Search PubMed⌕ Search

Biomedical subjects

K Asai

Publications and source records attributed to K Asai.

At least 235 records · Page 13Linked to original sources
PubMed1989

Fibrinogen is chemotactic for vascular smooth muscle cells.

We studied the effect of fibrinogen on the migration of bovine aortic smooth muscle cells in culture, using a Neuro Probe 48-well micro chemotaxis chamber. Fibrinogen stimulated the migration of the cells dose-dependently at concentrations from 30 to 1000 micrograms/ml. A modified checkerboard analysis of the response demonstrated that the effect was largely chemotactic in nature. The present results suggest that fibrinogen may play an important role in the pathogenesis of arterial intimal thickening and atherosclerosis.

Animals↗
PubMed1989

An epidemiological investigation of emotional and behavioral problems in primary school children in Japan. The report of the first phase of a WHO collaborative study in Western Pacific Region.

1860 primary school children, aged from 6 to 12 years, from urban suburban and rural areas in Japan were assessed by their school teachers according to the Rutter scale. The prevalence of children with deviant scores in the general population was 3% and this figure was lower than that for any other country assessed by the same scale. Eighty-four percent of the deviants were of an antisocial type but only 7% were neurotic. The ratio of antisocial to neurotic was higher than those from other countries. The prevalence of children with deviant scores was higher in boys than in girls, and also higher in early and middle school years than in late school years. Area, family occupation, sibship size, birth order and one-parent family had only limited effects on the deviant behaviour of the children.

Affective Symptoms↗
PubMed1989

Characteristics of collagenase in experimental periapical granulomas from the teeth of dogs.

Periapical granulomas were induced, with a success rate of about 60% (66 granulomas produced out of 109 roots treated) in mandibular premolars. The average wet weight of the granulomas, 46.1 +/- 34.5 mg (mean +/- SD, n = 22), was sufficient to allow individual specimens to be used for most of the biochemical analyses. High collagenase activity was extracted directly from the granulomas with 4 M urea solution. The enzyme was a typical animal collagenase (EC 3.4.24.7) which clove native collagen molecules into three-quarter (alpha A) and one-quarter (alpha B) length fragments. The collagenase was activated by 1 mM p-aminophenylmercuric acetate. This activated enzyme broke down collagen I rather than collagen III preferentially, which is similar to the activity of human polymorphonuclear leucocyte collagenase. The molecular weights of the latent and activated collagenases were 67 and 49 K, respectively.

Animals↗
PubMed1989

Beta-migrating very low density lipoprotein attenuates endothelium-dependent relaxation in rabbit atherosclerotic aortas.

We studied the effects of beta-migrating very low density lipoprotein (beta-VLDL) on the vascular responses of isolated thoracic aortic preparations taken from normal and hypercholesterolemic rabbits. The endothelium-dependent relaxation induced by acetylcholine or adenosine triphosphate (ATP) was attenuated in the arteries from hypercholesterolemic rabbits that were fed a cholesterol-rich diet for 12 weeks. In these aortas, the lesional circumference of the atherosclerotic plaques (fatty streaks) was only 12.18 +/- 1.98%. The relaxation induced by the Ca2+ ionophore A23187 or nitroglycerin was not altered. Preincubation with beta-VLDL significantly inhibited the relaxation due to acetylcholine, ATP, or A23187, especially in the aortas of hypercholesterolemic rabbits. However, beta-VLDL did not alter the response to nitroglycerin. Preincubation with high density lipoprotein had no significant effect on vessel relaxation. These results indicated that endothelium-dependent relaxation was already inhibited in the early stages of atherosclerosis, and that the atherogenic lipoprotein, beta-VLDL, further inhibited endothelium-dependent relaxation in atherosclerotic aortas. It may be that beta-VLDL also plays a role in determining the level of vascular tonus in atherosclerosis.

Acetylcholine↗
PubMed1989

Identification of benzoylcarnitine in the urine of a patient of hyperammonemia.

Benzoylcarnitine was identified in the urine of a patient with a carbamoyl-phosphate synthase I deficiency for whom sodium benzoate and L-carnitine had been used to treat hyperammonemia. This is a newly identified metabolite of benzoate. Its excretion in the urine was increased day by day at the administration of both sodium benzoate and L-carnitine from 0.10 to 2.25 mmol/g creatinine. Since there is the possibility of a secondary carnitine deficiency and an increase of benzoyl toxicity after long-term therapy with benzoate supplementation and protein restriction, it is important to monitor the urinary excretion of benzoylcarnitine.

Ammonia↗
PubMed1989

Vascular endothelial cell migration in vitro roles of cyclic nucleotides, calcium ion and cytoskeletal system.

According to the response to injury hypothesis, endothelial migration and repair may play an important role in the initiation and progression of atherosclerosis. In this study, we examined the regulatory mechanisms of endothelial cell migration in vitro, using cultured endothelial cells from fetal bovine aortas. Dibutyryl cyclic AMP, 8-bromo cyclic GMP, and theophylline (each at concentrations of 10(-4) to 10(-3) M) inhibited the migration of endothelial cells. Migration was not significantly affected by the Ca2+ channel blockers diltiazem (10(-6) to 10(-4) M) and nicardipine (10(-6) to 10(-5) M) or by La3+ (10(-4) to 10(-3) M), an inorganic Ca2+-antagonist, TMB-8 (10(-6) to 5 x 10(-5) M), an intracellular Ca2+ blocker, or the calmodulin inhibitors W-7 (10(-6) to 5 x 10(-5) M) and trifluoperazine (10(-7) to 10(-5) M). At the extracellular Ca2+ concentrations of less than 0.2 mEq/l, the migration was inhibited significantly. In addition, migration was markedly suppressed by colchicine (10(-8) to 10(-5) M), an inhibitor of tubulin polymerization, and by cytochalasin B (10(-7) to 10(-5) M), an inhibitor of actin polymerization. These results suggest that cyclic nucleotides, such as cyclic AMP and GMP, may regulate the migration of vascular endothelial cells. Although a low concentration of extracellular Ca2+ is essential to their migration, participation of the intracellular Ca2+-calmodulin system was not evident in this study. It appears that the cytoskeletal system, including microtubules and microfilaments, is involved in the mechanisms of migration.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

Role of platelet secretory products in modified lipoprotein metabolism in macrophages.

Macrophage-derived foam cells and platelets are found in many lesions of atherosclerosis. Macrophages possess scavenger receptors that take up modified low density lipoproteins (LDL) like acetylated or acetoacetylated LDL (aLDL, aaLDL) resulting in accumulation of esterified cholesterol (EC) and acquisition of the characteristics of foam cells. We obtained a certain platelet secretory product from washed platelet-rich plasma which had been frozen and thawed three times (PSP alpha). We studied the effect of PSP alpha in modified lipoprotein metabolism in macrophages. When mouse or human macrophages were incubated with aaLDL and PSP alpha, much more EC was accumulated than with aaLDL only. Though the increase in EC of macrophages was dependent on the concentration of PSP alpha, it declined in high concentrations of PSP alpha. PSP alpha moderately increased 125I-aaLDL binding and cellular metabolism. PSP alpha also affected 125I-oxidized LDL binding and cellular metabolism, but it did not affect the metabolism of 125I beta-migrating very low density lipoprotein (beta VLDL). These results suggest that substances shed by activated platelets play a role in atherosclerosis as potent mediators of EC accumulation in macrophages and by affecting the receptor-mediated endocytosis of modified lipoproteins.

Animals↗
PubMed1988

Evidence for the expression of a primitive intestinal-like alkaline phosphatase in the intestinal 407 cell line.

Intestinal-like alkaline phosphatase was found to be expressed in the intestinal 407 cell line. This enzyme was identified by use of monoclonal antibodies specific for human placental (H7 and HPMS-1) and intestinal alkaline phosphatase (2HIMS-1 and 2HIMS-3) separately. Purification of this isozyme by use of two different monoclonal antibody immunoaffinity chromatographies demonstrates a single protein band on SDS-polyacrylamide gel electrophoresis indicating that this enzyme is not formed as a heterodimer. The apparent monomer subunit molecular weight and the dimer molecular weight of this isozyme were determined to 70000 and 160000, respectively. The enzyme is a homodimer according to molecular weight determinations. Furthermore, this isozyme is neuraminidase sensitive and comparatively heat stable, properties also characteristic for the placental enzyme. Our data suggest that the intestinal-like alkaline phosphatase in the intestinal 407 cell line displays properties intermediate of the intestinal and placental isozymes which may reflect the existence and reexpression of a new primitive isozyme.

Alkaline Phosphatase↗
PubMed1988

Urinary acylcarnitines in a patient with neonatal multiple acyl-CoA dehydrogenation deficiency, quantified by a carboxylic acid analyzer with a reversed-phase column.

A quantitative analysis for urinary acylcarnitines in a patient with neonatal multiple acyl-CoA dehydrogenation deficiency is described. This method (liquid chromatography) can quantify twelve acylcarnitines including glutarylcarnitine and 3 isomeric acylcarnitines (butyryl-1, valeryl- and octanoylisomer) in urine. Before and up to the 15th hour of DL-carnitine therapy, isovalerylcarnitine was the largest single component existing in urinary acylcarnitines. Its excretion increased approximately 10 times within 1 day of DL-carnitine therapy. However, the acetyl-, the isobutyryl- and the butyrylcarnitine values increased gradually. From the 8th day of the therapy, the isobutyrylcarnitine value exceeded the isovalerylcarnitine. The patient's dominant urinary specific acylcarnitine derived from amino acids oxidation deficiency was changed from isovalerylcarnitine(leucine) to isobutyrylcarnitine(valine) during the early period of DL-carnitine therapy. Glutarylcarnitine was a minor component in the urine. Its degree of increase was as small as that of octanoylcarnitine. 2-Methylbutyrylcarnitine and propionylcarnitine were not detected.

Acyl-CoA Dehydrogenase↗
PubMed1988

Chemotactic response of vascular smooth muscle cells to acetoacetylated low-density lipoprotein.

We studied the effect of acetoacetylated low-density lipoprotein (LDL), which is recognized by the scavenger receptor, on the migration of fetal bovine aortic smooth muscle cells in culture, using a Neuro Probe 48-well microchemotaxis chamber. Acetoacetylated LDL is chemotactic and chemokinetic for the smooth muscle cells, and the effect is maximal with 50 micrograms/ml of protein, while native LDL has no significant chemotactic activity. These results suggest that denatured LDL might play an important role in the recruitment of smooth muscle cells from the media into the intima in atherosclerosis.

Animals↗
PubMed1988

Effects of splenectomy on serum lipids and experimental atherosclerosis.

The authors examined the effects of splenectomy on serum lipids in patients with hematologic disease, in rabbits, and also in cholesterol-fed rabbits with experimental atherosclerosis. Serum cholesterol was determined in patients with hypersplenism before and after splenectomy. Meanwhile serum lipids were determined in two groups of rabbits: splenectomy group (Spx group, n = 19), and sham operation group (Sham group, n = 14) before and after the operation. Then the rabbits were divided into four subgroups: cholesterol-fed groups--Spx-C (n = 12) and Sham-C (n = (9), and normal-chow-fed groups--Spx-N (n = 7) and Sham-N (n = 5). The Spx-C and the Sham-C rabbits were fed 1% cholesterol diet and the Spx-N and Sham-N rabbits were fed normal chow for twelve weeks. In patients preoperative serum cholesterol levels were low, and significant increase in serum cholesterol was observed following splenectomy. In rabbits, the Spx-C group showed significantly higher levels of serum cholesterol, triglycerides, and phospholipids in contrast to lower levels of high density lipoprotein cholesterol, as compared with the Sham-C group. The percentage of aortic plaque area in the Spx-C group tended to be higher than that in the Sham-C group. On the other hand, the Spx-N and the Sham-N group showed no difference in serum lipids during twelve weeks. The worsening of atherosclerosis in the Spx-C group was considered to be mainly due to an enhanced hyperlipidemia. Their results suggest a possible role of the spleen in lipid metabolism, in particular the existence of a splenic factor that can cause hypocholesterolemia in hyperplenism and can suppress hyperlipidemia.

Adolescent↗
PubMed1988

Cholesterol metabolism in inherently scorbutic rats (ODS rats).

We observed the cholesterol metabolism of a colony of Wistar rats with a hereditary defect in vitamin C synthesizing ability (the ODS (osteogenic disorder-Shionogi) rats) in six kinds of experiments. Female ODS rats aged 36 days had a low HDL (high-density lipoprotein)-cholesterol level in serum as compared with age-matched control rats in spite of the absence of scorbutic symptoms. Female ODS rats aged 63 days which revealed severe scorbutic symptoms had a very low HDL-cholesterol level (mean value; 17 mg/dl). And male ODS rats, whose lives had been prolonged by supplementing with L-ascorbic acid, also had lower serum HDL-cholesterol and had increased total cholesterol in serum and liver when the acid supplement dose was relatively insufficient. On the other hand, we examined HDL2- and HDL3-cholesterol levels in serum to determine the mechanism of low HDL-cholesterol. As a result, we observed a low HDL2-cholesterol level in ODS rats but normal HDL3-cholesterol level. But the authors observed no decrease of LCAT (lecithin: cholesterol acyltransferase) activity in serum of ODS rats. These results could be due to disturbance of lipid metabolism in a vitamin C-deficient condition, that is to say, there might be abnormalities of the cholesterol excretion pathway of bile acid from liver, and maturity of the HDL-cholesterol particle due to other factors except that of LCAT activity.

Animals↗
PubMed1987

Risk factors of atherogenicity in inherently scorbutic rats (OD rats).

We observed the pathophysiological state of a colony of Wistar rats with a hereditary defect in vitamin C-synthesizing ability (the OD rat) in three kinds of experiments. In experiment 1, OD rats that were not supplemented with L-ascorbic acid (ASA) were killed 36 days after birth. In experiment 2, OD rats that were not supplemented with AsA were killed 63 days after birth. In experiment 3, OD rats that were supplemented with sufficient ASA (100 mg/100 g body weight/day) for 16 days from 47 days after birth were assayed 63 days after birth. From analyses of serum chemistry, platelet aggregability and counts of blood cells, some atherogenic risk factors were elucidated, that is, there was a decrease of high density lipoprotein in serum and an increase of platelet aggregability. Furthermore, it was observed that OD rats have some characteristics different from latent vitamin C-deficient animals from the viewpoint of malnutrition.

Alanine Transaminase↗