نتایج جستجو برای: alpha 1 antitrypsin a1at

تعداد نتایج: 2882257  

2010
Mary Ann Comunale Lucy Rodemich-Betesh Julie Hafner Mengjun Wang Pamela Norton Adrian M. Di Bisceglie Timothy Block Anand Mehta

BACKGROUND We previously reported increased levels of protein-linked fucosylation with the development of liver cancer and identified many of the proteins containing the altered glycan structures. One such protein is alpha-1-antitrypsin (A1AT). To advance these studies, we performed N-linked glycan analysis on the five major isoforms of A1AT and completed a comprehensive study of the glycosylat...

2009
Irina Petrache Joud Hajjar Michael Campos

Alpha-1-antitrypsin deficiency (AATD), also known as alpha1-proteinase inhibitor deficiency, is an autosomal co-dominant condition. The genotypes associated with AATD include null, deficient, and dysfunctional alpha-1-antitrypsin (A1AT) variants, which result in low levels of circulating functional A1AT, unbalanced protease activity, and an increased risk of developing lung emphysema, the leadi...

ژورنال: :hepatitis monthly 0
ignacio blanco the principality of asturias biomedical research office (oib-ficyt), oviedo, spain and alpha1-antitrypsin deficiency spanish registry, spain +34-985252481, [email protected]; uluhqsmoo}yu~yt{iofdew}w{mosyb{mom{ka~ewmsus{ch office (oib-ficyt), oviedo, spain and alpha1-antitrypsin deficiency spanish registry, spain +34-985252481, [email protected]; the principality of asturias biomedical research office (oib-ficyt), oviedo, spain and alpha1-antitrypsin deficiency spanish registry, spain +34-985252481, [email protected] frederick j. de serres national institute of environmental health sciences, research triangle park, nc, usa, usa victoriano cárcaba department of internal medicine, ‘valle del nalón hospital, principado de asturias, spain, spain beatríz lara hospital universitario arnau de vilanova, avda, institut de recerca biomédica de lleida (irb), ciberes instituto salud carlos iii, pneumology service, institut de recerca hospital universitari vall d’hebron, spain enrique fernández-bustillo biostatistics unit, central university hospital of asturias, spain

background currently, there is a remarkable lack of genetic epidemiological studies on alpha 1-antitrypsin (aat) deficiency in about half of the 193 countries of the world. this fact impedes the establishment of a true prevalence pattern of this deleterious hereditary disorder in extensive regions of human population. objectives the aim of the present study was to generate detailed maps of the ...

Journal: :Gut 2002
D Yoon F Kueppers R M Genta G B Klintmalm V I Khaoustov B Yoffe

BACKGROUND Alpha-1-antitrypsin (A1AT) deficiency is the most common inherited metabolic disorder with the potential to cause injury in the lung and liver. Recent reports suggested that alpha-1-antichymotrypsin (A1AC) deficiency may also be a possible cause of chronic liver disease. However, it has received little attention and is rarely investigated in the clinical setting. AIMS To assess the...

Journal: :The Journal of clinical investigation 1988
M D Wewers D J Herzyk J E Gadek

We characterized the elastase and antielastase activity of the alveolar fluid of seven patients with the adult respiratory distress syndrome (ARDS) and thirteen normal volunteers. Alpha-1-antitrypsin (A1AT) concentrations were 60-fold higher in ARDS as compared to normal lavage fluid (2,140 +/- 498 nM; 36.1 +/- 4.2 nM, respectively). ARDS fluid antineutrophil elastase activity was also consider...

2011
Michael R Ringenbach Erin Banta Melissa R Snyder Timothy J Craig Faoud T Ishmael

Alpha-1-antitrypsin (A1AT) deficiency is a genetic disease characterized by low levels and/or function of A1AT protein. A1AT deficiency can result in the development of COPD, liver disease, and certain skin conditions. The disease can be diagnosed by demonstrating a low level of A1AT protein and genotype screening for S and Z mutations, which are the most common. However, there are many genetic...

Journal: :Lancet 1979
P Isaacson D B Jones M A Judd

Preliminary studies have suggested that alpha-1-antitrypsin (A1AT) is a useful immunohistochemical marker of histiocytes (monocytes/macrophages) and malignant tumours derived from them. To confirm the reliability of this marker a wide variety of benign and malignant lymphoreticular cells and tissues have been stained by the immunoperoxidase technique for A1AT and positive staining was found to ...

2017
Yu-Sheng Chang Chih-Hong Pan Che-Chang Chang Kai-Leun Tsai Wen Chou Jin-Hua Chen Sheng-Hong Lin Yi-Ying Lu Chih-Chun Tai Fang Lin Ching-Yu Lin

61 The aim of this study was to examine oxidative stress and low level of alpha62 1-antitrypsin (A1AT) in primary Sjögren's syndrome (pSS), and evaluate the 63 associated autoreactivity against unmodified and their 4-hydroxy-2-nonenal (HNE)64 modified peptides with pSS. Two differentially expressed proteins, alpha-1-acid 65 glycoprotein 1 (A1AG1) and A1AT, exhibited 2-fold differences, and thei...

Journal: :Thorax 2011
Richard I Carter Richard A Mumford Kelly M Treonze Paul E Finke Phillip Davies Qian Si John L Humes Asger Dirksen Eeva Piitulainen Ali Ahmad Robert A Stockley

BACKGROUND Alpha-1-antitrypsin (A1AT) deficiency is the only recognised genetic risk factor for chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. Since A1AT is the major inhibitor of neutrophil elastase (NE), this enzyme has become widely implicated in the pathogenesis of COPD in general; however, there is currently no specific biomarker for its...

2008
Patrick Geraghty Mark P. Rogan Catherine M. Greene Mark L. Brantly Shane J. O’Neill Clifford C. Taggart Noel G. McElvaney

Neutrophil elastase (NE) activity is increased in lung diseases such as alpha-1-antitrypsin (A1AT) deficiency and pneumonia. We have recently demonstrated that NE can induce expression of cathepsin B and MMP 2 in vitro and in a mouse model. We postulated that increased Cathepsin B and MMP-2 in acute and chronic lung diseases are due to the presence of high levels of extracellular NE and that ex...

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