This text helps the reader determine whether or not the gastrointestinal mucosa ulcerates can be viewed as a balance between aggressive factors present in the lumen and the mucosal defence system. Several of these aggressive factors, such as acid, bile and pepsin, are endogenous substances. Similarly, several endogenous substances exert control over mucosal blood flow and secretion and thus are important mediators of mucosal defence. In this volume, experts in this field have contributed chapters on some of the most important of these endogenous mediators, including histamine, prostaglandins, leukotrienes and platelet-activating factor. The potential contribution of these mediators to gastrointestinal disease has been assessed. Also discussed is the role these mediators play in gastrointestinal side effects of drugs (i.e. non-steroidal anti-inflammatory drugs). Also covered are the mechanisms of action of endogenous mediators relative to the the drugs used clinically for the treatment of maladies of the digestive system. This volume will be of interest to the basic scientist, the clinical investigator and to students of pathophysiology and medicine.

Gastritis presents a thorough review of current concepts in gastric inflammation. The book includes reviews of basic scientific research on the cell biology and pathophysiology of gastric inflammation. Results of up-to-date clinical research are considered within the context of basic science information. The book also considers inflammatory problems through the electron microscope and the endoscope. Inflammatory mediators, neutrophils, and other causes of stomach inflammation are only a few of the subjects covered in this superb reference volume for gastroenterologists and scientists studying gastric pathophysiology.

This book provides readers with an up-to-date and comprehensive view on the resolution of inflammation and on new developments in this area, including pro-resolution mediators, apoptosis, macrophage clearance of apoptotic cells, possible novel drug developments.

Over the past decade a great deal of research activity has occurred on either side of the gastroduodenal epithelial interface, with the common goal of elucidating the mechanisms of mucosal protection and how these may be compromised in peptic ulcer disease. A prime stimulus to such research has been the realization that abnormal acid secretion or its delivery into the duodenum in excessive amount cannot fully explain ulcer pathogenesis in the majority of patients. One may envisage the stomach and proximal duodenum as being in a dynamic equilibrium, with aggressive luminal factors, such as acid and pepsin, being counteracted by protective mucosal mechanisms. Until recently, the mechanisms involved in mucosal protection had been poorly defined while the physiology and pathophysiology of acid and pepsin secretion had been elucidated. The impression that gastroduodenal mucosa was protected by a single mechanism has at last been replaced by a more realistic view, suggesting a number of protective zones acting in series. Some of these zones may act as first or second line defences against aggressive factors while certain zones may specifically protect against certain aggressors.

An explosive increase in the knowledge of the effects of chemical and physical agents on biological systems has led to an increased understanding of normal cellular functions and the consequences of their perturbations. The 14-volume Second Edition of Comprehensive Toxicology has been revised and updated to reflect new advances in toxicology research, including content by some of the leading researchers in the field. It remains the premier resource for toxicologists in academia, medicine, and corporations. Comprehensive Toxicology Second Edition provides a unique organ-systems structure that allows the user to explore the toxic effects of various substances on each human system, aiding in providing diagnoses and proving essential in situations where the toxic substance is unknown but its effects on a system are obvious. Comprehensive Toxicology Second Edition is the most complete and valuable toxicology work available to researchers today. Contents updated and revised to reflect developments in toxicology research Organized with a unique organ-system approach Features full color throughout Available electronically on sciencedirect.com, as well as in a limited-edition print version

In recent years, there have been significant advances both in understanding the mechanisms involved in gastrointestinal mucosal injury and protection, as well as in the development of successful strategies for prevention and treatment of gastrointestinal injury. Nevertheless, many people worldwide still suffer from gastrointestinal damage.This book contains contributions by an international panel of researchers in the form of up-to-date reviews on the mechanisms of gastrointestinal injury and protection. These are complemented by papers discussing how these new findings about cell/tissue injury and cytoprotection/organoprotection can be applied to the prevention and treatment of tissue damage in the gastrointestinal tract. Moreover, the publication includes a special chapter on Andre Robert, who has discovered the phenomenon of gastric cytoprotection.This publication will be of great interest for both basic and clinical researchers in gastroenterology and pharmacology, reviewing the advances made so far and pointing towards future developments.

Three distinct types of contractions perform colonic motility functions. Rhythmic phasic contractions (RPCs) cause slow net distal propulsion with extensive mixing/turning over. Infrequently occurring giant migrating contractions (GMCs) produce mass movements. Tonic contractions aid RPCs in their motor function. The spatiotemporal patterns of these contractions differ markedly. The amplitude and distance of propagation of a GMC are several-fold larger than those of an RPC. The enteric neurons and smooth muscle cells are the core regulators of all three types of contractions. The regulation of contractions by these mechanisms is modifiable by extrinsic factors: CNS, autonomic neurons, hormones, inflammatory mediators, and stress mediators. Only the GMCs produce descending inhibition, which accommodates the large bolus being propelled without increasing muscle tone. The strong compression of the colon wall generates afferent signals that are below nociceptive threshold in healthy subjects. However, these signals become nociceptive; if the amplitudes of GMCs increase, afferent nerves become hypersensitive, or descending inhibition is impaired. The GMCs also provide the force for rapid propulsion of feces and descending inhibition to relax the internal anal sphincter during defecation. The dysregulation of GMCs is a major factor in colonic motility disorders: irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and diverticular disease (DD). Frequent mass movements by GMCs cause diarrhea in diarrhea predominant IBS, IBD, and DD, while a decrease in the frequency of GMCs causes constipation. The GMCs generate the afferent signals for intermittent short-lived episodes of abdominal cramping in these disorders. Epigenetic dysregulation due to adverse events in early life is one of the major factors in generating the symptoms of IBS in adulthood.