Hideyuki Oniki

National Cerebral and Cardiovascular Center, Ōsaka, Ōsaka, Japan

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Publications (15)36.32 Total impact

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    ABSTRACT: Several studies have documented an association between serum uric acid (SUA) concentration and cardiac hypertrophy in hypertensive patients; however, the association remains unclear in chronic kidney disease (CKD) patients. If there is an association between SUA and hypertrophy in these patients, it is unknown whether the association is different between men and women. Our aim in this study is to determine whether SUA is associated with cardiac hypertrophy in CKD patients, focusing on any sex differences. Two hundred sixteen CKD patients (117 men and 99 women) were enrolled in this cross-sectional study. Patients prescribed uric acid-lowering agents and those with congestive heart failure, valvular heart disease, or ischemic heart disease were excluded from this study. Left ventricular mass index (LVMI) and left ventricular hypertrophy (LVH) were assessed using echocardiography. The prevalence of LVH was 58% in men and 47% in women. In multivariate linear regression analysis, SUA levels did not correlate with LVMI in men, whereas SUA was independently associated with LVMI in women (β=0.27, P=0.02). Multivariate logistic regression analysis also revealed that diabetes mellitus (odds ratio (OR), 4.41; P=0.01) was associated with LVH in men, whereas age (OR, 1.13; P<0.01), hypertension (OR, 7.38; P=0.03) and SUA (OR, 1.91; P=0.03) were associated with LVH in women. In female CKD patients, SUA levels were associated with LVMI and LVH, whereas there was no association in male patients. These observations suggest that an association between SUA levels and the development of cardiac hypertrophy is more likely in women than in men.Hypertension Research advance online publication, 3 October 2013; doi:10.1038/hr.2013.134.
    Hypertension Research 10/2013; · 2.79 Impact Factor
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    ABSTRACT: Perioperative blood pressure (BP) management is important to prevent cardiovascular complication, especially for hypertensive patients. In the present study, we investigated perioperative BP variability and contributing factors in hypertensive patients. Subjects were 28 treated hypertensive patients who underwent total or subtotal gastrectomy. Ambulatory BP monitoring was carried out before and after (16 days in average) the surgery. Angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and diuretics were withdrawn on the previous day, while other drugs were administered until the day of surgery. BP, body weight, blood chemistry, as well as the use of intravenous vasopressor or vasodepressor agents during the perioperative period were investigated. The 24-hour BP before surgery was 124 ± 19/70 ± 12 mm Hg, and the number of antihypertensive drugs was 1.8. In 22 patients, intravenous vasopressor agents were used during surgery, while another patient received intravenous vasodepressor agents after surgery. The 24-hour BP significantly decreased after surgery (-8.2 ± 14.7/-2.6 ± 7.3 mm Hg). Body weight, serum Na, and hematocrit also decreased. There were nine patients whose 24-hour systolic BP decreased by more than 10 mm Hg and for two patients more than 20 mm Hg. The decrease in BP correlated with the change in serum Na. Forty-three percent of the patients who took ACE inhibitors/ARBs showed BP reduction greater than 10 mm Hg, while 25% of the patients without these drugs showed such BP reduction. Our findings suggest that 24-hour BP decreases after gastrectomy. Patients taking ACE inhibitors or ARBs may need careful monitoring to prevent excessive BP fall.
    Clinical and Experimental Hypertension 03/2013; · 1.28 Impact Factor
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    ABSTRACT: Objective Uric acid (UA) has shown to be a causal risk factor for the development and progression of renal disease. The aim of this study was to investigate the relationship between changes in the level of UA and trends in the renal function among hypertensive patients during a 10-year observation period. Methods The subjects included 104 hypertensive outpatients (60 women and 44 men, mean age 60±9 (SD) years at the first visit) who had undergone at least five instances of successful 24-hour home urine collection, with the first examination completed between 1998 and 2000 and the last examination completed between 2008 and 2010. Results The estimated glomerular filtration rate (eGFR) significantly decreased over the 10.4-year observation period, with an average change in eGFR of -0.66/mL/min/year. The uric acid clearance at the last examination was significantly lower than that observed at the first visit, while there were no significant differences in the serum UA levels during this period. The change in serum UA exhibited a significant negative correlation with the change in eGFR (r=-0.34, p<0.01). The patients whose UA level decreased more than 0.5 mg/dL during the observation period demonstrated significantly smaller declines in eGFR compared to those whose UA level increased more than 0.5 mg/dL. In the multivariate analysis, the change in serum UA and the average urinary salt excretion during the observation period were found to be significantly associated with the change in eGFR, independent of age, sex, BP changes or an increased number of antihypertensive drugs. Conclusion Based on the findings observed over a 10-year observation period, increased UA is suggested to promote decline of the renal function in hypertensive patients. Controlling the level of UA as well as intensively restricting salt intake is required in order to preserve the renal function.
    Internal Medicine 01/2013; 52(13):1467-72. · 0.97 Impact Factor
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    ABSTRACT: We investigated the influence of long-term salt load on renal function in hypertensive patients. The subjects were 133 hypertensive patients (80 women and 53 men, mean age 60±9 years) who underwent at least five successful 24 h home urine collections during the 10-year observation period. Blood pressure (BP) and 24-h urinary salt and creatinine excretion levels were measured. BP decreased from 143±12/85±8 to 129±14/68±11 mm Hg during the 10.5-year observation period, and this decrease was associated with patients taking an increased number of antihypertensive drugs (1.3±1.0 to 2.2±1.1). The estimated glomerular filtration rate (eGFR) also significantly decreased from 71.7±14.6 to 64.7±16.5 ml min(-1) (P<0.01), and the change in eGFR was -0.68 ml min(-1) per year on average. The average salt excretion was 8.6±2.2 g per day and showed a significant negative correlation with the change in eGFR (r=-0.21, P=0.02). Subjects with an average salt excretion<8 g per day showed a significantly slower decline in renal function than those with an average salt excretion 8 g per day (the change in eGFR: -0.41±1.10 vs. -0.83±1.19 ml min(-1) per year, P<0.05). In the multivariate analysis, the average salt excretion (partial r=-0.19, P=0.03) and baseline eGFR (partial r=-0.23, P=0.01) were significantly associated with the change in eGFR. This association was independent of BP change or an increased number of antihypertensive drugs. The results suggest that long-term salt load promotes a decline in renal function in hypertensive patients; thus, salt restriction is encouraged, to prevent renal damage.Hypertension Research advance online publication, 11 October 2012; doi:10.1038/hr.2012.155.
    Hypertension Research 10/2012; · 2.79 Impact Factor
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    ABSTRACT: Endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization and relaxation, and endothelium-independent relaxations to the nitric oxide donor sodium nitroprusside and the adenosine 5'-triphosphate (ATP)-sensitive K(+)-channel opener levcromakalim were both impaired in mesenteric arteries of type II diabetic Goto-Kakizaki rats. The treatment with the superoxide dismutase mimetic tempol or its combination with the angiotensin II type 1 receptor blocker candesartan failed to improve EDHF-mediated responses, although both treatments partially improved endothelium-independent relaxations. These findings suggest that increased oxidative stress may in part account for the impaired endothelium-independent relaxations in diabetes, while it does not play a major role in the impaired EDHF-mediated responses.
    Clinical and Experimental Hypertension 07/2012; · 1.28 Impact Factor
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    ABSTRACT: Blood pressure (BP) control in hypertensives has improved; however, it still remains to be insufficient. We have investigated the trend in BP control status of the hypertensive patients followed for 10 years in hypertension clinic. Subjects included 133 patients who have been followed from the first visit during 1998-2000 to the last visit during 2008-2010. During the mean follow-up period of 10.5 years, average BP and body weight significantly (P < .01) decreased from 143 ± 12/85 ± 8 mm Hg to 129 ± 14/68 ± 11 mm Hg, and from 59.8 ± 9.9 kg to 58.7 ± 10.6 kg, respectively. The achievement rate of good BP control defined as <140/90 mm Hg and the number of antihypertensive drugs also increased significantly during this period (39.1%-77.5% and 1.3 ± 1.0-2.2 ± 1.1, respectively, P < .01). Blood pressure control improved and the number of antihypertensive drugs also increased in 45 patients who were older than 65 years at the last visit. The use of Ca channel blockers (CCBs), angiotensin II receptor antagonists, and diuretics increased significantly during this period. Results suggest that lifestyle modification including body weight reduction as well as intensive antihypertensive treatment contributed to the improved BP control in hypertensive patients including the elderly.
    Clinical and Experimental Hypertension 05/2012; 34(4):258-63. · 1.28 Impact Factor
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    ABSTRACT: This study was designed to determine whether a high-salt diet would alter endothelial function and, if so, the relative contributions of endothelium-derived hyperpolarizing factor (EDHF) and nitric oxide (NO) to any changes in vasomotor responses. Male Dahl salt-sensitive (DS) rats were given either a high-salt diet (8% NaCl, DS-H) or a low-salt diet (0.4% NaCl, DS-L) for 6 weeks. Membrane potentials and contractile responses were recorded from the isolated superior mesenteric arteries. After salt loading, DS-H developed hypertension, while DS-L remained normotensive. No difference was found in acetylcholine (ACh)-induced, endothelium-dependent relaxation between the groups. However, after treatment with indomethacin and NO synthase inhibitor, EDHF-like relaxation was significantly greater in DS-H than in DS-L. In contrast, NO-mediated relaxation was significantly smaller in DS-Hthan in DS-L. Iberiotoxin (IbTx), a specific blocker of large-conductance calcium-dependent potassium (BKCa) channels, attenuated EDHF-like relaxation in DS-H but not in DS-L. IbTx marginally inhibited EDHF-mediated hyperpolarization only in DS-H. Endothelium-independent relaxation in response to sodium nitroprusside or levcromakalim was similar in both groups. In conclusion, EDHF-like relaxation is upregulated through the activation of BKCa channels in the mesenteric arteries of DS-H. As the overall relaxation in response to ACh did not differ between the groups, the upregulation of EDHF appears to compensate for the loss of NO in the mesenteric arteries of DS-H.
    Hypertension Research 04/2012; 35(8):849-54. · 2.79 Impact Factor
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    ABSTRACT: It has been shown that aging and hypertension are important risk factors to promote renal damage. However, little data are available on the effect of obesity on the progression of renal damage, especially in young and middle-aged individuals. The aim of this study was to determine the association between body mass index (BMI) and renal function evaluated by estimated glomerular filtration rate (eGFR) in Japanese men. We studied the cross-sectional association of BMI with eGFR in 3872 Japanese men in a work-site population (18-64 y; mean age 42.1 ± 0.2 y). Estimated glomerular filtration rate was calculated by a novel equation for Japanese men. Estimated glomerular filtration rate was negatively correlated with age, systolic blood pressure (SBP), hemoglobin A1c (HbA1c), and BMI. We performed multiple regression analysis, controlling for factors, such as SBP, low-density lipoprotein-cholesterol, gamma-glutamyl transpeptidase, age, HbA1c, and uric acid. The association between age and eGFR was highly statistically significant. In addition, BMI was still significantly associated with eGFR independently of SBP. Moreover, mean eGFR, which was adjusted for age, SBP, HbA1c, serum uric acid, and gamma-glutamyl transpeptidase, decreased from 88.9 mL/min/1.73 m(2) in the first quartile of BMI to 87.5 mL/min/1.73 m(2) in the second, 86.9 mL/min/1.73 m(2) in the third, and 85.9 mL/min/1.73 m(2) in the fourth quartile (test for trend, P < .0001). These results show that a close relationship is present between obesity and decreased eGFR in Japanese men. Keeping appropriate body weight, in addition to appropriate blood pressure, in young and middle age may be important to prevent renal damage in older age.
    Clinical and Experimental Hypertension 10/2011; 34(2):140-4. · 1.28 Impact Factor
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    ABSTRACT: To determine whether polymorphisms at codon 487 (*1, GAA=Glu; *2, AAA=Lys) of mitochondrial aldehyde dehydrogenase 2 (ALDH2) influence nitroglycerine (glyceryl trinitrate (GTN))-induced vasodilation, and whether GTN or isosorbide dinitrate (ISDN) is a more effective antianginal agent in each ALDH2 genotype. A randomised, open-label, crossover trial with 117 healthy Japanese (20-39 years) whose genotypes were determined (*1/*1, n=47; *1/*2, n=48; *2/*2, n=22) was performed at Kyushu University Hospital, Fukuoka, Japan. Participants were randomly assigned to treatment: sublingual spray of GTN (0.3 mg) or ISDN (1.25 mg). After ≥ 1 week, measurements were repeated using the other drug. The main outcome measures were the maximal rate of increase in the brachial artery diameter determined by ultrasonography, the time required to attain maximal dilation (T(max)) and the time required to attain 90% maximal dilation (T(0.9)). The maximal artery diameter increase in response to GTN or ISDN did not differ among genotypes. However, GTN T(max) was significantly longer for *2/*2 (299.7 s, 269.0-330.4) than *1/*1 (254.7 s, 238.6-273.4; p=0.0190). GTN T(0.9) was significantly longer in the *1/*2 (206.1 s, 191.7-219.3) and *2/*2 (231.4 s, 211.8-251.0) genotypes than *1/*1 (174.9 s, 161.5-188.3; p=0.0068, p<0.0001, respectively). In contrast, the time-course of ISDN-induced vasodilation did not differ among genotypes. GTN T(max) and T(0.9) among *1 allele carriers (*1/*1 and *1/*2) were significantly shorter than those of ISDN, whereas the time course of GTN and ISDN vasodilation did not differ among participants carrying *2/*2. The amplitude of GTN-induced vasodilation was not influenced by the ALDH2 genotype, but the response was significantly delayed in *2 allele carriers, especially *2/*2. GTN dilated the artery more quickly than ISDN in *1/*1 and *1/*2, but not in *2/*2. Trial registration number UMIN000001492 (UMIN-CTR database).
    BMJ Open 01/2011; 1(1):e000133. · 1.58 Impact Factor
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    ABSTRACT: 1. Non-nitric oxide/prostaglandin-mediated endothelium-derived hyperpolarization (EDH) is considered to be mediated, in part, by gap junctions and it has been suggested that cAMP increases endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation through the modulation of gap junctions. Cilostamide, which inhibits phosphodiesterase III, has been suggested to augment EDHF-type relaxation by increasing the concentration of cAMP. 2. In the present study, we investigated the effect of cilostamide on EDH per se in mesenteric arteries of Wistar rats using a conventional microelectrode technique. 3. The resting membrane potential of the mesenteric arteries was significantly more negative in the presence of 10(-6) mol/L cilostamide compared with control conditions. Furthermore, EDH in response to 10(-6) mol/L acetylcholine (ACh) in the presence of 10(-5) mol/L indomethacin and 10(-4) mol/L N(G)-nitro-L-arginine was decreased in the presence of 10(-6) mol/L cilostamide by approximately 5 and 3.5 mV in proximal and distal arteries, respectively. 4. Glibenclamide (10(-5) mol/L), an ATP-sensitive potassium channel (K(ATP)) inhibitor, abolished the hyperpolarization to 10(-6) mol/L cilostamide. Furthermore, in the presence of glibenclamide, ACh-induced EDH was unaffected by cilostamide, suggesting that the inhibition of ACh-induced hyperpolarization by cilostamide in the absence of glibenclamide may be due to the smaller driving force for hyperpolarization because of the more negative membrane potential under such conditions. 5. The findings of the present study suggest that cilostamide produces hyperpolarization by activating K(ATP) channels, presumably by increasing cAMP. However, cilostamide alone may not directly affect EDH.
    Clinical and Experimental Pharmacology and Physiology 02/2009; 36(7):729-33. · 2.41 Impact Factor
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    ABSTRACT: 1. In the present study, we investigated the effects of chronic treatment of stroke-prone spontaneously hypertensive rats (SHRSP) with the statin fluvastatin on vascular Rho/Rho-kinase pathway mediated contraction, which has been shown to be upregulated in hypertension. 2. Contribution of the Rho/Rho-kinase pathway to noradrenaline-induced contraction of arteries from SHRSP was assessed by the inhibitory effect of Y-27632, a Rho/Rho-kinase inhibitor. Stroke-prone spontaneously hypertensive rats were treated with fluvastatin (10 mg/kg per day) for 1 month. 3. Treatment with fluvastatin tended to attenuate the contraction to noradrenaline and significantly decreased the Y-27632-sensitive component of the contraction in controls compared with fluvastatin-treated rats. 4. RhoA, as assessed by western blotting, was also reduced by fluvastatin treatment. 5. These findings suggest that chronic treatment with fluvastatin reduces the contractile response associated with Rho/Rho-kinase in arteries of hypertensive rats.
    Clinical and Experimental Pharmacology and Physiology 09/2006; 33(8):673-8. · 2.41 Impact Factor
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    ABSTRACT: The aim of the present study was to determine whether sex differences contribute to the association of serum uric acid and left ventricular hypertrophy in individuals with hypertension. Seventy participants with essential hypertension (34 men, 36 women; 54.4 +/- 1.6 years old) were enrolled to undergo echocardiography to calculate the left ventricular mass index (LVMI). Twenty-four-hour ambulatory blood pressure monitoring was done to assess blood pressure level precisely. The LVMI was significantly correlated with serum uric acid (r = 0.295, p = 0.013) in all participants. After controlling for factors such as age, sex, mean 24-h systolic blood pressure, creatinine clearance, and duration of hypertension, serum uric acid was still found to be significantly and independently associated with LVMI. Because serum uric acid was significantly higher in men than in women (6.8 +/- 0.3 and 5.1 +/- 0.2 mg/dl, respectively), subsequent analysis was performed by gender. Multiple regression analysis revealed that the LVMI was significantly and independently associated with serum uric acid in women, but not in men. The potential effect of uric acid on LV hypertrophy is more pronounced in female than in males with essential hypertension.
    Circulation Journal 08/2006; 70(7):885-8. · 3.58 Impact Factor
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    ABSTRACT: Diabetes mellitus is an important risk factor for cardiovascular diseases, and vasodilator dysfunction may contribute to vascular complications in diabetes. We previously demonstrated that the angiotensin II receptor blocker (ARB) corrected the impaired endothelium-derived hyperpolarizing factor (EDHF)-mediated arterial hyperpolarization and relaxation associated with hypertension or aging, partially independently of blood pressure. To test whether EDHF-mediated, as well as endothelium-independent, relaxations would be altered in arteries from type II diabetic Goto-Kakizaki rats, and whether ARB would correct these alterations. Goto-Kakizaki rats were treated with either the ARB candesartan or a combination of hydralazine and hydrochlorothiazide for 8 weeks, beginning at 10 weeks of age. Membrane potentials and contractile responses were recorded from the isolated mesenteric arteries. The two treatments lowered blood pressure comparably. Acetylcholine-induced, EDHF-mediated hyperpolarization and relaxation in mesenteric arteries were markedly impaired in untreated Goto-Kakizaki rats compared with age-matched Wistar rats, and neither ARB nor the combination therapy improved these responses. On the other hand, relaxations to endothelium-derived nitric oxide, assessed in rings precontracted with high potassium solution, were similar among the four groups. Relaxation to the nitric oxide donor sodium nitroprusside and that to levcromakalim, an ATP-sensitive K-channel opener, were also impaired in untreated Goto-Kakizaki rats, and the response to sodium nitroprusside was partially improved in treated Goto-Kakizaki rats. These findings suggest that EDHF-mediated hyperpolarization and relaxation and endothelium-independent relaxations are both impaired in arteries of type II diabetic rats, and antihypertensive treatment with or without ARB partially corrects endothelium-independent relaxations to the nitric oxide donor but not EDHF-mediated responses.
    Journal of Hypertension 03/2006; 24(2):331-8. · 4.22 Impact Factor
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    ABSTRACT: Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patients. A total of 25 patients with primary aldosteronism caused by Conn's adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects. The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 +/- 7.7, 142.3 +/- 7.2, and 115.2 +/- 7.2 g/m(2), respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism. These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage.
    American Journal of Hypertension 02/2006; 19(1):13-8. · 3.67 Impact Factor
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    ABSTRACT: Blockade of the renin-angiotensin system improves the impaired endothelium-dependent relaxations associated with hypertension and aging, partly through amelioration of endothelium-derived hyperpolarizing factor (EDHF)-mediated responses. Although the nature of EDHF is still controversial, recent studies have suggested the involvement of gap junctions in EDHF-mediated responses. Gap junctions consist of connexins (Cx), and we therefore tested whether the expression of Cx in vascular endothelial cells would be altered by hypertension and antihypertensive treatment. Spontaneously hypertensive rats (SHR) were treated with either the angiotensin II type 1 receptor antagonist candesartan or the combination of hydralazine and hydrochlorothiazide for 3 mo from 5 to 8 mo of age. Confocal laser scanning microscopy after immunofluorescent labeling with antibodies against Cx37, Cx40, and Cx43 revealed that the expression of Cx37 and Cx40 in endothelial cells of the mesenteric artery was significantly lower in SHR than in WKY. Treatment with candesartan, but not the combination of hydralazine and hydrochlorothiazide, significantly increased the expression of Cx37 and Cx40, although blood pressure decreased similarly. On the other hand, the expression of Cx43, though scarce and heterogeneous, was increased in SHR compared with WKY, and candesartan treatment lowered the expression of Cx43. These findings suggest that renin-angiotensin system blockade corrects the decreased expression of Cx37 and Cx40 in arterial endothelial cells of hypertensive rats, partly independently of blood pressure, whereas the expression of Cx43 changed in the opposite direction. It remains to be clarified whether these changes in Cx37 and Cx40 are related to endothelial function, particularly that attributable to EDHF.
    AJP Heart and Circulatory Physiology 08/2004; 287(1):H216-24. · 4.01 Impact Factor

Publication Stats

137 Citations
36.32 Total Impact Points

Institutions

  • 2013
    • National Cerebral and Cardiovascular Center
      Ōsaka, Ōsaka, Japan
  • 2004–2013
    • Kyushu University
      • • Graduate School of Medical Sciences
      • • Department of Clinical Medicine
      Fukuoka-shi, Fukuoka-ken, Japan
  • 2012
    • Kyushu Medical Center
      Hukuoka, Fukuoka, Japan
    • Fukuoka Dental College
      Hukuoka, Fukuoka, Japan