The effects of anticoagulants on the determination of both trypsin inhibitory capacity and the concentration of alpha 1-antitrypsin measured by radial immunodiffusion, and on the alpha 1-antitrypsin phenotype were investigated. These results were compared with those obtained for serum. The following anticoagulants were investigated: sodium citrate; sodium oxalate; buffered citrate; potassium oxalate/sodium fluoride; sodium heparin; and potassium EDTA. It was found that plasmas from all of the anticoagulants, except sodium heparin, resulted in apparently significant decreases of both trypsin inhibitory capacity and concentration of alpha 1-antitrypsin measured by radial immunodiffusion, relative to serum. These decreases were not simply due to dilution by anticoagulants. Using both acid starch gel electrophoresis followed by immunofixation and isoelectric focusing in agarose, no interference was found in the phenotype determination. It is concluded that serum should be used to measure the trypsin inhibitory capacity or the concentration of alpha 1-antitrypsin by radial immunodiffusion, although plasma is also suitable provided that sodium heparin is used as the anticoagulant. The alpha 1-antitrypsin phenotype can be determined with either serum or any of the plasma. None of the anticoagulants employed in this study was present in excess.
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http://dx.doi.org/10.1515/cclm.1985.23.5.277 | DOI Listing |
Rationale: Individuals homozygous for the Alpha-1 Antitrypsin (AAT) Z allele (Pi*ZZ) exhibit heterogeneity in COPD risk. COPD occurrence in non-smokers with AAT deficiency (AATD) suggests inflammatory processes may contribute to COPD risk independently of smoking. We hypothesized that inflammatory protein biomarkers in non-AATD COPD are associated with moderate-to-severe COPD in AATD individuals, after accounting for clinical factors.
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Department of Pharmaceutics, College of Pharmacy, University of Florida, Gainesville, FL 32610, USA.
Endosomal toll-like receptors (TLRs) TLR7, TLR8, and TLR9 play an important role in systemic lupus erythematosus (SLE) pathogenesis. The proteolytic processing of these receptors in the endolysosome is required for signaling in response to DNA and single-stranded RNA, respectively. Targeting this proteolytic processing may represent a novel strategy to inhibit TLR-mediated pathogenesis.
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Pneumology Department, Hospital Universitari Vall d'Hebron/Vall d'Hebron Research Institute (VHIR), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain.
Respir Res
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Department of Respiratory Medicine, St Vincent's University Hospital, Elm Park Dublin 4, Dublin, Ireland.
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January 2025
Shum Yiu Foon Shum Bik Chuen Memorial Centre for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Alpha-1 antitrypsin (AAT) is a key serine protease inhibitor for regulating proteases such as neutrophil elastase. AAT restrains the pulmonary matrix from enzymatic degradation, and a deficiency in AAT leads to inflammatory tissue damage in the lungs, resulting in chronic obstructive pulmonary disease. Due to the crucial biological function of AAT, the emerging research interest in this protein has shifted to its role in cancer-associated inflammation and the dynamics of the tumor microenvironment.
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