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Articles by H Kato
Total Records ( 8 ) for H Kato
  N Takatsuka , A Hasegawa , A Takamori , Y Shimizu , H Kato , T Ohashi , T Amagasa , T Masuda and M. Kannagi

Human T-cell leukemia virus type I (HTLV-I) is associated with adult T-cell leukemia, HTLV-I-associated myelopathy/tropical spastic paraparesis and various autoimmune-like disorders. T-cell immune suppression is also associated with HTLV-I infection. Mechanisms of diverse immune dysregulation in HTLV-I infection are obscure. Here, we investigated a potential link between autoimmunity and immune suppression in HTLV-I infection. G14, an IL-2-dependent HTLV-I-negative CD4+CD8+ T-cell line previously established from an HTLV-I-infected rat, constantly proliferated and produced IFN-. IFN- production by G14 cells was dependent on interactions between CD4 and MHC-II, suggesting that G14 cells recognized self-antigens presented by MHC-II on themselves. To examine immune response to G14 cells, we inoculated G14 cells into syngeneic naive rats. Interestingly, T-cells isolated from these rats vigorously proliferated when stimulated with G14-Tax cells that stably expressed HTLV-I Tax, but not with G14 cells. G14-Tax-mediated T-cell proliferation was abrogated by antibodies to CD80 and CD86 that were up-regulated in G14-Tax cells. T-cells propagated by repetitive G14-Tax cell stimulations in culture with IL-2 expressed CD4, CD25 and cytolytic T lymphocyte-associated antigen 4 (CTLA-4), produced abundant amounts of IL-10 and IFN- in response to G14 cells and suppressed growth of G14 cells mainly through supernatant-mediated mechanisms. Similar IL-10- and IFN--producing CD4+CD25+CTLA-4+ T-cells were predominantly induced in culture of splenocytes from HTLV-I-infected rats following stimulation with G14-Tax cells. These results implied that expression of Tax in the otherwise low immunogenic autoreactive T-cells induced IL-10- and IFN--producing T-cell responses with regulatory effects against the autoreactive cells. Our findings provide new insights into the complex immune conditions underlying HTLV-I-associated diseases.

  H Kato , A Sato , H Fukuda , Y Kagami , H Udagawa , A Togo , N Ando , O Tanaka , M Shinoda , H Yamana and S. Ishikura

The study objective was to evaluate the efficacy and toxicity of chemoradiotherapy with 5-fluorouracil (5-FU) plus cisplatin in patients with Stage I esophageal squamous cell carcinoma (ESCC). The primary endpoint was proportion of complete response (%CR).


Patients with Stage I (T1N0M0) ESCC, aged 20–75 years, without indication of endoscopic mucosal resection were eligible. Treatment consisted of cisplatin 70 mg/m2 (day 1) and 5-FU 700 mg/m2/day (days 1–4) combined with 30 Gy radiotherapy (2 Gy/day, 5 days/week, days 1–21). The cycle was repeated twice with 1-week split. Salvage surgery was recommended for residual tumor or local recurrence.


From December 1997 to June 2000, 72 patients were enrolled. No ineligible patient or major protocol violation was observed. There were 63 CRs for %CR of 87.5% [95% confidence interval (CI): 77.6–94.1]. Six patients with residual tumor successfully underwent esophagectomy. There was no Grade 4 toxicity. Four-year survival proportion was 80.5% (95% CI: 71.3–89.7), and 4-year major relapse-free survival proportion was 68% (95% CI: 57.3–78.8) (mucosal recurrence removed by endoscopy was not counted as an event).


High CR proportion and survival proportion with mild toxicity suggest that this regimen could be considered as a candidate of new standard treatment to be compared with surgery in patients with Stage I ESCC.

  A Kamei , Y Watanabe , T Ishijima , M Uehara , S Arai , H Kato , Y Nakai and K. Abe

Anemia can be induced by dietary iron deficiency, as well as by hemorrhagia. It may also be associated with changes in lipid metabolism. However, no global analysis detailing the consequences of iron deficiency in the liver has yet been conducted. Since the liver is a metabolically important organ and also a major iron-storing organ, we performed a comprehensive transcriptome analysis to determine the effects of iron deficiency on hepatic gene expression. Four-week-old rats were fed an iron-deficient diet, ~3 ppm iron, ad libitum for 16 days. These rats were compared with similar rats pair-fed a control diet with a normal iron level, 48 ppm iron. The 16-day iron-deficient diet apparently induced anemia. On day 17, the rats were killed under anesthesia, and their livers were dissected for DNA microarray analysis. We identified 600 upregulated and 500 downregulated probe sets that characterized the iron-deficient diet group. In the upregulated probe sets, genes involved in cholesterol, amino acid, and glucose metabolism were significantly enriched, while genes related to lipid metabolism were significantly enriched in the downregulated probe sets. We also found that genes for caspases 3 and 12, which mediate endoplasmic reticulum (ER)-specific apoptosis, were upregulated in the iron-deficient group. Combined, these results suggest that iron deficiency exerts various influences, not only on nutrient metabolism but also on apoptosis, as a consequence of ER stress in the liver.

  A Fukumura , H Tsujii , T Kamada , M Baba , H Tsuji , H Kato , S Kato , S Yamada , S Yasuda , T Yanagi , R Hara , N Yamamoto , J Mizoe , K Akahane , S Fukuda , Y Furusawa , Y Iwata , T Kanai , N Kanematsu , A Kitagawa , N Matsufuji , S Minohara , N Miyahara , H Mizuno , T Murakami , K Nishizawa , K Noda , E Takada and S. Yonai

The features of relativistic carbon-ion beams are attractive from the viewpoint of radiotherapy. They exhibit not only a superior physical dose distribution but also an increase in biological efficiency with depth, because energy loss of the beams increases as they penetrate the body. This paper reviews clinical aspects of carbon-beam radiotherapy using the experience at the National Institute of Radiological Sciences. The paper also outlines the dosimetry related to carbon-beam radiotherapy, including absolute dosimetry of the carbon beam, neutron measurements and radiation protection measurements.

  T Fujibuchi , N Funabashi , M Hashimoto , H Kato , M Kurokawa , H. M Deloar , E Kunieda , I Komuro and T. Sakae

Organ absorbed doses in computed tomography (CT) scans can be measured with anatomical phantoms but not inside the human body. In this study, a straightforward method was investigated to estimate organ doses in clinical CT using the radiation treatment planning system (RTPS) and compared them with experimental results of photoluminescence dosemeters (PLD). In a heterogeneous phantom, the average difference between PLD and RTPS values were –5.0 % for the body and 7.1 % for the lung. Using CT data, organ doses in 30 clinical cases were then calculated. There was a significant inverse correlation between the calculated values of organ doses and body mass index (BMI, correlation coefficients (r)=–0.69 (whole body), –0.80 (right lung), –0.81 (left lung), –0.76 (spinal cord), –0.74 (vertebra bone), –0.74 (heart), and –0.79 (oesophagus), all p < 0.01). An RTPS can be a simple and useful tool for estimating equivalent doses inside the human body, during whole-body CT scans.

  N Iwasaki , H Kato , T Kamishima and A. Minami

The goal of osteochondral mosaicplasty (mosaicplasty) against osteochondritis dissecans of the humeral capitellum (capitellar OCD) is to allow patients to return to their sports activities without functional disturbance of the affected elbow. Consequently, the rehabilitation protocol and the interval before returning to sports activities must be established. Although surgeons need this type of data for establishing sequential alterations of grafts in the elbow, no such data have been published.


The findings of magnetic resonance imaging (MRI) improve with increasing time after mosaicplasty for capitellar OCD.

Study Design

Case series; Level of evidence, 4.


Ten young male athletes with advanced lesions of capitellar OCD, treated with mosaicplasties, underwent MRI scans at 3, 6, and 12 months, postoperatively. The surgical technique involved obtaining small-sized cylindrical osteochondral grafts from the lateral periphery of the femoral condyle at the level of the patellofemoral joint and transplanting them to the capitellar lesion. The MRI findings were semiquantitatively assessed according to the scoring system of Henderson et al (4, normal; 16, no repair).


At 12 months, all patients returned to their competitive level of sports without any disturbances of the operated elbow. Fluid surrounding the graft was found in all patients at 3 months and 4 patients at 6 months. The grafts were all well seated within the recipient sites, with no MRI evidence of graft loosening at 12 months. The overall MRI scores significantly improved from 3 to 12 months.


The MRI findings indicate that the graft incorporation to the surrounding tissues occurs around or after 6 months, postoperatively. This finding suggests that rehabilitation precautions be taken for up to 6 months after mosaicplasty for young athletes with capitellar OCD.

  Y Kamenisch , M Fousteri , J Knoch , A. K von Thaler , B Fehrenbacher , H Kato , T Becker , M. E.T Dolle , R Kuiper , M Majora , M Schaller , G. T.J van der Horst , H van Steeg , M Rocken , D Rapaport , J Krutmann , L. H Mullenders and M. Berneburg

Defects in the DNA repair mechanism nucleotide excision repair (NER) may lead to tumors in xeroderma pigmentosum (XP) or to premature aging with loss of subcutaneous fat in Cockayne syndrome (CS). Mutations of mitochondrial (mt)DNA play a role in aging, but a link between the NER-associated CS proteins and base excision repair (BER)-associated proteins in mitochondrial aging remains enigmatic. We show functional increase of CSA and CSB inside mt and complex formation with mtDNA, mt human 8-oxoguanine glycosylase (mtOGG)-1, and mt single-stranded DNA binding protein (mtSSBP)-1 upon oxidative stress. MtDNA mutations are highly increased in cells from CS patients and in subcutaneous fat of aged Csbm/m and Csa–/– mice. Thus, the NER-proteins CSA and CSB localize to mt and directly interact with BER-associated human mitochondrial 8-oxoguanine glycosylase-1 to protect from aging- and stress-induced mtDNA mutations and apoptosis-mediated loss of subcutaneous fat, a hallmark of aging found in animal models, human progeroid syndromes like CS and in normal human aging.

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