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This volume contains the papers presented at the International
Symposium on "Cirrhosis, Hyperammonemia and Hepatic
Encephalopathy," held in Valencia, Spain, De- cember 2nd_4th, 1996.
Liver cirrhosis is one of the main causes of death in occidental
countries. There are other hepatic dysfunctions such as fulminant
hepatic failure, Reye's syndrome, or congenital deficiencies of
urea cycle enzymes which can also lead to hepatic encephalopathy,
coma and death. However, the molecular bases ofthe pathogenesis of
hepatic encephalopathy remain unclear. One ofthe consequences of
hepatic failure is the reduced ability to detoxify ammonia by
incorporating it into urea. This leads to increased blood ammonia
levels. Hyperam- monemia is considered one of the main factors
responsible for the mediation of hepatic encephalopathy and
classical clinical treatments are directed towards reducing blood
ammo- nia levels. Altered neurotransmission is an essential step in
the pathogenesis of hepatic encephalopathy. The first part of the
book is devoted to the discussion of the recent advances in the
understanding of the alterations of different neurotransmitter
systems in hepatic encephalopathy. The alterations of tryptophan
metabolism and neurotransmission in hepatic encephalopathy and the
implications for the clinical use of neuropsychoactive drugs are
reviewed. The alterations in glutamate transport and
neurotransmission in hepatic encephal- opathy due to acute liver
failure are also reviewed. The role of NMDA receptors in the
molecular mechanism of acute ammonia toxicity is discussed as well
as its modulation by metabotropic glutamate receptors and
muscarinic receptors.
Given the latest advances in cancer research, which includes basic
research and its derived diagnostic, clinical, and therapeutic
applications, the book New Trends in Cancer for the 21st Century is
written by individuals such as molecular biologists, whose tasks
are to decipher, after sequencing the human genome, those new genes
and pathways involved in the carcinogenesis process; clinical and
molecular pathologists, who apply these discoveries for the
molecular diagnosis and characterization of the tumor; and clinical
oncologists, who treat patients. Pharmacogenetics introduces new
perspectives in the translational fields with the design of drugs
against specific targets, which at this moment are in clinical
trials phases. This book achieves a state of the art in every field
of cancer research and discusses the new perspectives that will
open the future for cancer treatment (basic research, new
technologies, new drugs, therapies...). For this reason, the book
is intended for pathologists, clinicians, and biologists, as well
as fellows and students of physiology and medicine.
This volume contains the papers presented in the International
Summer Course on "Cirrhosis, Hyperammonemia and Hepatic
Encephalopathy," which was one of the prestigious Summer Course, of
the Complutense University of Madrid held in EI Escorial, Spain,
during August 10-14, 1992. Liver cirrhosis is one of the main
causes of death in western countries. In addition there is a series
of liver dysfunctions including fulminant hepatic failure, Reye's
syndrome and congenital defects of urea cycle enzymes that could
lead to hepatic encephalopathy, coma and death. As a consequence of
impaired liver function, the ability to detoxify ammonia by its
incorporation into urea is diminshed, resulting in increased
ammonia levels in blood and brain. Hyperammonemia is considered one
of the main factors in the mediation of hepatic encephalopathy and
the classical clinical treatments are directed towards reducing
blood ammonia levels. A part of the book is therefore devoted to
the study of certain aspects of ammonia metabolism such as the
regulation of the urea cycle, the main mechanism of ammonia
detoxification in mammals, which is located mainly in the liver.
The metabolism of ammonia in other tissues, including brain, is
also presented, as well as the effects of hyperammonemia on brain
metabolism and function and on brain microtubules. The control of
cerebral protein breakdown is reviewed. The classical and some
recently proposed clinical treatments as well as nutritional
considerations in the management of patients with liver failure are
also discussed.
This volume contains the papers presented at the International
Symposium on "Cirrhosis, Hyperammonemia and Hepatic
Encephalopathy," held in Valencia, Spain, January 24th-27th, 1994.
Liver cirrhosis and other hepatic dysfunctions such as fulminant
hepatic failure and congenital defects of urea cycle enzymes can
lead to hepatic encephalopathy, coma and death. Hepatic
encephalopathy is one of the main causes of death in western
countries. The ability to detoxify ammonia by its incorporation
into urea is diminished by impaired liver function, resulting in
increased ammonia levels in blood and brain. Hyperammonemia is
considered one of the main factors in the mediation of hepatic
encephalopathy and the classical clinical treatments are directed
towards reducing blood ammonia levels. However, the molecular bases
of the pathogenesis of hepatic encephalopathy and the role of
hyperammonemia in this process remain unclear and several
hypotheses have been proposed. To clarify the mechanisms involved
in hepatic encephalopathy and hyperammonemia suitable animal models
are necessary. The animal models available and the ideal features
of an animal model are presented in the initial part of the book.
This volume contains the text of the presentations delivered at the
International Symposium on Rare Diseases "Inherited Neuromuscular
Diseases: Translation from Pathomechanisms to Therapies," held in
Valencia, Spain, from November 16 to 18, 2008. The symposium
represents a part of the continuous efforts on dif- sion of science
to the society of the Catedra Santiago Grisolia and the Fundacion
Ciudad de las Artes y las Ciencias -Comunitat Valenciana. More than
200 inter- tional scientists from different countries of Europe,
the USA, and Australia attended the meeting. The venue was the
Auditorium of the Science Museum Principe Felipe. Ten years ago
Alan Emery wrote in the preface of Neuromuscular Disorders:
Clinical and Molecular Genetics the following comments: "It has
been estimated that more than one person in every 3,000 has a
serious disabling inherited n- romuscular disorder. The suffering
caused by these disorders is considerable, but, until the last
decade or so, virtually nothing was known of their pathogenesis.
Any rationale approach to treatment was therefore out of the
question. However, matters are now changing rapidly. The genes for
many of these disorders have been localised and characterised and
their gene products identi ed and studied. The detection of
preclinical disease, the identi cation of heterozygous carriers and
prenatal di- nosis are all becoming possible, and, hopefully,
effective treatments may no be too far distant."
This volume contains the papers presented at the Inter- national
Symposium on "Cirrhosis, Hepatic Encephalopathy and Ammonium
Toxicity", held in Valencia, Spain, November 27-29, 1989. Hepatic
cirrhosis as well as other liver failures usual- ly lead to hepatic
encephalopathy which is an important cause of death in occidental
countries. However the molecular bases of the pathogenesis of
hepatic encephalopathy remain unclear and several hypotheses have
been proposed. Hyperammonemia is considered one of the main factors
responsible for the mediation of hepatic encephalopathy. Therefore,
a part of the book is devoted to the effects of hyperammonemia on
cerebral function, ammonia and amino acid metabolism, brain
microtobules, astrocytes and synaptic trans- mission and their
possible role in the pathogenesis of hepatic encephalopathy.
Carnitine has a remarkable protective effect against acute ammonium
intoxication. Thus some results regarding this effect are also
presented, as well as the clinical use of car- nitine. The
alterations of the metabolism of ammonia and of seda- tives in
liver diseases and their clinical implications are also discussed.
The possible role of altered GABA-ergic neurotransmission on the
pathogenesis of hepatic encephalopathy has received considerable
attention recently. Results of these studies and those on
benzodiazepine receptor ligands are presented as well as those on
the hypothesis of the role of altered synaptic plasma membrane on
the pathogenesis of hepatic encephalopathy.
It is difficult to imagine anyone who has not heard of cancer.
This disease can affect families, friends or any one of us at any
time in our lives. Every year nearly 3 million Europeans are
diagnosed with cancer, leading to around 800,000 deaths per year.
These deaths occur not only in aging populations, but also in
children and adults who are in the most active period of their
lives. This represents a tremendous problem that cannot be ignored
by politicians or citizens. Fortunately, there is a constantly
growing awareness that although cancer is a problem to be dealt
with by clinicians, it should also be the concern of everyone. This
volume contains the lectures held at the International Symposium on
Cancer "New Trends in Cancer for the 21st Century." Fundamental
researchers, politicians and representatives from patient
coalitions share here their knowledge and interests as well as
their concerns and experiences. Not only do these papers provide
state-of-the-art information on cancer, they are also an
opportunity to look at the problem from different points of view.
It can be encouraging to realise that we are not alone in this
fight.
This volume contains the text of the presentations delivered at the
International Symposium on Rare Diseases "Inherited Neuromuscular
Diseases: Translation from Pathomechanisms to Therapies," held in
Valencia, Spain, from November 16 to 18, 2008. The symposium
represents a part of the continuous efforts on dif- sion of science
to the society of the Catedra Santiago Grisolia and the Fundacion
Ciudad de las Artes y las Ciencias -Comunitat Valenciana. More than
200 inter- tional scientists from different countries of Europe,
the USA, and Australia attended the meeting. The venue was the
Auditorium of the Science Museum Principe Felipe. Ten years ago
Alan Emery wrote in the preface of Neuromuscular Disorders:
Clinical and Molecular Genetics the following comments: "It has
been estimated that more than one person in every 3,000 has a
serious disabling inherited n- romuscular disorder. The suffering
caused by these disorders is considerable, but, until the last
decade or so, virtually nothing was known of their pathogenesis.
Any rationale approach to treatment was therefore out of the
question. However, matters are now changing rapidly. The genes for
many of these disorders have been localised and characterised and
their gene products identi ed and studied. The detection of
preclinical disease, the identi cation of heterozygous carriers and
prenatal di- nosis are all becoming possible, and, hopefully,
effective treatments may no be too far distant."
It is difficult to imagine anyone who has not heard of cancer. This
disease can affect families, friends or any one of us at any time
in our lives. Every year, nearly 3 million Europeans are diagnosed
with cancer, leading to around 800,000 deaths per year. These
deaths occur not only in aging populations, but also in children
and adults who are in the most active period of their lives. This
represents a tremendous problem that cannot be ignored by
politicians or citizens. Fortunately, there is a constantly growing
awareness that although cancer is a problem to be dealt with by
clinicians, it should also be the concern of everyone. This volume
contains the lectures held at the International Symposium on Cancer
New Trends in Cancer for the 21st Century. Fundamental researchers,
politicians and representatives from patient coalitions share here
their knowledge and interests as well as their concerns and
experiences.
Given the latest advances in cancer research, which includes basic
research and its derived diagnostic, clinical, and therapeutic
applications, the book New Trends in Cancer for the 21st Century is
written by individuals such as molecular biologists, whose tasks
are to decipher, after sequencing the human genome, those new genes
and pathways involved in the carcinogenesis process; clinical and
molecular pathologists, who apply these discoveries for the
molecular diagnosis and characterization of the tumor; and clinical
oncologists, who treat patients. Pharmacogenetics introduces new
perspectives in the translational fields with the design of drugs
against specific targets, which at this moment are in clinical
trials phases. Several organizations such as the EORTC (European
Organization for Research and Treatment of Cancer) and the OECI
(Organization of European Cancer Institutes) and comprehensive
cancer centers play a crucial role in focusing cancer research on
all these areas.
This book achieves a state of the art in every field of cancer
research and discusses the new perspectives that will open the
future for cancer treatment (basic research, new technologies, new
drugs, therapies...). For this reason, the book is intended for
pathologists, clinicians, and biologists, as well as fellows and
students of physiology and medicine.
Brain Tryptophan Perturbation in Hepatic Encephalopathy:
Implications for Effects by Neuropsychoactive Drugs in Clinical
Practice; F. Bengtsson, et al. Hepatic Encephalopathy in Acute
Liver Failure: Role of the Glutamate System; A. Michalak, et al.
Glutamate and Muscarinic Receptors in the Molecular Mechanisms of
Acute Ammonia Toxicity and of Its Prevention; M.D. Minana, et al.
Studies on the Pharmacological Properties of Oxindole
(2-Hydroxyindole) and 5-Hydroxyindole: Are They Involved in Hepatic
Encephalopathy?; F. Moroni, et al. The Involvement of Ammonia with
the Mechanisms That Enhance GABA-ergic Neurotransmission in Hepatic
Failure; E.A. Jones, A.S. Basile. Direct Enhancement of GABA-ergic
Neurotransmission by Ammonia; J.-H. Ha, et al. The Peripheral
Benzodiazepine Receptor and Neurosteroids in Hepatic
Encephalopathy; M.D. Norenberg, et al. Ornithine Aminotransferase
as a Therapeutic Target in Hyperammonemias; N. Seiler. Sparse-Fur
(spf) Mouse as a Model of Hyperammonemia: Alterations in the
Neurotransmitter Systems; I.A. Qureshi, K.V.R. Rao. Abnormal Gene
Expression Causing Hyperammonemia in Carnitine-Deficient Juvenile
Visceral Steatosis (JVS) Mice; T. Saheki, et al. 7 Additional
Articles. Index.
Control of Urea Synthesis and Ammonia Detoxification.- Brain
Metabolism in Hepatic Encephalopathy and Hyperammonemia.- Ammonia
Metabolism in Mammals: Interorgan Relationship.- Clinical
Manifestations and Therapy of Hepatic Encephalopathy.- Nutritional
Considerations in Patients with Hepatic Failure.- Do Benzodiazepine
Ligands Contribute to Hepatic Encephalopathy?.- Effects of
Hyperammonemia on Neuronal Function: NH4+, IPSP Cl-Extrusion.-
Activation of NMDA Receptor Mediates the Toxicity of Ammonia and
the Effects of Ammonia on the Microtubule-Associated Protein
MAP-2.- Modulation of the Exocytotic Release of Neurotransmitter
Glutamate by Protein Kinase C.- Controls of Cerebral Protein
Breakdown.- Two Different Families of NMDA Receptors in Mammalian
Brain: Physiological Function and Role in Neuronal Development and
Degeneration.- Glanglioside GM1 and its Semisynthetic
Lysogangliosides Reduce Glutamate Neurotoxicity by a Novel
Mechanism.- Contributors.
Animal Models of Hepatic Encephalopathy and Hyperammonemia.- Brain
Metabolism in Encephalopathy Caused by Hyperammonemia.- In Vivo
Brain Magnetic Resonance Imaging (MRI) and Magnetic Resonance
Spectroscopy (MRS) in Hepatic Encephalopathy.- Role of the Cellular
Hydration State for Cellular Function: Physiological and
Pathophysiological Aspects.- Astrocyte-Neuron Interactions in
Hyperammonemia and Hepatic Encephalopathy.- Spinal Seizures in
Ammonia Intoxication.- Molecular Mechanism of Acute Ammonia
Toxicity and of its Prevention by L-Carnitine.- Portal-Systemic
Encephalopathy: a Disorder of Multiple Neurotransmitter Systems.-
The GABA Hypothesis: State of the Art.- Neuropharmacologic
Modulation of Hepatic Encephalopathy: Experimental and Clinical
Data.- S-Adenosyl-L-Methionine Synthetase and Methionine Metabolism
Deficiencies in Cirrhosis.- Diagnosis and Therapy of Hepatic
Encephalopathy.- Neomycin Reduces the Intestinal Production of
Ammonia from Glutamine.- N-Acetylglutamate Synthetase (NAGS)
Deficiency.- Ornithine Transcarbamylase Deficiency: A Model for
Gene Therapy.- Retroviral Gene Transfer for LDL Receptor Deficiency
into Primary Hepatocytes.- The Carnitine System: Recent Aspects.-
Use of Hepatocyte Cultures for Liver Support Bioreactors.-
Hepatitis C Viral infection after Orthotopic Liver
Transplantation.- Exercise-Induced Hyperammonemia: Skeletal Muscle
Ammonia Metabolism and the Peripheral and Central Effects.-
Possible Role of Ammonia in the Brain in Dementia of Alzheimer
Type.- Contributors.
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