Biomedical subjects

Y Higashimoto

Publications and source records attributed to Y Higashimoto.

At least 55 records · Page 3Linked to original sources

PubMed1997

Mucosal interleukin-1 beta production and acid secretion in enlarged fold gastritis.

BACKGROUND: We have previously shown that eradication of Helicobacter pylori increases acid secretion in H. pylori-associated enlarged fold gastritis. AIM: To investigate whether locally produced interleukin-1 beta is possibly involved in the inhibition of acid secretion in H. pylori gastritis. METHODS: IL-1 beta release from the gastric body mucosa was determined by short-term culture of biopsy specimens in 13 patients with enlarged fold gastritis (all H. pylori-positive), five H. pylori-positive and 10 H. pylori-negative patients without enlarged folds. The acid-inhibitory effect of locally produced IL-1 beta was examined by [14C]-aminopyrine uptake assay using isolated rabbit gastric glands. RESULTS: IL-1 beta release was significantly greater in patients with enlarged fold gastritis, significantly correlated with both basal and tetragastrin-stimulated acid outputs in the H. pylori-positive patients (r = -0.591 and r = -0.641, respectively; P < 0.01), and significantly decreased with concomitant increases in acid secretions after eradication of H. pylori. [14C]-aminopyrine uptake was inhibited by IL-1 beta in a dose-dependent manner. CONCLUSIONS: Increased production of IL-1 beta caused by H. pylori infection is possibly involved in the inhibition of acid secretion in enlarged fold gastritis.

Adult↗

PubMed1997

Biliary atresia: current management and outcome.

Between 1986 and 1994, 42 patients with BA were treated at the Kobe Children's Hospital. These patients underwent a wider excision of the hilar fibrous remnant with Roux-Y reconstruction (with or without intussuscepted valve) without stoma. Corticosteroids were used postoperatively when the stool was acholic or unsteadily cholic. The daily dose was reduced from 20 mg/day by half down. The patients were divided into two groups; in Group I (n = 17, before October 1990), a single course of corticosteroid therapy was employed. In Group II (n = 25, from November 1990 on), this regimen was repeated whenever the stool appeared less cholic. The bile flow improved significantly (excellent in 29% and 60%, and poor in 71% and 32% in Groups I and II, respectively.) Corticosteroids were used in 15 Group I patients with good response in 10 and in 21 Group II patients, 15 of whom had multiple courses. Sixteen of the 21 Group II patients had a good response. The incidence of the cholangitis was not significantly different between the 19 patients with valve and the 23 patients without valve. A 5 year survival significantly improved from 70% in Group I to 96% in Group II. In both groups, the survival rate significantly increased, when compared with the survival rate figured out with an assumption of OLT survivors as dead. On the same assumption, the survival rate of Group II is significantly more than that of the Group II. These suggest a positive contribution of liver transplantation and an aggressive corticosteroid therapy on better survival of Group II.

Anti-Inflammatory Agents↗

PubMed1996

Over-expression of bcl-xL gene in human gastric adenomas and carcinomas.

The present study was designed to clarify whether bcl-xL is involved in the development of carcinoma in the stomach. Levels of bcl-xL and bcl-2 mRNA were determined by a reverse-transcription/polymerase-chain reaction in endoscopic gastric biopsy specimens from 10 control subjects, 11 patients with adenomas and 14 patients with carcinomas. In 6 of 11 adenomas, 5 of 8 early carcinomas and 3 of 6 advanced carcinomas, the bcl-xL gene was over-expressed. In carcinomas, over-expression of the bcl-xL gene was observed in 6 of 9 intestinal-type carcinomas and 2 of 5 diffuse-type carcinomas. No correlation was observed between bcl-xL and bcl-2 gene expression. In cases in which the bcl-xL gene was over-expressed, an apparent increase in the protein level of Bcl-xL was observed by immunoblot analysis and intense Bcl-x immunoreactivity was detected immunohistochemically within the tumor cells. In conclusion, we showed that bcl-xL is over-expressed in gastric carcinomas at both the RNA and protein levels, suggesting that over-expression of bcl-xL may play a role in gastric carcinogenesis.

Adenoma↗

PubMed1996

Heparin-binding EGF-like growth factor is an autocrine growth factor for rat gastric epithelial cells.

We examined the biological action and expression of heparin-binding EGF-like growth factor (HB-EGF) in a rat gastric mucosal cell line, RGM1. HB-EGF stimulated DNA synthesis of RGM1 cells in a dose-dependent manner. Mitogenic effect of HB-EGF was as potent as that of other known mitogens for gastric epithelial cells, such as hepatocyte growth factor (HGF) and transforming growth factor (TGF)-alpha. Northern blot analysis showed that RGM1 cells as well as rat gastric mucosal tissue expressed a 2.5-kilobase transcript of HB-EGF. Not only HB-EGF and TGF-alpha but also HGF caused a rapid induction of HB-EGF mRNA in the cells. Treatment with heparitinase which destroys heparan sulfate proteoglycan (HSPG) or with chlorate which inhibits sulfation of HSPG diminished [3H]thymidine incorporation of RGM1 cells in serum-free medium. In addition, a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits the DNA synthesis of RGM1 cells in serum-free medium in a dose-dependent manner. These results suggest that HB-EGF is an autocrine and paracrine growth factor for gastric epithelial cells and may play significant roles in mucosal repair of the stomach in cooperation with other growth factors.

Amino Acid Sequence↗

PubMed1996

Successful endoscopic balloon dilatation for hypertrophic pyloric stenosis.

The authors successfully applied endoscopic balloon dilatation for the treatment of hypertrophic pyloric stenosis (HPS). The patient was an infant girl who had undergone repair of a giant omphalocele. Endoscopic balloon dilatation was performed using a 9-mm endoscope and an 8-mm polyethylene terephthalate (PET) balloon dilator. Dilatation was performed three times for 10 minutes. Vomiting continued after the dilatation. At the second session, dilatation was performed using a 12-mm PET balloon dilator. The 9-mm endoscope then passed through the pylorus. The patient has had no episodes of vomiting since the second treatment. This procedure is an important therapeutic option for selected patients with HPS.

Catheterization↗

PubMed1996

Chemical synthesis of phosphorylated peptides of the carboxy-terminal domain of human p53 by a segment condensation method.

A segment condensation method was developed for the chemical synthesis of large (> 90 amino acid) phosphopeptides and was used to produce phosphorylated and non-phosphorylated derivatives of the C-terminal tetramerization and regulatory domains of human p53 (residues 303-393). Efficient condensation synthesis of the 91 residue p53 domain was achieved in two steps. The non-phosphorylated N-terminal segment p53(303-334) (1) and its derivative phosphorylated at serine 315 (1P315), and the non-phosphorylated middle segment p53(335-360) (2), were synthesized as partially protected peptide thioesters in the solid phase using Boc chemistry. The C-terminal segment p53(361-393) (3) and its derivative phosphorylated at serine 392 (3P392) were synthesized as partially protected peptides in the solid phase using Fmoc chemistry. Phosphoamino acid was incorporated into the N-terminal segment (1P315) at the residue corresponding to p53 serine 315 as Boc-Ser(PO3(Bzl)2)-OH during synthesis. Serine 392 in the C-terminal segment was selectively phosphorylated after synthesis by phosphitylation followed by oxidation. A derivative phosphorylated at serine 378 was synthesized in a one-step condensation of the unphosphorylated N-terminal segment (1) and the phosphorylated long C-terminal segment p53(335-393) (2-3P378). Yields of the ligated peptides after removal of the protecting groups and HPLC purification averaged 60% for the first condensation and 35% for the second condensation. All five p53 peptides exhibited monomer-tetramer association as determined by analytical ultracentrifugation. Circular dichroism spectroscopy revealed that phosphorylation at Ser315 increased the alpha-helical content, which was abolished when Ser392 also was phosphorylated, suggesting an interaction between N-terminal and C-terminal residues of the C-terminal domain of p53.

Amino Acid Sequence↗

PubMed1996

Increased production of interleukin 1 beta and hepatocyte growth factor may contribute to foveolar hyperplasia in enlarged fold gastritis.

BACKGROUND AND AIMS: It has been reported that eradication of Helicobacter pylori improves fold width in H pylori associated enlarged fold gastritis. The aim of this study was to clarify the mechanism of fold thickening in this condition. PATIENTS AND METHODS: In eight patients with enlarged fold gastritis and 13 patients without enlarged folds, the presence of H pylori infection, inflammatory infiltrates, mucosal plasia, and epithelial cell proliferation in the body mucosa were investigated, and production of transforming growth factor alpha (TGF alpha), hepatocyte growth factor (HGF), and interleukin 1 beta (IL 1 beta) was determined by a competitive reverse transcription/polymerase chain reaction method and in vitro short-term culture of biopsy specimens. RESULTS: In the patients with enlarged fold gastritis, inflammatory infiltrates including macrophages increased with H pylori colonisation in the body. Foveolar thickness and proliferating cell nuclear antigen (PCNA) labelling index were increased. Messenger RNA levels of HGF, but not TGF alpha, were increased, and release of HGF and IL 1 beta was increased. HGF release, which was positively correlated with IL 1 beta release and foveolar thickness, decreased in the presence of IL 1 receptor antagonist. After eradication of H pylori, inflammatory infiltrates, IL 1 beta and HGF release decreased with concomitant decreases in PCNA labelling index, foveolar thickness and fold width. CONCLUSIONS: Increased IL 1 beta and HGF production caused by H pylori infection may contribute to fold thickening of the stomach by stimulating epithelial cell proliferation and foveolar hyperplasia in patients with enlarged fold gastritis.

Adult↗

PubMed1996

Role of prostaglandins in intestinal epithelial restitution stimulated by growth factors.

Mucosal integrity is reestablished after superficial injuries by a rapid resealing process, termed epithelial restitution, that is regulated by several growth factors and cytokines. Growth factors are also known to stimulate the synthesis of endogenous prostaglandins that mediate important functions in intestinal epithelial cells. Therefore, we examined the effect of endogenous eicosanoid production modulators, piroxicam, dexamethasone, and nordihydroguaiaretic acid (NDGA) on intestinal epithelial restitution using two cultured cell wound-resealing models, IEC-6 and Caco-2 cells. Epidermal growth factor, transforming growth factor-beta, hepatocyte growth factor, and fetal calf serum (FCS) accelerated intestinal epithelial restitution, and piroxicam significantly suppressed these stimulatory effects. Dexamethasone mimicked the action of piroxicam. No additive effect of piroxicam and dexamethasone was observed. NDGA did not affect epithelial restitution. Piroxicam abolished the increase in 6-ketoprostaglandin F1 alpha (PGF1 alpha) release induced by FCS. Furthermore, addition of a stable PGI2 analogue, OP-41483 [5(E)-6,9-deoxa-6,9-methylene-15-cyclopentyl-16,17,18,19,20-pen tanor-PGI2], reversed the slowing of epithelial restitution induced by piroxicam. These results suggest that endogenous prostaglandins play an important role in regulating intestinal epithelial restitution.

6-Ketoprostaglandin F1 alpha↗

PubMed1996

[Currarino triad : a case report].

The authors report a case of Currarino triad comprising anorectal malformations, sacral bony anomaly and presacral mass. A 1-year-old boy was presented with constipation as his chief complaint. No neurological deficit was found on admission. There was no cutaneous evidence of underlying spinal dysraphism. Lumbar X-ray films showed bony defect caudal to the third sacral vertebra. A barium-enema examination revealed an anterior displacement of the rectum. A myelography showed a presacral cavity filled with contrast medium. MRI demonstrated a thick filum terminale, and a round hypointense mass in the pelvis on T1 weighted images and hyperintense on T2 weighted images. Surgically we released the thick filum terminale, and obliterated the anterior sacral meningocele, because total removal would have been hazardous. Postoperatively transient dysuria was observed for a month, and the difficulty in defecation persisted. Recognition of this rare condition will lead to correct diagnosis and proper treatment.

Abnormalities, Multiple↗

PubMed1995

Mobilization of gastric histamine during repeated administration of a proton potassium adenosine triphosphatase inhibitor in intact and antrectomized rats.

Intact and antrectomized female rats were treated with the potent proton pump inhibitor, E3810 (daily 40 mg/kg weight, s.c.) for 4 weeks. Plasma gastrin concentration and urinary excretion of N-terminal big gastrin increased until day 14 and persisted at a high level in intact rats treated with E3810, but did not increase in antrectomized rats. Urinary excretion of histamine increased progressively and reached 7 times the control value following 4 weeks of treatment with E3810 in intact rats, but not in antrectomized rats. At the termination of the treatment, the endocrine cell density in the oxyntic mucosa of intact rats had increased by 85% with increased histamine content and elevated histidine decarboxylase activity, while antrectomized rats showed a low histamine level and low histidine decarboxylase activity. Administration of gastrin-17 I (10 micrograms/kg weight, sc) itself caused a significant increase in urinary excretion of histamine, which was inhibited by the specific gastrin receptor antagonist, L-365,260. These results suggests that the massive urinary excretion of histamine caused by the treatment with E3810 reflects gastrin-induced mobilization of gastric histamine and that neither E3810 itself nor E3810-induced luminal pH elevation has direct effects on mobilization of oxyntic mucosal histamine.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1995

Helicobacter pylori increases gene expression of hepatocyte growth factor in human gastric mucosa.

Helicobacter pylori (H. pylori) induces hyperproliferation of the gastric mucosa. This study was designed to clarify whether H. pylori infection is involved in the gene expression of hepatocyte growth factor (HGF), a potent stimulator of cell proliferation in gastric mucosa. Levels of HGF mRNA were determined by a reverse transcription-polymerase chain reaction in endoscopic gastric biopsy specimens from 9 control subjects and 9 patients with H. pylori infection. In patients with H. pylori infection, levels of HGF mRNA in gastric mucosa were significantly higher than those in control subjects. HGF mRNA levels in patients with H. pylori infection were correlated with the severity of gastric mucosal inflammation. Our observations indicate that H. pylori infection increases the expression of HGF gene in gastric mucosa probably through the mucosal inflammation.

Adult↗

PubMed1995

Posterior plication of the rectum for rectal prolapse in children.

Fourteen patients with rectal prolapse (age range, 1 to 12 years) underwent posterior plication of the rectum for rectal prolapse. The procedure consisted of (1) natal cleft incision, (2) midline separation of the levator muscle, (3) dissection of two thirds of the circumference of the rectum, (4) plication of the posterior wall of the rectum using U-shaped mattress sutures, and (5) fixation of the sutures of the rectal wall to the coccyx. There has been no recurrence of prolapse in any of the patients. The authors' experience suggests that an elongated rectum is responsible for prolapse. This simple but definitive technique is recommended.

Child↗

PubMed1995

Dietary regulation of glucose-dependent insulinotropic peptide (GIP) gene expression in rat small intestine.

The hormone, glucose-dependent insulinotropic peptide (GIP), is an important incretin regulator of the gastrointestinal tract. To investigate whether diet is important for the control of GIP gene expression in the small intestine, GIP messenger RNA (mRNA) levels were measured in rats during fasting and after glucose or fat administration. Ribonuclease protection analyses revealed that glucose and fat administration increased GIP mRNA levels by 4-fold and 2.5-fold, respectively, compared with the control, and that prolonged fasting decreased GIP mRNA levels to 44% of those of control animals. Glucose infusion increased plasma GIP levels and tended to stimulate an increase in the GIP hormone concentration in the mucosa of the small intestine. Administration of fat also stimulated an increase of plasma GIP levels but did not modify tissue GIP concentrations. Prolonged fasting tended to decrease plasma GIP levels, although GIP tissue concentrations did not change. These data suggest that dietary glucose or fat stimulates GIP synthesis and secretion, and that food deprivation causes a decrease in GIP synthesis and secretion. This regulation involves changes at the pretranslational level and is reflected by modifications of GIP mRNA expression.

Analysis of Variance↗

PubMed1995

Stimulatory effect of 1 alpha,25-dihydroxyvitamin D3 on mouse alveolar macrophage tumor necrosis factor-alpha production in vitro: involvement of protein kinase C and Ca2+/calmodulin-dependent kinase.

1 alpha,25-Dihydroxyvitamin D3 [1 alpha,25(OH)2D3, calcitriol] has been shown to modulate the immune function of peripheral monocytes and peritoneal macrophages. However, its effect on alveolar macrophage (AM) cytokine secretion has not been reported. We therefore investigated the influence of calcitriol on tumor necrosis factor (TNF-alpha) production by murine AMs and attempted to elucidate changes in the signal transduction system involved in such effects. Calcitriol significantly enhanced TNF-alpha secretion by AM stimulated with either lipopolysaccharide (LPS; 10 micrograms/ml; p < 0.005) or phorbol 12-myristate 13-acetate (PMA; 100 ng/ml; p < 0.05) at low doses (between 10(-11) and 10(-9) M). However the protein kinase C (PKC) inhibitor, H7 (10 microM), and the Ca2+/calmodulin inhibitor, W7 (25 microM), reversed such calcitriol effects. Calcitriol increased the total PKC activity of AMs. These findings indicate that calcitriol enhances both LPS- and PMA-stimulated TNF-alpha secretion through PKC- or Ca2+/calmodulin-dependent pathways.

Animals↗

PubMed1995

[A case of chronic hypersensitivity pneumonitis due to long term exposure to toluene diisocyanate].

A 55-year-old paint sprayer, who had been working with paint containing toluence diisocyanate since age 20, was admitted to our hospital with a complaint of exertional dyspnea. Physical examination revealed clubbed fingers, and fine crackles were audible in both lower lung fields. The thoracic CT film showed diffuse linear and ringed shadows in both lung fields. Open lung biopsy disclosed alveolitis and fibrosis as well as infiltration of mononuclear cells, but no Masson bodies or granulomas. Toluene diisocyanate-specific antibody was positive. Based on these results, we diagnosed chronic hypersensitivity pneumonitis due to the chemical. To our knowledge, there has been no previously reported case of chronic hypersensitivity pneumonitis due to isocyanate.

Alveolitis, Extrinsic Allergic↗

PubMed1994

Developmental expression of the glucose-dependent insulinotropic polypeptide gene in rat intestine.

The developmental expression of the glucose-dependent insulinotropic polypeptide (GIP) gene was investigated in rat intestine. Steady state levels of GIP mRNA were determined in the intestine during fetal and postnatal development by double ribonuclease protection assays. GIP mRNA could be detected as early as day 20 of embryonic development and very low levels remained until postnatal day 3. The GIP mRNA levels increased markedly in the period between days 3 and 5 of postnatal life and then gradually increased toward adult levels. Since intron 1 of the GIP gene contains putative TATA and CCAAT boxes, and some potential cis-acting promoter elements, we examined whether or not another transcript starting from exon 2 of the GIP gene is expressed during development of rat intestine. Ribonuclease protection assays suggested that although an abbreviated transcript might exist starting from exon 2, it appears to be minor and its relative abundance is unchanged during development or following intraduodenal glucose stimulation. These observations suggest that GIP may play an important role in early postnatal development probably associated with suckling.

Aging↗

PubMed1994

Effect of aging on plasma 1,5-anhydroglucitol levels in humans and rats.

Since normal reference values change with age in some clinical parameters, we measured the plasma levels of 1,5-anhydroglucitol (AG), a new marker of glycemic control in diabetes mellitus, in healthy subjects and in rats. Our results showed a significantly negative correlation of the marker with age in humans and that the plasma AG levels of older rats were markedly lower than those of younger counterparts. This remarkable reduction of AG in the older rat group can be partially explained by our finding that aged animals excreted AG more rapidly in the urine than younger ones, besides a decrease in food intake. We therefore suggest that normal clinical reference values for plasma AG levels should be modified according to age.

Adolescent↗

PubMed1994

Effect of chronic tobacco smoke exposure on the function of alveolar macrophages in mice.

We evaluated the effect of chronic tobacco smoke exposure on the function of the alveolar macrophage (AM) in mice. Tumor necrosis factor-alpha production of the AM triggered by lipopolysaccharides was smaller in smoke-exposed mice as compared to control mice but did not reach statistical significance (27.3 +/- 4.0 vs. 34.8 +/- 4.9 U/ml). The percentage of AM which did not phagocytize latex particles in the smoke-exposed mice was significantly larger than that in control mice (33.9 +/- 2.3 vs. 20.8 +/- 2.1%; p < 0.05). Ia antigen expression of the AM was significantly larger in smoke-exposed mice (cytotoxicity index: 0.180 +/- 0.033 vs. 0.038 +/- 0.0118; p < 0.01). The asialo-GM1 antigen expression was similar in both groups (0.949 +/- 0.007 vs. 0.961 +/- 0.011). Although the precise mechanisms of these functional changes of the AM by tobacco smoke exposure are not clear, they may have some immunological effects on the alveolar space.

Animals↗