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Biomedical subjects

T Chiba

Publications and source records attributed to T Chiba.

At least 541 records · Page 30Linked to original sources
PubMed1988

Dual action of protein kinase C activation in the regulation of insulin release by muscarinic agonist from rat insulinoma cell line (RINr).

The role of protein kinase C in muscarinic agonist-induced insulin release from rat insulinoma cells was investigated. The dose-dependent stimulation of insulin secretion by carbamylcholine (carbachol) was associated with dose-dependent increase in the release of 3H-inositolphosphates from prelabeled rat insulinoma cell line (RINr) cells. After preincubation with 32P-orthophosphates, carbachol also evoked a rapid decrease in 32P-labeling of phosphatidylinositol-4,5-bisphophate with concomitant increase in 32P-labeling of phosphatidic acid. Furthermore, carbachol significantly increased membrane-associated protein kinase C activity with a simultaneous decrease of its activity in cytosol. Although phorbol-12,13-dibutyrate (PDBu), a protein kinase C activator, also stimulated insulin release, insulin secretion induced by concomitant administration of carbachol and PDBu was clearly less than the level expected on the basis of an additive action. Moreover, PDBu significantly inhibited inositolphospholipid turnover stimulated by carbachol. Finally, PDBu inhibited the binding of 3H-scopolamine binding revealed that PDBu decreased the number of muscarinic receptors without altering its affinity. These findings suggest that activation of protein kinase C not only mediates muscarinic stimulation of insulin secretion from RINr cells but also operates a negative feedback mechanism in a signal transduction system, at least in part, via down-regulation of muscarinic receptors.

Adenoma, Islet Cell↗
PubMed1988

Calcitonin gene-related peptide stimulates adenylate cyclase activation via a guanine nucleotide-dependent process in rat liver plasma membranes.

To evaluate the functional relationship between the liver calcitonin gene-related peptide (CGRP) receptor and guanine nucleotide-binding proteins, we investigated the effects of nucleotides not only on adenylate cyclase activation by CGRP, but also on 125I-[Tyr0]rat CGRP binding to rat liver plasma membranes. In the presence of GTP, rat CGRP stimulated adenylate cyclase activity in a dose-dependent manner in rat liver plasma membranes, and this effect was reduced in the absence of GTP. Salmon calcitonin also enhanced adenylate cyclase activation in the presence of GTP, but only in higher concentrations. On the other hand, guanine nucleotides not only decreased 125I-[Tyr0]rat CGRP binding to rat liver plasma membranes, but also accelerated the dissociation of label binding, and the removal of Mg2+ from incubation medium attenuated this inhibitory action of GTP on 125I-[Tyr0]rat CGRP binding to membranes. Scatchard analysis of the data revealed that the reduction of 125I-[Tyr0]rat CGRP binding by GTP was due to the decrease in binding affinity without a significant change in binding capacity. These findings lead us to conclude that binding of CGRP to its receptors activates adenylate cyclase in rat liver plasma membranes via a guanine nucleotide-dependent process, suggesting the involvement of guanine nucleotide-binding stimulatory protein in the action of CGRP.

Adenylyl Cyclases↗
PubMed1988

Persistent jaundice after hepatic porto-jejunostomy in biliary atresia: are the patients' prognoses determined within 3 months after surgery?

Eighteen patients with biliary atresia who showed persistent jaundice after hepatic porto-jejunostomy were studied clinically. It was revealed that: 1) Patients who had abnormally high preoperative values of laboratory data showed persistent jaundice; 2) high portal pressure occurred frequently in patients with persistent jaundice; 3) most patients of persistent jaundice had a history of postoperative cholangitis; 4) in contrast to jaundice-free patients, those with persistent jaundice tended to show elevation in gamma-globulin, TTT and gamma-GTP in the early postoperative period. These results suggest that for patients showing an upward tendency in these laboratory data after surgery, carefully management should be taken, even if the serum bilirubin level continue to decrease.

Adolescent↗
PubMed1988

Improvement of in vivo stability of alginate-polylysine capsules.

Dextran (MW 70,000) and rat islets were encapsulated in alginate-polylysine membrane. The capsules were further coated with tolylene 2,4-diisocyanate. Both of positive and negative charges were detected on the surface of alginate-polylysine capsules, which were absent after coating the capsules with tolylene 2,4-diisocyanate. In the peritoneal cavity, alginate-polylysine capsules were entrapped by the peritoneum, and 89% of dextran was leaked out of the capsules. Alginate-polylysine capsules coated with tolylene 2,4-diisocyanate were present freely in the peritoneal cavity and no leakage of dextran from the capsules were detected. Insulin release from the encapsulated islets was almost the same in both of tolylene 2,4-diisocyanate-coated and uncoated capsules. This study demonstrates that in vivo stability of capsules is dependent on the charge on the surface and can be improved by coating with tolylene 2,4-diisocyanate.

Alginates↗
PubMed1988

[Clinical effect of combination chemotherapy with peplomycin and mitomycin C (PM therapy) in recurrent uterine cervical cancer].

Seventeen patients with recurrent uterine cervical cancer were treated with combination chemotherapy consisting of consecutive intravenous drip infusion of PEP 5 mg for 6 days and intravenous infusion of MMC 10 mg on the 6th day. Of twelve evaluable cases, 2 complete responses and 6 partial responses were obtained and the response rate was 67%. The median survival for responders was 61.3 weeks as compared with 28.0 weeks for non-responders. The initial clinical effect appeared after at least two courses. Pulmonary toxicity in the form of interstitial pneumonitis occurred in 8 cases (50%) including 2 cases of pulmonary fibrosis. This result suggests that PM therapy is a very useful treatment method for recurrent uterine cervical cancer which can be performed safely.

Aged↗
PubMed1988

[Amylase-producing ovarian cancer treated with postoperative QF chemotherapy--a case report].

A case of an amylase-producing ovarian cancer in 69-year-old woman has been investigated by light and electron microscopy, as well as by amylase isozyme analysis. Serum and urinary amylase levels were found to be elevated, especially by an amylase isozyme analysis of the tumor homogenate which revealed a salivary type of cancer. The serum amylase level and its isozyme pattern returned to normal following therapy. Pathological examination revealed a serous cystadenocarcinoma. The ultrastructure of this tumor resembled that of other ovarian serous cystadenocarcinomas. No zymogen granules were recognized. Thus, a biochemical analysis of amylase isozyme was found to be a useful tumor marker for diagnosis and treatment of an amylase-producing ovarian serous neoplasm.

Amylases↗
PubMed1987

Mechanisms for direct inhibition of canine gastric parietal cells by somatostatin.

To examine the potential mechanisms by which somatostatin inhibits gastric acid secretion we studied its effects on isolated canine gastric parietal cells. Using 125I-[Leu8-D-Trp22-Tyr25]somatostatin-28 as ligand, we identified somatostatin-binding sites in parietal cell-enriched fractions of fundic mucosa. Two binding sites with respective dissociation constants of 3.2 X 10(-9) and 2.1 X 10(-7) M were identified. Somatostatin-14 and -28 were equally potent both in displacing bound ligand and in inhibiting parietal cell activity as measured by [14C]aminopyrine uptake. Pertussis toxin reversed the ability of somatostatin to inhibit the uptake of [14C]aminopyrine and production of cAMP by parietal cells stimulated with histamine and forskolin but not with dibutyryl cAMP or pentagastrin. Furthermore, somatostatin had no effect on parietal cell membrane inositol phospholipid turnover or changes in protein kinase C (Ca2+/phospholipid-dependent enzyme) activity induced by carbachol or pentagastrin. These data indicate that somatostatin directly inhibits parietal cell activity via mechanisms both dependent on and independent of the pertussis toxin-sensitive inhibitory guanine nucleotide-binding protein.

Aminopyrine↗
PubMed1987

Mechanisms for the stimulatory and inhibitory effects of carbamoylcholine on canine gastric D-cells.

We have previously reported that carbamoylcholine (carbachol), a recognized inhibitor of somatostatin release from D-cells, can act as stimulant following pretreatment of cells with pertussis toxin. In the present studies we have observed that pertussis toxin reverses the inhibitory effects of carbachol on D-cell stimulated with either cAMP or 12-O-tetradecanoyl-phorbol 13-acetate. Furthermore, the stimulatory effects of carbachol on D-cells pretreated with pertussis toxin potentiated the actions of pentagastrin without further enhancing the release of 3H-inositol triphosphate from prelabeled cells. These studies suggest that carbachol exerts its inhibitory effects on D-cells via pertussis toxin sensitive guanine nucleotide binding proteins at a point distal to the activation of different signal transduction mechanisms and that the stimulatory effects of carbachol are mediated by mechanisms that are independent of membrane phosphoinositide turnover.

Animals↗
PubMed1987

Cerebroside sulfuric ester (sulfatide) induces oxygen radical generation in guinea-pig leukocytes.

Previous studies on experimental allergic encephalomyelitis have shown that a number of leukocytes appear in demyelinating lesions of guinea-pig brain. The present studies showed that cerebroside sulfuric ester (sulfatide), a typical component of myelin membranes, stimulated the oxidative metabolism of guinea-pig neutrophils and macrophages, leading to marked generation of oxygen radicals and light emission. Formation of a spin adduct of 5,5-dimethyl-1-pyrroline N-oxide by leukocytes was dependent on the concentration of sulfatide, and correlated well with the generation of superoxide anion and the intensity of chemiluminescence measured in the absence of luminol. The addition of myelin membranes to the sulfatide-stimulated neutrophils amplified the light emission, suggesting an interaction between myelin membranes and those of leukocytes. Assay of the thiobarbituric acid reaction in the mixture of membranes and cells showed that sulfatide-stimulated cells induced lipid peroxidation in myelin membranes. These results suggest that sulfatide released from demyelinating lesions stimulates leukocytes to release toxic oxygen radicals, which attack myelin membranes, leading to a chain reaction of demyelination.

Animals↗