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001-es BibID:	BIBFORM038629
035-os BibID:	PMID:9272279
Első szerző:	Csípő István (vegyész)
Cím:	Serum complement activation of SLE patients during plasmapheresis / Csipő I., Kávai M., Kiss E., Bedő Z., Csongor J., Szegedi Gy., Philbert F., Cohen J. H.
Dátum:	1997
ISSN:	0891-6934
Megjegyzések:	The erythrocyte complement receptor 1 (ECR1)-immune complex binding assay is a sensitive method for the determination of complement fragments which can be activated by bovine serum albumin (BSA)-anti-BSA in vitro. When the C3b/C4b containing bovine serum albumin (BSA)-anti-BSA was formed in the presence of the serum of patients with systemic lupus erythematosus (SLE) its binding to ECR1 was found to be lower than that formed in sera of normal volunteers. The plasmapheresis of SLE patients homozygous for the CR1/E high density allele displays a beneficial effect on the formation of C3b/C4b containing BSA-anti-BSA and its binding to ECR1. There was no significant correlation between the serum C3/C4 level and the percentage of C3b/C4b containing BSA-anti-BSA binding to the ECR1 of SLE patients during plasmapheresis. At the same time, there was an inverse correlation between the serum immune complex level and the ECR1 binding, which was significant in 3 of 5 cases. These data suggest that, besides the determination of different components of complement activation, the functional assay of complement activation might be useful in monitoring the effect of plasmapheresis in SLE.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény 0 (Antibodies) 0 (Antigen-Antibody Complex) 0 (Receptors, Complement 3b) 0 (Serum Albumin, Bovine) 80295-43-8 (Complement C3b) 80295-50-7 (Complement C4b) Adult Animals Antibodies/immunology Antigen-Antibody Complex/blood Cattle Complement Activation/immunology Complement C3b/immunology Complement C4b/immunology Erythrocytes/immunology Female Humans Lupus Erythematosus, Systemic/blood/immunology Male Middle Aged Plasmapheresis Receptors, Complement 3b/immunology Serum Albumin, Bovine/immunology
Megjelenés:	Autoimmunity. - 25 : 3 (1997), p. 139-146. -
További szerzők:	Kávai Mária (1930-) (vegyész) Kiss Emese (1960-) (belgyógyász, immunológus) Bedő Zoltán Csongor József Szegedi Gyula (1936-2013) (belgyógyász, immunológus) Philbert, F. Cohen, J. H. M.
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001-es BibID:	BIBFORM033375
035-os BibID:	WOS:000084138000021
Első szerző:	Csípő István (vegyész)
Cím:	Effect of plasmapheresis on ligand binding capacity and expression of erythrocyte complement receptor type 1 (CR1) of patients with systemic lupus erythematosus (SLE) / I. Csipő, E. Kiss, P. Soltész, P. Antal-Szalmás, Gy. Szegedi, J. H. M. Cohen, R. P. Taylor, M. Kávai
Dátum:	1999
Megjegyzések:	The functional activity and the expression of CR1 on the erythrocytes (E) of patients with SLE were, respectively, determined by measuring the binding to E of either complement-opsonized bovine serum albumin (BSA)-anti-BSA immune complexes (ICC) or specific anti-ECR1 MoAbs. We found that both the functional activity and levels of ECR1 in SLE patients homozygous for ECR1 high density allele were significantly lowered compared with healthy controls having the same allele. Soon after plasmapheresis there was a significant increase in E ICC binding activity, and this increased functional activity was stable. Moreover, plasmapheresis reduced the level of immune complexes demonstrable in the circulation of the patients. The expression of ECR1 determined with several different anti-CR1 MoAbs was also elevated as a consequence of plasmapheresis. This elevation was observed for both MoAb 1B4, which competes for the ICC binding site of ECR1, and for MoAb HB8592, which does not, but the time course for the increase in binding of the two MoAbs was different, in that the epitope recognized by MoAb 1B4 increased more rapidly. The present results, considered in the context of previous findings, suggest that more than one mechanism may be operative with respect to the effects of the plasmapheresis in increasing ECR1 levels defined by different epitopes on the molecule.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Clinical and Experimental Immunology 118 : 3 (1999), p. 458-464. -
További szerzők:	Kiss Emese (1960-) (belgyógyász, immunológus) Soltész Pál (1961-) (belgyógyász, kardiológus) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Szegedi Gyula (1936-2013) (belgyógyász, immunológus) Cohen, J. H. M. Taylor, R. P. Kávai Mária (1930-) (vegyész)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM038628
035-os BibID:	PMID:9161700
Első szerző:	Kiss Emese (belgyógyász, immunológus)
Cím:	CR1 density polymorphism and expression on erythrocytes of patients with systemic lupus erythematosus / Kiss E., Csipő I., Cohen J. H., Reveil B., Kávai M., Szegedi Gy.
Dátum:	1996
ISSN:	0891-6934
Megjegyzések:	The present study investigated the expressed number of CR1 on erythrocytes (E) in relationship of the CR1 density genotype from 46 patients with systemic lupus erythematosus (SLE) and 47 healthy volunteers. The CR1 genotype was determined by a method based on polymerase chain reaction (PCR) amplification of the genomic DNA fragment of 1.8 kb separated by HindIII endonuclease digestion and agarose gel electrophoresis. Our data supported the earlier results that the number of binding sites/E for monoclonal anti-CR1 decreased among SLE patients compared with normal individuals having the same alleles for the CR1/E density. At the same time the novelty of our recent results was that the decreased expression of CR1 on E correlated significantly with kidney involvement in patients homozygous for the CR1/E high density allele (HH). These data suggest that the deficiency of the detectable number of CR1 on erythrocytes is acquired in this SLE population.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény 0 (Receptors, Complement) 0 (Receptors, Complement 3b) Erythrocytes/chemistry/immunology Female Genotype Heterozygote Homozygote Humans Lupus Erythematosus, Systemic/genetics/metabolism/pathology Male Polymorphism, Genetic/genetics Polymorphism, Restriction Fragment Length Receptors, Complement/genetics Receptors, Complement 3b/biosynthesis/genetics/immunology Severity of Illness Index
Megjelenés:	Autoimmunity. - 25 : 1 (1996), p. 53-58. -
További szerzők:	Cohen, J. H. M. Reveil, B. Kávai Mária (1930-) (vegyész) Szegedi Gyula (1936-2013) (belgyógyász, immunológus) Csípő István (1953-) (vegyész)
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