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Articles by Y Yamazaki
Total Records ( 4 ) for Y Yamazaki
  Y Yamazaki , I Usui , Y Kanatani , Y Matsuya , K Tsuneyama , S Fujisaka , A Bukhari , H Suzuki , S Senda , S Imanishi , K Hirata , M Ishiki , R Hayashi , M Urakaze , H Nemoto , M Kobayashi and K. Tobe
 

Nonalcoholic fatty liver disease (NAFLD) is an abnormal liver metabolism often observed with insulin resistance and metabolic syndrome. Calorie restriction is a useful treatment for NAFLD and reportedly prolongs the life spans of several species in which sirtuin plays an important role. In this study, we examined whether the activation of SIRT1, a mammalian ortholog of sirtuin, may ameliorate the development of NAFLD. Monosodium glutamate (MSG) mice, which exhibited obesity and insulin resistance, were treated with SRT1720, a specific SIRT1 activator from the age of 6–16 wk. Sixteen-week-old MSG mice exhibited increased liver triglyceride content and elevated levels of aminotransferase. SRT1720 treatment significantly reduced these levels without affecting body weight or food intake. These results suggested that the administration of SRT1720 ameliorated the development of NAFLD in MSG mice. The expressions of lipogenic genes, such as sterol regulatory element-binding protein-1c, acetyl-CoA carboxylase, and fatty acid synthase, and the serum lipid profiles, including free fatty acids, were elevated in MSG mice and were reduced by SRT1720 treatment. SRT1720 treatment also reduced the expressions of lipogenic genes in cultured HepG2 cells. Furthermore, SRT1720 treatment decreased the expressions of marker genes for oxidative stress and inflammatory cytokines in the liver of MSG mice. Taken together, SRT1720 treatment may reduce liver lipid accumulation, at least in part, by directly reducing the expressions of lipogenic genes. The reduction of oxidative stress and inflammation may also be involved in the amelioration of NAFLD.

  H Ishikawa , E Yano , S Fujimori , M Kinoshita , T Yamanouchi , M Yoshikawa , Y Yamazaki and T. Teramoto
 

Background. Health literacy (HL), the capacity of individuals to access, understand and use health information to make informed and appropriate health-related decisions, is recognized as an important concept in patient education and disease management.

Objective. To examine the relation of three levels of HL (i.e. functional, communicative and critical HL) to patient–physician information exchange during a visit.

Methods. Participants were 134 outpatients with type 2 diabetes who were under continuous care by four attending physicians at a university-affiliated hospital. The visit communication was recorded and analysed using the Roter Interaction Analysis System. Patient HL was measured through a self-reported questionnaire using newly developed self-rated scales of functional, communicative and critical HL. Sociodemographic and clinical characteristics and patient's perception of the information exchange were assessed for each patient through self-reported questionnaires and review of electronic medical records.

Results. Patient HL levels were related to the information exchange process during the visit. Among the three HL scales, communicative HL (the capacity to extract information, derive meaning from different forms of communication and apply new information to changing circumstances) was related to patient's perceptions of the information exchange. Further, patient communicative HL had a modifying effect on the relationship between physician's information giving and patient's perception of it, suggesting that physician's communication may be perceived differently depending on the patient's HL.

Conclusion. The exploration of patient HL may provide a better understanding of potential barriers to patient–physician communication and patient's self-management of disease.

  T Yazawa , Y Inaoka , R Okada , T Mizutani , Y Yamazaki , Y Usami , M Kuribayashi , M Orisaka , A Umezawa and K. Miyamoto
 

Previously, we demonstrated that bone marrow-derived mesenchymal stem cells (MSCs) differentiate into steroidogenic cells such as Leydig and adrenocortical cells by the introduction of steroidogenic factor-1 (SF-1) and treatment with cAMP. In this study, we employed the same approach to differentiate umbilical cord blood (UCB)-derived MSCs. Despite UCB-MSCs differentiating into steroidogenic cells, they exhibited characteristics of granulosa-luteal-like cells. We found that peroxisome proliferator-activated receptor- coactivator-1 (PGC-1) was expressed and further induced by cAMP stimulation in UCB-MSCs. Consistent with these results, tissue-specific expression of Pgc-1 was observed in rat ovarian granulosa cells. PGC-1 binds to the NR5A family [SF-1 and liver receptor homolog-1 (LRH-1)] of proteins and markedly enhances their transcriptional activities. Reporter assays revealed that PGC-1 activated the promoter activities of SF-1 and LRH-1 target genes. Infection of KGN cells (a human cell line derived from granulosa cells) with adenoviruses expressing PGC-1 resulted in the induction of steroidogenesis-related genes and stimulation of progesterone production. PGC-1 also induced SF-1 and LRH-1, with the latter induced to a greater extent. Knockdown of Pgc-1 in cultured rat granulosa cells resulted in attenuation of gene expression as well as progesterone production. Transactivation of the NR5A family by PGC-1 was repressed by Dax-1. PGC-1 binds to the activation function 2 domain of NR5A proteins via its consensus LXXLL motif. These results indicate that PGC-1 is involved in progesterone production in ovarian granulosa cells by potentiating transcriptional activities of the NR5A family proteins.

  D Fujisawa , Y Yamazaki and T. Morita
 

Many anticoagulant proteins have been found from snake venoms. Recently, L-amino acid oxidase (LAO) from the venom of Gloydius blomhoffi, M-LAO, was reported to inhibit coagulation factor IX; however, the mechanism of its anticoagulant activity is still unclear. Here, we re-evaluated the anticoagulant activity of M-LAO. We first purified M-LAO from the venom of G. blomhoffi, and examined the effect of LAO inhibitors and the hydrogen peroxide scavenger, catalase, on the anticoagulant activity of M-LAO. We found that the isolated M-LAO fraction prolongs the APTT, PT and fibrinogen clotting time and cleaves the A-chain of fibrinogen. LAO inhibitors or catalase did not inhibit these effects. Detailed analysis revealed that the M-LAO fraction contained a small amount of 39-kDa metalloproteinase. The prolongation of clotting time and degradation of fibrinogen were inhibited by a metalloproteinase inhibitor. Therefore, we concluded that the anticoagulant activity of the M-LAO fraction was caused by the 39-kDa metalloproteinase.

 
 
 
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