The mechanism of liver injury by hepatitis B virus, using a novel adenovirus expressing HBV
The mechanism of liver injury by hepatitis B virus, using a novel adenovirus expressing HBV
批准号:
15590639
负责人:
MURATA Kazumoto
金额:
$2.24万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2003
资助国家:
日本
项目状态:
已结题
起止时间:
2003 至 2004
中文摘要
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英文摘要
Five days after intravenous injection of adenovirus expressing HBV (adeno-HBV) to BALB/c mice, serum HBsAg showed a peak whereas no elevation in adeno-GFP (control virus) injected mice during follow-up. The number of intrahepatic lymphocytes increased 1 day after injection in mice injected either adeno-HBV or adeno-GFP, suggesting that this effect is due to adenovirus itself. Howevr, 5 days after injection, the number of NK cells increased again whereas no increase in adeno-GFP injected mice. The number of CD1d tertramer positive cells decreased 1 day after injection by both adenovirus. The number of CD1d tetramer positive cells recovered in a few days in adeno-GFP injected mice. In contrast, it was not recovered until 10 days after injection of adeno-HBV. NK cytotoxicity using Yac-1 cells was up-regulated 1 day after injection of both virus. Then, it gradually went back to normal in adeno-GFP injected mice whereas iNK cytotoxicity up-regulated again in adeno-HBV injected mice. From the differences on Day 5 after injection, HBV may decrease the number of CD1d tetramer positive cells and increase the number of NK cells. Injection of adeno-HBV to GD1 knockout mice demonstrated the disappearance of NK cytotoxicity. These results may indicate that HBV up-regulated NK cells through NKT cells activation.
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Hepatocellular carcinoma presenting with obstructive jaundice : A clinico-pathological study of eight cases.
伴有梗阻性黄疸的肝细胞癌:八例临床病理研究。
DOI:
--
发表时间:
2003
期刊:
Hepato-Gastroenterology 50
影响因子:
--
作者:
[Yamamoto N, Murata K., Qio M, Murata K, Murata K, Murata K]
通讯作者:
Murata K
DOI:
10.1073/pnas.1131929100
发表时间:
2003-05-27
期刊:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
影响因子:
11.1
作者:
[Murata, K, Lechmann, M, Liang, TJ]
通讯作者:
Liang, TJ
Low-dose chemotherapy of cisplatin and 5-fluorouracil or doxorubicin via implanted infusion port for unresectable HCC
通过植入输注端口进行顺铂和 5-氟尿嘧啶或多柔比星低剂量化疗治疗不可切除的 HCC
DOI:
--
发表时间:
2003
期刊:
Anticancer Research 23
影响因子:
--
作者:
[Yamamoto N, Murata K., Qio M, Murata K]
通讯作者:
Murata K
Low-dose chemotherapy of cisplatin and 5-fluorouracil or doxorubic in via implanted infusion port for unresectable HCC
通过植入输注端口进行顺铂和 5-氟尿嘧啶或多柔比的低剂量化疗治疗不可切除的 HCC
DOI:
--
发表时间:
2003
期刊:
Anticancer Research 23
影响因子:
--
作者:
[Murata K, Shiraki K, Kawakita T, Yamamoto N, Okano H, et al., Murata K]
通讯作者:
Murata K
Tuberculous peritonitis during hemodialysis
血液透析期间结核性腹膜炎
DOI:
--
发表时间:
2004
期刊:
Gastroenterology 127
影响因子:
--
作者:
[Yamamoto N]
通讯作者:
Yamamoto N
共 8 条
Comprehensive analyses for the mechanism of PIVKA-II production from hepatocellular carcinoma
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批准号:23591005
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.41万
-
财政年份:2011
-
负责人:MURATA Kazumoto
-
依托单位:
The mechanism of chronicity of hepatitis B (inhibition of antigen presentation by HBX protein)
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批准号:17590631
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.24万
-
财政年份:2005
-
负责人:MURATA Kazumoto
-
依托单位:
海外基金