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Biomedical subjects

M Akagi

Publications and source records attributed to M Akagi.

At least 199 records · Page 11Linked to original sources
PubMed1984

Effect of histamine on the hippocampal neurons in guinea-pigs.

Histamine produced an excitatory effect on CA3 pyramidal cells in hippocampal slices of guinea-pigs. The amplitude of population spikes and EPSPs was augmented by histamine at concentrations of 10(-7) to 10(-6) M. Cimetidine but not pyrilamine prevented the stimulatory effect. The histamine effect was mimicked by dimaprit but not by 2-pyridylethylamine. It is concluded that histamine has a facilitatory influence on the hippocampal excitatory system via H2 receptor.

Animals↗
PubMed1984

Muscarinic cholinergic receptors in human gastric mucosa.

Muscarinic cholinergic receptor sites in human gastric mucosa were analyzed directly by using radioligand binding techniques with the specific muscarinic antagonist 3H-quinuclidinyl benzilate (QNB) as ligand. Specific binding of 3H-QNB to membrane preparations from human gastric mucosa was saturable, of high affinity (Kd = 4.17 +/- 1.94 nM, Bmax = 0.37 +/- 0.04 pmol/mg protein) and selectively inhibited by muscarinic antagonists (atropine, scopolamine) and agonists (acetylcholine, pilocarpine). These findings provide direct evidence for the existence of muscarinic cholinergic receptors in human gastric mucosa. The specific 3H-QNB binding to its receptor was blocked by atropine but not by histamine, cimetidine, pentagastrin, or synthetic human gastrin. The muscarine and histamine H2-receptor, or muscarine and gastrin receptor, probably do not share the same locus.

Acetylcholine↗
PubMed1984

A specific gastrin receptor in human gastric mucosa.

Biological active 125I-synthetic human gastrin (125I- SHG ) appeared to bind specifically on human gastric mucosal membrane preparations. Gastrin binding was reversible, saturable and of high affinity (Kd = 3.44 +/- 3.44 X 10(-10)M) with the binding site (3.66 +/- 0.34 fmol/mg protein) at 37 degrees C for 30 min (pH 7.4). Specific gastrin binding was present in the fundic mucosa and absent from the antral, duodenal, jejunal, and colonic mucosa. Gastrin analogues (tetragastrin, pentagastrin, caerulein, and synthetic human gastrin) inhibited 125I- SHG specific binding. However, the specific gastrin binding was not inhibited by glucagon, insulin, acetylcholine, atropine, histamine, or cimetidine. It was suggested that gastrin and histamine H2 receptor or gastrin and muscarinic cholinergic receptor did not share the same locus.

Adenylyl Cyclases↗
PubMed1984

Histopathologic study on development and extension of atrophic change in the gastric mucosa.

A histopathologic study was carried out on 30 resected stomachs with various gastric or duodenal diseases. Both the pyloric gland cells and the parietal cells were counted in serial sections of the surgically resected stomach. A good correlation (p less than 0.001) was found between the number of pyloric gland cells and parietal cells. The number of both glandular cells was greatest on the greater curvature and fewest at the part closer to the antrofundic mucosal border on the lesser curvature. In addition, a fairly uniform pattern was observed in the distribution of the parietal cells. The maximum density area of parietal cells was centered on the greater curvature of the stomach body, and this density decreased concentrically in proportion to the distance from the center. This uniform pattern was seen in almost all specimens, with or without atrophic change in the gastric mucosa. These results suggest that atrophic change does not develop in a particular part of the stomach but wholly and equally in the gastric mucosa.

Adult↗
PubMed1984

A study on the distribution of G-cells in human gastric mucosa.

The distribution of G-cells in the gastric glands was studied quantitatively using the indirect immunoperoxidase method in 37 resected stomachs: 11 for esophageal cancer, 14 for gastric cancer, 4 for gastric ulcer, 7 for duodenal ulcer, and 1 for atypical epithelium. G-cells were seen in the pyloric glands and in the pseudopyloric glands in the atrophic fundic gland area. No G-cells were found in the fundic glands or in the cardiac glands. There was a significant correlation between the number of G-cells and the pyloric and/or pseudopyloric glandular tubes (p less than 0.01). The number of G-cells per glandular tube was 1.9 +/- 0.5 in the pyloric glands and 1.2 +/- 0.4 in the pseudopyloric glands on the pyloric part of the atrophic fundic gland area. G-cells were rarely seen in the pseudopyloric glands on the cardiac part of the atrophic fundic gland area. It is suggested that the pseudopyloric glands without G-cells in the cardiac region are akin to cardiac glands.

Adult↗
PubMed1984

Estrogen-dependent plasminogen activator in 7,12-dimethylbenz[a]anthracene-induced rat mammary tumors in vivo and in vitro.

Hormonal regulation of plasminogen activator in rat mammary tumor induced by 7,12-dimethylbenz[a]anthracene (DMBA) was studied both in vivo and in vitro. Plasminogen activator activity in DMBA-induced tumor (DMBA-tumor) was markedly decreased by ovariectomy, and recovered in a dose-dependent fashion upon estradiol administration, reaching a maximal level at 12 hr. This estrogen-stimulated production of the enzyme was prevented by actinomycin D, cycloheximide, and tamoxifen, indicating that in DMBA-tumor, estrogen might regulate de novo synthesis of plasminogen activator at a transcriptional level via an estrogen receptor system. Furthermore, DMBA-tumor cells in primary culture displayed similar estrogen-dependency toward the production of the enzyme without any cell proliferation. This indicates that the action of estrogen is mediated neither by cell division nor by prolactin, another hormone pastulated to be responsible for the development and growth of DMBA-tumor. Taken together, the present results have led to support the view that the primary function of estrogen is to induce plasminogen activator, which is probably essential to maintain the malignant state of DMBA-tumor.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1984

Histochemical study of phosphorylase in proliferating cells of intestinal metaplasia and carcinoma of the human stomach.

A morphologic histochemical study of phosphorylase was carried out to investigate the relationship between gastric carcinoma and intestinal metaplasia. Intense phosphorylase activity was observed in the carcinoma cells, especially in well-differentiated adenocarcinoma, and in the proliferating cells of some intestinal metaplasias. Metaplastic epithelium other than the proliferating cells occasionally showed a positive reaction. Phosphorylase was negative in normal gastric epithelium, even in its proliferating cells. There was an apparent coincidence between the location of well-differentiated adenocarcinoma and the distribution of intestinal metaplasia, with the proliferating cells showing positive reaction for phosphorylase. These data suggest that the relationship between the proliferating cells of intestinal metaplasia showing phosphorylase activity and well-differentiated adenocarcinoma is apparently closer than the much-debated relationship between the epithelium of intestinal metaplasia and gastric carcinoma.

Adenocarcinoma↗
PubMed1984

Stimulation of ornithine decarboxylase activity and DNA synthesis by phorbol esters or bile acids in rat colon.

The changes of colonic epithelial ornithine decarboxylase (ODC) activity and DNA synthesis following intrarectal administration of a tumor-promoting agent, 12-O-tetradecanoylphorbol-13-acetate (TPA), or various bile acids to male noninbred rats were studied. A single instillation of TPA, at a dose as low as 16 nmol, led to a significant (about 10-fold) increase in colonic ODC activity. Peak ODC activity was observed at 4 hr, and the enzyme activity returned to the control level about 24 hr after intrarectal TPA. This pattern was almost the same as that observed after sodium deoxycholate treatment. TPA showed more potent induction of ODC activity than deoxycholate, although the maximal induction was greater in the case of deoxycholate treatment. Both TPA and deoxycholate stimulated DNA synthesis at 2 days after intrarectal instillation, after an initial depression at 4-12 hr. A structure-activity study of 26 bile acids revealed that 5 beta-cholanoic acid with alpha-hydroxy groups in two of the 3 alpha, 7 alpha, 12 alpha positions and 5 beta-cholanoic acid with a 3 alpha-hydroxy group induced colonic ODC activity significantly, while the 3 alpha, 6 alpha-dihydroxy acid did not. Replacement of hydroxy groups by keto groups or a change from alpha to beta configuration decreased the ODC-inducing activities. Tri-substituted 5 beta-cholanoic acid derivatives, whether hydroxy or keto, did not stimulate ODC. These data indicate that a specific bile acid structure with a definite spatial relationship of the hydroxy groups is required for induction of colonic ODC activity.

Animals↗
PubMed1983

beta-Galactosidase-neuraminidase deficiency (galactosialidosis): clinical, pathological, and enzymatic studies in a postmortem case.

Three male siblings in a Japanese family were affected with beta-galactosidase-neuraminidase deficiency (galactosialidosis). One patient died at 45 years of age, and postmortem liver and brain tissues were studied enzymatically. The residual activity of neuraminidase was relatively high in these tissues. Neuraminidase activity did not change in the tissues after repeated freezing and thawing of the homogenates, whereas this enzyme in control tissues lost 30 to 60% of its activity. There was a profound deficiency of beta-galactosidase in the tissues of the patient. Michaelis constant, pH profiles, and cryostability were identical for the patient and control patients. Cathepsin B was moderately increased in activity in the patient's tissues.

Adult↗
PubMed1983

Neuropathological findings of an autopsy case of adult beta-galactosidase and neuraminidase deficiency.

An autopsy case of a Japanese male with familial beta-galactosidase and neuraminidase deficiency is reported. The clinical picture was characterized by adult onset, a gargoyle-like face, cerebellar ataxia, myoclonus, convulsions, retinal degeneration and cortical blindness. Histopathologically, most neurons seemed to have become degenerated in the whole cerebral cortex. Moreover, the calcarine cortex appeared spongy with depopulation of nerve cells. Stuffed neurons or neuronal storage changes were found throughout the brain, especially in the motor nuclei of the spinal cord and brain stem. The inclusions in the stuffed neurons revealed various profiles on the electron microscope. They were composed of membranous lamellar and/or multilamellar structures, often accompanying vacuoles and reminiscent of lipofuscin-like profiles.

Age Factors↗
PubMed1983

Histamine release inhibition and prevention of the decrease in membrane fluidity induced by certain anti-allergic drugs: analysis of the inhibitory mechanism of NCO-650.

NCO-650 exerted a dose-dependent inhibition of histamine release from isolated rat mast cells without affecting the Ca-uptake and intracellular cAMP levels. When the membrane stabilizing action of NCO-650 was investigated with the liposomes prepared by various phospholipids with or without cholesterol, it became clear that compound 48/80 decreases the order parameter of liposomes and NCO-650 inhibits the decrease of order parameter. Histamine release from histamine-containing liposomes was brought about by compound 48/80 at concentrations higher than 0.5 micrograms/ml, and pretreatment of the liposomes with NCO-650 inhibited histamine release due to compound 48/80. The incorporation of NCO-650 in the liposomes was effective in abolishing the phase transition of the lipid bilayer membranes from crystalline gel to liquid crystalline phases, and decreased the phase transition temperature. Those changes in the lipid bilayer membranes correspond to those displayed by incorporation of cholesterol in the liposomes. An increase of permeability of lipid membrane by compound 48/80 may be due to partial loosening of the lipid order; NCO-650 rigidified the liposome membrane and as a result of this, it decreased histamine release.

Animals↗