6 research outputs found

    Analysis off Dependent Discrete Choices Using Gaussian Copula

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    A popular tool for analyzing product choices of consumers is the well-known conditional logit discrete choice model. Originally publicized by McFadden (1974), this model assumes that the random components of the underlying latent utility functions of the consumers follow independent Gumbel distributions. However, in practice the independence assumption may be violated and a more reasonable model should account for the dependence of the utilities. In this dissertation we use the Gaussian copula with compound symmetric and autoregressive of order one correlation matrices to construct a general multivariate model for the joint distribution of the utilities. The induced correlations on the utilities and the choice probabilities are studied using analytic expressions and simulations. For regression with consumer and product specic covariates, we derive expressions for the likelihood function and the score functions. We use numerical methods and computer code to obtain the maximum likelihood estimates of the regression and correlation parameters. The standard errors of the estimates were obtained using bootstrap. Comparison of our model with other competing methods and practical applicability is illustrated using both real world consumer preference and simulated data

    Saccharomyces Boulardii and Bismuth Subsalicylate as Low-Cost Interventions to Reduce the Duration and Severity of Cholera

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    We conducted a randomised single-blinded clinical trial of 100 cholera patients in Port-au-Prince, Haiti to determine if the probiotic Saccharomyces cerevisiae var. boulardii and the anti-diarrhoeal drug bismuth subsalicylate (BS) were able to reduce the duration and severity of cholera. Subjects received either: S. boulardii 250 mg, S. boulardii 250 mg capsule plus BS 524 mg tablet, BS 524 mg, or two placebo capsules every 6 hours alongside standard treatment for cholera. The length of hospitalisation plus the number and volume of emesis, stool and urine were recorded every 6 hours until the study subject was discharged (n=83), left against medical advice (n=11), or requested removal from the study (n=6). There were no reported deaths or adverse study-related events. There were no statistically significant differences between the study arms and the outcomes of interest

    Liver Perilipin 5 Expression Worsens Hepatosteatosis But Not Insulin Resistance in High Fat-Fed Mice

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    Perilipin 5 (PLIN5) is a lipid droplet (LD) protein highly expressed in oxidative tissues, including the fasted liver. However, its expression also increases in nonalcoholic fatty liver. To determine whether PLIN5 regulates metabolic phenotypes of hepatosteatosis under nutritional excess, liver targeted overexpression of PLIN5 was achieved using adenoviral vector (Ad-PLIN5) in male C57BL/6J mice fed high-fat diet. Mice treated with adenovirus expressing green fluorescent protein (GFP) (Ad-GFP) served as control. Ad-PLIN5 livers increased LD in the liver section, and liquid chromatography with tandem mass spectrometry revealed increases in lipid classes associated with LD, including triacylglycerol, cholesterol ester, and phospholipid classes, compared with Ad-GFP liver. Lipids commonly associated with hepatic lipotoxicity, diacylglycerol, and ceramides, were also increased in Ad-PLIN5 liver. The expression of genes in lipid metabolism regulated by peroxisome proliferator-activated receptor-alpha was reduced suggestive of slower mobilization of stored lipids in Ad-PLIN5 mice. However, the increase of hepatosteatosis by PLIN5 overexpression did not worsen glucose homeostasis. Rather, serum insulin levels were decreased, indicating better insulin sensitivity in Ad-PLIN5 mice. Moreover, genes associated with liver injury were unaltered in Ad-PLIN5 steatotic liver compared with Ad-GFP control. Phosphorylation of protein kinase B was increased in Ad-PLIN5-transduced AML12 hepatocyte despite of the promotion of fatty acid incorporation to triacylglycerol as well. Collectively, our data indicates that the increase in liver PLIN5 during hepatosteatosis drives further lipid accumulation but does not adversely affect hepatic health or insulin sensitivity
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