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Biomedical subjects

H Daida

Publications and source records attributed to H Daida.

At least 19 recordsLinked to original sources

Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta.

AIMS/HYPOTHESIS: Several epidemiological data suggest that patients with postprandial hyperglycaemia are at high risk of cardiovascular disease. The aim of this study was to elucidate the effect of a glucose 'spike' on monocyte adhesion to rat aortic endothelial cells. MATERIALS AND METHODS: Monocyte adhesion to endothelial cells in vivo was quantitated using an en face method for observation of endothelial surface after immunohistochemical staining for CD68 in the thoracic aortas of Sprague-Dawley rats after several kinds of blood glucose rises. RESULTS: The number of monocytes adhering to endothelial cells increased at 30 min after injection of glucose in 8-week-old Sprague-Dawley rats. The increased adhesion returned to the basal level at 120 min after glucose injection, concomitantly with the return of blood glucose levels to normal. The infusion of octreotide to inhibit endogenous insulin secretion did not prevent the glucose-induced increase in monocyte adhesion to endothelial cells. On the other hand, the number of monocytes adhering to endothelial cells did not increase in rats with streptozotocin-induced diabetes and sustained hyperglycaemia. CONCLUSIONS/INTERPRETATION: Our data demonstrate that a temporary rise in blood glucose levels can in itself promote a reversible increase in monocyte adhesion to arterial endothelial cells.

Animals↗

Adeno-associated virus-mediated human IL-10 gene transfer suppresses the development of experimental autoimmune orchitis.

Testicular germ cell-induced autoimmune orchitis is characterized by inflammatory cell infiltration followed by disturbance of spermatogenesis. Experimental autoimmune orchitis (EAO) is an animal model for human immunological male infertility; delayed-type hypersensitivity (DTH) response plays a key role in its induction. Interleukin-10 (IL-10) is a regulatory cytokine that is critical in preventing organ-specific autoimmune inflammation. To determine the effects on EAO of human IL-10 (hIL-10) gene transfer, C3H/He mice immunized by unilateral testicular injury were administered intramuscular (i.m.) injections of adeno-associated viral (AAV) vector-encoding hIL-10 on the day of immunization. Serum hIL-10 was detected beginning at 1 week postinjection, and peaked at 3 weeks. Histological examinations showed a significantly low incidence of orchitis and disturbance of spermatogenesis in AAV hIL-10-treated mice, and the DTH response to autologous testicular cells was significantly suppressed. Immunohistochemical analysis of IFN- and IL-2, T-cell-associated cytokines, in the spleen and testes revealed significantly fewer cytokine-expressing cells after treatment. We conclude that a single i.m. administration of AAV hIL-10 significantly suppresses EAO and hypospermatogenesis by regulating cell-mediated immunity in the testes.

Adenoviridae↗

Association of seropositivity for antibody to Chlamydia-specific lipopolysaccharide and coronary artery disease in Japanese men.

Recent studies suggest an association between Chlamydia pneumoniae infection and coronary artery disease (CAD). To examine this relationship in Japanese men, serum IgA and IgG antibodies to Chlamydia-specific lipopolysaccharide were measured by enzyme-linked immunosorbent assay in 507 patients with CAD and 200 age-matched controls. CAD patients were divided into (1) 269 patients with myocardial infarction (MI) and (2) 238 patients with chronic coronary heart disease (CCHD). Compared with the control group, the CAD group did not differ in the prevalences of both antibodies (IgA: 23.7 vs 18.0%, p=0.10; IgG: 52.7 vs 51.0%, p=0.6). The index of IgG antibody was not significantly different between CAD and control groups (median 1.19 vs 1.18, p=0.3), whereas the index of IgA antibody was significantly higher in CAD than control group (median 0.60 vs 0.46, p<0.0001). Compared with the control group, the MI group had a significantly higher prevalence of IgA antibody (28.6 vs 18.0%, p=0.007); however, there was no difference in the prevalence of IgG antibody (58.0 vs 51.0%, p=0.13). The CCHD group did not differ in the prevalences of both antibodies (IgA: 18.1 vs 18.0%, p=0.9; IgG: 45.6 vs 51.0%, p=0.2). After the adjustment for coronary risk factors, odds ratios (ORs) of seropositive antibodies for CAD were 1.59 [95% confidence interval (CI): 0.88-2.87, p=0.12] for IgA seropositivity and 0.92 (95%CI: 0.58-1.47, p=0.7) for IgG seropositivity in all cases. In the MI and control groups, ORs of seropositive antibodies for MI were 2.67 (95%CI: 1.32-5.38, p=0.007) for IgA seropositivity, and 1.36 (95%CI: 0.79-2.36, p=0.2) for IgG seropositivity. This study discovered that IgA antibody to Chlamydia was significantly associated with CAD, especially with MI, in Japanese Men and the findings suggest that chronic infection of Chlamydia may be linked to the pathogenesis of MI.

Aged↗

Potentially protective effects of the Ser447-Ter mutation of the lipoprotein lipase gene against the development of coronary artery disease in Japanese subjects via a beneficial lipid profile.

Several DNA variants at the lipoprotein lipase (LPL) gene locus have been found to be associated with the plasma lipid levels and the prevalence of coronary artery disease (CAD). In particular, the Ser447-termination (Ter) mutation at the exon 9 of the LPL gene has the potential to elevate the plasma high-density lipoprotein (HDL) levels, but it remains unknown in the Japanese population. The present study investigated 93 CAD patients and 96 age- and sex-matched healthy controls. The Ser447-Ter mutation was determined by polymerase chain reaction restriction fragment length polymorphism method. The allelic frequency of the Ser447-Ter mutation was 0.103 in all subjects. The Ser447-Ter (GG and CG) group was associated with significantly higher levels of plasma HDL-cholesterol (p<0.001) and lower levels of plasma triglyceride than the CC group (p<0.02). The peak particle size of low-density lipoprotein (LDL) was significantly larger in the Ser447-Ter (GG and CG) group than in CC group (p<0.05). The frequency of the Ser447-Ter genotype in GG and CG was significantly lower in CAD than in the controls (11.9% vs 26%, odds ratio = 0.38; 95% confidence interval, 0.18-0.81; p<0.02). These results suggest that the Ser447-Ter mutation of the LPL gene is associated with high plasma HDL-cholesterol levels, low plasma triglyceride levels and a larger LDL particle size. This mutation may have a protective effect against the development of CAD via its favorable lipoprotein profile.

Aged↗

Relationship between plasma homocysteine levels and saphenous vein graft disease after coronary artery bypass grafts.

The long-term efficacy of coronary artery bypass graft (CABG) surgery is limited by saphenous vein graft (SVG) disease. Elevated levels of plasma homocysteine are a known independent risk factor for cardiovascular disease. However, its influence on the patency of SVG is unknown. To determine whether plasma homocysteine levels are related to SVG disease after CABG we measured homocysteine levels in 80 patients who underwent CABG (age: 64+/-8, interval after bypass surgery: 6.4+/-3.1, range: 1-13 years). The patients were divided into a vein graft disease group (more than 50% angiographical stenosis in any vein graft, n=40) and a no-vein graft disease group (<50% stenosis in any vein graft, n=40). The presence of a mutation in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene was also determined by polymerase chain reaction. Homocysteine levels in the vein graft disease group were significantly higher than in the no-vein graft disease group (11.2 vs. 9.1 micromol/l, p=0.01). Multiple regression analysis showed that the interval after CABG was an independent factor for SVG disease (odds ratio: 1.014, 95% confidence intervals: 1.003-1.025, p=0.013) and elevated levels of homocysteine tended to be an independent factor for SVG disease (odds ratio: 1.098, 95% confidence intervals: 0.994-1.213, p=0.067). There was no significant difference in MTHFR genotypes between the two groups. These findings indicate that elevated levels of plasma homocysteine are related to SVG disease after CABG.

Case-Control Studies↗

Association of serum antioxidant capacity with coronary artery disease in middle-aged men.

The possible involvement of oxidative damage in the progression of atherosclerosis has been suggested. There is some evidence that antioxidant therapy may be beneficial for the prevention of coronary heart disease. In this study, we investigated the relationship between coronary artery disease (CAD) and serum antioxidative status by measuring the total antioxidant status (TAS). Other relevant antioxidants, such as retinol, alpha, gamma-tocopherol, ascorbic acid, alpha, beta-carotenoids, erythrocyte glutathione peroxidase (GSH-Px) and oxidative products, were also determined in 31 male CAD patients with angiographically defined CAD and 66 male controls, aged 40-70 years, in a case-control study. The TAS levels, ratio and the concentrations of retinol, albumin, total protein and HDL cholesterol were significantly lower in the CAD patients than in the controls (p<0.01), and alpha-tocopherol and alpha/gamma-tocopherol were significantly higher in the CAD patients than in the controls. The TAS level correlated positively with gamma-GTP, GPT, GOT and uric acid (p<0.01). A multiple regression analysis in the CAD patients revealed that the TAS levels correlated most negatively with the number of diseased vessels. The concentrations of carotenoids and GSH-Px, as well as the alpha/gamma-tocopherol ratio were also significantly associated. Although conditional logistic regression analysis suggested low levels of HDL-cholesterol to be a significant coronary risk factor (OR=5.1, 95% CI=1.09-24.3), the TAS level showed no significant independent contribution to CAD. This study demonstrated an association of antioxidant parameters with the atherosclerosis progression, however, it did not confirm antioxidants as an independent risk factor for CAD event.

Adult↗

Common polymorphism in the promoter of the CD14 monocyte receptor gene is associated with acute myocardial infarction in Japanese men.

We investigated whether C(-260)-->T polymorphism in the promoter of the CD14 monocyte receptor gene predisposed to coronary atherosclerosis and acute myocardial infarction (AMI) in Japanese men. The frequencies of T allele and T/T homozygotes in patients with AMI were significantly higher than in controls and in patients with angina without prior AMI, suggesting that the CD14 promoter polymorphism is associated with AMI rather than with coronary atherosclerosis, and this polymorphism may be one of the genetic risk factors for AMI in Japanese men.

Aged↗

Effect of probucol on repeat revascularization rate after percutaneous transluminal coronary angioplasty (from the Probucol Angioplasty Restenosis Trial [PART]).

To address the issue of whether probucol reduces clinical events after percutaneous transluminal coronary angioplasty (PTCA), we surveyed clinical status at 1 year after PTCA of 101 patients who had entered the Probucol Restenosis Angioplasty Trial. Repeat angioplasty at index lesions were required in 5 patients in the probucol group and in 12 in the control group, suggesting that probucol administered beginning 4 weeks before PTCA reduces repeat revascularization rates for 1 year.

Angioplasty, Balloon, Coronary↗

Thiazolidinediones, dyslipidaemia and insulin resistance syndrome.

Insulin resistance is known to unite several metabolic abnormalities. The associated dyslipidaemia appears to play a central role in this atherogenic syndrome. Thiazolidinediones, which are recently introduced insulin sensitizing agents, have been shown to be effective not only in reducing elevated glucose levels, but also in improving the other metabolic abnormalities that are associated with insulin resistance. The present review focuses on these potential effects of thiazolidinediones.

Chromans↗

High prevalence of seropositivity for antibodies to Chlamydia-specific lipopolysaccharide in patients with acute coronary syndrome.

BACKGROUND: Results of recent studies have demonstrated that there is an association between infection with Chlamydia pneumoniae and coronary artery disease (CAD). Inflammatory response caused by chlamydial infection has been considered to contribute to the development of atherosclerosis in coronary arteries. OBJECTIVE: The aim of this study was to investigate the specific relations between chlamydial infection and coronary events in patients with CAD. METHODS: We measured serum levels of immunoglobulin A and G antibodies against Chlamydia spp.-specific lipopolysaccharide in 155 patients with CAD and 60 age-matched and sex-matched healthy controls by enzyme-linked immunosorbent assay. CAD patients were divided into groups of the patients with acute coronary syndrome [(ACS), n = 35], old myocardial infarction [(OMI), n = 60] and chronic coronary heart disease [(CCHD), n = 60]. RESULTS: Prevalence of both seropositive antibodies in the control group and CCHD group were not different. In contrast, in ACS group there were significantly higher prevalences of seropositive immunoglobulin A (46 versus 12%, P = 0.0001) and G (74 versus 45%, P = 0.005) antibodies and in OMI group there was a significantly higher prevalence of seropositive immunoglobulin A antibodies (28 versus 12%, P = 0.02). Furthermore, compared with CCHD group, in ACS group there were significantly higher prevalences of seropositive immunoglobulin A (P = 0.00006) and G (P = 0.002) antibodies and in OMI group there was a higher prevalence of seropositive immunoglobulin A (P = 0.01). Adjustment for confounding factors did not change these findings. CONCLUSIONS: Infection with Chlamydia is significantly associated with ACS and OMI, but not with CCHD. These findings suggest that chronic and reactive infection with Chlamydia can lead to disruption of vulnerable plaque in patients with ACS.

Acute Disease↗

Arrhythmogenic right ventricular cardiomyopathy with an initial manifestation of severe left ventricular impairment and normal contraction of the right ventricle.

A case of arrhythmogenic right ventricular cardiomyopathy (ARVC) with an initial manifestation of severe impairment of the left ventricle (LV) and normal contraction of the right ventricle (RV) is presented. A 43-year-old man was admitted to hospital because of congestive heart failure following a common cold. The LV function was diffusely and severely hypokinetic. Coronary arteriogram revealed normal vessels. An endomyocardial biopsy specimen obtained from the RV septum revealed mild infiltration of lymphocytes with focal myocytes necrosis and so healing myocarditis was suspected. The specimen did not include any fatty replacement of myocytes. Since then, the patient suffered from recurrent congestive heart failure as well as nonsustained ventricular tachycardia and required frequent hospitalization. Progressive impairment, dilation, and thinning of both ventricles were observed on serial echocardiographic examinations. Although the RV gradually enlarged and became impaired, severe dilatation and impairment of the LV has always been predominant in the patient's clinical course. After medical follow-up for 10 years, he died suddenly of ventricular fibrillation and pump failure. The autopsy revealed extensive fibrofatty replacement of myocytes in both the ventricles, extending from the outer layer to the inner layer of myocardium in the RV and to the middle layer in the LV. These features were compatible with arrhythmogenic right ventricular cardiomyopathy or perimyocarditis, although only the rightsided bundle of the interventricular septum was completely replaced by fatty tissue, which can not be explained as a sequel of perimyocarditis. Moreover, apoptosis was present in the myocyte nuclei of the myocardial layers bordering the area of fatty replacement. Therefore, myocarditis may have triggered or accelerated the process of apoptosis leading to ARVC.

Adult↗

Characteristics of coronary heart disease in Japanese taxi drivers as determined by coronary angiographic analyses.

Several epidemiological studies have shown that the prevalence of ischemic heart disease is higher in occupational drivers than in people with other occupations. Although occupation categories can be surrogate measures for coronary risk factors, the relationships between taxi driving and severity of coronary heart disease (CHD) has not been investigated. Even more important, the contribution of risk factors to the severity of CHD in taxi drivers remains unclear. Our study tested the hypothesis that taxi driving could be associated with the severity of CHD. We also examined the relation between this occupation and risk factors and social lifestyle. We analyzed the coronary angiograms of 57 consecutive male taxi driver patients and compared them with those of 215 age-adjusted male non-taxi-driver patients. The number of diseased vessels and risk factors were compared between two groups. The prevalence of myocardial infarction and multi-vessel disease was higher in the taxi-driver patients than in the non-taxi-driver patients. The taxi-driver patients had higher prevalence of body mass index (BMI), diabetes, and smoking, higher levels of low-density lipoprotein cholesterol (LDL-C), and lower levels of apolipoprotein AI (ApoAI). Multiple logistic regression analysis showed that multi-vessel disease was associated with BMI and diabetes mellitus in taxi-driver patients. The taxi-driver patients were characterized by more extensive coronary atherosclerosis associated with higher prevalence of diabetes mellitus and obesity. These characteristics may be explained by in part their working environment.

Automobile Driving↗

Troglitazone improves endothelial dysfunction in patients with insulin resistance.

Insulin resistance is a possible major metabolic cause of atherosclerosis. Endothelial dysfunction is commonly found in patients with insulin resistance, and primary treatment of insulin resistance with troglitazone should improve such endothelial dysfunction. Thus, the effects of troglitazone on endothelial function were investigated. Thirteen non-diabetic male subjects with hyperinsulinemic response to oral glucose load (n = 7) and normal (n = 6) subjects were investigated. Flow-mediated dilatation (FMD) of the brachial artery was examined by high resolution ultrasonography before and after the administration of troglitazone of 400 mg for 4 weeks. In insulin resistant subjects, fasting glucose (4.9+/-0.3 to 4.7+/-0.3 mmol/L, p<0.05), insulin (45+/-30 to 25+/-15 pmol/L, p<0.05) and response to oral glucose load (AUC glucose: 15.0+/-3.5 to 13.0+/-2.2 mmol x h/L, p<0.05; AUC insulin: 965+/-560 to 475+/-275 pmol x h/L, p<0.05) were significantly reduced. FMD was significantly improved in insulin resistant subjects. A significant negative correlation was observed between FMD and AUC insulin (r=-0.64, p<0.05). The present study demonstrates that FMD is impaired in insulin resistant subjects, and troglitazone improves the blunted vascular response and impaired insulin response. This finding suggests that primary treatment of insulin resistance could prevent the development of atherosclerosis by improving endothelial dysfunction.

Adult↗

Prognostic significance of exercise-induced systemic hypertension in healthy subjects.

Exercise hypertension has been suggested to predict future resting hypertension, but its significance in terms of cardiovascular risk has not been defined. To assess the prognostic significance of exercise hypertension, 150 healthy, asymptomatic subjects with normal resting blood pressures and exercise systolic blood pressures > or =214 mm Hg (i.e., >90th percentile) on Bruce treadmill tests were identified retrospectively and age- and gender-matched with subjects with exercise systolic blood pressures of 170 to 192 mm Hg (40th to 70th percentiles). Subjects were contacted by survey a mean of 7.7+/-2.9 years after the index treadmill test. The survey response rate was 93%. There were 12 deaths, including 8 in the exercise hypertension group. A major cardiovascular event, defined as cardiovascular death, myocardial infarction, stroke, coronary angioplasty, or coronary bypass graft surgery occurred in 5 controls and 10 subjects with exercise hypertension. At follow-up, 13 controls and 37 subjects with exercise hypertension were now diagnosed as having resting hypertension. In multivariate analysis, exercise hypertension was not a significant predictor for death or any individual cardiovascular event, but was for total cardiovascular events and new resting hypertension. The multivariate risk ratio for exercise hypertension was 3.62 (p = 0.03) in predicting a major cardiovascular event. Other significant predictors included body mass index and age. For predicting new resting hypertension, the multivariate odds ratio for exercise hypertension was 2.41 (p = 0.02). These data suggest that exercise hypertension carries a small but significant risk for major cardiovascular events in healthy, asymptomatic persons with normal resting blood pressures.

Adult↗

Possible role of high susceptibility of high-density lipoprotein to lipid peroxidative modification and oxidized high-density lipoprotein in genesis of coronary artery spasm.

Recent study demonstrated high susceptibility of plasma LDL to lipid peroxidative modification in patients with variant angina. Oxidized stress state, especially oxidized LDL, may induce coronary artery spasm by its impairing effect of endothelium-dependent arterial relaxation, but precise mechanisms remain unclear. Study subjects included 93 patients who underwent coronary angiographic examination: 12 patients with coronary artery spasm provoked by ergonovine without organic stenosis (group I), 11 patients who did not demonstrate coronary artery spasm or organic stenosis (group II) and 70 patients with organic coronary artery stenosis (group III). Levels of plasma HDL-cholesterol and apoA-I in group I were similar to those in III but were significantly lower than those in II, although the other plasma lipid parameters were not different among the three groups. The levels of TBARS in plasma and HDL were significantly higher in group I than in II or III (2.94+/-1.56 vs. 1.91+/-0.35 or 2.23+/-0.89 nmol MDA/ml and 1.23+/-1.00 vs. 0.54+/-0.37 or 0.70+/-0.63 nmol MDA/mg protein; P < 0.05), although the levels of TBARS in LDL were not significantly different. In the monitoring curve of diene production during copper-induced lipid peroxidation of HDL, its propagation slope was steeper and levels of maximum diene absorbance was higher in group I as compared with that in II or III, but not found in those of LDL. These results suggested that high susceptibility of HDL to lipid peroxidative modification in group I may contribute to the genesis of coronary artery spasm, and oxidized HDL rather than oxidized LDL is more likely to be related to coronary artery spasm.

Copper↗