The University of Osaka · 의학
Tetsuya Tomita 교수의 연구실은 염증성 관절질환, 특히 류마티스성 관절염의 분자 기전과 유전자 치료 전략을 중심으로 연구를 진행하고 있습니다. NF-kappaB 및 EMMPRIN과 같은 핵심 분자 기전을 규명하며 관절 파괴를 억제할 수 있는 새로운 치료법 개발에 주력하고 있으며, 특히 관절 내 유전자 전달을 통한 치료 전략 개발에 뛰어난 기여를 하고 있습니다. 또한 PPARγ 수용체를 타겟으로 한 약물 개발을 통해 염증 조절 및 관절 보호 효과를 동시에 확보하고자 하는 다각적 접근을 펼치고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
The present results demonstrate that administration of NF-kappaB decoy ODN in arthritic joints of rats with CIA led to an amelioration of arthritis. These findings suggest that intraarticular transfection of NF-kappaB decoy ODN may provide a useful therapeutic approach for the treatment of inflammatory arthritis.
Myelography was performed in 535 patients at the Memorial Sloan-Kettering Hospital from January 1979 to December 1979. In 110 cases a complete block was demonstrated and of these, 78 had epidural metastases. A uniform treatment was applied using radiation therapy and high dose steroid. The neurologic outcome for each patient was evaluated, correlating pre-treatment neurologic status, pathologic type, nature of block (level, structural versus tumoral), and result of repeat fluoromyelography. Only
The results demonstrated in this study suggest the potential usefulness of NFkappaB decoy ODN for gene therapy of inflammatory synovitis of RA.
The transfection frequency and stability of expression recognized in this study indicate the possibility of a strategy for treatment of joint disorders, including arthritis, using direct gene transfer.
The expression of EMMPRIN stimulates the production of MMP-1 and MMP-3 in the synovial tissue of affected joints in RA. The results of this study suggest that EMMPRIN may be one of the important factors in progressive joint destruction in RA.
THR0921 is a novel peroxisome proliferator-activated receptor gamma (PPARgamma) agonist with potent anti-diabetic properties. Because of the proposed role of PPARgamma in inflammation, we investigated the potential of orally active THR0921 to inhibit the pathogenesis of collagen-induced arthritis (CIA). CIA was induced in DBA/1J mice by the injection of bovine type II collagen in complete Freund's adjuvant on days 0 and 21. Mice were treated with THR0921 (50 mg/kg/day) starting on the day of the