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Cytokines in Liver Injury and Repair [Hardcover]

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  • Category: Books (Medical)
  • ISBN-10:  0792387759
  • ISBN-10:  0792387759
  • ISBN-13:  9780792387756
  • ISBN-13:  9780792387756
  • Publisher:  Springer
  • Publisher:  Springer
  • Binding:  Hardcover
  • Binding:  Hardcover
  • Pub Date:  01-Feb-2002
  • Pub Date:  01-Feb-2002
  • Pages:  377
  • Pages:  377
  • SKU:  0792387759-11-SPRI
  • SKU:  0792387759-11-SPRI
  • Item ID: 100751516
  • List Price: $169.99
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This book, the proceedings of Falk Symposium No. 125 on 'Cytokines in Liver Injury and Repair' (Progress in Gastroenterology and Hepatology Part II), held in Hannover, Germany, on September 30 - October 1, 2001, provides an update of our current knowledge on the role of cytokines in various human and experimental liver diseases and on their present and prospective use in therapeutic trials.

The book contains chapters by most well-known experts in the field who have contributed significantly to our present knowledge on cytokines in liver injury and repair.

This book, the proceedings of Falk Symposium No. 125 on 'Cytokines in Liver Injury and Repair' (Progress in Gastroenterology and Hepatology Part II), held in Hannover, Germany, on September 30 - October 1, 2001, provides an update of our current knowledge on the role of cytokines in various human and experimental liver diseases and on their present and prospective use in therapeutic trials.

Developments in recent years include: Since the first report of a cytokine knockout mouse for IL-2 in 1991 a large number of cytokine and cytokine receptor genes have been inactivated in mouse germlines and the corresponding mutant mice have provided a wealth of novel information. In addition, targeted-gene disruption techniques (e.g. cre-loxP) and liver-specific overexpression of certain cytokines have provided clues for the understanding of their role in the pathophysiology of liver diseases.

The number of well-characterized cytokines, chemokines, and growth factors is ever growing and it becomes increasingly evident that they are effective in a complex network of positive and negative signals. A disruption of this homeostatic balance is a direct cause of disease, determines its complications, and is related to its progression, e.g. in inflammation and fibrogenesis.

Signaling pathways from receptors to target genes have beenlƒ+

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