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1.

001-es BibID:BIBFORM046367
Első szerző:Halloran, Margaret M.
Cím:Cellular adhesion molecules in rat adjuvant arthritis / Halloran M. M., Szekanecz Z., Barquin N., Haines G. K., Koch A. E.
Dátum:1996
ISSN:0004-3591
Megjegyzések:To examine adhesion molecule expression during the progression of inflammation in a rheumatoid arthritis model of adjuvant-induced arthritis (AIA) in rats. METHODS: Immunohistochemical analysis was used to determine the distribution of the following adhesion molecules: lymphocyte function-associated antigen 1 (LFA-1; CD11a/CD18), Mac-1 and p150/95 (CD11bc/CD18), intercellular adhesion molecule 1 (ICAM-1), and CD44 in tissue sections from the ankle joints of rats with AIA. Control animals and those with AIA were killed at intervals over a 54-day period after injection with mineral oil and Mycobacterium butyricum, respectively. RESULTS: CD44 and LFA-1 were expressed on lymphocytes, macrophages, and synovial (ST) lining cells. CD44 expression on macrophages was found to be increased compared with control animals by day 18, and was significantly increased by day 41. CD44 expression on lymphocytes significantly increased earlier, on days 11-18. Increased LFA-1 expression on macrophages occurred late, on day 41. LFA-1 expression on lymphocytes was significantly increased on days 25, 47, and 54. ST lining cells exhibited two distinct periods of increased expression, one early, on days 11-25 and one later, on days 41-54. CD11b/c was expressed on macrophages and ST lining cells, showing a significant increase on AIA rat ST lining cells compared with control animals on day 4. No differences in ICAM-1 expression on endothelial cells between rats with AIA and controls were found on any of the days examined. CONCLUSION: CD44 expression is up-regulated on macrophages and lymphocytes during the early development of AIA, while LFA-1 expression is up-regulated later in the development of AIA. The up-regulation of CD44 and LFA-1 at different times in the development of AIA suggests an important role for these adhesion molecules in establishing and sustaining an inflammatory response in the AIA joint.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arthritis and Rheumatism. - 39 : 5 (1996), p. 810-819. -
További szerzők:Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Barquin, Nora Haines, G. Kenneth Koch, Alisa E.
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2.

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
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3.

001-es BibID:BIBFORM007072
Első szerző:Koch, Alisa E.
Cím:In situ expression of cytokines and cellular adhesion molecules in the skin of patients with systemic sclerosis : their role in early and late disease / Koch, A. E., Kronfeld-Harrington, L. B., Szekanecz, Z., Cho, M. M., Haines, G. K., Harlow, L. A., Strieter, R. M., Kunkel, S. L., Massa, M. C., Barr, W. G., Jimenez, S. A.
Dátum:1993
ISSN:1015-2008 (Print)
Megjegyzések:Cytokines and cellular adhesion molecules (CAMs) may play a role in the inflammatory and fibrotic processes underlying systemic sclerosis (SSc). We compared the immunohistological distribution of cytokines and CAMs in skin biopsies from 12 SSc patients and 14 normal (NL) individuals. Among CAMs, vascular cell adhesion molecule-1 (VCAM-1), which mediates leukocyte-endothelial adhesion, showed increased expression on SSc versus NL endothelium and stratum granulosum. P-selectin was up-regulated in SSc versus NL stratum granulosum. The CD44 lymphocyte homing receptor showed the most striking differences between SSc and NL: its expression was increased in SSc stratum granulosum, stratum spinosum, on lymphocytes, and macrophages. Regarding cytokines, interleukin-6 (IL-6) expression was increased on SSc versus NL endothelium and fibroblasts. Tumor necrosis factor-alpha (TNF-alpha) reactivity was more prevalent in SSc than NL stratum granulosum, whereas IL-8 expression was higher on SSc compared to NL endothelium. Some CAMs, such as VCAM-1 and P-selectin, and cytokines, namely TNF-alpha and IL-8, were more commonly found in skin biopsies taken from early (< or = 1 year's duration) SSc, while others, such as IL-6, showed up-regulation in the late stage of the disease. The results suggest that certain CAMs and cytokines may play a differential role in both the early, inflammatory, and the late, fibrotic stage of SSc.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adult
Aged
Antigens, CD44
Biopsy
Carrier Proteins
Cell Adhesion
Cell Adhesion Molecules
Cytokines
Endothelium
Female
Fibroblasts
Humans
Immunohistochemistry
Interleukin-6
Interleukin-8
Male
Middle Aged
P-Selectin
Platelet Membrane Glycoproteins
Receptors, Cell Surface
Receptors, Lymphocyte Homing
Scleroderma, Systemic
Skin
Tumor Necrosis Factor-alpha
Vascular Cell Adhesion Molecule-1
Megjelenés:Pathobiology. - 61 : 5-6 (1993), p. 239-246. -
További szerzők:Kronfeld-Harrington, Lisa B. Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Cho, Michael M. Haines, G. Kenneth Harlow, Lisa A. Strieter, Robert M. Kunkel, Steven L. Massa, Mary C. Barr, Walter G. Jimenez, Sergio A.
Internet cím:elektronikus változat
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4.

001-es BibID:BIBFORM046369
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Differential distribution of intercellular adhesion molecules (ICAM-1, ICAM-2, and ICAM-3) and the MS-1 antigen in normal and diseased human synovia : their possible pathogenetic and clinical significance in rheumatoid arthritis / Szekanecz Z., Haines G. K., Lin T. R., Harlow L. A., Goerdt S., Rayan G., Koch A. E.
Dátum:1994
ISSN:0004-3591
Megjegyzések:Cellular adhesion and differentiation molecules (CAMs) may play a role in the recruitment and retention of inflammatory cells into rheumatoid arthritis synovial tissue (RA ST). In order to determine if certain CAMs are up-regulated in RA ST compared with normal ST, we studied the distribution of intercellular adhesion molecules (ICAMs) 1, 2, and 3 in ST. We also studied the MS-1 antigen since it is preferentially expressed on discontinuous endothelia, such as those found in RA ST; MS-1 is also expressed differentially upon cytokine activation of cells in vitro or in pathologic conditions in situ. Thus, we postulated a possible similarity between MS-1 and ICAM-1 expression in inflamed ST. METHODS. Immunohistochemical analysis was used to determine the distribution of ICAMs and MS-1 in ST from 10 patients with RA, 10 with osteoarthritis (OA), and 4 normal individuals. RESULTS. ICAM-1 expression was found on significantly more RA ST endothelial cells compared with normal cells, as well as on RA ST macrophages and lining cells. ICAM-2, also found on endothelial cells, showed no differential staining pattern. ICAM-3 was present on RA ST macrophages and lining cells as well as on some RA and OA endothelial cells. The MS-1 antigen was present on most RA and OA ST endothelia, lining cells, and macrophages. ICAM-1 expression and MS-1 expression in the lining layer were positively correlated in both RA and OA. CONCLUSION. ICAM-1, while found mainly on endothelial cells, is up-regulated on RA ST macrophages and lining cells, suggesting a role for these cells in the infiltration and tissue damage seen in the RA ST. ICAM-3, which is present mainly on normal resting leukocytes but not on normal endothelium, is expressed by some diseased ST leukocytes and endothelial cells. MS-1 is also found on the RA ST specialized, fenestrated endothelium, on macrophages, and in the lining layer. These results suggest that the differential expression of ICAMs and MS-1 in RA ST compared with normal ST might play a special role in the pathogenesis of RA.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arthritis and Rheumatism. - 37 : 2 (1994), p. 221-231. -
További szerzők:Haines, G. Kenneth Lin, Theodore R. Harlow, Lisa A. Goerdt, Sergij Rayan, Ghazi Koch, Alisa E.
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5.

001-es BibID:BIBFORM018159
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Temporal expression of cytokines and chemokines in rat adjuvant-induced arthritis / Szekanecz, Z., Halloran, M. M., Woods, J. M., Volin, M. V., Haines, G. K., Koch, A. E.
Dátum:2001
ISSN:1465-9905
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
Megjelenés:Arthritis Research. - 3 : Suppl. A. (2001), p. 9. -
További szerzők:Halloran, Margaret M. Woods, James M. Volin, Michael V. Haines, G. Kenneth Koch, Alisa E.
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DOI
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6.

001-es BibID:BIBFORM007105
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Differential expression of the urokinase receptor (CD87) in arthritic and normal synovial tissues / Szekanecz, Z., Haines, G. K., Koch, A. E.
Dátum:1997
ISSN:0021-9746 (Print)
Megjegyzések:To determine whether the urokinase plasminogen activator receptor (u-PAR; CD87) exhibits a possible pathogenic role in rheumatoid and osteoarthritis. METHODS: A semiquantitative, indirect immunoperoxidase histochemical analysis was performed on frozen synovial tissue sections. The recently characterised monoclonal antibody 10G7 recognising transfectants bearing u-PAR was used. Synovial tissue was obtained from 10 patients with rheumatoid arthritis, 10 patients with osteoarthritis, and four normal subjects. RESULTS: u-PAR was expressed on 70-90% of synovial tissue lining cells and subsynovial, interstitial macrophages from the arthritis patients, but only on a few myeloid cells from the normal subjects. It was also present on more endothelial cells from the rheumatoid and osteoarthritis patients, than from normal synovial tissue. CONCLUSIONS: Plasminogen activators are important in joint destruction underlying arthritis. The up-regulated expression of u-PAR in diseased versus normal synovial tissue suggests a role for this antigen in the inflammatory and angiogenic mechanisms underlying rheumatoid and osteoarthritis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Arthritis, Rheumatoid
Humans
Immunohistochemistry
Macrophages
Osteoarthritis
Receptors, Cell Surface
Receptors, Urokinase Plasminogen Activator
Synovial Membrane
Megjelenés:Journal of Clinical Pathology. - 50 : 4 (1997), p. 314-319. -
További szerzők:Haines, G. Kenneth Koch, Alisa E.
Internet cím:elektronikus változat
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7.

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
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8.

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
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