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Louis J Elsas - One of the best experts on this subject based on the ideXlab platform.

  • verbal dyspraxia and galactosemia
    Pediatric Research, 2003
    Co-Authors: Amy L Webb, Mary Jane Kennedy, Rani H. Singh, Louis J Elsas
    Abstract:

    Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: Cumulative Percentage dose (CUMPCD) of 13CO2 in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a 13C-galactose bolus, and the (CUMPCD) of 13CO2 in expired air was determined. Patients with 2.7 mg/dL, and mean urinary galactitol levels >135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO2 in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.

  • Verbal Dyspraxia and Galactosemia
    Pediatric Research, 2003
    Co-Authors: Amy L Webb, Mary Jane Kennedy, Rani H. Singh, Louis J Elsas
    Abstract:

    Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: Cumulative Percentage dose (CUMPCD) of ^13CO_2 in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a ^13C-galactose bolus, and the (CUMPCD) of ^13CO_2 in expired air was determined. Patients with 135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO_2 in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.

Amy L Webb - One of the best experts on this subject based on the ideXlab platform.

  • verbal dyspraxia and galactosemia
    Pediatric Research, 2003
    Co-Authors: Amy L Webb, Mary Jane Kennedy, Rani H. Singh, Louis J Elsas
    Abstract:

    Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: Cumulative Percentage dose (CUMPCD) of 13CO2 in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a 13C-galactose bolus, and the (CUMPCD) of 13CO2 in expired air was determined. Patients with 2.7 mg/dL, and mean urinary galactitol levels >135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO2 in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.

  • Verbal Dyspraxia and Galactosemia
    Pediatric Research, 2003
    Co-Authors: Amy L Webb, Mary Jane Kennedy, Rani H. Singh, Louis J Elsas
    Abstract:

    Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: Cumulative Percentage dose (CUMPCD) of ^13CO_2 in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a ^13C-galactose bolus, and the (CUMPCD) of ^13CO_2 in expired air was determined. Patients with 135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO_2 in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.

Mary Jane Kennedy - One of the best experts on this subject based on the ideXlab platform.

  • verbal dyspraxia and galactosemia
    Pediatric Research, 2003
    Co-Authors: Amy L Webb, Mary Jane Kennedy, Rani H. Singh, Louis J Elsas
    Abstract:

    Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: Cumulative Percentage dose (CUMPCD) of 13CO2 in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a 13C-galactose bolus, and the (CUMPCD) of 13CO2 in expired air was determined. Patients with 2.7 mg/dL, and mean urinary galactitol levels >135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO2 in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.

  • Verbal Dyspraxia and Galactosemia
    Pediatric Research, 2003
    Co-Authors: Amy L Webb, Mary Jane Kennedy, Rani H. Singh, Louis J Elsas
    Abstract:

    Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: Cumulative Percentage dose (CUMPCD) of ^13CO_2 in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a ^13C-galactose bolus, and the (CUMPCD) of ^13CO_2 in expired air was determined. Patients with 135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO_2 in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.

Rani H. Singh - One of the best experts on this subject based on the ideXlab platform.

  • verbal dyspraxia and galactosemia
    Pediatric Research, 2003
    Co-Authors: Amy L Webb, Mary Jane Kennedy, Rani H. Singh, Louis J Elsas
    Abstract:

    Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: Cumulative Percentage dose (CUMPCD) of 13CO2 in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a 13C-galactose bolus, and the (CUMPCD) of 13CO2 in expired air was determined. Patients with 2.7 mg/dL, and mean urinary galactitol levels >135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO2 in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.

  • Verbal Dyspraxia and Galactosemia
    Pediatric Research, 2003
    Co-Authors: Amy L Webb, Mary Jane Kennedy, Rani H. Singh, Louis J Elsas
    Abstract:

    Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: Cumulative Percentage dose (CUMPCD) of ^13CO_2 in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a ^13C-galactose bolus, and the (CUMPCD) of ^13CO_2 in expired air was determined. Patients with 135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO_2 in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.

Xiaoyan Shi - One of the best experts on this subject based on the ideXlab platform.

  • In vitro-in vivo correlations for three different commercial immediate-release indapamide tablets
    Drug development and industrial pharmacy, 2013
    Co-Authors: Peter Yaro, Weijun Liu, Mingjin Xun, Xiaoyan Shi
    Abstract:

    The objective of this study was to develop and validate the in vitro-in vivo correlations (IVIVCs) of three commercially available immediate-release solid dosage forms of indapamide using drug dissolution/absorption simulating system (DDASS). The in vitro dissolution profiles of three brands of immediate-release tablets were obtained using the USP I basket method and DDASS. A single-dose, three-way, crossover pharmacokinetic study for the tablets was carried out in six beagle dogs. Correlation models were developed for each immediate release formulation using Cumulative Percentage dissolved/eluted (Fd) versus Cumulative Percentage absorbed (Fa) and Cumulative Percentage permeated (Fp) versus Cumulative Percentage absorbed (Fa). Prediction errors were estimated for the Cmax and AUC to determine the validity of the correlation. Level A IVIVCs were established for the three brands between in vitro (dissolution and permeation) data from DDASS and in vivo data from dogs. Predicted plasma concentrations of each commercial brand were obtained from the dissolution and permeation profile data using the correlation models. A percent prediction error of