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Articles by Y Kimura
Total Records ( 8 ) for Y Kimura
  Y Kimura , F. T Nishimura , S Abe , T Fukunaga , H Tanii and K. Saijoh
 

Aims: To assess the effect of the –360G/A polymorphism in the promoter region of the human aldehyde dehydrogenase-2 (ALDH2) gene on its transcription, basal and acetaldehyde/ethanol-induced gene expression was examined by in vivo and in vitro experiments. Methods: Human peripheral blood leukocytes were collected before and after alcohol ingestion (0.4 g/kg body weight) in 21 healthy young Japanese volunteers with a deficient phenotype of ALDH2 (487Glu/Lys), and the levels of ALDH2 mRNA were quantified by real-time RT-PCR. The transcriptional activity of the ALDH2 promoter was investigated by a reporter assay using HepG2 cells in the presence or absence of acetaldehyde/ethanol. Results: The basal level of ALDH2 mRNA was significantly higher in –360A heterozygous subjects than in –360G homozygous subjects. In all subjects, regardless of the genotype, ALDH2 mRNA increased following ethanol ingestion. The promoter activity of a reporter plasmid for –360G was significantly lower than that of a reporter plasmid for –360A. Exposure to acetaldehyde induced a significant increase in the transcriptional activity of the –360G reporter, but not the –360A reporter. Conclusions: In vivo and in vitro experiments showed that the –360G allele has lower basal transcriptional activity than the –360A allele, whereas acetaldehyde/ethanol-induced gene expression, in general, seems to be more enhanced in individuals homozygous for the –360G allele than in those with the –360A allele. Thus, the promoter polymorphism may be involved in individual differences in acetaldehyde elimination.

  Y Takemoto , H Kawata , T Soeda , K Imagawa , S Somekawa , Y Takeda , S Uemura , M Matsumoto , Y Fujimura , J. i Jo , Y Kimura , Y Tabata and Y. Saito
 

Background— In-stent thrombosis is mainly triggered by adenosine diphosphate (ADP)-dependent platelet aggregation after percutanous coronary stent implantation. Ectonucleoside triphosphate diphosphohydrolase (E-NTPDase) rapidly hydrolyzes ADP to adenosine monophosphate, inhibiting platelet aggregation. We tested the hypothesis that local delivery of human placental E-NTPDase (pE-NTPDase) gene into injured arteries via gene-eluting stent could prevent subacute in-stent thrombosis.

Methods and Results— We generated gene-eluting stents by coating bare metal stents with cationic gelatin hydrogel containing pE-NTPDase cDNA (pE-NTPDase stent), and implanted the stents into rabbit femoral arteries (FA) prone to production of platelet-rich thrombi due to repeated balloon injury at 4-week intervals. After the second injury, E-NTPDase gene expression was severely decreased; however, the implantation of pE-NTPDase stent increased E-NTPDase mRNA levels and NTPDase activity to higher level than normal FA. The FAs with pE-NTPDase stents maintained patency in all rabbits (P<0.01), whereas the stent-implanted FAs without pE-NTPDase gene showed low patency rates (17% to 25%). The occlusive platelet-rich thrombi, excessive neointimal growth, and infiltration of macrophages were inhibited in stent implanted FA with pE-NTPDase gene, but not without pE-NTPDase gene.

Conclusions— Human pE-NTPDase gene transfer via cationic gelatin-coated stents inhibited subacute in-stent thrombosis and suppressed neointimal hyperplasia and inflammation without antiplatelet drugs.

  Y Kimura , Y Ishibashi , E Tsuda , Y Yamamoto , H Tsukada and S. Toh
  Introduction

A high incidence of anterior cruciate ligament (ACL) injuries related to sports activities has been reported; however, the injury situation of ACL injury in badminton has not been elucidated. This study investigated the mechanism of ACL injury in badminton using a questionnaire.

Methods

Information on injury mechanism was gathered from interviews with six male and 15 female badminton players who received a non-contact ACL injury playing badminton and underwent ACL reconstruction.

Results

The most common injury mechanism (10 of 21 injuries) was single-leg landing after overhead stroke. Nine of 10 players had injured the knee opposite to the racket-hand side. The second most frequent injury mechanism (eight of 21 injuries) was plant-and-cut while side-stepping or backward stepping. All eight players injured the knee of the racket-hand side. Eleven injuries occurred in the rear court, and six of the 11 injuries occurred during single-leg landing after an overhead stroke.

Conclusion

The knee opposite to the racket-hand side tended to sustain the ACL injuries during single-leg landing after a backhand overhead stroke, whereas the knee of the racket-hand side tended to be injured by plant-and-cut during side or backward stepping. These injury patterns appear to be due to specific movements during badminton.

  M Takaoka , D Nagata , S Kihara , I Shimomura , Y Kimura , Y Tabata , Y Saito , R Nagai and M. Sata
 

Rationale: Obesity is associated with a high incidence of cardiovascular complications. However, the molecular link between obesity and vascular disease is not fully understood. Most previous studies have focused on the association between cardiovascular disease and accumulation of visceral fat. Periadventitial fat is distributed ubiquitously around arteries throughout the body.

Objective: Here, we investigated the impact of obesity on inflammation in the periadventitial adipose tissue and on lesion formation after vascular injury.

Methods and Results: High-fat, high-sucrose feeding induced inflammatory changes and decreased adiponectin expression in the periadventitial adipose tissue, which was associated with enhanced neointima formation after endovascular injury. Removal of periadventitial fat markedly enhanced neointima formation after injury, which was attenuated by transplantation of subcutaneous adipose tissue from mice fed on regular chow. Adiponectin-deficient mice showed markedly enhanced lesion formation, which was reversed by local delivery, but not systemic administration, of recombinant adiponectin to the periadventitial area. The conditioned medium from subcutaneous fat attenuated increased cell number of smooth muscle cells in response to platelet derived growth factor-BB.

Conclusions: Our findings suggest that periadventitial fat may protect against neointimal formation after angioplasty under physiological conditions and that inflammatory changes in the periadventitial fat may have a direct role in the pathogenesis of vascular disease accelerated by obesity.

  T Iyoda , M Ushida , Y Kimura , K Minamino , A Hayuka , S Yokohata , H Ehara and K. Inaba
 

V14 TCR expressing invariant NK T (iNKT) cells recognize -galactosylceramide (GC)/CD1d complex and produce large amounts of various cytokines before the onset of the adaptive immunity. After stimulation with a high dose (2–5 µg) of GC in vivo, iNKT cells in the spleen and liver become anergic in terms of the proliferation and cytokine production to subsequent stimulation. In this study, we monitor how iNKT anergy is induced. Anergized iNKT cells dramatically reduced the expression of IL-2R, and exogenous IL-2 restored the ability to proliferate and produce IL-4 but not to produce IFN-. Anergized iNKT cells expressed high levels of programmed death-1 (PD-1). However, iNKT cells in PD-1-deficient mice became anergic as a result of GC injection, as do normal mice. Furthermore, anti-PD-1 blocking mAb was unable to restore their responsiveness. When iNKT cells were stimulated with immobilized anti-CD3 in the presence or absence of anti-CD28, they produced cytokines in a dose-dependent manner. Unlike in naive CD4 T cells, the strong TCR-mediated signaling with co-stimulation renders them anergic to any subsequent stimulation with GC and spleen dendritic cells (DCs). Moreover, iNKT cells also became anergic after stimulation with phorbol-12-myristate-13-acetate + ionophore. Finally, the injection of GC-pulsed DCs was more potent in inducing anergy than B cells. These results indicate that strong TCR-mediated activation with co-stimulation provides signals that induce the anergic state in iNKT cells.

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

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

Methods

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.

Results

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.

Conclusions

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.

  K Nagao , Y Zhao , K Takahashi , Y Kimura and K. Ueda
 

ABCA1 plays a major role in HDL metabolism. Cholesterol secretion by ABCA1 is dependent on the presence of extracellular acceptors, such as lipid-free apolipoprotein A-I (apoA-I). However, the importance of the direct interaction between apoA-I and ABCA1 in HDL formation remains unclear. In contrast, ABCB4 mediates the secretion of phospholipids and cholesterol in the presence of sodium taurocholate (NaTC) but not in the presence of apoA-I. In this study, we analyzed apoA-I binding and NaTC-dependent lipid efflux by ABCA1. ABCA1 mediated the efflux of cholesterol and phospholipids in the presence of NaTC as well as in the presence of apoA-I in an ATP-dependent manner. The Tangier disease mutation W590S, which resides in the extracellular domain and impairs apoA-I-dependent lipid efflux, greatly decreased NaTC-dependent cholesterol and phospholipid efflux. However, the W590S mutation did not impair apoA-I binding and, conversely, retarded the dissociation of apoA-I from ABCA1. These results suggest that the W590S mutation impairs ATP-dependent lipid translocation and that lipid translocation or possibly lipid loading, facilitates apoA-I dissociation from ABCA1. NaTC is a good tool for analyzing ABCA1-mediated lipid efflux and allows dissection of the steps of HDL formation by ABCA1.

  N Shibuya , Y Mikami , Y Kimura , N Nagahara and H. Kimura
 

Hydrogen sulfide (H2S) has been recognized as a smooth muscle relaxant. Cystathionine -lyase, which is localized to smooth muscle, is thought to be the major H2S-producing enzyme in the thoracic aorta. Here we show that 3-mercaptopyruvate sulfurtransferase (3MST) and cysteine aminotransferase (CAT) are localized to vascular endothelium in the thoracic aorta and produce H2S. Both 3MST and CAT were localized to endothelium. Lysates of vascular endothelial cells produced H2S from cysteine and -ketoglutarate. The present study provides a new insight into the production and release of H2S as a smooth muscle relaxant from vascular endothelium.

 
 
 
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