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Biomedical subjects

T Miida

Publications and source records attributed to T Miida.

At least 37 records · Page 2Linked to original sources

High prebeta1-HDL levels in hypercholesterolemia are maintained by probucol but reduced by a low-cholesterol diet.

Previous study has shown that prebeta1-HDL levels increase in hypercholesterolemia, or high cholesteryl ester transfer protein (CETP) activity. To determine how prebeta1-HDL levels change after treatment with probucol or by following a low-cholesterol diet, we randomly assigned 24 hypercholesterolemic patients to either the probucol (P), or low-cholesterol diet group (D), and measured prebeta1-HDL levels before and after treatments using native two-dimensional gel electrophoresis. We also examined 12 subjects with normolipidemia (N). At baseline, prebeta1-HDL levels were higher in P (P < 0.05) and D (P < 0.05) than in N (9.2 +/- 4.3, 10.4 +/- 5.5, and 5.9 +/- 2.3 mg/dl apo A-I). After a 4-week treatment, prebeta1-HDL levels were still high in P (10.5 +/- 4.2 mg/dl apo A-I, N.S.), but reduced in D (7.7 +/- 3.0 mg/dl apo A-I, P < 0.001). Delta prebeta1-HDL (Y) was positively correlated with deltaCETP mass (X) in P (y = 7.83x - 1.93; r = 0.584, P < 0.05). In summary, high prebeta1-HDL levels in hypercholesterolemia are maintained by probucol but reduced by a low-cholesterol diet. These findings suggest that prebeta1-HDL levels may be regulated by cholesterol and CETP levels.

Aged↗

Plasma lipoprotein profiles change significantly during cardiac catheterization.

Most patients in acute myocardial infarction (AMI) undergo emergent coronary angiography (CAG). However, when to analyze lipoprotein profiles in AMI is not clear. To determine whether lipoprotein profiles change during catheterization, we measured serum lipid and apolipoprotein concentrations in 65 patients (51 men and 14 women) before and after catheterization. Heparin was injected at 50 units/kg for CAG and 200 units/kg for percutaneous transluminal coronary angioplasty (PTCA). We found that cholesterol and triglyceride decreased by 9.4% (P < 0.001) and 53.1% (P < 0.001), respectively, after catheterization. Apolipoproteins also decreased significantly. Variables decreased two to five times more after PTCA than after CAG. Lipoprotein lipase mass was higher after PTCA (267.8 +/- 135.3 micrograms/L) than after CAG (93.3 +/- 48.4 micrograms/L; P < 0.05). In conclusion, lipoprotein profiles change during catheterization. We recommend avoiding analysis of lipoprotein profiles after emergent CAG in AMI.

Adult↗

[Circadian changes in remnant-like particle-cholesterol (RLP-C), and its diagnostic value for postprandial increase in remnant lipoprotein in diabetes mellitus].

To investigate whether remnant-like particle-cholesterol (RLP-C) increases in the postprandial state, and if so, whether such response can be used for detecting postprandial increase in remnant lipoprotein, we measured RLP-C levels at two points (before breakfast, and after lunch), or seven points (before and after each meal, and midnight) in 36 diabetic patients. delta RLP-C was calculated by subtracting RLP-C level before breakfast from that at each point. delta RLP-C after lunch was defined as delta RLP-CL and maximum delta RLP-C as delta RLP-Cmax. Daily profiles of RLP-C (n = 22) showed that RLP-C increased during the daytime in 6 patients (27.3%; responders), but not in the others (nonresponders). In the histogram of delta RLP-Cmax, we could easily distinguish responders (delta RLP-Cmax = 6 approximately 12 mg/dl) from nonresponders (< 4 mg/dl). By using delta RLP-CL of 4 mg/dl as the cut-off value, we could also separate two groups without overlap. With this cut-off value, 11 out of 36 patients (30.6%) were diagnosed as responders. High performance liquid chromatography (HPLC) analysis with cholesterol-monitoring revealed that VLDL-sized RLP increased markedly after lunch in responders. In conclusion, RLP-C increases in some diabetic patients, and delta RLP-CL is useful for detecting postprandial increase in remnant lipoprotein.

Aged↗

[The measurement of antioxidant activity in human plasma using cumene hydroperoxide].

We describe a new method using cumene hydroperoxide to determine antioxidant activity (AO) in human plasma. We used a kit (Determiner LPO: Kyowa Medex Co., LTD. Tokyo Japan) for the determination of lipid peroxides in plasma or serum. 30 microliters 1 of sample was mixed with 70 microliters 1 of cumene hydroperoxide (50 nmol/ml) and incubated at 30 degrees C for 120 min before analysis. Samples were mixed with 1.0 ml of reagent-I (Determiner LPO) and incubated at 30 degrees C for 5 min. Then 2.0 ml of reagent-II (Determiner LPO) was added and incubated at 30 degrees C for 10 min, at which time the absorbance at 675 nm was measured. AO were calculated using the following formula: AO nmol/ml = 35 nmol/ml-(Es-Eb)/(Estd-Eb) x 35 nmol/ml (Es = sample abs., Eb = blank abs., Estd = standard abs.). Within-run precision for plasma AO was 2.3%. AO in plasma samples stored for 4 h at 4 degrees C was decreased by 1 nmol/ml. After 3 h at room temperature, AO was decreased by the same amount. Because this method measured ascorbic acid, alpha-tocopherol, glutathione peroxidase and quercetin as antioxidant compounds, we were able to measure antioxidant activity in human plasma. Our reference values were calculated from the volunteers group which consisted of 172 students and 82 soldiers. The reference intervals for plasma AO by this procedure were 15.4-20.9 nmol/ml.

Adult↗

[Assessment of diabetic cardiovascular autonomic neuropathy by heart rate variability and pulse wave velocity].

Neuropathy is a frequent complication in diabetes mellitus. Since the involvement of the autonomic nervous system indicates a poor prognosis, early detection and subsequent management are important. Analysis of heart rate variability (HRV) provides a quantitative measure of sympathovagal modulation activities on the heart and has been proven to be useful for the early assessment of the diabetic autonomic neuropathy. We recently developed a simple method of measuring pulse wave velocity (PWV) to evaluate sympathetic nervous activity in the vascular system. In this paper, we examined 33 diabetic patients with and without peripheral neuropathy (15 and 18 respectively) using these methods. In time domain analysis, the mean heart rate, standard deviation and coefficient of variation of HRVs significantly differed between these two groups, whereas the indices of PWVs did not show a significant difference. In frequency domain analysis of HRV, both low and high frequency components were decreased, and the low frequency component in normalized unit did not increase after standing in patients with peripheral neuropathy. We previously reported that the mean PWV decreased after standing in patients with diabetic neuropathy. This disagreement suggests that beta sympathetic dysfunction precedes alpha sympathetic dysfunction in diabetic neuropathy.

Adult↗

LpA-I levels do not reflect pre beta1-HDL levels in human plasma.

High-density lipoprotein (HDL) containing apo A-I but no apo A-II (LpA-I) can promote cholesterol efflux from cells, while HDL containing apo A-I and apo A-II can not. Pre beta1-HDL, a minor fraction of LpA-I, is the initial acceptor of cellular cholesterol. To determine whether the pre beta1-HDL:LpA-I ratio is constant in human plasma, we measured LpA-I levels by differential electroimmunoassay, and HDL subfraction levels by nondenaturing 2-dimensional gel electrophoresis in 26 subjects. We found that the pre beta1-HDL:LpA-I ratio was higher in hypercholesterolemia (0.21+/-0.09; n = 11, P < 0.05), coronary artery disease (0.26+/-0.13; n = 5, P = 0.08) and hypertriglyceridemia (0.39+/-0.22; n = 3, P = 0.16) than in normolipidemia (0.11+/-0.03, n = 5). LpA-I levels were significantly correlated with HDL2b (r = 0.771, P=0.000001), HDL2a (r = 0.438, P < 0.01), and pre beta2-HDL levels (r = 0.496, P < 0.005) but not with pre beta1-HDL or HDL3 levels. In conclusion, the pre beta1-HDL:LpA-I ratio is not constant in human plasma. These findings strongly suggest that size distribution of LpA-I may change in various disorders.

Adult↗

Two families of Lowe oculocerebrorenal syndrome with elevated serum HDL cholesterol levels and CETP gene mutation.

The ocuolocerebrorenal syndrome of Lowe (OCRL) is an X-linked recessive disorder which is characterized by renal tubular dysfunction, congenital cataracts, and cognitive impairment. In a review article by Charnas et al. (N Engl J Med 1991; 324: 1318-25), hypercholesterolemia, due to elevated high-density lipoprotein cholesterol (HDL-C) levels, was described as being highly prevalent in OCRL patients. This report prompted us to examine three OCRL children in two unrelated families and we confirmed the high prevalence of high serum HDL-C levels in the patients (3/3). In addition, we found that their normal family members also had high serum HDL-C levels (5/7). Analysis of cholesteryl ester transfer protein (CETP) genes, which are now recognized as one of factors increasing serum HDLC levels, revealed the D442G mutation in exon 15 in 5 of 10 family members (1/3 of OCRL patients and 4/7 healthy family members), and no mutation of intron 14 G(+1)-to-A. The detected D442G mutation may be one of the causes in our two OCRL families; however, further studies, based on larger numbers of subjects, are needed to confirm these findings.

Adolescent↗

Structural changes in oxidative modification of low-density lipoprotein: investigation using lipid peroxidation products, surface charge, and spectrophotometric patterns.

It is well recognized that oxidative modification of low-density lipoprotein (LDL) accelerates atherogenesis of the arterial vascular wall. In this study, we examined the relationship between various methods of measuring the extent of oxidation, namely lipid peroxidation products, surface charge, and spectrophotometric patterns. LDL was isolated from fresh human normal plasma by centrifugation and was oxidized by incubating with copper ions. Apolipoprotein B was isolated from the LDL solution. We also prepared artificial lipid particles composed of cholesterol linolenate, triolein, and phosphatidylcholine. Our results suggest that lipid peroxidation begins drastically in 30-60 min, while the abolition of the positive charge on apoliproproteins is accelerated after 60 min. We found a characteristic change in the spectrophotometric pattern during the process and conclude that the spectrophotometric absorption ration at 232 and 203 nm is a useful measure of in vitro oxidation of LDL.

Electrophoresis, Polyacrylamide Gel↗

An autopsied case of acute myocarditis with myocardial calcification.

A 47-year-old woman was admitted with fever, hypotension, an elevated serum creatinine kinase level, and electrocardiographic abnormalities, which led to the diagnosis of acute myocarditis. She was placed on percutaneous cardiopulmonary support because of hemodynamic collapse on the third hospital day. Serial echocardiography showed gradual recovery of profound hypokinesis and edematous thickening of the left ventricle, but she died of sepsis on the 17th day without overt renal insufficiency or electrolytic abnormalities. Autopsy revealed myocardial necrosis with lymphocytic infiltrates and extensive myocardial calcification. Calcification was dense in the area of severe myocardial necrosis, and the distribution of calcium deposits suggested that the calcification was a consequence of significant inflammation of the myocardium. Recovery of regional wall motion was prominent in the area of severe inflammatory change. Dissociation between the pathologic and echocardiographic findings suggested the possibility of functional reversibility of severely damaged myocardium and possible mechanisms of abnormal contractile function other than inflammatory change.

Acute Disease↗

Effect of serum amyloid A on cellular affinity of low density lipoprotein.

Serum amyloid A, an apolipoprotein of high density lipoproteins, is also present to a lesser degree in low density lipoproteins and is co-localized with apolipoprotein B in atherosclerotic lesions. This study examined the effect of serum amyloid A on cellular affinity of low density lipoprotein in vitro. 125I-labelled low density lipoprotein, when loaded with recombinant serum amyloid A1 (acute phase isotype) or recombinant serum amyloid A4 (constitutive isotype), had enhanced binding to both human skin fibroblasts and a murine macrophage cell line, J774, while its degradation was slightly increased in both cells. The binding of oxidized low density lipoprotein to J774 cells was also enhanced by addition of recombinant serum amyloid A1 or serum amyloid A4, and degradation of oxidized low density lipoprotein was moderately enhanced by recombinant serum amyloid A1. The effects of recombinant serum amyloid A on cellular binding of labelled low density lipoprotein were not competed by non-labelled low density lipoprotein and were diminished in the presence of high density lipoprotein. These findings suggest that serum amyloid A in low density lipoprotein may promote association of low density lipoprotein with cells by non-specific adsorption, and high density lipoprotein may prevent such interactions by removal of serum amyloid A.

Adult↗

A case of nonpenetrating traumatic aortic regurgitation detected by transesophageal echocardiography.

A 67-year-old man, who had fell 5 meters, landing on his back, one month before, was referred because of heart failure due to aortic regurgitation (AR). Transesophageal echocardiogram (TEE) confirmed injuries in the aortic valve and the Valsalva sinus of the aorta before the surgery: the intimal flap in the Valsalva sinus of right coronary cusp (RCC), the prolapse of the RCC, and the dissection by longitudinal length of 3 cm in the Valsalva sinus of noncoronary cusp (NCC), ending as a blind pouch. Postoperative TEE confirmed the dissection was not repaired in the Valsalva sinus of the NCC. In this instance, TEE was extremely useful, compared with transthoracic echocardiography, computed tomography and magnetic resonance imaging, to assess the mechanism of AR following a nonpenetrating trauma, and to know to what degree the aortic valve and the Valsalva sinus of the aorta were destroyed.

Aged↗

Differences in the effects of cytokines on the expression of adhesion molecules in endothelial cells.

OBJECTIVES: Expressions of adhesion molecules on arterial endothelial cells are crucial events in initiation of atherosclerosis. Our recent study has shown that endothelial cells express endothelial leukocyte adhesion molecule-1 (ELAM-1) significantly due to stimulation with oxidized LDL, H2O2, or hypoxia. This current study is aimed at investigating temporal relations of the induction of ELAM-1, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in cultured endothelial cells of the human thoracic aorta. METHODS: The activators examined were interleukin 1 alpha (IL-1 alpha), tumor necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma). Cells were incubated with each of the cytokines at 10 ng/ml for 0.5-48 hours. The adhesion molecules were determined by enzyme immunoassay. RESULTS: ELAM-1 appeared after stimulations by IL-1 and TNF alpha; ELAM-1 was induced by IL-1 after one hour, while it rose sharply after a 30-min stimulation by TNF alpha. The ICAM-1 expression was observed even in non-stimulated cells and further increased in proportion to duration of stimulation. No significant difference occurred between the effects of IL-1 and TNF alpha on the ICAM-1 expression. Weak expression of VCAM-1 was observed only by TNF alpha after 4-through 24-h stimulation. IFN gamma did not cause any changes in the expression of ELAM-1, VCAM-1, and ICAM-1. CONCLUSIONS: The present data indicate a specific time course for each induction of ELAM-1 and VCAM-1, but not ICAM-1. Therefore, the combination of molecules may play a role for endothelial cells to discriminate monocytes from such other cells as neutrophils and lymphocytes.

Aorta↗

[Serum apolipoprotein E-rich HDL-C levels in the subjects with hyperalphalipoproteinemia].

To clarify an increasing factor of serum apolipoprotein E-rich HDL-C(apo E-rich HDL-C) level in the patients with hyperalphalipoproteinemia(HALP), we characterized the relationships between the serum apo E-rich HDL-C levels and, apolipoprotein E genotypes and cholesteryl ester transfer protein(CETP) gene mutations using healthy(n = 46) and HALP subjects(HDL-C > or = 100 mg/dl, n = 67). Serum apo E-rich HDL-C level of healthy subjects was significantly different from that of HALP subjects. Frequencies of apo E allele of all subjects studied were consistent with previous other reports. It was, however, demonstrated that apo epsilon 4 allele decreases the apo E-rich HDL-C level in all HALP subjects. On the other hand, the G to A mutation in the intron 14 splice donor site(114A) and Asp442 to Gly mutation in the exon 15(D442G), were analysed by polymerase chain reaction-single strand conformation polymorphism(PCR-SSCP) method. Then we compared the apo E-rich HDL-C levels between the HALP subjects in the almost general population of apo E 3/3 with and without CETP gene mutation. There was strong tendency that the existence of CETP mutations increased the serum apo E-rich HDL-C level, comparing with the HALP subjects without these mutations. Therefore, we suggested that the increasing of serum apo E-rich HDL-C level was caused by the CETP deficiency and its level was affected by apo E genotypes.

Apolipoproteins E↗

Efficacy of marker wire for intracoronary stenting.

The Marker Wire was used for Palmaz-Schatz coronary stent implantation. The Marker Wire is useful in estimating lesion length and in determining the number of stents required, in addition to facilitating stent positioning.

Aged↗

[Usefulness of PCR-SSCP using non-RI coloration method as a routine genetic analysis].

The polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis is considered as one of useful routine genetic analyses. However, that PCR-SSCP has been analyzed using radioisotope (RI) such as [32P] labeled compounds. So that, it was difficult to use this method routinely at clinical laboratories. In this paper, we compared with an RI mediated and a non-RI coloration mediated PCR-SSCP analysis regarding to those of sensitivity, time and money cost, respectively. The coloration method had enough sensitivity to detect one of cholesteryl ester transfer protein gene mutations. The time and money cost of non-RI coloration mediated method were more advantageous than the RI mediated one. Therefore, it is shown that the non-RI coloration mediated PCR-SSCP analysis is very useful for the routine genetic analysis at clinical laboratories.

Carrier Proteins↗

Development of coronary atherosclerosis in asymptomatic heterozygous patients with familial hypercholesterolemia.

To determine whether coronary atherosclerosis develops with age in asymptomatic patients with familial hypercholesterolemia (FH) and whether long-term cholesterol-lowering therapy is effective for primary prevention of coronary artery disease (CAD) in such patients, 13 patients with heterozygous FH (10 men, 3 women, aged 34 to 66 years) were examined by coronary angiography, and followed up for 5.8 +/- 3.4 years. The extent of coronary atherosclerosis was expressed as the coronary score (CS) by scoring (0 to 5) points in each of 15 American Heart Association segments. The mean CS was 2.4 times higher in men than in women (11.5 +/- 7.9 vs 4.7 +/- 4.2) although the mean age was lower in the former than in the latter (51.2 +/- 8.4 vs 57.7 +/- 0.6 years). In men, CS correlated significantly with age (CS = 0.682 x age-24.4; r = 0.800, p < 0.01). All patients except one had received cholesterol-lowering agents throughout the follow-up period. The untreated patient developed CAD 7 years later. One treated patient also developed CAD, but within 6 months of enrollment in this study. The other 11 treated patients did not develop CAD. Reexamination by coronary angiography in two of these patients revealed no significant progression after 6-year treatment. Coronary atherosclerosis develops with age in asymptomatic FH patients and long-term cholesterol-lowering therapy may be effective for primary prevention of CAD in such patients.

Adult↗