Seitaro Maruyama

Niigata University, Niahi-niigata, Niigata, Japan

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Publications (10)23.54 Total impact

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    ABSTRACT: We report a case of Graves' disease in a patient on regular hemodialysis. The patient also suffered from Wolff-Parkinson-White (WPW) syndrome and paroxysmal atrial fibrillation, which may both have been manifestations of the Graves' disease because of the increased oxygen demand. To our knowledge, this is the first case to illustrate the usefulness of the antithyroid agent propylthiouracil for Graves' disease complicated by endstage renal disease (ESRD) and WPW syndrome.
    Clinical and Experimental Nephrology 04/2004; 8(1):71-4. · 1.25 Impact Factor
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    ABSTRACT: The beta(2)-adrenergic receptor (B2AR) is expressed in pancreatic beta-cells and modulates insulin secretion. The purpose of the present study was to evaluate the influence of the Arg16Gly variant allele of B2AR on insulin secretion in patients with type 2 diabetes. We used minimal model analysis of the frequently sampled insulin-modified intravenous glucose tolerance test (FSIGT) and polymerase chain reaction (PCR)-restriction fragment length polymorphism to examine differences of insulin secretion and insulin resistance among three genotypes. There were no significant differences in baseline clinical characteristics, HbA1c, uric acid, CRP or lipid profiles among the three groups. The Gly/Gly group had significantly higher levels of fasting insulin (38.2+/-4.7 pmol/l versus 23.6+/-3.5 pmol/l) and homeostasis model assessment of insulin resistance (HOMA-R) (1.90+/-0.19 versus 1.32+/-0.24), compared with the Arg/Arg group, but there were no significant differences in acute insulin response to glucose (AIRg) bolus, insulin sensitivity (Si), or glucose effectiveness (Sg) among the three genotypes. Several reports have speculated that the Gly16 allele of B2AR exhibits agonist-promoted downregulation, but our findings, elevated fasting insulin concentrations, and previous clinical studies of blood pressure and lypolysis are controversial. The direct mechanism by which the Gly16 allele of B2AR may influence insulin secretion of pancreatic beta-cells is unknown. Further studies of the expression of the allelic receptor in islet cells may help to resolve the role of B2AR in insulin secretion. However, increased sensitivity to catecholamine-induced lipolysis of the Gly allele promotes higher free fatty acids concentrations in the portal system, which could enhance the higher levels of fasting insulin.
    Diabetes Research and Clinical Practice 02/2004; 63(1):11-8. · 2.74 Impact Factor
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    ABSTRACT: Postextrasystolic potentiation is the phenomenon in which ventricular contractile force is strengthened by a preceding premature beat. However, the response of diastolic function after an extrasystole is unknown. We studied 58 patients with chronic heart failure (CHF) and two control subjects to evaluate the response of relaxation following extrasystole. At cardiac catheterization, from the derivative of the left ventricular (LV) pressure, the ratio of LV peak negative dP/dt (-dP/dt) of a postextrasystole to a basal beat was calculated and defined as the postextrasystolic relaxation response (PRR). PRR was compared with parameters of left ventriculography: LV end-diastolic volume index (EDVI), LV end-systolic volume index (ESVI), and LV ejection fraction (EF). The PRRs of the two control subjects were 0.80 and 0.84. The mean PRR of the CHF patients was 0.99 +/- 0.15. In all subjects, including patients and controls, correlation analysis between (EDVI, ESVI, and EF) and PRR yielded the following: (a) EDVI vs. PRR: R = 0.273, p = 0.036; (b) ESVI vs. PRR: R = 0.446, p < 0.001; and (c) EF vs. PRR: R = -0.520, p < 0.001. Thus, normal or non-failing human hearts showed a decline of -dP/dt in postextrasystole compared with the basal beats, but failing hearts had potentiated relaxation following an extrasystole.
    Molecular and Cellular Biochemistry 09/2003; 251(1-2):43-6. · 2.33 Impact Factor
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    ABSTRACT: Experimental autoimmune myocarditis (EAM) induced in rats by injection of cardiac myosin is an animal model of human myocarditis and post-myocarditis dilated cardiomyopathy. It has been reported that proinflammatory cytokines play crucial roles in the induction of EAM and in the progression of myocardial injury in this disease. FR167653 (1-[7-(4-fluorophenyl)-1,2,3,4-tetrahydro-8-(4-pyridyl) pyrazolo [5,1-c] [1,2,4] triazin-2-yl]-2-phenylethanedione sulfate monohydrate) as been reported to suppress tumor necrosis factor-alpha (TNF-alpha). We hypothesized that FR167653 would suppress the progression of EAM if TNF-alpha and/or interleukin-1 beta (IL-1beta) were the culprit cytokines in EAM. To investigate the effects of FR167653 in EAM, FR167653 was given to rats for 4 weeks, immediately after they had been immunized with cardiac myosin. The ratio of heart weight to body weight and the area of inflammatory lesions were less in the FR167653 groups than in the control rats. FR167653 reduced serum sialic acid levels significantly. The control group showed a deterioration in cardiac function. The FR167653 groups had significantly better hemodynamic parameters, including improved left ventricular end-diastolic pressure, central venous pressure, aortic pressure, and positive and negative left ventricular pressure derivatives. mRNA expression of IL-1beta in the heart was significantly lower in rats given FR167653. However, mRNA of TNF-alpha was not detected in any groups. Our results suggest that FR167653 suppresses the development of myocarditis by suppression of IL-1beta.
    Molecular and Cellular Biochemistry 05/2003; 246(1-2):39-44. · 2.33 Impact Factor
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    ABSTRACT: Genetic responses that characterize experimental autoimmune myocarditis (EAM) have not yet been determined. To investigate gene expression in the myocardium of EAM, absolute copy numbers of 44 mRNA species [calcium-handling proteins, contractile proteins, natriuretic peptides (NPs), cytokines, chemokines, growth factors, renin-angiotensin-aldosterone (RAA) system, endothelins (ETs) and extracellular matrix] in synthesized cDNA from a fixed quantity of total heart RNA were assessed using real-time reverse-transcriptase PCR at days 0, 14, 21 and 28 after immunization. alpha-Cardiac myosin showed a 26.3-fold decrease and beta-cardiac myosin a 3.75-fold increase at day 14. Atrial NP and brain NP increased 47.7- and 6.35-fold at days 21 and 14 respectively. Angiotensin II type 1 receptor, angiotensin-converting enzyme and ET1 increased 22.3-fold at day 21, 6.30-fold at day 21 and 16.8-fold at day 14 respectively. Aldosterone receptor decreased 2.15-fold at day 14, but aldosterone synthetase was detected only at days 14 and 21. Interleukin (IL)-2, IL-10, interferon-gamma and monocyte chemo-attractant protein-1 increased 9.08-fold at day 14, 398-fold at day 21, 43.1-fold at day 14 and 142-fold at day 14 respectively. Collagen type 3, collagen type 1 and fibronectin increased 34.6-, 1.74- and 44.4-fold respectively at day 21. Interestingly, osteopontin showed a 4540-fold increase and it was the highest mRNA of all at day 14. An isoform of cardiac myosin and NP are dramatically changed in EAM. RAA system and ET expressions are changed differently during the EAM time course. Cytokine, chemokine and extracellular matrix greatly increase and, in particular, large numbers of osteopontin mRNA are expressed in early EAM.
    Clinical Science 01/2003; 103(6):623-32. · 4.86 Impact Factor
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    ABSTRACT: Brain-derived neurotrophic factor (BDNF) reduces plasma glucose levels in obese db/db diabetic mice and is speculated to produce its effects via the hypothalamus, the regulatory centre of satiety and the autonomic nervous system. The potential effect of BDNF directly on peripheral endocrine organs, however, remains to be clarified. Here we report the effects of BDNF on hormonal secretion from pancreatic islets of Langerhans using their isolated culture. In an immunohistochemical study, mouse pancreatic alpha cells were stained specifically with the anti-TrkB (a specific receptor for BDNF) antibody. After 7 days culture of isolated islets of the normal mouse pancreas, 10 ng/ml BDNF decreased the secretion of glucagon per 6 h significantly less than that of the control (p = 0.016). In contrast, there were no significant changes in insulin secretion or glucagon and insulin contents in the islets cultured under the same conditions. In vivo administration of BDNF (10 mg/kg/day) to normal mice for 7 days significantly decreased their food consumption (p < 0.05). The fasting plasma glucose levels were decreased on day 7 compared with day 1 more significantly in BDNF-treated mice (p = 0.043) than in pair-fed control mice (p = 0.14). In newborn BDNF-knockout mice, fasting plasma glucose levels increased in the order of homozygote, heterozygote and wild type (p = 0.033). No apparent immunohistochemical abnormality was observed for pancreatic glucagon in the BDNF-knockout mice. These data suggest that BDNF affects glucose metabolism not only with its anorectic effect but also with modulated glucagon secretion from pancreatic alpha cells.
    Diabetes Obesity and Metabolism 01/2003; 5(1):27-37. · 5.18 Impact Factor
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    ABSTRACT: Homogenous assays for LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) are highly accurate, with little interference from triglyceride. Using these methods, we measured postprandial LDL-C and HDL-C. Earlier studies suggested a postprandial decrease in LDL-C. To elucidate whether LDL-C and HDL-C decrease significantly during the day, we determined daily profiles of LDL-C and HDL-C using homogeneous assays in subjects with normal coronary arteries (N; n=10), and subjects with coronary artery disease (CAD; n=23). In both groups, LDL-C and HDL-C were significantly lower from after breakfast until midnight than they were before breakfast. The next morning, they returned to baseline levels. The mean reduction in LDL-C was 0.09-0.13 mmol/L in N and 0.05-0.20 mmol/L in CAD, while that in HDL-C was 0.02-0.06 mmol/L in N and 0.00-0.05 mmol/L in CAD. LDL-C and HDL-C decrease significantly over the course of the day.
    Annals of Clinical Biochemistry 06/2002; 39(Pt 3):241-9. · 1.92 Impact Factor
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    ABSTRACT: Experimental autoimmune myocarditis (EAM) in rats is an animal model of human giant cell myocarditis and postmyocarditis dilated cardiomyopathy. As the heart consumes large amounts of energy, heart diseases such as myocarditis and dilated cardiomyopathy are associated with abnormal fatty acid metabolism. Peroxisome proliferator-activated receptor alpha (PPARalpha) is a regulator of the oxidative degradation of fatty acids. To investigate the role of PPARalpha in EAM, fenofibrate (a PPARalpha activator) was administered to rats with EAM for 4 weeks. Reductions in the ratios of both ventricular weight to body weight and the area of inflammatory lesions to the total area of heart sections were observed in fenofibrate-treated rats when compared with controls. Fenofibrate ameliorated changes in serum albumin and sialic acid, which are markers of inflammation. Cardiac expression of interleukin-10 (IL-10) mRNA was more pronounced in the fenofibrate group than in the control group (1.3 +/- 0.2 vs 0.7 +/- 0.1; p < 0.01), and the area of intact myocardium correlated with the IL-10 mRNA level (p = 0.0297, r = 0.620). We suggest that PPARalpha activators may prevent the progression of myocarditis through increased expression of the gene encoding the anti-inflammatory cytokine IL-10, although the mechanisms involved remain to be determined.
    Journal of atherosclerosis and thrombosis 01/2002; 9(2):87-92. · 2.93 Impact Factor
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    ABSTRACT: Dual-chamber (DDD) pacing is a therapeutic strategy for hypertrophic obstructive cardiomyopathy (HOCM), but some patients show deterioration after implantation of the DDD pacemaker. We report a case of HOCM with shortness of breath upon physical exertion. To evaluate the suitability of pacing therapy, the acute effects of DDD pacing and short-term results using temporary VDD pacing were examined. The acute study demonstrated a mild reduction in the pressure gradient within the left ventricle. After 1 week of VDD pacing, a left ventriculography showed apical dyskinesis, with no effect on subjective symptoms or the blood concentration of brain natriuretic peptide (BNP) observed. Newly developed asynergy may be caused by changes in the contractile pattern. The patient underwent a myotomy-myectomy. After the operation, her subjective symptoms disappeared, and the hemodynamic parameters and blood concentration of BNP improved compared with those before the operation. The response to 1-week temporary VDD pacing can provide valuable data such as hemodynamics and neurohormonal changes in distinguishing between responders and nonresponders for pacing therapy.
    01/2001;
  • Journal of Cardiac Failure - J CARD FAIL. 01/1999; 5(3):44-44.