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Articles by T Nakajima
Total Records ( 4 ) for T Nakajima
  H Ozaki , M Miyachi , T Nakajima and T. Abe

High-intensity resistance training increases muscle size, but reduces arterial compliance. Muscular blood flow reduction (BFR) during low-intensity training has been shown to elicit muscle hypertrophy. However, the effect on arterial compliance is unknown. We examined the effects of walk training with BFR on carotid arterial compliance and muscle size in the elderly adults. Both BFR-walk training (BFR-W, n = 13, 66 ± 1 year) and control-walk training (CON-W, n = 10, 68 ± 1 year) groups performed 20 minutes treadmill walking at an exercise intensity of 45% of heart rate reserve, 4 days/week for 10 weeks. The BFR-W group wore pressure cuffs on both legs during training. Maximum knee joint strength (~15%) and MRI-measured thigh muscle cross-sectional area (3%) increased in the BFR-W, but not in the CON-W. Carotid arterial compliance improved in both BFR-W (50%) and CON-W (59%) groups. Walk training with blood flow reduction can improve thigh muscle size/strength as well as carotid arterial compliance, unlike high-intensity training, in the elderly.

  K Onoue , S Uemura , Y Takeda , S Somekawa , H Iwama , K Imagawa , T Nishida , Y Morikawa , Y Takemoto , O Asai , T Soeda , S Okayama , K Ishigami , K Nakatani , H Kawata , M Horii , T Nakajima , Y Akai , M Iwano and Y. Saito

Background— Renal dysfunction is commonly accompanied by a worsening of atherosclerosis; however, the underlying molecular mechanism is not fully understood. We examined the role played by soluble fms-like tyrosine kinase-1 (sFlt-1), an endogenous antagonist of the proatherogenic cytokine placental growth factor (PlGF), in the worsening of atherosclerosis in patients with renal dysfunction and in an animal model of renal failure.

Methods and Results— In this study, 329 patients who received cardiac catheterization and 76 patients who underwent renal biopsy were enrolled. Both plasma sFlt-1 levels and renal sFlt-1 mRNA expression were positively correlated with estimated glomerular filtration rate (P<0.01). The PlGF/sFlt-1 ratio was negatively correlated with estimated glomerular filtration rate (P<0.01), whereas plasma PlGF levels were not affected by it. The PlGF/sFlt-1 ratio was significantly higher in patients with multivessel coronary artery disease than in patients with single-vessel or no coronary artery disease. The reduction of circulating sFlt-1 and renal sFlt-1 mRNA levels was confirmed in five-sixths (5/6)–nephrectomized apolipoprotein E–deficient mice that developed experimental renal dysfunction. Atherosclerotic plaque area and macrophage infiltration into the plaque were significantly higher in 5/6–nephrectomized apolipoprotein E–deficient mice than in control mice, but replacement therapy with recombinant sFlt-1 significantly reduced both plaque formation and macrophage infiltration.

Conclusions— The present study demonstrates that a reduction in the circulating levels of sFlt-1 is associated with the worsening of atherosclerosis that accompanies renal dysfunction.

  S Somekawa , K Imagawa , N Naya , Y Takemoto , K Onoue , S Okayama , Y Takeda , H Kawata , M Horii , T Nakajima , S Uemura , N Mochizuki and Y. Saito

Aldosterone synthase (CYP11B2) and 11β-hydroxylase (CYP11B1) regulate aldosterone and cortisol production, respectively. The expression of these enzymes is promoted by calcium influx through Cav3.2, a T-type calcium channel. Neuron-restrictive silencer factor (NRSF) binds to neuron-restrictive silencer element (NRSE) to suppress the transcription of NRSE-containing genes. We found a NRSE-like sequence in human CYP11B2 and CYP11B1 genes as well as the CACNA1H gene of many mammalian species. The CACNA1H gene encodes the -subunit of Cav3.2. Here we investigated how NRSF/NRSE regulates aldosterone and cortisol synthesis. Inhibition of endogenous NRSF by an adenovirus-expressing dominant-negative NRSF (AD/dnNRSF) increased human CYP11B2 and CYP11B1 mRNA expression, leading to aldosterone and cortisol secretion in human adrenocortical (H295R) cells. In reporter gene experiments, NRSE suppressed luciferase reporters driven by CYP11B2 and CYP11B1 promoters and dnNRSF enhanced them. Moreover, cotransfection of dnNRSF increased luciferase activity of reporter genes after deletion or mutation of NRSE, suggesting that NRSF/NRSE regulates transcription of CYP11B2 and CYP11B1 genes indirectly. AD/dnNRSF augmented mRNA expression of rat CYP11B2 and CYP11B1 genes, neither of which contains a NRSE-like sequence in rat adrenal cells. AD/dnNRSE also significantly increased CACNA1H mRNA in H295R and rat adrenal cells. Efonidipine, a T/L-type calcium channel blocker, significantly suppressed dnNRSF-mediated up-regulation of CYP11B2 and CYP11B1 expression. Moreover, NRSF/NRSE is also involved in angiotensin II- and K+-stimulated augmentation of CYP11B2 and CYP11B1 gene transcription. In conclusion, NRSF/NRSE controls aldosterone and cortisol synthesis by regulating CYP11B2 and CYP11B1 gene transcription mainly through NRSF/NRSE-mediated enhancement of the CACNA1H gene.

  K Kiyota , T Nakajima and K. G. Nishimura

This article presents a new simple econometric framework for the estimation of individual firms’ markup over their marginal cost, taking account of firm heterogeneity, demand-driven cyclical price changes, and the limited availability of firm-level information. The framework is applied to study markup of Japanese firms in manufacturing and wholesale/retail trade for 1994–2002. The results indicate that, on average, the Japanese markets become more competitive in the 1990s than before even in non-manufacturing industries. We also find sizable heterogeneity and non-negligible pro-cyclicality in the markup of the Japanese firms.

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