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Titlebook: HCV/Oxidative Stress and Liver Disease; Kiwamu Okita (Professor and Chairman) Conference proceedings 2003 Springer Japan 2003 DNA.RNA.canc

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發(fā)表于 2025-3-21 18:55:09 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱HCV/Oxidative Stress and Liver Disease
編輯Kiwamu Okita (Professor and Chairman)
視頻videohttp://file.papertrans.cn/421/420173/420173.mp4
概述Including information on new aspects of oxidative stress and liver disease
圖書封面Titlebook: HCV/Oxidative Stress and Liver Disease;  Kiwamu Okita (Professor and Chairman) Conference proceedings 2003 Springer Japan 2003 DNA.RNA.canc
描述.Since the discovery of superoxide dismutase more than three decades ago, there has been rapid growth in the knowledge of oxidative stress and disease. This volume containing the proceedings of the 13th Yamaguchi Symposium on Liver Disease includes discussion of the direct cellular effects of hepatitis C virus (HCV) proteins on hepatocytes and reviews evidence that oxidative stress caused primarily by the HCV core protein plays a key role in disease pathogenesis. Also included are chapters on new aspects of oxidative stress and liver disease such as carbon monoxide as a regulator of liver microcirculation, hepatic iron accumulation and the incidence of hepatocellular carcinoma, and oxidative stress in the absence of inflammation in hepatocarcinogenesis. This collection of papers from the Yamaguchi Symposium creates a valuable reference resource for physicians and hepatologists..
出版日期Conference proceedings 2003
關(guān)鍵詞DNA; RNA; cancer; cell; gene; gene expression; hepatitis; interferon; liver; liver disease; mutation; oxidative
版次1
doihttps://doi.org/10.1007/978-4-431-67005-6
isbn_softcover978-4-431-67007-0
isbn_ebook978-4-431-67005-6
copyrightSpringer Japan 2003
The information of publication is updating

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發(fā)表于 2025-3-21 22:07:14 | 只看該作者
Role of Core Protein-Induced Oxidative Stress in the Pathogenesis of Hepatitis C,of core-induced oxidative stress include DNA damage, lipid peroxidation, cell cycle dysregulation, and stellate cell activation. These in turn contribute to cell death, fibrogenesis, and carcinogenesis, as seen in patients with chronic hepatitis C. Modulation of oxidative stress may therefore have t
板凳
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地板
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Role of Hepatitis C Virus in Hepatocarcinogenesis: Oxidative Stress in the Absence of Inflammation,ample, colorectal cancer, the accumulation of a set of genetic aberrations may also be necessary for the multistage development of HCC. However, the HCV core protein, to which an oncogenic potential is ascribed, may allow some of the multiple stages of hepatocarcinogenesis to be skipped. Unlike in t
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發(fā)表于 2025-3-22 16:42:40 | 只看該作者
,Reduced Chemical Hepatocarcinogenesis in Interferon-γ Receptor Knockout Mice,wer hepatocellular carcinomas than IFN-α/βR KO and wild-type (wt) mice, although the diameters of the largest liver tumors were not significantly different among the three lineages. Interestingly, immunohistochemical studies demonstrated that the proportions of monocytes/macrophages were greatly red
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發(fā)表于 2025-3-22 19:00:57 | 只看該作者
Fewer Somatic Mutations of Mitochondrial DNA in Noncancerous Liver Tissue of Patients with Hepatoce larger group, some had been treated with IFN, but none had the desired response. The number of mutations in cancerous tissues was significantly smaller for patients with a biochemical or complete response to IFN than for patients with no response to IFN or no history of treatment with IFN. At prese
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發(fā)表于 2025-3-23 00:05:54 | 只看該作者
Hepatic Iron Staining in Chronic Hepatitis C Patients with Low HCV RNA Levels as a Predictive Markenalysis showed that TIS was an independent factor relating to the response to IFN therapy . 0.0062). The TIS correlated significantly with serum ferritin levels (. = 0.637, . < 0.001), but not with any other parameter. Conclusions: Among CH-C patients with low HCV RNA levels, the TIS of the liver ma
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發(fā)表于 2025-3-23 08:08:06 | 只看該作者
ocellular carcinoma, and oxidative stress in the absence of inflammation in hepatocarcinogenesis. This collection of papers from the Yamaguchi Symposium creates a valuable reference resource for physicians and hepatologists..978-4-431-67007-0978-4-431-67005-6
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