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Biomedical subjects

O Yasuda

Publications and source records attributed to O Yasuda.

29 records · Page 2Linked to original sources
PubMed1993

Effects of beraprost sodium, a stable analogue of prostacyclin, on hyperplasia, hypertrophy and glycosaminoglycan synthesis of rat aortic smooth muscle cells.

The effects of beraprost sodium, a stable analogue of prostacyclin, on the syntheses of DNA, protein and glycosaminoglycans (GAG) of cultured vascular smooth muscle cells (SMC) were studied. SMC were isolated from the thoracic aorta of male Wistar rats. The syntheses of DNA, protein and GAG of SMC were determined by incorporations of [3H]thymidine, [3H]leucine and [35S]sulfuric acid, respectively. Insulin at a concentration of 10(-6) M stimulated DNA synthesis 4 fold compared to control. Beraprost sodium suppressed the insulin-stimulated DNA synthesis dose-dependently at concentrations greater than 10(-7) M and suppressed it by 68% at 10(-5) M. Platelet derived growth factor (PDGF) at a concentration of 20 ng/ml stimulated DNA synthesis 6 fold compared to control. Beraprost sodium suppressed the PDGF-stimulated DNA synthesis dose-dependently at concentrations greater than 10(-7) M and suppressed it by 51% at 10(-5) M. Beraprost sodium suppressed GAG synthesis dose-dependently at concentrations greater than 10(-7) M and suppressed it by 49% at 10(-5) M. However, beraprost sodium at concentrations up to 10(-5) M did not affect protein synthesis. These results indicate that beraprost sodium suppressed the proliferation and GAG synthesis of SMC but did not affect hypertrophy. Beraprost sodium may be a potent antiarteriosclerotic agent through suppression of hyperplasia of SMC and modification of matrix protein.

Animals↗
PubMed1992

Effect of ipriflavone on bone mineral density and calcium-related factors in elderly females.

The effects of ipriflavone (7-isopropoxy-3-phenyl-4H-1-benzopyran-4-one) on bone mineral density (BMD) of the 3rd lumbar vertebra and on calcium (Ca)-related factors, including serum calcitonin (CT) levels before and after rapid calcium infusion (4 mg/kg for 5 minutes), were studied in 11 elderly female subjects (80 +/- 2 years of age, mean +/- SE). Ipriflavone (IP) administration (600 mg/day, 7 months) resulted in inhibition of BMD loss in 7 patients (responders, mean change of BMD value 2.2 +/- 2.3%), whereas 4 patients showed a loss of BMD (nonresponders, mean change of BMD value -13.1 +/- 2.6%) compared with pretreatment values. The responder group showed a significant increase in mean pretreatment serum CT levels (from 20 +/- 2 pg/ml to 42 +/- 7 pg/ml, P < 0.05) after treatment with IP, and a significant decrease in the mean basal serum level of corrected Ca (from 9.6 +/- 0.2 mg/dl to 8.7 +/- 0.1 mg/dl, P < 0.01) after treatment with IP; nonresponders did not show these changes. For responders, both the percentage of change and the maximal value of serum CT in response to Ca infusion were maintained at rather high levels, both before and after IP treatment; nonresponders showed almost no response to a stimulation test for CT. These findings suggest that IP inhibits bone loss in elderly female subjects possibly through the mechanism of increasing CT secretion.

Aged↗
PubMed1992

Circulating suppressing factor for the muscarinic acetylcholine receptor in patients with senile dementia of the Alzheimer type.

Circulating suppressing factor for the binding of quinuclidinyl benzilate (QNB), an antagonist for the muscarinic acetylcholine receptor, to the synaptic membranes was evaluated in 48 patients with senile dementia of the Alzheimer type (SDAT), in 17 patients with the vascular type dementia (VTD) and in 11 nondemented elderly subjects (NE). The mean suppression rate on the binding in the SDAT group was significantly greater than that in the NE group, although that in the VTD group was similar to that in the NE group. Moreover, the percent QNB binding was significantly (p < 0.05) correlated with the score of the mini-mental state in the SDAT group. The circulating suppressing factor may participate in the pathogenesis of SDAT.

Aged↗
PubMed1992

Bradykinin suppresses endothelin-induced contraction of coronary, renal and femoral arteries through its B2-receptor on the endothelium.

Effect of bradykinin (BK) on endothelin-1 (ET-1)-induced vasoconstriction and its mechanism were investigated. The development of isometric force of arterial rings of canine coronary, renal and femoral arteries was recorded using a organ bath containing Krebs-Henseleit buffer aerated with 95% O2 and 5% CO2. ET-1 at more than 10(-9) M dose-dependently induced vascular contraction similarly among the three arteries. BK at more than 10(-8) M dose-dependently suppressed the ET-1-induced vasoconstriction only in the presence of endothelium, and the effect of BK was largest in the coronary arteries. The BK-induced suppression was not affected by addition of des-Arg9-[Leu8]-BK, an antagonist for B1-receptor, but did be completely reversed by addition of B2-receptor antagonist (10(-6) M) [D-Arg0,Hyp3,Thi5,8,D-Phe7]-BK. The BK's suppression of the ET-1-induced vasoconstriction was partly reversed by additions of each 10(-5) of Ng-nitro-L-arginine, a substrate inhibitor of nitric oxide, methylene blue, an inhibitor of soluble guanylate cyclase, or indomethacin, an inhibitor of cyclooxygenase. The reversing effects of methylene blue and indomethacin were additive. BK suppresses the ET-1-induced vasoconstriction through B2-receptor on the endothelium. Both endothelial nitric oxide and prostaglandin(s) are participated in the BK's effect.

Animals↗
PubMed1992

Effects of manidipine hydrochloride on proliferation and glycosaminoglycan synthesis of cultured vascular smooth muscle cells.

The effects of manidipine hydrochloride, a calcium channel blocker, on the proliferation and the synthesis of glycosaminoglycans (GAG) in cultured rat aortic vascular smooth muscle cells (VSMC) were studied. Mandipine hydrochloride suppressed the DNA synthesis of VSMC dose dependently at concentrations of more than 10(-8) M. Mandipine hydrochloride 10(-6) M suppressed proliferation of VSMC to 50% of the control value. Manidipine hydrochloride stimulated the synthesis of GAG at concentrations above 10(-11) M. Manidipine hydrochloride 10(-8) M stimulated synthesis of GAG to 450% of control. Our findings suggest that because mandipine hydrochloride suppresses proliferation and stimulates GAG synthesis of VSMC, it may be an anti-arteriosclerotic agent.

Animals↗
PubMed1992

EDTA induces differentiation and suppresses proliferation of promyelocytic leukemia cell line HL-60--possible participation of zinc.

Effects of ethylenediaminetetraacetic acid (EDTA), a chelator of divalent cations, on the proliferation and differentiation of human promyelocytic leukemia cell line HL-60 were examined. Incubation of HL-60 cells with 200 microM of EDTA suppressed cell proliferation, and induced differentiation assessed by reductivity of nitro blue tetrazolium and activity of alpha-naphthyl butyrate esterase. These effects were inhibited by zinc (Zn) dose-dependently at concentrations of up to 20 microM, but not by other divalent cations including Ca, Mg, Fe, Cu, Ni, or Cd. Although addition of 200 microM EDTA for 24 hr decreased the c-myc mRNA level of HL-60 cells, coaddition of 20 microM of Zn also reversed this effect on c-myc mRNA level. Treatment with EDTA did not change the half-life time of degradation of c-myc mRNA after addition of actinomycin D (5 micrograms/ml). These findings suggest that Zn deficiency suppresses c-myc gene transcription which is followed by suppression of proliferation and induction of differentiation of HL-60 cells.

Blotting, Northern↗
PubMedDate not supplied

Relation between low serum cholesteryl-ester transfer activity and abdominal aortic calcification in normolipidemic elderly subjects.

We studied the relation between cholesteryl-ester transfer activity (CETA) and abdominal aortic calcification in elderly subjects. Compared with 10 young healthy subjects (mean +/- S.D. age, 27 +/-2 years) and to 26 elderly subjects without abdominal aortic calcification (79 +/- 7 years), 16 elderly patients with abdominal aortic calcification (82 +/- 6 years) had significantly lower levels of serum CETA. However, there were no differences in the levels of serum lipids and apolipoproteins, including total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol and apolipoproteins A-I, A-II, B, C-II and E, between the two elderly groups. When the two groups of elderly subjects were considered together, the level of serum CETA did not correlate significantly with any lipids and apolipoproteins. These results provide evidence that CETA may prevent the development of aortic calcification in normolipidemic elderly people.

Journal Article↗
PubMedDate not supplied

Differential expression of the alpha1 type VIII collagen gene by smooth muscle cells from atherosclerotic plaques of apolipoprotein-E-deficient mice.

We have investigated the morphology, growth and gene expression of smooth muscle cell (SMC) cultures derived from advanced atherosclerotic plaques and from non-plaque-containing aorta of individual apolipoprotein-E-deficient mice. The initial outgrowth of cells was faster from plaques (P) than from non-plaque segments (NP), but the cells in P cultures divided more slowly than NP cells in subcultures. By the 6th passage, the general growth pattern, morphology, ploidy and response to mitogenic factors of the cells were no longer consistently different in P and NP cultures. However, by the use of differential display, several transcripts were identified that were differentially expressed in three independent pairs of P and NP cultures. One of the transcripts, from a type VIII collagen gene, was elevated in all the P cultures compared to their NP counterparts even at the 40th passage. The alpha1 type VIII collagen transcripts were also readily detectable by RT-PCR in freshly dissected plaques, but not in the normal parts of aortas from the apolipoprotein-E-deficient mice. In situ hybridization showed that the transcripts were limited to the fibrous cap of plaques. Thus, SMCs from atherosclerotic plaques produce type VIII collagen and this differential expression continues when the cells are maintained in tissue culture.

Animals↗