Gamma radiation-induced thermoluminescence, trace element and paramagnetic defect of quartz from the Sambagawa metamorphic belt, Central Shikoku, Japan.

This study analyzes the Thermoluminescence (TL) emissions for five emission bands, trace element concentrations and defects in quartz grains extracted from metamorphic rocks and quartz veins in the Sambagawa metamorphic belt, central Shikoku. An emission of 500nm with 195, 245, and 320-325°C glow peaks are observed through the lowest to highest grade samples. A 450nm emission band with intense 195 and 245°C glow peaks and a 320-325°C shoulder peak is found in the higher grade samples. A 570nm emission band with a 170°C glow peak is observed in the samples derived from the lower grade zones. These characteristics of TL emissions of quartz suggest that they can be an indicator for the identification of rock derived from different metamorphic grades. The higher metamorphic grade samples with 450nm emission bands in particular show higher intensities of the E1' center. This relation indicates that the activation of the E1' center in higher metamorphic conditions possibly contributed to the 450nm emission band. Also, the 500nm emission band is generally observed in the samples with the signal intensities of the Aluminum hole center, suggesting that the center is the source of this emission band. We also observed that the lower metamorphic grade samples contain lower signal intensities of the Aluminum hole center, despite higher aluminum concentrations. This inconsistency indicates that the formation of interstitial aluminum ions cause local lattice distortion regions, where self-trapped excitons can be formed and presumably provide the 570nm emissions.

A child with adrenocortical adenoma accompanied by congenital hemihypertrophy: report of a case.

We report herein the findings of a 7-year-old male child with a ruptured adrenocortical adenoma and congenital hemihypertrophy which was incidentally detected after suffering a trauma. A review of 21 pediatric cases of adrenocortical neoplasms in the literature was made. The patient showed precocious puberty such as pubis and advanced bone age, but an endocrinological examination revealed no definite abnormalities. The right adrenal tumor with hematoma was resected after these evaluations. Adrenocortical adenoma is considered to occur more frequently in female children. However, the incidence of adrenocortical tumors accompanied by congenital hemihypertrophy does not differ between males and females. The outcomes were relatively good, although the observation periods were short in some patients. A large number of patients presented with a tumor and hemihypertrophy on the same side. This finding is of interest when considering the possible association between hemihypertrophy of the organs and tumor proliferation. However, their association in terms of development was unclear. It is necessary for patients with hemihypertrophy to have regular examinations for the possible development of malignant tumors, especially in the kidney, adrenal gland, and liver.

Effect of vitamin E on lipid metabolism and atherosclerosis in ESRD patients.

BACKGROUND: Oxidative stress is enhanced in patients with end-stage renal disease (ESRD) undergoing hemodialysis (HD). Bioincompatibility represents an important source of reactive oxygen species. HD patients exhibit altered anti-oxidative defences and anti-oxidative vitamins such as vitamin E and C are altered in uremia. Frequently, HD patients also suffer from atherosclerotic cardiac disease. We have previously reported that low density lipoprotein (LDL) of HD patients is rich in malondialdehyde (MDA), an end product of lipid peroxidation. MDA rich LDL is thought to be an atherogenic lipoprotein due to its enhancement of macrophage foam cell formation. METHODS: We conducted a controlled study for two years comparing the effects of a vitamin E coated cellulose membrane dialyzer and an ordinary cellulose membrane dialyzer on lipid metabolism and the progress of atherosclerosis. LDL-MDA and oxidized LDL (ox-LDL) were measured in HD patients using these two types of dialyzers. Plasma vitamin E and lipid concentrations were also evaluated. The aortic calcification index (ACI) was evaluated by CT scan to assess the progress of atherosclerosis before and for every year after treatment. RESULTS: Use of a vitamin E coated cellulose membrane dialyzer for six months, one year and two years resulted in a significant reduction in LDL-MDA and ox-LDL compared to the ordinary cellulose membrane dialyzer. Treatment with a vitamin E-coated dialyzer significantly reduced the percentage increase in ACI after 24 months compared to the control. There were no significant changes in plasma vitamin E and lipid concentrations between the two groups. CONCLUSIONS: These results suggest that the oxidative stress could be one of the stimulating factors of abnormal lipid metabolism and atherosclerosis in ESRD patients.

Effect of simvastatin on the lipid profile of hemodialysis patients.

BACKGROUND: Simvastatin, a 3-hydroxy 3-methylglutaryl co-enzyme A (HMG-CoA) reductase inhibitor, is used widely for treatment of hypercholesterolemia. Simvastatin may be a suitable treatment for dyslipidemia in hemodialysis (HD) patients. However, investigation of the side-effects and safety of long-term administration of simvastatin to HD patients has been limited. In this study, we investigated the effects and safety of simvastatin and its effects on lipoprotein metabolism in hypercholesterolemic patients on HD. METHODS: Simvastatin was administered at a dosage of 5 mg/day for 24 weeks to 38 HD patients with high serum total cholesterol (TC) levels (200 mg/dl) or low high-density lipoprotein cholesterol (HDL-C) levels (35 mg/dl). Every four weeks, serum lipids, apolipoprotein, lipoprotein (a) [Lp(a)] and malondialdehyde (MDA) levels were measured. In addition, lipid levels were determined in each lipoprotein fraction separated by ultracentrifugation. RESULTS: After 24 weeks of simvastatin administration, TC significantly decreased by 25.7%, and low-density lipoprotein cholesterol (LDL-C) was significantly decreased by 33.6%. Triglyceride (TG) and HDL-C showed no significant changes. Apolipoprotein (apo) B significantly decreased by 24.5% and apo E by 30.0%. No significant changes were observed in the other apolipoproteins. MDA was also significantly decreased, whereas Lp(a) was not significantly altered. In the lipoprotein fractions, very LDL cholesterol (VLDL-C), intermediate-density lipoprotein cholesterol (IDL-C), LDL1 cholesterol (LDL1-C), and LDL2 cholesterol (LDL2-C) showed significant decreases. No particular side-effects were observed during the 12 months of simvastatin administration. CONCLUSIONS: These results suggest that simvastatin appears to be safe and effective in HD patients with hypercholesterolemia.

[Effects of hemodialysis membrane on serum lipid profile of maintenance hemodialysis patients].

Atherosclerosis and lipid abnormalities are still insuperable complications for maintenance hemodialysis patients. We observed the serum lipid profile of 27 maintenance hemodialysis patients (M : F; 20 : 7, age; 54.9 +/- 6.2 y. o., hemodialysis duration; 10.8 +/- 4.9 years, body weight; 53.6 +/- 4.4 kg) using a low flux cellulose membrane, cellulose (1.5 m2), a vitamin-E-modified dialysis membrane, CL-15E (CL- 15E 1.5 m2, Terumo), and polysulfon, PS (PS-1.3UW 1.3 m2, Fresenius) dialysers. Each membrane dialyzer was used for 3 months. The blood flow rate was 200 ml/min, and hemodialysis time, 4 hours. When the dialyzers were replaced, fasting blood was collected at the beginning of hemodialysis and serum lipid parameters were measured. Seven additional maintenance hemodialysis patients were selected and TC, TG, HDL-C were measured as controls, because their dialyzers (low flux cellulose 1.5 m2) and hemodialysis conditions were not changed during the study. TC was decreased by PS and there were significant differences between cellulose and PS, and between CL-15E and PS. However, these changes were conducted within the normal range of TC. TG was not significantly changed during the study. HDL-C was decreased by CL-15E and PS as well as TC. There were significant differences in HDL-C between cellulose and CL-15E, and between cellulose and PS. Apo B, Apo B/A-I were decreased by PS and there were significant differences between cellulose and PS, respectively, LP(a) was not changed during the study. RLP-C (Cellulose vs. PS, CL-15E vs. PS), VLDL-C (Cellulose vs PS), and LDL-C (cellulose vs. PS, CL-15E vs. PS) were significantly decreased between membranes, respectively. Although the precise mechanism is yet unknown, the uptake of LDL and remnant into receptors of the liver might be improved by PS hemodialysis. In conclusion, these data suggest that PS decreased the serum levels of the lipid profile in maintenance hemodialysis patients and may be effective in improving their lipid abnormality.

Reproduction of progressive retinal degeneration (bright blindness) in sheep by administration of ptaquiloside contained in bracken.

The process of occurrence of bright blindness, progressive retinal degeneration (PRD), in sheep was observed using two Suffolk ram lambs fed on a diet containing bracken powder. The first sign of the bright blindness was detected 4 months after the start of experiment. Based on these preliminary results, the amount of bracken powder necessary to induce PRD was estimated (experiment I). In the following experiment, ptaquiloside (PT), a norsesquiterpene glucoside of the illudane type isolated from bracken, which is a bracken carcinogen and a causative principle of cattle bracken poisoning was administered to two Suffolk ram lambs. It was clearly demonstrated in this experiment (experiment II) that PT present in bracken is also a causative principle of PRD.

Effect of platelet-activating factor on lipoprotein lipase and blood lipids.

We investigated the effect of platelet-activating factor (PAF) and of the PAF specific antagonist CV-6209 on plasma lipid metabolism, and particularly on post-heparin plasma lipolytic activity in male Wistar rats. Lipoprotein lipase (LPL) activity was enhanced by intravenous injection of PAF before intravenous injection of heparin when the PAF dose was low (0.2 micrograms/kg). PAF activated hepatic triacylglycerol lipase (HTGL) activity dose-dependently. Plasma triacylglycerols (TG) significantly decreased with the activation of LPL and/or HTGL. Plasma total cholesterol (TC) and phospholipid (PL) levels decreased at a low dose of PAF (0.2 micrograms/kg), but increased when higher doses were used. The PAF antagonist CV-6209 partially reversed the PAF induced effects on HTGL, TC and PL.

Enhancement of non-polar lipid transfer reaction through stabilization of substrate lipid particles with apolipoproteins.

Transfer of lipids was studied between human plasma low density lipoproteins (LDL) and triolein particles coated with an egg phosphatidylcholine monolayer, with diameter of 27 +/- 4 nm. The lipid particles were unstable and seemed to aggregate to LDL when incubated with LDL either in the presence or the absence of bovine serum albumin. Human apolipoproteins A-I, A-II, C-II, C-III, and E stabilized the lipid particles and completely prevented this process. Cholesterol rapidly appeared in the lipid particles to reach homogeneous distribution among the phospholipid surfaces of LDL and the lipid particles regardless of whether apolipoproteins were present or absent. Cholesteryl ester spontaneously appeared in the lipid particles to some extent in the absence of the apolipoproteins, and human plasma lipid transfer protein enhanced this reaction only to a very limited extend. When the lipid particles were stabilized with the apolipoproteins, spontaneous cholesteryl ester transfer was minimized and the lipid transfer protein catalyzed the transfer of cholesteryl ester markedly. There was no specific difference among the apolipoproteins in stabilizing the particles and enhancing the transfer reaction. Reciprocal decrease in volume of triglyceride was observed at the same time in the lipid particles until the relative content of cholesteryl ester in the cores of LDL was the same as in the lipid particles. The kinetics of the cholesteryl ester and triglyceride transfer was consistent with the model that the reaction is bidirectional in equilibrium and takes both non-polar lipids as substrate in a single pool.

Probucol prevents lipid storage in macrophages.

Effects of probucol on lipid storage in macrophages in vitro in the presence of acetylated low density lipoprotein (acetyl-LDL) were observed using macrophage-like cells (UE-12) established from a human histiocytic lymphoma cell line (U-937). Under ordinary light microscopy as well as under electron microscopy we found that probucol added to the medium, either in ethanolic solution or bound to LDL, markedly prevented the development of macrophages into foam cells. Microscale enzymatic assay of cholesterol also showed that the intracellular accumulation of esterified cholesterol caused by acetyl-LDL was markedly decreased by the addition of probucol. The concentration of probucol added to the medium was almost comparable to the plasma concentration of the drug usually obtained in patients under treatment with probucol. The possibility that probucol interferes with the binding of acetyl-LDL to the receptors on the cell surface was suggested. The results of the present investigation coincide with the clinical findings that probucol causes a more marked regression of xanthomas than would be expected from the extent of lowering of LDL cholesterol.

High density lipoproteins with poor reactivity to cholesteryl ester transfer reaction observed in a homozygote of familial hyperalphalipoproteinemia.

A homozygous patient of familial hyperalphalipoproteinemia was found impaired in cholesteryl ester transfer between high and low density lipoproteins (HDL and LDL) in the plasma (T. Kurasawa et. al. J. Biochem. 98: 1499-1508 (1985)). None of the heterozygotes investigated in his family was shown decreased in the transfer rate in spite of their moderately elevated HDL levels. Plasma d = 1.21 bottom fraction of the patient contained substantial transfer activity with normal HDL, while HDL from the patient showed poor reactivity with the d = 1.21 bottoms of the normal plasma and the patient's plasma. HDL from the patient increased the reactivity to the transfer reaction upon occasion without significant change in its physical and chemical properties.

A method for direct incorporation of radiolabeled cholesteryl ester into human plasma low-density-lipoproteins: preparation of tracer substrate for cholesteryl ester transfer reaction between lipoproteins.

[14C]Cholesteryl ester was directly incorporated into human plasma low-density lipoproteins (LDL) for the purpose of preparing a tracer substrate for investigation of the cholesteryl ester transfer reaction between plasma lipoproteins. The radiolabeled cholesteryl oleate was sonicated with egg phosphatidylcholine to form cholesteryl ester-containing liposomes. The liposomes were incubated with plasma fraction of density greater than 1.006 at 37 degrees C in the presence of dithionitrobenzoic acid. When the distribution of the radiolabeled cholesteryl ester was equilibrated among liposomes and lipoprotein fractions, the mixture was applied to an affinity chromatography column of dextran sulfate-cellulose (LA01) (Arteriosclerosis 4, 276-282). LDL was eluted by increasing the NaCl concentration and was finally isolated as a floating fraction by ultracentrifugation at a solvent density of 1.063 (adjusted with NaCl). The chemical composition, electrophoretic mobility and density of the labeled LDL were consistent with those of the native LDL. Radioactivity in this preparation was present exclusively in cholesteryl ester. Apolipoprotein B100 was preserved intact throughout the procedure. When the rate of cholesteryl ester transfer was measured between LDL and high-density lipoproteins by using this labeled LDL, the kinetics was consistent with the equilibrium transfer model, but the apparent rate measured was slightly higher than that measured with the labeled LDL prepared by the method using the intrinsic cholesterol esterification reaction of plasma.