Keisuke Itoh

Multicenter, prospective trial of white-light imaging alone versus white-light imaging followed by magnifying endoscopy with narrow-band imaging for the real-time imaging and diagnosis of invasion depth in superficial esophageal squamous cell carcinoma.

BACKGROUND Magnifying endoscopy with narrow-band imaging (ME-NBI) has been used to estimate the invasion depth of superficial esophageal squamous cell carcinoma (SESCC), but the real diagnostic power of ME-NBI remains unclear because of few prospective studies. OBJECTIVES To evaluate whether ME-NBI adds additional information to white-light imaging (WLI) for the diagnosis of invasion depth of SESCC. DESIGN Multicenter, prospective trial using real-time imaging and diagnosis. SETTING Seven Japanese institutions. PATIENTS Fifty-five patients with SESCC were enrolled from June 2011 to October 2013, and the results for 49 lesions were analyzed. INTERVENTIONS Patients underwent primary WLI followed by ME-NBI, and reports of primary WLI (WLI alone) were completed before secondary ME-NBI (WLI followed by ME-NBI). To standardize diagnosis among examiners, this trial was started after achievement of a mean κ value≥.6 among 11 participating endoscopists. MAIN OUTCOME MEASUREMENTS Diagnosis of invasion depth by each tool was divided into cancer limited to the epithelium and the lamina propria mucosa and cancer invading beyond the muscularis mucosae (≥T1a-MM) and then collated with the final pathologic diagnosis by an independent pathologist blinded to the clinical data. RESULTS The accuracy of invasion depth in WLI alone and WLI followed by ME-NBI was 71.4% and 65.3% (P=.375), respectively. Sensitivity for ≥T1a-MM was 61.1% for both groups (P=1.000), and specificity for ≥T1a-MM was 77.4% for WLI alone and 67.7% for WLI followed by ME-NBI (P=.375). LIMITATION Open-label trial. CONCLUSIONS ME-NBI showed no additional benefit to WLI for diagnosis of invasion depth of SESCC. (University Hospital Network Clinical Trials Registry number: UMIN000005632.).

Efficacy of famotidine and omeprazole in healing symptoms of non-erosive gastro-oesophageal reflux disease: randomized-controlled study of gastro-oesophageal reflux disease

Background : The epidemiology and pathophysiology of non‐erosive gastro‐oesophageal reflux disease differs from erosive gastro‐oesophageal reflux disease. There is a possibility that non‐erosive gastro‐oesophageal reflux disease treatment requires a different regimen/approach but it is not yet acknowledged.

A case of pancreaticoduodenal artery aneurysm causing pancreatic pseudotumour and duodenal obstruction

This case report describes a ruptured pancreaticoduodenal artery aneurysm (PDAA) causing pancreatic pseudotumour and duodenal obstruction. A 59-year-old man was referred to our hospital with a chief complaint of frequent vomiting without abdominal pain. Because a mass lesion 10 cm in diameter was palpated in the right para-umbilical region and found in the head of the pancreas on computerized tomography (CT) and ultrasonography, malignant tumour of the pancreas or tumour-forming pancreatitis was strongly suspected, and further examination was performed.Magnetic resonance imaging (MRI) results suggested subacute haematoma inside the mass. On angiography, an aneurysm 8 mm in diameter was found in the posterior superior pancreaticoduodenal artery (PSPD). Since an ultrasound-guided percutaneous needle biopsy from the solid part of the mass indicated no malignancy, the lesion was considered an inflammatory pseudotumour in the head of pancreas due to ruptured aneurysm. Bypass surgery was planned, but the tumour shrank significantly with conservative treatment. Obstruction disappeared completely without surgery 4 weeks after the first symptom.

Oral Vaccination Against Helicobacter pylori with Recombinant Cholera Toxin B‐Subunit

Background.  The innocuous pure recombinant cholera toxin B‐subunit (rCTB) is very attractive as a strong adjuvant for host immunization, but little is known about rCTBs gastric mucosal immunoadjuvanticity against Helicobacter pylori. The immunoadjuvanticity of rCTB against H. pylori was tested.

Bone morphogenetic protein 2 induced differentiation toward superficial epithelial cells in the gastric mucosa

BackgroundEpithelial–mesenchymal interactions are important for maintenance of the gastrointestinal tract mucosa. Moreover, diffusible factors from the underlying mesenchyme control the proliferation and differentiation of the epithelial cells. However, the details of the associated signaling remain unknown.MethodsTwo novel cell lines, designated MSE1 (mouse stomach epithelium) and MSMF1 (mouse stomach myofibroblast) cells, were established from mouse glandular stomach and cocultured in three-dimensional collagen gels in vitro.ResultsMSE1 cells formed dramatic branching tubular structures upon coculture with MSMF1 cells. In contrast, they formed spherical cyst structures in the absence of fibroblast support or the presence of Swiss 3T3 cells. Since bone morphogenetic protein 2 (BMP2) was expressed by MSMF1 cells but not Swiss 3T3 cells, we investigated whether it induced the morphological differentiation. Addition of BMP2 to MSE1 cells induced the formation of branching tubular structures, even in the absence of MSMF1 cells. Noggin, a BMP2 antagonist, blocked the MSMF1-induced tubular branch formation by MSE1 cells. MSE1 cells were induced to express mRNA of MUC5AC, an important marker for gastric superficial epithelium in the upper part of pits, upon branching tubule formation after BMP2 addition. Coculture with MSMF1 cells or BMP2 addition induced Smad1 phosphorylation in MSE1 cells. Furthermore, BMP2 inhibited MSE1 cell proliferation in MTS assays and suppressed AKT phosphorylation.ConclusionsBMP2 stimulated MSE1 cells to form branching duct-like structures and differentiate toward superficial epithelium in three-dimensional cocultures in vitro, suggesting that it may act as a morphogen and differentiation inducer in epithelial–mesenchymal interactions of gastric mucosa.

Helicobacter pylori eradication decreases blood neutrophil and monocyte counts.

Background : The effect of Helicobacter pylori infection on systemic disorders is not well understood.

Helicobacter pylori eradication decreases the expression of glycosylphosphatidylinositol-anchored complement regulators, decay-accelerating factor and homologous restriction factor 20, in human gastric epithelium.

Background: It has previously been reported that there is a strong correlation between the expression of glycosylphosphatidylinositol (GPI)‐anchored complement membrane inhibitor in gastric epithelium and the severity of inflammation of gastric mucosa. To investigate the regulation of complement activity in gastric epithelium during Helicobacter pylori (H. pylori)‐associated gastritis, the expression of GPI‐anchored complement membrane inhibitors, decay‐accelerating factor (DAF) and 20‐kDa homologous restriction factor 20 (HRF20), and membrane cofactor protein (MCP), which is a transmembrane protein, were evaluated after removal of the H. pylori stimulus. Furthermore, the expression of the complement fragment, C3c, was also investigated.