Frequency of nonsteroidal anti-inflammatory drug-associated ulcers.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for treatment of orthopedic diseases, inflammatory diseases, etc., and low-dose aspirin is a common antiplatelet therapy given mainly for secondary prevention of atherothrombosis (e.g.

Surface potential studies on adsorption processes of clay nanosheets onto a floating molecular film of an amphiphilic alkylammonium cation.

A floating molecular film was formed when a chloroform solution of dimethyldioctadecylammonium bromide (DMDOA(+)Br(-)) was spread on an aqueous dispersion of a clay mineral (sodium montmorillonite). At a low concentration (<50 ppm: ppm = mg dm(-3)), a clay mineral was exfoliated into negatively charged layers (denoted by clay nanosheets). Clay nanosheets in a dispersion were adsorbed onto a floating film because of electrostatic interactions.

[Strategy to manage low dose aspirin-induced gastrointestinal injury].

Low dose aspirin, as an anti-platelet medication, has been increasingly prescribed to elderly patients for primary and secondary prevention of cardio- and cerebro-vascular events. Nonetheless, aspirin's effectiveness in such disease prevention is limited by the risk of upper and lower gastrointestinal (GI) complications such as ulceration, hemorrhage and perforation. Aspirin administration is associated with 2-fold increase in the GI risk in middle-aged users without prior history of peptic ulcer and without concomitant medications.

[Role of proton pump inhibitor in the management of low dose aspirin related ulcerations].

Aspirin, as an anti-platelet medication, has been increasingly prescribed to elderly patients for primary and secondary prevention of cardio--and cerebro--vascular events. Nonetheless, aspirin's effectiveness in such disease prevention is limited by the risk of gastrointestinal (GI) complications such as ulceration, hemorrhage and perforation. Aspirin administration is associated with 2-fold increase in GI risk in middle-aged users without prior history of peptic ulcer and without concomitant medications.

[PPARgamma agonists for the diseases of gastrointestinal tract and liver].

Peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear receptor superfamily, is expressed in colonic epithelial cells at high levels and is assumed to play an important physiological role in the gut. In vitro as well as animal model experiments showed considerable anti-cancer and anti-inflammatory effects of thiazolidinedione (TZD) PPARgamma agonists in the colon. Therefore, in the gastroenterology field, much attention has been focused on the efficacy of TZD on the treatment of colorectal cancer and inflammatory bowel diseases (IBD).

Proton pump inhibitors and recurrent bleeding in peptic ulcer disease.

Peptic ulcer disease (PUD) is one of the main lesions responsible for upper gastrointestinal (GI) bleeding, as well as esophageal varices and Mallory-Weiss tear. Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs)/aspirin are the major responsible causes. In cases of upper GI bleeding, urgent endoscopy is performed after stabilization of vital signs.

[Iron deficiency anemia and H. pylori].

Although Helicobacter pylori (H. pylori) is a causative agent for chronic gastritis, peptic ulcer, and gastric carcinoma, this pathogen is also responsible for some extra-gastric diseases. Both epidemiologic and clinical studies suggest that H.

[Role of Helicobacter pylori eradication in the prevention of peptic ulcer in NSAID users].

Helicobacter pylori (H. pylori) and non-steroidal anti-inflammatory drug (NSAID) are independent risk factors for peptic ulcers and ulcer complications and they have additive or synergistic effects. A meta-analysis showed that the OR for the incidence of peptic ulcer was 61.

[Guideline for prophylaxis and treatment of NSAID-associated gastric ulcerations].

Both Helicobacter pylori (H. pylori) infection and non-steroidal anti-inflammatory drug (NSAID) administration independently and significantly increase the risk of peptic ulceration and ulcer bleeding as its complication. Because of increasing ratio of the senior generation in Japan, the relative role of NSAID including low-dose aspirin as an anti-platelet therapy, will be more important in the pathogenesis of peptic ulcerations.

Up-regulation of TFF1 (pS2) expression by TNF-alpha in gastric epithelial cells.

Background And Aim: TFF1 (pS2) is expressed at a high level in gastric epithelial cells and plays an important role in protecting the gastric mucosa. However, the regulatory mechanisms of TFF1 expression are not fully understood. The aim of this study was to investigate the effect of TNF-alpha, a representative proinflammatory cytokine, on TFF1 expression.

Comparison between endoscopic papillary balloon dilatation and endoscopic sphincterotomy for the treatment of common bile duct stones.

Background: This study was designed to evaluate the therapeutic outcome and early postoperative complications, especially pancreatitis, of endoscopic papillary balloon dilation (EPBD) and endoscopic sphincterotomy (EST) in patients with common bile duct stones in our department.

Methods: One hundred eighty patients with common bile duct stones were randomized to undergo EPBD or EST. An 8-mm dilatation balloon was used for EPBD.

Regulation of TFF3 expression by homeodomain protein CDX2.

Although trefoil factor family 3 (TFF3) plays an important role in protecting the intestinal mucosa, the regulatory mechanisms of its expression are not fully understood. Since homeodomain protein CDX2 has been reported to be critically involved in the development and differentiation of intestinal epithelium, we examined whether CDX2 affects the expression of TFF3. The transcription of human TFF3 reporter genes was significantly up-regulated by the transient overexpression of CDX2 in COS-7 cells and AGS gastric cells.

Peroxisome proliferator-activated receptor gamma (PPARgamma) regulates trefoil factor family 2 (TFF2) expression in gastric epithelial cells.

Although trefoil factor family 2 (TFF2) plays a critical role in the defense and repair of gastric mucosa, the regulatory mechanism of TFF2 expression is not fully understood. In this study, we investigated the regulation of TFF2 expression by peroxisome proliferator-activated receptor gamma (PPARgamma) in gastric epithelial cells. MKN45 gastric cells were used.

Central thyrotropin-releasing hormone increases hepatic cyclic AMP through vagal-cholinergic and prostaglandin-dependent pathways in rats.

Central neuropeptides play roles in many physiologic regulations through the autonomic nervous system. We have demonstrated that central thyrotropin-releasing hormone (TRH), one of neuropeptides, induces a stimulation of hepatic proliferation through vagal-cholinergic pathways. Since cAMP is known to play an important role in the hepatic proliferation, effect of central TRH on hepatic cAMP was investigated.

Thyrotropin-releasing hormone in the dorsal vagal complex stimulates pancreatic blood flow in rats.

Central administration of thyrotropin-releasing hormone (TRH) enhanced pancreatic blood flow in animal models. TRH nerve fibers and receptors are localized in the dorsal vagal complex (DVC), and retrograde tracing techniques have shown that pancreatic vagal nerves arise from the DVC. However, nothing is known about the central sites of action for TRH to elicit the stimulation of pancreatic blood flow.

Protective effect of central thyrotropin-releasing hormone analog on cerulein-induced acute pancreatitis in rats.

Central neuropeptides play a role in many physiological functions through the autonomic nervous system. We have recently demonstrated that central injection of a thyrotropin-releasing hormone (TRH) analog increases pancreatic blood flow through vagal and nitric oxide-dependent pathways. In this study, the central effect of a TRH analog on experimental acute pancreatitis was investigated in rats.

Intraportal nicotine infusion in rats decreases hepatic blood flow through endothelin-1 and both endothelin A and endothelin B receptors.

Smoking has been demonstrated to aggravate liver injury. Nicotine, a major pharmacological component of tobacco smoke, affects a multitude of functions. Smoking and nicotine induce synthesis of endothelin (ET)-1.

PPARgamma mediates NSAIDs-induced upregulation of TFF2 expression in gastric epithelial cells.

Trefoil factor family (TFF) is a group of peptides that play critical roles in maintaining gastric mucosal integrity. In real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and reporter gene assays, we show that indomethacin and aspirin upregulate TFF2 expression in MKN45 gastric cells. These drugs also activated peroxisome proliferator-activated receptor gamma (PPARgamma) at concentration ranges that increase TFF2 expression, and upregulated TFF2 expression was suppressed by GW9662, a specific inhibitor of PPARgamma.

[Guidelines in the management of Helicobacter pylori infection in Japan--in comparison with the guidelines published in other countries].

Helicobacter pylori(H. pylori) is a causative agent for chronic gastritis and is an important risk factor for peptic ulcers, gastric carcinomas, and gastric MALT lymphomas. In 2000, the Japanese Society for Helicobacter Research published a guideline on the diagnosis and treatment of H.