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Articles by T Ninomiya
Total Records ( 3 ) for T Ninomiya
  J. J Brugts , T Ninomiya , E Boersma , W. J Remme , M Bertrand , R Ferrari , K Fox , S MacMahon , J Chalmers and M. L. Simoons

Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce cardiovascular risk in different groups of patients. Whether these effects can be generalized to the broad group of patients with vascular disease is unknown. Therefore, we undertook a combined analysis using individual data from ADVANCE, EUROPA, and PROGRESS to determine the consistency of the treatment effect of perindopril-based regimen in patients with vascular disease or at high risk of vascular disease.

Methods and results

We studied all-cause mortality and major cardiovascular outcomes during a follow-up of about 4 years in the 29 463 patients randomly assigned a perindopril-based treatment regimen or placebo. The perindopril-based regimens were associated with a significant reduction in all-cause mortality [hazard ratio (HR) 0.89; 95% confidence interval (CI) 0.82–0.96; P = 0.006], cardiovascular mortality (HR 0.85; 95% CI 0.76–0.95; P = 0.004), non-fatal myocardial infarction (HR 0.80; 95% CI 0.71–0.90; P < 0.001), stroke (HR 0.82; 95% CI 0.74–0.92; P = 0.002), and heart failure (HR 0.84; 95% CI 0.72–0.96; P = 0.015). Results were consistent in subgroups with different clinical characteristics, concomitant medication use, and across all strata of baseline blood pressure.


This study provides strong evidence for a consistent cardiovascular protection with an ACE-inhibitor treatment regimen (perindopril–indapamide) by improving survival and reducing the risk of major cardiovascular events across a broad spectrum of patients with vascular disease.

  H Nakamura , A Yukita , T Ninomiya , A Hosoya , T Hiraga and H. Ozawa

We elucidated the localization of Thy-1–positive cells in the perichondrium of fetal rat limb bones to clarify the distribution of osteogenic cells in the process of endochondral ossification. We also examined the formation of calcified bone-like matrices by isolated perichondrial cells in vitro. At embryonic day (E) 15.5, when the cartilage primodia were formed, immunoreactivity for Thy-1 was detected in cells of the perichondrium adjacent to the zone of hypertrophic chondrocytes. At E17.5, when the bone collar formation and the vascular invasion were initiated, fibroblast-like cells at the sites of vascular invasion, as well as in the perichondrium, showed Thy-1 labeling. Double immunostaining for Thy-1 and osterix revealed that Thy-1 was not expressed in the osterix-positive osteoblasts. Electron microscopic analysis revealed that Thy-1–positive cells in the zone of hypertrophic chondrocytes came in contact with blood vessels. Perichondrial cells isolated from limb bones showed alkaline phosphatase activity and formed calcified bone-like matrices after 4 weeks in osteogenic medium. RT-PCR demonstrated that Thy-1 expression decreased as calcified nodules formed. Conversely, the expression of osteogenic marker genes Runx2, osterix, and osteocalcin increased. These results indicate that Thy-1 is a good marker for characterizing osteoprogenitor cells. (J Histochem Cytochem 58:455–462, 2010)

  S Kikuchi , T Ninomiya , H Tatsumi , N Sawada and T. Kojima

Autotypic tight junctions are formed by tight junction–like structures in three regions of myelinating Schwann cells, the paranodal loops, Schmidt–Lanterman incisures, and outer/inner mesaxons, and various tight junction molecules, including claudin-19 and junctional adhesion molecule (JAM)-C. Our findings demonstrate the identification and subcellular distribution of a novel tricellular tight junction protein, tricellulin (TRIC), in the autotypic tight junctions of mouse myelinating Schwann cells, compared with the autotypic adherens junction protein E-cadherin and the autotypic tight junction protein JAM-C, which are expressed in the paranodal loops, Schmidt–Lanterman incisures, and mesaxons. In real-time RT-PCR, the expression level of TRIC mRNA was about 10-fold higher in the sciatic nerve than in the spinal cord or cerebrum. In immunostaining, TRIC signals were completely restricted to the peripheral nervous system (PNS) and strongly concentrated at the paranodal loops, Schmidt–Lanterman incisures, and mesaxons of myelinating Schwann cells. In addition, TRIC was expressed in the thin region of the paranode and there was a gap between TRIC and the Na+ channel. Furthermore, TRIC was more distally located from the node than E-cadherin and was colocalized with JAM-C. It is possible that TRIC may be a component to maintain the integrity for PNS myelin function and morphology. This manuscript contains online supplemental material at Please visit this article online to view these materials. (J Histochem Cytochem 58:1067–1073, 2010)

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