Objective: βig-h3 is an extracellular matrix protein, which is overexpressed in synovial tissues of rheumatoid arthritis (RA) similar to adhesive glycoproteins. We sought to evaluate the compensatory role of βig-h3 with adhesive glycoproteins in mediating the adhesion of fibroblastlike synoviocytes (FLS) and to confirm the inhibitory effect of YH18 peptide of the 2nd fas-1 domain in βig-h3-mediated adhesion.Methods: The adhesion of FLS isolated from synovial tissues of RA, was evaluated in 96 well microtiter plate coated with matrix proteins. Inhibitory effect of YH18 peptides from the 2nd and 4th fas-1 domains was estimated in βig-h3-mediated adhesion of FLS. Results:The adhesion of FLS on βig-h3 was weaker than that of fibronectin and vitronectin.The βig-h3-mediated adhesion was enhanced by the stimulation with phorbol myristate acetate (PMA), but not by cytokines and growth factors. Combination of fibronectin with βig-h3 synergistically enhanced the adhesion of FLS, in contrast to the additive effect of vitronectin combined with βig-h3. YH18 peptide of the 2nd fas-1 domain did not block the βig-h3-mediated

No abstract

Objectives: To investigate the regulatory role of TWEAK on production of effector molecules from fibroblast‐like synoviocytes (FLS) in rheumatoid arthritis (RA).Methods: The expression of TWEAK and Fn14 was evaluated using immunohistochemical study. After stimulation of FLS with TWEAK, gene expression microarray assay was performed. The expression of Fn14 and effector molecules was determined by RT‐PCR, Western blot analysis, and flow cytometry. Results: The expression of TWEAK and Fn14 was up‐regulated within synovial tissues of RA. The expression of Fn14 on the FLS was induced by PMA but not by FGF‐acidic or ‐basic. When the expression gene profile was evaluated, transcripts of MMPs were down‐regulated with TWEAK treatment. To confirm the results, FLS was stimulated with soluble TWEAK (100ng/ml), which increased ICAM‐1 and VCAM‐1, but down‐regulated MMP‐1 and TIMP‐1 slightly. TWEAK showed an additive effect on IL‐1¥â‐ and IFN‐¥ã‐induced up‐regulation of ICAM‐1 & VCAM‐1, but no additional effects on the TNF‐¥á‐induced up‐regulation. TWEAK significantly inhibited IL‐1¥â‐induced production of MMP‐1 and TIMP‐1. Although COX‐2 expression was highly upregulated by IL‐1¥â, Tweak did not make any additional changes. Conclusions: Our data showed that the interaction between TWEAK and Fn14 may involve in the pathogenesis of RA by differentially regulating the synthesis of effector molecules from FLS.

Hypothenar hammer syndrome (HHS) is a non-atherosclerotic, non-inflammatory vascular disease that causes a digital ischemia as a result of the occlusion of distal ulnar artery adjacent to the hook of hamate. This syndrome is usually observed in men who use the hypothenar eminence of the hand to grip devices such as a hammer. As a consequence of repeated blunt trauma, the ulnar artery beneath hypothenar eminence may lead to pathologic changes, such as intima-medial hyperplasia and reactive inflammatory infiltrates, which lead to the digital ischemia. We experienced a case of HHS with digital ulcerations which occurred after intensive work with nail remover for 10 days. Selective angiography of right forearm showed complete occlusion of the ulnar artery at the level of hook of hamate with deficient superficial palmar arch. After treatment with intravenous prostaglandin E1 and heparin, the ulcerative lesions of fingers improved without surgical intervention, which implicates that medical management of HHS should be considered prior to the surgical treatment.