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Biomedical subjects

Y Abiko

Publications and source records attributed to Y Abiko.

At least 217 records · Page 12Linked to original sources
PubMed1989

Regeneration of periodontal tissues following experimentally induced periodontitis in rats: a comparison of sucrose-rich and conventional diets.

The purpose of the present study is to elucidate influences of diet on periodontal regeneration following experimental periodontitis in rats. S-D rats were divided into two groups, which were fed either a conventional diet (group A) or a sucrose-rich diet (group B). Experimental periodontitis was produced by placement of elastic bands between maxillary molar teeth. After one week, the elastic bands were removed and the animals were sacrified by perfusion fixation with formalin immediately, 1, 3, or 5 days, or 1, 2, 3, 4, 6, or 8 weeks after the removal. Sections of the teeth and surrounding tissue were examined by light microscopy. Three days after the removal, in both groups, granulation tissues with many inflammatory cells were covered by epithelial cells; the attachment site to the root surface was located more apically than the cemento-enamel junction. Distinct periodontal pockets were formed by five days after the removal in group A. In group B, the infiltrations of inflammatory cells were more prominent than in group A. Six weeks after the removal in both groups, an epithelium which resembled long junctional epithelium rather than pocket epithelium became thicker. Eight weeks after the removal, the findings were similar to those of six weeks in group A. However, a severe inflammatory cell concentration was found in group B. These results suggest that periodontal wound healing is markedly influenced by diet, and that this experimental system is useful for studying dynamic changes in both pocket and long junctional epithelia.

Animals↗
PubMed1989

[Statistical study of epulis, especially in general pathology].

This report contains a statistical study of 874 cases of epulis diagnosed by the Department of Pathology of Tokyo Dental College from 1966 to 1986. 1. Of the 874 cases, 344 were epulis fibrosa, 217 were epulis granulomatosa, 78 were epulis fibromatosa, 74 were epulis fibrosaosteoplastica, 51 were epulis hemangiomatosa, 43 were epulis fibrosa teleangiectaticum, 15 were epulis cementoplastica, 14 were epulis osteomatosa, 3 were congenital epulis, 2 were giant cell epulis, and 1 was epulis cementomatosa. 2. As has been reported in other literature, there is a marked tendency for this condition to occur in females (331 male cases and 539 female cases). 3. Our data indicate a higher occurrence rate in people in their fifties, although the occurrence rates were similar in people in their twenties and in people in their sixties. 4. The epulis was observed most frequently in the maxillary incisor region.

Adolescent↗
PubMed1988

Phospholipase A2 in macrophage plasma membrane releases arachidonic acid from phosphatidylinositol.

A high level of arachidonic acid release from [2-14C]arachidonylphosphatidylinositol (PI) was observed at neutral pH (6.0-7.0) in the presence of purified plasma membranes of guinea pig peritoneal macrophages. This activity was at least 10-fold higher than that with arachidonylphosphatidylcholine (PC) or phosphatidylethanolamine (PE) as substrate. The accumulation of [14C]diacylglycerol and [14C]phosphatidic acid was not detected at any time, and arachidonic acid release from [14C]arachidonyldiacylglycerol was not detectable either. The data suggest that arachidonic acid release from PI may not occur via the phospholipase C pathway. In this paper, we demonstrate the possibility that arachidonic acid release from PI at neutral pH in the macrophage plasma membrane is dependent on the action of phospholipase A2 (EC 3.1.1.4) -like activity. The maximum arachidonic acid release was dependent upon both pH and substrate. Particularly, the activity of arachidonic acid release from PI at neutral pH was very high compared with that from PC or PE. We suggest that phosphatidylinositol phospholipase A2 (EC 3.1.1.52) may play an important role in providing arachidonic acid for subsequent metabolic activity in the macrophages.

Animals↗
PubMed1988

Propranolol inhibits accumulation of non-esterified fatty acids in the ischemic dog heart.

The effects of propranolol and d-propranolol on the accumulation of non-esterified fatty acids (NEFA) induced by complete occlusion of the left anterior descending coronary artery (LAD) for 90 min, were investigated in dogs anesthetized with pentobarbital. The myocardial levels of eight NEFA (lauric, myristic, palmitic, palmitoleic, stearic, oleic, linoleic and arachidonic acids) were determined after fluorescent labelling of the NEFA with 9-anthryldiazomethane. LAD occlusion increased the myocardial levels of NEFA, especially those of arachidonic and palmitoleic acids; arachidonic acid increased by 3.5 times and palmitoleic acid by 2.9 times. Pretreatment with propranolol (1 mg/kg) inhibited almost completely the accumulation of NEFA induced by occlusion of the LAD, whereas pretreatment with d-propranolol (1 mg/kg) did not inhibit the accumulation of NEFA, although it tended to inhibit the accumulation of palmitoleic, stearic and arachidonic acids. These results suggest that the inhibitory action of propranolol on the accumulation of NEFA in the myocardium during ischemia is mainly due to its antagonistic effect at beta-adrenoceptors and probably partly due to its effect as a local anesthetic.

Animals↗
PubMed1988

Binding site of alpha 2-plasmin inhibitor to plasminogen.

Peptide T-11, a carboxyl terminal tryptic fragment of alpha 2-plasmin inhibitor, inhibits the reversible first step of the reaction between plasmin and alpha 2-plasmin inhibitor. To elucidate which amino-acid residues played a important role in the inhibitory activity of peptide T-11, we prepared the various synthetic derivatives of peptide T-11 and determined the peptide concentration that inhibited the apparent rate constant of the reaction between plasmin and alpha 2-plasmin inhibitor by 50% (IC50). Peptide III, which lacked the residues Gly-1 to Pro-7 of peptide I (peptide T-11), had a strong inhibitory activity, like peptide I (IC50: peptide I, 7 microM; peptide III, 13 microM). The peptides that lacked the Leu-9 and Lys-10 or Lys-26 of peptide III showed much weaker activity, and the loss or amidation of the C-terminal lysine of peptide III also markedly reduced the inhibitory activity. Peptide III competitively inhibited the binding of [14C]tranexamic acid to kringle 1 + 2 + 3 (K1-3) and kringle 4 (K4) in a binding assay performed by the gel-diffusion method. The respective dissociation constants (Kd) of peptide III for K1-3 and K4 were 0.85 microM and 35.2 microM. These data suggest that the amino residue of Lys-10 and the carboxylic acid of Lys-26 in peptide T-11 play crucial roles in the ionic binding of alpha 2-plasmin inhibitor to the tranexamic acid-binding site (lysine-binding site) of plasminogen. Peptide T-11: H-G-D-K-L-F-G-P-D-L-K-L-V-P-P-M-E-E-D-Y-P-Q-F-G-S-P-K-OH.

Amino Acid Sequence↗
PubMed1988

Cardiac metabolism as an indicator of oxygen supply/demand ratio.

We evaluated the anti-ischemic effect of drugs by using the inhibition of glycolytic flux at the level of the phosphofructokinase (PFK) reaction, caused by ischemia, as an indicator of the oxygen supply/demand ratio in the ischemic myocardium. Ischemia was induced by ligating the left anterior descending coronary artery in the open-chest dog. After 3 min of coronary ligation, the ischemic myocardium was removed. The endocardial portion of the myocardial sample was used to determine the levels of glucose-6-phosphate (G6P), fructose-6-phosphate (F6P) and fructose-1,6-diphosphate (FDP), and the ratio of [( G6P] + [F6P])/[FDP] was calculated in order to assess the rate of glycolytic flux at the PFK stage. Either saline or drug (propranolol, 1 mg/kg; carteolol, 100 micrograms/kg; nadolol, 1 mg/kg; nifedipine, 10 micrograms/kg; diltiazem, 100 micrograms/kg; verapamil, 100 micrograms/kg; and flunarizine, 1 mg/kg) was injected intravenously 5 min before coronary ligation. In the saline-treated heart, ischemia increased the levels of G6P and F6P, whereas it decreased the level of FDP. The ratio of ([G6P] + [F6P])/[FDP] was increased by ischemia from 2.2 to 23.6, suggesting the inhibition of glycolytic flux at the level of the PFK reaction. In the drug-treated heart, ischemia increased the levels of G6P and F6P, but the increases were smaller than those in the saline-treated heart. Pretreatment with propranolol, nadolol, diltiazem, verapamil, flunarizine attenuated the increase in the ratio of ([G6P] + [F6P])/[FDP] caused by ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Recognition of acidic phospholipase A2 activity in plasma membranes of resident peritoneal macrophages.

Phospholipase (PLase) activities in the plasma membrane of guinea pig peritoneal macrophages were studied, as these enzymes having such activity may be candidates for the release of arachidonic acid (AA) from phosphatidylcholine (PC). An AA release system operating at acidic pH was identified in the macrophage plasma membrane and characterized. This membrane-bound acidic PLase A2 had an optimum pH at 4.5, and enzyme activation was observed in Ca++-free medium; but the maximum activity was found at 0.5 mM Ca++ concentration. The Km value for PC of acidic PLase A2 was 4.2 microM, and a Michaelis-Menten relationship was evident. Calcium might act as a cofactor at some intermediate step during the activation of acidic PLase A2 in light of the uncompetitive manner of Ca++ action. Furthermore, the release of [3H]-AA from preradiolabelled macrophage plasma membranes occurred with the addition of Ca++ at pH 4.5. These data suggest that the acid PLase A2 is a component of the plasma membrane and is not due to lysosomal contamination since membrane-bound acidic PLase A2 properties are opposite to those found for lysosomal PLase A2.

Animals↗
PubMed1988

Inhibition of human gingival carcinoma cell growth by prostaglandins.

The inhibitory effects of various prostaglandins (PGA2, PGD2 and PGE2) on the growth of human gingival carcinoma cell line Ca 9-22 and human cervical carcinoma cell line HeLa were studied in vitro. 1. PGA2 and PGD2 significantly depressed Ca 9-22 cell proliferation in dose and time related fashion. 2. The inhibitory rate by PGs for Ca 9-22 cells exceeded than HeLa-cells. 3. IC50 value of PGD2 on growth of Ca 9-22 was calculated to be 4 micrograms/ml.

Cell Division↗
PubMed1988

[Effects of cibenzoline on myocardial ischemia].

The effect of cibenzoline, an antiarrhythmic drug, on myocardial ischemia was studied in the anesthetized open-chest dog. Ischemia was induced by completely ligating or partially occluding the left anterior descending coronary artery. The levels of ATP and creatine-phosphate decreased, and the ADP and AMP levels increased during ischemia. The level of glycogen was also decreased, and that of lactate was increased by ischemia, resulting in myocardial acidosis. Pretreatment with either 2 mg/kg or 8 mg/kg of cibenzoline prevented the decrease in ATP level and the increase in lactate level. These results suggest that cibenzoline reduces the influence of ischemia on the myocardium.

Adenosine Diphosphate↗
PubMed1988

MCl-176, a novel calcium channel blocker, attenuates the ischemic myocardial acidosis induced by coronary artery occlusion in dogs.

The effect of MCl-176 [2-(2,5-dimethoxyphenylmethyl)-3-(2-dimethylaminoethyl)-6- isopropoxy-4(3H)-quinazolinone hydrochloride], a novel calcium channel blocker, on ischemic myocardial acidosis was studied in the dog heart, in which the left anterior descending coronary artery was partially occluded for 90 min (partial occlusion). Myocardial pH (measured by a micro glass pH electrode) was about 7.60 in the nonischemic normal heart. The myocardial pH decreased rapidly in response to partial occlusion, and reached the steady state of about 6.85 within 30 min (i.e., the myocardial [H+] increased after partial occlusion). Saline or drug was injected i.v. 30 min after partial occlusion, and the drug effect was observed till the end of partial occlusion. Myocardial [H+], that had been increased by partial occlusion, restored slightly after the saline injection, and the restoration was about 30% 60 min after the injection. MCl-176 increased this spontaneous restoration of myocardial [H+] with a decrease in blood pressure and heart rate; the restoration induced by 0.1 mg/kg of MCl-176 was 74% 60 min after the injection. Even in the paced heart, MCl-176 (0.1 mg/kg) attenuated the ischemia-induced myocardial acidosis. Propranolol (1 mg/kg) also attenuated the myocardial acidosis, the restoration being 82%. These results indicate that MCl-176 attenuates the myocardial acidosis during ischemia as does propranolol, and that the mechanism of action of MCl-176 is not due primarily to a decrease in heart rate.

Acidosis↗
PubMed1987

Effects of kringles derived from human plasminogen on fibrinolysis in vitro.

Plasminogen kringle 1+2+3 (K1-3) containing lysine-binding sites inhibited the reaction of plasmin with alpha 2-plasmin inhibitor (alpha 2PI), in a rate assay using a synthetic chromogenic substrate, S-2251. However, K1-3 did not inhibit the reaction to any degree between alpha 2PI and mini-plasmin which lacked the kringle 1 to 4 portion of plasmin. These results suggest that K1-3 blocked the binding of alpha 2PI to the lysine-binding site of plasmin. In the urokinase (UK)-induced fibrinolysis, K1-3 shortened the human plasma clot lysis time at low concentration (0.5-6 microM), and prolonged the lysis time at a high concentration (20 microM). Similar results were obtained in the lysis time of a fibrin clot consisting of plasminogen, fibrinogen and alpha 2PI isolated from human plasma. The kringle 4 (K4) of human plasminogen did not accelerate human plasma clot lysis at any concentration (1.2-24.1 microM). Furthermore, in the tissue plasminogen activator (TPA)-induced fibrinolysis, K1-3 also shortened both the lysis time of human plasma clot and fibrin clot as observed in UK-induced fibrinolysis, but K4 did not. The above findings indicate that the reaction of alpha 2PI with the lysine-binding site of plasmin is involved in the inhibition of plasmin activity by alpha 2PI, and in the presence of an inhibitor of this reaction, the balance of coagulofibrinolytic activity in plasma will be shifted towards the fibrinolytic side.

Fibrinolysin↗
PubMed1987

Accumulation of nonesterified fatty acids in the dog myocardium during coronary artery occlusion determined by a method using 9-anthryldiazomethane.

The levels of nonesterified fatty acids (NEFA) in the myocardium during ischemia were determined by a simple method, which requires neither previous separation with thin-layer chromatography nor heating. After being extracted with Folch's solution, NEFA were subjected to fluorescent labeling with 9-anthryldiazomethane at room temperature, separation with high-pressure liquid chromatography, and then detection by a flow-through fluorometer. Calibration and validation studies revealed that this method was satisfactory. The left anterior descending coronary artery was completely occluded for 90 min in dogs anesthetized with pentobarbital. In the nonischemic myocardium, the levels of lauric, myristic, palmitic, palmitoleic, stearic, oleic, linoleic, and arachidonic acids were 5.31, 15.85, 47.06, 2.59, 23.92, 37.90, 38.69, and 3.99 nmol/g wet tissue, respectively, and those in the ischemic myocardium 5.67, 22.16, 75.94, 6.65, 42.67, 61.75, 70.06, and 13.39 nmol/g wet tissue, respectively, the total NEFA in the former being 175.3 and that in the latter 298.3 nmol/g wet tissue. The increase in myocardial NEFA during ischemia was significant except for lauric and myristic acids, and the increase in arachidonic acid was the greatest. The ratio of the level of arachidonic acid in the ischemic myocardium to that in the nonischemic myocardium was 335.6%.

Animals↗
PubMed1987

Relationship between coronary flow and adenosine release during severe and mild hypoxia in the isolated perfused rat heart with special reference to time-course change.

The contribution of endogenous adenosine to coronary vasodilation induced by global myocardial hypoxia was examined. In isolated rat hearts perfused by means of Langendorff's technique, the relationship between chronological changes in coronary flow and adenosine release during hypoxia was analyzed. The oxygenation level of myoglobin (MbO2), myocardial oxygen uptake, lactate release, and left ventricular pressure (LVP) was also measured. Adenosine was determined by radioimmunoassay, and the MbO2 levels by the optical method. Severe hypoxia (20% O2 + 75% N2 + 5% CO2) increased coronary flow, adenosine release, and lactate release and decreased both myocardial oxygen uptake and LVP. Mild hypoxia (50% O2 + 45% N2 + 5% CO2) also increased coronary flow, adenosine release, and lactate release, while it affected neither myocardial oxygen uptake nor LVP. These results suggest that the oxygen supply is compensated by an increase in coronary flow in mild hypoxia, whereas this does not occur in severe hypoxia. Changes in MbO2 were the reverse of those in coronary flow during severe hypoxia, confirming that a decrease in intracellular oxygen correlates well with an increase in coronary flow. The pattern of changes in adenosine release, however, was not identical with that in coronary flow in severe and mild hypoxia, indicating that there is no significant relationship between coronary flow and adenosine release in either severe or mild hypoxic hearts. These findings suggest that adenosine is not the only metabolic mediator of regulation of coronary flow in hypoxic hearts.

Adenosine↗
PubMed1987

Rapid procedure for preparation of macrophage plasma membrane.

This report describes a simple and efficient procedure for the isolation of plasma membrane from guinea pig peritoneal macrophages. The use of polycationic beads (Affi-gel 731 beads) facilitates rapid and high-clear separation of plasma membrane within 30 min. The final plasma membrane coated beads fraction has high specific activities of marker enzymes with little contamination with mitochondrial, lysosomal or cytoplasmal markers.

Animals↗
PubMed1987

Effect of nadolol, a beta-adrenoceptor blocking agent, on myocardial metabolism in the dog ischaemic heart.

The effect of nadolol at a dose of 1 mg kg-1, i.v. on the ischaemic myocardial metabolism has been examined in the dog. Ischaemia was induced by ligating the left anterior descending coronary artery for 3 min, and nadolol was injected 5 min before ligation. Ischaemia caused myocardial metabolic changes; it decreased energy charge potential and inhibited glycolytic flux through phosphofructokinase reaction. Pretreatment with nadolol lessened the decrease in energy charge potential and the inhibition of glycolytic flux being caused by ischaemia. Nadolol may have a beneficial effect on the ischaemic myocardium.

Adenine Nucleotides↗
PubMed1987

Cloning and characterization of Streptococcus mutans LM7 plasmid pAM7.

The 5.6-kilobase-pair cryptic plasmid, pAM7, of Streptococcus mutans LM7 was cloned into Escherichia coli plasmids or a shuttle plasmid to examine whether the plasmid encodes bacteriocin. Plasmid pAM7 encoded proteins with molecular weights of 30,000, 22,000, and 12,000, but none of them appeared to be bacteriocin.

Bacterial Proteins↗