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Articles by M Hayashi
Total Records ( 7 ) for M Hayashi
  H Ishii , T Toriyama , T Aoyama , H Takahashi , T Amano , M Hayashi , M Tanaka , Y Kawamura , Y Yasuda , Y Yuzawa , S Maruyama , S Matsuo , T Matsubara and T. Murohara
 

Background— Percutaneous coronary intervention (PCI) using drug-eluting stents significantly reduces the risk of restenosis in the general population. However, in patients on hemodialysis, adverse cardiac events are frequently seen even if treated with drug-eluting stents. Recent studies suggest that C-reactive protein (CRP) reflects vascular wall inflammation and can predict adverse cardiac events. We evaluated possible prognostic values of CRP on outcomes in patients on hemodialysis undergoing PCI with drug-eluting stents.

Methods and Results— A total of 167 patients undergoing PCI with sirolimus-eluting stents for stable angina (322 lesions) were enrolled. They were divided into tertiles according to serum CRP levels. We analyzed the incidence of major adverse cardiovascular events including cardiovascular death, nonfatal myocardial infarction, and target lesion revascularization after PCI as well as quantitative coronary angiographic data. The mean follow-up was 31 months (SD, 14). Major adverse cardiac events occurred in 11 patients (19.6%) of the lowest tertile, in 22 patients (39.3%) of the middle tertile, and in 28 patients (50.9%) of the highest tertile during follow-up period (P=0.0009). There was a progressive increase in neointimal growth after sirolimus-eluting stent implantation during follow-up because preprocedural CRP levels were higher, despite similar angiographic data just after PCI. Angiographic restenosis at 6 to 8 months after PCI was seen in 10.6% in the lowest tertile, 17.9% in the middle tertile, and 32.0% in the highest tertile (P=0.0007).

Conclusions— Increased preprocedural serum CRP levels would predict higher major adverse cardiac events and restenosis rates after sirolimus-eluting stents implantation in patients on hemodialysis.

  S Yamada , H Ishii , H Takahashi , T Aoyama , Y Morita , H Kasuga , K Kimura , Y Ito , R Takahashi , T Toriyama , Y Yasuda , M Hayashi , H Kamiya , Y Yuzawa , S Maruyama , S Matsuo , T Matsubara and T. Murohara
 

Background and objectives: Cardiac failure is directly affected by left ventricular (LV) dysfunction, and particularly LV systolic dysfunction is strongly associated with survival in ESRD patients. The aim of this study was to determine the prognostic value of reduced LV ejection fraction (LVEF) measured at the time of initiation of hemodialysis (HD) in incident HD patients.

Design, setting, participants, & measurements: 1254 consecutive ESRD patients who electively started HD therapy were screened by echocardiography within 1 month after its inception. They were divided into five groups according to LVEF levels with a decrease of 0.1 each and were followed up for up to 7 years. Survival was examined with the Kaplan-Meier method and compared using the log-rank test.

Results: Among the 1254 patients, LVEF levels ≥0.6, 0.5 to 0.6, 0.4 to 0.5, 0.3 to 0.4, and <0.3 were seen in 842 (67.1%), 247 (19.7%), 107 (8.5%), 41 (3.3%), and 17 (1.4%) patients, respectively. On Kaplan-Meier analysis, 7-year event-free rates from cardiovascular death were 84.2, 83.7, 73.6, 59.4, and 30.9% in order of groups with decreasing LVEF of 0.1 each, respectively. Seven-year event-free rates from all-cause death were 69.2, 61.7, 57.1, 45.9, and 23.1% in the respective groups. Even after adjustment for other risk factors, decreasing LVEF was a strong independent predictor for cardiovascular death.

Conclusions: Reduced LVEF on starting HD therapy could stratify risk of cardiovascular and all-cause mortality in ESRD patients. Screening by echocardiography at start of HD therapy might be recommended to predict prognosis in patients with ESRD.

  C Li , M Kuchimanchi , D Hickman , L Poppe , M Hayashi , Y Zhou , R Subramanian , G Kumar and S. Surapaneni
 

Motesanib diphosphate is a novel, investigational, highly selective oral inhibitor of the receptor tyrosine kinases vascular endothelial growth factor receptors 1, 2, and 3, the platelet-derived growth factor receptor, and the stem cell factor receptor (Kit). The in vitro metabolic profiles of [14C]motesanib were examined by using microsomes and hepatocytes from preclinical species and humans. Several oxidative metabolites were observed and characterized by tandem mass spectrometry, nuclear magnetic resonance spectroscopy, and coinjection with authentic standards. Cytochrome P450 (P450) 3A4 is the major isozyme involved in the oxidative biotransformation of motesanib, but the CYP2D6 and CYP1A isozymes also make minor contributions. In hepatocyte incubations, oxidative and conjugative pathways were observed for all species examined, and indoline N-glucuronidation was the dominant pathway. Three less common and novel phase II conjugates of the indoline nitrogen were detected in hepatocytes and in microsomes supplemented with specific cofactors, including N-carbamoyl glucuronide, N-glucose, and N-linked β-N-acetylglucosamine. An N-glucuronide metabolite was the most frequently observed phase II conjugate in liver microsomes of all species, whereas the N-acetylglucosamine conjugate was observed only in monkey liver microsomes. Incubations with recombinant human UDP-glucuronosyltransferases (UGTs) and inhibition by the UGT1A4 and UGT1A1 substrates/inhibitors imipramine and bilirubin suggested that UGT1A4 is the major UGT isozyme catalyzing the N-glucuronidation of motesanib, with a minor contribution from UGT1A1. The in vitro metabolic profiles were similar between the human and preclinical species examined. All metabolites found in humans were also detected in other species.

  C Li , M Kuchimanchi , D Hickman , L Poppe , M Hayashi , Y Zhou , R Subramanian , G Kumar and S. Surapaneni
 

Motesanib diphosphate is a novel, investigational, highly selective oral inhibitor of the receptor tyrosine kinases vascular endothelial growth factor receptors 1, 2, and 3, the platelet-derived growth factor receptor, and the stem cell factor receptor (Kit). The in vitro metabolic profiles of [14C]motesanib were examined by using microsomes and hepatocytes from preclinical species and humans. Several oxidative metabolites were observed and characterized by tandem mass spectrometry, nuclear magnetic resonance spectroscopy, and coinjection with authentic standards. Cytochrome P450 (P450) 3A4 is the major isozyme involved in the oxidative biotransformation of motesanib, but the CYP2D6 and CYP1A isozymes also make minor contributions. In hepatocyte incubations, oxidative and conjugative pathways were observed for all species examined, and indoline N-glucuronidation was the dominant pathway. Three less common and novel phase II conjugates of the indoline nitrogen were detected in hepatocytes and in microsomes supplemented with specific cofactors, including N-carbamoyl glucuronide, N-glucose, and N-linked β-N-acetylglucosamine. An N-glucuronide metabolite was the most frequently observed phase II conjugate in liver microsomes of all species, whereas the N-acetylglucosamine conjugate was observed only in monkey liver microsomes. Incubations with recombinant human UDP-glucuronosyltransferases (UGTs) and inhibition by the UGT1A4 and UGT1A1 substrates/inhibitors imipramine and bilirubin suggested that UGT1A4 is the major UGT isozyme catalyzing the N-glucuronidation of motesanib, with a minor contribution from UGT1A1. The in vitro metabolic profiles were similar between the human and preclinical species examined. All metabolites found in humans were also detected in other species.

  S Takatsuki , F Extramiana , M Hayashi , A Haggui , A Messali , P Milliez , A Leenhardt and B. Cauchemez
  Aims

Creation of complete linear lesions in the lateral mitral isthmus (LMI) by catheter ablation for treating atrial fibrillation remains technically challenging. We aimed to clarify whether a high take-off left inferior pulmonary vein (LIPV) can hamper the creation of a complete block at the LMI.

Methods and results

We included 81 consecutive patients who underwent linear ablation at the LMI and cardiac computed tomography (CT) before ablation. We defined a high take-off LIPV when the level of the lower edge of the LIPV ostium was higher than that of the top of mitral annulus on CT. The clinical backgrounds, parameters, and long-term follow-up were then compared between the success (successful creation of a complete LMI block) and failure groups. A complete LMI block was obtained in 60/81 (76%) patients. In the failure group, a high take-off LIPV was noted more commonly and the LMI tended to be longer than the success group. Multivariate analysis revealed that a high take-off LIPV was an independent predictor of failure to achieve a complete LMI block. The sinus rhythm maintenance rate was not different between the success and failure groups.

Conclusion

A high take-off LIPV hampered the creation of complete linear lesions in the LMI.

  M Yamaguchi , M Hayashi , S Fujita , T Yoshida , T Utsunomiya , H Yamamoto and K. Kasai
 

It has previously been reported that low-energy laser irradiation stimulated the velocity of tooth movement via the receptor activator of nuclear factor kappa B (RANK)/RANK ligand and the macrophage colony-stimulating factor/its receptor (c-Fms) systems. Matrix metalloproteinase (MMP)-9, cathepsin K, and alpha(v) beta(3) [(v)β3] integrin are essential for osteoclastogenesis; therefore, the present study was designed to examine the effects of low-energy laser irradiation on the expression of MMP-9, cathepsin K, and (v)β3 integrin during experimental tooth movement.

Fifty male, 6-week-old Wistar strain rats were used in the experiment. A total force of 10g was applied to the rat molars to induce tooth movement. A Ga-Al-As diode laser was used to irradiate the area around the moving tooth and, after 7 days, the amount of tooth movement was measured. To determine the amount of tooth movement, plaster models of the maxillae were made using a silicone impression material before (day 0) and after tooth movement (days 1, 2, 3, 4, and 7). The models were scanned using a contact-type three-dimensional (3-D) measurement apparatus. Immunohistochemical staining for MMP-9, cathepsin K, and integrin subunits of (v)β3 was performed. Intergroup comparisons of the average values were conducted with a Mann–Whitney U-test for tooth movement and the number of tartrate-resistant acid phosphatase (TRAP), MMP-9, cathepsin K, and integrin subunits of (v)β3-positive cells.

In the laser-irradiated group, the amount of tooth movement was significantly greater than that in the non-irradiated group at the end of the experiment (P < 0.05). Cells positively stained with TRAP, MMP-9, cathepsin K, and integrin subunits of (v)β3 were found to be significantly increased in the irradiated group on days 2–7 compared with those in the non-irradiated group (P < 0.05).

These findings suggest that low-energy laser irradiation facilitates the velocity of tooth movement and MMP-9, cathepsin K, and integrin subunits of (v)β3 expression in rats.

  M Hayashi , K Kitamura and K. Harada
 

Soy protein consists of mainly 7S globulin (β-conglycinin) and 11S globulin (glycinin). The 7S globulin exerts favorable and unfavorable effects on human nutrition, food processing, and human health. Therefore, it is important for the improvement of the soy protein to control the content of 7S globulin. A mutant line lacking the 7S globulin was induced by -ray irradiation, and the deficiency is controlled by a single recessive gene, cgdef. The Cgdef gene, despite its potential for improvement of the soy protein, has not been assigned to a linkage group of a soybean genetic map. We crossed "Mo-shi-dou Gong 503" with plants homozygous or heterozygous for the Cgdef allele and screened an F2 mapping population that segregated with the cgdef allele to locate the Cgdef gene on a soybean genetic map. By linkage analysis, we assigned the Cgdef gene to chromosome 19 at the position between the Satt523 and Sat_388 simple sequence repeat (SSR) markers. Six SSR markers (Sat_134, Sat_405, Satt143, Satt398, Sat_195, and Satt694) and 2 amplified fragment length polymorphism markers identified previously were mapped at the same position of the Cgdef gene. These markers should enable to conduct map-based cloning of the Cgdef gene.

 
 
 
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