Three RFLP's at the 3' end of the cystatin C gene, the disease gene in hereditary cystatin C amyloid angiopathy (HCCAA) in Iceland
(1990) In Nucleic Acids Research 18(24). p.7471-7471- Abstract
- Sputum samples from 25 patients with bronchiectasis were assayed enzymatically for myeloperoxidase, neutrophil elastase and cathepsin B, and immunologically for cystatin A, cystatin B, cystatin C, cystatin S and kininogen. High myeloperoxidase and neutrophil elastase levels were found in those sputum samples that were assessed visually to be purulent. These samples were also found to contain high levels of cathepsin B activity and cystatin A, but low levels of cystatin S and of the most effective cathepsin B inhibitor, cystatin C. In contrast, sputum samples that were low in myeloperoxidase and neutrophil elastase activities had low levels of cathepsin B and cystatin A, but high cystatin C and S levels. It is concluded that cathepsin B... (More)
- Sputum samples from 25 patients with bronchiectasis were assayed enzymatically for myeloperoxidase, neutrophil elastase and cathepsin B, and immunologically for cystatin A, cystatin B, cystatin C, cystatin S and kininogen. High myeloperoxidase and neutrophil elastase levels were found in those sputum samples that were assessed visually to be purulent. These samples were also found to contain high levels of cathepsin B activity and cystatin A, but low levels of cystatin S and of the most effective cathepsin B inhibitor, cystatin C. In contrast, sputum samples that were low in myeloperoxidase and neutrophil elastase activities had low levels of cathepsin B and cystatin A, but high cystatin C and S levels. It is concluded that cathepsin B activity in sputum is positively correlated with the degree of inflammation and neutrophil recruitment. Although this may be due in part to reduced amounts of cathepsin B inhibitors, particularly cystatin C, theoretical considerations suggest that factors other than the gross level of inhibitors must be involved in the control of cathepsin B activity. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1105573
- author
- Palsdottir, A ; Jonsdottir, S ; Abrahamson, Magnus LU ; Grubb, Anders LU and Jensson, O
- organization
- publishing date
- 1990
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Nucleic Acids Research
- volume
- 18
- issue
- 24
- pages
- 7471 - 7471
- publisher
- Oxford University Press
- external identifiers
-
- pmid:1979681
- scopus:0025603140
- ISSN
- 1362-4962
- DOI
- 10.1093/nar/18.24.7471-a
- language
- English
- LU publication?
- yes
- id
- d35559fa-5a6f-4f90-acd2-6867ef0823e8 (old id 1105573)
- alternative location
- http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=332913&blobtype=pdf
- date added to LUP
- 2016-04-01 11:59:31
- date last changed
- 2021-01-03 04:47:54
@article{d35559fa-5a6f-4f90-acd2-6867ef0823e8, abstract = {{Sputum samples from 25 patients with bronchiectasis were assayed enzymatically for myeloperoxidase, neutrophil elastase and cathepsin B, and immunologically for cystatin A, cystatin B, cystatin C, cystatin S and kininogen. High myeloperoxidase and neutrophil elastase levels were found in those sputum samples that were assessed visually to be purulent. These samples were also found to contain high levels of cathepsin B activity and cystatin A, but low levels of cystatin S and of the most effective cathepsin B inhibitor, cystatin C. In contrast, sputum samples that were low in myeloperoxidase and neutrophil elastase activities had low levels of cathepsin B and cystatin A, but high cystatin C and S levels. It is concluded that cathepsin B activity in sputum is positively correlated with the degree of inflammation and neutrophil recruitment. Although this may be due in part to reduced amounts of cathepsin B inhibitors, particularly cystatin C, theoretical considerations suggest that factors other than the gross level of inhibitors must be involved in the control of cathepsin B activity.}}, author = {{Palsdottir, A and Jonsdottir, S and Abrahamson, Magnus and Grubb, Anders and Jensson, O}}, issn = {{1362-4962}}, language = {{eng}}, number = {{24}}, pages = {{7471--7471}}, publisher = {{Oxford University Press}}, series = {{Nucleic Acids Research}}, title = {{Three RFLP's at the 3' end of the cystatin C gene, the disease gene in hereditary cystatin C amyloid angiopathy (HCCAA) in Iceland}}, url = {{http://dx.doi.org/10.1093/nar/18.24.7471-a}}, doi = {{10.1093/nar/18.24.7471-a}}, volume = {{18}}, year = {{1990}}, }