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Biomedical subjects

C Kawanami

Publications and source records attributed to C Kawanami.

At least 19 recordsLinked to original sources
PubMed1998

Severe muscle damage induced by high carbohydrate intake from elemental diet in a patient with Crohn's disease.

Crohn's disease is associated with complications in multiple organs. However, there are very few reported cases of patients with Crohn's disease with muscle symptoms and/or high serum creatine phospho-kinase (CPK) levels. We report here a patient with Crohn's disease who experienced skeletal muscle damage with extremely high serum CPK level during treatment with an elemental diet. The non-parenteral administration of large amounts of carbohydrate and limited glycogen degradation capability may be a possible causative mechanism for this elemental diet-induced muscle damage.

Adult↗
PubMed1998

Comparison of the signal transduction pathways activated by gastrin in enterochromaffin-like and parietal cells.

BACKGROUND & AIMS: Gastrin stimulates acid secretion from parietal cells and histamine release from enterochromaffin-like (ECL) cells through identical gastrin receptors. However, gastrin has been shown to have a trophic effect only on ECL cells. The aim of this study was to compare gastrin-induced signal transduction pathways in the ECL and parietal cells of Mastomys natalensis, an African rodent. METHODS: Both ECL and parietal cells were isolated from the gastric mucosa of M. natalensis, and intracellular signal transduction events in response to gastrin were investigated. RESULTS: Gastrin elicited histamine release from ECL cells and acid secretion from parietal cells in association with enhanced inositol phospholipid turnover. Although gastrin increased [3H]thymidine incorporation into ECL cells, it had no effect on parietal cells. Moreover, tyrosine phosphorylation and activation of mitogen-activated protein (MAP) kinase as well as c-fos and c-jun gene expression were augmented only in ECL cells. In addition, gastrin increased the formation of guanosine triphosphate-Ras with a simultaneous decrease in guanosine diphosphate-Ras levels in ECL but not in parietal cells. CONCLUSIONS: Although gastrin receptors are present in both ECL and parietal cells, they activate the Ras-MAP kinase pathway only in ECL cells.

Animals↗
PubMed1998

Rat gastric mucosal cells express ICAM-1 and proinflammatory cytokines during indomethacin-induced mucosal injury.

Adhesion molecules and cytokines are known to be involved in the formation of acute gastric mucosal injury. However, it is not clear whether the gastric mucosal cells express these molecules and modulate the inflammation. To clarify whether gastric mucosal cells express intercellular adhesion molecule-1 (ICAM-1) and proinflammatory cytokines (tumor necrosis factor-alpha (TNF-alpha), interleukin-1-alpha (IL-1-alpha), and cytokine-induced neutrophil chemoattractant-2-beta (CINC-2-beta)) in the formation of gastric mucosal injury, we have used rat indomethacin-induced gastric mucosal lesions as an in vivo model. The gene expression of all cytokines and ICAM-1 increases at the early stages of indomethacin-induced gastritis (TNF-alpha and IL-1-alpha gene expression began to increase earlier than that of ICAM-1 and CINC-2-beta) and can mainly be detected in the gastric epithelial layer. To further identify the source of those molecules, the epithelial cells were separated into seven fractions according to their sizes by a counterflow elution. ICAM-1 and CINC-2-beta gene expressions are particularly enhanced in the middle-sized cell fractions that are rich in gastric mucous-producing cells. The effect of TNF-alpha or IL-1-alpha on the gene expression of ICAM-1 and cytokines was examined by using RGM-1 cells as a model for gastric mucosal cells. RGM-1 cells show an augmented ICAM-1 and proinflammatory cytokine expression in response to TNF-alpha or IL-1-alpha stimulation. Moreover, immunohistochemical staining also reveals an increase in ICAM-1 and CINC protein production in RGM-1 cells in response to TNF-alpha stimulation. We conclude that gastric mucosal cells express various cytokines and an adhesion molecule during the formation of acute gastric mucosal injury and that they may modulate the inflammation.

Animals↗
PubMed1998

Effect of aging on gastrin receptor gene expression in rat stomach.

Gastrin is a pivotal humoral factor which regulates gastric acid secretion through its receptors. There is no report, however, concerning the age-related changes of gastrin receptor gene expression in the stomach. Northern blot analysis and in situ hybridization were performed to clarify the changes of gastrin receptor expression during the aging. In situ hybridization clarified that gastrin receptor mRNA was expressed mainly in enterochromaffin-like (ECL) cells in adult rat gastric mucosa. With aging, gastrin receptor gene expression in the stomach increased with the concomitant increase in histidine decarboxylase mRNA. Since histidine decarboxylase is a marker of gastric ECL cells, the augmented gastrin receptor mRNA in aged rats may be caused by the increased ECL cells in gastric mucosa during the aging.

Aging↗
PubMed1998

Expression of protooncogene c-kit and its ligand stem cell factor (SCF) in gastric carcinoma cell lines.

We examined 13 human gastric carcinoma cell lines for the expression of both c-kit and stem cell factor (SCF). Expression of mRNAs was detected by both Northern blot analysis and reverse transcriptase-polymerase chain reaction (RT-PCR), and expression of translated proteins was detected by western blotting. Using RT-PCR we confirmed the expression of c-kit in five (ECC12, TMK1, MKN7, GCIY, and HGC27) cell lines. Northern blot analysis showed coexpression of both c-kit and SCF in ECC12 and expression of SCF in five other (MKN74, MKN1 OKAJIMA, KATOIII, and TMK1) cell lines. SCF stimulated both tyrosine phosphorylation of c-kit and growth of ECC12, whereas it did not stimulate those of GCIY. The sizes of c-kit transcript and protein in GCIY were slightly smaller than those of the reported ones, suggesting the presence of a biologically inactive truncated form of c-kit in GCIY. The present study suggests that c-kit/SCF system might play an important role in the carcinogenesis and tumor growth of ECC12 and that the truncated form of c-kit in GCIY might not be associated with malignant transformation.

Blotting, Northern↗
PubMed1997

Pepsinogen C gene product is a possible growth factor during gastric mucosal healing.

We isolated, by the subtraction cloning method, a pepsinogen C (PGC) gene fragment (the sequence between the 968th and 1179th base pairs) from a rat gastric mucosal cDNA library as a cDNA clone encoding a substance that promotes growth of the normal rat gastric mucosal cell line RGM1. Northern blot analysis revealed that PGC gene expression was enhanced not only in acetic acid-induced chronic gastric ulcers but also in indomethacin-induced gastric mucosal lesions. PGC gene expression was also increased in the Helicobacter felis-infected stomachs. Thus, the PGC gene may play a role in gastric epithelial cell growth during gastric mucosal healing.

Acetic Acid↗
PubMed1997

Developmental gene expression of gastrin receptor in rat stomach.

Gastrin, which is present in fetal plasma, may have important roles in the development of gastric mucosa, since it is not only a potent stimulator of gastric acid secretion but also a growth promoting factor. Gastrin regulates various cellular functions via its receptors on cell membrane. Therefore, in order to elucidate a role for gastrin in the development of gastrointestinal system during gestation, Northern blot analysis was performed. The results of the study suggested that gastrin receptor is mainly present on parietal cells. Furthermore, proton pump and gastrin receptor gene expressions in parietal cells were strongly stimulated by the administration of exogenous gastrin. In conclusion, gastrin may be involved in the developmental change of parietal cells through its receptors.

Animals↗
PubMed1997

Regenerating gene expression in normal gastric mucosa and indomethacin-induced mucosal lesions of the rat.

Regenerating (reg) gene expression was tested in rat gastrointestinal mucosa to investigate the role played by this gene in the healing of mucosal lesions. Expression of reg mRNA was higher in the stomach than in any other region of the gastrointestinal tract. The gastric cells that expressed reg mRNA were located in the deepest mucosal layer and were small in diameter. In an injured state following indomethacin treatment, reg gene expression was markedly augmented, accompanied by an increase of c-fos expression and healing of the mucosal lesions. These results suggest a role of the reg gene in the healing of gastrointestinal mucosal lesions.

Animals↗
PubMed1997

Helicobacter pylori induces proinflammatory cytokines and major histocompatibility complex class II antigen in mouse gastric epithelial cells.

Although Helicobacter pylori has been reported to stimulate the release of various cytokines from gastric tissue, it remains unknown whether normal and nontumorous gastric epithelial cells produce these cytokines. Therefore, in this study, we used a normal mouse gastric surface mucous cell line (GSM06) to determine whether gastric epithelial cells produce proinflammatory cytokines in response to H. pylori. The expression of MHC class II antigen was also examined, to investigate whether gastric epithelial cells participate in the immune response to H. pylori. In the study, GSM06 cells were incubated with H. pylori or its lipopolysaccharide (LPS). Proinflammatory cytokines were detected by Northern and Western blot analysis. The expression of MHC class II antigen was examined by fluorescence activated cell sorter (FACS) analysis. Genetic expression of proinflammatory cytokines such as interleukin-1alpha, tumor necrosis factor-alpha, and cytokine-induced neutrophil chemoattractant-2beta was enhanced by both intact and sonicated H. pylori, but not by H. pylori LPS. The expression of MHC class II antigen was induced by H. pylori more strongly than by interferon-gamma. We conclude that H. pylori induces the expression of proinflammatory cytokines and MHC class II antigen in gastric epithelial cells. Gastric epithelial cells may act as antigen-presenting cells and participate in the immune response to H. pylori infection.

Animals↗
PubMed1997

Distribution of prostaglandin E receptors in the rat gastrointestinal tract.

AIMS: In order to study the role of prostaglandin in the regulation of the gastrointestinal functions, gene expression of prostaglandin receptors along the rat gastrointestinal tracts were investigated. METHODS: Rats were used for the study. The combination of counterflow elutriation separation of mucosal cells and Northern blot analysis was used to detect the gene expression of prostaglandin receptors in gastrointestinal tracts. RESULTS: In small intestine and colon, prostaglandin E2 EP1 and EP3 receptor mRNAs were mainly localized in the deeper intestinal wall containing muscle layers. EP4 receptor gene expression, on the other hand, was detected in the intestinal mucosal layer. In the stomach, EP1 mRNA was detected in gastric muscle layers, whereas EP3 and EP4 receptor gene expression was mainly present in the gastric mucosal layer containing epithelial cells. In gastric epithelial cells, parietal cells were found to have both EP3 and EP4 receptors. At lower concentrations, prostaglandin E2 inhibited gastric acid secretion by parietal cells probably through EP4 receptors. At higher concentrations, however, it stimulated it. On the other hand, mucous cells possessed only EP4 receptor mRNA. CONCLUSIONS: Thus, it is suggested that prostaglandin E2 modulates gastrointestinal functions through at least three different prostaglandin receptors (EP1, EP3, and EP4), each of which has a distinct contribution in the gastrointestinal tract.

Aminopyrine↗
PubMed1997

Intragastric distribution of nonsteroidal anti-inflammatory drug-related ulcers in patients without collagen diseases.

During the long-term administration of nonsteroidal anti-inflammatory drugs (NSAIDs), approximately 3% of patients have gastric ulcers develop in each year. Although much is known about the endoscopic characteristics of NSAID-induced gastric ulcers in patients with rheumatoid arthritis (RA), it is not clear where in the stomach NSAIDs induce ulcers in patients without RA. We looked at that question. During the 1-year study period, 29 patients with gastric ulcer, who had been taking NSAIDs regularly for more than 4 weeks mainly for osteoarthritis, were identified. Seventy-five patients with gastric ulcers who had not taken NSAID also were found. The sites of gastric ulcers of these two groups were quite different. The NSAID-induced ulcers mainly were found in the gastric antrum, whereas the majority of NSAID-unrelated ulcers were in the gastric corpus. We conclude that NSAID-induced ulcers in non-RA patients mainly are formed in the gastric antrum.

Adult↗
PubMed1997

Helicobacter pylori independent chronological change in gastric acid secretion in the Japanese.

BACKGROUND: Gastric acid secretion in Japanese subjects decreases with aging. One of the possible causative mechanisms of this attenuated acid secretion is speculated to be a Helicobacter pylori induced chronic gastritis. The infection rate of this microorganism has decreased recently in Japan. AIMS: To investigate whether gastric acid secretion has altered over the past 20 years, and if so, what the influence of H pylori infection might be in the Japanese population. SUBJECTS AND METHODS: Gastric acid secretion, serum gastrin and pepsinogen I and II concentrations, and H pylori infection were determined in 110 Japanese subjects in both the 1970s and 1990s. RESULTS: Basal acid output as well as maximal acid output have greatly increased over the past 20 years, not only in individuals with H pylori infection but also in those without infection. Furthermore, subjects with H pylori infection tended to show decreased gastric acid secretion in comparison with those without infection, particularly in geriatric subjects. There was a positive correlation between gastric acid secretion and serum pepsinogen I concentrations. CONCLUSIONS: In Japan, both basal and stimulated gastric acid secretion have increased over the past 20 years; some unknown factors other than the decrease in H pylori infection may play an important role in this phenomenon.

Adult↗
PubMed1996

Reg gene expression is increased in rat gastric enterochromaffin-like cells following water immersion stress.

BACKGROUND & AIMS: Reg gene has been isolated from regenerating rat pancreatic islets, and subsequent studies have shown a trophic effect of Reg protein on islet cells. However, little is known about the role of Reg protein in the stomach. The aim of this study was to clarify the localization of Reg messenger RNA (mRNA) and its product in the stomach and to examine changes in the level of their expression during regeneration of gastric mucosal cells. METHODS: Gastric lesions were experimentally induced in Sprague-Dawley rats by water immersion stress. Northern blot analysis and in situ hybridization studies were performed to examine changes in mRNA levels. Immunohistochemical studies were performed to identify the cellular localization and to investigate the change in Reg protein level. RESULTS: Reg mRNA and its product were distributed in the basal part of the oxyntic mucosa and were expressed mainly in enterochromaffin-like cells. Levels of both Reg mRNA and its product were markedly increased in the water immersion-induced gastric lesions. CONCLUSIONS: Reg mRNA and its product are expressed in gastric enterochromaffin-like cells, and their levels are increased during the healing process of water immersion-induced gastric lesions.

Animals↗
PubMed1996

Erythropoietin stimulates proliferation of rat-cultured gastric mucosal cells.

Most anemic patients with chronic renal failure have gastric mucosal lesions. However, these gastric lesions are often improved after the administration of recombinant human erythropoietin (rHuEPO). We have used the rat gastric mucosal cell line RGM-1, to examine the possibility that rHuEPO might directly stimulate the growth of gastric mucosal cells in vitro. Our results show that rHuEPO dose-dependently increased [3H]thymidine incorporation into RGM-1 cells and their expression of c-myc gene. In addition, 125I-rHuEPO specifically bound to RGM-1 cells, and moreover, erythropoietin receptor gene expression was detected by RT-PCR. We conclude that rHuEPO has a direct growth-promoting effect on RGM-1 cells, suggesting possible usefulness of rHuEPO administration for the treatment of gastric mucosal damage in patients with chronic renal failure.

Animals↗
PubMed1996

"Mediterranean lymphoma" treated with antibiotics.

We report a case of Mediterranean lymphoma treated with antibiotics. A 74-year-old woman visited the hospital due to abdominal pain. Endoscopic examination showed erosions and ulcerations on duodenal mucosa. Biopsy specimens histologically revealed massive infiltration of small-sized lymphocytes and plasma cells in subepithelial mucosa. Immunoperoxidase staining showed that the infiltrating cells were positively stained with anti-alpha heavy chain. Serum IgA concentration was elevated and immunoelectrophoresis of the serum demonstrated monoclonal protein composed of alpha heavy chain. During the antibiotic treatment her symptoms disappeared and serum IgA concentration was normalized. Endoscopic examination also showed healing of the duodenal ulceration. The similarities between Mediterranean lymphoma and gastric mucosa-associated lymphoid tissue (MALT) type lymphoma, both of which may be related to bacterial infection and can be treated with antibiotics, are discussed in this report.

Aged↗