12 research outputs found

    <i>H</i>. <i>pylori</i> antibody status, proportion of metabolic syndrome and HOMA-IR in subjects greater or less than 50 years of age.

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    <p>† MS: metabolic syndrome</p><p>‡ <i>p</i>-value of Cochran-Mantel-Haenszel test for the independence of age and <i>H</i>. <i>pylori</i> antibody controlling for the factor of metabolic syndrome.</p><p><i>H</i>. <i>pylori</i> antibody status, proportion of metabolic syndrome and HOMA-IR in subjects greater or less than 50 years of age.</p

    Correlations among metabolic syndrome, <i>H</i>. <i>pylori</i> status and other factors.

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    <p>† data expressed as coefficient (<i>p</i> value)</p><p>Correlations among metabolic syndrome, <i>H</i>. <i>pylori</i> status and other factors.</p

    Characteristics of metabolic syndrome status between different age groups.

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    <p>† data expressed as No (%)</p><p>Characteristics of metabolic syndrome status between different age groups.</p

    Predictors of metabolic syndrome by multivariate logistic regression analysis.

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    <p>†95% CI: 95% confidence interval</p><p>Predictors of metabolic syndrome by multivariate logistic regression analysis.</p

    Characteristics of Study Subjects.

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    <p>*: mean±standard deviation (SD)</p><p><i>H</i>. <i>pylori</i> Ab: <i>Helicobacter pylori</i> antibody</p><p>HOMA-IR: Homeostasis model assessment of insulin resistance</p><p>BMI: body mass index</p><p>SBP: systolic blood pressure</p><p>DBP: diastolic blood pressure</p><p>TG: triglyceride</p><p>HDL: high density lipoprotein</p><p>LDL: low density lipoprotein</p><p>VLDL: very low density lipoprotein</p><p>TCHOL: total cholesterol</p><p>FBG: fasting blood glucose</p><p>HbA1c: glycosylated hemoglobin</p><p>AG: average glucose</p><p>AST: aspartate aminotransferase</p><p>ALT: alanine aminotransferase</p><p>HS-CRP: high sensitivity C-reactive protein</p><p>TNF-α: tumor necrosis factor α</p><p>Characteristics of Study Subjects.</p

    Effect of lipopolysaccharides (LPS) on resting pH<sub>i</sub> and NHE activity in HRASMCs superfused with HEPES-buffered Tyrode solution.

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    <p><b>A, C, E:</b> The top bar shows the buffer system used in the superfusate. The periods of application of NH<sub>4</sub>Cl and LPS (1∼10000 ng/ml) are shown with bars above or below the trace. Traces A represents experiments showing the effect of different concentrations of LPS (1∼10000 ng/ml) on resting pH<sub>i</sub> in HEPES-buffered Tyrode solution in HRASMCs (pH<sub>o</sub>  = 7.4, 37°C). The left part of traces C and E shows a typical pH<sub>i</sub> recovery from an intracellular acidosis induced by a 7 min NH<sub>4</sub>Cl (20 mM) pre-pulse in HEPES-buffered solution (pH<sub>o</sub>  = 7.4, 37°C) in HRASMCs. The right part of traces C and E represents experiment showing the effect of different concentrations of LPS (1∼10000 ng/ml) on pH<sub>i</sub> recovery in HRASMCs. B, D: Histograms, showing the change in resting pH<sub>i</sub> and pH<sub>i</sub> recovery slope of acid extrusion after NH<sub>4</sub>Cl-induced intracellular acidosis averaged for 7 and 6 experiments similar to those shown in A and C (measured at the range between the two dash lines of the figure), respectively. *: p<0.01 vs. control.</p

    Effect of lipopolysaccharides (LPS) on NBC activity in HRASMCs superfused with 5% CO2/HCO3<sup>−</sup> Tyrode solution plus 30 μM HOE 694.

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    <p>The top bar shows the buffer system used in the superfusate. The periods of application of NH<sub>4</sub>Cl and LPS (1000 and 10000 ng/ml) are shown with bars above or below the trace. The left part of traces shows a typical pH<sub>i</sub> recovery from an intracellular acidosis induced by a NH<sub>4</sub>Cl (20 mM) pre-pulse in 5% CO<sub>2</sub>/HCO<sub>3</sub><sup>−</sup> Tyrode solution plus 30 μM HOE 694 (pH<sub>o</sub>  = 7.4, 37°C) in HRASMCs. The middle part of trace represents experiment showing the effect of 2 different concentrations of LPS (1000 ng/ml and 10000 ng/ml) on pH<sub>i</sub> recovery in HRASMCs.</p

    Effect of 30 μM HOE 694, Na<sup>+</sup>-free and 0.2 mM DIDS on pHi recovery from induced acidosis in HRASMCs superfused with 5% CO2/HCO3<sup>−</sup> Tyrode solution.

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    <p><b>A and C:</b> The top bar shows the buffer system used in the superfusate. The periods of application of NH<sub>4</sub>Cl and tested drugs (30 μM HOE 694, Na<sup>+</sup>-free solution, 0.2 mM DIDS and HOE 694 pulse DIDS) are shown with bars above or below the trace. The left part of traces A and C shows a typical pH<sub>i</sub> recovery from an intracellular acidosis induced by a 10 min NH<sub>4</sub>Cl (20 mM) pre-pulse in 5% CO<sub>2</sub>/HCO<sub>3</sub><sup>−</sup> Tyrode solution (pH<sub>o</sub>  = 7.4, 37°C) in HRASMCs. For details of mechanism of the pre-pulse technique, please see the <i>Materials and Methods</i> section. The right part of traces A and C represents experiments showing the effect of 30 μM HOE 694 (a NHE exchanger inhibitor), Na<sup>+</sup>-free solution 0.2 mM DIDS (a NBC exchanger inhibitor) and HOE 694 plus DIDS on pH<sub>i</sub> recovery, respectively, in HRASMCs. B and D: Histograms, showing the pH<sub>i</sub> recovery slope of acid extrusion after NH<sub>4</sub>Cl-induced intracellular acidosis averaged for several experiments similar to those shown in A and C respectively. **: p<0.01 vs. control.</p

    Effect of Na<sup>+</sup>-free and 30 μM HOE 694 on pHi recovery from induced acidosis (evidence of Na<sup>+</sup>-H<sup>+</sup> exchanger) in HRASMCs superfused with HEPES-buffered Tyrode solution.

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    <p><b>A:</b> Top bar shows buffer system used in the superfusate. The periods of application of NH<sub>4</sub>Cl and tested drugs (30 μM HOE 694, a NHE exchanger inhibitor, and Na<sup>+</sup>-free solution) are indicated with bars above or below the trace. The left part of trace A show a typical recovery of pH<sub>i</sub>-recovery from an intracellular acidosis induced by a 10 min NH<sub>4</sub>Cl (20 mM) pre-pulse in HEPES-buffered Tyrode solution (pHo  = 7.4, 37°C) in HRASMCs. For details of the mechanism of the pre-pulse technique, please see the <i>Materials and Methods</i> section. The right part of trace A represents experiments showing the effect of Na<sup>+</sup>-free and 30 μM HOE 694 on pH<sub>i</sub> recovery, respectively, in HRASMCs. <b>B:</b> Histograms, showing the pH<sub>i</sub> recovery slope of acid extrusion after NH<sub>4</sub>Cl-induced intracellular acidosis averaged for 6 experiments similar to those shown in A. *: p<0.01 vs. control.</p

    The effect of LPS on protein expression of NHE, NBC and intracellular resting pH in HRASMCs.

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    <p><b>A</b>: The figure shows the result of Western blot analysis for β-actin, NHE 1, 2 and 3, from the bottom to the top, respectively, before (left part) and after (right part) the 1000 ng/ml LPS treatment (n = 4). <b>B</b>: The histogram shows relative protein expression, as an average of 6 experiments, which is similar to that shown in A. Data is shown as the mean ± SEM (p<0.01; n = 6). <b>C</b>: The figure shows the result of Western blot analysis for β-actin, SLC4A8 (NBCBE), SLC4A7 (NBCn1), SLC4A5 (NBCe2) and SLC4A4 (NBCe1), from the bottom to the top, respectively, before (left part) and after (right part) the 1000 ng/ml LPS treatment (n = 4). <b>D</b>: The histogram shows the protein expression, as an average of 4 experiments, which is similar to that shown in C. Data is shown as the mean ± SEM (p<0.01; n = 4). <b>E</b>: Gene expression of mRNA of different members of SLC4 family: NBCe1 (SLC4A4; 336 bp), NBCe2 (SLC4A5; 650 bp and 1 kb), NBCn1 (SLC4A7; 328 bp) and NDCBE1 (SLC4A8; 243 bp) extracted from HRASMCs by RT-PCR. Actin expression was used as control (373 bp). bp denotes base pairs; M denotes marker; + denotes the presence of template; − denotes the absence of template (negative control).</p
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