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001-es BibID:BIBFORM054216
Első szerző:Ajzner Éva (laboratóriumi szakorvos)
Cím:Anti-factor V auto-antibody in the plasma and platelets of a patient with repeated gastrointestinal bleeding / É. Ajzner, I. Balogh, G. Haramura, Z. Boda, K. Kalmár, G. Pfliegler, B. Dahlbäck, L. Muszbek
Dátum:2003
ISSN:1538-7933
Megjegyzések:Development of autoantibody against coagulation factor V (FV) is a rare clinical condition with hemorrhagic complications of varying severity. The aim of this study was to establish the pathomechanism of an acquired FV deficiency and characterize the FV inhibitor responsible for the clinical symptoms. A 78-year-old female was admitted to hospital with severe gastrointestinal bleeding. General clotting tests and determination of clotting factors were performed by standard methods. FV antigen and FV containing immune complexes were measured by ELISA. The FV molecule was investigated by Western blotting and by sequencing the f5 gene. The binding of patient's IgG to FV and activated FV (FVa) was demonstrated in an ELISA system and its effect on the procoagulant activity of FVa was tested in clotting tests and in a chromogenic prothrombinase assay. Localization of the epitope for the antibody was performed by blocking ELISA. FV activity was severely suppressed both in plasma and platelets. FV antigen levels were normal by ELISA using polyclonal anti-FV antibody or monoclonal antibody against the connecting region of FV, but depressed when HV1 monoclonal antibody against the C2 domain in the FV light-chain was used as capture antibody. The FV molecule was found intact. An IgG reacting with both FV and FVa was present in the patient's plasma and its binding to FV was inhibited by HV1 antibody. FV-containing immune complexes were detected in the patient's plasma and platelet lysate. The patient's IgG inhibited the procoagulant function of FVa. An anti-FV IgG was present in the patient's plasma and platelets. The autoantibody reacted with an epitope in the C2 domain of FV light chain and neutralized the procoagulant function of FVa.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of thrombosis and haemostasis. - 1 : 5 (2003), p. 943-949. -
További szerzők:Balogh István (1972-) (molekuláris biológus, genetikus) Haramura Gizella (1957-) (vezető analitikus) Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus) Kalmár Kálmán Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Dahlbäck, Björn Muszbek László (1942-) (haematológus, kutató orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM038137
Első szerző:Balogh István (molekuláris biológus, genetikus)
Cím:Analysis of Gas6 in human platelets and plasma / Istvan Balogh, Sassan Hafizi, Jonas Stenhoff, Karin Hansson, Björn Dahlback
Dátum:2005
ISSN:1079-5642
Megjegyzések:OBJECTIVE: Gas6 is a member of the vitamin K-dependent protein family. Gas6-deficient mice were found to be resistant to thrombosis because of defective platelet function. Mouse Gas6 was demonstrated to be present in platelets and found to be involved in platelet aggregation. The aim of this study was to investigate the presence of Gas6 in human platelets and plasma and determine its role in platelet function. METHODS AND RESULTS: The presence of Gas6 in human platelets and plasma was analyzed using sensitive immunologic methods. Mass spectrometry and ELISA were used to identify and quantify Gas6 in plasma. Gas6 was demonstrated to be present in human plasma, at a concentration determined to be 13 to 23 ng/mL (0.16 to 0.28 nM). Furthermore, plasma Gas6 levels were found to be lower in patients administered with warfarin. However, Gas6 was undetectable in human platelets. CONCLUSIONS: This is the first report to identify and quantify Gas6 in human plasma. However, Gas6 protein was not detected in human platelets, suggesting that any potential platelet-specific function could be because of Gas6 from the circulation. These findings open up new directions regarding the role of Gas6 in normal and pathophysiological situations such as inflammation, autoimmune disease, thrombosis and arteriosclerosis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arteriosclerosis Thrombosis And Vascular Biology. - 25 : 6 (2005), p. 1280-1286. -
További szerzők:Hafizi, Sassan Stenhoff, Jonas Hansson, Karin Dahlbäck, Björn
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3.

001-es BibID:BIBFORM016361
Első szerző:Lindqvist, Pelle G.
Cím:Umbilical cord plasma levels of growth-arrest specific protein 6 in intrauterine growth restriction / Lindqvist Pelle G., Balogh Istvan, Dahlbäck Björn
Dátum:2010
ISSN:0001-6349
Megjegyzések:Growth arrest specific protein 6 (GAS6) is a newly discovered antiapoptotic protein related to cell survival. We hypothesized that GAS6 might be involved in the fetal adaptation to intrauterine growth restriction (IUGR). Design. A nested case-control study. Setting. A retrospective study of 25 small-for-gestational age and 36 appropriate-for-gestational age pregnancies. Sample. Frozen samples from cases and controls in a prospective cohort study. Methods. GAS6 was measured with an enzyme-linked immunosorbent assay method in umbilical cord plasma taken immediately after delivery. Main outcome measure. Differences in GAS6 levels between pregnancies with placental insufficiency and those without. Results. GAS6 levels were significantly higher among newborns with abnormal umbilical cord Doppler tracings (19.5 ? 5.3 vs. 15.0 ? 3.2, p = 0.02). Among those with abnormal umbilical cord tracings (n = 9), the two with umbilical venous pulsations had significantly lower GAS6 levels (mean 14.4 vs. 21.1, p = 0.04) and one of them died after delivery. Conclusions. GAS6 levels are raised in IUGR fetuses and we speculate that GAS6 might be involved in the fetal adaptation to placental insufficiency.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Acta Obstetricia Et Gynecologica Scandinavica. - 89 : 1 (2010), p. 22-26. -
További szerzők:Balogh István (1972-) (molekuláris biológus, genetikus) Dahlbäck, Björn
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