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mg-egta-gvbs  (CompTech Computer Technologies)

 
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    CompTech Computer Technologies mg-egta-gvbs
    Functional hemolytic assays of complement activation. (A) CH50-type antibody-initiated complement assays incubating antibody-sensitized erythrocytes (EA) with 0.2% human serum for 1 hour at 31-41°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There is 2-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01) (P ≤ 0.05 for the comparisons 31 vs. 37, 31 vs. 39, 31 vs. 41, 33 vs. 37, 33 vs. 39, 33 vs. 41, 35 vs. 39, 35 vs. 41, with significantly more hemolysis at lower temperatures) Data are mean ± SEM for 4 independent experiments. (B) Evaluating antibody-initiated complement activation from 0-37°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There was 2.5-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01). (P ≤ 0.05 for the comparisons 31 vs. 37, 24 vs. 37, 19 vs. 37, with significantly more hemolysis at lower temperatures). The trend of increased complement activation was reversed at 13°C. (No statistical difference between hemolysis at 13 vs. 37 or 7 vs. 37). Data are mean ± SEM for 4 independent experiments. (C) AP50-type alternative complement pathway assays, incubating rabbit erythrocytes with 4% human serum in <t>Mg-EGTA-GVBS</t> for 30 minutes at 31-41°C showed that temperature did not influence complement-mediated cell lysis over therapeutic hypothermia temperatures (ANOVA P = 0.45). Data are mean ± SEM for 4 independent experiments. (D) Evaluating alternative pathway activation from 0-37°C showed that alternative pathway activation was significantly inhibited at 24°C and below. There was no difference in the degree of hemolysis at 31°C vs. 37°C) Data are mean ± SEM for 4 independent experiments.
    Mg Egta Gvbs, supplied by CompTech Computer Technologies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Clinical hypothermia temperatures increase complement activation and cell destruction via the classical pathway"

    Article Title: Clinical hypothermia temperatures increase complement activation and cell destruction via the classical pathway

    Journal: Journal of Translational Medicine

    doi: 10.1186/1479-5876-12-181

    Functional hemolytic assays of complement activation. (A) CH50-type antibody-initiated complement assays incubating antibody-sensitized erythrocytes (EA) with 0.2% human serum for 1 hour at 31-41°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There is 2-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01) (P ≤ 0.05 for the comparisons 31 vs. 37, 31 vs. 39, 31 vs. 41, 33 vs. 37, 33 vs. 39, 33 vs. 41, 35 vs. 39, 35 vs. 41, with significantly more hemolysis at lower temperatures) Data are mean ± SEM for 4 independent experiments. (B) Evaluating antibody-initiated complement activation from 0-37°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There was 2.5-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01). (P ≤ 0.05 for the comparisons 31 vs. 37, 24 vs. 37, 19 vs. 37, with significantly more hemolysis at lower temperatures). The trend of increased complement activation was reversed at 13°C. (No statistical difference between hemolysis at 13 vs. 37 or 7 vs. 37). Data are mean ± SEM for 4 independent experiments. (C) AP50-type alternative complement pathway assays, incubating rabbit erythrocytes with 4% human serum in Mg-EGTA-GVBS for 30 minutes at 31-41°C showed that temperature did not influence complement-mediated cell lysis over therapeutic hypothermia temperatures (ANOVA P = 0.45). Data are mean ± SEM for 4 independent experiments. (D) Evaluating alternative pathway activation from 0-37°C showed that alternative pathway activation was significantly inhibited at 24°C and below. There was no difference in the degree of hemolysis at 31°C vs. 37°C) Data are mean ± SEM for 4 independent experiments.
    Figure Legend Snippet: Functional hemolytic assays of complement activation. (A) CH50-type antibody-initiated complement assays incubating antibody-sensitized erythrocytes (EA) with 0.2% human serum for 1 hour at 31-41°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There is 2-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01) (P ≤ 0.05 for the comparisons 31 vs. 37, 31 vs. 39, 31 vs. 41, 33 vs. 37, 33 vs. 39, 33 vs. 41, 35 vs. 39, 35 vs. 41, with significantly more hemolysis at lower temperatures) Data are mean ± SEM for 4 independent experiments. (B) Evaluating antibody-initiated complement activation from 0-37°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There was 2.5-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01). (P ≤ 0.05 for the comparisons 31 vs. 37, 24 vs. 37, 19 vs. 37, with significantly more hemolysis at lower temperatures). The trend of increased complement activation was reversed at 13°C. (No statistical difference between hemolysis at 13 vs. 37 or 7 vs. 37). Data are mean ± SEM for 4 independent experiments. (C) AP50-type alternative complement pathway assays, incubating rabbit erythrocytes with 4% human serum in Mg-EGTA-GVBS for 30 minutes at 31-41°C showed that temperature did not influence complement-mediated cell lysis over therapeutic hypothermia temperatures (ANOVA P = 0.45). Data are mean ± SEM for 4 independent experiments. (D) Evaluating alternative pathway activation from 0-37°C showed that alternative pathway activation was significantly inhibited at 24°C and below. There was no difference in the degree of hemolysis at 31°C vs. 37°C) Data are mean ± SEM for 4 independent experiments.

    Techniques Used: Functional Assay, Activation Assay, Lysis



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    Functional hemolytic assays of complement activation. (A) CH50-type antibody-initiated complement assays incubating antibody-sensitized erythrocytes (EA) with 0.2% human serum for 1 hour at 31-41°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There is 2-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01) (P ≤ 0.05 for the comparisons 31 vs. 37, 31 vs. 39, 31 vs. 41, 33 vs. 37, 33 vs. 39, 33 vs. 41, 35 vs. 39, 35 vs. 41, with significantly more hemolysis at lower temperatures) Data are mean ± SEM for 4 independent experiments. (B) Evaluating antibody-initiated complement activation from 0-37°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There was 2.5-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01). (P ≤ 0.05 for the comparisons 31 vs. 37, 24 vs. 37, 19 vs. 37, with significantly more hemolysis at lower temperatures). The trend of increased complement activation was reversed at 13°C. (No statistical difference between hemolysis at 13 vs. 37 or 7 vs. 37). Data are mean ± SEM for 4 independent experiments. (C) AP50-type alternative complement pathway assays, incubating rabbit erythrocytes with 4% human serum in <t>Mg-EGTA-GVBS</t> for 30 minutes at 31-41°C showed that temperature did not influence complement-mediated cell lysis over therapeutic hypothermia temperatures (ANOVA P = 0.45). Data are mean ± SEM for 4 independent experiments. (D) Evaluating alternative pathway activation from 0-37°C showed that alternative pathway activation was significantly inhibited at 24°C and below. There was no difference in the degree of hemolysis at 31°C vs. 37°C) Data are mean ± SEM for 4 independent experiments.
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    Functional hemolytic assays of complement activation. (A) CH50-type antibody-initiated complement assays incubating antibody-sensitized erythrocytes (EA) with 0.2% human serum for 1 hour at 31-41°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There is 2-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01) (P ≤ 0.05 for the comparisons 31 vs. 37, 31 vs. 39, 31 vs. 41, 33 vs. 37, 33 vs. 39, 33 vs. 41, 35 vs. 39, 35 vs. 41, with significantly more hemolysis at lower temperatures) Data are mean ± SEM for 4 independent experiments. (B) Evaluating antibody-initiated complement activation from 0-37°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There was 2.5-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01). (P ≤ 0.05 for the comparisons 31 vs. 37, 24 vs. 37, 19 vs. 37, with significantly more hemolysis at lower temperatures). The trend of increased complement activation was reversed at 13°C. (No statistical difference between hemolysis at 13 vs. 37 or 7 vs. 37). Data are mean ± SEM for 4 independent experiments. (C) AP50-type alternative complement pathway assays, incubating rabbit erythrocytes with 4% human serum in <t>Mg-EGTA-GVBS</t> for 30 minutes at 31-41°C showed that temperature did not influence complement-mediated cell lysis over therapeutic hypothermia temperatures (ANOVA P = 0.45). Data are mean ± SEM for 4 independent experiments. (D) Evaluating alternative pathway activation from 0-37°C showed that alternative pathway activation was significantly inhibited at 24°C and below. There was no difference in the degree of hemolysis at 31°C vs. 37°C) Data are mean ± SEM for 4 independent experiments.
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    Functional hemolytic assays of complement activation. (A) CH50-type antibody-initiated complement assays incubating antibody-sensitized erythrocytes (EA) with 0.2% human serum for 1 hour at 31-41°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There is 2-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01) (P ≤ 0.05 for the comparisons 31 vs. 37, 31 vs. 39, 31 vs. 41, 33 vs. 37, 33 vs. 39, 33 vs. 41, 35 vs. 39, 35 vs. 41, with significantly more hemolysis at lower temperatures) Data are mean ± SEM for 4 independent experiments. (B) Evaluating antibody-initiated complement activation from 0-37°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There was 2.5-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01). (P ≤ 0.05 for the comparisons 31 vs. 37, 24 vs. 37, 19 vs. 37, with significantly more hemolysis at lower temperatures). The trend of increased complement activation was reversed at 13°C. (No statistical difference between hemolysis at 13 vs. 37 or 7 vs. 37). Data are mean ± SEM for 4 independent experiments. (C) AP50-type alternative complement pathway assays, incubating rabbit erythrocytes with 4% human serum in Mg-EGTA-GVBS for 30 minutes at 31-41°C showed that temperature did not influence complement-mediated cell lysis over therapeutic hypothermia temperatures (ANOVA P = 0.45). Data are mean ± SEM for 4 independent experiments. (D) Evaluating alternative pathway activation from 0-37°C showed that alternative pathway activation was significantly inhibited at 24°C and below. There was no difference in the degree of hemolysis at 31°C vs. 37°C) Data are mean ± SEM for 4 independent experiments.

    Journal: Journal of Translational Medicine

    Article Title: Clinical hypothermia temperatures increase complement activation and cell destruction via the classical pathway

    doi: 10.1186/1479-5876-12-181

    Figure Lengend Snippet: Functional hemolytic assays of complement activation. (A) CH50-type antibody-initiated complement assays incubating antibody-sensitized erythrocytes (EA) with 0.2% human serum for 1 hour at 31-41°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There is 2-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01) (P ≤ 0.05 for the comparisons 31 vs. 37, 31 vs. 39, 31 vs. 41, 33 vs. 37, 33 vs. 39, 33 vs. 41, 35 vs. 39, 35 vs. 41, with significantly more hemolysis at lower temperatures) Data are mean ± SEM for 4 independent experiments. (B) Evaluating antibody-initiated complement activation from 0-37°C showed that hemolysis of antibody-sensitized erythrocytes in human serum differed significantly as a function of temperature (ANOVA P < 0.01). There was 2.5-fold more hemolysis at 31°C vs. 37°C (* t -test P = 0.01). (P ≤ 0.05 for the comparisons 31 vs. 37, 24 vs. 37, 19 vs. 37, with significantly more hemolysis at lower temperatures). The trend of increased complement activation was reversed at 13°C. (No statistical difference between hemolysis at 13 vs. 37 or 7 vs. 37). Data are mean ± SEM for 4 independent experiments. (C) AP50-type alternative complement pathway assays, incubating rabbit erythrocytes with 4% human serum in Mg-EGTA-GVBS for 30 minutes at 31-41°C showed that temperature did not influence complement-mediated cell lysis over therapeutic hypothermia temperatures (ANOVA P = 0.45). Data are mean ± SEM for 4 independent experiments. (D) Evaluating alternative pathway activation from 0-37°C showed that alternative pathway activation was significantly inhibited at 24°C and below. There was no difference in the degree of hemolysis at 31°C vs. 37°C) Data are mean ± SEM for 4 independent experiments.

    Article Snippet: Alternative complement pathway hemolytic assays were performed by incubating rabbit erythrocytes (CompTech, Tyler, TX) with 4% NHS in Mg-EGTA-GVBS at temperatures ranging from 0°C to 37°C.

    Techniques: Functional Assay, Activation Assay, Lysis