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Biomedical subjects

C Naito

Publications and source records attributed to C Naito.

At least 19 recordsLinked to original sources
PubMed1991

Plasmapheresis in conjunction with the dextran sulfate cellulose column for hypertriglyceridemic patient: a comparison with familial hypercholesterolemia.

For assessment of the usefulness of a dextran sulfate cellulose (DSC) column in the conduct of plasmapheresis (DSC lipoprotein adsorption, DSC-LA) for patients with hypertriglyceridemia on hemodialysis, a study was conducted to determine whether the adsorption of lipoproteins on a column varies in response to a variation in the lipoprotein composition. A patient with type V hyperlipoproteinemia on hemodialysis, a patient with type IIa homozygous, and a patient with type IIa heterozygous familial hypercholesterolemia were used in this study. In all patients, apolipoprotein B- and E-containing lipoproteins were removed preferentially by a DSC column. Following DSC-LA, abdominal pain before DSC-LA in a patient with type V hyperlipoproteinemia subsided, and regression of tuberous and tendinous xanthomas was induced in familial hypercholesterolemia. In cases of hyperlipoproteinemia, this column thus appears to exert a therapeutic effect regardless of the type of disease.

Achilles Tendon↗
PubMed1991

Long term effect of LDL apheresis in Japan. LDL Apheresis Study Group.

LDL-apheresis is introduced in many cases all over Japan. Among them, evaluation of long-term effect on ischemic heart disease (IHD) has made on 10 cases with homozygous familial hypercholesterolemia (FH) and 49 cases with heterozygous FH. As to homozygous FH, 3 patients had angina pectoris. Mean duration of treatment was 26 months (52 treatments). The changes in total cholesterol (TC) in each treatment was from 426 mg/dl to 151 mg/dl. Improvement in IHD was observed in 5 out of 10 cases. As to heterozygous FH, 17 cases had history of myocardial infarction and 12 had angina pectoris. Mean duration of treatment was 13 months (19 treatments). Mean TC was decreased from 271 mg/dl to 126 mg/dl by each treatment. Regression in Achilles tendon thickenting or skin and palpebral xanthomas was observed. Frequency of anginal attacks decreased in 8 out of 17 cases. Ischemic change in ECG were improved in 3 out of 26 cases. Coronary angiography performed with 2 to 3 years of interval in some cases revealed regression or no progression in coronary stenosis. As a whole, IHD improved in 15 cases and exacerbated in 2 cases. Main side effect was hypotension attack. Bradycardia and anginal attack during treatment were observed in some cases. LDL-apheresis was judged as effective in 25 out of 44 patients with IHD or xanthoma.

Blood Component Removal↗
PubMed1990

The effect of pravastatin in relation to low density lipoprotein receptor activity.

Pravastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, suppresses new synthesis of cholesterol via HMG-CoA in hepatocytes. As a result, low density lipoprotein (LDL) receptor activity in the liver is enhanced, which leads to lowering of plasma cholesterol. Inhibitors are shown to be effective in heterozygous familial hypercholesterolaemia (FH). Although FH heterozygotes are defined genetically as possessing half the normal LDL receptor activity, some heterogeneity of LDL receptor activity is observed in these patients. To see whether the effect of an inhibitor is related to LDL receptor activity in each patient, pravastatin was administered to 7 FH heterozygotes for 3 months at a daily dose of 10 mg; their mean LDL receptor activities measured before the therapy were 45.0 +/- 9.9% of the normal control. After medication, mean serum total cholesterol decreased from 349.0 to 279.7 mg/dl (p less than 0.05), and LDL-cholesterol decreased from 272.6 to 207.7 mg/dl (p less than 0.05). A significant correlation between the initial LDL receptor activity and the effect of pravastatin was not proved. However, the pre-treatment level of LDL-cholesterol was positively correlated (r = 0.795) with the absolute decrement of LDL-cholesterol after 3 months (p less than 0.05). This implies that the more LDL-cholesterol was elevated, the more pravastatin was effective.

Adult↗
PubMed1989

Selective removal of triglyceride-rich lipoproteins by plasmapheresis in diabetic patients with severe hypertriglyceridemia.

Two diabetic patients with marked intractable hypertriglyceridemia under treatment with hemodialysis for chronic renal failure were treated by either an apolipoprotein B-dependent removal of lipoproteins using dextran sulfate cellulose column plasmapheresis or a size-dependent removal of lipoproteins using hollow-fiber filtration plasmapheresis. In one patient, a column packed with hollow fibers was used as a plasma separator and a dextran sulfate cellulose column as an adsorbent. In another patient, because the hollow-fiber column did not separate plasma from whole blood, a centrifuge-type blood cell separator was used for the plasma separation. The amounts of plasma cholesterol, triglycerides, and phospholipids removed by plasmapheresis were 30%, 33%, and 30%, respectively, when the combination of a hollow-fiber column and a dextran sulfate cellulose column was used. Corresponding values were 31%, 29%, and 27%, respectively, when the combination of the centrifuge-type blood cell separator and the hollow-fiber column was used. The efficiency of lipid removal was almost the same with both techniques. As for plasma separation, the centrifuge-type blood cell separator was more efficient than the hollow-fiber column. Some losses of albumin and platelets were observed when combination plasmapheresis using the centrifuge-type blood cell separator and the hollow-fiber column was performed. In conclusion, we prefer the centrifuge-type blood cell separator to the hollow-fiber column for plasma separation of marked hypertriglyceridemia. The second filter must be chosen for each patient according to the size of the lipoproteins.

Adult↗
PubMed1988

Dose-dependent hypolipidemic effect of an inhibitor of HMG-CoA reductase, pravastatin (CS-514), in hypercholesterolemic subjects. A double blind test.

The hypolipidemic effect of a new HMG-CoA reductase inhibitor, pravastatin, was examined. The reductions of serum cholesterol and LDL-cholesterol were dose-dependent and significant differences were observed between placebo and 10 or 20 mg groups (P less than 0.01), and 10 and 20 mg (P less than 0.05) groups. The reduction rate of cholesterol after 8 weeks during medication was 16.1% in the 10 mg group, 20.5% in the 20 mg group compared to baseline serum cholesterol levels. LDL-cholesterol decreased by 23.9% in the 10 mg group, and 29.8% compared to baseline LDL-cholesterol in the 20 mg group. The lowering of total cholesterol was entirely attributed to a reduction in LDL-cholesterol.

Adult↗
PubMed1988

Activity of low-density lipoprotein receptors as estimated from concentrations of apolipoprotein B and C-II in serum.

The correlation between low-density lipoprotein (LDL) receptor activity and concentrations of lipids and apolipoproteins in serum was examined in 12 subjects with heterozygous familial hypercholesterolemia (FH) and in four with non-FH type II hyperlipoproteinemia. Concentrations of high-density lipoprotein cholesterol and of apolipoproteins (apo) A-I, C-II, and C-III were significantly positively correlated with LDL receptor activity, whereas LDL receptor activity was significantly inversely correlated with LDL cholesterol and apo B concentrations, and with apo ratios B/A-I and B/A-II. Neither total serum cholesterol, triglyceride, phospholipid, apo A-I, nor apo E concentrations correlated significantly with LDL receptor activity. Multiple regression analysis, with LDL receptor activity as the dependent variable, revealed concentrations of apo B and apo C-II to be the principal determinant factors. To confirm this, we subsequently calculated the LDL receptor activities before and after administration of CS-514, an inhibitor of hydroxymethylglutaryl-CoA reductase (EC 1.1.1.88), which increases the hepatic LDL receptor activity and decreases the concentration of cholesterol in serum. This drug increased calculated LDL receptor activities significantly, with a significant decrease in serum cholesterol.

Apolipoprotein C-II↗
PubMed1987

Enhanced degradation of low density lipoprotein in human monocyte-derived macrophages associated with an increase in its free fatty acid content.

Low density lipoprotein (LDL) rich in oleic acid (designated FFA-rich LDL) was produced by the reconstitution technique. FFA-rich LDL, like acetyl LDL, moved faster than native LDL in agarose gel electrophoresis. While FFA-rich LDL was observed to degrade far less than natural LDL in lymphocytes, its degradation in monocyte-derived macrophages was three times higher than that of natural LDL or LDL reconstituted without the addition of oleic acid. A competitive study showed that the catabolism of FFA-rich LDL in macrophages may be influenced by systems other than the acetyl LDL receptor.

Cells, Cultured↗
PubMed1987

Effect of dietary cholesterol on production of lipoproteins and apolipoproteins by perfused livers from Japanese monkeys (Macaca fuscata).

Isolated livers from Japanese monkeys were perfused for the purpose of characterizing low density lipoprotein (LDL) secreted directly by the liver, and for determining whether cholesterol feeding affects the hepatic production of LDL. Perfusate containing [3H]leucine was recirculated for 60 min, followed by perfusion with fresh perfusate for two additional 2-h periods. Radiolabelled lipoproteins, which are isolated by ultracentrifugation as very low density lipoprotein (VLDL), LDL, and high density lipoprotein were 0.87 +/- 0.74, 1.83 +/- 1.47, and 0.44 +/- 0.33%, respectively, of total radiolabelled protein in the medium of the last 2-h period. Subfractionation of perfusate LDL by high performance liquid chromatography, and by concanavalin A sepharose chromatography, revealed that the newly synthesized LDL were secreted as apo E-rich particles. Cholesterol feeding resulted in a four-fold increase in hepatic secretion of newly synthesized VLDL, but not of the LDL. The distribution of radioactivity among VLDL apolipoproteins was not affected by cholesterol feeding. Incorporation of radioactivity into apo B100 of LDL decreased significantly, but that into apo E did not change. These results suggested that (i) the elevation of serum LDL in cholesterol-fed monkeys is not due to enhanced hepatic production of LDL, but probably results from intravascular metabolism of VLDL, which is of hepatic origin, and (ii) cholesterol feeding affects the hepatic apo B100 synthesis and/or release but not apo E.

Animals↗
PubMed1986

Calmodulin-independent inhibition of platelet phospholipase A2 by calmodulin antagonists.

We tested the effects of calmodulin, two types of calmodulin antagonists, and various phospholipids on the phospholipase A2 activities of intact platelets, platelet membranes, and partially purified enzyme preparations. Trifluoperazine, chlorpromazine (phenothiazines) and N-(6-amino-hexyl)-5-chloro-1-naphthalenesulfonamide (W-7), at concentrations which antagonize the effects of calmodulin, significantly inhibited thrombin- and Ca2+ ionophore-induced production of arachidonic acid metabolites by suspensions of rabbit platelets and Ca2+-induced arachidonic acid release from phospholipids of membrane fractions, but not phospholipase A2 activity in purified enzyme preparations. The addition of acidic phospholipids, but not calmodulin, stimulated phospholipase A2 activity in purified enzyme preparations while decreasing its Km for Ca2+. The dose-response and kinetics of inhibition by calmodulin antagonists of acidic phospholipid-activated phospholipase A2 activity in purified preparations were similar to those of Ca2+-induced arachidonic acid release from membrane fractions. Calmodulin antagonists were also found to inhibit Ca2+ binding to acidic phospholipids in a similar dose-dependent manner. Our results suggest that the platelet phospholipase A2 is the key enzyme involved in arachidonic acid mobilization in platelets and is regulated by acidic phospholipids in a Ca2+-dependent manner and that calmodulin antagonists inhibit phospholipase A2 activity via an action on acidic phospholipids.

Animals↗
PubMed1986

The basic apolipoprotein A-I in the patients with familial lecithin:cholesterol acyltransferase deficiency.

The apolipoprotein A-I (apo A-I) from the patients with familial lecithin: cholesterol acyltransferase (LCAT) deficiency has been characterized. More than 10% of total serum apo A-I was recovered in the bottom fraction (d greater than 1.21 g/ml) of the patients' sera, while in normal sera, only 4.3 +/- 2.7% (Mean +/- SD) of apo A-I was found in the bottom fraction. The lipoproteins of the sera from the patients were analysed by density gradient ultracentrifugation and by high performance liquid chromatography (HPLC). Our HPLC analysis has revealed that the association of apo A-I with a lipid-poor HDL, observed in the patients, is not due to ultracentrifugal artifacts. The serum apo A-I isoproteins and their relative concentrations in the three patients were analysed by two dimensional electrophoresis. The isoprotein distribution for each of the three patients was as follows: isoproteins 2 and 3; 12.3, 21.2 and 25.7%, suggesting that the basic isoforms (isoproteins 2 and 3) were increased compared to normal controls (3.5 + 2.3%). The profile of apo A-I isoproteins of the bottom fraction was almost the same as that of the patient's HDL, indicating the equivalent affinity of each isoprotein with lipid and/or protein of HDL. These observations are compatible with the suggestion that the reduction of HDL-cholesterol in familial LCAT deficiency may be due to rapid catabolism of HDL, resulting in the increase in the ratio of apo A-I isoprotein 2 and 3 (immature form of isoprotein A-I) to isoprotein 4 and 5 (mature form of apo A-I).

Adult↗