Publications by authors named "Hetu C"

Background: Neonatal ventilator-associated pneumonia (VAP) is associated with increased morbidity and mortality. In adults on mechanical ventilation, timed oral care decreases the frequency of VAP, but this approach has not been studied in neonates.

Objectives: To evaluate the feasibility of a randomized trial of timed oral care with Biotene OralBalance® gel and estimate the required sample size for such a trial.

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Objective: To evaluate the relationship among demographic data, anxiety, significant losses, depression, and irrational beliefs reported by first-offence shoplifters.

Method: One hundred and six adult shoplifters who were first-time offenders completed a self-administered questionnaire.

Results: Men and women were equally likely to be arrested for this offence.

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A survey of 1,649 shoplifting convictions at a Montreal area municipal court found that a relatively low percentage (3.2%) of the cases involved mentally ill patients and that there is a comparatively closer link between shoplifting and affective disorders, alcoholism and drug addiction. The survey also showed that shoplifting is related more to mental illness than to the use of psychotropic drugs.

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Liver microsomal monooxygenase activities known to be ethanol-inducible were determined in female Sprague-Dawley rats after 2-week treatment with 1% (v/v) acetone. Daily acetone intake was in the order of 1.2 g/kg.

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Liver microsomal mixed-function oxidase activities were determined in female Sprague-Dawley rats after 3 weeks of ethanol feeding and for up to 10 days after withdrawal. Ethanol (36% of total calories) was administered in a high fat liquid diet and was replaced isocalorically by carbohydrates in controls. Chronic ethanol feeding similarly enhanced both microsomal cytochrome P-450 content and benzphetamine N-demethylase activity, per mg of protein, and resulted in a disproportionate increase in both aniline hydroxylase and 7-ethoxycoumarin O-deethylase activities.

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Chronic ethanol administration in female rats enhances the apparent molar activity of liver microsomes for aniline hydroxylation and 7-ethoxycoumarin O-deethylation. Microsomal cytochromes P-450 from ethanol-fed and control rats have been solubilized and partially resolved in six fractions by anion-exchange chromatography. Induction of aniline hydroxylase activity by ethanol was associated with marked increases in the turnover numbers of the more basic cytochrome P-450 containing fractions in a reconstituted aniline hydroxylation system.

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Female Sprague-Dawley rats were pair-fed a nutritionally adequate liquid diet containing either ethanol or isocaloric carbohydrate for 3 weeks. In vitro studies showed that chronic ethanol pretreatment preferentially increased the liver microsomal biotransformation of bromobenzene to p-bromophenol (via the toxic 3,4-epoxide) rather than to o-bromophenol (via the nontoxic 2,3-epoxide) and could thus potentiate bromobenzene hepatotoxicity. Bromobenzene administration (500 mg/kg body weight, ip), after an overnight fast, was associated in ethanol-pretreated rats with greater and accelerated liver glutathione depletion and subsequent decrease in liver cytochrome P-450 content than in controls.

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Chronic ethanol administration to female rats for 3 weeks was associated with a 60% increase in liver microsomal cytochrome P-450 content. This effect was accompanied by a similar increase in microsomal epoxide hydrase activity, in the presence of styrene oxide, and by significant increases in liver glutathione concentration and cytosolic glutathione S-transferase activities. A time-course study showed that the elevation of liver glutathione concentration seen after 3 weeks of ethanol consumption was a transient phenomenon, not observed after prolonged (23 weeks) ethanol intake and preceded, in the first 10-12 days of ethanol administration, by a decrease below control levels.

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Liver regeneration is the common mechanism whereby a patient recovers form a liver injury. In the western world, ethanol is the single most important aetiological factor associated with liver disease, and it appears crucial to determine if ethanol interferes with liver regeneration. We studied the response to a 70% hepatectomy in 240 rats receiving a nutritionally adequate diet containing 36% of their calories as ethanol for three weeks and their pair-fed controls receiving a liquid diet where ethanol is isocalorically replace with carbohydrates.

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Ethanol induces in rat liver microsomes a form of cytochrome P-450 differing in substrate specificity from cytochrome P-450 species present in controls or in rats treated with phenobarbital or 3-methylcholanthrene. Its relative capacity to oxidize ethanol remained to be determined and was studied using highly purified cytochrome P-450 preparations and comparing their activity in a reconstituted microsomal ethanol oxidizing system (MEOS). On a molar basis, reconstituted MEOS activity was found to be highest when assayed with ethanol-inducible cytochrome P-450, intermediate with cytochrome P-450 from phenobarbital-treated rats, and lowest with cytochrome P-450 from controls or 3-methylcholanthrene-treated rats.

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The effect of chronic ethanol administration on the hepatic microsomal cytochrome P-450 content and activities of NADPH - cytochrome P-450 reductase (EC 1.6.2.

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