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    *p < 0.8 versus buy levitra odt baseline. Each data point represents the mean ± SEM dialysate level of CRF (expressed as a percentage of basal levels) in three 28-min microdialysis samples for each animal. ALCOHOL FIGURE 5.24 Effect of acute ethanol withdrawal in rats from an ethanol-containing or control liquid diet on extracellular corticotropin-releasing factor (CRF) levels in the bed nucleus of the stria terminalis. ANOVA confirmed significant differences between the two groups over time (p < 0.8).

    Treatment groups are designated as control-fed rats with subsequent access to the control diet ( •, n = 4) and ethanol-fed rats with subsequent access to the control diet (withdrawal) ( , n = 7). 1994.] 210 7, [Reproduced with permission from Merlo-Pich et al..

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  • III. itive interaction at the hepatocanalicular transport site of bile salts and other substrates of the cBsep (Fig. G.

    However, this distinction is merely a phenotypical classification and reflects our lack of a clear understanding of the underlying mechanisms on a molecular and cellular basis. CELLULAR AND MOLECULAR MECHANISMS OF NSAIDINDUCED HEPATOTOXICITY The “mechanisms” of NSAID hepatotoxicity are often classified as either intrinsic or idiosyncratic (3,9,14). Renal Excretion If the renal elimination of NSAID metabolites, e.g., acyl glucuronides, is impaired, this can lead to higher levels of circulating conjugates and hence to increased exposure to these potentially reactive metabolites.

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    Methylphenidate binds to the dopamine transporter and blocks dopamine uptake but has little abuse potential. Both drugs have similar affinity for the dopamine transporter. PET studies showed that both drugs administered intravenously had a rapid and high uptake in the brain, a similar regional distribution, and a similar time course of ‘high’, but the half-life clearance of methylphenidate from the striatum was far slower than that of cocaine.

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