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Articles by Y Kodama
Total Records ( 3 ) for Y Kodama
  J. e Obata , T Nakamura , Y Kitta , Y Kodama , K Sano , K. I Kawabata , Y Saitoh , D Fujioka , T Kobayashi , T Yano , Y Watanabe , K Watanabe and K. Kugiyama

Background— Sirolimus-eluting stent (SES) implantation aggravated endothelial vasomotor dysfunction in infarct-related coronary arteries.

Methods and Results— This study examined the effect of SES implantation on the duration of reperfusion-induced endothelial vasomotor dysfunction in infarct-related coronary arteries and on postinfarct left ventricular dysfunction in acute myocardial infarction (AMI). Patients with a first AMI due to occlusion of the left anterior descending coronary artery and successful reperfusion using SES (n=15) or bare metal stents (BMS; n=18) were examined. The vasomotor response of the left anterior descending coronary artery to acetylcholine and left ventriculography were examined 2 weeks and 6 months after AMI. At 6 months after AMI, the impairment of epicardial coronary artery dilation and coronary blood flow increase in response to acetylcholine was recovered from 2 weeks after AMI in BMS-treated patients, whereas the responses of SES-treated patients improved but remained impaired compared with BMS-treated patients (% increase in blood flow, 77±12% in SES versus 116±15% in BMS at 10 µg/min of acetylcholine, P<0.01). Left ventricular regional wall dysfunction in the left anterior descending coronary artery territory improved from 2 weeks to 6 months after AMI in BMS-treated patients but not in SES-treated patients (% improvement of average SD/chord, 6% in SES versus 19% in BMS, P<0.05), although left ventricular global ejection fraction was similar between the groups at any time points.

Conclusions— SES implantation may delay recovery of reperfusion-induced endothelial vasomotor dysfunction in infarct-related coronary arteries and left ventricular regional dysfunction for at least 6 months after AMI.

  Y Kodama , M Takita , S Kawagoe , S Hirahara , Y Kimura , S Onozawa , T Wada , K Nakano , M Kami , T Matsumura and K. Yuji

There is a lack of sufficient information on the employment of home care for the treatment of hematologic malignancies.


We provided home care to 580 patients from 1 January through 31 October 2007. Patients with hematologic malignancies were selected from these 580 patients; subsequently, by reviewing their medical records.


The main clinical condition in 15 (2.6%) of 580 patients was hematologic malignancies. The median age of the patients was 78 years (range, 64–92). Of the 15 patients, 12 showed a performance status (PS) of 3–4, and the condition of 6 patients was complicated with dementia. Food intake via the oral route was possible in 14 patients. These patients were administered palliative care. Among the seven patients who required pain control, four had been opioid users; however, none had used anticancer drugs for pain relief. Furthermore, three patients received blood transfusion. Although three patients developed severe complications (acute appendicitis, pneumonia and hyperglycemia), we were able to treat all cases adequately. Eight patients died at home due to aggravation of the primary diseases. The remaining seven patients were transferred to other hospitals for the treatment of complications or for the convenience of their respective families.


Even patients with hematologic malignancies could be candidates for home care if their underlying diseases are slowly progressive, and they can sustain themselves by oral intakes. Dementia and poor PS are not contraindicated to it.

  H Hatanaka , F Omura , Y Kodama and T. Ashikari

The maltose transporter gene is situated at the MAL locus, which consists of genes for a transporter, maltase, and transcriptional activator. Five unlinked MAL loci (MAL1, MAL2, MAL3, MAL4, and MAL6) constitute a gene family in Saccharomyces cerevisiae. The expression of the maltose transporter is induced by maltose and repressed by glucose. The activity of the maltose transporter is also regulated post-translationally; Mal61p is rapidly internalized from the plasma membrane and degraded by ubiquitin-mediated proteolysis in the presence of glucose. We found that S. cerevisiae strain ATCC20598 harboring MAL21 could grow in maltose supplemented with a non- assimilable glucose analogue, 2-deoxyglucose, whereas strain ATCC96955 harboring MAL61 and strain CB11 with MAL31 and AGT1 could not. These observations implied a Mal21p-specific resistance against glucose-induced degradation. Mal21p found in ATCC20598 has 10 amino acids, including Gly-46 and His-50, that are inconsistent with the corresponding residues in Mal61p. The half-life of Mal21p for glucose-induced degradation was 118 min when expressed using the constitutive TPI1 promoter, which was significantly longer than that of Mal61p (25 min). Studies with mutant cells that are defective in endocytosis or the ubiquitination process indicated that Mal21p was less ubiquitinated than Mal61p, suggesting that Mal21p remains on the plasma membrane because of poor susceptibility to ubiquitination. Mutational studies revealed that both residues Gly-46 and His-50 in Mal21p are essential for the full resistance of maltose transporters against glucose-induced degradation.

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