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Articles by Y Sakata
Total Records ( 2 ) for Y Sakata
  J. S Burchfield , J. W Dong , Y Sakata , F Gao , H. P Tzeng , V. K Topkara , M. L Entman , N Sivasubramanian and D. L. Mann

Background— Activation of both type 1 and type 2 tumor necrosis factor (TNF) receptors (TNFR1 and TNFR2) confers cytoprotection in cardiac myocytes. Noting that the scaffolding protein TNF receptor–associated factor 2 (TRAF2) is common to both TNF receptors, we hypothesized that the cytoprotective responses of TNF were mediated through TRAF2.

Methods and Results— Mice with cardiac-restricted overexpression of low levels of TNF (MHCsTNF3) and TRAF2 (MHC-TRAF2LC) and mice lacking TNFR1, TNFR2, and TNFR1/TNFR2 were subjected to ischemia (30 minutes) reperfusion (30 minutes) injury ex vivo using a Langendorff apparatus. MHCsTNF3 mice were protected against ischemia-reperfusion injury as shown by a significant 30% greater left ventricular developed pressure, 80% lower creatine kinase release, and Evans blue dye uptake compared with littermates. The extent of ischemia-reperfusion induced injury was similar in wild-type, TNFR1, and TNFR2 deficient mice; however, mice lacking TNFR1/TNFR2 had a significant 40% lower left ventricular developed pressure, a 65% greater creatine kinase release, and 40% greater Evans blue dye uptake compared with littermates. Interestingly, MHC-TRAF2LC mice had a significant 50% lower left ventricular developed pressure, a 70% lower creatine kinase release, and 80% lower Evans blue dye uptake compared with littermate controls after ischemia-reperfusion injury. Biochemical analysis of the MHC-TRAF2LC hearts showed that there was activation of nuclear factor-kappaB but not c-Jun N-terminal kinase activation.

Conclusion— Taken together, these results suggest that TNF confers cytoprotection in the heart through TRAF2-mediated activation of nuclear factor-B.

  I Okamoto , M Munakata , M Miyazaki , T Satoh , T Takahata , Y Takamatsu , O Muto , K Koike , K Ishitani , T Mukaiyama , Y Sakata , K Nakagawa and K. Tamura

Hormonal imbalance characterized by excessive production of growth hormone (GH) and a low circulating concentration of insulin-like growth factor (IGF)-1 has been demonstrated in individuals with various serious conditions. However, little is known about changes in the GH–IGF-1 axis in cancer patients.


We prospectively examined the circulating levels of several hormones in 58 patients with solid tumors who were classified according to Eastern Cooperative Oncology Group performance status (PS): PS 0–1, n = 15; PS 2, n = 15; PS 3, n = 15; and PS 4, n = 13. The relations of hormone concentrations, with a focus on the GH–IGF-1 system, to PS were evaluated by Spearman's rank correlation test and regression analysis.


The circulating levels of IGF-1, IGF-binding protein-3 and thyroid hormones (total T3 and T4) were inversely correlated with PS score. The concentration of GH was increased irrespective of PS but not statistically significant. The ratio of IGF-I to GH was inversely correlated with PS. The levels of GH and IGF-1 in all patients were also inversely correlated.


The present study suggests that the GH–IGF-1 axis is disturbed in patients with cancer.

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