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Comparative safety study on severe anemia by simeprevir versus telaprevir‐based triple therapy for chronic hepatitis C 下载免费PDF全文
Eiichi Ogawa Norihiro Furusyo Eiji Kajiwara Hideyuki Nomura Akira Kawano Kazuhiro Takahashi Kazufumi Dohmen Takeaki Satoh Koichi Azuma Makoto Nakamuta Toshimasa Koyanagi Kazuhiro Kotoh Shinji Shimoda Jun Hayashi The Kyushu University Liver Disease Study Group 《Journal of gastroenterology and hepatology》2015,30(8):1309-1316
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Yoshinori Yanai Takeo Kosaka Kohei Nakamura Eriko Aimono Kazuhiro Matsumoto Shinya Morita Shuji Mikami Hiroshi Nishihara Mototsugu Oya 《Cancer science》2020,111(12):4652
Cyclin‐dependent kinase 12 (CDK12), one of the key factors associated with DNA damage response pathways, is located on chromosome 17 proximal to Erb‐B2 receptor tyrosine kinase 2 (ERBB2). In this report, CDK12 and ERBB2 coamplification was detected by targeted next‐generation sequencing in two urothelial carcinomas. The staining intensity of the CDK12 and human epidermal growth factor receptor‐2 proteins was associated with the prognosis of each urothelial carcinoma case. Our results suggest that CDK12 coamplification with ERBB2 might be associated with tumor aggressiveness and contribution to cancer pathogenesis. Therapies targeting CDK12 should be developed for these patients. 相似文献
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Shoji Kubo Hiroaki Kinoshita Kazuhiro Hirohashi Takatsugu Yamamoto 《Journal of Hepato-Biliary-Pancreatic Surgery》1995,2(1):85-89
A case of cystadenocarcinoma of the liver is reported. The patient was a 73-year-old woman in whom a tumor was detected in
the lateral segment of the liver during a health examination. Ultrasonograms and computed tomograms showed a multilocular
cystic mass. Magnetic resonance imaging (MRI) showed a multilocular lowintensity mass, including a high-intensity portion
and a portal branch compressed by the tumor. MRI with gadolinium showed an enhanced cyst wall. The cystic part of the tumor
became smaller and the solid part became larger over a 1-month period, indicating that the tumor was malignant. Subsegmentectomy
(S3) was performed and cystadenocarcinoma with cystadenoma was diagnosed by histopathological examination. Identification of
changes in the appearance of a tumor should be helpful for the differential diagnosis of cystadenoma and cystadenocarcinoma. 相似文献
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Shinsuke Hamaguchi Yasuhisa Okuda Toshimitsu Kitajima Nobuhide Masawa 《Journal canadien d'anesthésie》2002,49(7):745-748
PURPOSE: To clarify the appropriate concentration and dose of hypertonic saline solution (HSS) for preventing delayed neuronal death in the hippocampal CA1 subfield after transient forebrain ischemia in gerbils. METHODS: Thirty gerbils were randomly assigned to five groups: physiological saline solution (PSS) group, ischemia/reperfusion treated with PSS 2 mL x kg(-1); 5% HSS group, treated with 5% HSS 2 mL x kg(-1); 7.5% HSS group, treated with 7.5% HSS 2 mL x kg(-1); 10% HSS group, treated with 10% HSS 2 mL x kg(-1); 20% HSS group, treated with 20% HSS 2 mL x kg(-1). Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes. Five days later, histopathological changes in the hippocampal area were examined, and the degenerative ratio of the pyramidal cells were measured according to the following formula: (number of degenerative pyramidal cells/total number of pyramidal cells per 1 mm of hippocampal CA1 subfield) x 100. RESULTS: In PSS and 20% groups, neuronal cell damage was observed five days after ischemia. In the other three groups, these changes were not observed. The degenerative ratios of pyramidal cells were as follows; PSS group: 91.6 +/- 5.6%, 5% HSS group: 7.2 +/- 1.6%, 7.5% group: 8.3 +/- 1.4%, 10% HSS group: 6.2 +/- 1.1%, 20% HSS group: 85.8 +/- 8.7% (P < 0.05; PSS and 20% HSS vs three other groups). CONCLUSION: This study demonstrates that 5, 7.5 or 10% HSS 2 mL x kg(-1) may prevent delayed neuronal death in the hippocampal CA1 subfield after cerebral ischemia/reperfusion in gerbils. 相似文献
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Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies. 相似文献