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Biomedical subjects

O Yamamoto

Publications and source records attributed to O Yamamoto.

At least 91 records · Page 5Linked to original sources

Inhibition of phase III activity by acid in canine stomach.

Very few phase III activity of the interdigestive migrating contractions (phase III) occurs in the stomach of fasted duodenal ulcer patients. But the mechanism is not well understood. In this study, we studied the effect of gastric and duodenal acidification on the spontaneous phase III activity in the upper gastrointestinal tract of conscious dogs. Gastric and duodenal motor activity in 5 conscious dogs was monitored by means of chronically implanted force transducers. Intragastric pH changes were measured by placing a pH glass electrode in the gastric antrum. Intragastric and intraduodenal acidification was achieved by i.v. infusion of histamine, and by intragastric and intraduodenal instillation of acidic solutions of different pHs. The plasma motilin concentrations were measured by radioimmunoassay. Histamine (40 micrograms/kg/h) inhibited spontaneous phase III activity, but the histamine-induced inhibition was completely prevented by pretreatment with famotidine, a potent histamine H2 receptor antagonist (0.3 mg/kg, i.v.). Intragastric acidification at pH 1.0 strongly inhibited spontaneous phase III activity, but an acidic solution at pH 2.0 had no effect in inhibiting phase III activity. Intraduodenal acidification at pH 1.0 also inhibited spontaneous phase III activity. Histamine injection and gastric and duodenal acidification at pH 1.0 strongly suppressed motilin release. It is concluded that gastric and duodenal acidification at pH 1.0 inhibits the occurrence of the spontaneous phase III activity, and the suppression of endogenous release of motilin due to gastric and duodenal acidification at pH 1.0 is involved in this inhibitory mechanism.

Animals↗

Identification of a vitamin D-responsive element in the 5'-flanking region of the rat 25-hydroxyvitamin D3 24-hydroxylase gene.

The 5'-flanking region of the rat vitamin D3 24-hydroxylase (P450cc24) gene was examined and a vitamin D-responsive element (VDRE) responsible for the 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3) enhancement was identified. Unidirectional deletion analyses of the 5'-flanking region indicated that the region [-167/-102] is involved in vitamin D responsiveness. Further functional analyses showed that the segment [-204/-129] conferred the hormone responsiveness in an orientation-independent manner when it was placed upstream to the heterologous thymidine kinase promoter or the rabbit beta-globin promoter. The segment [-204/-129] contained two direct repeat motifs homologous to other VDREs found in the osteocalcin and osteopontin genes. Synthetic oligonucleotides containing the putative VDRE were used for functional analyses and gel mobility shift assays. The proximal [-151/-137], but not the distal [-169/-155] direct repeat activated the transcription in response to 1,25-(OH)2D3 through the beta-globin promoter. Furthermore, the proximal direct repeat formed a complex with the vitamin D receptor and a nuclear accessory factor(s) from COS cells (or retinoid X receptor) in the presence of 1,25-(OH)2D3. These results indicate that a direct repeat motif, AGGTGAgt-gAGGGCG, located at -151 base pairs upstream in the antisense strand binds to a heterologous dimer consisting of the VDR occupied with 1,25-(OH)2D3 and the nuclear accessory factor and that it plays a critical role in mediating the vitamin D enhancement of the rat P450cc24 gene expression.

Animals↗

Inhibition of phase III activity by acidifying stomach in vagally denervated and innervated dogs with gastric pouches.

BACKGROUND/AIMS: Intragastric acidification at pH 1.0 strongly inhibits phase III contractions in the dog, but this mechanism is not well known. We studied the mechanism in conscious dogs. METHODS: Vagally denervated and innervated gastric pouch dogs were prepared. Force transducers were chronically implanted on the serosa of the pouch, main stomach, and mid-duodenum. The pH of the perfusate was monitored. RESULTS: Administration of histamine (40 micrograms.kg-1.h-1 intravenously [i.v.]) and instillation of acidic saline at pH 1.0, but not pH 2.0, into the main stomach strongly inhibited the motilin-induced (0.1 microgram/kg i.v.) phase III activity in the main stomach and the innervated pouch but did not influence contractions in the extrinsically denervated pouch. Famotidine completely reversed the histamine-induced inhibition of phase III in the main stomach and Pavlov pouch. Acidification of the pouch itself or duodenum at pH 1.0 did not affect contractions in the main stomach and pouch of either type. CONCLUSIONS: The mechanism of inhibition of motilin-induced phase III activity by acid in the stomach involves the intact vagovagal reflex, but sympathetic participation is not completely ruled out. The inhibition of motilin-induced phase III activity may originate in the antral mucosa of the stomach.

Acids↗

Giant folliculosebaceous cystic hamartoma.

We report a case of a giant cystic cutaneous adnexal hamartoma which showed fibrofollicular units embedded in the stroma with aberrant fat tissue. There were many sebaceous lobules in the fibrofollicular units, and its histologic features were consistent with conventional folliculosebaceous cystic hamartoma. Given the unique clinical history and appearance, this lesion is considered to be a congenital variant.

Adult↗

Three modes of melanosome transfers in Caucasian facial skin: hypothesis based on an ultrastructural study.

The transfer mechanism of melanosome from the melanocyte into the keratinocyte was investigated in mildly photodamaged Caucasian facial skin by electron microscopy. Three ways of transfer are suggested by our observations. The first mechanism probably occurs through the following process: 1) protrusion and insertion of the thick dendrite of the melanocyte into the basal keratinocyte, 2) formation of sac-dendrite complex in the subnuclear region, 3) digestion and segregation of the enclosed dendrite, 4) formation of the cistern in the paranuclear region, and 5) pinching-off of the melanosomes in single or aggregated form from the tip of the cistern. The second mechanism probably takes place through a membrane fusion between the melanocyte and the keratinocyte. Such a membrane fusion possibly forms a passage way for release of the melanosome from the former cell to the latter. The third mechanism is considered to include exocytosis of the single melanosome from the melanocyte followed by the endocytosis through the formation of coated-pit in the keratinocyte.

Adult↗

Vagovagal inhibition of motilin-induced phase III contractions by antral acidification in dog stomach.

Gastric acidification at pH 1.0 strongly inhibits the spontaneously occurring and motilin-induced phase III contractions in canine and human stomach. In this study, we examined inhibition by gastric acidification in dogs following gastrojejunostomy, truncal vagotomy, and antrectomy. As a result, gastric acidification with 0.1 N HCl solution at pH 1.0 for 30 min at a rate of 1.0 ml/min significantly inhibited motilin-induced phase III activity to 23.5 +/- 5.9% of the control in the normal intact dogs and to 17.2 +/- 3.4% in the gastrojejunostomized dogs. In the antrectomized dogs, gastric acidification did not significantly inhibit the action of motilin (81.7 +/- 10%), but, in the vagotomized dogs, gastric acidification inhibited the action of motilin to 72.0 +/- 4.9%; the inhibition was much weaker than in the intact and gastrojejunostomized dogs but was significant. The duodenal acidification had no effect at all on the action of motilin (94.6 +/- 12.5%) in the gastrojejunostomized dogs. These findings strongly suggest the existence of a vagovagal reflex in the inhibition of motilin-induced phase III contractions by gastric antral acidification, although the involvement of sympathetic regulation cannot be completely ruled out.

Animals↗

Influence of efonidipine hydrochloride, calcium antagonist on the epithelium of prostates in spontaneously hypertensive rats.

The hypertensive effect on the development of the prostatic abnormality in spontaneously hypertensive rats (SHRs) was examined using Efonidipine hydrochloride, a calcium antagonist. The control SHRs were given a high sodium and potassium diet (SP-diet) alone, and the treated SHRs were given a SP-diet with 0.15% Efonidipine hydrochloride from 8 to 28 weeks of age. The systolic blood pressure (SBP) in the control SHRs increased with age, while the elevation of SBP was significantly prevented in the treated SHRs. Light-microscopically, the prostatic lesion was observed both in the control and treated SHRs. The glandular lumen was narrowed with papillary protrusions, and the epithelium was composed of tall columnar epithelial cells. However, hypertension-induced complications in kidneys and hearts were not observed in the treated SHRs. These results suggested that the prostatic abnormality of SHRs might not be the consequent lesions upon hypertension.

Animals↗

Beta-adrenergic regulation of gap-junctional intercellular communication in cultured rabbit gastric epithelial cells.

The effect of a beta-adrenergic agonist, isoproterenol, on gap-junctional intercellular communication (GJIC) and intracellular cyclic AMP (cAMP) content was investigated in cultured rabbit gastric epithelial cells. Isoproterenol rapidly enhanced GJIC determined by the Lucifer yellow transfer at 10(-6) and 10(-5) M but the effect at 10(-6) M was variable. The enhancement of GJIC by 10(-5) M isoproterenol, which disappeared within 10 or 30 min, was inhibited by a beta blocker, propranolol. Isoproterenol (10(-6) M) greatly increased cAMP at 5 min and much more so at 20 min after its addition. Colforsin (also known as forskolin) and 3-isobutyl-1-methylxanthine (IBMX) enhanced GJIC until 16 and 20 min after their addition, respectively. Both colforsin and IBMX increased the cAMP content by a lesser extent than 10(-6) M isoproterenol. Isoproterenol (10(-5) M) inhibited the GJIC enhanced by colforsin or IBMX. Propranolol abolished the inhibition of GJIC by isoproterenol in the presence of IBMX. Both amiloride, an inhibitor of the Na+/H+ exchanger, and nigericin, a K+/H+ antiporter, inhibited the GJIC enhanced by isoproterenol, IBMX, colforsin and irsogladine. An inhibitor of cAMP-dependent protein kinase A, H-89 (N-[2-((3-(4- bromophenyl)-2-propenyl)-amino)-ethyl]-5-isoquinolinesulfonamide), abolished the enhancement of GJIC by colforsin and IBMX but did not abolish that by isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗

Hydrated electron-induced inactivation of tyrosinase in aqueous solution by exposure to cobalt-60 gamma-rays. I. Cresolase activity.

Tyrosinase (0.2 mg/ml of 0.1 M phosphate buffer solution, pH 6.5) which has cresolase and catecholase activities was irradiated with 60Co gamma-rays. The cresolase activity was measured at varying radiation doses under various atmospheric conditions. D0 was found to be 350 Gy in N2-saturated solution. The OH radical has been shown to be the main species involved in radiation-induced enzyme inactivation. However, in this study, OH radical scavengers, t-BuOH and MeOH, had no effect. O2 which acts generally as an enhancer of OH-induced enzyme inactivation also had little effect, but N20 ae aq scavenger, and Cu++ markedly inhibited the inactivation indicating that e aq is the main species involved in inactivating the cresolase activity, reducing Cu++ as the active center.

Basidiomycota↗

Hydrated electron-induced inactivation of tyrosinase in aqueous solution by exposure to cobalt-60 gamma-rays. II. Catecholase activity.

Tyrosinase (0.2 mg/ml) was irradiated with 60Co gamma-rays. The catecholase activity was measured at varying radiation doses under various atmospheric conditions. D0 was found to be 1.25 kGy and hit number to be 2 in N2-saturated solution. OH radical scavengers, t-BuOH and MeOH, had no effect. O2 which is an enhancer of OH-induced enzyme inactivation had little effect. But N2O as a e aq scavenger and Cu++ markedly protected against the inactivation indicating that e aq was the main species to inactivate the enzymatic activity. By Ultrogel chromatography, it was found that the enzymatic activity was lost when this enzyme dissociated into its subunits. Thus, it was concluded that the radiation-induced inactivation was due to the reduction of Cu++ as the active center and the chelater with e aq followed by the dissociation.

Amino Acids↗

[A case of fistula-cancer response to arterial chemoembolization].

Arterial chemoembolization was performed three times preoperatively for cancer associated with fistula-in-ano for diminishing the postoperative surgical tissue defect of the perineum. Partial response of the tumor to this treatment was confirmed by computed tomography. A sixty-two-year-old male patient recognized a mass in the perineum one and a half years ago. He had suffered from fistula-in-ano for thirty years. The mass increased its size and formed a tumor in the bilateral buttocks (12 x 9 cm and 9 x 9 cm in diameter). Biopsy specimen showed a moderately differentiated adenocarcinoma. Angiography showed a hypervascular tumor stain. The main feeders to the tumor were the superior rectal artery and bilateral internal iliac artery. Arterial chemoembolization was performed three times through the right and left internal iliac artery with Gelfoam particle. Arterial infusion chemotherapy was added through inferior mesenteric artery and bilateral internal iliac artery with a total 120 mg of adriamycin and 1,500 mg of 5-FU simultaneously. The tumor decreased in size to 44% of the preoperative size by the treatment. A radical operation was performed following the preoperative treatment. Preoperative arterial chemoembolization for cancer associated fistula-in-ano was considered to be helpful for local control.

Adenocarcinoma↗

Inhibition of motilin-induced phase III contractions by pentagastrin in Heidenhain pouch dogs.

We compared the inhibitory effects of histamine and pentagastrin (PG) on motilin-induced upper gastrointestinal phase III activity in conscious dogs that had surgically prepared Heidenhain pouchs (HP). Contractile activity was measured by means of chronically implanted force transducers, and changes in pH of the perfusate through the HP were monitored simultaneously. Intravenous infusion of PG (4 micrograms/kg-hr) inhibited motilin-induced phase III activity both in the main stomach and in the HP, whereas histamine (40 micrograms/kg-hr) inhibited activity only in the main stomach. Famotidine (0.3 mg/kg, i.v., the dose that completely inhibited gastric acid secretion by PG or histamine) blocked the inhibition of phase III activity induced by histamine but did not affect PG-induced inhibition. L-364,718 (1 mg/kg, i.v.), which had no effect on the PG-induced decrease in the pH of the perfusate lowered by PG, reversed the inhibition of phase III activity by PG in the HP but not in the main stomach. However, L-364,718, when combined with famotidine, potently reversed the PG-induced inhibition of phase III activity both in the main stomach and in the HP. These results show that the inhibitory effect of PG on motilin-induced phase III activity is brought about by two distinctive mechanisms, gastric acid and the cholecystokinin receptors-dependent mechanism, whereas the histamine-induced inhibition is mediated only by gastric acid. In the vagally denervated HP, however, gastric acid is not involved in an inhibitory effect of PG.

Animals↗

Mechanism of motilin-induced contractions in isolated perfused canine stomach.

BACKGROUND: Motilin is known to induce gastric phase III contractions via neural pathways in vivo, but the local mechanism of action is not clearly determined. METHODS: An isolated perfused canine stomach was used to demonstrate the mechanism of motilin. Synthetic canine motilin at doses of 0.1, 0.3, 1.0, and 3.0 micrograms/h was infused intra-arterially, and effects of several receptor antagonists on motilin-induced contractions were examined. RESULTS: The immunoreactive motilin concentration of venous effluent showed that motilin at doses of 0.1 and 0.3 microgram/h was within the physiological range. Each dose of motilin induced phasic contractions in the isolated stomach, and a dose-related increase in frequency was observed, but not their mean amplitude. Atropine, hexamethonium, ICS205-930, BRL43694, phentolamine, yohimbine, and propranolol significantly inhibited motilin-induced contractions. Naloxone, methysergide, and timolol did not affect the response of motilin. Prazosin significantly increased the mean amplitude of motilin-induced contractions. CONCLUSIONS: Physiological dose of motilin can initiate phasic contractions in the stomach independently of the presence of the extrinsic nerves. The results suggest that cholinergic pathway, 5-hydroxytryptamine (HT)3 receptors, and alpha receptors are involved in the motilin-induced contractions.

Animals↗

A combined occurrence of neuroendocrine carcinoma of the skin and a benign appendageal neoplasm.

A 76-year-old Japanese male presented with a subcutaneous nodule in the dorsal cubital region of the right arm. The center of the nodule showed typical features of neuroendocrine carcinoma of the skin. The peripheral portion showed epithelial islands of squamoid cells with horn cysts suggestive of benign appendageal tumor with pilar differentiation. The coexistence of two skin neoplasms in the same lesion would suggest that both tumors developed from common pluripotential stem cell.

Aged↗