PubMed Health⌕ Search

Biomedical subjects

T Miida

Publications and source records attributed to T Miida.

At least 19 recordsLinked to original sources
PubMed2001

Cholesteryl ester transfer protein deficiency causes slow egg embryonation of Schistosoma japonicum.

In our attempt to discover a potential cause for accumulation of cholesteryl ester transfer protein (CETP) deficiency in Eastern Asia, we studied the association of CETP deficiency with pathogenesis of Schistosoma japonicum, a life-threatening parasite peculiar to this region. The eggs of S. japonicum showed slow embryonation when cultured in CETP-deficient human plasma. Restoration of CETP to the deficient plasma rescued it, while inhibition of CETP in normal plasma did not cause slow embryonation of the cultured eggs. The egg embryonation was also retarded in the liver but not in the intestine of wild-type mice in comparison to the CETP-transgenic mice. The granulomatous lesion around the parasite eggs in the liver was less in the wild-type than in the CETP-transgenic mice. Thus, CETP deficiency may act against Schistosomiasis japonica by retarding egg embryonation, a potential cause of liver granulomatosis. It does not seem directly due to the lack of CETP activity in plasma but to abnormal lipoprotein generated by chronic CETP deficiency.

Animals↗
PubMed2001

Novel glomerular lipoprotein deposits associated with apolipoprotein E2 homozygosity.

BACKGROUND: Hyperlipoproteinemia is occasionally associated with severe glomerular injury caused by abnormal accumulation of lipid in glomeruli, which occurs in conditions such as lipoprotein glomerulopathy (LPG). This study investigates the cases of two siblings with homozygous apolipoprotein (apo) E2 who show unique histologic features, massive proteinuria, and dysbetalipoproteinemia. METHODS: Histologic studies were performed using renal biopsy specimens. Plasma lipoproteins were extensively characterized. The exons of the apo E genes were sequenced to avoid missing any mutations. RESULTS: Histologically, the siblings' condition resembled LPG by light microscopy studies. Electron microscopy studies revealed large lipoid deposits in the paramesangium, subendothelium, and subepithelium of the glomeruli, which were different from LPG in terms of not forming the layered structure resembling a fingerprint even in large lipoprotein thrombi, and mesangial foam cells. Immunohistochemically, the lipoid deposits contained apo E and apo B. These patients did not have either diabetic nephropathy or other known forms of glomerulonephritis. The sequence of exons of the apo E genes revealed homozygosity for apo E2 in both cases. CONCLUSION: The extensive lipoprotein deposition in glomeruli, which resembles LPG, can also occur in apo E2 homozygous individuals, but in a distinct fashion. Because the two cases were siblings, they may have other shared alleles, in addition to the apo E2 allele, that negatively affect processing of lipoproteins and lead to abnormal accumulation of lipoprotein deposits in glomeruli.

Amino Acid Sequence↗
PubMed2001

LR11, a mosaic LDL receptor family member, mediates the uptake of ApoE-rich lipoproteins in vitro.

Since the molecular identification of the low density lipoprotein receptor (LDLR), an ever increasing number of related proteins have been discovered. These receptors belonging to the LDLR family are thought to play key roles in lipoprotein metabolism in a variety of tissues, including the arterial wall. We have discovered that the expression of a 250-kDa mosaic LDLR-related protein, which we termed LR11 for the presence of 11 LDLR ligand-binding repeats, is markedly induced in smooth muscle cells in the hyperplastic intima of animal models used for the study of atherosclerosis. Here, we demonstrate that the human LR11, when overexpressed in hamster cells, binds and internalizes 39-kDa receptor-associated protein (RAP), an in vitro ligand for all receptors belonging to the LDLR family. Furthermore, LR11 binds the apolipoprotein E (apoE)-rich lipoproteins, beta-very low density lipoproteins (VLDLs), with a high affinity similar to that of other members, such as the LDLR and VLDL receptor. RAP and beta-VLDL compete with each other; however, other serum lipoproteins are not able to inhibit their binding. LR11 shows specific binding of apoE-enriched HDL prepared from human cerebrospinal fluid as well as of beta-VLDL, suggesting that the apoE content of lipoproteins is most likely important for mediating the high-affinity binding to the receptor. LR11-overexpressing cells are able to internalize and degrade the bound beta-VLDL; these cells also show increased accumulation of cholesteryl esters when incubated with beta-VLDL. Incubation for 48 hours with beta-VLDL of LR11-overexpressing cells, but not of control cells, promotes the appearance of numerous intracellular lipid droplets. Taken together, LR11, a mosaic LDLR family member whose expression in smooth muscle cells is markedly induced in atheroma, has all the properties of a receptor for the endocytosis of lipoproteins, particularly for the incorporation of apoE-rich lipoproteins.

Animals↗
PubMed2001

Th1/Th2 balance alteration in the clinical course of a patient with acute viral myocarditis.

Cytokines have an important role in the pathogenesis and pathophysiology of myocarditis. In this study, subsets of peripheral helper T lymphocytes (Th) in a patient with acute viral myocarditis were analyzed by 3-color flow cytometry. During the clinical course of myocarditis, the Th1/Th2 ratio of peripheral lymphocytes changed. Th1 was dominant in the acute inflammatory phase during which levels of creatine kinase (CK) increased (day 6), then Th2 levels overtook those of Th1 in the recovery phase during which levels of CK decreased (day 13 and 20). At the time of discharge (day 35), Th1 and Th2 had normalized. Thus, it was speculated that the induction of lymphocytic myocarditis was associated with Th1 dominant status, and recovery was related to Th2 polarity. Th subset imbalances may play an important role in the pathogenesis of acute viral myocarditis and these analyses may be useful for understanding the disease activity of myocarditis.

Adult↗
PubMed2001

[Pre beta-HDL].

Explore the source record for details and available documents.

Animals↗
PubMed2000

Prebeta1-high-density lipoprotein (prebeta1-HDL) concentration can change with low-density lipoprotein-cholesterol (LDL-C) concentration independent of cholesteryl ester transfer protein (CETP).

To clarify whether prebeta1-high-density lipoprotein (prebeta1-HDL) concentration changes with low-density lipoprotein-cholesterol (LDL-C) concentration independent of cholesteryl ester transfer protein (CETP), we determined prebeta1-HDL concentration by native two-dimensional gel electrophoresis in 58 subjects with normal triglyceride and HDL-cholesterol concentrations. We also measured LDL-C and CETP concentrations. In 17 subjects, a second blood sample was taken 1-6 months after the first. We found that prebeta1-HDL concentration was positively correlated with LDL-C concentration (r=0.529, P<0.0001) and with CETP mass (r=0.398, P<0.01). In 17 patients, Deltaprebeta1-HDL was positively correlated with DeltaLDL-C (r=0.635, P<0.01), but not with DeltaCETP mass (r=0.275). In conclusion, prebeta1-HDL concentration changes with LDL-C concentration independent of CETP. These results suggest that prebeta1-HDL concentration may reflect the balance between several regulatory factors, including LDL-C and CETP concentrations.

Adult↗
PubMed2000

Exercise induced atrioventricular block with gap phenomenon in atrioventricular conduction.

A 54-year-old man with normal atrioventricular (AV) conduction at rest gave a 4-year history of presyncope during exercise. Treadmill testing showed exercise induced AV block. Electrophysiological study demonstrated rate dependent infranodal AV block and abnormal refractory period of the His-Purkinje system. The gap phenomenon in AV conduction occurred during the programmed stimulation. Supernormal conduction could be considered as the mechanism of the gap phenomenon in this patient.

Atrioventricular Node↗
PubMed2000

Bezafibrate increases prebeta 1-HDL at the expense of HDL2b in hypertriglyceridemia.

Prebeta1-high density lipoprotein (prebeta1-HDL), the initial acceptor of cell-derived cholesterol, can be generated from HDL(2) by hepatic lipase. Because bezafibrate elevates lipase activity, it may increase prebeta1-HDL at the expense of HDL(2). To answer this question, we determined the apolipoprotein A-I (apoA-I) distribution in 20 hypertriglyceridemics (triglycerides>2.26 mmol/L) and 20 sex-matched normolipidemics by native 2-dimensional gel electrophoresis. At baseline, prebeta1-HDL was 70% higher in hypertriglyceridemics than in normolipidemics (123.5+/-49.9 versus 72.5+/-34.1 mg/L apoA-I, P<0.01). Prebeta1-HDL was positively correlated with triglyceride (r=0.624, P<0.0001). A 4-week bezafibrate treatment (400 mg daily) increased prebeta1-HDL by 30% (160.2+/-64.5 mg/L apoA-I, P<0.05) but decreased HDL(2b) by 31% (from 188.8+/-94.9 to 129.3+/-78.7 mg/L apoA-I, P<0.05). Hepatic lipase activity increased by 24% (P<0.005). Prebeta1-HDL was generated either from ultracentrifugally isolated HDL(2) or from plasma during incubation with triglyceride lipase. In conclusion, bezafibrate increases prebeta1-HDL at the expense of HDL(2). We speculate that such an effect might partly contribute to the antiatherogenic action of bezafibrate.

Adult↗
PubMed2000

Capillary isotachophoretic analysis of serum lipoproteins using a carrier ampholyte as spacer ion.

We have developed a novel analytical method for serum lipoproteins using a commercially available capillary electrophoresis apparatus, BioFocus 3000 (Bio-Rad Laboratories Co Ltd, USA). The analytical principle is isotachophoresis (ITP), using a carrier ampholyte, BioLyte 7/9, as a spacer ion. The method allows a much higher resolution of lipoproteins than of amino acid mixtures. Serum lipoproteins are normally separated into 13-15 peaks, including some shoulder peaks. The reproducibility of repeated analysis within a day was relatively good with the coefficient of variation within the range 0.9-1.1%. VLDL, LDL and HDL prepared by discontinuous density ultracentrifugation could be further separated by capillary ITP. This high-resolving ability of our method enabled detection of small amounts of abnormal lipoprotein species. For example, small dense LDL, which is thought to be an atherogenic lipoprotein, could be detected within the LDL group peak. Moreover, an abnormal HDL, apolipoprotein E-rich HDL, was also detected by a single analysis. These findings suggest that our capillary ITP method is a useful means for detailed analysis of lipoproteins and thus for clinical diagnosis of hyperlipoproteinaemic subjects.

Ampholyte Mixtures↗
PubMed2000

Autoantibodies against oxidized low-density lipoprotein correlate with Achilles tendon xanthomas.

Although there is increasing evidence for anti-oxidized low-densitiy lipoprotein (LDL) autoantibodies in human sera, their diagnostic utility remains controversial. We examined the difference in autoantibody titers between patients with Achilles tendon xanthoma and control subjects. Fifteen hyperlipidemic patients with Achilles tendon xanthoma (group A+) and 94 hyperlipidemic patients without Achilles tendon xanthoma (group A-) were studied. Quantification of anti-oxidized LDL and anti-native LDL autoantibodies was performed using an ELISA method. To calculate antibody titers, we used the ratio between the spectrophotometric reading of anti-oxidized LDL and anti-native LDL wells. Using oxidized LDL that was purified by gel-permeation chromatography as antigen, immunoglobulin G level differed significantly between groups A+ and A- (p < 0.01). In contrast, using native and oxidized LDL as antigens without chromatographical purification revealed no significant difference between the two groups. Furthermore, immunoglobulin autoantibody titer did not correlate with age, body mass index, total cholesterol, high-density lipoprotein cholesterol, LDL cholesterol, or triglyceride in the entire group of subjects. Thus, immunoglobulin G autoantibody values appear to correlate with Achilles tendon xanthoma.

Achilles Tendon↗
PubMed2000

Possible risk factors of carotid artery atherosclerosis in the Japanese population: a primary prevention study in non-diabetic subjects.

OBJECTIVE: Hyperinsulinemia has been associated with the risk of coronary heart disease, stroke, and renal disease in nondiabetic subjects. However, direct evidence that hyperinsulinemia per se is directly associated with atherosclerosis has been conflicting. The present study was designed to investigate the cross-sectional association of carotid artery atherosclerosis with insulin, independent of well-known cardiovascular risk factors, in nondiabetic subjects. METHODS AND SUBJECTS: Between 1996 and 1997, 1,335 subjects (620 men and 715 women) were recruited from one Japanese community, interviewed, and examined. Clinical measurements in the study included intimal-medial thickness (IMT) of the carotid artery, fasting plasma insulin, serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), fasting plasma glucose (FPG), hemoglobin type HbA1c, systolic blood pressure (SBP), diastolic blood pressure (DBP), and body mass index (BMI). We divided the subjects of both genders into three subgroups according to age (40-49 years of age; 50-59; and 60-69). RESULTS: Using simple regression analysis, we found that IMT was significantly correlated with at least one of TC, LDL-C, HbA1c, SBP, DBP, and BMI in each subgroup. The results of multivariate analysis showed that IMT was independently correlated with TC, HDL-C, LDL-C, SBP and BMI in males and with TC, TG, HDL-C, LDL-C, HbA1c, SBP, DBP, and BMI in females. Insulin levels showed no correlation with IMT in either males or females. CONCLUSION: Fasting hyperinsulinemia does not appear to be correlated with carotid artery atherosclerosis based on the present cross-sectional results.

Adult↗
PubMed2000

A new sandwich enzyme immunoassay for measurement of plasma pre-beta1-HDL levels.

Pre-beta1-HDL, a putative discoid-shaped high density lipoprotein (HDL) of approximately 67-kDa mass that migrates with pre-beta mobility in agarose gel electrophoresis, contains apolipoprotein A-I (apoA-I), phospholipids, and unesterified cholesterol. It participates in the retrieval of cholesterol from peripheral tissues. In this study we established a new sandwich enzyme immunoassay (EIA) for measuring plasma pre-beta1-HDL using mouse anti-human pre-beta1-HDL monoclonal antibody (MAb 55201) and goat anti-human apoA-I polyclonal antibody. MAb 55201 reacted with apoA-I in lipoprotein [A-I] with molecular mass less than 67 kDa, and with pre-beta1-HDL separated by nondenaturing two-dimensional electrophoresis, whereas it did not react with apoA-I in alpha-HDL. Pre-beta1-HDL levels measured by this method declined when incubated at 37 degrees C for 2 h, whereas this decrease was not observed in the presence of 2 mM lecithin:cholesterol acyltransferase inhibitor 5,5'-dithiobis (2-nitrobenzoic acid). To clarify the clinical significance of measuring pre-beta1-HDL by this method, 47 hyperlipidemic subjects [male/female 22/25; age 55 +/- 14 years; body mass index 25 +/- 4.5 kg/m(2); total cholesterol (TC) 245 +/- 64 mg/dl; triglyceride (TG) 232 +/- 280 mg/dl; HDL cholesterol (HDL-C) 51 +/- 23 mg/dl] and 25 volunteers (male/female 15/10; age 36 +/- 9.3 years; body mass index 23 +/- 3.5 kg/m(2); TC 183 +/- 28 mg/dl; TG 80 +/- 34 mg/dl; HDL-C 62 +/- 15 mg/dl) were involved. Plasma pre-beta1-HDL levels were significantly higher in hyperlipidemic subjects than in volunteers (39.3 +/- 10.1 vs. 22.5 +/- 7.5 mg/ml, P < 0.001) whereas plasma apoA-I levels did not differ (144.2 +/- 28.4 vs. 145.3 +/- 16.3 mg/dl). These results indicate that this sandwich EIA method specifically recognizes apoA-I associated with pre-beta1-HDL.

Adult↗
PubMed1999

Serum amyloid A protein generates pre beta 1 high-density lipoprotein from alpha-migrating high-density lipoprotein.

Serum amyloid A protein (SAA), an acute-phase reactant in reactive amyloidosis, has high affinity for high-density lipoprotein (HDL). When SAA is added to HDL, SAA displaces apolipoprotein A-I (apoA-I) and phospholipid from the HDL particles. These dissociated components may form prebeta1-HDL because free apoA-I can associate with phospholipid to become a lipoprotein having prebeta mobility. To determine whether SAA generates prebeta1-HDL from alpha-migrating HDL, we investigated the effects of recombinant SAA on HDL subfraction concentration using nondenaturing two-dimensional gradient gel electrophoresis. When we added SAA (0.5 mg/mL) to plasma, the prebeta1-HDL concentration increased by 164% (from 4.7% +/- 1.3% to 12.4% +/- 3.2% of apoA-I, p < 0.005). The increase in prebeta1-HDL was proportional to the dose of SAA. When we added SAA to a column of Sepharose beads coupled to the isolated HDL (alpha-migrating HDL), prebeta1-HDL was dissociated from the column together with the SAA-associated HDL. In summary, we demonstrate that SAA generates prebeta1-HDL from alpha-migrating HDL. We speculate that SAA-mediated HDL remodeling may take place in inflammation.

Adult↗
PubMed1999

In vitro examination of the safety of rotational atherectomy of side branches jailed by stents.

In vitro experimental models of branch orifices jailed by various stents were created to estimate the safety and the efficacy of rotational atherectomy when rotational burrs were advanced through the struts of stents. The scaffolding structures of the stents were destroyed due to loss and deflection of the struts, and the size of ablated stent-particles differed: the maximal size was 1.7 mm in slotted stents, and 17.6 mm in coiled stents. Thus, there is a definite potential for ablating stents when rotational atherectomy of restenotic lesions of side-branch orifices jailed by stents is performed.

Angioplasty, Balloon, Coronary↗