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T Chiba

Publications and source records attributed to T Chiba.

At least 523 records · Page 29Linked to original sources
PubMed1989

Autoregulation of muscarinic and gastrin receptors on gastric parietal cells.

In previous studies we demonstrated that parietal cell stimulation with gastrin and carbamoylcholine (carbachol) is accompanied by increased turnover of membrane inositol phospholipids. We conducted the present studies to examine whether membrane-associated protein kinase C activity is enhanced as a consequence of these events and to explore the role of this enzyme in regulating parietal cell function. We observed that carbachol and gastrin dose dependently increased membrane-associated protein kinase C activity while histamine did not. Furthermore, compounds such as phorbol esters and diacylglycerol, which are known to be direct stimulants of protein kinase C activity, also stimulated parietal cell aminopyrine uptake. In contrast, the phorbol ester 12-O-tetradecanoylphorbol-13-acetate and the synthetic diacylglycerol 1-oleoyl-2-acetyl-sn-glycerol inhibited both aminopyrine uptake and membrane inositol phospholipid turnover in parietal cells induced by carbachol and gastrin. The inhibitory effect appeared to result from reduction in the quantity of muscarinic and gastrin receptors without alterations in their specific affinities. These data suggest that protein kinase C mediates stimulation of parietal cells by gastrin and carbachol but also activates an autoregulatory mechanism via downregulation of muscarinic and gastrin receptors.

Aminopyrine↗
PubMed1989

Somatostatin receptors on canine fundic D-cells: evidence for autocrine regulation of gastric somatostatin.

Somatostatin is known to have inhibitory effects on the release and action of a wide variety of gut peptides. Previous studies in vivo have suggested a potential inhibitory role for somatostatin even on its own secretion. To determine whether this autoregulatory effect is the result of a direct action of the peptide on the cell that is responsible for its secretion, we examined the effect of a non-immunoreactive but biologically active analogue of somatostatin ([Leu8-D-Trp22-Tyr25]S28) on release of somatostatin-like immunoreactivity (SLI) from isolated canine fundic D-cells. We identified somatostatin binding sites with dissociation constants of 1.2 X 10(-9) and 3.8 X 10(-8) M that coenriched with D-cells. Somatostatin 14, somatostatin 28, and [Leu8-D-Trp22-Tyr25]S28 were equivalent in displacing 125I-[Leu8-D-Trp22-Tyr25]S28 from the binding sites. [Leu8-D-Trp22-Tyr25]S28 inhibited SLI release from D-cells stimulated with (DBcAMP), and pentagastrin. Pertussis toxin pretreatment prevented the inhibitory effects of [Leu8-D-Trp22-Tyr25]S28 on both SLI secretion and cAMP accumulation by on both SLI secretion and cAMP accumulation by D-cells stimulated with epinephrine and forskolin. In contrast, [Leu8-D-Trp22-Tyr25]S28 inhibition of SLI release induced by DBcAMP and pentagastrin was not altered by pertussis toxin. Our data suggest that somatostatin autoregulates its own secretion via specific receptors on D-cells. This inhibitory effect is mediated by mechanisms that are both dependent on and independent of pertussis toxin-sensitive inhibitory guanine nucleotide binding proteins.

Amino Acid Sequence↗
PubMed1989

Carbachol inhibits stimulant-induced increases in fundic D-cell cytosolic Ca2+ concentration.

We undertook these studies to examine the mechanisms by which carbachol inhibits somatostatin release. For these studies, we utilized cultured D-cells isolated from the canine gastric fundus. Carbachol inhibited somatostatin release induced by both pentagastrin and 12-O-tetradecanoyl-phorbol-13-acetate but did not alter the redistribution of protein kinase C induced by these agents. In contrast, carbachol diminished the increase in D-cell cytosolic free calcium levels ([Ca2+]i) induced by pentagastrin, and this effect was no longer evident after pretreatment of D-cells with pertussis toxin. Although carbachol by itself had no effect on [Ca2+]i, after pretreatment of D-cells with pertussis toxin, carbachol both enhanced [Ca2+]i and stimulated somatostatin release. These data indicate that carbachol activates signals in D-cells that result in both increase and decrease in [Ca2+]i. The latter effect, which appears to be mediated via a pertussis toxin-sensitive guanine nucleotide binding protein, may be one mechanism responsible for cholinergic inhibition of somatostatin release.

Animals↗
PubMed1989

Autonomic neurons and paraneurons (SIF cells) in the sympathetic ganglia regulating guinea pig proximal colon: immunohistochemical studies.

Additional evidence for the existence of subclasses of SIF cells is described. Type II SIF cells in the inferior mesenteric ganglia contain enkephalin, vasoactive intestinal polypeptide (VIP), somatostatine (SOM), neuropeptide tyrosine (NPY), or dynorphin (DYN) in variable combinations in addition to noradrenalin. These transmitters or modulators can affect the autoreceptors of the SIF cell themselves or modify the synatpic transmission and the activity of sympathetic ganglionic neurons through portal blood vessels. Tyrosine hydroxylase/NPY immunoreactive nerve terminals from sympathetic ganglia innervate blood vessels and both submucous and myenteric ganglia. DYN/VIP/cholecystokinin neurons in the nerve plexus send axon collaterals to the inferior mesenteric ganglia and form a feedback loop. Substance P (SP) and calcitonin gene related peptide may exist in sensory nerve terminals. SP neurons in the myenteric ganglia innervate smooth muscles. SOM neurons inhibitory interneurons in the ganglia. SIF cells act as secretory paraneurons, the effect being long-lasting and nonspecific, while sympathetic neurons innervate both nerve plexus and intestinal tissues, and the effects in this case are specific, fast and of short duration.

Animals↗
PubMed1989

Localization of beta II subspecies of protein kinase C in beta-cells.

Protein kinase C (PKC) has been generally accepted to play a key role in stimulus-response coupling in various secretory cells, including pancreatic islets and pancreatic acini. The enzyme exists as a large family of multiple subspecies with highly related structures (alpha-, beta I-, beta II-, gamma-, delta-, epsilon-, and zeta-PKC). With an immunocytochemical procedure with subspecies-specific antibodies, beta II-PKC-like immunoreactivity was identified to localize in the beta-cells of the rat pancreatic islets. Neither beta I- nor gamma-PKC-like immunoreactivity was found in both islets and acini. Biochemical analysis confirmed that the rat whole pancreatic tissues contain a significant amount of alpha-PKC and a minute amount of beta II-PKC but neither beta I- nor gamma-PKC. On the other hand, beta II-PKC-like immunoreactivity was not detected in rat insulinoma cells, in which insulin secretion was induced in response to 12-O-tetradecanoylphorbol-13-acetate and carbachol but not in response to glucose. These findings suggest that beta II-PKC is the major, if not the sole, subspecies of PKC in beta-cells of rat pancreatic islets and a possible candidate for involvement in glucose-induced insulin secretion.

Animals↗
PubMed1989

[The present status and problems in the treatment of biliary atresia with special reference to surgical and long-term results].

The surgical results are not satisfactory yet in Japan and only 46% of the patients are free of jaundice 3 years ago. However, we found many presentations which reported jaundice disappearance rate with more than 80% in the last several years. The main cause of death in jaundiced patients with the failed hepatic portoenterostomy was hepatic failure. Other causes of deaths in these patients, including those died within one month after operation, were peritonitis, cardiac and/or renal failure, hemorrhagic tendency and lung edema. The main cause of death in jaundice-free patients was rupture of the esophageal varices. We examined 48 long-term survivors ranging in age from 10 to 33 years. There were 41 cases without and 7 with jaundice. Thirty-seven (77%) of 48 cases were leading their normal lives. Among them, 6 cases were enjoying their lives after overcoming the sequelae, such as portal hypertension. The morbidities of the remaining 11 (23%) long-term survivors were jaundice in 7, portal hypertension in 5, encephalopathy after splenorenal shunt in 1 and so on. The cured states of most cases without jaundice are satisfactory and eventually these former patients can achieve a favorable quality of life.

Adolescent↗
PubMed1988

Receptors for calcitonin gene-related peptide on the rat liver plasma membranes.

Specific binding sites for calcitonin gene-related peptide (CGRP) were identified in the rat liver plasma membrane. The binding of 125I-[TyrO]rat CGRP to rat liver plasma membrane was time dependent, saturable and reversible. Scatchard analysis of the data revealed a single class of binding sites with apparent dissociation constant of 260.8 pM and a maximal binding capacity of 26.6 fmol/mg of protein. Rat, chick, and human CGRP and their synthetic analogues inhibited label binding in a dose-dependent manner with relative potencies as follows; chick greater than rat greater than human greater than [TyrO]rat CGRP. Salmon, human and [Asu1'7]eel calcitonin also inhibited label binding but only at higher concentrations. These results clearly indicate the presence of specific binding sites for CGRP in rat liver plasma membrane and suggest that CGRP has possible biological actions on the rat liver.

Animals↗
PubMed1988

Disturbances of voluntary control of saccadic eye movements in schizophrenic patients.

To study whether or not schizophrenic patients have disturbances in voluntary control of saccades, we examined visually elicited saccade and antisaccade tasks in 10 normal control subjects and 12 schizophrenic patients. The latencies of saccades in the schizophrenic patients were not significantly different from those of normal controls. However, 6 of the 12 schizophrenics showed significant abnormalities in the antisaccade task; 6 made more errors and 3 of them showed longer latencies than normal controls. Five of these 6 patients revealed an atrophy of the frontal cortex on computed tomography (CT) scans. These results indicate that many schizophrenics show difficulties in voluntary control of saccades, suggesting a dysfunction of the frontal cortex.

Adult↗
PubMed1988

Projection pathways, co-existence of peptides and synaptic organization of nerve fibers in the inferior mesenteric ganglion of the guinea-pig.

The presence of immunoreactive enkephalin, dynorphin, vasoactive intestinal polypeptide, cholecystokinin, substance P and neuropeptide Y in nerve fibers that project to the guinea-pig inferior mesenteric ganglion was analysed, after different denervation and ligation procedures. A quantitative analysis demonstrates that enkephalin- and substance P fibers reach the ganglion mainly via lumbar splanchnic and partly via intermesenteric nerves. Dynorphin-, vasoactive intestinal polypeptide- and cholecystokinin fibers reach the ganglion mainly via colonic and partly via hypogastric or intermesenteric nerves. Neuropeptide Y fibers enter via intermesenteric, lumbar splanchnic and hypogastric nerves and pass through the ganglion. Analysis of serial 0.5 micron sections tends to confirm co-existence: of dynorphin, vasoactive intestinal polypeptide and cholecystokinin in fibers projecting from the colon; of dynorphin with substance P in the lumbar splanchnic nerves; and of neuropeptide Y with substance P in the hypogastric and colonic fibers. Synaptic contacts, predominantly axodendritic, onto the ganglion cells from enkephalin-, vasoactive intestinal polypeptide-, and substance P-containing terminals were revealed by electron microscopy. Enkephalin-immunoreactive axon varicosities are filled with small, clear vesicles with a few large, cored vesicles and form asymmetric synapses; dynorphin-, vasoactive intestinal polypeptide- and cholecystokinin-immunoreactive axon varicosities are rich in large, dense-cored vesicles and form symmetric synapses.

Animals↗
PubMed1988

A patient with biliary atresia who died 28 years after hepatic portojejunostomy.

A patient who died of hepatic failure nearly 29 years after hepatic portojejunostomy is reported. His death may be attributed to several faults in treatment. From our experiences it can be said that biliary atresia is a curable disease, although liver-transplantation is required in some patients in whom hepato portoenterostomy is unsuccessful.

Adult↗
PubMed1988

Tolbutamide inhibits gastrin release in man.

Tolbutamide significantly decreased fasting plasma gastrin after 5 min of intravenous infusion in patients with atrophic gastritis, duodenal ulcer, or insulin-dependent diabetes mellitus (IDDM) as well as in healthy volunteers. Increased plasma insulin and decreased blood glucose were observed in patients with atrophic gastritis, duodenal ulcer and healthy volunteers, but not in patients with IDDM. Suppression of plasma gastrin in healthy volunteers was also observed following oral administration of tolbutamide. Despite the observed decrease in plasma gastrin, neither basal nor tetragastrin-stimulated acid output was changed for 30 min following tolbutamide infusion in healthy volunteers. Thus, our data suggest that tolbutamide inhibits gastrin release in man via mechanisms independent of changes in plasma insulin, blood glucose or acid secretion.

Adult↗
PubMed1988

Studies on subtype "d" biliary atresia.

Nine cases of specific type (subtype d) biliary atresia were experienced at the Tohoku University Hospital and were classified into three groups on the basis of their clinical and pathological findings. Group 1 cases were defined as cases showing obstruction on the side of the hepatic duct and cystic dilatation, communicating with the gallbladder, in the common bile duct. Group 2 cases were those showing dilatation similar to Group 1, but measuring less than 20 mm, the dilated part being covered with thick connective tissue. Group 3 cases were those showing isolated dilatation in the common hepatic duct or the common bile duct and having no communication with the gallbladder. The postoperative course was good in Group 1 patients, while jaundice was prolonged in Group 2 patients. In Group 3, jaundice disappeared in one patient who died later, while the other patient showed recurrence of slight jaundice.

Bile Ducts↗
PubMed1988

Problems involved in re-laparotomy for congenital biliary atresia: with special reference to postoperative ascending cholangitis.

Problems involved in re-laparotomy, particularly ascending cholangitis, were investigated in 129 patients with biliary atresia treated in Tohoku University Hospital in and after 1972. The occurrence of cholangitis after re-laparotomy for re-obstruction of the hepatic port, for peritonitis, for intestinal obstruction, for portal hypertension and after surgery for external fistula is not necessarily frequent. Surgery, if necessary, should be employed in these patients, paying careful attention to those who show cholangitis after the first operation.

Biliary Atresia↗
PubMed1988

Carbamoylcholine and gastrin induce inositol lipid turnover in canine gastric parietal cells.

The potential role of inositol phospholipid turnover in mediating acid secretion was examined in a preparation enriched for isolated canine gastric parietal cells. The stimulatory effects of carbamoylcholine (carbachol) and gastrin on parietal cell uptake of [14C]aminopyrine were linked to dose- and time-dependent selective reduction in cellular phosphatidylinositol content, although the specific fatty acid composition of the phosphoinositides was not altered. Analysis of [3H]inositol phosphates accumulated in cells prelabeled with [3H]inositol revealed an increase in labeled inositol trisphosphate by 5 min of incubation with either carbachol or gastrin. Furthermore, after preincubation of parietal cells in medium containing [32P]orthophosphate, the two secretagogues elicited a time-dependent decrease in 32P labeling of phosphatidylinositol 4,5-bisphosphate and concomitant increase in labeling of phosphatidic acid. These data demonstrate that the acid secretagogue actions of carbachol and gastrin are correlated with turnover of cellular inositol phospholipids in a preparation consisting predominantly of parietal cells.

Aminopyrine↗
PubMed1988

Biosynthesis of somatostatin in canine fundic D cells.

The observation that virtually all of the somatostatin-like immunoreactivity in the stomach consists of somatostatin-14 (S14), to the exclusion of somatostatin-28 (S28), suggests a unique pattern of prosomatostatin posttranslational processing. In order to examine the mechanisms by which S14 is produced from its precursor in the stomach, we investigated the biosynthesis of somatostatin in isolated canine fundic D cells. D cells pulse-labeled with [35S]cysteine revealed a cycloheximide inhibitable time-dependent incorporation of radioactivity into S14. A small fraction of radioactivity was incorporated into S28 but not into larger precursors. However, when the cells were incubated with monensin (1 microM), incorporation of radioactivity into a presumed somatostatin precursor was noted. Upon transfer of [35S]cysteine prelabeled cells to radioactivity-free medium, no conversion of S28 to S14 could be detected and the decrease of labeled S14 in cells correlated with a complimentary increase in the culture medium. Exogenous somatostatin inhibited somatostatin biosynthesis in a fashion that could be blocked by pertussis toxin pretreatment. Stimulation of prelabeled D cells with tetradecanoyl phorbol 13-acetate (10(-7) M) or forskolin (10(-4) M) for 2 h resulted in release of 41 and 33% of the newly synthesized radioactive S14, respectively, while only 9 and 6% of the total cell content of radioimmunoassayable somatostatin was secreted. These data suggest that: (a) somatostatin is synthesized in fundic D cells primarily as S14, (b) S14 is produced by rapid processing of a larger precursor but there is little, if any, conversion of S28 to S14, (c) somatostatin biosynthesis is autoregulated, and (d) newly synthesized S14 is preferentially released from D cells in response to stimulation.

Animals↗