Effects of hyaluronic acid on the release of proteoglycan from the cell matrix in rabbit chondrocyte cultures in the presence and absence of cytokines

Objective. To investigate the effects of hyaluronic acid (HA) on the release of proteoglycan by cultured rabbit chondrocytes. Methods. Articular cartilage chondrocytes were isolated from the knee joints of New Zealand white rabbits. Proteoglycan synthesis after incubation with HA was determined by measuring ³⁵S-sulfate incorporation. Cells incubated with HA were labeled with ³H-glucosamine and applied to a Sepharose CL-2B column. After incubation of confluent cells with ³⁵S-sulfate and then with HA in various concentrations in the presence or absence of cytokines, proteoglycan release from the cell matrix layer was measured. Results. HA (M_r 3 × 10⁵ to 19 × 10⁵), at 10 μg/ml to 1 mg/ml, had little effect on the incorporation of ³⁵S-sulfate or ³H-glucosamine into cartilage matrix proteoglycans, or on the hydrodynamic size of proteoglycan monomers, in rabbit chondrocyte cultures. However, at 10–1,000 μg/ml, HA suppressed the release of ³⁵S-proteoglycans from the cell matrix layer into the medium in the presence and absence of interleukin-1, tumor necrosis factor α, or basic fibroblast growth factor. Conclusion. These results suggest that HA is a potent inhibitor of the displacement of matrix proteoglycan into culture medium.     

ULTRASTRUCTURE OF THE MOUSE SYNOVIAL MEMBRANE

The synovial membrane of the mouse knee joint was examined by electron microscopy and electron microscopic histochemistry, with special reference to the development of the extracellular matrix. In the embryonic synovium, the intercellular spaces were filled with hyaluronate and chondroitin sulfate. The formation of the early joint cavity appeared to be initiated by accumulation of hyaluronate and chondroitin sulfate in the synovial primordium. At the postnatal stage, the synovial primordium differentiated into a true synovial intima that could be easily identified by the presence of two distinct lining cells: fibroblast-like cells (B cells) and phagocytic cells (A cells). Simultaneously, the synovial intima provided the specialized extracellular matrix that was characterized by organized structures of micro-fibrils, collagen fibers, and fibrous long spacing fibers embedded in a large number of glycoproteins.     

A case of refractory cutaneous polyarteritis nodosa in a patient with hepatitis B carrier status successfully treated with tumor necrosis factor alpha blockade

We describe a patient with refractory cutaneous polyarteritis nodosa (CPAN) with hepatitis B virus (HBV) carrier status who was successfully treated with tumor necrosis factor alpha (TNF-α) blockade, using etanercept, and we review 5 similar cases. We administered etanercept because of the occurrence of repeated flares despite aggressive therapy. C-reactive protein normalization; prednisolone dose-sparing; and absence of any adverse events, including HBV reactivation with nucleotide analogue administration, or renal dysfunction, have been achieved for 8 months. TNF-α blockade should be considered for intractable CPAN.     

Nucleotide sequence of the adenovirus type 40 inverted terminal repeat: close relation to that of adenovirus type 5

Human adenovirus type 40 (Ad40) is a pathogen that causes acute infantile gastroenteritis. Ad40 has the distinct characteristic of being difficult to propagate in conventional cultured human cells. The nucleotide sequence of the inverted terminal repeat (ITR) of Ad40, which includes the origin of adenoviral DNA replication, was determined using recombinant plasmid DNA. By using our newly developed program to express the ITR homologies simply, we found that the ITR of Ad40, which is 163 nucleotides long, was related most closely to that of adenovirus type 5, which replicates efficiently.     

Estrogen receptor alpha polymorphism as a genetic marker for bone loss, vertebral fractures and susceptibility to estrogen

OBJECTIVE: The purpose of the present study was to investigate the possible roles of PvuII and XbaI polymorphisms of the estrogen receptor alpha (ER(alpha)) in bone mineral density (BMD), vertebral fracture, bone loss rate after menopause and response to hormone replacement therapy (HRT). METHODS: All 286 women were grouped according to the genotypes of PvuII or XbaI polymorphisms of the ER(alpha) gene. We compared the BMD Z-score, incidence of vertebral fracture, changes in Z-score after menopause and response of BMD to HRT among the genotypes. RESULTS: Subjects with the PPxx genotype had significantly (P<0.05) lower Z-scores than did subjects with the other genotypes. A negative correlation was observed between the length of time after menopause and the decrease of the Z-score only in women with the pp genotype, suggesting faster bone loss in this group. In the analysis of the ER(alpha) polymorphism with regard to the effect of HRT on BMD, there appears to be a significantly greater increase of BMD (P<0.01 and 0.05) in women with the pp genotype than in those with the Pp or PP genotype. CONCLUSIONS: PvuII and XbaI polymorphisms of the ER(alpha) gene were associated with BMD in postmenopausal Japanese women. Also, the polymorphisms may be useful genetic markers for predicting vertebral fracture in relatively young postmenopausal women. The PvuII polymorphism may be associated with susceptibility to changes in estrogen level.     

Usefulness of coronary angioscopy for the evaluation of hyperlipidemia

Hyperlipidemia is one of the major coronary risk factors, which leading to the clinical worse outcome in patients with coronary artery disease, that is, acute coronary syndrome. Coronary plaque rupture followed by the formation of thrombus has been revealed to be a major cause of acute coronary syndrome. It would be important to detect the vulnerable plaque before its rupture, but there were no ways to detect by the conventional methods except coronary angioscopy. Yellow plaque and thrombus are mostly observed at the culprit lesion by the coronary angioscopy, which suggests that vulnerable plaque is dark yellow. Coronary angioscopy may diagnose the high-risk group among patients with hyperlipidemia.