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aat plasma concentrations  (Hycult Biotech)


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    Structured Review

    Hycult Biotech aat plasma concentrations
    <t>PR3,</t> NE, <t>AAT</t> and hsCRP plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. a PR3 plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. b NE plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. c AAT plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. d PR3 to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. e NE to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. f hsCRP concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. Data is represented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, NS = p > 0.05
    Aat Plasma Concentrations, supplied by Hycult Biotech, 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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    Average 90 stars, based on 1 article reviews
    aat plasma concentrations - by Bioz Stars, 2025-05
    90/100 stars

    Images

    1) Product Images from "Increased proteinase 3 and neutrophil elastase plasma concentrations are associated with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes"

    Article Title: Increased proteinase 3 and neutrophil elastase plasma concentrations are associated with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes

    Journal: Molecular Medicine

    doi: 10.1186/s10020-019-0084-3

    PR3, NE, AAT and hsCRP plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. a PR3 plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. b NE plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. c AAT plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. d PR3 to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. e NE to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. f hsCRP concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. Data is represented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, NS = p > 0.05
    Figure Legend Snippet: PR3, NE, AAT and hsCRP plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. a PR3 plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. b NE plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. c AAT plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. d PR3 to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. e NE to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. f hsCRP concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. Data is represented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, NS = p > 0.05

    Techniques Used:

    PR3, NE and AAT plasma concentrations in patients with type 2 diabetes. a NE plasma concentrations in patients that didn't use insulin drugs versus patients that also used insulin. b NE plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. c PR3 plasma concentrations in patients that didn't use insulin versus patients that also used insulin. d PR3 plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. e AAT plasma concentrations in patients that didn't use insulin versus patients that also used insulin. f AAT plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. Data is represented as mean ± SEM. ** p < 0.01, NS= p > 0.05
    Figure Legend Snippet: PR3, NE and AAT plasma concentrations in patients with type 2 diabetes. a NE plasma concentrations in patients that didn't use insulin drugs versus patients that also used insulin. b NE plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. c PR3 plasma concentrations in patients that didn't use insulin versus patients that also used insulin. d PR3 plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. e AAT plasma concentrations in patients that didn't use insulin versus patients that also used insulin. f AAT plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. Data is represented as mean ± SEM. ** p < 0.01, NS= p > 0.05

    Techniques Used:



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    Hycult Biotech aat plasma concentrations
    <t>PR3,</t> NE, <t>AAT</t> and hsCRP plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. a PR3 plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. b NE plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. c AAT plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. d PR3 to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. e NE to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. f hsCRP concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. Data is represented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, NS = p > 0.05
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    <t>PR3,</t> NE, <t>AAT</t> and hsCRP plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. a PR3 plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. b NE plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. c AAT plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. d PR3 to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. e NE to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. f hsCRP concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. Data is represented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, NS = p > 0.05
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    Beckman Coulter aat circulating plasma concentration
    <t>PR3,</t> NE, <t>AAT</t> and hsCRP plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. a PR3 plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. b NE plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. c AAT plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. d PR3 to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. e NE to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. f hsCRP concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. Data is represented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, NS = p > 0.05
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    Beckman Coulter plasma aat concentration
    Effects of <t>AAT</t> infusion on macrophage control of M. intracellulare infection. (A) Mean plasma AAT levels ± SD, measured by nephelometry, pre- and post-AAT infusion of 10 PiZZ subjects. The normal range for plasma AAT at National Jewish Health is 0.72–1.92 mg/mL. (B) Quantitation of M. intracellulare in MDM cultured in plasma, both obtained before and after AAT infusion from PiZZ patients. Data shown are the mean ± SEM of cells from 10 subjects. (C) Pre-AAT infused MDM + post-AAT infused plasma (10 or 50%) vs. post-AAT infused MDM + pre-AAT infused plasma (10 or 50%) were infected with M. intracellulare . One hour, 2 and 4 days after infection, the cells were washed, lysed, and M. intracellulare quantified. Data shown are the mean ± SEM of cells from five subjects. (D) AAT (1, 2, 3, or 5 mg/mL) was incubated with a liquid culture of 5 × 10 5 M. intracellulare /mL without macrophages for 2 and 4 days and M. intracellulare quantified. Data shown are the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, NS, non-significant; Pre M+P, pre-AAT infused MDM + plasma; Post M+P, post-AAT infused MDM + plasma; AAT, alpha-1-antitrypsin; M. intra, M. intracellulare .
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    Randox plasma a1 antitrypsin aat concentration
    Effects of <t>AAT</t> infusion on macrophage control of M. intracellulare infection. (A) Mean plasma AAT levels ± SD, measured by nephelometry, pre- and post-AAT infusion of 10 PiZZ subjects. The normal range for plasma AAT at National Jewish Health is 0.72–1.92 mg/mL. (B) Quantitation of M. intracellulare in MDM cultured in plasma, both obtained before and after AAT infusion from PiZZ patients. Data shown are the mean ± SEM of cells from 10 subjects. (C) Pre-AAT infused MDM + post-AAT infused plasma (10 or 50%) vs. post-AAT infused MDM + pre-AAT infused plasma (10 or 50%) were infected with M. intracellulare . One hour, 2 and 4 days after infection, the cells were washed, lysed, and M. intracellulare quantified. Data shown are the mean ± SEM of cells from five subjects. (D) AAT (1, 2, 3, or 5 mg/mL) was incubated with a liquid culture of 5 × 10 5 M. intracellulare /mL without macrophages for 2 and 4 days and M. intracellulare quantified. Data shown are the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, NS, non-significant; Pre M+P, pre-AAT infused MDM + plasma; Post M+P, post-AAT infused MDM + plasma; AAT, alpha-1-antitrypsin; M. intra, M. intracellulare .
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    Image Search Results


    PR3, NE, AAT and hsCRP plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. a PR3 plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. b NE plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. c AAT plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. d PR3 to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. e NE to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. f hsCRP concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. Data is represented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, NS = p > 0.05

    Journal: Molecular Medicine

    Article Title: Increased proteinase 3 and neutrophil elastase plasma concentrations are associated with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes

    doi: 10.1186/s10020-019-0084-3

    Figure Lengend Snippet: PR3, NE, AAT and hsCRP plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. a PR3 plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. b NE plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. c AAT plasma concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. d PR3 to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. e NE to AAT ratio in patients with liver steatosis and type 2 diabetes versus lean and obese controls. f hsCRP concentrations in patients with liver steatosis and type 2 diabetes versus lean and obese controls. Data is represented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, NS = p > 0.05

    Article Snippet: PR3, NE and AAT plasma concentrations were quantified using sandwich ELISAs (enzyme-linked immunosorbent assay; cat# HK384, HK319 and HK387 respectively, Hycult Biotech, Uden, The Netherlands) according to manufacturer’s instructions.

    Techniques:

    PR3, NE and AAT plasma concentrations in patients with type 2 diabetes. a NE plasma concentrations in patients that didn't use insulin drugs versus patients that also used insulin. b NE plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. c PR3 plasma concentrations in patients that didn't use insulin versus patients that also used insulin. d PR3 plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. e AAT plasma concentrations in patients that didn't use insulin versus patients that also used insulin. f AAT plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. Data is represented as mean ± SEM. ** p < 0.01, NS= p > 0.05

    Journal: Molecular Medicine

    Article Title: Increased proteinase 3 and neutrophil elastase plasma concentrations are associated with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes

    doi: 10.1186/s10020-019-0084-3

    Figure Lengend Snippet: PR3, NE and AAT plasma concentrations in patients with type 2 diabetes. a NE plasma concentrations in patients that didn't use insulin drugs versus patients that also used insulin. b NE plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. c PR3 plasma concentrations in patients that didn't use insulin versus patients that also used insulin. d PR3 plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. e AAT plasma concentrations in patients that didn't use insulin versus patients that also used insulin. f AAT plasma concentrations between patients with well controlled glycaemia versus patients with a poor control of glycaemia. Data is represented as mean ± SEM. ** p < 0.01, NS= p > 0.05

    Article Snippet: PR3, NE and AAT plasma concentrations were quantified using sandwich ELISAs (enzyme-linked immunosorbent assay; cat# HK384, HK319 and HK387 respectively, Hycult Biotech, Uden, The Netherlands) according to manufacturer’s instructions.

    Techniques:

    Effects of AAT infusion on macrophage control of M. intracellulare infection. (A) Mean plasma AAT levels ± SD, measured by nephelometry, pre- and post-AAT infusion of 10 PiZZ subjects. The normal range for plasma AAT at National Jewish Health is 0.72–1.92 mg/mL. (B) Quantitation of M. intracellulare in MDM cultured in plasma, both obtained before and after AAT infusion from PiZZ patients. Data shown are the mean ± SEM of cells from 10 subjects. (C) Pre-AAT infused MDM + post-AAT infused plasma (10 or 50%) vs. post-AAT infused MDM + pre-AAT infused plasma (10 or 50%) were infected with M. intracellulare . One hour, 2 and 4 days after infection, the cells were washed, lysed, and M. intracellulare quantified. Data shown are the mean ± SEM of cells from five subjects. (D) AAT (1, 2, 3, or 5 mg/mL) was incubated with a liquid culture of 5 × 10 5 M. intracellulare /mL without macrophages for 2 and 4 days and M. intracellulare quantified. Data shown are the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, NS, non-significant; Pre M+P, pre-AAT infused MDM + plasma; Post M+P, post-AAT infused MDM + plasma; AAT, alpha-1-antitrypsin; M. intra, M. intracellulare .

    Journal: Frontiers in Immunology

    Article Title: Alpha-1-Antitrypsin Enhances Primary Human Macrophage Immunity Against Non-tuberculous Mycobacteria

    doi: 10.3389/fimmu.2019.01417

    Figure Lengend Snippet: Effects of AAT infusion on macrophage control of M. intracellulare infection. (A) Mean plasma AAT levels ± SD, measured by nephelometry, pre- and post-AAT infusion of 10 PiZZ subjects. The normal range for plasma AAT at National Jewish Health is 0.72–1.92 mg/mL. (B) Quantitation of M. intracellulare in MDM cultured in plasma, both obtained before and after AAT infusion from PiZZ patients. Data shown are the mean ± SEM of cells from 10 subjects. (C) Pre-AAT infused MDM + post-AAT infused plasma (10 or 50%) vs. post-AAT infused MDM + pre-AAT infused plasma (10 or 50%) were infected with M. intracellulare . One hour, 2 and 4 days after infection, the cells were washed, lysed, and M. intracellulare quantified. Data shown are the mean ± SEM of cells from five subjects. (D) AAT (1, 2, 3, or 5 mg/mL) was incubated with a liquid culture of 5 × 10 5 M. intracellulare /mL without macrophages for 2 and 4 days and M. intracellulare quantified. Data shown are the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, NS, non-significant; Pre M+P, pre-AAT infused MDM + plasma; Post M+P, post-AAT infused MDM + plasma; AAT, alpha-1-antitrypsin; M. intra, M. intracellulare .

    Article Snippet: Plasma AAT concentration was measured by turbidimetry using goat anti-human AAT antiserum with a chemistry analyzer according to manufacturer's instructions (Beckman Coulter AU480).

    Techniques: Infection, Quantitation Assay, Cell Culture, Incubation