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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 33 (1961), S. 468-470 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 31 (1959), S. 1862-1867 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 41 (1994), S. C185 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stimulation of human neutrophils with zymosan particles resulted in a dose-response release of IL-8 in the 24 h culture supernatant, measured using a specific radioimmunoassay. IL-8 was detected after 8 h (0.11±0.08 nM) and peaked at 24 h (2.81±0.85 nM). Two distinct PAF receptor antagonists, WEB 2086 and UK 74505 produced a dose-dependent inhibition of zymosan-induced IL-8 release. This inhibitory action was maximal (68% 10−6 M WEB 2086; 71% 10−8 M UK 74505) when the drug was co-administered with zymosan, becoming progressively less effective when administered at increasing intervals after addition of zymosan. In contrast, a specific LTB4 antagonist, LY 255283, an IL-1 receptor antagonist and an anti-human TNFα antibody were unable to modulate the response indicating that these mediators are not involved. This study provides the first direct evidence of a central role for the phospholipid mediator PAF in the pathway of IL-8 release, following neutrophil activation by a particulate stimulusin vitro.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Rabbits ; diabetes ; hypercholesterolaemia ; lipoproteins ; cholesterol metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Serum lipoproteins and key hepatic and intestinal enzymes regulating cholesterol synthesis, esterification and catabolism, namely 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase, acyl coenzyme A: cholesterol-o-acyltransferase (ACAT) and cholesterol 7α-hydroxylase respectively, were compared in two hypercholesterolaemic rabbit models — the cholesterol-fed animal and the hypercholesterolaemic diabetic animal. Hypercholesterolaemia in the cholesterol-fed animals was reflected in the VLDL and LDL fractions, whereas VLDL and HDL2 cholesterol levels were elevated in the diabetic animals. The lipoproteins of the cholesterol-fed animals were enriched with cholesterol but the lipoprotein fractions in the diabetic animals were enriched with triacylglycerol. While hepatic HMGCoA reductase activity was significantly reduced in both groups, the activities of hepatic ACAT and cholesterol 7α-hydroxylase were significantly increased in the cholesterol-fed animals and significantly reduced in the diabetic animals compared with controls. In the intestine, the activity of HMGCoA reductase was increased and ACAT reduced in the diabetic animals. By contrast, in the cholesterol-fed group, HMGCoA reductase activity was lower and ACAT activity was higher in comparison with the control group. These differences in lipoproteins and cellular cholesterol metabolism between the hypercholesterolaemic rabbit models may explain the differences in susceptibility to atherosclerosis, previously reported in these two animal models.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; LDL ; cholesterol ; esterification ; glycosylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study investigates the relationship between Type 2 (non-insulin-dependent) diabetes mellitus and hypercholesterolaemia with regard to delivery of cholesterol to cells and regulation of endogenous cholesterol synthesis. The ability of LDL, from hypercholesterolaemic and Type 2 diabetic patients, to suppress cellular cholesterologenesis and to enhance mitogen-stimulated lymphocyte proliferation was compared. Cholesterol synthesis was estimated by measuring [14C]-acetate incorporation into cholesterol and lymphocyte proliferation was assessed by [3H]-thymidine incorporation into mitogen-stimulated normal lymphocytes. The results indicate that LDL from both Type 2 diabetic patients in poor metabolic control and hypercholesterolaemic patients was significantly less effective (p 〈 0.001) than LDL from non-diabetic normocholesterolaemic subjects in suppressing cholesterol synthesis in lymphocytes. LDL from all hypercholesterolaemic patients enhanced lymphocyte proliferation to a greater extent than LDL from normocholesterolaemic subjects and this effect was significantly increased using LDL from Type 2 diabetic, hypercholesterolaemic patients. Both suppression of [14C]-acetate incorporation and enhancement of [3H]-thymidine uptake could be related to an increased esterified/free cholesterol ratio in the LDL particle. The fact that cholesterol synthesis and cell proliferation were markedly altered by the above changes in LDL composition suggests a mechanism for cellular cholesterol accumulation in the Type 2 diabetic patient, even in the absence of elevated serum cholesterol levels.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Key words Apolipoprotein B-48 ; triglyceride-rich lipoproteins ; NIDDM ; cholesterol ; triglyceride.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The intestine is a major site of cholesterol synthesis and produces apolipoprotein B-48, which is critical for intestinal cholesterol absorption and secretion. The purpose of this study was to examine postprandial changes in apolipoprotein B-48 in diabetes. Six non-insulin-dependent diabetic patients and six non-diabetic control subjects were given a high-fat meal (1300 kcal) and blood samples were taken pre- and postprandially, from which the triglyceride-rich lipoprotein fraction was isolated by ultracentrifugation (density 〈 1.006 g/ml). Apolipoprotein B-48 was separated on 4–15 % gradient gels and quantified as a percentage of the fasting concentration by densitometric scanning. Total protein, triglyceride and cholesterol in the triglyceride-rich lipoprotein fraction, blood glucose, and serum insulin were also measured. Diabetic patients exhibited a postprandial triglyceride-rich apolipoprotein B-48 profile significantly different from that of control subjects (p 〈 0.05). The triglyceride and total protein concentration in the triglyceride-rich lipoprotein fraction mirrored the post-prandial profile and apolipoprotein B-48 in both groups. Significantly different patterns for triglyceride (p 〈 0.02) and total protein (p 〈 0.05) following the fat-rich meal were observed in the two groups. Fasting and postprandial triglyceride-rich lipoprotein cholesterol and total apolipoprotein B were significantly higher in diabetic patients than in control subjects (p 〈 0.05). Since apolipoprotein B-48 is the structural protein of intestinally-derived lipoprotein particles, these studies suggest an abnormality in intestinal lipoprotein metabolism in diabetes. [Diabetologia (1994) 37: 1259–1264]
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Non-insulin-dependent diabetes mellitus ; low density lipoprotein oxidation ; low density lipoprotein fatty acids ; lipid peroxidation ; conjugated dienes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Oxidation of low density lipoprotein (LDL) plays an important role in the pathogenesis of atherosclerosis and is related to the fatty acid composition which is altered in diabetes mellitus. This study examines the relationship between the fatty acid composition of LDL and high density lipoprotein (HDL) and lipoprotein oxidation. A group of nine non-insulin-dependent diabetic (NIDDM) patients were compared to seven healthy control subjects before and after a high monounsaturated diet. Lipoproteins were isolated and oxidisability was measured by conjugated diene formation and lipid peroxide analysis. Serum HDL cholesterol was significantly lower in the diabetic patients. LDL cholesteryl ester linoleic acid in the diabetic patients was significantly higher at baseline and decreased after diet (p〈0.05) while oleic acid increased in both diabetic and non-diabetic subjects (p〈0.05). HDL cholesteryl ester oleic acid was lower in the diabetic patients compared with control subjects (p〈0.05) before diet and it increased significantly after diet (p〈0.05). LDL lipid peroxides and conjugated diene formation were related to LDL glycation (r=0.46, p〈0.05 and r=0.49, p〈0.05, respectively). Both decreased following diet (lipid peroxides for diabetic patients from 476±30 to 390±20 nmol/mg protein p〈0.05 and for control subjects from 350±36 to 198±30 nmol/mg protein p〈0.05). HDL conjugated diene formation decreased in both groups after diet but only significantly in the control group (55.4±7.5 to 53.2±6.7 nmol/mg protein for diabetic patients and 45.8±6.4 to 31.6±4.8 nmol/mg protein p〈0.05 for control subjects). There was a positive correlation between LDL lipid peroxide formation and percentage of cholesteryl ester linoleic acid in LDL from diabetic patients (r=0.61, p〈0.05) and control subjects (r=0.91, p〈0.01). Fatty acid composition of LDL was reflected in the composition of HDL. In the presence of HDL lipoprotein peroxidation decreased. This decrease in lipoprotein peroxidation was positively related to the percentage of linoleic acid in LDL (r=0.71, p〈0.05). This study confirms the close relationship between the fatty acid composition of LDL and HDL and demonstrates the importance of the fatty acid composition of the cholesteryl ester fraction in relation to LDL oxidation in diabetes. Linoleic acid in HDL appears to be a protecting factor against oxidation.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Keywords: Key words Non-insulin-dependent diabetes mellitus ; low-density lipoprotein oxidation ; dietary fatty acids ; low-density lipoprotein composition ; glycated low-density lipoprotein.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The increased risk of atherosclerotic disease in diabetic subjects may be due to enhanced foam cell formation following an increased susceptibility of low density lipoprotein to oxidative modification. This study has compared fatty acid content and lipoprotein oxidisability in 10 non-insulin-dependent diabetic subjects with that in 10 control subjects. Both groups were normocholesterolaemic and the diabetic subjects had higher triglyceride levels (2.2 ± 0.4 vs 1.2 ± 0.2 mmol/l, p 〈 0.05). The fatty acid composition was compared in low density lipoprotein following Folch extraction, separation by thin layer chromatography (for the lipid classes) and analysis by gas liquid chromatography. Low density lipoprotein oxidisability was assessed by conjugated diene and thiobarbituric acid reacting substance formation in the presence of copper ions. The esterified/free cholesterol ratio was higher in the low density lipoprotein from patients compared to control subjects (2.9 ± 0.1 vs 1.9 ± 0.3, p 〈 0.05). Linoleic acid in the cholesteryl ester fraction of the lipoprotein was higher in the patients than in the control subjects (48.2 ± 2.2 % vs 42.4 ± 3.4 %, p 〈 0.05) as was the total quantity of linoleic acid in the cholesteryl ester fraction (317.8 ± 68.0 vs 213.2 ± 28.0 μg/mg protein, p 〈 0.05) and in the low-density lipoprotein as a whole (443.2 ± 70.0 vs 340.2 ± 28.2 μg/mg protein, p 〈 0.05). Lipoprotein oxidisability was also increased in the diabetic group with increased formation of thiobarbituric acid reacting substances (35.6 ± 7.2 vs 22.3 ± 3.5 nmol/mg protein, p 〈 0.05, increased total diene formation (502 ± 60 vs 400 ± 30 nmol/mg protein, p 〈 0.05) and increased rate of diene formation (7.2 ± 0.6 vs 5.1 ± 0.9 nmol diene · mg protein–1· min–1, p 〈 0.05). This study indicates that low-density lipoprotein from diabetic subjects is more susceptible to oxidation. This could, in vivo, accelerate foam-cell formation thereby increasing atherosclerotic risk in diabetic subjects. [Diabetologia (1995) 38: 1300–1306]
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0428
    Keywords: Keywords Non-insulin-dependent diabetes mellitus ; low density lipoprotein oxidation ; low density lipoprotein fatty acids ; lipid peroxidation ; conjugated dienes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Oxidation of low density lipoprotein (LDL) plays an important role in the pathogenesis of atherosclerosis and is related to the fatty acid composition which is altered in diabetes mellitus. This study examines the relationship between the fatty acid composition of LDL and high density lipoprotein (HDL) and lipoprotein oxidation. A group of nine non-insulin-dependent diabetic (NIDDM) patients were compared to seven healthy control subjects before and after a high monounsaturated diet. Lipoproteins were isolated and oxidisability was measured by conjugated diene formation and lipid peroxide analysis. Serum HDL cholesterol was significantly lower in the diabetic patients. LDL cholesteryl ester linoleic acid in the diabetic patients was significantly higher at baseline and decreased after diet (p 〈 0.05) while oleic acid increased in both diabetic and non-diabetic subjects (p 〈 0.05). HDL cholesteryl ester oleic acid was lower in the diabetic patients compared with control subjects (p 〈 0.05) before diet and it increased significantly after diet (p 〈 0.05). LDL lipid peroxides and conjugated diene formation were related to LDL glycation (r = 0.46, p 〈 0.05 and r = 0.49, p 〈 0.05, respectively). Both decreased following diet (lipid peroxides for diabetic patients from 476 ± 30 to 390 ± 20 nmol/mg protein p 〈 0.05 and for control subjects from 350 ± 36 to 198 ± 30 nmol/mg protein p 〈 0.05). HDL conjugated diene formation decreased in both groups after diet but only significantly in the control group (55.4 ± 7.5 to 53.2 ± 6.7 nmol/mg protein for diabetic patients and 45.8 ± 6.4 to 31.6 ± 4.8 nmol/mg protein p 〈 0.05 for control subjects). There was a positive correlation between LDL lipid peroxide formation and percentage of cholesteryl ester linoleic acid in LDL from diabetic patients (r = 0.61, p 〈 0.05) and control subjects (r = 0.91, p 〈 0.01). Fatty acid composition of LDL was reflected in the composition of HDL. In the presence of HDL lipoprotein peroxidation decreased. This decrease in lipoprotein peroxidation was positively related to the percentage of linoleic acid in LDL (r = 0.71, p 〈 0.05). This study confirms the close relationship between the fatty acid composition of LDL and HDL and demonstrates the importance of the fatty acid composition of the cholesteryl ester fraction in relation to LDL oxidation in diabetes. Linoleic acid in HDL appears to be a protecting factor against oxidation. [Diabetologia (1996) 39: 667–676]
    Type of Medium: Electronic Resource
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