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Articles by M Miyachi
Total Records ( 2 ) for M Miyachi
  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.

  M Miyachi , N Kakazu , S Yagyu , Y Katsumi , S Tsubai Shimizu , K Kikuchi , K Tsuchiya , T Iehara and H. Hosoi
 

Purpose: Seventy to eighty percent of rhabdomyosarcoma (RMS) tumors retain wild-type p53. The tumor suppressor p53 plays a central role in inducing cell cycle arrest or apoptosis in response to various stresses. p53 protein levels are regulated by MDM2 through ubiquitin-dependent degradation. In this study, we evaluated whether nutlin-3, a recently developed small-molecule antagonist of MDM2, has an effect on p53-dependent cell cycle arrest and apoptosis in cultured human RMS cell lines.

Experimental Design: Five RMS cell lines with different p53 statuses and MDM2 expression levels were treated with nutlin-3. Gene expression patterns, cell viability, cell cycle, and apoptosis after nutlin-3 treatment, and antitumor activity of combination treatment with vincristine or actinomycin D were assessed.

Results: Significant p53 activation was observed in wild-type p53 cell lines after nutlin-3 treatment. p53 activation led to cell cycle arrest in parallel with increased p21 expression. Furthermore, these cell lines underwent p53-dependent apoptosis, concomitant with elevation of proapoptotic genes and activation of caspase-3. The effect of nutlin-3 was almost the same in terms of half maximal inhibitory concentration and apoptosis whether or not MDM2 was overexpressed. Nutlin-3 did not induce either cell cycle arrest or apoptosis in p53 mutant cell lines. A combination of vincristine or actinomycin D with nutlin-3 enhanced the antitumor activity in RMS cell lines with wild-type p53.

Conclusions: Nutlin-3 effectively restored p53 function in both normal MDM2 expression and MDM2 overexpression RMS cell lines with wild-type p53. p53 restoration therapy is a potential therapeutic strategy for refractory RMS with wild-type p53.

 
 
 
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