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Biomedical subjects

Y Abiko

Publications and source records attributed to Y Abiko.

At least 145 records · Page 8Linked to original sources
PubMed1994

Newly discovered photodegradation products of nifedipine in hospital prescriptions.

New photodegradation products of nifedipine (1) have been isolated. They were found in tablets dispensed in the pulverized form by hospitals. 1 decomposed concurrently into six components after storage of 30 days under exposure to normal room light. The main photoproduct was a nitroso derivative (2) and others were minor. Preparative thin-layer chromatography has been used to isolate the six photodegradation products. The chemical structures of these isolated compounds were identified or estimated by comparison with authentic samples and/or using UV, IR, 1H NMR, mass spectroscopy, melting point determination, and elementary analysis. From these analyses, it was found that 1 was converted into a cis-azoxy derivative (4), a trans-azoxy derivative (5), a N,N'-dioxide derivative (6) and a lactam derivative (7) in addition to 2 and a nitro derivative (3). Furthermore, it is proposed that 2 is mainly responsible for the formation of these new products (4-7) by photochemical condensation.

Chromatography, High Pressure Liquid↗
PubMed1994

Stimulation of interleukin-6 production of periodontal ligament cells by Porphyromonas endodontalis lipopolysaccharide.

Interleukin-6 (IL-6), which is a multifunctional cytokine, has important roles in acute and chronic inflammation and may also be implicated in bone resorption. We examined the IL-6 production in periodontal ligament (PDL) cells which were treated with lipopolysaccharide (LPS) from several oral inflammatory pathogens. The LPS from Porphyromonas endodontalis, which was isolated from infected root canals and radicular cyst fluids, was more potent than the LPS from any other periodontal organisms examined. P. endodontalis LPS stimulated IL-6 release from PDL cells in a time- and dose-dependent manner. Northern blot hybridization analysis revealed that the IL-6 mRNA level in PDL cells was increased by P. endodontalis LPS. These results suggest that stimulation of the IL-6 release of PDL cells by P. endodontalis LPS may have a role in the progression of inflammation and alveolar bone resorption in periodontal and periapical diseases.

Blotting, Northern↗
PubMed1994

Effect of different magnitudes of tension force on prostaglandin E2 production by human periodontal ligament cells.

Periodontal ligament (PDL) cells are known to produce prostaglandin E2 (PGE2) in response to mechanical stress. However, the rate of PGE2 production from PDL cells in response to different magnitudes of tension forces has not been examined. This study, therefore, was undertaken to determine the effect of different magnitudes of tension forces on PGE2 production and inositol trisphosphate (IP3) levels in PDL cells in vitro. Human PDL cells were cultured on flexible-bottomed plates and placed on a Flexercell strain unit. Cells were flexed at six cycles (5-s strain, 5-s relaxation) at six steps of tension force (9, 12, 15, 18, 21, 24% increase in surface area) for 5 days. PGE2 production and IP3 levels were determined by radioimmunoassay. There was a 6- and 25-fold increase in the rate of PGE2 production by cells exposed to low (9%) and high (24%) tension forces, respectively, and these increases were tension force-dependent. Tension force also induced increases in the intracellular levels of IP3 that did not seem to be directly related to the production of PGE2. The different rates of PGE2 production by PDL cells in response to different magnitudes of mechanical stress may be of importance in PDL and alveolar bone metabolism.

Adult↗
PubMed1994

Enhancement of ischemic myocardial metabolic derangement by glibenclamide.

We examined whether opening of the ATP-sensitive potassium (KATP) channels in the ischemic myocardium plays an important cardioprotective role during ischemia. Dogs were anesthetized with sodium pentobarbital (30 mg/kg, i.v.). Sixty minutes after treatment of the dog with glibenclamide (0.3 or 3 mg/kg, i.v.), the LAD was ligated. At 3 or 15 min after LAD ligation, left ventricular tissue was taken from the ischemic region to measure tissue metabolite levels. After ischemia, the tissue levels of ATP and creatine phosphate decreased to 49-74% and 26-34%, respectively, and lactate level increased to 380-660%. Ischemia (either 3 or 15 min) increased the levels of G6P and F6P and decreased the FDP level, indicating the inhibition of glycolysis. Glibenclamide at either dose decreased the level of blood glucose by 20-30% and increased the blood insulin level twice. The decrease in ATP and increase in lactate due to ischemia were significantly enhanced by glibenclamide at a dose of 3 mg/kg. The increase in G6P due to 15 min of ischemia were also enhanced significantly by 0.3 and 3 mg/kg of glibenclamide. Glibenclamide worsened the metabolic alterations produced by ischemia. These results suggest that KATP channels that can be inhibited by glibenclamide may perform some functions in the ischemic myocardium.

Adenosine Monophosphate↗
PubMed1994

Laminin localization and gelatinolytic activity of epithelial rest of Malassez grown on titanium.

The purpose of this study was to examine laminin localization in epithelial rests of Malassez grown on titanium and their gelatinase activity. Laminin localization was confirmed by immunocytochemistry in all epithelial cells grown on titanium. The conditioned medium from the epithelial cells grown on titanium exhibited 72kD- and 92 kD-gelatinase activities by gelatin zymography. Those results suggest that laminin contributes to the epithelial cell attachment to titanium and that gelatinases may be mobilized for epithelial cell movement on titanium.

Animals↗
PubMed1993

Cardioprotective effect of d-propranolol in ischemic-reperfused isolated rat hearts.

In the isolated, perfused working rat heart, ischemia (15 min) decreased mechanical function and also the tissue levels of ATP and creatine phosphate, and increased the tissue levels of lactate and free fatty acids including arachidonic acid. Reperfusion (20 min) did not restore mechanical function, but restored changes of metabolites incompletely except for free fatty acids, which changed further during reperfusion. Drugs were given 5 min before ischemia until the end of ischemia or for the first 10 min after reperfusion. Both dl- and d-propranolol (10 and 30 microM) decreased mechanical function, accelerated the recovery of mechanical function during reperfusion following ischemia, and attenuated ischemia reperfusion-induced metabolic changes. The attenuation of reperfusion-induced metabolic changes was more marked when these drugs were present during reperfusion. d-Propranolol showed a cardioprotection similar to that by dl-propranolol. Timolol (50 microM) did not accelerate the recovery of mechanical function during reperfusion, and did not attenuate the reperfusion-induced metabolic changes. These results suggest that d-propranolol, like dl-propranolol, has a cardioprotective effect which is probably due to its membrane stabilizing (or sodium channel blocking) action.

Adenosine Triphosphate↗
PubMed1993

Effects of iloprost, a PGI2 derivative, on ischemic myocardial energy and carbohydrate metabolism in dogs.

Effects of iloprost, which is a stable prostacyclin analogue, on the ischemic myocardium were examined in the open-chest dog heart in terms of biochemical parameters. Ischemia was initiated by ligating the left anterior descending coronary artery. When the coronary artery was ligated for 3 min, the levels or glycogen, fructose-1,6-diphosphate (FDP), adenosine triphosphate and creatine phosphate decreased, and the levels of glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), lactate, adenosine diphosphate and adenosine monophosphate increased. During ischemia, therefore, energy charge potential was significantly decreased from 0.89 +/- 0.01 to 0.82 +/- 0.01, and ([G6P] + [F6P])/[FDP] and [lactate]/[pyruvate] ratios were significantly increased from 1.75 +/- 0.30 to 29.05 +/- 5.70 and 13 +/- 3 to 393 +/- 112, respectively. Iloprost (0.1, 0.3, or 1 microgram.kg-1) was injected intravenously 5 min before the onset of ischemia. Iloprost (0.1, 0.3, and 1 micrograms.kg-1) reduced the ischemia-induced decrease in energy charge potential to 94, 74, and 86%, respectively, the increase in ([G6P] + [F6P])/[FDP] to 38, 29, 32%, respectively, and the increase in [lactate]/[pyruvate] to 67, 45, 65%, respectively. These results suggest that iloprost lessens the myocardial metabolic derangements produced by ischemia, and the most potent effect was obtained at the dose of 0.3 microgram.kg-1.

Adenosine Diphosphate↗
PubMed1993

Suppression of proliferation of a human B-cell leukaemic cell line derived from acute lymphoblastic leukaemia by soluble factor(s) from Campylobacter rectus.

Soluble sonic extracts of several strains were examined for their ability to alter proliferation of a cell line derived from acute lymphoblastic leukaemia (BALL-1). Extracts of all strains tested caused dose-dependent suppression of proliferation when assessed by DNA (tritiated thymidine incorporation), RNA (tritiated uridine incorporation) and protein (tritiated leucine incorporation) synthesis. There was no effect on the viability of BALL-1 as measured by either trypan-blue exclusion or extracellular release of the cytoplasmic enzyme lactate dehydrogenase. The suppressive factor(s) was separated in a well-defined peak by high-pressure liquid DEAE ion-exchange chromatography, which revealed a single active peak with a molecular mass of 48 kDa. Characterization of the peak indicated that the suppressive factor(s) was heat labile (activity destroyed at 80 degrees C) and sensitive to the proteolytic enzyme pronase P. The soluble suppressive factor(s) from Campylobacter rectus thus has protein-like properties and no cytotoxicity to a human B-cell leukaemic cell line.

B-Lymphocytes↗
PubMed1993

Effects of transforming growth factor-beta on collagen gene expression and collagen synthesis level in mineralizing cultures of osteoblast-like cell line, MC3T3-E1.

1. High levels of type I collagen mRNA and [3H]proline incorporation into collagenase digestable protein by MC3T3-E1 cells were detected during the first 7 days of culture, after which they declined. 2. Type I collagen gene expression was stimulated by TGF-beta in the early culture stage when the collagen gene expression was fully functioning. 3. However, these stimulatory effects disappeared at the differentiation stages. Although collagen gene expression was stimulated by TGF-beta (2.0 ng/ml) in early culture, collagen synthesis in medium was not. 4. This study shows that collagen synthesis and collagen gene expression were affected by the state of differentiation in MC3T3-E1 cells and that the rate of stimulation by TGF-beta in collagen gene expression decreased over time in culture.

Animals↗
PubMed1993

Stimulation of plasmin activity in cultured human fibroblast cells by Porphyromonas endodontalis.

1. Plasmin activity in the conditioned medium of Gin-1 cells, a human gingival fibroblast cell line, was stimulated by Porphyromonas endodontalis, a putative pathogen of oral submucous abscesses, in a time- and dose-dependent manner. 2. P. endodontalis stimulated the activity of plasminogen activator in both the conditioned medium and the cell lysate. The plasminogen activator in Gin-1 cells was approx. 50 kDa by zymography. 3. The conditioned medium of Gin-1 cells exposed to P. endodontalis stimulated the conversion of human serum prekallikrein to kallikrein. 4. These results suggested that P. endodontalis stimulates the plasminogen activator-plasmin system in Gin-1 cells, and that activated plasmin plays a role in the progress of periodontal tissue inflammation.

Amino Acid Sequence↗
PubMed1993

Influences of pravastatin and simvastatin, HMG-CoA reductase inhibitors, on myocardial stunning in dogs.

We examined the effects of pravastatin and simvastatin, HMG-CoA reductase inhibitors, on stunned myocardium in vivo. Pravastatin and simvastatin were given orally 2 mg/kg for 3 weeks. After 3 weeks of administration, pentobarbital-anesthetized dogs were subjected to 15-min left anterior descending (LAD) coronary artery occlusion followed by 2-h reperfusion. Myocardial segment function was determined by sonomicrometry. The tissue energy and carbohydrate metabolites were determined in the 2-h-reperfused hearts. Administration of pravastatin and simvastatin for 3 weeks decreased serum cholesterol level and blood pressure (BP). Simvastatin resulted in a worsening of segment shortening in the reperfused myocardium as compared with control and pravastatin groups. The level of ATP in the simvastatin group was significantly lower as compared with that in the control group. The other metabolite levels were not significantly altered by either pravastatin or simvastatin. These results suggest that simvastatin enhances stunning of the myocardium in association with ATP reduction after reperfusion subsequent to ischemia.

Adenosine Triphosphate↗
PubMed1993

Modulation by histamine of the delayed outward potassium current in guinea-pig ventricular myocytes.

1. Histamine receptor-mediated modulation of the delayed outward potassium current (IK) was investigated in guinea-pig single ventricular cells by the whole-cell voltage clamp. 2. Histamine increased IK in a dose- dependent manner with a half-maximum dose of 3.8 x 10(-8) M. Histamine (10(-6) M) increased IK by a factor of 3.02 without a significant change in the current kinetics. The threshold dose of histamine for increasing IK was 10(-9) M and this value was similar to that for calcium current. 3. Cimetidine decreased IK in the presence of histamine, by shifting the dose-response curve to histamine to the right. The pA2 value of cimetidine against histamine was 6.38. 4. Forskolin did not increase IK after application of 10(-6) M histamine, and histamine scarcely increased IK in the presence of a heat-stable inhibitor of cyclic AMP-dependent protein kinase (PKI). 5. We conclude that stimulation by histamine of IK is mainly by way of the H2-receptor, and is mediated by cyclic AMP-dependent phosphorylation.

Animals↗
PubMed1993

Effects of LP-805, a newly developed vasodilator, on myocardial metabolism in ischaemic dog hearts.

The effects of LP-805, a newly developed vasodilator, on changes in the myocardial energy and carbohydrate metabolism induced by ischaemia were studied in open-chest anaesthetized dogs. Ischaemia was induced by ligating the left anterior descending coronary artery for 3 min. The myocardial energy stores were depleted, and the levels of glycolytic intermediates were altered 3 min after the onset of ischaemia. Energy change potential was decreased, and ([G6P] + [F6P])/[FDP] and [lactate]/[pyruvate] ratios were increased by ischaemia. These findings indicated that the myocardial metabolism was converted from an aerobic to an anaerobic type by ischaemia. LP-805 (10, 30, or 100 micrograms kg-1) was injected intravenously 5 min before the onset of ischaemia. LP-805 prevented the myocardial energy depletion and alterations of myocardial carbohydrate metabolism due to ischaemia, indicating that it appeared to convert the anaerobic metabolism back to aerobic metabolism in the ischaemic myocardium. In conclusion, LP-805 may reduce the ischaemic influence on the myocardium.

Adenine Nucleotides↗
PubMed1993

Lidocaine attenuates both mechanical and metabolic changes induced by hydrogen peroxide in the rat heart.

The effect of lidocaine on the hydrogen peroxide (H2O2)-induced mechanical and metabolic changes was studied in the Langendorff rat heart, which was perfused aerobically at a constant flow rate and paced electrically. H2O2 (600 microM) increased the left ventricular end-diastolic pressure (i.e., mechanical dysfunction), decreased the tissue levels of ATP and creatine phosphate (i.e., metabolic change), and increased the tissue level of malondialdehyde (MDA). The mechanical and metabolic alterations induced by H2O2 were attenuated by lidocaine (50 or 200 microM). Lidocaine also attenuated the H2O2-induced increase in MDA. Nevertheless, lidocaine modified neither the myocardial ferrylmyoglobin level that was increased by H2O2 nor the H2O2 concentration in vitro and did not affect the mechanical function and energy metabolism of the normal heart. These results suggest that lidocaine attenuates both mechanical and metabolic changes induced by exogenous H2O2. The protective action of lidocaine on the H2O2-induced changes is due to neither energy-sparing nor H2O2-scavenging effect, but probably due to its effect to reduce the H2O2-induced lipid peroxidation.

Adenosine Triphosphate↗
PubMed1993

Cloning of a Streptococcus sobrinus oligo-isomaltosaccharide synthase gene and characterization of its product.

A Streptococcus sobrinus gene coding for a glucosyltransferase (GTF)-S was cloned into Escherichia coli, using the bacteriophage lambda L47.1 and the plasmid vector pACYC184. The MD124 clone obtained expressed a 155 kDa GTF-S which did not react with any antisera against GTF-S1, -S2 and -I enzymes. The recombinant enzyme (designated rGTF-S3) was homogeneously purified from the MD124 cell-extract and characterized. The purified rGTF-S3 synthesized primer-independently alpha-1,6-linked linear oligosaccharides from sucrose. The dependence upon the sucrose concentration was diphasic, and the respective Km values were 1.3 and 25 mM. The properties except the Km values were similar to those of oligo-isomaltosaccharide synthase from S. sobrinus AHT.

Chromatography, High Pressure Liquid↗
PubMed1993

Protective effect of crataegus extract on the cardiac mechanical dysfunction in isolated perfused working rat heart.

The effect of the water-soluble fraction of Crataegus (Crataegus extract) on the cardiac mechanical and metabolic function was studied in the isolated, perfused working rat heart during ischemia and reperfusion. Ischemia (15 min) was produced by removing afterload pressure, and reperfusion (20 min) was produced by returning it to the original pressure. In the control (no drug) heart, ischemia decreased mechanical function to the lowest level, which did not recover even after the end of reperfusion. Crataegus extract (0.01 or 0.05%) was applied to the heart from 5 min before ischemia through the first 10 min after reperfusion. With the high concentration of Crataegus extract (0.05%) the mechanical function recovered during reperfusion incompletely without increasing coronary flow, but the low concentration of Crataegus extract (0.01%) did not. In the heart treated with the high concentration of Crataegus extract, the reperfusion-induced recovery of the energy metabolism was accelerated, and the level of lactate during ischemia was lower than that in the control heart, although the myocardial levels of free fatty acids during ischemia and reperfusion were not greatly affected. These results demonstrate that Crataegus extract (0.05%) has a cardioprotective effect on the ischemic-reperfused heart, and that the cardioprotective effect is not accompanied by an increase in coronary flow.

Adenine Nucleotides↗
PubMed1993

Large cyst formation in pleomorphic adenoma.

The aim of this study was to examine about the etiology of large cyst formation in pleomorphic adenoma from the histopathological standpoint by examining four cases of our own as well as previously reported ones. In the first of our cases, a large cyst wall lined with keratinized squamous epithelium was observed. In the second, a large cyst containing mucinous material was lined with a single cell layer of squamous epithelium-like cells. The third case was a carcinoma in pleomorphic adenoma with some large cysts lined with multiple layers of atypical epithelial cells. In the fourth case, a hemorrhagic portion were seen on a large cyst wall without a lining of epithelial cells. From these histopathological observations and the suggestions of previous authors, we surmised that the large cyst formation in pleomorphic adenoma might originate from the squamous metaplasia of tumor cells and the enlargement of duct-like structures by outstanding secretion from tumor cells or salivary gland tissues, hemorrhagic portions, or necrosis in the malignant tumor.

Adenoma, Pleomorphic↗