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Articles by K Kondo
Total Records ( 4 ) for K Kondo
  K Kondo , R Shibata , K Unno , M Shimano , M Ishii , T Kito , S Shintani , K Walsh , N Ouchi and T. Murohara
 

Background— Adiponectin plays a protective role in the development of obesity-linked disorders. We demonstrated that adiponectin exerts beneficial actions on acute ischemic injury in mice hearts. However, the effects of adiponectin treatment in large animals and its feasibility in clinical practice have not been investigated. This study investigated the effects of intracoronary administration of adiponectin on myocardial ischemia-reperfusion (I/R) injury in pigs.

Methods and Results— The left anterior descending coronary artery was occluded in pigs for 45 minutes and then reperfused for 24 hours. Recombinant adiponectin protein was given as a bolus intracoronary injection during ischemia. Cardiac functional parameters were measured by a manometer-tipped catheter. Apoptosis was evaluated by terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling staining. Tumor necrosis factor- and interleukin-10 transcripts were analyzed by real-time polymerase chain reaction. Serum levels of derivatives of reactive oxygen metabolites and biological antioxidant potential were measured. Adiponectin protein was determined by immunohistochemical and Western blot analyses. Intracoronary administration of adiponectin protein led to a reduction in myocardial infarct size and improvement of left ventricular function in pigs after I/R. Injected adiponectin protein accumulated in the I/R-injured heart. Adiponectin treatment resulted in decreased tumor necrosis factor- and increased interleukin-10 mRNA levels in the myocardium after I/R. Adiponectin-treated pigs had reduced apoptotic activity in the I/R-injured heart and showed increased biological antioxidant potential levels and decreased derivatives of reactive oxygen metabolite levels in the blood stream after I/R.

Conclusions— These data suggest that adiponectin protects against I/R injury in a preclinical pig model through its ability to suppress inflammation, apoptosis, and oxidative stress. Administration of intracoronary adiponectin could be a useful adjunctive therapy for acute myocardial infarction.

  K Yamaji , T Kimura , T Morimoto , Y Nakagawa , K Inoue , Y Soga , T Arita , S Shirai , K Ando , K Kondo , K Sakai , M Goya , M Iwabuchi , H Yokoi , H Nosaka and M. Nobuyoshi
  Background—

We previously reported that the long-term luminal response after coronary bare metal stenting is triphasic, with an early restenosis phase spanning the 6 months after the index procedure, an intermediate-term regression phase from 6 months to 3 years, and a late renarrowing phase beyond 4 years. However, the clinical significance of late luminal renarrowing remains unknown.

Methods and Results—

Angiographic and clinical follow-up of the same cohort of 405 patients with successful Palmaz-Schatz stent placement was extended beyond 15 years. Clinical follow-up was completed in 98% of patients at 5 years and in 81% at 15 years. The incidence of death and cardiac death at 15 years was 45.4% and 20.6%, respectively. Paired long-term (4 to 10 years) and very long-term (>10 years) angiographic studies without intercurrent target lesion revascularization were performed in 55 lesions, and minimal luminal diameter further decreased from 1.88±0.50 mm to 1.60±0.73 mm (P=0.002). Late target lesion revascularization after initial stabilization of the stented segments occurred rarely within 4 years. Beyond 4 years, however, the incidence of late target lesion revascularization increased steadily from 3.3% at 4 years to 24.7% at 15 years. The incidence of definite very late stent thrombosis was low (1.5% at 15 years).

Conclusions—

Luminal renarrowing of the stented segment beyond 4 years was a progressive process extending beyond 10 years. The angiographic observation of late in-stent restenosis was clinically relevant because a corresponding progressive increase in the incidence of late target lesion revascularization was observed beyond 4 years and up to 15 to 20 years after bare metal stent implantation.

  R Yamaguchi , M Tanaka , K Kondo , T Yokoyama , Y Kaneko , M Yamaguchi , Y Ogata , O Nakashima , M Kage and H. Yano
  Objective

Invasive micropapillary carcinoma of the breast is a distinct variant of breast cancer. In the present study, we analyzed potential immunophenotypic changes in invasive micropapillary carcinoma.

Methods

Specimens from 15 patients with invasive micropapillary carcinoma were analyzed using clinicopathological and immunohistochemical methods. We also examined the relationship between clinicopathological factors using the Ki-67 labeling index.

Results

Immunohistochemical staining for cytoplasmic p63 expression was seen in four (27%) tumors, and p63 nuclear expression was also observed in four (27%) tumors. Involucrin and 34betaE12 were expressed in the invasive micropapillary carcinoma component of nine (60%) and four (27%) tumors, respectively. Cytokeratin 5/6 was expressed in three (20%) tumors and cytokeratin 14 staining was negative in all tumors. In one tumor (case 3), vimentin, epithelial membrane antigen and cytokeratin 8/18 were co-expressed. Four tumors (27%) were negative for the estrogen receptor/progesterone receptor/HER2. However, 11 out of 15 (73%) tumors were positive for the estrogen receptor. The Ki-67 labeling index was significantly higher in cases with p63 tumor expression than in those without (P < 0.0001), and also higher in cases with lymph node metastasis than in cases without (P = 0.0029).

Conclusions

Nuclear expression of p63, involucrin and 34betaE12 were detected indicating squamous differentiation. Cytoplasmic p63 expression was also identified. The fact that the Ki-67 labeling index was significantly higher in such cases may have been associated with the aggressive behavior of these tumors. Our findings suggest that the characteristic morphology of invasive micropapillary carcinomas may be due to immunophenotypical and oncogenic changes.

  H Shishido , M. D Yamada , K Kondo and S. Maruta
 

Calmodulin (CaM), a physiologically important Ca2+-binding protein, participates in numerous cellular regulatory processes. It is dumbbell shaped and contains two globular domains connected by a short -helix. Each of the globular domains has two Ca2+-binding sites, the EF hands. CaM undergoes a conformational change upon binding to Ca2+, which enables it to bind to specific proteins for specific responses. Here, we successfully photocontrolled CaM binding to its target peptide using the photochromic compound N-(4-phenylazophenyl) maleimide (PAM), which reversibly undergoes cis–trans isomerization upon ultraviolet (UV) and visible (VIS) light irradiation. In order to specifically incorporate PAM, CaM mutants having reactive cysteine residues in the functional region were prepared; PAM was stoichiometrically incorporated into the cysteine residues in these mutants. Further, we prepared the target peptide, M13, fused with yellow fluorescent protein (YFP) to monitor the CaMM13 peptide interaction. The binding of the PAMCaM mutants, N60C, D64C and M124C, to M13YFP was reversibly photocontrolled upon UVVIS light irradiation at appropriate Ca2+ concentrations.

 
 
 
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