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  • Articles: DFG German National Licenses  (3)
  • 1995-1999  (2)
  • 1965-1969  (1)
  • dietary fatty acids  (2)
  • low-density lipoprotein composition  (2)
  • Actin  (1)
  • 1
    ISSN: 1432-0428
    Keywords: 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.
    Type of Medium: Electronic Resource
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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 12 (1969), S. 218-226 
    ISSN: 1432-0533
    Keywords: Muscle ; Actin ; Z-Line ; Myofibril ; Loss of Myofilaments
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Verlust der I-Band-Myofilamente und des Materials im Z-Streifen werden bei drei verschiedenen pathologischen Zuständen beschrieben. dystrophischer Myotonie, subakuter spinaler Strangdegeneration und myatrophischer Lateralsklerose. Im Falle einer myatrophischen lateralsklerose wird auch eine Hypertrophie des Z-Streifens beschrieben. Es wird eine mögliche cyclische Alteration des Z-Streifens als Reaktion auf verschiedene, bisher unbekannte pathologische Reize und in Verbindung damit ein Verlust der Myofilamente des I-Bandes vermutet.
    Notes: Summary Loss of I-band myofilaments and Z-line material is described in three different pathological conditions; namely, dystrophia myotonica, sub-acute combined degeneration of the spinal cord and amyotrophic lateral sclerosis. In the case of amyotrophic lateral sclerosis hypertrophy of the Z-line is also described. A possible cyclical alteration in the Z-line in response to, so far unknown, pathological stimuli is suggested and in conjunction with this possible loss of I-band myofilaments.
    Type of Medium: Electronic Resource
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