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001-es BibID:	BIBFORM007073
Első szerző:	Koch, Alisa E.
Cím:	Effects of thrombospondin-1 on disease course and angiogenesis in rat adjuvant-induced arthritis / Koch, A. E., Szekanecz, Z., Friedman, J., Haines, G. K., Langman, C. B., Bouck, N. P.
Dátum:	1998
ISSN:	0090-1229 (Print)
Megjegyzések:	Leukocyte extravasation into the synovium is important in rheumatoid arthritis (RA). Thrombospondin (TSP)-1 mediates cell adhesion and migration and inhibits angiogenesis, and it has been implicated in RA. However, little information is available on the role of TSP-1 in arthritis-associated inflammation and neovascularization. Therefore, we analyzed the effects of TSP-1 in adjuvant-induced arthritis (AIA), a rat model for RA. Hydron pellets containing TSP-1 were implanted in one ankle of AIA rats post-adjuvant injection, while the contralateral ankle received sham implants. Body weight loss and joint swelling were determined in comparison to nonimplanted AIA controls. In addition, synovial vessel counts were obtained in TSP-1-versus sham-implanted ankles of the same rat. The implantation of TSP-1 pellets into one ankle resulted in an enhancement of swelling in both ankles. Furthermore, TSP-1 exhibited a biphasic modulatory effect on synovial vessel counts (P < 0.05). In conclusion, TSP-1 implanted into one ankle of AIA rats may augment the severity of the disease. One possible explanation, among others, for the modulating effect of TSP-1 on inflammation may be its effect on arthritis-related angiogenesis.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Arthritis, Experimental Arthritis, Rheumatoid Body Weight Disease Models, Animal Dose-Response Relationship, Drug Joints Neovascularization, Pathologic Rats Rats, Inbred Lew Tarsus, Animal Thrombospondin 1
Megjelenés:	Clinical Immunology and Immunopathology. - 86 : 2 (1998), p. 199-208. -
További szerzők:	Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Friedman, J. Haines, G. Kenneth Langman, C. B. Bouck, N. P.
Internet cím:	DOI elektronikus változat Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM007104
Első szerző:	Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:	Increased synovial expression of transforming growth factor (TGF)-beta receptor endoglin and TGF-beta 1 in rheumatoid arthritis : possible interactions in the pathogenesis of the disease / Szekanecz, Z., Haines, G. K., Harlow, L. A., Shah, M. R., Fong, T. W., Fu, R., Lin, S. J., Rayan, G., Koch, A. E.
Dátum:	1995
ISSN:	0090-1229 (Print)
Megjegyzések:	The ingress of inflammatory cells into the rheumatoid (RA) synovial tissue (ST) plays a role in the pathogenesis of this disease. Transforming growth factor beta (TGF-beta) may play a role in this process. We have investigated the distribution of endoglin, a newly described receptor for TGF-beta 1 and -beta 3, in RA compared to osteoarthritis (OA) or normal ST. Immunohistochemical analysis was carried out using an anti-TGF-beta 1 monoclonal antibody (mAb) as well as 10 mAbs raised against various epitopes of endoglin. This study was performed on ST from 10 patients with RA, 10 with OA, and 4 normal individuals. TGF-beta 1 expression was significantly up-regulated on RA compared to OA and normal ST lining cells, interstitial macrophages, and endothelial cells (P < 0.05). All anti-endoglin mAbs uniformly reacted with endothelial cells in RA, OA, and normal STs. However, 3 out of 10 anti-endoglin mAbs reacted with significantly more RA versus normal ST lining cells (P < 0.05), as well as RA compared to OA and normal macrophages (P < 0.05). There was a positive correlation between TGF-beta 1 and endoglin reactivity on the synovial lining layer and subsynovial macrophages (P < 0.05). These results indicate that TGF-beta 1 and certain epitopes of endoglin, a TGF-beta 1 and -beta 3 receptor, are up-regulated on myeloid elements in RA compared to normal ST. Endoglin is also present on ST endothelia, and its expression may also be increased on OA compared to normal ST lining cells. These findings implicate endoglin in the pathogenesis of RA.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Antibodies, Monoclonal Antigens, CD Arthritis, Rheumatoid Humans Membrane Glycoproteins Osteoarthritis Receptors, Cell Surface Synovial Membrane Transforming Growth Factor beta Vascular Cell Adhesion Molecule-1
Megjelenés:	Clinical Immunology and Immunopathology. - 76 : 2 (1995), p. 187-194. -
További szerzők:	Haines, G. Kenneth Harlow, Lisa A. Shah, M. R. Fong, T. W. Fu, Rao Lin, S. J. Rayan, Ghazi Koch, Alisa E.
Internet cím:	elektronikus változat DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM007103
Első szerző:	Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:	Increased synovial expression of the adhesion molecules CD66a, CD66b, and CD31 in rheumatoid and osteoarthritis / Szekanecz, Z., Haines, G. K., Harlow, L. A., Shah, M. R., Fong, T. W., Fu, R., Lin, S. J., Koch, A. E.
Dátum:	1995
ISSN:	0090-1229 (Print)
Megjegyzések:	Leukocyte-endothelial interaction mediated by adhesion molecules may play a role in the ingress of inflammatory cells into the rheumatoid (RA) synovial tissue (ST). A number of these molecules have been shown to be up-regulated in the inflamed compared to normal ST. We studied the distribution of two members of the CD66 carcinoembryonic antigen adhesion molecule family, as well as that of CD31, an antigen structurally related to CD66, on various cell types in the RA compared to osteoarthritic (OA) and normal ST. Immunoperoxidase histochemistry was carried out using monoclonal antibodies to CD66a, CD66b, and CD31. This study was performed on ST from 10 patients with RA, 10 with OA, and 4 normal individuals. CD66a, and CD66b were expressed on RA and OA ST myeloid cells but not on normal ST lining cells and interstitial macrophages, suggesting that these antigens may be specific markers of diseased compared to normal ST macrophages (P < 0.05). CD31 was present on more RA and OA than on normal ST macrophages. Also, CD31 was present on most RA, OA, and normal ST endothelial cells. Our results indicate that the expression of CD66a, CD66b, and CD31, members of the immunoglobulin superfamily of adhesion receptors, is up-regulated on cells of myeloid origin in the inflamed compared to normal ST. These results suggest that the CD66 antigens and CD31 may be involved in the adhesive events in the inflamed synovium.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Antigens, CD Antigens, CD31 Antigens, Differentiation Antigens, Differentiation, Myelomonocytic Arthritis, Rheumatoid Cell Adhesion Molecules Humans Osteoarthritis Synovial Membrane
Megjelenés:	Clinical Immunology and Immunopathology. - 76 : 2 (1995), p. 180-186. -
További szerzők:	Haines, G. Kenneth Harlow, Lisa A. Shah, M. R. Fong, T. W. Fu, Rao Lin, S. J. Koch, Alisa E.
Internet cím:	elektronikus változat DOI Intézményi repozitóriumban (DEA) tárolt változat
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