Helicobacter infections with rare bacteria or minimal gastritis: Expecting the unexpected.

Background: The routine use of special stains for detection of Helicobacter remains controversial.

Aims: To determine the frequency of histologically atypical Helicobacter infection.

Methods: All gastric biopsies received at a large pathology reference laboratory over a 6-month period were stained for Helicobacter, and the histologic and clinicopathologic parameters evaluated.

Significant increase in IgG4+ plasma cells in gastric biopsy specimens from patients with pernicious anaemia.

Aim: To investigate the presence of IgG4+ plasma cells in gastric mucosal biopsy samples from patients with atrophic gastritis (AG) and a history of pernicious anaemia (PA) (AG+PA+).

Methods: Gastric mucosal biopsy specimens from 46 patients with AG+PA+ were investigated. As controls, we evaluated specimens from patients with AG but no history of PA (AG+ PA-) (n=25), normal histology (n=25), mild chronic inactive gastritis (MCIG) (n=25) or Helicobacter pylori gastritis (HP) (n=25).

Toxicant-associated steatohepatitis in vinyl chloride workers.

Unlabelled: Although nonalcoholic steatohepatitis (NASH) is typically associated with obesity, it has also been reported to occur in lean individuals exposed to industrial chemicals. Occupational exposure to vinyl chloride (VC) is a well-documented risk factor for hemangiosarcoma, but has not previously been associated with steatohepatitis. Here we evaluate liver biopsies from 25 nonobese, highly exposed VC workers for steatohepatitis.

The use of dynamic positron emission tomography imaging for evaluating the carcinogenic progression of intestinal metaplasia to esophageal adenocarcinoma.

Background: In this study, we investigate the use of PET scanning in the carcinogenic progression of reflux esophagitis to Barrett's esophagus to high grade dysplasia to esophageal adenocarcinoma, and correlate the uptake levels of 18F-FDG related to histological changes, and the rates of proliferation and apoptosis.

Methods: An established esophagoduodenal anastomsis rat model in conjunction with micro-PET scanning at 1 week, 1 month, 3 month, and 6 month after procedure was performed.

Results: Increased uptake levels of 18F-FDG were observed in the esophagi after EDA procedure.

Chemoprevention of carcinogenic progression to esophageal adenocarcinoma by the manganese superoxide dismutase supplementation.

Purpose: Oxidative stress is related to the carcinogenic pathway of reflux esophagitis to Barrett's metaplasia to esophageal adenocarcinoma (EAC). Recent studies have shown that a decreased manganese superoxide dismutase (MnSOD) level is associated with the increased incidences of Barrett's esophagus (BE) and EAC. The aim of this study was to investigate MnSOD supplementation as a chemopreventive agent to prevent oxidative injury and subsequent BE and EAC formation.

Alterations in manganese superoxide dismutase expression in the progression from reflux esophagitis to esophageal adenocarcinoma.

Background: Comprehensive understanding of the basic mechanisms in the progression of esophagitis, Barrett esophagus (BE), and esophageal adenocarcinoma (EAC) is urgently needed to develop a management strategy for an effective screening of BE and management of EAC. The aim of this study is to provide a detailed insight of the histology and the cellular and molecular events associated with the genesis of BE and EAC under the esophagoduodenal reflux conditions.

Methods: Esophagoduodenal anastomosis (EDA) was performed on rats.

Loss of manganese superoxide dismutase expression and activity in rat esophagus with external esophageal perfusion.

Background: Manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme that scavenges superoxide radicals found in the mitochondria, has been shown to protect oxygen-utilizing cells from the toxicity of the reactive oxygen species (ROS). Current studies in the animal esophageal reflux model are limited, and the reports on the relevance of protein expression level and enzymatic antioxidative activity of MnSOD in esophageal mucosal defense are controversial. Thus, the aim of this study is to investigate the role of MnSOD expression and activity in rats with esophageal perfusion injury.

Morphological transformation in esophageal submucosa by bone marrow cells: esophageal implantation under external esophageal perfusion.

Accumulating clinical and experimental studies indicate that Barrett's esophagus might arise through multipotential stem cells under the stress of gastroesophageal reflux. Previously, we have presented a novel external pump perfusion rat model and demonstrated that perfusion with both acid and bile can induce severe esophagitis in 1 week with a similarly pathological change seen in humans. The aim of this study was to investigate the histological changes of esophagus after bone marrow cell engraftment with bile and acid perfusion.

A novel external esophageal perfusion model for reflux esophageal injury.

The current animal models of esophagitis and Barrett's esophagus consist of surgeries that divert the gastroduodenal contents to the esophagus. The limitations of these models are the inability to control the amount and concentration of the refluxate and the causing of significant postoperative stress and morbidity. Eighteen adult rats were cannulated at the upper esophagus and connected to a subcutaneous osmotic micropump to perfuse the esophageal lumen with bile and acid.

Cyclooxygenase-2 and epithelial growth factor receptor up-regulation during progression of Barrett's esophagus to adenocarcinoma.

Aim: To investigate the expression of cyclooxygenase-2 (COX-2) and epithelial growth factor receptor (EGFR) throughout the progression of Barretts esophagus (BE).

Methods: COX-2 and EGFR protein expressions were detected by using immunohistochemical method. A detailed cytomorphological changes were determined.

Rosai-Dorfman disease of the gastrointestinal tract: report of a case and review of the literature.

Rosai-Dorfman disease (RDD) is a rare, acquired disease of unknown etiology that affects primarily children and young adults. It is characterized by a proliferation of distinctive histiocytes in the lymph nodes and/or extranodal sites. Involvement of the gastrointestinal tract is rare.

Association of manganese superoxide dismutase expression with progression of carcinogenesis in Barrett esophagus.

Hypothesis: The down-regulation of manganese superoxide dismutase (MnSOD) expression plays a role in the progression of Barrett esophagus (BE).

Design: An evaluation of 92 esophageal samples, including 17 patients with normal esophagus, 22 with intestinal metaplasia, 22 with indefinite/low-grade dysplasia, 16 with high-grade dysplasia (HGD), and 15 with esophageal adenocarcinoma were evaluated for MnSOD expression. We evaluated MnSOD expression using immunohistochemistry and graded it separately on a 2-category ordinal scale in relation to the mucosa and submucosa that ranged from 0 (no staining) to 3 (strong staining).

Slow transit colon constipation is not related to the number of interstitial cells of Cajal.

Background And Aims: Recent studies have demonstrated decreased numbers of interstitial cells of Cajal in patients suffering from severe chronic constipation as measured by c-Kit (CD117) and CD34 immunohistology. In this study, we wished to determine whether there were abnormalities in the number of neurons of the Auerbach's plexus, their CD117 and CD34 immunoreactivity, or the thickness of colon wall sections in patients with refractory slow transit colonic constipation as compared with control subjects.

Patients And Methods: Specimens from 13 patients who had undergone subtotal colectomy for severe chronic constipation refractory to medical treatment were compared with normal controls.

Esophageal injury with external esophageal perfusion.

Background: External esophageal perfusion (EEP) with the idea that esophageal perfusion can be controlled with a single ingredient at a constant rate and concentration, might be used to dissect the injurious role of gastro-duodenal secretions for the progression from esophagitis to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). This study is to evaluate the EEP rat model for esophagitis induced by using a micro-osmotic pump with bile perfusion.

Methods: Eighteen adult rats underwent the EEP procedure.

Diverse antioxidants protect against acetaminophen hepatotoxicity.

The reactive oxygen species-sensitive transcription nuclear factor-kappaB (NF-kappaB) plays a pivotal role in the development of acetaminophen (APAP) hepatotoxicity. We investigated the efficacy of a diverse series of antioxidants in preventing APAP-induced hepatotoxicity. BALB/c mice were divided into four groups and provided with antioxidants incorporated into chow as follows: (1) control diet; or diet supplemented with (2) S-adenosylmethionine (SAMe); (3) green tea polyphenols (GrTP); or (4) (RS)-n-propylthiazolidine-4(R)-carboxylic acid (PTCA).

Preconditioning of NOD mice with anti-CD8 mAb and costimulatory blockade enhances chimerism and tolerance and prevents diabetes, while depletion of alpha beta-TCR+ and CD4+ cells negates the effect.

Bone marrow transplantation blocks diabetes pathogenesis and reverses autoimmunity in nonobese diabetic (NOD) mice. However, there is a greater barrier to engraftment in the context of autoimmunity. In the present study, we characterized which recipient cells influence engraftment in prediabetic NOD mice, with the goal to replace myelotoxic conditioning with antigen-specific deletion of reactive host cells.

Flt3-ligand treatment prevents diabetes in NOD mice.

The mechanism by which mixed chimerism reverses autoimmunity in type 1 diabetes has not been defined. NOD mice have a well-characterized defect in the production of myeloid progenitors that is believed to contribute significantly to the autoimmune process. We therefore investigated whether chimerism induces a correction of this defect.

p-Aminophenol-induced hepatotoxicity in hamsters: role of glutathione.

p-Aminophenol (PAP) is a widely used industrial chemical and a known nephrotoxin. Recently, it was found to also cause hepatotoxicity and glutathione (GSH) depletion in mice. The exact mechanism of liver toxicity is not known.

Efficacy of a transforming growth factor beta 2 containing nutritional support formula in a murine model of inflammatory bowel disease.

Objective: Dietary, environmental and genetic events may influence host susceptibility to inflammatory bowel diseases (IBD). Transforming growth factor beta 2 (TGF-beta 2), a multifunctional polypeptide (cytokine) present in human and bovine milk, plays a critical role in the development of tolerance, the prevention of autoimmunity, and in anti-inflammatory responses. TGF-beta 2 is a potent inhibitor of intestinal epithelial cell (IEC) growth and stimulates IEC differentiation.

Association of metallothionein expression and lack of apoptosis with progression of carcinogenesis in Barrett's esophagus.

Barrett's esophagus is the transformation of normal esophageal squamous epithelium to specialized intestinal metaplasia (SIM). Among the Barrett's specialized cells, those that can develop protective mechanisms against apoptosis may have potential to become malignant. Studies have shown that overexpression of metallothionein (MT), low molecular protein that protects cells from apoptotic stimuli, appears to be associated with more advanced, highly malignant tumors.

Targeting of glycosaminoglycan-cytokine interactions as a novel therapeutic approach in allotransplantation.

Background: Glycosaminoglycans (GAGs) are heteropolysaccharides present as integral components of the extracellular matrix (ECM), cell and basement membranes. GAGs play an important role in immune and inflammatory responses because of their ability to interact with cytokines and chemokines, promoting the localization of these molecules onto the ECM or cell membranes at specific anatomical sites. The main goal of these studies was to test the hypothesis that interference with the binding of cytokines/chemokines to GAGs will interfere with a graft rejection response.