Accession Number
Upcoming SlideShare
Loading in...5

Like this? Share it with your network


Accession Number






Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Microsoft Word

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

Accession Number Document Transcript

  • 1. <1> Accession Number 1999377328 Authors Banerjee S. Michetti P. Institution Dr. P. Michetti, Div. of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215; United States. E-Mail: Title Strategies for developing a Helicobacter pylori vaccine. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 557-561), 1999. Abstract Novel strategies are needed to control infection with Helicobacter pylori. Prophylactic and therapeutic immunization against this gastric pathogen is possible in animal models, and initial human studies in H. pylori- infected subjects showed that immunization with H. pylori urease is both safe and immunogenic. In rodents, gastric protection against Helicobacter species infection does not depend on the humoral immune response, and a prominent role of the major histocompatibility complex II- restricted CD4+ T-cell response is recognized; however, much remains to be learned about the mechanisms of effective bactericidal response. A clear understanding of the basic mechanisms of gastric immune protection in humans is of the utmost importance for the development of an effective human vaccine. More potent vaccines are likely to be required to induce protection in humans. The availability of two complete genome sequences of H. pylori represents a unique opportunity to identify novel vaccine antigens. Multivalent vaccines delivered by recombinant attenuated bacteria or administered with nontoxic adjuvants need to be evaluated in relevant models. [References: 45] <2> Accession Number 1999377327 Authors Mowat AMcI. Institution A.McI. Mowat, Department of Immunology, University of Glasgow, Western Infirmary, Glasgow G11 6NT; United Kingdom. E-Mail: Title
  • 2. Basic mechanisms and clinical implications of oral tolerance. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 546-556), 1999. Abstract Oral tolerance is the physiologic mechanism that prevents hypersensitivity to food proteins and probably to commensal bacteria. It has also attracted attention as a means of administering therapy for autoimmune and inflammatory diseases. Although evidence indicates that both clonal inactivation and active regulatory mechanisms may play a role and that the induction of these may be determined selectively by the feeding regimen used to induce tolerance, the exact mechanisms of oral tolerance remain unclear. Here, we discuss recent evidence that fed antigens are presented to CD4+ T cells by antigen-presenting cells (APCs) that lack costimulatory activity, resulting in partial activation of T cells followed by a state of unresponsiveness. This seems to occur in many tissues of the immune system but may be particularly important in the draining mesenteric lymph node. Resting dendritic cells may be the predominant population of APCs involved in oral tolerance, and conditions that activate dendritic cells allow the induction of productive immunity. Conventionally, presentation of antigen in the absence of costimulation is thought to induce T-cell anergy, but evidence now indicates that anergic T cells can also act as regulatory cells via the production of inhibitory mediators or via cognate interactions with APCs and other T cells. We discuss how an ability to deactivate APCs may explain bystander suppressor activity in oral tolerance, and we consider how the production of transforming growth factor-beta or interleukin-10 by Th3 or T regulatory 1 cells may contribute to tolerance in vivo. We speculate that both the production of inhibitory mediators and the delivery of suppression via cognate interactions may be properties of otherwise 'anergic' T cells. [References: 100] <3> Accession Number 1999377326 Authors Acheson DWK. Institution
  • 3. Dr. D.W.K. Acheson, Div. of Geographic Med./Infect. Dis., New England Medical Center, 750 Washington Street, Boston, MA 02111; United States. E- Mail: Title Foodborne infections. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 538-545), 1999. Abstract The role of foodborne infections in the health of the population has become of major concern recently. Numerous agents are transmitted in food and water and typically result in acute gastroenteritis, although long-term complications such as reactive arthritis (due to Salmonella, Yersinia, and Shigella organisms), Guillain-Barre syndrome (due to Campylobacter organisms), and renal failure (due to Escherichia coli) are now well recognized. The development of FoodNet to follow the epidemiology of select foodborne infections in the United States has been a major advance in recent years and is now beginning to show interesting trends. Our understanding of the pathogenesis of some of the major foodborne pathogens, especially Salmonella, is advancing and the genome sequencing of these organisms will advance the field further. Of particular concern of late is the increasing number of antibiotic-resistant bacterial isolates, especially for Salmonella and Campylobacter. Irrespective of their cause, these changes in susceptibility patterns pose a major threat to the appropriate treatment of patients. Overall, our knowledge of foodborne infections is advancing rapidly, but new factors such as the emergence of antibiotic resistance means that vigilance must be maintained. [References: 60] <4> Accession Number 1999377325 Authors Isolauri E. Institution Dr. E. Isolauri, Department of Paediatrics, University of Turku, 20520 Turku; Finland. E-Mail: Title Probiotics and gut inflammation. Source Current Opinion in
  • 4. Gastroenterology. Vol 15(6) (pp 534-537), 1999. Abstract The intestine's mucosal surface provides a defense barrier against antigens encountered by the enteric route. In this system a balance is generated and maintained between host and microfloral bacteria. In intestinal inflammation, the integrity of the barrier is disrupted, a greater amount of antigens traverses the mucosal barrier, and the routes of transport are altered, possibly evoking aberrant immune responses and release of proinflammatory cytokines with further impairment of the barrier function. Nutritional therapy remains an attractive tool in the management of intestinal inflammation. The advances this past year are related to the ecologic system provided by specific strains of gut microflora, the concept of healthy microflora, and ways in which gut barrier function could be strengthened by consumption of mono- and mixed cultures of beneficial live microorganisms as probiotics. [References: 18] <5> Accession Number 1999377324 Authors Hai Ning Shi. Nagler-Anderson C. Institution Dr. H.N. Shi, Mucosal Immunology Laboratory, Massachusetts General Hospital East, Building 149, 3 West, 13th Street, Charlestown, MA 02129; United States. E-Mail: Title Mucosal T-cell responses to enteric infection. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 529-533), 1999. Abstract Although immunologists typically examine immune responses in peripheral lymphoid tissues, mucosal surfaces are the first sites at which most antigens are encountered. The role of lymphocytes in the gut-associated lymphoid tissue (GALT) in the production of secretory IgA has been well characterized. Although T cells of the GALT are located in areas likely to have a key role in cell-mediated immunity at mucosal surfaces, the ways in which these cells help defend against mucosal infection are only beginning to be understood. This review examines mucosal T-cell responses to enteric infection with bacteria, viruses, and parasites. [References: 20]
  • 5. <6> Accession Number 1999377323 Authors Fasano A. Institution Dr. A. Fasano, Div. of Pediat. Gastroenterol./Nutr., Univ. of Maryland School of Medicine, HSF Building, 685 West Baltimore Street, Baltimore, MD 21201; United States. E-Mail: Title Intestinal toxins. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 523-528), 1999. Abstract The application of molecular techniques to the study of bacterial pathogenesis has made possible discoveries that are changing the way scientists view the bacterium-host interaction. Today, research on the molecular basis of the pathogenesis of infective diarrheal diseases of necessity transcends established boundaries between cell biology, bacteriology, intestinal pathophysiology, and immunology. A comprehensive approach has been taken here to outline the most recent findings on the interaction between enteric pathogens and their target eukaryotic cells through the elaboration of toxins. [References: 44] <7> Accession Number 1999377322 Authors Baldeon ME. Walker WA. Institution Dr. W.A. Walker, Mucosal Immunology Laboratory, Harvard Medical School, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129; United States. Title Luminal regulators of intestinal immune responses. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 521-522), 1999. <8> Accession Number 1999377321 Authors Louis-Jacques O. Perman JA. Institution Dr. J.A. Perman, Department of Pediatrics, 22 South Greene Street, Baltimore, MD 21201; United States. E-Mail: Title Disorders of the stomach and duodenum in children.
  • 6. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 516-520), 1999. Abstract Over the past year, there have been continued efforts to increase our understanding of the epidemiology, natural history, and pathogenic mechanisms of Helicobacter pylori infection in children. In an attempt to delineate the spectrum of disease associated with this organism, several teams of investigators have also examined the association of H. pylori infection with other disorders, from food allergy to inflammatory bowel disease. Developmental aspects of gastric and duodenal motility, risk factors for gastrointestinal bleeding in pediatric intensive care unit patients, and the use of uncooked cornstarch in the treatment of dumping syndrome are among other topics covered in this review. [References: 34] <9> Accession Number 1999377320 Authors Moesinger RC. Bender J. Duncan M. Magnuson T. Harmon JW. Institution Dr. J.W. Harmon, Department of Surgery, Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21224; United States. Title Surgical intervention and understanding of diseases of the stomach and duodenum. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 509-515), 1999. Abstract The stomach and duodenum are organs of complex physiology and cell biology. Neoplastic disease of these organs represents a difficult surgical challenge, and gastric and duodenal cancer mortality rates remain high despite advances in surgical technique, perioperative care, and adjuvant therapy. True 'cures' elude the surgeon all too often. Fortunately, our understanding of the genetics and molecular biology of upper gastrointestinal neoplasms is increasing and is now significantly affecting the clinical management of these tumors as surgical therapies continue to improve. The care of benign disease of the stomach and duodenum is also evolving as medical therapy and
  • 7. surgical technology improve to lessen the morbidity associated with peptic ulcer disease and other benign conditions. The event that may have the greatest effect on surgical intervention in peptic ulcer disease is the Centers for Disease Control and Prevention launching of an educational campaign to promote treatment of Helicobacter pylori. This article reviews the most significant advances published in the past year on surgical intervention of the stomach and duodenum. [References: 74] <10> Accession Number 1999377319 Authors Church NI. Palmer KR. Institution N.I. Church, Western General Hospital, Gastrointestinal Unit, Crewe Road, Edinburgh EH4 2XU; United Kingdom. Title Diagnostic and therapeutic endoscopy. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 504-508), 1999. Abstract Endoscopic therapy improves the outcome of nonvariceal upper gastrointestinal hemorrhage. Routine second-look procedures may not improve outcome. Patients who rebleed after endoscopic therapy for ulcer hemorrhage should be treated by further endoscopic therapy, rather than urgent surgery. Thinner endoscopes offer adequate visualization with improved patient tolerance, and new endoscopic therapeutic methods continue to be evaluated. Stigmata of recent hemorrhage and their endoscopic interpretation remain a topic for discussion. The Rockall scoring system is validated. Percutaneous endoscopic gastrostomy insertion may be possible without prior transillumination of the stomach. Routine use of antibiotics prior to insertion reduces wound infection. Percutaneous endoscopic gastrostomy feeding is well established, and follow-up studies confirm its value. Endoscopic ultrasound is a rapidly developing technique. Its uses and potential have evolved, resulting in wider applications in benign disease of the esophagus, biliary tree, and pancreas, in addition to its increasing role in the diagnosis and staging of malignancy. [References: 43] <11> Accession Number
  • 8. 1999377318 Authors Louw JA. Marks IN. Institution Dr. J.A. Louw, University of Cape Town, E23 Gastrointestinal Clinic, New Groote Schuur Hospital, Observatory, Cape Town 7925; South Africa. E- Mail: Title The treatment of peptic ulcer disease. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 497-503), 1999. Abstract The literature published in the period under review identified some areas of key clinical and scientific importance in the treatment of peptic ulcer disease. Attention was drawn to the possibility that Helicobacter pylori may be less important as an etiologic factor in ulcer disease in the United States than in the rest of the world. The usual large number of papers addressed various treatment regimens, and the issue of H. pylori resistance to antibiotics was prominent. The introduction of the cyclooxygenase enzyme 2 (COX-2)-specific inhibitors promises to significantly affect nonsteroidal anti-inflammatory drug (NSAID) gastropathy. The review period produced some excellent papers (mainly review papers) on this topic, but there is a paucity of peer-reviewed data on the clinical application of COX-2 NSAIDs. Perhaps more important is that some authors, using a variety of animal models, protested the blithe acceptance of the COX-2 concept, questioning the idea of 'specificity' and identifying possible problems with respect to ulcer healing. Observations of potential clinical importance with regard to the phenomenon of acid rebound after proton-pump inhibitor therapy were presented, and the role of H. pylori in the management of nonulcer dyspepsia remains controversial, despite the publication of three of the best- designed studies to date on this important topic. [References: 59] <12> Accession Number 1999377317 Authors Hammer J. Talley NJ. Institution
  • 9. Dr. N.J. Talley, University of Sydney, Clinical Sciences Building, P.O. Box 63, Penrith, NSW 2751; Australia. Title Nonulcer dyspepsia. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 492-496), 1999. Abstract Nonulcer dyspepsia, characterized by unexplained persistent or recurrent epigastric pain or discomfort, affects approximately 20% of the general population. Symptom-based diagnostic criteria, first developed by an international group of experts, have been refined in the past year in an effort to increase the applicability of the criteria (Rome II criteria). New disease-specific questionnaires that were developed to measure quality of life in patients with dyspepsia are now available and are expected to be widely used in clinical research studies. Studies on the pathophysiology and management of nonulcer dyspepsia were other major topics in the past year, including three large, well- conducted randomized controlled trials of Helicobacter pylori eradication and symptom resolution. [References: 51] <13> Accession Number 1999377316 Authors Quigley EMM. Institution Dr. E.M.M. Quigley, Department of Medicine, Clinical Sciences Building, Cork University Hospital, Cork; Ireland. E-Mail: Title Gastroduodenal motility. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 481-491), 1999. Abstract Several major themes emerged over the past year in the area of gastroduodenal motility. Mostly, these themes represented extensions of research areas discussed in prior reviews in this series rather than the emergence of completely new concepts. Thus, for example, considerable emphasis has again been placed on regional gastric motor function in dyspepsia and on the role of fundic relaxation and accommodation, in particular. Not surprisingly,
  • 10. basic physiologic research has also shown a keen interest in the regulation of fundic relaxation. One new and exciting development is the recognition of the stomach's role in satiety. The spectrum of gastric motor dysfunction in diabetes mellitus continues to be explored, and the important role of hyperglycemia in regulating gastric function has been further emphasized. More data have been provided on noninvasive alternatives to gastric motor function testing, and several studies have looked at factors that may influence variability in these various tests. There have been few innovations over the past year in the therapeutic arena; rather, the indications and limitations of current therapies have been further developed. [References: 172] <14> Accession Number 1999377315 Authors Cryer B. Institution Dr. B. Cryer, Dallas VA Medical Center, 4500 South Lancaster Road (111B1), Dallas, TX 75216; United States. E-Mail: Title Nonsteroidal anti-inflammatory drug gastrointestinal toxicity. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 473-480), 1999. Abstract Nonsteroidal anti-inflammatory drugs (NSAIDs) are currently the most widely used class of therapeutic agents. By inhibiting cyclooxygenase (COX) and reducing gastrointestinal prostaglandins, they provide effective analgesia and suppress inflammation in a variety of conditions. However, through the same mechanism of COX inhibition, they also cause significant gastrointestinal toxicity. One of the most common methods to reduce NSAID- induced gastrointestinal toxicity has been to co- prescribe prophylactic therapies such as acid-reducing agents or the synthetic prostaglandin analogue, misoprostol. More recently safer NSAIDs, such as the COX-2 specific NSAIDs or the nitric oxide-releasing NSAIDs, have been developed or are currently in development. This article reviews mechanisms of NSAID-induced gastrointestinal toxicity. Also reviewed are data on the gastrointestinal consequences of the prophylactic co-therapies, COX-2 specific NSAIDs and nitric oxide-releasing NSAIDs. [References: 60]
  • 11. <15> Accession Number 1999377314 Authors Lichtenberger LM. Institution Dr. L.M. Lichtenberger, Department of Integrative Biology, University of Texas Medical School, 6431 Fannin Street, Houston, TX 77030; United States. Title Gastroduodenal mucosal defense. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 463-472), 1999. Abstract Research performed in the laboratory and the clinic over the past several years has added to our understanding of the mechanisms that are operative in protecting the epithelial lining of the stomach and duodenum from injury and ulceration, most frequently caused by necrotic agents in the lumen. The defensive mechanism of the gastroduodenal mucosa comprises a series of physical, chemical, biologic, and immunologic barriers or mechanisms that act in concert to either prevent or limit cellular injury or transformation. The field of gastroduodenal defense can be subdivided into the following four areas: extracellular mucus barrier properties; membrane and ion transport properties; cellular factors promoting growth and restitution; and vascular, neural, and inflammatory factors ensuring optimal tissue perfusion and immune responsiveness, respectively. In addition, a great deal can be learned about gastroduodenal defense by studying the effects of ulcerogenic factors and conditions on the defensive mechanisms described here and specifically how they may be compromised by nonsteroidal anti-inflammatory drugs and Helicobacter pylori infection. This review presents interesting and noteworthy findings impacting on these properties contributing to gastroduodenal defense since the prior review article on this subject appearing in this journal. [References: 79] <16> Accession Number 1999377313 Authors Schubert ML.
  • 12. Institution Dr. M.L. Schubert, McGuire VAMC, Code 111N, Gastroenterology Division, 1201 Broad Rock Boulevard, Richmond, VA 23249; United States. E-Mail: Title Regulation of gastric acid secretion. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 457-462), 1999. Abstract This paper summarizes important developments, published over the past year, that improve our understanding of the regulation of gastric acid secretion at the central, peripheral, and intracellular levels and mechanisms by which various neuro-transmitters, paracrine agents, and hormones regulate gastric secretion and are themselves regulated. The main stimulants of acid secretion from the parietal cell are histamine, gastrin, and acetylcholine. Histamine, released from fundic enterochromaffinlike cells, interacts with H2 receptors on parietal cells that are coupled via separate G proteins to activation of adenylate cyclase and phospholipase C. The antral hormone gastrin, released by activation of cholinergic and bombesin/gastrin-releasing peptide neurons, acts mainly by release of histamine from enterochromaffinlike cells. Acetylcholine, released from gastric intramural neurons, interacts with muscarinic M3 receptors on parietal cells and has little, if any, effect on histamine secretion. The main inhibitor of acid secretion is somatostatin, which, acting via sst2 receptors, exerts a tonic restraint on parietal, enterochromaffinlike, and gastrin cells. In patients with duodenal ulcer, infection with Helicobacter pylori is associated with increased basal and stimulated plasma gastrin concentrations and acid outputs. The precise mechanisms mediating the effects are not known, but evidence suggests that both products of the bacteria and the inflammatory infiltrate are capable of stimulating gastrin and acid secretion. [References: 44] <17> Accession Number 1999377312 Authors Schubert ML. Institution
  • 13. Dr. M.L. Schubert, McGuire VAMC, Code 111N, Gastroenterology Division, 1201 Broad Rock Boulevard, Richmond, VA 23249; United States. E-Mail: Title Stomach and duodenum. Source Current Opinion in Gastroenterology. Vol 15(6) (pp 455-456), 1999.