Masaru Kato

Our data provide the first evidence of a dual role of autophagy in the regulation of death pathways in RASFs. A reduced expression of ALFY and the formation of p62-positive polyubiquitinated protein aggregates promote cell death in RASFs under severe ER stress.

In cases of aortic dissection, the stent-graft is an effective tool for closing the entry site and promoting clot formation in the false lumen and for reducing the size of the false lumen within 6 months of the onset of dissection if the entry site has been closed.

The treatment of rheumatoid arthritis (RA) is now entering a new era, the era of Janus kinase (JAK) inhibitors. JAK inhibitors target multiple cytokines including IL-6 and exhibit a beneficial treatment effect in patients with RA and inadequate response to conventional synthetic or biologic disease-modifying anti-rheumatic drugs. Since the treatment effect of JAK inhibitors is promising even for patients refractory to anti-IL-6 therapy, it needs to be considered how multiple cytokines play roles

The effect of light on respiration of intact mouse liver mitochondria was examined at various temperatures using various interference filters. State 3 respiration, namely, O 2 consumption in the presence of ADP, was clearly activated by visible light around 600 nm (orange-red) and 420 nm. This photosensitivity was also observed for ascorbate-tetramethyl-p-phenylene-diamine (TMPD) oxidation by the intact mitochondrial preparation in the presence of antimycin A. These results clearly show that the

We aimed to investigate the involvement of macroautophagy/autophagy in autoimmunity in rheumatoid arthritis (RA) through citrullination of VIM (vimentin) and its interaction with MHC class II in synovial fibroblasts (SFs). The cell surface expression of MHC class II and B7 costimulatory molecules on SFs was analyzed by flow cytometry after treatment with IFNG/IFN-γ (interferon gamma). Intracellular citrullinated autoantigens in SFs were analyzed by immunoblotting using serum from anti-citrullina

Reactivation of resolved HBV can occur during standard immunosuppressive therapy for autoimmune diseases. The low titer of baseline anti-HBs may carry its risk.

Pulmonary arterial hypertension (PAH) is a life-threatening complication in connective tissue diseases (CTD). It remains controversial whether immunosuppressive therapy is useful for PAH associated with CTD (PAH-CTD). The Dana Point algorithm does not refer such treatments in patients with PAH-CTD due to the lack of evidence. However, some case reports have shown the potential efficacy of immunosuppression for PAH-CTD. Here we report five cases of PAH-CTD treated with corticosteroids and discuss

We newly identified high aPL-S as an important risk factor for ION development in SLE, suggesting the involvement of aPL-induced coagulopathy in the pathophysiology of lupus ION.

Recent studies have clarified that pulmonary arterial hypertension associated with connective tissue diseases (CTD-PAH) has some distinctive clinical aspects from other PAH, such as high prevalence, venous and cardiac involvement, less favourable outcome, helpfulness of detection algorithm, response to immunosuppression, pre-PAH conditions in borderline pulmonary arterial pressure and coexistence of interstitial lung disease. In this review, by focusing on these distinctive aspects, we discuss h

A chiral stationary phase (CSP 1) derived from an (S)-N-3,5-dinitrobenzoyl-1-naphthylglycine showed excellent enantiomeric separation for amino acid derivatives with a fluorogenic reagent, 4-fluoro-7-nitro-2,1,3-benzoxadiazole (NBD-F), in high-performance liquid chromatography (HPLC). We compared elution profiles (separation factor and elution order) of NBD-amino acids and their analogs on HPLC, to determine the diastereomeric complex between the chiral moiety of CSP 1 and NBD-amino acid, which

Objective Optineurin ( OPTN ) is an autophagy adaptor/receptor that acts as an intrinsic negative regulator of osteoclast differentiation. RANKL expressed by rheumatoid arthritis synovial fibroblasts ( RASF s) is primarily responsible for the development of bone erosions in patients with RA . The aim of the present study was to explore the role of OPTN in the pathogenesis of joint destruction in RA . Methods RASF s were left untreated or incubated with tumor necrosis factor ( TNF ) or interferon