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18篇 您的检索式:作者名="Hiroyo"
    题名 作者 年代 出处 被引量
1Cryptogenic cirrhosis in the region where obesity is not prevalent显示文摘瞄准:最近的研究证明了肥胖是起因不明的肝硬化(CC ) 和非酒精的 steatohepatitis 的普通特征。然而,几乎在肥胖不是流行的区域的 CC 上没有很少信息。方法:CC 的临床的特征,和肝相关的病态和死亡在肥胖的流行是低的日本被分析。在 652 个肝脏硬化症的病人之中,我们与 CC 识别了 29 个病人(4.4%) 。这些,被跟随在上面因为超过 6 个月在盒子控制被比较的 24 个 CC 病人与年龄学习 -- ,性别 -- ,并且病毒的病原学的孩子呸匹配分数的控制有肝硬化。结果:肥胖(BMI>or=25 kg/m (2 )) ,糖尿病,和 hypertriglyceridemia 是更经常的,并且内脏的胖区域比在控制在 CC 病人是更大的。抗胰岛素性的索引更高,浆液 aminotransferase 层次比在控制在 CC 病人是更低的。逻辑回归分析作为 CC 的独立预言者识别了提高的血红素 A1c, BMI>or=25 kg/m (2 ) ,和正常 aminotransferase 层次。Kaplan-Meier 分析与在那些组之间的肝相关的病态的类似的累积概率相对照比在控制在 CC 表明了肝细胞癌和更高的幸存率的更低的出现。结论:CC 更经常甚至在肥胖不是流行的区域与控制相比与非酒精的 steatohepatitis 暗示的临床的特征介绍。肝细胞癌和更高的幸存率的更低的出现可以作为与病毒的肝硬化相比在 CC 显示一堂懒惰临床的功课。Hideyuki Kojima Shinya Sakurai Masahiko Matsumura Norie Umemoto Masahito Uemura Hiroyo Morimoto Yasuhiro Tamagawa Hiroshi Fukui 2006World Journal of Gastroenterology2006,12,13:3
2A New MIC Magic-T Using Coupled Slot Lines显示文摘Masayoshi Aikawa and Hiroyo Ogawa 1980IEEE Transaction on Microwave Theory and Technology1980,28,6:1
3Patterning of hybrid titania film using photopolymerization显示文摘Hiroyo S Kanayo T Yasuhiko A 2004Thin Solid Films2004,466,12:1
4Patterning of hybrid titania film using photopolymerization 显示文摘Hiroyo S Kanayo T Yasuhiko A 2004Thin Solid Films2004,466,:1
5Male Sterility-Inducing Mitochondrial Genomes: How Do They Differ?显示文摘Tomohiko Kubo Kazuyoshi Kitazaki Muneyuki Matsunaga Hiroyo Kagami Tetsuo Mikami 2011Critical Reviews in Plant Sciences2011,,4:1
6Patterning of Hybrid Titania Film Using Photopolymerization显示文摘 Kanayo T Yasuhiko A 2004Thin Solid Films2004,466,:1
7显示文摘Hiroyo Segawa Satoshi Ogata Naoto Hirosaki 2010Opti- cal Materials2010,33,:1
8Influence of CO2, SO2and NO in flue gas on Microalgae productivity 显示文摘Hiroyo M Akihiro H and Norio S 2004Journal of Chemical Engineering of Japan2004,64,5:1
9Deterioration of soil fertility by land use changes in South Sumatra, Indonesia:from 1970 to 1990显示文摘Jamalam L Tamaluddin S Hiroyo N 1998Hydrological Processes1998,12,:1
10Supplementation with branched-chain amino acids attenuates hepatic apoptosis in rats with chronic liver disease显示文摘Masashi Kuwahata Hiroyo Kubota Hiroaki Kanouchi Shunsuke Ito Aki Ogawa Yukiko Kobayashi Yasuhiro Kido 2012Nutrition Research2012,,7:1
11显示文摘Hiroyo Segawa Kanayo Tateishi Yasuhiko Arai 2004Thin Solid Films2004,466,:1
12Elschnig pearl formation along the neodymium:YAG laser posterior capsulotomy margin显示文摘Daijiro Kurosaka Katsuhiko Kato Hiroyo Kurosaka Mami Yoshino Kunihiko Nakamura Kazuno Negishi 2002Journal of Cataract & Refractive Surgery2002,,10:1
13Exercise-induced lipid peroxidation and leakage of enzymes before and after vita- min E supplementation显示文摘SATOSHI S KIYOJI T HIROYO K 1989Int J Biochemistry1989,21,8:1
14Treatment for gastric carcinoma in the oldest old patients显示文摘Shunji Endo Yukinobu Yoshikawa Nobutaka Hatanaka Harumi Tominaga Yosuke Shimizu Kazuya Hiraoka Akiko Nishitani Toshimitsu Irei Shinsuke Nakashima Mi-Hwa Park Hiroyo Takahashi Makoto Wakahara Wataru Kamiike 2011Gastric Cancer2011,,2:1
15Fabrication of periodic arrays of top-gathering titania-organic hybrid pillars derived from multi-beam laser interference显示文摘HIROYO S HIROAKI M TETSUJI Y 2006Proc SPIE2006,6106,61:1
16Fabrication of glasses of dispersed yellow oxynitride phosphorfor white light-emitting diodes显示文摘Hiroyo Segawa Satoshi Ogata Naoto Hirosaki 2010Journal of the opticalmaterials2010,33,17:1
17Fungal pyrrolidine-containing metabolites inhibit alkaline phosphatase activity in bone morphogenetic protein-stimulated myoblastoma cells显示文摘Fibrodysplasia ossificans progressiva(FOP)is a rare autosomal dominant congenital disorder characterized by progressive heterotopic ossification in muscle tissues.A constitutively activated mutation of a bone morphogenetic protein(BMP)receptor,ALK2,has been identified in patients with FOP.We report here that four structurally related compounds,lucilactaene,hydroxylucilactaene,NG-391 and NG-393,produced by fungal strain Fusarium sp.B88,inhibit BMP signaling in vitro.Alkaline phosphatase activity,a marker enzyme of osteoblastic differentiation,was decreased in C2C12 myoblasts stably expressing mutant ALK2 by treatment with those compounds with IC_(50) values of 5.7,6.8,6.9 and 6.1 mM,respectively.Furthermore,NG-391 and NG-393 inhibited BMP-specific luciferase reporter activity,which is directly regulated by transcription factor Smads,with IC50 values of 1.4 and 2.1 mM,respectively.These findings suggest that these fungal metabolites may provide a new direction in the development of FOP therapeutics.Takashi Fukuda Ryuji Uchida Hiroyo Inoue Satoshi Ohte Hiroyuki Yamazaki Daisuke Matsuda Takenobu Katagiri Hiroshi Tomoda 2012Acta Pharmaceutica Sinica B2012,2,1:0
18Mutation analysis of ATP13A2 in early-onset parkinsonism patients显示文摘BACKGROUND: A recent study has found that ATP13A2 is the causative gene for PARK9-linked auto-somal recessive early-onset parkinsonism, described previously in Jordanian and Chilean families (Ku-for-Rakeb syndrome). OBJECTIVE: To screen eastern Asian patients with early-onset parkinsonism for mutations in ATP13A2 and to describe positron emission tomography (PET) findings of PARK9-linked parkinsonism. DESIGN, TIME AND SETTING: In total, 117 patients were selected from the Department of Neurology, Juntendo University, from February 2003 to October 2006, for this molecular genetics and case-control study. PARTICIPANTS: The patients with parkinsonism consist of two cohorts. Ninety four patients with onset age of less than 30 years were selected for the first cohort. They included 49 males and 44 females, comprising 73 Japanese, 9 Korean, 8 Taiwan Residents, and 4 Mainland Chinese. Eleven patients had parkinsonism complicated with dementia, 15 patients had family histories of parkinsonism (including 2 families), and 5 patients were from consanguineous parents (including one family). The second cohort of 23 patients was composed of patients with consanguineous parents (n = 15) or who had affected siblings (n = 6) or both (n = 2), but the age at onset ranged from 30 to 50 years. METHODS: In 117 patients with parkinsonism, direct sequencing of ATP13A2 exons 13, 16, and 26, in which mutations had been reported previously, were performed. Sequencing was also performed in all 29 exons, including splice sites, in 28 probands who showed homozygosity at the PARK9 locus by haplotype analysis. Mutation analysis was also performed in 150 normal people. Linkage analysis was performed on all 3 parkinsonism families using short tandem repeat markers flanking the PARK9 locus. For patients who had ATP13A2 mutation, we performed brain MRI and 18F-dopa PET scans. MAIN OUTCOME MEASURES: ATP13A2 DNA sequence, 18F-dopa PET scan and brain MRI findings. RESULTS: A novel F182L mutation in a consanguineous Japanese family was identified. The patient was homozygous for the F182L mutation and her unaffected parents and two unaffected siblings were heterozygous for the F182L mutation. The patient developed early-onset atypical parkinsonism, which resembled the originally reported Kufor-Rakeb syndrome. MRI examination showed spinal cord atrophy and 18F-dopa PET scan findings were similar to those of Parkinson’s disease. CONCLUSION: Detection of the new PARK9 mutation, together with the previously reported cases of PARK9-linked parkinsonism, expand the clinical phenotypic spectrum of levodopa-responsive parkinsonism.Yuping Ning Hiroyuki Tomiyama Yuanzhe Li Manabu Funayama Hiroyo Yoshino Shigeto Sato Yoshikuni Mizuno Nobutaka Hattori 2008Neural Regeneration Research2008,3,4:0
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