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Biomedical subjects

Hiroyuki Daida

Publications and source records attributed to Hiroyuki Daida.

63 records · Page 4Linked to original sources
PubMed2003

R/R genotype of human paraoxonase (PON1) is more protective against lipoprotein oxidation and coronary artery disease in Japanese subjects.

Human paraoxonase (PON1) is an high-density lipoprotein (HDL) -associated enzyme that is proposed to protect against the oxidation of lipoproteins. Recently, the association of coronary artery disease (CAD) and PON1 activity was reported. Furthermore, the R/R genotype of PON1 has been related to the risk for CAD. In this study we investigated the PON1 genotype and susceptibility to lipoprotein oxidation to elucidate the contribution of PON1 to atherosclerosis in Japanese subjects. We studied 179 patients who underwent coronary angiography and their PON1 genotypes were determined. Lipoproteins were obtained from a patient's blood after at least 12 hours fasting and were separated with sequential ultracentrifugation. We analyzed the thiobarbituric acid reactive substances (TBARS) and continuously monitored the copper-induced oxidation three genotype groups. Genotype frequencies of Q/Q, Q/R, and R/R were 21.2%, 36.9%, and 41.9%, respectively. PON1 polymorphism clearly determined the lipid oxidation. The R/R genotype of PON1 had significantly lower levels of plasma and HDL TBARS and significantly retarded the initiation of oxidation in HDL and low-density lipoprotein (LDL). The R/R genotype was related to the lower prevalence of CAD. The PON1 genotype clearly determined the oxidative modification of lipoproteins and may play a role in the pathogenesis of atherosclerosis via its protective effect against lipoprotein oxidation in Japanese subjects.

Adult↗
PubMed2003

[Coronary artery disease].

Hypertension are at high risk for cardiovascular morbidity and mortality in patients with coronary heart disease. Although the benefits of antihypertensive therapy in such patients are well established, control of high blood pressure still insufficient. In this review, we discussed about some problems in management of blood pressure especially in patients with coronary heart disease, contents; unique nature of coronary circulation, J-curve hypothesis, drug usage for special situations. We should understand the importance of antihypertensive therapy, and should perform positive treatment.

Antihypertensive Agents↗
PubMed2002

Platelets activated by collagen through immunoreceptor tyrosine-based activation motif play pivotal role in initiation and generation of neointimal hyperplasia after vascular injury.

BACKGROUND: Platelet adhesion on components of the extracellular matrix and platelet activation by those components are crucial for the arrest of posttraumatic bleeding, but they can also harm tissue by occluding diseased vessels. Recent studies have shown that the activation of platelets by collagen is mediated through the same pathway used by immune receptors, with an immunoreceptor tyrosine-based activation motif on the Fc receptor gamma chain (FcRgamma) playing a pivotal role. METHODS AND RESULTS: We examined the role of collagen-stimulated platelets in the development of injury-induced neointimal formation by using mice deficient in FcRgamma. The left femoral arteries of 8- to 12-week-old FcRgamma-deficient mice (n=16) and C57BL/6 (wild-type) mice (n=16) were injured by a straight spring wire (0.35-mm diameter). Segments of the injured and uninjured femoral arteries were excised at 7 days and 28 days after the vascular injury. Arterial segments were examined by immunohistochemistry and electron microscopy. Two hours after injury, electron microscopy showed marked decreases in platelet adhesion and neutrophil attachment to the vascular wall surface in FcRgamma-knockout mice compared with wild-type mice. At 7 days after injury, staining with anti-neutrophil antibody showed fewer neutrophils in FcRgamma-knockout mice than in wild-type mice. Computer-aided morphometry performed to measure the neointimal area, intima/media ratio, and stenotic area at 28 days after injury showed a significantly smaller ratio and area in FcRgamma-knockout mice than in wild-type mice (for neointimal area, 16 635 +/- 1406 versus 31 483 +/- 2309 microm2, respectively; for intima/media ratio, 1.25 +/- 0.40 versus 2.68 +/- 0.04, respectively; and for stenotic area, 26.8 +/- 2.1% versus 49.3 +/- 4.1%, respectively). CONCLUSIONS: These results demonstrate that FcRgamma may play important roles in the initiation and generation of neointimal hyperplasia after balloon injury through the activation of platelets by collagen.

Adaptor Proteins, Signal Transducing↗
PubMed2002

Effect of BO-653 and probucol on c-MYC and PDGF-A messenger RNA of the iliac artery after balloon denudation in cholesterol-fed rabbits.

Antioxidants have been proposed as a promising treatment for restenosis after percutaneous transluminal coronary angioplasty (PTCA), but their mechanism of action remains unclear. Here, we investigated the effect of antioxidants on gene expression in the artery after balloon denudation. We developed a sensitive ribonuclease (RNase) protection assay for the messenger RNA (mRNA) levels of immediate early (IE) genes (c-jun, c-fos and c-myc), as well as platelet-derived growth factor-A (PDGF-A), platelet-derived growth factor-beta receptor, transforming growth factor-beta 1, and vascular endothelial growth factor. New Zealand White rabbits were fed a 0.17% cholesterol diet containing vehicle, BO-653 or probucol, and balloon denudation for iliac arteries was performed. The iliac arteries were then removed at 4 h after the denudation, for IE genes, and 10 days after for growth factors and receptors. Both BO-653 and probucol significantly reduced neointimal thickening, compared with the control. In terms of gene expression, BO-653, but not probucol, significantly inhibited c-myc induction. On the other hand, probucol, but not BO-653, significantly inhibited PDGF-A expression. Neither treatment had any effect on the expression of other genes. These results suggest that antioxidants affect the gene expression of the neointimal response and that both BO-653 and probucol inhibit gene expression in specific manners.

Analysis of Variance↗
PubMed2002

Lipid compositional differences of small, dense low-density lipoprotein particle influence its oxidative susceptibility: possible implication of increased risk of coronary artery disease in subjects with phenotype B.

An increased susceptibility of low-density lipoprotein (LDL) to lipid peroxidative modification may be a key factor in the higher risk of coronary artery disease (CAD) among subjects with phenotype B. Compositional differences in the LDL particle may also be implicated in its atherogenicity and, in particular, may be associated with varying degrees of oxidative susceptibility of LDL, although this remains unclear. We hypothesized that the oxidative susceptibility of small, dense LDL was directly influenced by its lipid composition, which may lead to an increased risk of CAD in subjects with phenotype B. To test this hypothesis, we compared the differences in lipid compositions of LDL particles from subjects with phenotype A and those with phenotype B, and investigated the direct association of lipid composition with susceptibility to lipid peroxidative modification in 102 subjects who underwent a coronary angiographic examination. Subjects with phenotype B (n = 52) had a significantly higher incidence of CAD than subjects with phenotype A (77% v 44%; P <.005). In comparing the oxidative susceptibility of LDL, the lag time was significantly reduced in subjects with phenotype B compared to phenotype A (48.7 +/- 8.6 v 41.5 +/- 5.5 minutes; P <.0001). In addition, the lag time showed a positive correlation with LDL-peak particle diameter (PPD) (r = 0.324, P <.005). Lipid composition per LDL particle was expressed as the ratio of lipid content to apolipoprotein B (apoB) content (wt/wt). Subjects with phenotype B showed a significant depletion in the contents of free-cholesterol (FC), cholesterol ester (CE), and phospholipid (PL) per particle compared to subjects with phenotype A, although there was no significant difference in the triglyceride (TG) content per LDL particle. Except for TG, the lipid content per LDL particle showed a significant positive correlation with lag time in all subjects. Moreover, increased susceptibility of small, dense LDL to lipid peroxidative modification was most strongly associated with a depleted FC content per LDL particle. In conclusion, the greater risk of CAD in subjects with phenotype B may result, in part, from increased susceptibility to lipid peroxidative modification of LDL that is depleted in lipid contents, especially FC content per LDL particle.

Aged↗
PubMed2002

Triggers and circadian distribution of the onset of acute aortic dissection.

The purpose of this study was to clarify the activities that trigger the onset of acute aortic dissection (AAD) and their relation to the occurrence of AAD. The study group comprised 444 consecutive patients referred for spontaneous AAD. From the hospital medical records, the activities that triggered AAD could be identified in 307 of these: most (86.6%) AAD episodes occurred in relation to physical (73.6%) or mental (13%) activities. In the older (> or =61 years) population, AAD occurred significantly more frequent during sleep or rest than in the younger (< or =60 years) population (16.9% vs 7.6%, p=0.020). The relationship between the time of onset and the triggering activity of AAD could be assessed in 267 patients. The onset of AAD was predominantly during the day: 63.3% of the episodes occurred between 06.00h and 18.00h, and were significantly more related to physical or mental activities than the nighttime events (95.3% vs 70.4%, p<0.0001). Most (86.6%) of the AAD episodes were related to physical or mental stress, particularly those that occurred during the day.

Acute Disease↗
PubMed2002

Predictive value of the adipocyte-derived plasma protein adiponectin for restenosis after elective coronary stenting.

The purpose of this study was to test the hypothesis that plasma levels of adiponectin can predict angiographic in-stent restenosis after coronary stenting. We prospectively examined adiponectin levels in 127 consecutive patients undergoing elective coronary stenting. Restenosis was defined as more than 50% stenosis at follow-up study by quantitative coronary angiography. There were no significant differences in the clinical characteristics or angiographical findings between the groups with restenosis and no restenosis. The levels of adiponectin did not differ between the restenosis group and the no restenosis group (5.7 +/- 2.8 vs 5.9 +/- 3.6 microg/mL, p = 0.72). The plasma levels of adiponectin were not related with the late loss index after coronary stenting (r = 0.01, p = 0.89). The levels of adiponectin were significantly lower in men than in women (5.5 +/- 3.2 vs 8.8 +/- 3.7 microg/ mL, p < 0.001), and negatively correlated with body mass index (r = -0.21, p = 0.01). We analyzed adiponectin levels in male, female, obese, non-obese, diabetes, and non-diabetes patients, however, there were no significant differences between the restenosis group and no restenosis group. This study has demonstrated that the measurement of adiponectin could not predict angiographic restenosis after elective coronary stenting, whereas the plasma levels of adiponectin were associated with some coronary risk factors in patients with coronary artery disease.

Adiponectin↗