Search PubMed⌕ Search

Biomedical subjects

K Onodera

Publications and source records attributed to K Onodera.

At least 145 records · Page 8Linked to original sources
PubMed1996

Effects of dopamine antagonists on neuronal histamine release in the striatum of rats subjected to acute and chronic treatments with methamphetamine.

In this study, we examined the changes in neuronal histamine (HA) release in the rat striatum after acute and repeated administration of methamphetamine (METH). We studied the regulation of METH-induced HA release by dopamine receptors and the relationship between METH-induced HA release and stereotyped behavior. Acute administration of METH (1 mg/kg) significantly increased HA release 60 min later. Pretreatments with the dopamine D2 antagonists sulpiride and haloperidol blocked the METH-induced increase of HA release, whereas pretreatment with a dopamine D1 antagonist, SCH23390, did not. Moreover, repeated administration of METH (3 mg/kg) greatly enhanced the METH-induced increase of HA release 60, 80, 100, 120 and 180 min after rechallenge of METH (1 mg/kg). Repeated treatment with haloperidol and METH blocked the increase of HA release induced by the rechallenge of METH. The METH-induced increase of HA release was still found after the METH-induced stereotyped behavior decreased in both acute and repeated administrations of METH. These findings suggest that the METH-induced HA release in the striatum is controlled by dopamine D2 receptors and may play an important inhibitory role in the METH-induced stereotyped behavior. Furthermore, a persistent change in the HA neuron system through DA neurotransmission may be partially responsible for the METH-induced behavioral sensitization.

Animals↗
PubMed1996

Tissue factor pathway inhibitor production by human mesangial cells in culture.

Fibrin formation within the glomeruli has been observed in various forms of human and experimental glomerulonephritis and it may play an important role in progressive glomerular injury. Furthermore it has been hypothesized that glomerular fibrin deposition may occur through activation of either the intrinsic or extrinsic coagulation pathway. It has been demonstrated that a procoagulant activity (PCA) which is compatible with tissue factor is present in the glomeruli and becomes increased in human proliferative glomerulonephritis and in animal models of nephritis. Tissue factor pathway inhibitor (TFPI) regulates the extrinsic pathway of blood coagulation through its ability to inhibit tissue factor activity. TFPI is present in plasma and in platelets, and it is now thought to be produced mainly by endothelial cells. We examined whether human mesangial cells (HMC) could produce TFPI and attempted to clarify regulatory factors which affect TFPI production. Cultured HMC were used and TFPI in the cell supernatants was measured by ELISA using a specific antibody. Cultured HMC showed the production of TFPI. Immunoblot analysis revealed 40 kD protein of TFPI. The concentration of TFPI was significantly increased following the incubation with thrombin and heparin, including low molecular weight heparin, in a dose- and time-dependent manner. However, fetal calf serum, phorbol myristate acetate, lipopolysaccharide, IL-1 beta and tissue factor did not stimulate TFPI synthesis. Our data show that cultured HMC have the ability to produce TFPI which inhibits fibrin formation. It is possible that thrombin-induced enhancement of TFPI synthesis may be caused by the autoregulatory system of blood coagulation and that with heparin it may represent another anticoagulatory effect of heparin.

Anticoagulants↗
PubMed1996

Effects of theophylline in p-chlorophenylalanine-treated mice in a light/dark test.

The effects of theophylline were examined in a light/dark test in p-chlorophenylalanine (PCPA)-treated mice to investigate serotonergic contribution to its effects. Three consecutive treatments with PCPA (200 mg/kg once daily) barely affected parameters in the light/ dark test. In vehicle- and PCPA-treated mice, theophylline (100 mg/kg) significantly decreased time spent in the light zone, which suggested its anxiogenic-like activity. In PCPA-treated mice, theophylline (50 mg/kg) also tended to decrease the time spent in the light zone. The effects of theophylline on the contents of monoamines and their metabolites in the brains of vehicle- and PCPA-treated mice were also investigated. Treatment with PCPA significantly decreased the contents of serotonin (5-HT) and its metabolite, as well as the contents of the metabolites of noradrenaline (NA) and dopamine (DA). Theophylline increased the metabolites of 5-HT, NA and DA in the brains of vehicle-treated mice. The increases produced by theophylline in the metabolites of NA and 5-HT were extinguished in PCPA-treated mice. Behavioral and biochemical data in the present study demonstrate that theophylline-induced anxiogenic-like activity was not mediated by serotonergic neuronal systems and that NAergic neuronal systems also might not contribute to the activity.

Animals↗
PubMed1996

[Syndrome X].

Explore the source record for details and available documents.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Deterioration of urinary findings after tonsil stimulation in patients with IgA nephropathy.

We studied whether urinary findings are affected by stimulation of tonsils in patients with IgA nephropathy. In 62 patients with IgA nephropathy and 20 patients with other renal diseases tonsils were stimulated by an ultra short wave for 10 min. Changes in amount of urinary protein, urinary sediment, blood leucocyte count, concentrations of serum IgA and serum secretory IgA were evaluated after tonsil stimulation. Forty of 62 patients with IgA nephropathy (65%) showed deterioration of urinary findings after the stimulation compared with 6 of 20 patients with other renal diseases (30%). The deterioration was significantly more frequent in IgA nephropathy than in other renal diseases (p <0.005). Previous episodes of gross hematuria following upper respiratory tract infections had occurred in 17 of 40 patients who showed deterioration of urinary findings after tonsil stimulation (43%) as against in 4 of 22 without deterioration (18%). The level of serum secretory IgA was higher in patients who showed deterioration of urinary findings after tonsil stimulation than in those who did not show it. Though tonsil stimulation increased blood leucocyte count it did not affect the concentrations of serum IgA or secretory IgA. It is concluded that tonsil stimulation often deteriorates urinary findings in patients with IgA nephropathy; therefore chronic tonsillitis may play a part in the pathogenesis of IgA nephropathy.

Adolescent↗
PubMed1995

Long-term depletion of brain histamine induced by alpha-fluoromethylhistidine increases feeding-associated locomotor activity in mice with a modulation of brain amino acid levels.

We examined the long-term effects of administration of (S)-alpha-fluoromethylhistidine (FMH), a specific inhibitor of histidine decarboxylase, on the spontaneous locomotor activity, food intake and brain contents of histamine, catecholamines, serotonin and amino acids of ICR mice. The distance of ambulation and number of rearings significantly increased from 8 to 15 h (20.00-03.00 h) after treatment with FMH (100 mg/kg, i.p.) and the 24-h food intake also increased significantly. On FMH treatment, the locomotor activity in movements of 3-15 cm/0.5 s was greater than that of control mice, whereas the number of slight movements (0-1 cm/0.5 s) decreased, suggesting that once a mouse treated with FMH is in motion, it moves a longer distance than a control mouse. We sacrificed mice 12 or 24 h after FMH treatment to measure the brain contents of histamine, monoamines and amino acids. Decrease of the brain histamine content to 35% of the control level was observed until 24 h after FMH treatment, but no significant changes in the brain catecholamine and serotonin contents were detected. However, the brain GABA content of ICR mice decreased to 85% of control 12 h after FMH treatment. Moreover, decrease of the brain GABA content after FMH treatment was greater in mast cell-deficient W/Wv mice, being 70 and 62% of the control level 12 and 24 h after treatment, respectively. The present experiments support the idea that the locomotor activity is affected by the central histaminergic system, directly and/or indirectly.

Amino Acids↗
PubMed1995

Isolation and characterization of a yeast gene, MPD1, the overexpression of which suppresses inviability caused by protein disulfide isomerase depletion.

MPD1, a yeast gene the overexpression of which suppresses the inviability caused by the loss of protein disulfide isomerase (PDI) was isolated and characterized. The MPD1 gene product retained a single disulfide isomerase active site sequence (APWCGHCK), an N-terminal putative signal sequence, and a C-terminal endoplasmic reticulum (ER) retention signal, and was a novel member of the PDI family. The gene product, identified in yeast extract, contained core size carbohydrates. MPD1 was not essential for growth, but overexpression of the gene suppressed the maturation defect of carboxypeptidase Y caused by PDI1 deletion, indicative of the related function to PDI in the yeast ER.

Amino Acid Sequence↗
PubMed1995

Effects of the histaminergic system on the morphine-induced conditioned place preference in mice.

The effects of an H2 receptor antagonist, a histidine decarboxylase inhibitor and a histamine precursor on the morphine-induced place preference in mice were examined. Morphine (1-7 mg/kg) produced a place preference in a dose-dependent manner. This morphine-induced place preference was significantly antagonized by the dopamine (DA) D1 receptor antagonist SCH 23390. The histamine precursor, L-histidine, attenuated the morphine (7 mg/kg)-induced place preference. On the other hand, the histidine decarboxylase inhibitor, alpha-fluoromethylhistidine (alpha-FMH), significantly potentiated the morphine (1 mg/kg)-induced place preference. This potentiation was antagonized by SCH 23390. The H2 receptor antagonist zolantidine (0.3 mg/kg) significantly potentiated the morphine-induced place preference. Surprisingly, zolantidine (1 mg/kg) alone also produced a significant place preference. The zolantidine-induced place preference was antagonized by SCH 23390. In addition, zolantidine (1, 3 and 10 mg/kg) significantly increased DA turnover (DA ratio) in the limbic forebrain (nucleus accumbens and olfactory tubercle), implying that zolantidine may activate the mesolimbic DA system. Moreover, co-administration of zolantidine dose-dependently increased morphine (10 mg/kg)-induced DA turnover in the limbic forebrain. These results suggest that the activation of histaminergic neurons may attenuate the rewarding effect of morphine, while the inhibition of histaminergic neurons may potentiate the rewarding effect of morphine. Furthermore, potentiation of the morphine-induced rewarding effect by inhibition of histaminergic neurons may be mediated by D1 receptors. We also demonstrated that the H2 receptor antagonist zolantidine may activate the mesolimbic DA system, and as a result, zolantidine itself produces a rewarding effect and potentiates the morphine-induced rewarding effect.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Ameliorating effects of histidine on scopolamine-induced learning deficits using an elevated plus-maze test in mice.

We investigated the effects of histidine on scopolamine-induced learning deficits in the elevated plus-maze test in mice. In this test, transfer latency (TL), the time mice took to move from the open arm to the enclosed arm, was used as an index of learning and memory. Intraperitoneal administration of scopolamine (0.5 mg/kg) prolonged the TL on day 2 compared with that in the saline-treated group. Histidine loading (500, 800 and 1600 mg/kg) reversed the prolongation of the TL induced by scopolamine. This ameliorating effect of histidine was abolished by alpha-fluoromethylhistidine, an inhibitor of histidine decarboxylase, suggesting that histidine itself has no such ameliorating effect. Moreover, the ameliorating effect of histidine was antagonized by a histamine H1 receptor antagonist, pyrilamine. However, zolantidine, a histamine H2 receptor antagonist, showed no antagonism of the effect of histidine. Thus, histamine, a decarboxylated product of histidine, elicited an ameliorating effect on scopolamine-induced learning deficit via histamine H1 receptors in mice. These findings clearly indicated that there is a close relationship between histaminergic and cholinergic systems in the brain, and that histamine may play certain important roles in learning and memory.

Animals↗
PubMed1995

Effects of thioperamide, a histamine H3-receptor antagonist, on a scopolamine-induced learning deficit using an elevated plus-maze test in mice.

We examined the effects of thioperamide and (R)-alpha-methylhistamine, a histamine H3-receptor antagonist and an agonist, respectively, on a scopolamine-induced learning deficit using an elevated plus-maze test in mice. Thioperamide alone slightly improved the learning deficit induced by scopolamine, and pretreatment with zolantidine, a histamine H2-receptor antagonist, significantly enhanced the effect of thioperamide in this test. (R)-alpha-Methylhistamine, pyrilamine, ketotifen, terfenadine, and zolantidine alone at the doses tested had no effect. Moreover, the improvement by thioperamide plus zolantidine was antagonized by pretreatment with histamine H1-receptor antagonists such as pyrilamine or ketotifen, but not by terfenadine. Thus, thioperamide improved the scopolamine-induced learning deficit through central histamine H1 receptors in mice. The present results supported the hypothesis that histamine may play an important role in learning and memory.

Animals↗
PubMed1995

The immuno-stimulant OK-432 enhances liver regeneration after 70% hepatectomy.

The effect of reticuloendothelial system activation on hepatic regeneration after 70% hepatectomy was investigated. OK-432, a killed streptococcal preparation which increases reticuloendothelial system function, was administered to rats prior to 70% hepatectomy. Hepatic incorporation of 3H-thymidine 24 h after 70% hepatectomy was enhanced by OK-432 pretreatment. DNA synthesis was greater in pretreated than in control rats and correlated highly with reticuloendothelial system phagocytic activity prior to surgery. Methyl palmitate, which decreases reticuloendothelial system function, was administered to rats prior to 70% hepatectemy. Hepatic incorporation of 3H-thymidine 24 h after 70% hepatoctomy was significantly depressed by methylpalmitate-pretreatment. These data suggest that reticuloendothelial system plays a role in liver regeneration and that hepatocyte proliferation might be enhanced by protection from surgical stress and endotoxins with reticuloendothelial system stimulation by OK-432.

Adjuvants, Immunologic↗
PubMed1995

Cell-cycle dependent biosynthesis and localization of p53 protein in untransformed human cells.

Localization of p53 in human cultured lymphocytes and in cultured skin fibroblasts was studied by immuno-fluorescent microscopy and post-embedded immunoelectron microscopy using Lowicryl K4M. In quiescent lymphocytes, p53 was found in small amounts in both the cytoplasm and the nucleus. p53 in the nucleus was found associated with the non-chromatin structure. At 24 h or 72 h of PHA stimulation, p53 increased markedly just beneath the plasma membrane and in the nucleus, which stained diffusely with anti-p53. In resting fibroblasts, small amounts of p53 were present in both the cytoplasm and the nucleus. After 16 h of stimulation of confluent-resting fibroblasts by trypsinization and replating, a phase just prior to the initiation of DNA synthesis, p53 slightly increased in both the cytoplasm and the nucleus. Afterwards, p53 was present predominantly in the cytoplasm, closely associated with the cytoskeletal actin filaments. In mitotic cells, p53 was distributed throughout the cytoplasm. When fibroblasts were extracted with saponin, p53 was still associated with the actin filaments, as well as mitochondrial membranes and granular structures of the nuclear matrix. Our data suggest that the initial increase of p53 in cells that enter the cell cycle through G1 first bind to the actin cytoskeleton, and that some of the p53 then move into the nucleus to initiate gene activation and DNA synthesis for cell proliferation. This implies that there is some functionally significant interaction between p53 and actin in the cells.

Cell Cycle↗
PubMed1995

Production of monoclonal antibodies specific to the carboxyl terminal region of the 85 kDa subunit of phosphatidylinositol 3-kinase: use of the antibodies in recognition of mutant p85.

We have established two hybridomas producing mAb to the carboxyl terminal region of phosphatidylinositol-3 kinase 85 kDa subunit type alpha (p85 alpha). Analysis using deletion mutants of p85 revealed that epitopes for the two mAb were located on the border of the src homology 2 (SH2) sequence located at the carboxyl end of p85. They immunoprecipitated free p85 efficiently, but reactivity to p85 bound to p110 was very weak. Together with the mAb which we have reported previously, a panel of mAb that covered the various parts of p85 alpha was obtained. Using this panel, we characterized two mutants of p85 (70 and 50 kDa) expressed in the human colon carcinoma cell line, HCC2998. No wild-type p85 was detected in these cells. A mAb specific to the carboxyl terminal region detected p70 but not p50, suggesting that this region is missing in p50. The panel of mAb is a useful tool to use to analyse mutant forms of p85.

Animals↗
PubMed1995

An ultrasonically powered instrument for laparoscopic surgery: a brief technical report of preliminary success.

We report the use of an ultrasonically powered instrument (CUSA) for laparoscopic surgery. A total of 105 patients underwent laparoscopic or laparoscopic assisted surgical procedures. Ninety-one laparoscopic cholecystectomies (LC), 9 laparoscopic appendectomies (LA), 3 laparoscopic colon resections (LCR), and 2 laparoscopic partial gastrectomies (LPG) were done using CUSA. In LC, CUSA separates the areolar connective tissue between gallbladder and liver bed without dividing any sizable vessels or injuring the liver. In LA, LCR, and LPG, CUSA makes mesenteric vessel identification and division rapid and safe. We concluded that CUSA is useful for laparoscopic surgery.

Adult↗
PubMed1995

Purification and characterization of chitin deacetylase from Absidia coerulea.

Chitin deacetylase, which releases the acetyl groups of glycol chitin was purified from a fungus, Absidia coerulea, and characterized. The enzyme was purified 516-fold to homogeneity by means of 65-80% ammonium sulfate precipitation followed by chromatography on Butyl Toyoperal-650M, Gigapite (hydroxyapatite), and DEAE Toyopearl-650M. It had an apparent molecular weight of 75 kDa both on sodium dodecyl sulfate polyacrylamide gel electrophoresis and gel filtration chromatography, indicating that the enzyme exists as a monomer. The amino-terminal sequence was determined to be Gly-Glu-Tyr-Trp-Gln-Ser-Phe-. The enzyme is active on chitooligosaccharides with more than two N-acetylglucosamine residues (chitobiose) and is able to convert the nascent chitin synthesized by chitin synthase to chitosan in vitro. When O-hydroxyethylated chitin (glycol chitin) was used as a substrate, the optimum pH for enzyme activity was 5.0 and the optimum temperature was 50 degrees C. The enzyme was heat-stable and strongly inhibited by Fe3+. Furthermore, chitin deacetylase was demonstrated to be localized near the inner face of the cell wall (periplasmic space) in the mycelia by using immunoelectron microscopy.

Amidohydrolases↗