基本情報
研究キーワード
4研究分野
1委員歴
5-
2012年 - 2014年
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2014年
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2014年
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2014年
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2012年
受賞
7-
2010年3月
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2009年5月
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2006年11月
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2002年7月
論文
965-
Journal of the American Heart Association 14(2) e034627 2025年1月21日BACKGROUND: The effect of worsening renal function and baseline chronic kidney disease (CKD) on outcomes in patients with chronic coronary syndrome in the setting of optimal medical therapy remains unknown. METHODS AND RESULTS: The REAL-CAD (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy With Pitavastatin in Coronary Artery Disease) study is a prospective, multicenter, randomized trial of high-dose (pitavastatin 4 mg/day) or low-dose (pitavastatin 1 mg/day) statin therapy in 12 118 patients with chronic coronary syndrome. The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, stroke, or unstable angina requiring hospitalization (major adverse cardiac and cerebral events [MACCE]). CKD was defined as an estimated glomerular filtration rate [eGFR] <60 mL/min per 1.73 m2. WRF was defined as a decrease in eGFR ≥20% in the initial year; borderline renal function was an annual decrease of 0%<eGFR<20%, and stable renal function was no decrease. Of 12 118 patients, 4340 had baseline CKD and 7778 did not. The rate of MACCE at 5 years was significantly lower in those without (5.5%) versus with CKD (9.5%) (P<0.0001). After excluding 1247 patients who had MACCE, were censored, or missing eGFR within 1 year, 10 871 patients were included. Of these, 3885 were baseline CKD and the remaining 6986 did not have baseline CKD. Of the 10 871 patients, 577 patients had WRF, 6014 patients showed borderline renal function, and the remaining 4280 patients maintained stable renal function. In patients with CKD, WRF was an independent predictor for MACCE at 4 years as compared with stable renal function (hazard ratio [HR]: 1.67; [95% CI, 1.03-2.73; P=0.039]). In patients without CKD, borderline renal function was a significant predictor for MACCE at 4 years compared with stable renal function (HR: 1.40 [95% CI, 1.03-1.91; P=0.032]). CONCLUSIONS: Baseline CKD was an independent predictor for MACCE in patients with CCS. WRF was a significant predictor for MACCE in patients with CKD. Because borderline renal function was an independent predictor for MACCE even in patients without CKD, mild-to-moderate annual declines of eGFR should be carefully monitored (NCT01042730). REGISTRATION: URL: https://www.clinicaltrials.gov; Unique Identifier: NCT01042730.
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International Journal of Molecular Sciences 26(2) 556-556 2025年1月10日 査読有り
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IJC Heart & Vasculature 54 101507-101507 2024年10月
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Hypertension research : official journal of the Japanese Society of Hypertension 2024年9月19日The Japanese Society of Hypertension have established a blood pressure (BP) target of 130/80 mmHg for patients with coronary artery disease (CAD). We evaluated the data of 8793 CAD patients in the Clinical Deep Data Accumulation System database who underwent cardiac catheterization at six university hospitals and the National Cerebral and Cardiovascular Center (average age 70 ± 11 years, 78% male, 43% with acute coronary syndrome [ACS]). Patients were divided into two groups based on whether or not they achieved the guideline-recommended BP of <130/80 mmHg. We analyzed the relationship between BP classification and major adverse cardiac and cerebral event (MACCE) separately in two groups: those with ACS and those with chronic coronary syndrome (CCS). During an average follow-up period of 33 months, 710 MACCEs occurred. A BP below 130/80 mmHg was associated with fewer MACCEs in both the overall (hazard ratio [HR] 0.83, 95% confidence interval [CI] 0.70-1.00, p = 0.048) and the ACS group (HR 0.67, 95%CI 0.51-0.88, p = 0.003). In particular, stroke events were also lower among those with a BP below 130/80 mmHg in both the overall (HR 0.69, 95%CI 0.53-0.90, p = 0.006) and ACS groups (HR 0.44, 95%CI 0.30-0.67, p < 0.001). In conclusion, the achievement of BP guidelines was associated with improved outcomes in CAD patients, particularly in reducing stroke risk among those with ACS.
MISC
1923-
Circulation research 65(3) 684-94 1989年9月 査読有りThe effects of early coronary artery reperfusion on the relation between the extent of myocardial infarction and serum levels of cardiac myosin light chain II or plasma creatine kinase levels were evaluated in the conscious dog. Hydraulic occluders were placed on the left anterior descending arteries of 38 dogs. Seven to 10 days later, myocardial infarction was produced. Coronary reperfusion was performed 3 hours (group A1, n = 13) and 6 hours (group A2, n = 12) after the occlusion. In the other 13 dogs, coronary occlusion was sustained throughout the course of the experiment (group B). Seven days after the occlusion, the heart was cut from the apex to the base into 4-mm slices, and infarct size was determined macroscopically. Rapid appearance and early peaking of creatine kinase were observed in group A. Cumulative release of creatine kinase significantly correlated with infarct size in group A (infarct size ranged from 0.1 to 20.1 g, r = 0.90) and group B (from 0.6 to 26.8 g, r = 0.91). However, since creatine kinase release in group A was greater in comparison with that from infarcts of the same size in group B, the slope of the regression line for group A was significantly steeper (p less than 0.05). Cardiac myosin light chain II appeared as early as creatine kinase did and continued to be elevated for 7 days. A very close relation was observed between infarct size and total cardiac myosin light chain II release (r = 0.87 for group A, and r = 0.88 for group B) or peak level of light chain II (r = 0.85 for group A, and r = 0.81 for group B). In addition, the slopes of the regression lines for infarct size and both peak and total release of light chain II did not differ between group A and group B. On histological examination, viable myocardium was frequently observed in the epicardium of the ischemic area in group A1; therefore, infarct size was greater in group B than in group A1 (p less than 0.05). Also, myocardial creatine kinase content in the epicardium of the center of the ischemic area in group A1 was greater than that in group B. Cardiac myosin light chain II release in group A1 was less than that in group B, whereas no difference was found in plasma creatine kinase release among groups A1, A2, and B.(ABSTRACT TRUNCATED AT 250 WORDS)
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Japanese circulation journal 53(8) 903-903 1989年8月20日
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Japanese circulation journal 53(8) 903-904 1989年8月20日
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Japanese circulation journal 53(6) 522-522 1989年6月20日
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The Journal of biological chemistry 264(17) 9734-7 1989年6月15日 査読有りWe previously reported the characterization of a rabbit uterus cDNA clone (SMHC29) which encoded part of the light meromyosin of smooth muscle myosin heavy chain (Nagai, R., Larson, D.M., and Periasamy, M. (1988) Proc. Natl. Acad. Sci. U. S. A. 85, 1047-1051). We have now characterized a second cDNA clone (SMHC40) which also encodes part of the light meromyosin but differs from SMHC29 in the following respects. Nucleotide sequence analysis demonstrates that the two myosin heavy chain mRNAs are identical over 1424 nucleotides but differ in part of the 3'-carboxyl coding region and a portion of the 3'-nontranslated sequence. Specifically, SMHC40 cDNA encodes a unique stretch of 43 amino acids at the carboxyl terminus, whereas SMHC29 cDNA contains a shorter carboxyl terminus of 9 unique amino acids which is the result of a 39-nucleotide insertion. Recent peptide mapping of smooth muscle myosin heavy chain identified two isotypes with differences in the light meromyosin fragment that were designated as SM1 (204 kDa) and SM2 (200 kDa) type myosin (Eddinger, T. J., and Murphy, R.A. (1988) Biochemistry 27, 3807-3811). In this study we present direct evidence that SMHC40 and SMHC29 mRNA encode the two smooth muscle myosin heavy chain isoforms, SM1 and SM2, respectively, by immunoblot analysis using antibodies against specific carboxyl terminus sequences deduced from SMHC40 and SMHC29 cDNA clones.
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Proceedings of the National Academy of Sciences of the United States of America 86(8) 2966-70 1989年4月 査読有りThe sarcoplasmic reticulum (SR) and the contractile protein myosin play an important role in myocardial performance. Both of these systems exhibit plasticity--i.e., quantitative and/or qualitative reorganization during development and in response to stress. Recent studies indicate that SR Ca2+ uptake function is altered in adaptive cardiac hypertrophy and failure. The molecular basis (genetic and phenotypic) for these changes is not understood. In an effort to determine the underlying causes of these changes, we characterized the rabbit cardiac Ca2+-ATPase phenotype by molecular cloning and ribonuclease A mapping analysis. Our results show that the heart muscle expresses only the slow-twitch SR Ca2+-ATPase isoform. Second, we quantitated the steady-state mRNA levels of two major SR Ca2+ regulatory proteins, the Ca2+-ATPase and phospholamban, to see whether changes in mRNA content might provide insight into the basis for functional modification in the SR of hypertrophied hearts. In response to pressure overload hypertrophy, the relative level of the slow-twitch/cardiac SR Ca2+-ATPase mRNA was decreased to 34% of control at 1 week. The relative Ca2+-ATPase mRNA level increased to 167% of control after 3 days of treatment with thyroid hormone. In contrast, in hypothyroid animals, the relative Ca2+-ATPase mRNA level decreased to 51% of control at 2 weeks. The relative level of phospholamban mRNA was decreased to 36% in 1-week pressure overload. Hyperthyroidism induced a decrease to 61% in the phospholamban mRNA level after 3 days of treatment, while hypothyroidism had virtually no effect on phospholamban mRNA levels. These data indicate that the expression of SR Ca2+-ATPase and phospholamban mRNA may not be coordinately regulated during myocardial adaptation to different physiological conditions.
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The British journal of radiology 62(734) 189-91 1989年2月 査読有り
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Basic research in cardiology 84 Suppl 1 55-66 1989年 査読有りSome aspects of the genetic and non-genetic control of the amount and rate of calcium cycled during steady-state activation of papillary muscles from right ventricular rabbit myocardium are presented. Genetic reorganization of the intracellular structure of the myocardium is achieved by producing right ventricular pressure overload and thyrotoxic hypertrophy. The mechanical performance of the pressure overload heart is slowed while time to peak tension is increased. These changes are associated with an increase in myothermal economy. In thyrotoxic hypertrophy the rate of mechanical performance is increased while time to peak tension is decreased. These alterations are associated with a decrease in myothermal economy. Tension-independent heat is used as an index of calcium cycling. In pressure overload hearts the amount and rate of calcium cycling is decreased. In contrast in thyrotoxic hypertrophy the amount of calcium cycled is unchanged while the rate is increased. In the pressure overload hearts there is a decrease in sarcoplasmic reticular (SR) Ca++ ATPase, whereas in the thyrotoxic preparations the message is increased. The change in the rate of calcium uptake in pressure overload and thyrotoxic hearts is correlated with a change in the amount of SR Ca++ ATPase mRNA. Calcium cycling was also altered by non-genetic inotropic intervention. Isoproterenol (1 microM) increases the amount of calcium cycled during each contraction relaxation cycle and the rate at which it is removed. These alterations are associated with an increase in force and a foreshortened twitch. Incubating the papillary muscle in high calcium (11 mM) also increases the force and the amount of calcium released into the cytosol. Under these circumstances the rate of uptake is not significantly increased and, accordingly, the isometric twitch is not foreshortened. In the presence of verapamil (14 microM) the peak twitch force is decreased and the isometric myogram is foreshortened. These changes are associated with a decrease in the amount of calcium released during activation and the rate at which it is removed.
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Journal of cardiovascular pharmacology 13 Suppl 5 S132-7; discussion S142-S137 1989年 査読有りWe investigated the in vivo vasoconstrictor effects of endothelin-1 (ET-1) on canine coronary arteries and the regulation of ET-1 gene expression with special reference to the pathogenesis of coronary vasospasm. ET-1, administered into the coronary arteries of anesthetized dogs, produced a profound and long-lasting reduction in coronary blood flow with myocardial ischemia. Coronary angiography revealed delayed filling of the distal branches and, in some cases, total occlusion in the epicardial portions of coronary arteries. The coronary vasoconstriction induced by ET-1 subsided after intracoronary administration of nitroglycerin. Pretreatment with the Ca2+-channel antagonist, nitrendipine, suppressed ET-1-induced vasoconstriction. In cultured porcine aortic endothelial cells, ET-1 gene expression was induced by agents related to thrombus formation, such as thrombin and transforming growth factor beta (TGF beta). These findings suggest that ET-1, produced by vascular endothelial cells, may contribute to the regulation of coronary circulation and the pathogenesis of coronary vasospasm with respect to intimal injury and subsequent thrombus formation.
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Life sciences 44(25) 1937-43 1989年 査読有りEndothelin, administered into the coronary arteries of anesthetized dogs, produced a profound and long-lasting reduction in coronary blood flow with electrocardiographical evidence of myocardial ischemia. Coronary angiography revealed delayed filling of the distal branches and, in some cases, cessation of the blood flow distal to the epicardial portions of coronary arteries. The coronary vasoconstriction induced by endothelin subsided after intracoronary administration of nitroglycerin. Pretreatment with the Ca2+-channel antagonist, nitrendipine, suppressed endothelin-induced vasoconstriction. These findings suggest that endothelin, produced by vascular endothelial cells, may contribute to the pathogenesis of coronary vasospasm.
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Proceedings of the National Academy of Sciences of the United States of America 85(4) 1047-51 1988年2月 査読有りA cDNA clone, SMHC-29, encoding the light meromyosin of smooth muscle myosin heavy chain (MHC), was isolated from a rabbit uterus cDNA library constructed in phage lambda gt11. This smooth muscle MHC cDNA demonstrates significant nucleotide and amino acid sequence homologies with known sarcomeric MHC genes from rabbit, rat skeletal, and nematode body wall myosin, and even with nonmuscle MHC gene from a slime mold (Dictyostelium discoideum), suggesting that smooth muscle, striated muscle, and nonmuscle MHC genes diverged from a common ancestor. The deduced amino acid sequences of the smooth muscle light meromyosin show very similar periodic distributions of hydrophobic and charged residues as found for the light meromyosin of striated muscle MHCs together with a high potential for alpha-helical formation, indicating an alpha-helical coiled-coil structure for the smooth muscle light meromyosin sequences. Furthermore, S1 nuclease mapping has revealed that this smooth muscle MHC gene for SMHC-29 is specifically expressed in smooth muscles of vascular and nonvascular types but not in the striated muscles or nonmuscle cells.
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Am. J. Physiol. 255 325-328 1988年
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Circulation 76(6) 1251-61 1987年12月 査読有りTo estimate the extent of myocardial infarction after coronary artery reperfusion, serum levels of cardiac myosin light chain (LC) I and creatine kinase (CK) were determined serially in 49 patients with acute myocardial infarction. Intracoronary thrombolysis was successful in 25 patients (reperfusion group), and 24 patients were treated in a conventional manner (control group). The peak level of CK appeared significantly earlier in the reperfusion group (11.3 +/- 3.1 hr, mean +/- SD) than in the control group (21.6 +/- 7.2 hr). Cumulative release of CK was significantly related to angiographically determined left ventricular ejection fraction 1 month after the attack in both groups (r = -.50; -.45, respectively). However, the amount of cumulative release of CK in the reperfusion group was greater compared with that in those with the same left ventricular ejection fraction in the control group. Peak appearance time of LCI was almost equal in the two groups (3.8 +/- 1.4 vs 3.9 +/- 1.2 days). Peak levels of LCI were related to the left ventricular ejection fraction in the reperfusion group (r = -.63) and in the control group (r = -.74), and the slopes of their regression lines were similar. The cardiac index obtained on the day of onset in the two groups was related to peak levels of LCI but not to total release of CK. These results suggest that serum levels of LCI reflect the changes in left ventricular function after acute myocardial infarction, regardless of the presence of coronary reperfusion. Thus, serial determinations of LCI in serum facilitate noninvasive assessment of the effects of intracoronary thrombolysis on infarct size.
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Circulation research 60(5) 692-9 1987年5月 査読有りThe in vivo synthesis rates of myosin isozyme heavy chains beta and alpha were measured in right ventricular (RV) muscle at 2 and 4 days following pulmonary artery constriction in rabbits, together with measurements of their relative mRNA levels. The synthesis rate of beta-myosin heavy chains was elevated in 2-day (0.27 +/- 0.06 day-1 or 2.5 +/- 0.7 mg/g RV/day, mean +/- SD) and in 4-day (0.25 +/- 0.08 day-1 or 2.8 +/- 1.0 mg/g RV/day) pressure overload, when compared to untreated rabbits (0.15 +/- 0.04 day-1 or 1.5 +/- 0.4 mg/g RV/day). However, the synthesis rates of alpha-myosin heavy chains in the same hearts were not altered significantly. There was a differential increase in the fractional synthesis rate of beta vs. alpha heavy chains in 2-day and 4-day pressure overload and in 2-day shams, suggesting switching toward beta heavy chain synthesis had occurred at these time points. beta heavy chain synthesis, as a proportion of total (alpha + beta) heavy chain synthesis, was significantly higher in 4-day pressure overload (78 +/- 9%) than in 4-day sham rabbits (63 +/- 6%). This increase in relative beta-synthesis was associated with a significant increase in the relative proportion of beta heavy chain mRNA level (76 +/- 13% vs. 56 +/- 7%). Furthermore, relative beta-synthesis and the beta-mRNA levels correlated linearly with each other in all experimental groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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FEDERATION PROCEEDINGS 46(4) 1404-1404 1987年3月
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JAPANESE JOURNAL OF PHARMACOLOGY 43 P15-P15 1987年
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CIRCULATION 74(4) 260-260 1986年10月
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 50(6) 469-469 1986年6月
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 50(6) 549-549 1986年6月
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FEDERATION PROCEEDINGS 45(4) 774-774 1986年3月
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Circulation research 57(3) 406-14 1985年9月 査読有りA detailed study was carried out to measure the relative contents of V1 and V3 myosin isozymes in different regions of rabbit ventricle as a function of age, to assess animal-to-animal variability, and to compare different experimental approaches aimed at minimizing the effects of such variability. In addition, comparisons were made in normal developing hearts between ventricular isozyme composition and myofibrillar myosin calcium-stimulated adenosine triphosphatase. V1 isozyme predominated relative to V3 isozyme in the hearts of 2-week-old rabbits, decreasing to become a minor component in 10-week-old animals. Despite this trend, there was considerable variability in relative isozyme content of whole ventricular tissue among different rabbits of the same age. This variability was reduced in comparisons of littermates and by use of cardiac biopsies to measure changes in isozyme content in the same animal over time. Within different regions of a given heart, there also were small but significant differences in the percent V1 isozyme. The percent V1 was greatest for right ventricular papillary, followed by right ventricular free wall and then the left ventricle (free wall plus septum). There also were differences in the percent V1 within those regions, as exemplified by the significantly higher values for ventricular epicardium vs. endocardium. There was a linear correlation between the myofibrillar myosin calcium-stimulated adenosine triphosphatase and percent V1 of total isozyme for both right and left ventricles in normal and developing hearts. The regression lines for calcium-stimulated adenosine triphosphatase vs. percent V1 had a steeper slope in the left than in the right ventricle.
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Japanese circulation journal 49(7) 733-9 1985年7月 査読有りWe have developed anticardiac myosin antibodies, especially monoclonal antibodies, for helping in the diagnosis of heart disease. Our investigations were divided into three research projects. We visualized the distribution of myosin isozymes in human atrial and ventricular myocardium by an immunofluorescence staining method using monoclonal antibodies specific for individual human cardiac myosin isozymes. We also revealed the redistribution of these cardiac myosin isozymes in an overloaded condition. The isozymic pattern of cardiac myosin was changed from the atrial type to the ventricular type in the overloaded atrium. This isozymic redistribution can be considered as physiological adaptive mechanism to meet increased cardiac work during overload. We developed a new method of imaging for myocardial infarction by single photon emission tomography using labelled monoclonal antibody specific for cardiac myosin heavy chain. Specific localization of the labelled antibody was demonstrated in the infarcted area and no accumulation of radioactivity was shown in the bone matrix as observed in 99mTc pyrophosphate images. We developed a sensitive radioimmunoassay of cardiac myosin light chain I (LCI) and demonstrated that peak serum levels of LCI in the patients with acute myocardial infarction correlated well with the left ventricular ejection fraction. Furthermore, LCI release from the infarcted myocardium was not affected by coronary reperfusion due to intracoronary thrombolysis. Thus, serial determinations of serum LCI better quantify the extent of myocardial damage even after coronary reperfusion in acute myocardial infarction.
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Japanese circulation journal 49 168-168 1985年3月1日
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 49(8) 777-777 1985年
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CIRCULATION 72(4) 88-88 1985年
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 49(8) 870-870 1985年
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JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 17 73-73 1985年
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European heart journal 5 Suppl F 103-10 1984年12月 査読有りWe have prepared monoclonal antibodies specific for either atrial or ventricular myosin and defined the isomyosin composition of myocardium in normal and overloaded human hearts. In the atrial myocardium, normal isozymic pattern was V1 dominant which converted to being V3 dominant in an overloaded condition. In contrast, normal isomyosin pattern of the ventricular myocardium was exclusively V3 dominant, and only a small change in the proportion of isomyosin was observed in an overloaded condition. From this, we conclude that isozymic changes in cardiac myosin could occur in the human heart to meet increased work induced by cardiac overload. However, the physiological importance of these isomyosin redistributions in human myocardium seems to be much greater in the atrium than in the ventricle, since larger amounts of V1 isomyosin which could be transformed to V3 isomyosin were present in the atrial myocardium.
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Japanese circulation journal 48 33-33 1984年9月10日
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The American journal of cardiology 54(1) 211-6 1984年7月1日 査読有りThe effect of methylprednisolone sodium succinate (MP) on release of myosin light chain II (LCII) from the myocardium was studied in experimental myocardial infarction (MI). Acute MI was produced in conscious, closed-chest dogs by ligating the left anterior descending coronary artery beyond the first diagonal branch. MP, 30 mg/kg, was administered intravenously just before and 24 hours after MI. After MI, LCII levels in the serum were determined serially up to 240 hours. MI size was determined histologically 10 days after MI. In the MP group, LCII levels in the serum within 72 hours were lower than in the control, and cumulative LCII release for 3 days decreased from 530 +/- 159 to 310 +/- 101 ng/ml (mean +/- standard deviation) (p less than 0.001). However, the peak LCII level appeared later (control vs MP, 63 +/- 27 vs 122 +/- 25 hours, p less than 0.001), and the peak LCII level and cumulative LCII release for 10 days were not decreased by MP treatment. MI size also was not reduced by MP (11.0 +/- 4.4% vs 11.8% +/- 4.5% of the left ventricle, difference not significant). Since the rate of disappearance of LCII is rapid and was not affected by MP, these results suggest that MP treatment early after acute MI delays breakdown of myosin filaments, but cannot prevent it.
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 48(8) 838-838 1984年
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 48(8) 829-830 1984年
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 48(8) 887-888 1984年
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 48(8) 925-925 1984年
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CURRENT THERAPEUTIC RESEARCH-CLINICAL AND EXPERIMENTAL 35(5) 860-862 1984年
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Japanese circulation journal 47 229-229 1983年12月1日
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The American journal of physiology 245(3) H413-9-H419 1983年9月 査読有りThe relationship between histologically determined infarct size and release or peak levels of circulating cardiac enzymes and myosin light chain 2 (LC2) was studied. Myocardial infarction was produced by ligating the left anterior descending coronary artery in 18 conscious closed-chest dogs. Creatine phosphokinase (CPK), cytosolic and mitochondrial isozymes of aspartate transaminase (sAST and mAST) in the plasma, and LC2 in the serum were measured serially until 10 days after infarction, when infarct size was determined histologically [range 4.0-38.8% of the left ventricular weight (%LV)]. Infarct size correlated most closely with LC2 release (r = 0.82, P less than 0.001) and less closely with peak sAST (r = 0.59, P less than 0.01), peak mAST (r = 0.49, P less than 0.05), peak CPK (r = 0.22), and CPK release (r = 0.14). The correlation between infarct size and CPK release was improved by limiting the analysis to the dogs with infarct size of less than 20% LV (n = 11, r = 0.53, P less than 0.1). Because, among cardiac enzymes and LC2, CPK activity decayed most rapidly in the lymph fluid when incubated in vitro, degeneration of CPK in the lymph stream may contribute to the nonlinear relationship between infarct size and CPK release.
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Japanese circulation journal 47 39-39 1983年6月1日
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Japanese circulation journal 47 55-55 1983年6月1日
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 47(8) 992-992 1983年
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 47(8) 867-867 1983年
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JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 47(8) 1021-1021 1983年
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CIRCULATION 68(4) 393-393 1983年
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Japanese circulation journal 46(11) 1159-65 1982年11月 査読有りAn extensive myocardial fibrosis due to progressive systemic sclerosis (PSS) was described in a 36-year-old normotensive woman without pulmonary hypertension. An electrocardiogram showed low voltage and a pseudo-infarctional pattern in leads V1 through V3. Right ventricular dilatation and generalized left ventricular hypokinesis were present, but her pulmonary artery pressure was normal. Serum creatine kinase (CK) was elevated to 2305 U/L and CK-MB isoenzyme was as high as 7.1%. Simultaneously performed isoenzyme analysis of CK from the homogenate of the skeletal muscle of the patient showed a similar pattern, thus confirming that serum CK originated mainly from the skeletal muscle lesions. Autopsy findings demonstrated diffuse myocardial fibrosis and relatively unremarkable changes in the lungs and the kidneys. Our case serves as a warning that primary myocardial fibrosis could be, in some cases, so extensive that it might lead to a rapidly aggravated myocardial dysfunction and eventual death.
書籍等出版物
21-
Springer 2009年 (ISBN: 9784431877745)
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Signal Transduction and Cardiac Hypertrophy (Naranjan S. Dhalla, Larry Hryshko, Elissavet Kardami, Pawan K. Singal, KLUWER ACADEMIC PUBLISHERS) 2003年
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Signal Transduction and Cardiac Hypertrophy (Naranjan S. Dhalla, Larry Hryshko, Elissavet Kardami, Pawan K. Singal, KLUWER ACADEMIC PUBLISHERS) 2003年
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Rapid Cycle Real-Time PCR : methods and applications 2001年
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in"The Hypertrophied Heart" 2000年
共同研究・競争的資金等の研究課題
91-
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