Search

Your search keyword '"Hirata, Koji"' showing total 371 results
Start Over Author "Hirata, Koji"
371 results on '"Hirata, Koji"'

101. Impact ofUGT1A1genotype upon toxicities of combination with low-dose irinotecan plus platinum

Author

Takano, Masashi, primary, Yamamoto, Kaichiro, additional, Tabata, Tsutomu, additional, Minegishi, Yuji, additional, Yokoyama, Takuma, additional, Hirata, Eiji, additional, Ikeda, Takeshi, additional, Shimada, Muneaki, additional, Yamada, Kouzo, additional, Morita, Satoshi, additional, Ando, Yuichi, additional, Hirata, Koji, additional, Sugihara, Masahiro, additional, Sugiyama, Toru, additional, Ohashi, Yasuo, additional, and Sakata, Yuh, additional

Published
2016
Full Text
View/download PDF

103. Impact of Sox9 Dosage and Hes1-mediated Notch Signaling in Controlling the Plasticity of Adult Pancreatic Duct Cells in Mice

Author

Hosokawa, Shinichi, primary, Furuyama, Kenichiro, additional, Horiguchi, Masashi, additional, Aoyama, Yoshiki, additional, Tsuboi, Kunihiko, additional, Sakikubo, Morito, additional, Goto, Toshihiko, additional, Hirata, Koji, additional, Tanabe, Wataru, additional, Nakano, Yasuhiro, additional, Akiyama, Haruhiko, additional, Kageyama, Ryoichiro, additional, Uemoto, Shinji, additional, and Kawaguchi, Yoshiya, additional

Published
2015
Full Text
View/download PDF

104. Diffusion-weighted Line-scan Echo-planar Spectroscopic Imaging Technique to Reduce Motion Artifacts in Metabolite Diffusion Imaging

Author

BITO, Yoshitaka, primary, HIRATA, Koji, additional, EBISU, Toshihiko, additional, KAWAI, Yuko, additional, OTAKE, Yosuke, additional, HIRATA, Satoshi, additional, SHIRAI, Toru, additional, SOUTOME, Yoshihisa, additional, OCHI, Hisaaki, additional, YAMAMOTO, Etsuji, additional, UMEDA, Masahiro, additional, HIGUCHI, Toshihiro, additional, and TANAKA, Chuzo, additional

Published
2015
Full Text
View/download PDF

136. Small-Scale InGaP/GaAs Heterojunction Bipolar Transistors for High-Speed and Low-Power Integrated-Circuit Applications.

Author

Oka, Tohru, Hirata, Koji, Suzuki, Hideyuki, Ouchi, Kiyoshi, Uchiyama, Hiroyuki, Taniguchi, Takafumi, Mochizuki, Kazuhiro, and Nakamura, Tohru

Subjects
*BIPOLAR transistors, *INTEGRATED circuits, *DIGITAL electronics
Abstract

Small-scale InGaP/GaAs heterojunction bipolar transistors (HBTs) with high-speed as well as lowcurrent operation are demonstrated. To reduce the emitter size S[sub E] and the base-collector capacitance C[sub BC] simultaneously, the HBTs are fabricated by using WSi/Ti as the base electrode and by burying SiO[sub 2] in the extrinsic collector region. WSi/Ti metals simplify and facilitate processing to fabricate small base electrodes, and the buried SiO[sub 2] reduces the parasitic C[sub BC]: under the base electrode. The cutoff frequency ƒ[sub T] of 156 GHz and the maximum oscillation frequency ƒ[sub max] of 255 GHz were obtained at a collector current I[sub c] of 3.5 mA for the HBT with S[sub E] of 0.5 µm × 4.5 µm, and ƒ[sub T] of 114 GHz and ƒ[sub max] of 230 GHz were obtained at l[sub c] of 0.9 mA for the HBT with S[sub E] of 0.25 µm × 1.5 µrn. A 1/8 static frequency divider operated at a maximum toggle frequency of 39.5 GHz with a power consumption per flip-flop of 190 mW. A transimpedance amplifier provides a gain of 46.5 dB.Ω with a bandwidth of 41.6 GHz at a power consumption of 150 mW. These results indicate the great potential of our HBTs for high-speed, low-power integrated-circuit applications. [ABSTRACT FROM AUTHOR]

Published
2001
Full Text
View/download PDF

137. Enhanced Susceptibility of HLA-mediated Ticlopidine-induced Idiosyncratic Hepatotoxicity by CYP2B6Polymorphism in Japanese

Author

Ariyoshi, Noritaka, Iga, Yukako, Hirata, Koji, Sato, Yasunori, Miura, Go, Ishii, Itsuko, Nagamori, Seiji, and Kitada, Mitsukazu

Abstract

Hepatotoxicity is the most frequent adverse drug reaction (ADR) in Japanese treated with ticlopidine (TP). We investigated the relationship between CYP2B6haplotype and incidence of TP-induced hepatotoxicity in 114 Japanese patients. Although 4 haplotypes (* 1A,* 1H,* 1Jand *6B) accounted for more than 80% of the inferred haplotypes in both control (n=81) and case (n=22) subjects, the prevalence was apparently different: control, * 1A>*6B>* 1H>* 1Jand case, * 1J>* 1H>* 1A>* 6B.The reporter gene assay for the two SNPs, which comprise the * 1Hor * 1Jhaplotype, suggested that the * 1Hand * 1Jhaplotypes may be associated with the increased expression of CYP2B6, probably due to g. −2320T>C. Combination analysis of CYP2B6and human leukocyte antigen (HLA) haplotypes revealed that individuals possessing CYP2B6* 1Hor * 1Jwith HLA-A*3303have the highest susceptibility to TP-induced hepatotoxicity (odds ratio, 38.82; 95%CI, 8.08-196.0, P<0.001). Although this is a preliminary case-control study with some limitations, it is the first example that HLA-induced idiosyncratic ADR may be modified by individual variation in CYP activities.

Published
2010
Full Text
View/download PDF

142. Properties of α-Mannosidase Partially Purified from the Apple Snail, Pomacea canaliculata

Author

HIRATA, Koji, ASO, Yoichi, and ISHIGURO, Masatsune

Abstract

Pomacea canaliculataα-mannosidase (260 kDa), composed of at least two isoforms with different pI, was partially purified. The activity was maximum at pH 4 and unaltered after incubation at 60°C for 60 min. ZnCl2, CaCl2, NaCl, and SH-reagents increased the activity, while MnCl2and EDTA inhibited it. The enzyme catalyzed the hydrolysis of α1-2, α1-3, and α1-6 mannosidic linkages.

Published
1998
Full Text
View/download PDF

143. Purification of Pomacea canaliculataα-Fucosidase Isoforms with Different Thermostabilities

Author

HIRATA, Koji, ASO, Yoichi, YASUDA, Shoji, and ISHIGURO, Masatsune

Abstract

Two isoforms, F1 (pI4.7) and F2 (pI4.9), of α-fucosidase were purified from the viscera of Pomacea canaliculata.The thermostability of F1 was higher than that of F2. Both were 260-kDa proteins containing polypeptides (55 and 52 kDa) and sugar. There were small differences between F1 and F2 in the optimum conditions for the enzyme reaction and pH stability.

Published
1998
Full Text
View/download PDF

144. Risk factors for recurrent biliary obstruction following endoscopic biliary stenting in patients with unresectable ampullary cancer: A multicenter retrospective study.

Author

Sugiura, Ryo, Kuwatani, Masaki, Kin, Toshifumi, Matsumoto, Ryusuke, Ikeda, Yuki, Sano, Itsuki, Hirata, Koji, Yoshida, Makoto, Masaki, Yoshiharu, Ono, Michihiro, Hirata, Hajime, Yamato, Hiroaki, Onodera, Manabu, Nakamura, Hideaki, Taya, Yoko, Ehira, Nobuyuki, Nakajima, Masahito, Kawabata, Hidemasa, Ihara, Hideyuki, and Kudo, Taiki

Subjects
*GALLSTONES, BILIARY tract cancer
Abstract

Objectives: Unresectable ampullary cancer (AC) is a rare disease entity. The risk factors for recurrent biliary obstruction (RBO) following endoscopic biliary stenting (EBS) for unresectable AC remain unknown. In this study we aimed to evaluate the cumulative RBO rate and to identify risk factors for RBO following palliative EBS in patients with unresectable AC. Methods: This multicenter retrospective observational study enrolled consecutive patients with unresectable AC who had undergone palliative EBS between April 2011 and December 2021. The cumulative rate of and risk factors for RBO following palliative EBS were evaluated via multivariate analysis. Results: The study analysis comprised 107 patients with a median age of 84 years (interquartile range 79–88 years). Plastic stents (PSs) and self‐expandable metal stents (SEMSs) were placed in 53 and 54 patients, respectively. Functional success was accomplished in 104 (97.2%) patients. Of these, RBO occurred in 62 (59.6%) patients, with obstruction and complete/partial migration occurring in 47 and 15 patients, respectively. The median time to RBO was 190 days. Multivariate analysis showed that PS was associated with a higher rate of RBO compared to SEMS (hazard ratio [HR] 2.48; P < 0.01) and that the presence of common bile duct stones/sludge immediately after EBS was an independent risk factor for RBO (HR 1.99; P = 0.04). Conclusions: The use of SEMS compared to PS during EBS reduced the time to RBO in patients with unresectable AC. Common bile duct stones/sludge immediately after EBS was a risk factor for RBO. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

145. Exocrine tissue-driven TFF2 prevents apoptotic cell death of endocrine lineage during pancreas organogenesis.

Author

Hirata, Koji, Kodama, Sota, Nakano, Yasuhiro, Minaki-Nakagawa, Yasuko, Aoyama, Yoshiki, Sakikubo, Morito, Goto, Toshihiko, Yoshida, Masahiro, Masui, Toshihiko, Yamamoto, Takuya, Uemoto, Shinji, and Kawaguchi, Yoshiya

Abstract

During embryogenesis, exocrine and endocrine pancreatic tissues are formed in distinct regions within the branched ductal structure in mice. We previously reported that exocrine-specific inactivation of Pdx1 by Elastase-Cre caused not only hypoplastic exocrine formation but also substantial endocrine defects resulting in diabetic phenotype, indicating the existence of an exocrine-driven factor(s) that regulates proper endocrine development. In this study, we identified Trefoil Factor 2 (TFF2) as an exocrine gene expressed from embryonic day 16.5 to adulthood in normal mice but significantly less in our Pdx1 mutants. Using in vitro explant culture of embryonic pancreatic tissue, we demonstrated that TFF2 prevented the apoptosis of insulin-producing cells but that antagonizing CXCR4, a known TFF2 receptor, suppressed this anti-apoptotic effect in the mutants. Furthermore, the antagonist in normal pancreatic tissue accelerated the apoptosis of insulin-producing cells, indicating that the TFF2/CXCR4 axis maintains embryonic insulin-producing cells in normal development. TFF2 also suppressed the apoptosis of Nkx6.1+ endocrine precursors in mutant pancreata, but this effect was unperturbed by the CXCR4 antagonist, suggesting the existence of an unknown receptor for TFF2. These findings suggest TFF2 is a novel exocrine factor that supports the survival of endocrine cells in the multiple stages of organogenesis through distinct receptors. [ABSTRACT FROM AUTHOR]

Published
2019
Full Text
View/download PDF

146. Ptf1a inactivation in adult pancreatic acinar cells causes apoptosis through activation of the endoplasmic reticulum stress pathway.

Author

Sakikubo, Morito, Furuyama, Kenichiro, Horiguchi, Masashi, Hosokawa, Shinichi, Aoyama, Yoshiki, Tsuboi, Kunihiko, Goto, Toshihiko, Hirata, Koji, Masui, Toshihiko, Dor, Yuval, Fujiyama, Tomoyuki, Hoshino, Mikio, Uemoto, Shinji, and Kawaguchi, Yoshiya

Abstract

Pancreas transcription factor 1 subunit alpha (PTF1A) is one of the key regulators in pancreatogenesis. In adults, it transcribes digestive enzymes, but its other functions remain largely unknown. Recent conditional knockout studies using Ptf1aCreER/floxed heterozygous mouse models have found PTF1A contributes to the identity maintenance of acinar cells and prevents tumorigenesis caused by the oncogenic gene Kras. However, Ptf1a heterozygote is known to behave differently from homozygote. To elucidate the effects of Ptf1a homozygous loss, we prepared Elastase-CreERTM; Ptf1afloxed/floxed mice and found that homozygous Ptf1a deletion in adult acinar cells causes severe apoptosis. Electron microscopy revealed endoplasmic reticulum (ER) stress, a known cause of unfolded protein responses (UPR). We confirmed that UPR was upregulated by the activating transcription factor 6 (ATF6) and protein kinase RNA (PKR)-like endoplasmic reticulum kinase (PERK) pathways, but not the inositol requiring enzyme 1 (IRE1) pathway. Furthermore, we detected the expression of CCAAT-enhancer-binding protein (C/EBP) homologous protein (CHOP), a pro-apoptotic factor, indicating the apoptosis was induced through UPR. Our homozygous model helps clarify the role PTF1A has on the homeostasis and pathogenesis of exocrine pancreas in mice. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results