Leukotrienes (LTs) are known to act as a mediator provoking tissue response in inflammation. LTs, particularly type B4 (LTB4) as chemotactic factor of neutrophil are released from neutrophils and gastric mucosal cells when these cells are stimulated by Helicobacter pylori. The present study was performed to test a possibility that eupatilin may prevent the H. pylori-induced gastric cell damage by observing whether this chemical inhibit the release of LTB4 from H. pylori-stimulated gastric cells (Kato III) and neutrophils. As observed in the previous study, H. pylori induced the release of LTB4 from these cells and at the same influx of Ca2+ into the cells. In the presence of eupatilin, the release of LTB4 was inhibited whereas Ca2+ influx was not affected. Probably eupatilin may inhibit the release of LTB4 by preventing the synthesis of LTs. These results suggest that eupatilin can has a therapeutic effect on H. pylori-induced gasric cell damage.
Helicobacter pylori* ; Helicobacter* ; Inflammation ; Leukotriene B4* ; Leukotrienes ; Neutrophils*

It has been implicated that leukotrienes play roles in the pathogenesis of gastritis and gastric ulceration associated with Helicobacter pylori (H. pylori). Rebamipide is being used as an antiulcer drug but it's mechanism of action has not been understood well. One possible mechanism of action of this drug is to inhibit the cellular release of leukotrienes by various stimuli, particularly H. pylori. In the present study, attempts were made to test this possibility and the results are as follows. When Kato III cells (gastric adenoma cells) were stimulated by H. pylori, leukotriene D4 (LTD4) was released and rebamipide inhibited this release dose-dependently. Similar experiment was performed on neutrophils because the infilteration of neutrophils is a common phenomenon in H. pylori-infected gasrtric tissues. Neutrophils released LTD4 when these cells were stimulated by H. pylori and rebamipide also inhibited this release. Furthermore, rebamipide inhibited the release of LTD from neutrophils induced by calcium ionophore A23187 and arachidonic acid. The results suggest that rebamipide has the action to inhibit the release of LTD4 from various cells and this action may contribute in part to prevent the ulcerogenesis induced by H. pylori.
Adenoma ; Arachidonic Acid ; Calcimycin ; Calcium ; Gastritis ; Helicobacter pylori* ; Helicobacter* ; Leukotriene D4* ; Leukotrienes ; Neutrophils ; Stomach Ulcer

Antifungal properties of methyl 2-benzimidazole carbamate (BMC) were investigated using 16 fungi. Cytotoxicity test of BMC revealed that the morphology of HeLa cells was considerably deformed even at the concentrations as low as 0.1 ppm. Minimum inhibitory concentration (MIC) values of BMC for 7 fungi among the 16 tested ones were lower than 1.95x10(-4) microg/ml, while Aspergillus flavus showed an MIC value higher than 1.0 microg/ml. Tolerance induction against BMC was successful only for Paecilomyces farinosus LAR10, contrary to the expectation that tolerance would be induced for the fungi having high MIC values such as Aspergillus niger ATCC 9642 and A. flavus ATCC 9643. Spore germination of A. niger ATCC 9642 was suppressed by BMC. However the mycelial growth of the fungus once germinated was not retarded at all by BMC up to 8 MIC. Addition of lanosterol provided a remedy for the reduced germination rate of A. niger ATCC 9642 spores.
Aspergillus flavus ; Aspergillus niger ; Fungi ; Germination ; HeLa Cells ; Humans ; Lanosterol ; Microbial Sensitivity Tests ; Niger ; Paecilomyces ; Spores

In this report, the inhibitory action of eupatilin was investigated by using leukotriene D4 in the human neutrophils and Kato III cells (Gastric adenoma cells as a substitute for gastric mucosal cells) stimulated by Helicobacter pylori. Leukotriene D4 (LTD4) was released from both neutrophils and Kato III cells when these cells were incubated with H. pylori. The release of LTD4 increased time-dependently and the maximum release of LTD4 was 2.3-2.5 pmol. But in the presence of eupatilin, the release of LTD4 from these cells was inhibited in a dose-dependent manner. In the neutrophils, die release of LTD4 was suppressed to 70% and 50% of the control levels when neutrophils was incubated with 0.01 and 0.1 mM of eupatilin. In the Kato III cells, the release of LTD4 was suppressed to 59% and 27% of the control levels by adding 0.01 and 0.1 mM of eupatilin. We estimated the intracellular Ca2+ levels when Kato III cells and neutrophils were stimulated by H. pylori using 45Ca. But the suppressive effect of eupatilin on Ca2+ influx into these cells was not significant. We also obtained the results that H. pylori induced Ca2+ influx into these cells by confocal microscopy, however there was no differences in the dose level of eupatilin. These results were confirmed by 1H Nuclear Magnetic Resonance(NMR) spectroscopy. The NMR patterns of eupatilin in the absence of Ca2+ was changed compare with when Ca2+ was present, but its effect was not strong.
Adenoma ; Helicobacter pylori ; Helicobacter* ; Humans* ; Leukotriene D4* ; Microscopy, Confocal ; Neutrophils* ; Spectrum Analysis

Fitz-Hugh-Curtis (FHC) syndrome is hepatitis characterized by severe right upper abdominal pain associated with pelvic inflammatory disease (PID), mimicking the symptoms of acute abdomen, such as in acute cholecystitis. FHC syndrome is becoming more common with the increasing incidence of PID in Korea. We treated eight patients with FHC syndrome, who visited our hospital with right upper quadrant abdominal pain. We emphasize the importance of spiral computed tomography (CT) in the diagnosis of right upper quadrant abdominal pain in sexually active young women.
Abdomen, Acute ; Abdominal Pain ; Chlamydia Infections ; Cholecystitis, Acute ; Female ; Hepatitis ; Humans ; Incidence ; Korea ; Pelvic Inflammatory Disease ; Peritonitis ; Tomography, Spiral Computed

Intestinal pseudo-obstruction (IPO) is an uncommon, severe complication that occurs in a small subgroup of patients with systemic lupus erythematosus (SLE). To our knowledge, approximately 30 cases of IPO in SLE have been reported in the literature. Moreover, IPO is rare as an initial manifestation of SLE. We report a case of a 43-year-old woman with SLE who initially presented with IPO.
Adult ; Female ; Humans ; Intestinal Pseudo-Obstruction* ; Lupus Erythematosus, Systemic*

Leukotrienes (LTs) are known to act as a mediator provoking tissue response in inflammation. This finding implicates that LTs also play important roles in the pathogenesis of H. pylori-induced gastritis and gastric ulceration. Rebamipide is being currently used as a therapeutics for gastritis and peptic ulcer, but their mechanisms of action have not been known clearly yet. One possibility is that their therapeutic effects are ascribed to interfering with the H. pylori-induced release of LTs from neutrophils and gastric mucosal cells. In the present study, this possibility was tested using LTB4 as the test material in human neutrophils and Kato III cells(gastric adenoma cells as a substitute for gastric mucosal cells). The release of LTB4 from both neutrophils and Kato III cells was time and H. pylori-dose dependent. The maximum release of LTB4 was induced by neutrophils and Kato III cells when these cells incubated with H. pylori 4.8 X 108 cells/ml for 30 min. But in the presence of rebamipide the release of LTB4 from these cells was suppressed in dose dependent manners. The release was completely suppressed at 1.0 mM of rebamipide in neutrophils and 2.0 mM of this drug in Kato III cells, respectively. We also obtained the results that the release of LTB4 was induced by A23187 (Ca2+ ionophore) and the A23187-induced release was also inhibited by rebamipide. It seems that the mechanism of action of rebamipide is through its interaction with the level of intracellular Ca2+. In view of the roles of LTB4 in inflammatory reaction and the roles of H. pylori in gastritis and peptic ulcer, the effects of this drug observed in this study may contribute to their therapeutic action in these gastric disorders.
Adenoma ; Calcimycin ; Gastritis ; Helicobacter pylori* ; Helicobacter* ; Humans ; Inflammation ; Leukotriene B4* ; Leukotrienes ; Neutrophils ; Peptic Ulcer ; Stomach Ulcer