[Small nuclear U-RNP antibodies].
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Animals↗
Biomedical subjects
Y Okano
Publications and source records attributed to Y Okano.
[Regulation of platelet functions].
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Animals↗
A major role for phospholipase A2 in antigen-induced arachidonic acid release in rat mast cells.
Cross-linking of IgE receptors by antigen stimulation leads to histamine release and arachidonic acid release in rat peritoneal mast cells. Investigators have reported a diverse distribution of [3H]arachidonate that is dependent on labelling conditions. Mast cells from rat peritoneal cavity were labelled with [3H]arachidonic acid for different periods of time at either 30 or 37 degrees C. Optimum labelling was found to be after 4 h incubation with [3H]arachidonate at 30 degrees C, as judged by cell viability (Trypan Blue uptake), responsiveness (histamine release) and distribution of radioactivity. Alterations in 3H-radioactivity distribution in mast cells labelled to equilibrium were examined on stimulation with antigen (2,4-dinitrophenyl-conjugated Ascaris suum extract). The results indicated that [3H]arachidonic acid was lost mainly from phosphatidylcholine and, to a lesser extent, from phosphatidylinositol. A transient appearance of radiolabelled phosphatidic acid and diacylglycerol indicated phosphatidylinositol hydrolysis by phospholipase C. Pretreatment with a phospholipase A2 inhibitor, mepacrine, substantially prevented the antigen-induced liberation of [3H]arachidonic acid from phosphatidylcholine. It can be thus concluded that, in the release of arachidonic acid by antigen-stimulated mast cells, the phospholipase A2 pathway, in which phosphatidylcholine is hydrolysed, serves as the major one, the phospholipase C/diacylglycerol lipase pathway playing only a minor role.
Animals↗
Guanosine 5'-(gamma-thio)triphosphate stimulates arachidonic acid liberation in permeabilized rat peritoneal mast cells.
The exocytotic histamine secretion from ATP-permeabilized and Mg-resealed rat peritoneal mast cells is markedly enhanced by the addition of guanosine 5'-(gamma-thio)triphosphate (GTP gamma S) at a concentration of 100 uM. GTP gamma S also caused a great enhancement of arachidonic acid liberation from these cells. The level of released arachidonic acid in permeabilized cells enhanced by GTP gamma S in the absence of Ca2+ was nearly equal to the level of permeabilized cells incubated in the presence of Ca2+ but without GTP gamma S, suggesting the Ca2+ sparing effect of GTP gamma S. From the time sequential changes in the [3H]arachidonate radioactivities in various phospholipids, it is conceivable that nucleotide-dependent arachidonic acid release was mediated via phospholipase A2 pathway. The entrapment of a diacylglycerol (DG) lipase inhibitor, RHC 80267, caused suppression of both Ca2+- and guanine nucleotide-dependent arachidonic acid liberation in mast cells, indicating contribution of DG lipase pathway for arachidonic acid generation.
Adenosine Triphosphate↗
Arachidonic acid release in BW755C-pretreated rat peritoneal mast cells stimulated with A23187, concanavalin A and compound 48/80.
Rat peritoneal mast cells respond to various secretagogues, such as ionophore A23187, concanavalin A (Ig E receptor cross-bridging) and compound 48/80 (membrane perturbing), to secrete histamine and to liberate arachidonic acid. Arachidonic acid release was made identifiable by pretreatment with BW755C, an inhibitor of both lipoxygenase and cyclo-oxygenase. The extent of arachidonic acid release varied among these three secretagogues. A23187 appeared to be most potent, whereas compound 48/80 was weakest. The sources of released arachidonic acids may be different depending on the types of stimulants. The stimulation with A23187 released arachidonic acid mainly from phosphatidylcholine and triacylglycerol. After treatment with concanavalin A and compound 48/80, in addition to phosphatidylcholine, phosphatidylinositol also appeared to serve as a donor of arachidonic acid.
4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
Identification and quantification of 5-hydroxypipecolic acid and hydroxyproline in mammalian brain and blood by selected ion monitoring.
A method for the analysis of 5-hydroxypipecolic acid and 4-hydroxyproline in mammalian brain and blood is reported. The identification and quantification of the two hydroxyimino acids were accomplished with gas chromatography/mass spectrometry including a selected ion-monitoring technique following HPLC prepurification. The lower limit of detection for the method is 2 to 10 pmol. The amounts of 5-hydroxypipecolic acid and 4-hydroxyproline in blood were 20 to 30 pmol/ml and 3 to 6 nmol/ml, respectively. Their concentrations in the rabbit whole brain were determined to be 5 and 120 pmol/g, respectively.
Adult↗
Piperidine: a microelectrophoretic study in the mammalian brain.
Using unit recording and electrophoretic techniques, the action of piperidine on unit activity of the brain of the rat was studied. Piperidine excited 31%, and inhibited 4% of cortical cells tested. In the hippocampus and caudate nucleus, piperidine excited larger proportions of the cells tested. The actions of piperidine were blocked by tetraethylammonium but not by scopolamine.
Acetylcholine↗
Effects of synthetic omega-conotoxin GVIA (omega-CgTX GVIA) on the membrane calcium current of an identifiable giant neurone, d-RPLN, of an African giant snail (Achatina fulica Ferussac), measured under the voltage clamp condition.
1. The sodium and the calcium inward currents (INa and ICa) of an identifiable giant neurone, d-RPLN (dorsal-right parietal large neurone), of an African giant snail (Achatina fulica Férussac), were measured separately under the voltage clamp condition. 2. The effects of synthetic omega-conotoxin GVIA (omega-CgTX GVIA) on the calcium current of the neuromembrane were examined. 3. omega-CgTX GVIA is a peptide venom originally isolated from a fish-hunting marine snail (Conus geographus L.); the peptide venom has been demonstrated to block markedly calcium channels in vertebrates. 4. In the case of the d-RPLN membrane, the ICa was much larger than INa. The command voltage (Vc) to get the ICa in maximum was about 0 mV; the maximum value of ICa in a representative experimental case, was measured as approximately 0.8 microA. 5. With respect to the ICa of a molluscan giant neurone, d-RPLN, synthetic omega-CgTX GVIA at a high concentration, 5 X 10(-5) M, showed almost no effect, in spite of reporting the peptide venom affecting the ICa in vertebrate preparations.
Amino Acid Sequence↗
[The effects of cefoperazone on the intestinal bacterial flora and the incidence of diarrhea in children].
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Adolescent↗
Secretomotor and mucolytic effects of mabuterol, a novel bronchodilator.
Action of mabuterol, a novel bronchodilator, on the respiratory secretion system was investigated, and the following effects were confirmed: 1) increase of output volume, amounts of protein and pulmonary surfactant in respiratory fluid; 2) decrease of sputum viscosity; 3) fragmentation of the sputum structure and 4) promotion of the mucociliary transport of particles. The results in the present study may, at least partly, substantiate clinical efficacy such as improvement of pulmonary function, favourable effects on expectoration and amelioration of symptoms observed in patients with chronic obstructive pulmonary disease.
Adrenergic beta-Agonists↗
Plasma lipoproteins and transferrin regulate the proliferation of a continuous T lymphocyte cell line.
Lipoproteins of hydrated densities less than 1.063 g/ml, very low density (VLDL) and low density (LDL) lipoproteins, could both enhance and suppress the proliferation of T lymphocyte cell lines. Enhancement and suppression were dependent on lipoprotein and transferrin concentrations. Enhancement occurred at low lipoprotein and high transferrin; suppression, at high lipoprotein and low transferrin. Lipoprotein suppression required a constituent of cell-conditioned medium as evidenced by the fact that lipoproteins did not suppress the replicative response of the IL-2-dependent murine cell line CTLL-2 to purified IL-2 but could suppress the response to cell-conditioned medium IL-2. For lipoprotein suppression and its relief by transferrin, both growth-regulating factors were required early in the cell cycle, suggesting that events important to progression through G1 are influenced. The data establish that the interplay between plasma lipoproteins, transferrin, and an unknown constituent of cell-conditioned medium can regulate the proliferation of T lymphocytes.
Animals↗
Biphasic effect of phorbol myristate acetate on histamine secretion induced by compound 48/80 in rat peritoneal mast cells.
Rat peritoneal mast cells which had been preincubated with phorbol myristate acetate (PMA, 100 ng/ml) for 30 sec elicited an enhanced histamine secretion induced by a potent secretagogue, compound 48/80. But a longer (5 min) preincubation with PMA followed by the agonist-stimulation induced a suppressed histamine secretion. A 5 min-PMA-pretreatment inhibited the compound 48/80-mediated hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) in [32P]-labeled cells. PMA-treatment alone for 5 min induced an activation of Ca2+-efflux monitored by 45Ca2+. The inhibition of histamine secretion induced by a 5 min-PMA-pretreatment followed by the agonist-stimulation may partly be attributed to the decreased intracellular Ca2+ concentration, [Ca2+]i, probably due to the depressed PIP2 breakdown and enhanced Ca2+-efflux. On the other hand, a 30 sec-preincubation with PMA followed by compound 48/80-stimulation induced a slight but significant increase in histamine secretion. In this case, neither breakdown of PIP2 nor Ca2+-influx was enhanced to raise the [Ca2+]i. Although we are unable to explain the mechanism for the enhancement of histamine secretion by a short (30 sec) PMA-preincubation, these results suggest that the biphasic effects of PMA on histamine secretion are mediated by intracellular Ca2+ mobilization probably via protein kinase C activation.
Animals↗
Inhibitory action of cyclic GMP on secretion, polyphosphoinositide hydrolysis and calcium mobilization in thrombin-stimulated human platelets.
The effect of cyclic GMP (cGMP) on human platelet activation was investigated, using its metabolically stable analogue, 8-bromo cGMP (8-bcGMP). Thrombin-induced serotonin secretion was inhibited by pretreatment with 8bcGMP in a dose-dependent manner. Production of inositol trisphosphate (IP3), a Ca2+ releaser was inhibited by 8bcGMP pretreatment of platelets. Preincubation of platelets with 8bcGMP was without effect on the basal level of cytosolic free Ca2+, measured by fluorescent indicator quin2, but suppressed its thrombin-induced enhancement independently of extracellular Ca2+. These results indicate that cGMP may be implicated in phospholipase C activation and Ca2+ mobilization (both influx through the plasma membrane and efflux from internal stores) in thrombin-activated human platelets.
Aminoquinolines↗
Early diagnosis of hepatocellular carcinoma: usefulness of ultrasonically guided fine-needle aspiration biopsy.
The results of various diagnostic procedures performed on six cases with solitary and minimal (less than 2 cm) hepatocellular carcinoma (HCC) that was later surgically resected were comparatively reviewed. The tumor was detected in 6/6 patients by ultrasonography, 1/6 by scintigraphy, 2/6 by CT, and 4/6 by angiography, and hepatocellular carcinoma was diagnosed in 3/6 by angiography and 6/6 by ultrasonically guided fine-needle aspiration biopsy. Since there are not a few HCCs that can be detected only by ultrasonography, fine-needle aspiration biopsy with ultrasound guidance is strongly recommended to confirm cases with a minimal lesion in the liver visualized only on a sonogram.
Aged↗
Effects of phenylalanine loading on protein synthesis in the fetal heart and brain of rat: an experimental approach to maternal phenylketonuria.
Pregnant rats were loaded with L-phenylalanine, and the distributions of [14C]leucine and [14C]urea into fetal plasma and tissues were examined. Uptake of [14C]leucine into the supernatant and protein fractions of fetal plasma and tissues was low in the rats loaded with phenylalanine. In contrast, [14C]urea was distributed identically in both groups, indicating that maternal hyperphenylalaninemia did not affect blood flow across the placenta. Administration of phenylalanine and p-chlorophenylalanine produced amino acid imbalance in fetal tissues. Along with these changes, polysomes of the affected fetal heart and brain disaggregated without changes in the ribonuclease activity. These results indicate that high phenylalanine levels in maternal plasma disturb the active transport of amino acids across the placenta, causing an amino acid imbalance and disaggregation of polysomes in fetal heart and brain. These changes may contribute to the congenital heart disease and mental retardation of maternal phenylketonuria.
Animals↗
An infant with Beckwith-Wiedemann syndrome and chromosomal duplication 11p13----pter.: correlation of symptoms between 11p trisomy and Beckwith-Wiedemann syndrome.
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Abnormalities, Multiple↗
Plasma lipoproteins can suppress accessory cell function and consequently suppress lymphocyte activation.
The low density classes of plasma lipoproteins (d less than or equal to 1.063 g/ml) suppress mitogenic activation and proliferation of peripheral blood T lymphocytes. Here we demonstrate that lipoprotein suppression can be directed against the accessory cells (greater than 85% monocytes) required for optimal activation of lymphocytes by polyclonal mitogens. Preincubation of accessory cells for 24 h with very low (VLDL) and low (LDL) density lipoproteins suppressed their ability to enhance lymphocyte activation, whereas preincubation of T lymphocytes with lipoproteins did not alter their responsiveness to mitogens. The phenotypic distribution of the accessory cell population was not specifically altered by the lipoproteins, nor did loss of viability account for the suppressive effect of the lipoproteins. Furthermore, the lipoprotein-preincubated accessory cells did not secrete stable inhibitory substances, nor was their ability to produce interleukin 1 diminished. The results of mixing experiments indicate that VLDL-incubated accessory cells had not differentiated into suppressor cells. The lipoprotein-incubated accessory cells appeared to induce the interleukin 2-responsive state in the mitogen-activated lymphocytes, but could not deliver a signal or signals required for the further progression of the activated lymphocytes through the cell cycle. These important findings define at least two types of accessory cell function in the in vitro activation of T lymphocytes.
Cell Survival↗
Pipecolic acid enhancement of GABA response in single neurons of rat brain.
Using unit recording and microelectrophoresis, influence of pipecolic acid (PA), a major metabolite of lysine in the brain, on GABA and glycine responses was studied in the cerebral cortical and hippocampal pyramidal neurons of rats. With small currents, PA had no effect on the single neuron activities but enhanced GABA response without affecting glycine response. The finding provides a new evidence that PA may have a connection with central GABA system.
Action Potentials↗