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Biomedical subjects

M Asahara

Publications and source records attributed to M Asahara.

At least 19 recordsLinked to original sources
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

[Pathophysiological background of transient hyperphosphatasemia].

We studied the relationship between 23 cases with transient hyperphosphatasemia (TH) and viral infection. Many of the patients appeared to be suffering from viral infection. Measurement of antibody in the titer revealed increases in antibody to Echo 22, Entero 71 and Coxsackie B5 in 20.0%, 11.1% and 11.1% of patients, respectively.

Alkaline Phosphatase↗
PubMed1998

[Sex and age distribution of patients with macroamylasemia found in the daily isoenzyme analysis].

We studied distributions of sex and age for 102 patients with macroamylasemia found in routine isoenzyme analysis. This study was based on a questionnaire to promote understanding of the clinical significance of macroamylase. More than half of the physicians received our report evaluated the information on macroamylase in the questionnaire. Macroamylasemia found in this study consisted of IgA type immunoglobulin in 92% and mostly had high activities in the serum. The back-ground of these patients with macroamylasemia were 10 cases of hepato-biliary disease, 9 cases of diabetes mellitus, 8 cases of autoimmune disease and so on. The frequency of macroamylasemia in males was double than in females and age distribution was not significant in statistic analysis.

Adolescent↗
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

Production and activation of hepatocyte growth factor during the healing of rat gastric ulcers.

The hepatocyte growth factor has been reported to be a potent mitogen of various epithelial cells, including gastric mucosal cells. Therefore, production and activation of hepatocyte growth factor in the gastric wall were investigated to speculate on the possible role of this factor in the healing of gastric ulcer in rats. Indomethacin-induced gastric mucosal lesions and acetic acid induced ulcers were employed as models of acute gastric lesions and chronic ulcer, respectively. Immunoblot and Northern blot analyses indicate that experimentally induced gastric mucosal lesions stimulate not only the production of hepatocyte growth factor, but also the conversion to its active form. This conversion was accompanied by increased gene expression of hepatocyte growth factor activator in the stomach. In rats with acute mucosal lesions, hepatocyte growth factor activator mRNA was most abundant 6 h after induction of mucosal lesions. On the other hand, hepatocyte growth factor and hepatocyte growth factor activator mRNA levels were elevated until 15 days after the induction of chronic ulcers. In summary, it has been clarified that not only production, but also activation of hepatocyte growth factor is stimulated during gastric ulcer healing.

Animals↗
PubMed1996

Nerve growth factor (NGF) induces increase in multi-ubiquitin chains and concomitant decrease in free ubiquitin in nuclei of PC12h.

Changes in Ubiquitin-immunoreactivity after nerve growth factor (NGF) treatment were investigated in PC12h cells. Ubiquitin-immunoreactivity was increased in the nucleus of NGF-treated cells. The quantitative analysis revealed that, after 7 days of NGF treatment, almost 20% of cells had ubiquitin-immunoreactive nuclei and the frequency was increased thereafter. Levels of free ubiquitin and multi-ubiquitin chains were measured by radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA), respectively. Measurements were carried out for four subcellular fractions: urea- and water-soluble extracts of nuclei and cytoplasm. Decrease in free ubiquitin was observed in water-soluble cytoplasmic extracts of NGF-treated cells, though increase in multi-ubiquitin chains in the same fraction was not observed. As for nuclei, increase in multi-ubiquitin chains and concomitant decrease in free ubiquitin were found in the water-soluble extracts after NGF treatment. Levels of multi-ubiquitin chains did not change in urea-soluble cytoplasmic extracts as well as nuclear urea-soluble ones after NGF treatment. These results indicated that multi-ubiquitination of nuclear proteins is increased during NGF-induced neuronal differentiation of PC12h cells.

Animals↗
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

Presence of prostaglandin EP4 receptor gene expression in a rat gastric mucosal cell line.

RGM-1 is an epithelial cell line established from gastric mucosa of adult Wistar rats. In this study, we characterized this newly established cell line by Northern blot analysis. We also investigated deoxyribonucleic acid (DNA) synthesis and hexosamine production in RGM-1 by PGE2. Northern blot analysis did not detect any transcript of proton pump, gastrin receptor, histidine decarboxylase, somatostatin and pepsinogen 1, indicating the absence of characteristics of parietal, ECL, D and chief cells in RGM-1 cells. However, this periodic acid-Schiff (PAS)-positive cell line expressed prostaglandin EP4 receptor mRNA but not EP1 and EP3 receptor mRNAs. [3H]-thymidine incorporation into DNA of the cells was not increased by PGE2. In contrast, PGE2 increased hexosamine content in RGM-1 cells. These results suggest that RGM-1 may be a useful model of gastric mucosal cells and that PGE2 plays a role on mucin synthesis in RGM-1 cells possibly via EP4 receptors.

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

A rare case of severe acute pancreatitis complicated with pancreatic pseudocysts, obstructive jaundice and intraperitoneal hemorrhage.

A 58-year-old man visited our hospital because of back pain. Blood examinations revealed the presence of acute inflammation and an increase of pancreatic enzymes. Abdominal computed tomography indicated pseudocysts in the pancreas. The patient was diagnosed as having acute pancreatitis with pseudocysts formation. During the course of the disease, a newly formed pseudocyst in the pancreatic head compressed the common bile duct, leading to the obstructive jaundice. In addition, the rupture of a pseudocyst in the pancreatic tail caused intraperitoneal hemorrhage. This is an interesting case of acute pancreatitis with pseudocysts in which two rare complications developed.

Acute Disease↗
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↗
PubMed1995

Establishment of primary epithelial cell culture from elutriated rat gastric mucosal cells.

Proliferating cells in the gastric mucosal epithelium were successfully enriched by counterflow elutriation in a medium-sized cell fraction. When inoculated on culture plates coated with E-C-L cell attachment matrix, these cells differentiated into mucus-producing cells after reaching confluence. Northern blot analysis did not detect any transcript of the proton pump, histidine decarboxylase, somatostatin, or pepsinogen I, indicating the absence of parietal, ECL, D, and chief cells in the confluent monolayer. These mucus-producing cell monolayers that respond to various growth factors may be a suitable model with which to investigate the function of gastric mucus cells in vitro.

Animals↗
PubMed1995

Gene expression of keratinocyte and hepatocyte growth factors during the healing of rat gastric mucosal lesions.

BACKGROUND & AIMS: The factors that stimulate the growth of gastric mucosal cells during gastric mucosal healing are not completely understood. This study was designed to investigate the gene expression of keratinocyte growth factor (KGF) and hepatocyte growth factor (HGF) in the healing of gastric mucosal lesions. METHODS: Northern blot analysis and reverse-transcription polymerase chain reaction were used to show HGF and KGF messenger RNA. RESULTS: Transcripts of HGF and KGF were not shown in rat gastric mucosal epithelium but were found in submucosal and muscular layers under normal conditions. When acute gastric mucosal lesions were induced by indomethacin treatment, expression of HGF messenger RNA was augmented in submucosal, muscular, or serosal layers, whereas the transcript of KGF was not influenced. When rat gastric mucosal epithelial cell line RGM1 and rat gastric mucosal primary culture cells were incubated with HGF or KGF, their proliferation was enhanced. CONCLUSIONS: The results showed increased gene expression of HGF together with constant production of KGF during gastric mucosal healing.

Acetates↗
PubMed1994

Gastrin receptor genes are expressed in gastric parietal and enterochromaffin-like cells of Mastomys natalensis.

Although gastric enterochromaffin-like (ECL) carcinoid tumors are known to develop in patients with long-standing hypergastrinemia, the expression of the gastrin receptor gene in ECL cells has not yet been demonstrated. Therefore, this study was designed to examine gastrin receptor gene expression in ECL cells. Mastomys gastric mucosal cells isolated by enzyme dispersion were separated into 10 fractions (F1-10) by centrifugal elutriation. Each fraction was examined histologically to determine whether they contained ECL and/or parietal cells and Northern blot analysis was used to confirm the presence of histidine decarboxylase and H+, K(+)-ATPase gene expression. ECL cells were found only in fractions 1 and 2, whereas parietal cells were detected in fractions 6-10. Gastrin receptor gene expression was demonstrated in both parietal cell-rich and ECL cell-rich fractions. In addition, the gastrin receptor cDNA sequences obtained from the two of the fractions (F1 and 8) were identical. These results suggest that gastrin receptor genes are expressed in ECL cells as well as in parietal cells and that these receptors are identical.

Animals↗
PubMed1994

Gastrin receptor gene expression in several human carcinomas.

Gastrin has been shown to enhance the growth of various human tumors. The present study was designed to examine the gastrin receptor gene expression in various human carcinoma cell lines and in surgically resected carcinoma tissues. By Northern blot analysis, gastrin receptor mRNA was detected in 3 out of 7 small cell lung carcinoma cell lines. Gastrin receptor mRNA was also expressed in one out of 8 colon carcinoma cell lines and 2 out of 10 colon carcinoma tissues. Moreover, one of two small cell carcinoma cell lines of the stomach clearly expressed gastrin receptor mRNA. However, none of the gastric adenocarcinoma cell lines or surgically resected gastric adenocarcinomas tested had any detectable expression of gastrin receptor gene. These findings may suggest a role of gastrin receptor in the growth and differentiation of certain human carcinomas.

Adenocarcinoma↗
PubMed1994

Sarcoidosis with hypercalcemia--successful treatment of renal insufficiency and renal calcification with prednisolone.

A case of muscular sarcoidosis accompanied by severe hypercalcemia (serum calcium 15.5 mg/dl), renal insufficiency and renal calcification is reported. Sarcoid granulomas were found in the biopsy specimens of the lung and the muscle. The administration of prednisolone effectively improved not only muscle weakness but also hypercalcemia, renal insufficiency and renal calcification. This is a rare case of sarcoidosis in which renal calcification remitted after treatment with prednisolone. It is thus suggested that prednisolone treatment should be considered not only for hypercalcemia, but also for renal insufficiency caused by renal calcification in patients with sarcoidosis.

Calcinosis↗