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Articles by M Yoshizawa
Total Records ( 3 ) for M Yoshizawa
  A Miyaki , S Maeda , M Yoshizawa , M Misono , Y Saito , H Sasai , T Endo , Y Nakata , K Tanaka and R. Ajisaka
 

Obesity and reduction in central arterial distensibility, respectively, have been identified as powerful and independent risk factors for cardiovascular disease. However, the effect of weight reduction on central arterial function in obese subjects has not yet been clarified. We investigated whether low-calorie diet-induced weight reduction affects central arterial distensibility and endothelial function in middle-aged obese men. Twelve obese men (age: 45+2 yrs, BMI: 30+1 kg/m 2) completed a 12-week dietary intervention. Caloric restriction induced significantly weight loss and decrease in BMI. After the program, carotid arterial compliance significantly increased and b-stiffness index and aortic pulse-wave velocity remarkably decreased. Concentrations of plasma endothelin-1 (ET-1) significantly decreased and plasma nitric oxide (NO) markedly increased after the program. Weight reduction by low-calorie diet in obese men increases central arterial distensibility, which may contribute to the improvement in endothelial function, as noted by a decrease in ET-1 and an increase in NO.

  M Yoshizawa
  Background:

Resistance training has been increasingly incorporated into the overall exercise programme because of its effect on muscle strength, functional capacity and osteoporosis. High-intensity resistance training increases arterial stiffness. However, the effect of moderate-intensity resistance training on arterial stiffness is unknown.

Objective:

To determine whether 12 weeks of moderate-intensity resistance training increases arterial stiffness in middle-aged women.

Methods:

35 middle-aged women (age range 32 to 59 years) volunteered to participate. The subjects were randomly assigned to one of three groups: resistance training (RT) group, aerobic exercise training (AET) group or control group. The RT and AET groups performed 12 weeks of moderate-intensity resistance training or aerobic exercise training (two days/week).

Results:

In the RT group, one-repetition maximum strength significantly increased after the intervention. Interestingly, aortic (carotid–femoral) pulse wave velocity (PWV; an index of arterial stiffness), and peripheral (femoral–ankle) PWV did not change with moderate-intensity resistance training. In contrast, in the AET group, carotid–femoral PWV significantly decreased after the intervention. Resistance training and aerobic exercise training did not affect blood pressure.

Conclusions:

This study found that moderate-intensity resistance training did not increase arterial stiffness in middle-aged women, which may have great importance for health promotion with resistance training.

  K Takeda , N. H Takahashi , M Yoshizawa and S. Shibahara
 

Lipocalin-type prostaglandin D synthase (L-PGDS) catalyses the formation of prostaglandin D2 (PGD2) and also functions as a transporter for lipophilic ligands, including all-trans retinoic acid (RA). Here, we show that human epidermal melanocytes produce and secrete L-PGDS and PGD2 in culture medium, whereas L-PGDS is not expressed in human melanoma cell lines, HMV-II, SK-MEL-28, 624 mel and G361. Treatment with RA (1 or 10 µM) for 4 days decreased the proliferation of melanocytes (30% decrease), but not melanoma cells. We therefore isolated L-PGDS-expressing cell lines from 624 mel cells. Treatment with RA decreased the proliferation of L-PGDS-expressing cells by 20%, but not mock-transfected cell lines lacking L-PGDS expression. RA induced expression of a cyclin-dependent kinase inhibitor p21Cip1 in L-PGDS-expressing cells, but not mock-transfected cells. Moreover, RA increased the transient expression of a reporter gene carrying the RA-responsive elements in L-PGDS-expressing cell lines (at least 5-fold activation), compared to the 2-fold activation in mock-transfected cell lines, suggesting that L-PGDS may increase the sensitivity to RA. Lastly, the knockdown of L-PGDS expression by RNA interference was associated with the restoration of the RA-mediated decrease in proliferation of human and mouse melanocytes. In conclusion, L-PGDS may fine-tune the RA signalling in melanocytes.

 
 
 
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