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Acetaldehyde–Related Pathology: Bridging the Trans–Disciplinary Divide - ISBN 9780470057667

Acetaldehyde–Related Pathology: Bridging the Trans–Disciplinary Divide

ISBN 9780470057667

Autor: Derek J. Chadwick, Jamie A. Goode

Wydawca: Wiley

Dostępność: 3-6 tygodni

Cena: 848,40 zł

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ISBN13:      

9780470057667

ISBN10:      

0470057661

Autor:      

Derek J. Chadwick, Jamie A. Goode

Oprawa:      

Hardback

Rok Wydania:      

2007-04-20

Ilość stron:      

286

Wymiary:      

234x157

Tematy:      

MB

Acetaldehyde contributes to pathologies ranging from cancer to asthma. It affects the whole body, the architecture of the cell and molecular control mechanisms. The origins of acetaldehyde vary from bacteria in the oral cavity and intestinal tract to atmospheric acetaldehyde as an environmental pollutant. Significant amounts of acetaldehyde are also derived from cigarette smoke and alcohol, both of which are major contributors to disease globally.
Acetaldehyde has deleterious effects in the liver, brain and skeletal muscle. It has also been shown that bacteria can generate significant amounts of acetaldehyde in the gastrointestinal tract, thus contributing to carcinogenesis in this tissue.  Many of the toxic effects of ethanol ingestion are mediated through acetaldehyde and there is increasing awareness that acetaldehyde is a principal disease–forming agent in tobacco–related illnesses.
Alcohol is metabolized by conversion to acetaldehyde, which in turn is converted to acetate by aldehyde dehydrogenase (ALDH).  There are a number of forms of ALDH of which the mitochondrial isoform (ALDH2) is particularly important. The ALDH2 gene has a functional polymorphism: homozygous subjects have little or no ALDH2 activity compared to their wild–type counterparts. Heterozygotes generally also have low ALDH2 activity. Epidemiological studies have found increased risk of certain diseases, including cancer of the gastrointestinal tract, alcoholic liver disease and late–onset Alzheimer’s disease in subjects with ALDH2 deficiency. 
This book features contributions from researchers working on all aspects of acetaldehyde–related pathology. From their expert accounts and the lively discussions accompanying each chapter, we can derive a better understanding of the pathogenesis of diseases in which acetaldehyde, from whichever source, is implicated.

Spis treści:
Symposium on Acetaldehyde–r elated pathology: bridging the trans–disciplinary divide, held at the Novartis Foundation, London 5–7th September.
Editors: Derek J. Chadwick (Organizer) and Jamie Goode
This symposium is based on a proposal made by Victor Preedy, Peter Emery and Mikko Salaspuro
Peter Emery Chair’s introduction.
David W. Crabb and Suthat Liangpunsakul Acetaldehyde generating enzyme systems: roles of alcohol dehydrogenase, CYP2E1 and catalase, and speculations on the role of other enzymes and processes.
Discussion.
Richard A. Deitrich, Dennis Petersen and Vasilis Vasiliou Removal of acetaldehyde from the body.
Discussion.
Shih–Jiun Yin and Giia–Sheun Peng Acetaldehyde, polymorphisms and the cardiovascular system.
Discussion.
Jun Ren Acetaldehyde and alcoholic cardiomyopathy: lessons from the ADH and ALDH2 transgenic models.
Discussion.
Mikko Salaspuro Interrelationship between alcohol, smoking, acetaldehyde and cancer.
Discussion.
Hiroto Matsuse, Chizu Fukushima, Terufumi Shimoda, Sadahiro Asai and Shigeru Kohno Effects of acetaldehyde on human airway constriction and infl ammation.
Discussion.
Helmut K. Seitz The role of acetaldehyde in alcohol–associated cancer of the gastrointestinal tract.
Discussion.
Robert Tardif The determination of acetaldehyde in exhaled breath.
Discussion.
Mostofa Jamal, Kiyoshi Ameno, Mitsuru Kumihashi, Weihuan Wang, Ikuo Uekita and Iwao Ijiri Ethanol and acetaldehyde: in vivo quantitation and effects on cholinergic function in rat brain.
Discussion.
Ville Salaspuro Pharmacological treatments and strategies for reducing oral and intestinal acetaldehyde.
Discussion.
Victor R. Preedy, David W. Crabb, Jaume Farrés and Peter W. Emery Alcoholic myopathy and acetaldehyde.
Discussion.
Onni Niemelä Acetaldehyde adducts in circulation.
Discussion.
General discussion.
M. Apte, J. McCarroll, R. Pirola and J. Wilson Pancreatic MAP kinase pathways and acetaldehyde.
Discussion.
Shivendra D. Shukla, Youn Ju Lee, Pil–hoon Park and Annayya R. Aroor Acetaldehyde alters MAP kinase signalling and epigenetic histone modifi cations in hepatocytes.
Discussion.
Paul J. Thornalley Endogenous α–oxoaldehydes and formation of protein and nucleotide advanced glycation endproducts in tissue damage.
Discussion.
C. J. Peter Eriksson Measurement of acetaldehyde: what levels occur naturally and in response to alcohol?
Discussion.
Final discussion.
Contributors Index.
Subject Index.

Nota biograficzna:
The Novartis Foundation is an international scientific and educational charity which promotes the study and general knowledge of science and in particular encourages international co–operation in scientific research.
Chairman: Peter Emery

Okładka tylna:
Acetaldehyde contributes to pathologies ranging from cancer to asthma. It affects the whole body, the architecture of the cell and molecular control mechanisms. The origins of acetaldehyde vary from bacteria in the oral cavity and intestinal tract to atmospheric acetaldehyde as an environmental pollutant. Significant amounts of acetaldehyde are also derived from cigarette smoke and alcohol, both of which are major contributors to disease globally.
Acetaldehyde has deleterious effects in the liver, brain and skeletal muscle. It has also been shown that bacteria can generate significant amounts of acetaldehyde in the gastrointestinal tract, thus contributing to carcinogenesis in this tissue.  Many of the toxic effects of ethanol inge stion are mediated through acetaldehyde and there is increasing awareness that acetaldehyde is a principal disease–forming agent in tobacco–related illnesses.
Alcohol is metabolized by conversion to acetaldehyde, which in turn is converted to acetate by aldehyde dehydrogenase (ALDH).  There are a number of forms of ALDH of which the mitochondrial isoform (ALDH2) is particularly important. The ALDH2 gene has a functional polymorphism: homozygous subjects have little or no ALDH2 activity compared to their wild–type counterparts. Heterozygotes generally also have low ALDH2 activity. Epidemiological studies have found increased risk of certain diseases, including cancer of the gastrointestinal tract, alcoholic liver disease and late–onset Alzheimer’s disease in subjects with ALDH2 deficiency. 
This book features contributions from researchers working on all aspects of acetaldehyde–related pathology. From their expert accounts and the lively discussions accompanying each chapter, we can derive a better understanding of the pathogenesis of diseases in which acetaldehyde, from whichever source, is implicated.

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