PubMed · 4129491
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Z Abedin, R P Sapru. 1974-02-04. His bundle ectopic beats. His bundle electrocardiographic study.. https://pubmed.ncbi.nlm.nih.gov/4129491/
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OBJECTIVES: To determine whether routine oral and enteral nutritional supplementation can improve the weight, anthropometry, and survival of adult patients. DESIGN: Systematic review of randomised controlled trials of oral or enteral protein supplementation in adults. Trials were identified from Medline (Silver Platter 3.11, 1966-96), reference lists of identified studies and review articles, and communication with feed manufacturers. SUBJECTS: Randomised controlled trials comparing oral or enteral protein supplementation with no routine supplementation. All trials of adult subjects were included except those addressing nutrition in pregnancy. MAIN OUTCOME MEASURES: Change in body weight and anthropometry (mid-arm muscle circumference), and all cause case fatality recorded at the end of scheduled follow up. Body weight and anthropometry were analysed as the weighted mean difference and 95% confidence intervals of the percentage change in these variables. Case fatality was analysed with odds ratio and 95% confidence intervals. RESULTS: 32 eligible reports (2286 randomised patients) published between February 1979 and July 1996 were identified, of which 30 (93.8%) (2062 randomised patients) reported outcomes of interest. Case fatality data were available for 1670 (81%) patients, and continuous variable data for up to 1607 (78%) patients. The treatment group receiving routine nutritional supplementation showed consistently improved changes in body weight and anthropometry compared with controls; weighted mean difference 2.06% (95% confidence interval 1.63% to 2.49%) and 3.16% (2.43% to 3.89%) respectively. The pooled odds ratio for death in the treatment group was 0.66 (0.48 to 0.91, 2P<0.01). Apparent benefits were observed in several prespecified subgroups of patients, treatment settings, and interventions, but were not evident if trials with less robust methodology were excluded. CONCLUSIONS: Routine oral or enteral supplementation seems to improve the nutritional indices of adult patients, but there are insufficient data in trials which meet strict methodological criteria to be certain if mortality is reduced. Benefits were not restricted to particular patient groups. Further large pragmatic randomised controlled trials of routine nutritional supplementation are justified.
The effect of pre- and postnatal ethanol exposure on protein kinase C (PKC) activity, immunochemical analysis of PKC alpha, betaI, betaII, gamma, delta, epsilon, eta, and zeta by isoform-specific antibodies, and in vitro phosphorylation of endogenous substrate proteins was investigated in rat cerebral cortex. The PKC activity was increased throughout the development. However, the activity at the age of 8 days was significantly high in cytosolic and membrane fractions from ethanol-treated rats. Immunochemical analysis showed increased levels of PKC betaI and betaII at the age of 8 days, and a decrease in delta isoform at 8, 30, and 90 days of age. PKC isoforms alpha, gamma, epsilon, and eta showed no appreciable change in ethanol-treated rats. PKC zeta levels were high in the cytosolic fraction from ethanol-treated samples of 90 days age. In vitro phosphorylation of endogenous substrate proteins in the presence of Ca2+/phospholipid showed increased phosphorylation of selective membrane and cytosolic proteins with 87, 65, 50, 43, 36, and 29 kDa in ethanol-treated rats. The phosphorylation of these proteins decreased in the presence of staurosporine, which also supported PKC-mediated phosphorylation. Increased PKC activity, activation of betaI and betaII isoforms, decreased levels of delta isoform, and phosphorylation of selective substrate proteins in cerebral cortex due to alcohol exposure might be relevant in ethanol-induced central nervous system dysfunction and fetal alcohol syndrome.
Large numbers of injection drug users (IDUs) are infected with HIV and receive both methadone and zidovudine (ZDV) therapy. Pharmacokinetic interactions between these agents may effect drug efficacy, toxicity, and compliance. To confirm and expand previous studies that identified a potential interaction between ZDV and methadone, we performed a within-subject study to determine oral and intravenous ZDV pharmacokinetics in 8 recently detoxified, heroin-addicted patients with HIV disease before and after initiation of methadone treatment. Acute methadone treatment increased oral ZDV in the area under the curve (AUC) by 41% (p = .03) and intravenous ZDV AUC by 19% (p = .06). Clearance was reduced by 21% (p = .007) and 19% (p = .04), respectively. Chronic methadone treatment increased oral ZDV AUC by 29% (p = .15) and intravenous ZDV AUC by 41% (p = .05). Clearance was decreased by 26% for both routes (p = .02). Methadone levels remained in the therapeutic range during ZDV treatment. These effects resulted primarily from inhibition of ZDV glucuronidation, but also from decreased renal clearance of ZDV. This study confirms that methadone-maintained patients receiving standard ZDV doses experience greater ZDV exposure and may be at increased risk for ZDV side effects and toxicity. Increased toxicity surveillance and possibly reduction in ZDV dose are indicated when these two agents are given concomitantly.