Titlebook: Drug-Induced Liver Toxicity; Minjun Chen,Yvonne Will Book 2018 Springer Science+Business Media, LLC, part of Springer Nature 2018 Acute li

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Reactive Metabolite Assessment in Drug Discovery and Development in Support of Safe Drug Designnowledged as an important determinant of drug failure. Reasons for individual susceptibilities of patients that result in various forms and severities of adverse drug reactions are manifold. They involve factors such as the underlying diseases, individual genotypes of the immune system, and drug spe

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High Content Screening for Prediction of Human Drug-Induced Liver Injurycombines automated imaging with image analysis to assess cell health and customized parameters in a multiparametric fashion, enabling coverage over several mechanisms important for DILI. In simple two-dimensional cell models, various HCS assays typically show a sensitivity of ~50% with a high specif

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1557-2153 s, from basic research through to clinical actionThis book provides a comprehensive view of the methodologies used for the study of liver toxicity encountered throughout the whole life cycle of a drug, from drug discovery, to clinical trial, post-marketing, and even clinical practice. Organized into

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Sensors,tigate these hazards. Alternatively, these stress responses may predict the development of idiosyncratic drug-induced liver injury (IDILI). Current evidence supports the hypothesis that IDILI is often mediated by adaptive immunity in genetically susceptible individuals which is modulated by the robustness of immune tolerance.

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Adaptive Reactive Rich Internet ApplicationsILI has lately expanded into complex three-dimensional models to further improve predictivity. The wealth of HCS data make it particularly amenable for machine learning and systems biology approaches for building rational models for prediction of DILI.

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Overview of Mechanisms of Drug-Induced Liver Injury (DILI) and Key Challenges in DILI Researchtigate these hazards. Alternatively, these stress responses may predict the development of idiosyncratic drug-induced liver injury (IDILI). Current evidence supports the hypothesis that IDILI is often mediated by adaptive immunity in genetically susceptible individuals which is modulated by the robustness of immune tolerance.