检索结果-南通市图书馆

新乡医学院学报 2000年第4期17卷 229-236页

作者：李同光 O’Brien KF naves jl Wiley Jr.AL 东卡罗来纳大学Brody医学院 Leo W Jenkins癌症中心放射肿瘤科北卡罗来纳大学公共卫生学院生物统计室 Watson医院Jere W.Annis放疗中心

目的　进一步验证微核率作为测量生物照射剂量的可行性。方法　 8例未经放疗 (xRT)和化疗的前列腺癌 ,经标准分区骨盆xRT治疗方案 ,收集前列腺癌患者xRT前和xRT中外周血 ,测定阻滞胞质分裂的外周血淋巴细胞 (PBL)微核率。检测项目包括 :... 详细信息

目的　进一步验证微核率作为测量生物照射剂量的可行性。方法　 8例未经放疗 (xRT)和化疗的前列腺癌 ,经标准分区骨盆xRT治疗方案 ,收集前列腺癌患者xRT前和xRT中外周血 ,测定阻滞胞质分裂的外周血淋巴细胞 (PBL)微核率。检测项目包括 :(1)检查微核率和估计的等效全身吸收剂量之间的关系 ;(2 )评价xRT前PBL微核率的辐射剂量效应关系的个体差异。结果　 (1)患者PBL微核率随估算的全身吸收射线量 [y =1.46 + 9.2D (R2 =0 .7,P =0 .0 72 ) ]增加而呈线性增加 ;微核呈广泛分布 ;每10 0 0个双核PBL微核率相应增加的比例分别高于基线水平 0 .9～ 8.2倍 (中位数 4.1)。 (2 )xRT前 ,微核率也随体外照射剂量增加而增加 ,每 1照射剂量下 ,大多数患者微核率呈高度离散分布。 3例因xRT引起的早期副反应患者中 ,2例的PBL微核率明显高于无xRT引起副反应者。结论　PBL微核率可用来测定体外生物照射剂量。因xRT前PBL微核率与体外辐射剂量效应关系存在着显著的个体差异 ,开始应用xRT前可用PBL微核率判定患者个体固有的放射敏感性。

关键词：微核淋巴细胞前列腺癌放射剂量效应治疗

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Dissecting the molecular pathophysiology of drug-induced liver injury

引用

World Journal of Gastroenterology 2018年第13期24卷 1373-1385页

作者： Hui Ye Leonard J Nelson Manuel Gómez del Moral Eduardo Martínez-naves Francisco Javier Cubero Department of Immunology Ophtalmology and ORLComplutense University School of MedicineMadrid 28040Spain 12 de Octubre Health Research Institute(imas12) Madrid 28041Spain Institute for BioEngineering(Human Liver Tissue Engineering Faraday BuildingThe University of EdinburghThe King BuildingsMayfield RoadEdinburgh EH9 3 JLScotlandUnited Kingdom Department of Cell Biology Complutense University School of MedicineMadrid 28040Spain

Drug-induced liver injury(DILI) has become a major topic in the field of Hepatology and Gastroenterology. DILI can be clinically divided into three phenotypes: hepatocytic, cholestatic and mixed. Although the clinical manifestations of DILI are variable and the pathogenesis complicated, recent insights using improved preclinical models, have allowed a better understanding of the mechanisms that trigger liver damage. In this review, we will discuss the pathophysiological mechanisms underlying DILI. The toxicity of the drug eventually induces hepatocellular damage through multiple molecular pathways, including direct hepatic toxicity and innate and adaptive immune responses. Drugs or their metabolites, such as the common analgesic, acetaminophen, can cause direct hepatic toxicity through accumulation of reactive oxygen species and mitochondrial dysfunction. The innate and adaptive immune responses play also a very important role in the occurrence of idiosyncratic DILI. Furthermore, we examine common forms of hepatocyte death and their association with the activation of specific signaling pathways.

关键词： signaling pathways acetaminophen Drug-induced liver injury cell death reactive oxygen species

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Alcoholic liver disease:Utility of animal models

引用

World Journal of Gastroenterology 2018年第45期24卷 5063-5075页

作者： Arantza Lamas-Paz Fengjie Hao Leonard J Nelson Maria Teresa Vázquez Santiago Canals Manuel Gómez del Moral Eduardo Martínez-naves Yulia A Nevzorova Francisco Javier Cubero Department of Immunology Ophthalmology and ORLComplutense University School of MedicineMadrid 28040Spain 12 de Octubre Health Research Institute(imas12) Madrid 28041Spain Institute for Bioengineering(IBioE) School of EngineeringFaraday BuildingThe University of EdinburghEdinburgh EH9 3 JLScotlandUnited Kingdom Department of Human Anatomy and Embryology Complutense University School of MedicineMadrid 28040Spain Instituto de Neurociencias Consejo Superior de Investigaciones CientíficasUniversidad Miguel HernándezSan Juan de Alicante 03550Spain Department of Cell Biology Complutense University School of MedicineMadrid 28040Spain Department of Genetics Physiology and MicrobiologyFaculty of BiologyUniversidad ComplutenseMadrid 28040Spain Department of Internal Medicine Ⅲ University Hospital RWTH AachenAachen 52062Germany

Alcoholic liver disease(ALD) is a major cause of acute and chronic liver injury. Extensive evidence has been accumulated on the pathological process of ALD during the past decades. However, effective treatment options for ALD are very limited due to the lack of suitable in vivo models that recapitulate the full spectrum of ALD. Experimental animal models of ALD, particularly rodents, have been used extensively to mimic human ALD. An ideal animal model should recapitulate all aspects of the ALD process, including significant steatosis, hepatic neutrophil infiltration, and liver injury. A better strategy against ALD depends on clear diagnostic biomarkers, accurate predictor(s) of its progression and new therapeutic approaches to modulate stop or even reverse the disease. Numerous models employing rodent animals have been established in the last decades to investigate the effects of acute and chronic alcohol exposure on the initiation and progression of ALD. Although significant progress has been made in gaining better knowledge on the mechanisms and pathology of ALD, many features of ALD are unknown, and require further investigation, ideally with improved animal models that more effectively mimic human ALD. Although differences in the degree and stages of alcoholic liver injury inevitably exist between animal models and human ALD, the acquisition and translational relevance will be greatly enhanced with the development of new and improved animal models of ALD.

关键词： Steatohepatitis Cirrhosis Hepatocellular carcinoma Alcoholic liver disease Reactive oxygen species

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：