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1.

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:BIBFORM035503
Első szerző:Balogh István (molekuláris biológus, genetikus)
Cím:High frequency of factor V Leiden mutation and prothrombin 20210A variant in Romanies of Eastern Hungary / Balogh I., Póka R., Losonczy G., Muszbek L.
Dátum:1999
Tárgyszavak:Orvostudományok Elméleti orvostudományok szerkesztői levél
Megjelenés:Thrombosis and Haemostasis. - 82 : 5 (1999), p. 1555-1556. -
További szerzők:Póka Róbert (1960-) (szülész-nőgyógyász, klinikai onkológus) Losonczy Gergely (1977-) (szemész) Muszbek László (1942-) (haematológus, kutató orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM034619
035-os BibID:PMID:10235459 WOS:000079748300036
Első szerző:Balogh István (molekuláris biológus, genetikus)
Cím:High prevalence of factor V Leiden mutation and 20210A prothrombin variant in Hungary / I. Balogh, R. Póka, G. Pfliegler, M. Dékány, Z. Boda, L. Muszbek
Dátum:1999
ISSN:0340-6245
Tárgyszavak:Orvostudományok Klinikai orvostudományok levél
egyetemen (Magyarországon) készült közlemény
Megjelenés:Thrombosis And Haemostasis 81 : 4 (1999), p. 660-661. -
További szerzők:Póka Róbert (1960-) (szülész-nőgyógyász, klinikai onkológus) Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Dékány Miklós Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus) Muszbek László (1942-) (haematológus, kutató orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM058218
Első szerző:Losonczy Gergely (szemész)
Cím:A novel homozygous mutation (1619delC) in GPIIb gene associated with Glanzmann thrombasthenia, the decay of GPIIb-mRNA and the synthesis of a truncated GPIIb unable to form complex with GPIIIa / Gergely Losonczy, Nurit Rosenberg, Csongor Kiss, János Kappelmayer, György Vereb, Adrienne Kerényi, István Balogh, László Muszbek
Dátum:2005
ISSN:0340-6245
Megjegyzések:The absence of agonist-induced platelet aggregation and the lack of fibrinogen receptor (GPIIb/IIIa) on the platelet surface demonstrated that the severe hemorrhagic complications of a child of Romany descent were caused by Glanzmann thrombasthenia. DNA sequencing revealed a novel homozygous deletion of a cytosine (1619delC) in the GPIIb gene causing a frameshift and predicting a novel stop codon at position 533 following 24 altered amino acids. Both parents possessed the same deletion in heterozygous form. The amount of GPIIb mRNA in the patient's platelets was 0.06% of the amount measured in control platelets. Neither GPIIb nor its truncated form could be detected in the platelets of the patient by Western blotting, while a small amount of GPIIIa was demonstrated. Quantitative flowcytometric analysis showed an elevated number of vitronectin receptors, a component of which is GPIIIa, on the patient's platelets. The surface expression of vitronectin receptor on thrombasthenic, but not on normal platelets was further increased by activation with thrombin receptor agonist peptide. BHK cells transfected with wild type GPIIIa andmutated GPIIb failed to express any mature GPIIb or pro-GPIIb. Immunoprecipitation with a polyclonal antibody recognizing both GPIIb and GPIIIa recovered a 60 kDa truncated form of GPIIb. This band was absent when immunoprecipitation was carried out with an antibody recognizing GPIIIa, suggesting that the truncated protein, lacking calf-1, calf-2 domains and major part of the thigh domain, is unable to form complex with GPIIIa.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Amino Acids
analysis
Animals
Antibodies
biosynthesis
Blood Platelets
Blotting, Western
Case Report
Cell Line
Cells
chemistry
Child
Cricetinae
Cytosine
Dna
Electrophoresis, Polyacrylamide Gel
Exons
Family Health
Female
Flow Cytometry
Gene Deletion
genetics
Homozygote
Humans
Hungary
Immunoprecipitation
Integrin alphaVbeta3
Integrin beta3
Male
metabolism
Mutagenesis, Site-Directed
Mutation
Platelet Aggregation
Platelet Glycoprotein GPIIb-IIIa Complex
Platelet Membrane Glycoprotein IIb
Polymerase Chain Reaction
Protein Binding
Protein Structure, Tertiary
Research
RNA, Messenger
Sequence Analysis, DNA
Support
Thrombasthenia
Thrombin
Transfection
Megjelenés:Thrombosis and Haemostasis. - 93 : 5 (2005), p. 904-909. -
További szerzők:Rosenberg, Nurit Kiss Csongor (1956-) (hematológus, onkológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Vereb György (1965-) (biofizikus, orvos) Kerényi Adrienne (1970-) (laboratóriumi szakorvos) Balogh István (1972-) (molekuláris biológus, genetikus) Muszbek László (1942-) (haematológus, kutató orvos)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM001211
035-os BibID:PMID:17598012
Első szerző:Nagy Béla Jr. (labordiagnosztikai szakorvos)
Cím:Investigation of Thr715Pro P-selectin gene polymorphism and soluble P-selectin levels in type 2 diabetes mellitus / Béla Nagy, Éva Csongrádi, Harjit Pal Bhattoa, István Balogh, György Blaskó, György Paragh, János Kappelmayer, Miklós Káplár
Dátum:2007
Megjegyzések:Increased levels of soluble P-selectin (sP-selectin) have been shown in a number of different disorders, e.g. diabetes mellitus (DM) and cardiovascular disease (CVD). Several studies have attempted to demonstrate the association of the most intensively examined variant of P-selectin gene polymorphism (Thr715Pro) with sP-selectin levels in healthy subjects and in CVD, but contradictory data have been reported.To clarify the effect of Pro715 allele on the sP-selectin levels in type 2 DM, we analysed this polymorphism in diabetic patients and compared these data with sP-selectin levels. Type 2 DM patients (n=119), 48 BMImatched non diabetic individuals - consisting mostly of overweight subjects - and 57 healthy volunteers were included in the study.TheThr715Pro polymorphism was analysed by PCR-RFLP, while sP-selectin levels were measured by ELISA. Significantly elevated sP-selectin levels were found in both DM and in overweight subjects compared to healthy controls. We confirmed previous reports that in healthy Pro715 allele carriers lower sPselectin levels could be measured; however, this difference was only significant in case of lean subjects. No significant difference was detected in sP-selectin level among DM and overweight individuals according to this genotype. However, significant difference was observed in sP-selectin levels in older DM patients compared to younger ones,but these levels were not accounted for by the Thr715Pro polymorphism.We suggest that in type 2 DM individuals, the significantly elevated sP-selectin levels are not due to the Thr715Pro P-selectin gene polymorphism.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Platelet activation
soluble P-selectin
Thr715Pro P-selectin polymorphism
type 2 DM
PADGEM protein
proline
threonine
adult
aged
allele
article
controlled study
DNA polymorphism
enzyme linked immunosorbent assay
female
genetic analysis
genotype
human
human cell
major clinical study
male
non insulin dependent diabetes mellitus
obesity
polymerase chain reaction
priority journal
protein blood level
restriction fragment length polymorphism
thrombocyte activation
Adolescent
Adult
Age Factors
Aged
Amino Acid Substitution
Case-Control Studies
Diabetes Mellitus, Type 2
Female
Humans
Male
Middle Aged
Mutation, Missense
Overweight
P-Selectin
Polymorphism, Genetic
Solubility
egyetemen (Magyarországon) készült közlemény
Megjelenés:Thrombosis and Haemostasis. - 98 (2007), p. 186-191. -
További szerzők:Csongrádi Éva (1969-) (szakorvos) Bhattoa Harjit Pal (1973-) (laboratóriumi szakorvos) Balogh István (1972-) (molekuláris biológus, genetikus) Blaskó György (1947-) (belgyógyász, klinikai farmakológus) Paragh György (1953-) (belgyógyász) Kappelmayer János (1960-) (laboratóriumi szakorvos) Káplár Miklós (1965-) (belgyógyász, diabetológus)
Internet cím:elektronikus változat
DOI
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6.

001-es BibID:BIBFORM058217
Első szerző:Wartiovaara, Ulla
Cím:Effect of Val34Leu polymorphism on the activation of the coagulation factor XIII-A / U. Wartiovaara, H. Mikkola, G. Szőke, G. Haramura, L. Kárpáti, I. Balogh, R. Lassila, L. Muszbek, A. Palotie
Dátum:2000
ISSN:0340-6245
Megjegyzések:Coagulation factor XIII (FXIII) is a protransglutaminase involved in the last step of the coagulation cascade by stabilising the fibrin clot. Recently, a common variation (FXIII Val34Leu) has been associated with a decreased risk of myocardial infarction and deep venous thrombosis. Val34Leu is critically located near the thrombin activation site of FXIII-A. In this study we investigated its effects on the activation of FXIII. Both recombinant and platelet-derived FXIII Val34Leu variants were shown to be more susceptible to thrombin cleavage than the wild type FXIII. The rate of enzymatic activation of FXIII Val34Leu was found increased, however, the specific activity of fully activated wild type FXIII and the Val34Leu mutant did not differ. During the course of thrombin-induced activation of FXIII fibrin gamma-chain dimerisation and alpha-chain polymerisation developed more rapidly with the Val34Leu mutant. The increased rate of fibrin stabilisation brought about by the Val34Leu FXIII seems to be paradoxically associated with a protective effect against pathological thrombosis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Factor XIII
Factor XII Val34Leu
thrombin
peptide
Megjelenés:Thrombosis and Haemostasis. - 84 : 4 (2000), p. 595-600. -
További szerzők:Mikkola, Hanna Szőke Gabriella Haramura Gizella (1957-) (vezető analitikus) Kárpáti L. Balogh István (1972-) (molekuláris biológus, genetikus) Lassila, Riitta Muszbek László (1942-) (haematológus, kutató orvos) Palotie, Aarno
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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