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1.
Hori Hiroki Ohta Asuka Matsui Honami Yano Kanako Morita-Tominaka Miyuki Linn Zayar Masumoto Daisuke Okumura Yosuke Okamura Satoshi Kurihara Kosuke Hayakawa Akira Rikiishi Takeshi Kobayashi Kyoko 《International journal of clinical oncology / Japan Society of Clinical Oncology》2022,27(1):245-252
International Journal of Clinical Oncology - The practice of cancer diagnosis disclosure to children has been changed with the times. The regulations of clinical trials in the 2000s might change... 相似文献
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Comparative safety study on severe anemia by simeprevir versus telaprevir‐based triple therapy for chronic hepatitis C
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![点击此处可从《Journal of gastroenterology and hepatology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
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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Induction of endothelium-dependent relaxation in the rat aorta by IRL 1620, a novel and selective agonist at the endothelin ETB receptor. 总被引:3,自引:2,他引:1
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![点击此处可从《British journal of pharmacology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
H. Karaki S. A. Sudjarwo M. Hori M. Takai Y. Urade T. Okada 《British journal of pharmacology》1993,109(2):486-490
1. The effects of a novel and selective agonist at the endothelin ETB receptor, IRL 1620 (Suc-[Glu9, Ala11,15] endothelin-1 (8-21)), were examined in the isolated aorta of the rat. 2. IRL 1620 (1-300 nM) changed neither the resting tone nor the cytosolic Ca2+ level ([Ca2+]i) of the aorta without endothelium. In the presence of endothelium, however, IRL 1620 increased endothelial [Ca2+]i with little effect on the muscle tone. In the absence of external Ca2+, IRL 1620 still induced a transient increase in endothelial [Ca2+]i. 3. Noradrenaline (100 nM) increased both muscle [Ca2+]i and tension. IRL 1620 (1-300 nM) relaxed the muscle with an increase in endothelial [Ca2+]i only in the presence of endothelium. An inhibitor of nitric oxide synthase, 100 microM NG-monomethyl-L-arginine, inhibited the relaxant effect of IRL 1620 but not the increase in endothelial [Ca2+]i. 4. In resting and noradrenaline-stimulated aorta, the effects of IRL 1620 were inhibited by a selective antagonist of the ETB receptor, IRL 1038 (0.3-3 microM), although a selective antagonist of the ETA receptor, BQ-123 (3 microM), was ineffective. Verapamil (10 microM) did not alter the effects of IRL 1620. 5. A muscarinic receptor agonist, carbachol (1 microM), also induced endothelium-dependent relaxation with an increase in endothelial [Ca2+]i. However, the effects of carbachol were not inhibited by the ETB antagonist, IRL 1038 (3 microM).(ABSTRACT TRUNCATED AT 250 WORDS) 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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Immunosuppressive activities of the newly discovered FK506, isolated from Streptomyces tsukubaensis, were examined by using cardiac allotransplantation in the rat, and the mechanisms underlying induction and maintenance of FK506-induced long-term allograft survival were studied. Male rats of WKA (RT1k) and F344 (RT1lvl) strains were used as recipients and donors, respectively, and those of BN (RT1n) strain were used as third-party donors. Treatment with FK506, beginning from the day of allografting for 14, 10, or as few as 4 days, prolonged allograft survival significantly across the major histocompatibility barrier. The minimum doses for prolonging graft survival were 0.1 mg/kg/day by intramuscular treatment and 1.0 mg/kg/day by oral treatment. Treatment with FK506 at a dose of 0.32 mg/kg/day from day 4 until day 10 resulted in all the grafts surviving indefinitely and from days 5 to 10, half the grafts survived indefinitely, suggesting that the agent inhibited ongoing rejection. On the other hand, cyclosporine treatment at a dose of 20 mg/kg/day from day 2 did not prolong graft survival time statistically significantly. Induction of prolonged graft survival was not obtained by pretreatment of the prospective donor or recipient; prolonging effects were observed only when the agent was administered after allografting. Thus, the primary effect of the agent is exerted on responder lymphocytes reacting to the donor antigens in the induction phase of long-term graft acceptance. The mechanisms underlying the maintenance of long-term grafts were analyzed by testing the capacity of lymphocytes or serum of long-term graft-bearing rats to inhibit graft rejection in irradiated grafted hosts. Transfer of 2 x 10(8) lymphocytes from FK506-induced long-term F344 graft-bearing WKA rats resulted in indefinite survival of F344 heart allografts, but it did not prolong survival of third-party BN hearts. Transfer of 2.5 ml serum from long-term graft-bearing rats also prolonged graft survival of F344 hearts, but not BN hearts. These results suggest that donor strain-specific suppressor cells and humoral factor(s) are induced by treatment with FK506 in the presence of allografts, and that they play at least partial roles in the maintenance of long-term allograft acceptance. 相似文献