Oscillation Reduction of an Anode-Layer-Type Hall Thruster by Azimuthal Propellant onuniformity

Discharge current oscillation in the frequency range of 10-100 kHz causes serious problems in using anode layer type Hall thrusters in space. As a novel approach to stabilize the discharge, azimuthally nonuniform propellant flow was created in an acceleration channel. A plenum chamber and hollow anodes were azimuthally divided into two or four sections and xenon flow rates supplied to them were controlled. As a result, the oscillation amplitude significantly decreased and oscillation-free operation was achieved at all magnetic flux densities

クサギカメムシの家屋などへの越冬飛来消長

金沢大学留学生センターFrom 1988 through 1992 we studied the overwintering number of brown-marmorated stink bugs (Halyomorpha mista), at Unazuki Spa Town in Toyama Prefecture, Japan, where the overwintering flight of Halyomorpha mista has been observed every year. The flight of H. mista to the wall surface of buildings starts usually at the end of September and reaches a peak around the 3rd week of October. The coming-fly of bugs ceases at the end of November. The flight of stink bugs started in the daytime when the maximum temperature reached nearly 25℃ after overnight minimum temperature of about 15℃; the maximum number of bugs was recorded on an autumn day after the minimum temperature fell below 10℃. Regarding the slit traps which were set on the building roofs, more bugs were attracted to the slit traps which faced riverside than to those which faced the mountains. The natural wood-color board (coated with clear lacquer) attracted more bugs than boards painted in black or white. The bugs attached to the slit traps were observed 1 or 2 weeks after the onset of their flying to the wall surface of buildings

Bile Acids Induce Cdx2 Expression Through the Farnesoid X Receptor in Gastric Epithelial Cells

Clinical and experimental studies showed that the reflux of bile into the stomach contributes to the induction of intestinal metaplasia of the stomach and gastric carcinogenesis. Caudal-type homeobox 2 (Cdx2) plays a key role in the exhibition of intestinal phenotypes by regulating the expression of intestine-specific genes such as goblet-specific gene mucin 2 (MUC2). We investigated the involvement of the farnesoid X receptor (FXR), a nuclear receptor for bile acids, in the chenodeoxycholic acid (CDCA)-induced expression of Cdx2 and MUC2 in normal rat gastric epithelial cells (RGM-1 cells). RGM-1 cells were treated with CDCA or GW4064, an FXR agonist, in the presence or absence of guggulsterone, an FXR antagonist. CDCA induced dose-dependent expression of Cdx2 and MUC2 at both the mRNA and protein levels. The maximum stimulation of Cdx2 and MUC2 mRNA induced by CDCA was observed at 3 h and by 6 h, respectively. GW4064 also induced expression of these molecules. The effects of CDCA and GW4064 on expression of Cdx2 and MUC2 were abolished by guggulsterone. These findings suggest that bile acids may induce gastric intestinal metaplasia and carcinogenesis through the FXR

Lansoprazole, a Proton Pump Inhibitor, Suppresses Production of Tumor Necrosis Factor-α and Interleukin-1β Induced by Lipopolysaccharide and Helicobacter Pylori Bacterial Components in Human Monocytic Cells via Inhibition of Activation of Nuclear Factor-κB and Extracellular Signal-Regulated Kinase

Pathogenic bacterial components play critical roles in initiation of gastrointestinal inflammation via activation of intracellular signaling pathways which induce proinflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β. Lansoprazole (LANSO), a proton pump inhibitor, has been widely used for the treatment of peptic ulcers and reflux esophagitis due to its potent acid-suppressive effect. It has also been reported to have anti-inflammatory effects. In this study we investigated the effects of LANSO on the production of TNF-α and IL-1β induced by lipopolysaccharide (LPS) and Helicobacter pylori water-soluble extract (HpWE) in the human monocytic cell line (THP-1). LANSO (100 µM) significantly reduced mRNA expression and production of TNF-α and IL-1β by THP-1 cells stimulated by LPS and HpWE. LANSO inhibited phosphorylation and degradation of inhibitory factor κB-α (IκB-α) and phosphorylation of extracellular signal-regulated kinase (ERK) induced by LPS and HpWE in THP-1 cells. These findings suggest that LANSO exerts anti-inflammatory effects by suppressing induction of TNF-α and IL-1β via inhibition of nuclear factor (NF)-κB and ERK activation

Mitochondrial disorders in NSAIDs-induced small bowel injury

Recent studies using small bowel endoscopy revealed that non-steroidal anti-inflammatory drugs including low-dose aspirin, can often induce small bowel injury. Non-steroidal anti-inflammatory drugs-induced small bowel mucosal injury involves various factors such as enterobacteria, cytokines, and bile. Experimental studies demonstrate that both mitochondrial disorders and inhibition of cyclooxygenases are required for development of non-steroidal anti-inflammatory drugs-induced small bowel injury. Mitochondrion is an organelle playing a central role in energy production in organisms. Many non-steroidal anti-inflammatory drugs directly cause mitochondrial disorders, which are attributable to uncoupling of oxidative phosphorylation induced by opening of the mega channel called mitochondrial permeability transition pore on the mitochondrial membrane by non-steroidal anti-inflammatory drugs. Bile acids and tumor necrosis factor-α also can open the permeability transition pore. The permeability transition pore opening induces the release of cytochrome c from mitochondrial matrix into the cytosol, which triggers a cascade of events that will lead to cell death. Therefore these mitochondrial disorders may cause disturbance of the mucosal barrier function and elevation of the small bowel permeability, and play particularly important roles in early processes of non-steroidal anti-inflammatory drugs-induced small bowel injury. Although no valid means of preventing or treating non-steroidal anti-inflammatory drugs-induced small bowel injury has been established, advances in mitochondrial studies may bring about innovation in the prevention and treatment of this kind of injury

Rebamipide, a mucoprotective drug, inhibits NSAIDs-induced gastric mucosal injury: possible involvement of the downregulation of 15-hydroxyprostaglandin dehydrogenase

Prostaglandin E2 plays an important role in the maintenance of gastric mucosal integrity. The level of biologically active prostaglandin E2 in the tissue is regulated by the balanced expression of its synthetic enzymes, such as cyclooxygenase, and its catabolic enzyme, 15-hydroxyprostaglandin dehydrogenase. We examined the effect of rebamipide, a mucoprotective drug, on prostaglandin E2 production and metabolism in the gastric tissue and its effect on indomethacin-induced gastric mucosal injury in mice. Rebamipide suppressed indomethacin-induced gastric mucosal injury. Suppressive effect of rebamipide on indomethacin-induced gastric mucosal injury was also observed in cyclooxygenase-2-knockout mice. The mice that were treated with rebamipide showed a 2-fold increase in cyclooxygenase-2 mRNA expression in the gastric tissue, whereas 15-hydroxyprostaglandin dehydrogenase mRNA expression markedly decreased as compared to vehicle-treated control mice. Rebamipide did not affect the expression of cyclooxygenase-1 in the gastric tissue. Rebamipide did not increase prostaglandin E2 production in the gastric tissue; however, it induced a 1.4-fold increase in the concentration of prostaglandin E2 in the gastric tissue as compared to vehicle-treated control mice. These results suggest that the suppressive effect of rebamipide on non-steroidal anti-inflammatory drugs-induced gastric mucosal injury can be attributed to reduced 15-hydroxyprostaglandin dehydrogenase expression, which increases the prostaglandin E2 concentration in the gastric tissue

Ectopic Varices Rupture in the Gastroduodenal Anastomosis Successfully Treated with N-butyl-2-cyanoacrylate Injection

The term &#34;ectopic varices&#34; is used to describe dilated portosystemic collateral veins in unusual locations other than the gastroesophageal region. We recently experienced a rare case of ectopic varices that developed in the gastroduodenal anastomosis after subtotal gastrectomy. A 70-year-old male with liver cirrhosis due to hepatitis C virus infection was admitted for hematemesis and tarry stool. He had received a subtotal gastrectomy with the Billroth-I method for gastric ulcer at 46 years of age. Although emergency endoscopy revealed esophageal and gastric fundal varices, there were no obvious bleeding points. After removal of the coagula, ectopic varices and a fibrin plug were observed on the gastroduodenal anastomosis. During the observation, blood began to spurt from the fibrin plug. N-butyl-2-cyanoacrylate with lipiodol injection succeeded in hemostasis. Splenic angiography showed gastric varices feeding from a short gastric vein and the posterior gastric vein. The blood flow around the bleeding point, as indicated by lipiodol deposition, had decreased, and no feeding vein was observed. Endoscopic and angiographic findings are shown and the treatment for such lesions is discussed.</p