42 research outputs found

    Serum levels of protein degradation products.

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    <p>Relative levels of serum protein degradation products, including acetylated amino acids, dipeptides, and urea cycle intermediates. Serum levels of each metabolite were compared using paired Welch's <i>t</i> tests, and <i>q</i> values were calculated to account for false discovery rates to correct for multiple comparisons.</p><p>Serum levels of protein degradation products.</p

    Global network analysis of relative measured metabolites in patients with alcoholic cirrhosis and severe AAH.

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    <p>Red nodes depict metabolites that are increased in severe AAH when compared to alcoholic cirrhosis; yellow nodes depict metabolites that are decreased in severe AAH when compared to alcoholic cirrhosis.</p

    Clinical and Demographic Characteristics of Patients.

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    <p>Baseline characteristics of patients. All values are expressed as medians and IQRs unless otherwise specified. Continuous variables were compared with Mann-Whitney <i>U</i> test. Categorical variables were compared with Fisher's exact test. N/A: not applicable; NS: not signifnicant (<i>p</i>>0.05).</p><p>Clinical and Demographic Characteristics of Patients.</p

    Characterization of ACP KD.

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    <p>A) Relative expression of ACP in control siRNA-treated and ACP siRNA-treated cells as measured by Taqman assay. B) Western blot using anti-lipoate antibody to compare protein from control siRNA-treated, negative control METTL9 siRNA-treated, and ACP siRNA-treated cells at 96 h and 168 h. C) Western blot using OXPHOS antibody cocktail to compare protein from control siRNA-treated, negative control METTL9 siRNA-treated, and ACP siRNA-treated cells at 96 h and 168 h.</p

    GSH/GSSG ratios are altered by changes in mtFASII function.

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    <p>GSH and GSSG levels in ACP KD cells, MECR OX cells, and their respective controls were determined by metabolomics analysis using UHLC/MS/MS, as described in Experimental Procedures. From these data, GSH/GSSG ratios were calculated. n = 6 and ** p < 0.01.</p

    Alterations in serum bile acid levels in patients with severe acute alcoholic hepatitis (hepatitis) and stable alcoholic cirrhosis (control).

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    <p>(A) Secondary bile acids. (B) Sulfated bile acids. (C) Products of gut microbial bile acid metabolism. (D) Schematic representation of altered bile acid turnover in severe AAH. * <i>p</i><0.05, ** <i>p</i><0.01, *** <i>p</i><0.001.</p

    Metabolic predictors of 180-day survival in severe AAH by logistic regression analysis.

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    <p>Univariable logistic regression analysis for metabolic predictors of 180-day survival in severe AAH. AA, amino acid; BCAA, branched-chain amino acid; FA, fatty acid; O.R., odds ratio; C.I., confidence interval.</p><p>Metabolic predictors of 180-day survival in severe AAH by logistic regression analysis.</p

    Pentose phosphate pathway metabolites are reduced in ACP KD cells and elevated in MECR OX cells.

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    <p>Levels of metabolites from the pentose phosphate pathway were analyzed in whole ACP KD and MECR OX cells and their respective controls using metabolomics, which included UHLC/MS/MS and GC/MS, as described in Experimental Procedures. Pentose phosphate pathway intermediates that were identified are indicated with arrows and a corresponding box plot. Y-axes for box plots indicate scaled intensity. Direction of metabolite level change compared to control in ACP KD cells is indicated by gray arrows, and direction of metabolite level change relative to control in MECR OX cells is indicated by blue arrows. In box plots, metabolite levels are shown for ACP KD cells, MECR OX cells, and their respective controls. For each box, n = 6 and open circles indicate extreme data points.</p
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