurred because of a large difference in density, Increasing the freestream enthalpy reduced the difference between the initial air temperature and the adiabatic flame temperature, which in turn reduced the heat addition, and subsequently, the amount of pressure rise in the duct.

Deaths from cirrhosis in Poland and Hungary: The impact of different alcohol policies during the 1980s

Objective - To compare patterns of deaths from cirrhosis in Poland and Hungary in the context of differing alcohol policies in the 1980s. Design - Cohort analysis of deaths from chronic Liver disease and cirrhosis between 1959 and 1992 using mortality data from the World Health Organization database. Results - The pattern of alcohol related mortality in these countries is quite different. In both countries, death rates increased in the 1960s and 1970s. In Poland, this increase was arrested in 1980 and death rates have levelled out, with the exception of those in young females. In Hungary, rates have continued to climb, although the rate of increase decreased in the 1980s. This change coincides with the introduction of a policy, following the introduction of martial law, to reduce alcohol consumption. Conclusions - The countries of central and eastern Europe display many similarities in both political history and measures of health such as overall life expectancy. When examined more closely, substantial differences emerge. Policy makers must be cautious about adopting global solutions to health challenges that fail to take into account national variations.

Is alcohol a cofactor of HIV and AIDS? Evidence from immunological and behavioral studies

The authors aim to critically examine empirical research on the effects of alcohol on HIV and AIDS from the immunological and behavioral fields. In vitro immunological studies demonstrate that social drinking increases the susceptibility of human cells to HIV infection. Animal studies show that acute and chronic alcohol ingestion increases rare of progression from retrovirus to clinical illness. In humans with HIV, no experimental evidence shows that alcohol is a cofactor of AIDS. Findings from behavioral studies show that a link between social drinking and risk of HIV is weak. No experimental evidence demonstrates that chronic drinking influences rate and course of disease progression to AIDS in humans who are HIV+. It is premature to promote the role of alcohol as a cofactor in HIV and AIDS.

The alcohol withdrawal syndrome

The alcohol withdrawal syndrome (AWS) is a set of signs and symptoms that typically develops in alcohol-dependent people within 6–24 h of their last drink. It may occur unintentionally if abstinence is enforced by illness or injury, or deliberately if the person voluntarily stops drinking because of an alcohol-related illness, or as a prelude to becoming and remaining abstinent. The signs and symptoms of the syndrome (panel) are largely, but not exclusively, those of autonomic hyperactivity, the reverse of the effects of alcohol intoxication. They represent a homoeostatic readjustment of the central nervous system (CNS) to the neuroadaptation that occurs with prolonged alcohol intoxication.1 RC Turner, PR Lichstein and JG Peden et al., Alcohol withdrawal syndromes: a review of pathophysiology, clinical presentation and treatment, J Gen Intern Med 4 (1989), pp. 432–444. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (39)1 They vary in severity from mild to severe.1