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  • 1
    Electronic Resource
    Electronic Resource
    COMPARATIVE EXPERIMENTS UPON CHEMICAL PRESERVATIVES IN MILK. (1905)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 27 (1905), S. 1060-1068 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja01987a004
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  • 2
    Electronic Resource
    Electronic Resource
    Insulin increases cyclic nucleotide content in human vascular smooth muscle cells: a mechanism potentially involved in insulin-induced modulation of vascular tone (1995)
    Springer
    Diabetologia 38 (1995), S. 936-941 
    Details
    ISSN: 1432-0428
    Keywords: Insulin ; arterial hypertension ; vasodilation ; vascular smooth muscle cells ; cyclic adenosine monophosphate ; cyclic guanosine monophosphate ; nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been suggested that insulin exerts a vasodilating effect, but the mechanisms involved are not completely understood. Since cyclic nucleotides mediate the vasodilation induced by endogenous substances, such as prostacyclin and nitric oxide, we aimed to investigate the influence of insulin (concentration range 240–960 pmol/l) on both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) content in human vascular smooth muscle cells. Insulin dose-dependently increased both nucleotides (cAMP: from 0.7±0.1 to 2.6±0.4 pmol/106 cells, p=0.0001; cGMP: from 1.3±0.2 to 3.4±0.7 pmol/106 cells, p=0.033). This increase is receptor-mediated, since it was blunted when cells were preincubated with the tyrosine kinase inhibitor genistein. The effect of insulin remained significant (p=0.0001) when preincubation with the phosphodiesterase inhibitor theophylline prevented cyclic nucleotide catabolism. The increase of cGMP was blunted when the cells were preincubated with the guanylate cyclase inhibitor methylene blue, and with the nitric oxide-synthase inhibitor NG-monomethyl-l-arginine. At all the concentrations tested, insulin potentiated the increase of cAMP induced by the stable prostacyclin analogue Iloprost (p=0.0001), whereas only at 1920 pmol/l did it potentiate the cGMP increase induced by glyceryltrinitrate (p=0.05). This study demonstrates that the vasodilating effects exerted by insulin may at least in part be attributable to an increase of both cGMP and cAMP via a receptor-mediated activation of adenylate and guanylate cyclases in human vascular smooth muscle cells and that the insulin effect on cGMP is mediated by nitric oxide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400582
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  • 3
    Electronic Resource
    Electronic Resource
    Insulin increases cyclic nucleotide content in human vascular smooth muscle cells: a mechanism potentially involved in insulin-induced modulation of vascular tone (1995)
    Springer
    Diabetologia 38 (1995), S. 936-941 
    Details
    ISSN: 1432-0428
    Keywords: Key words Insulin ; arterial hypertension ; vasodilation ; vascular smooth muscle cells ; cyclic adenosine monophosphate ; cyclic guanosine monophosphate ; nitric oxide.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been suggested that insulin exerts a vasodilating effect, but the mechanisms involved are not completely understood. Since cyclic nucleotides mediate the vasodilation induced by endogenous substances, such as prostacyclin and nitric oxide, we aimed to investigate the influence of insulin (concentration range 240–960 pmol/l) on both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) content in human vascular smooth muscle cells. Insulin dose-dependently increased both nucleotides (cAMP: from 0.7 ± 0.1 to 2.6 ± 0.4 pmol/106 cells, p = 0.0001; cGMP: from 1.3 ± 0.2 to 3.4 ± 0.7 pmol/106 cells, p = 0.033). This increase is receptor-mediated, since it was blunted when cells were preincubated with the tyrosine kinase inhibitor genistein. The effect of insulin remained significant (p = 0.0001) when preincubation with the phosphodiesterase inhibitor theophylline prevented cyclic nucleotide catabolism. The increase of cGMP was blunted when the cells were preincubated with the guanylate cyclase inhibitor methylene blue, and with the nitric oxide-synthase inhibitor NG-monomethyl-l-arginine. At all the concentrations tested, insulin potentiated the increase of cAMP induced by the stable prostacyclin analogue Iloprost (p = 0.0001), whereas only at 1920 pmol/l did it potentiate the cGMP increase induced by glyceryltrinitrate (p = 0.05). This study demonstrates that the vasodilating effects exerted by insulin may at least in part be attributable to an increase of both cGMP and cAMP via a receptor-mediated activation of adenylate and guanylate cyclases in human vascular smooth muscle cells and that the insulin effect on cGMP is mediated by nitric oxide. [Diabetologia (1995) 38: 936–941]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400582
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  • 4
    Electronic Resource
    Electronic Resource
    Influence of protamine on adhesion, chemotaxis and proliferation of human vascular smooth muscle cells (1997)
    Springer
    Diabetologia 40 (1997), S. 67-75 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Protamine ; insulin ; heparin ; vascular smooth muscle cells ; diabetic angiopathy ; atherosclerosis.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been shown that, in streptozotocin diabetic rats, protamine-retarded insulin administered in vivo stimulates intimal hyperplasia in balloon-injured carotid artery. The aim of this study was to evaluate the influence of protamine on cultured human vascular smooth muscle cells (hVSMC), by observing its effects on adhesion, chemotaxis and proliferation. hVSMC were isolated during abdominal surgery, cultured and utilized at passages 6–10. We observed that protamine stimulates: 1) cell adhesion in the concentration range 0.04–20 μg/ml (analysis of variance, ANOVA, p 〈 0.0001); 2) cell chemotaxis in the absence of fetal calf serum (FCS) in the concentration range 1–200 μg/ml (ANOVA, p 〈 0.0001) and in the presence of 1 % FCS in the concentration range 5–200 μg/ml (ANOVA, p 〈 0.0001), further enhancing the chemotaxis induced by 10 % FCS in the concentration range 20–200 μg/ml (ANOVA, p 〈 0.0001); 3) cell proliferation and 3H-thymidine incorporation from 1 to 5 μg/ml (ANOVA, p 〈 0.0001); 4) cell c-fos oncoprotein nuclear expression. We also observed that protamine effects on chemotaxis, proliferation and c-fos expression are inhibited by heparin that human insulin stimulates cell proliferation and 3H-thymidine incorporation (ANOVA, p 〈 0.0001) at concentrations equal to or greater than 480 pmol/l and that these effects of insulin persist in the presence of protamine. In conclusion, protamine influences hVSMC behaviour by interfering with biological functions involved in atherogenesis. The concentrations used in this short-term in vitro study were higher than those probably occurring in vivo in patients chronically treated by protamine-retarded insulin preparations: further studies, therefore, are needed to evaluate the safety of protamine as a retardant of insulin action in vivo. [Diabetologia (1997) 40: 67–75]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050644
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  • 5
    Electronic Resource
    Electronic Resource
    The AB-variant of metachromatic leukodystrophy (Postulated activator protein deficiency) (1981)
    Springer
    Acta neuropathologica 55 (1981), S. 281-287 
    Details
    ISSN: 1432-0533
    Keywords: AB-variant metachromatic leukodystrophy ; Activator protein deficiency ; Ultrastructure of sulfatide inclusions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The histopathological findings in a sural nerve biopsy of a new distinct variant of metachromatic leukodystrophy (MLD) are compared to those of classical MLD. The clinical and histological features are typical of a sulfatide lipidosis, yet in vitro activities of arylsulfatases A and B and cerebroside sulfatase are normal. Intact skin fibroblasts, when cultured in a medium supplemented with labelled sulfatide, show impaired in vivo sulfatide hydrolysis. A deficiency of the requisite activator protein is postulated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690991
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  • 6
    Electronic Resource
    Electronic Resource
    Intraneural injection of lymphocytes in experimental allergic neuritis (1983)
    Springer
    Acta neuropathologica 61 (1983), S. 61-64 
    Details
    ISSN: 1432-0533
    Keywords: Experimental allergic neuritis ; Lymphocytes ; Passive transfer ; Intraneural injection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Passive transfer of experimental allergic neuritis (EAN) lymph node cells (LNC) by intraneural injection did not produce significant demyelination. EAN-LNC stimulated with myelin in vitro produced mild demyelination while those incubated with Concanavalin A had no effect. The lack of demyelination by unstimulated EAN-LNC is in contrast to the marked demyelination produced by intraneural injection of EAN serum. The mononuclear cell infiltration and demyelination of classical EAN seem to require both cellular and humoral immune responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688387
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  • 7
    Electronic Resource
    Electronic Resource
    P2-peptide induced experimental allergic neuritis: a model to study axonal degeneration (1991)
    Springer
    Acta neuropathologica 82 (1991), S. 60-65 
    Details
    ISSN: 1432-0533
    Keywords: Experimental allergic neuritis: P2 myelin peptide ; Demyelination ; Axonal degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In experimental allergic neuritis (EAN) severity of clincal disease and pathology correlate with the dose of antigen (Hahn et al., Lab Invest 59:115–125, 1988). To avoid axonal membrane contamination of the antigen, EAN was induced with a synthetic peptide, corresponding to residues 53–78 of bovine P2 myelin protein. Severity of EAN correlated with the dose of peptide in the inoculate. The relationship between demyelination, inflammation and axonal degeneration was studied. Low doses resulted in pure demyelination. Axonal degeneration occurred only with high doses of inflammation. The role of macrophages in producing axonal damage is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310924
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  • 8
    Electronic Resource
    Electronic Resource
    Nerve biopsy findings in Niemann-Pick type II (NPC) (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 149-154 
    Details
    ISSN: 1432-0533
    Keywords: Key words: Niemann-Pick type II – Niemann-Pick type C – Peripheral neuropathy – Nerve biopsy ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The severe infantile form of Niemann-Pick disease type II was diagnosed in a 4-year-old girl and confirmed by demonstrating in cultured skin fibroblasts a deficiency of low-density lipoprotein-stimulated cholesterol ester synthesis of 〈5% of normal. Electrodiagnostic studies revealed changes of a predominantly demyelinating motor and sensory polyneuropathy. Light microscope and ultrastructural examination of a peroneal nerve biopsy showed unique changes. Compacted myelin sheaths were disproportionately thin with marked globular irregularities in single teased nerve fibres and evidence of chronic demyelination. The majority of axons were preserved but axonal spheroids and cytoskeletal abnormalities akin to neuroaxonal dystrophy were noted. Membrane-bound multilobulated lysosomal inclusions of floccular and electron-dense material were present in Schwann cells (SC), endoneurial fibroblasts, macrophages, pericytes and endothelial cells. SC of myelinated fibres were stuffed with whorls of concentric osmiophilic membranous profiles and electron-lucent material. The findings are diagnostic and differ from those of classical Niemann-Pick disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296184
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  • 9
    Electronic Resource
    Electronic Resource
    Neuropathy in igMλ paraproteinemia (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 57-64 
    Details
    ISSN: 1432-0533
    Keywords: Neuropathy ; IgMλ paraproteinemia ; Antigen-specificity ; Endoneurial compartment ; Endothelial-perineurial barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In axonal neuropathies associated with IgM paraproteinemia, reports of antigen specificity of the M-protein are few. A patient with IgM paraproteinemia presented with progressive mononeuritis multiplex. IgM was found deposited in striking amounts in endoneurium and shown to bind specifically to neural proteins and chondroitin sulfates. Direct immune mechanisms, as well as the physical effects of IgM deposition, likely contributed to the development of the neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687403
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  • 10
    Electronic Resource
    Electronic Resource
    Adoptive transfer of experimental allergic neuritis in the immune suppressed host (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 596-601 
    Details
    ISSN: 1432-0533
    Keywords: Experimental allergic neuritis ; Demyelination ; T cell immunity ; Irradiation ; Myelin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Experimental allergic neuritis (EAN) was induced in normal and irradiated Lewis rats by passively transferring T cells sensitized to SP-26, a peptide fragment of P2 myelin protein. The recipients became sick 4–8 days post transfer and the degree of disability correlated directly with the dose of T cells. Smaller doses caused demyelination of nerve roots and sciatic nerves and larger doses produced more severe demyelination and significant axonal degeneration. Irradiated recipients developed similar clinical EAN and showed macrophage-mediated demyelination despite severe suppression of the host inflammatory response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294298
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