Intestinal metaplasia (IM) of the stomach is a risk factor in developing intestinal-type gastric cancer and hence the question of reversibility is vital. There is emerging epidemiological evidence that with long term follow up, IM may be reversible although a combination of antioxidant agents and eradication of H pylori may be necessary to achieve this. The pathogenesis of IM is currently being elucidated and it is likely that a combination of bacterial, host, and environmental factors will be shown to lead to IM. In assessing gastric cancer risk, histochemical typing of IM will most probably be replaced by molecular markers.

Functional heartburn is a common disorder and appears to be composed of several distinct subgroups. Identifying the different subgroups based on clinical history only is not achievable at present. The mechanisms responsible for pain, clinical characteristics, and the optimal therapeutic approach remain poorly understood. Response to potent antireflux treatment is relatively limited. Current and future treatment strategies for functional heartburn patients who have failed standard dose proton pump inhibitors (PPIs) include increased PPI dose in some, as well as addition of pain modulators in others.

Retreatment with a combination of alpha interferon (IFN) plus ribavirin of patients with chronic hepatitis C who did not respond to IFN monotherapy has not been assessed in large controlled studies.

Peripheral and central effects of enteric infection are considered. Nerves play a vital part in the immediate response to enteric infection, promoting pathogen expulsion by orchestrating intestinal secretion and propulsive motor patterns. Laboratory studies indicate that therapeutic agents aimed at modulating the neural response can profoundly alter the outcome of infection. As our understanding of the role of nerves increases, exciting new targets for therapeutic intervention will emerge in both acute and chronic disorders induced by enteric infection.

Breast feeding and weaning are important physiologically significant luminal events that influence the growth of the small intestine in humans. A variety of factors including genetic preprogramming, systemic and local hormones, and permissive factors contribute and modulate intestinal growth. Here, we offer a view that integrates some of these factors, especially those relating to breast feeding and weaning.

Progress in the management of hepatocellular carcinoma (HCC) has been slow and has limited impact on outcome. Most patients with HCC have two diseases--chronic liver disease and HCC--and complex interactions between the two have major implications for diagnosis and prognosis as well as the management of HCC. The disease is most prevalent in those areas of the world where the infrastructure for clinical trials is least developed. Also, the aetiology of the disease varies around the world and it is still not known whether HCCs of different aetiologies have different prognoses. Current treatment is making an impact on the management of HCC but further progress awaits not only the development of more effective treatments but also the development of adequate methodologies to assess the impact of these treatments.

Classical descriptions of gut development specify subdivision into foregut, midgut, and hindgut together with their derivatives. This is based on the anatomical localisation of the anterior and posterior intestinal portals separating the roof of the yolk sac from the foregut and hindgut diverticulae. When considering the molecular basis of intestinal differentiation, it is necessary to think in terms of the genes involved, and in this respect those containing the homeobox motif are important players in specifying the fate of both the endodermal and mesodermal components of the gut. In this review, evidence is considered for their role, with particular regard to the acquisition of positional information.

Our current understanding of iron absorption under normal conditions is presented, together with an overview of the clinical disorders of iron overload and the molecular processes that contribute to increased iron deposition in iron overload. Recently, a number of new genes involved in iron metabolism have been identified which is allowing the molecular mechanisms of iron absorption to be elucidated.

We report a very rare case of primary low grade mucosa associated lymphoid tissue (MALT) lymphoma of the oesophagus. An 83 year old woman was referred to our hospital in June 1999 for further examination and treatment of oesophageal tumour. Although a physical examination and laboratory data showed no significant abnormalities, endoscopic observation revealed two slightly elevated submucosal tumour-like lesions of the oesophagus. Tissue specimens were obtained by endoscopic mucosal resection of the oesophagus using a cap fitted panendoscope. The lesions were composed of diffuse small atypical lymphoid cells--that is, centrocyte-like cells--which were stained with CD20, L26, BCL-2, and kappa, but not with CD3, CD5, CD10, or cyclin D1. Monoclonality was detected by polymerase chain reaction analysis using the primer for CDR-3 of immunoglobulin H and diagnosed as low grade MALT lymphoma of the oesophagus. The tumours were considered to be completely resected and therefore additional treatment was not administered. The patient is alive and well 22 months after treatment and diagnosis.

Alcohol is a major aetiological factor in hepatocarcinogenesis but our understanding of its importance as a modulating factor is just beginning to emerge. In the present review, a number of possible cofactors and mechanisms are discussed by which alcohol may enhance the development of hepatoma. These include dietary or environmental carcinogens ingested along with alcoholic beverages, alcoholic cirrhosis as a precancerous condition, and the effects of alcohol metabolism.