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  • 1
    ISSN: 1432-1920
    Keywords: udragit-E ; Embolic material
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have developed a new liquid material for embolisation of arteriovenous malformations: a mixture of methyl and butyl methacrylate, plus dimethylaminoethyl methacrylate copolymer (Eudragit-E) in a solvent consisting of ethanol and iopamidol. Upon contact with aqueous substances, Eudragit-E precipitates rapidly and forms a soft elastic sponge within 3 s, as the ethanol diffuses. In blood, the positively charged Eudragit-E aggregates the negatively charged blood elements. Transcatheter embolisation of 4 canine and 52 rat renal arteries was feasible. Histological studies revealed no acute inflammatory reaction within 1 week, but mild to moderate reactions in the subacute and chronic stages. No recanalisation was seen. Because of its unique properties and excellent thrombogenicity the Eudragit-E mixture seems a promising embolic material.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 109 (1987), S. 4157-4162 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Key words Glucagon ; insulin secretion ; exendin (9 ; 39) ; GLP-1 ; pancreas perfusion.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since glucagon-like peptide-1 (7–36) amide (7–37) (GLP-1) has been found to be a potent insulinotropic hormone, it has been postulated that glucagon stimulates insulin secretion from islet beta cells through the GLP-1 receptor. We therefore examined the effects of a GLP-1 receptor antagonist, exendin (9–39) amide, on glucagon- or GLP-1-stimulated insulin release from isolated perfused rat pancreas. When infusion of 100 nmol/l exendin (9–39) amide was started 5 min before that of 1 nmol/l glucagon, the stimulation of insulin release by glucagon was similar to that found in the control situation (preinfusion with vehicle alone). By contrast, when 0.3 nmol/l GLP-1 was used in the same experimental setting, exendin (9–39) amide clearly inhibited insulin release. These results indicate that glucagon stimulates insulin release mainly through glucagon receptors but not GLP-1 receptors on islet beta cells. [Diabetologia (1995) 38: 274–276]
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Key words Transgenic mice ; aldose reductase ; diabetic angiopathies ; diabetic retinopathy ; diabetic nephropathies.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the role of human aldose reductase (hAR) in the pathogenesis of diabetic complications, we generated transgenic mice carrying hAR cDNA driven by the murine MHC class I molecule promoter (hAR-Tg). Northern and Western blot analyses and immunoassay of hAR revealed that both hAR mRNA and the protein were expressed in all tissues tested. Thrombosis in renal vessels and fibrinous deposits in Bowman's capsule were observed in 6-week-old hAR-Tg mice fed a normal diet. Ingestion of a 30 % glucose diet for 5 days caused sorbitol concentrations in the liver, kidney, and muscle of hAR-Tg mice to be elevated significantly. Seven-week-old hAR-Tg mice fed a 20 % galactose diet for 7 days developed cataracts and occlusion of the retinochoroidal vessels, in addition to pathological changes in the kidney. Despite an elevated aldose reductase level in hAR-Tg mice and their intake of an aldose diet, no histopathological changes were found in other tissues, including the brain, lungs, heart, thymus, spleen, intestine, liver, muscle, spinal cord, or sciatic nerve. Results suggest that target organs of diabetic complications, such as the kidney, lens, and retina are sensitive to damage associated with a high level of AR expression, but other organs are not; the susceptibility of each organ to diabetic complications is determined by not only hAR but also other factors. [Diabetologia (1995) 38: 255–261]
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Keywords Vascular endothelial growth factor ; vascular permeability factor ; Goto-Kakisaki rat ; diabetic retinopathy ; ELISA ; immunohistochemistry.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Vascular endothelial growth factor (VEGF) is a potent angiogenic factor. VEGF levels in ocular tissue of 6-, 12-, 18- and 28-week-old Goto-Kakizaki (GK) rats, a well-known model of non-insulin-dependent diabetes, were evaluated by highly sensitive ELISA. VEGF concentrations in the GK rat as well as in non-diabetic Wistar rat significantly decreased from the age of 6 weeks to 18 weeks. However, although VEGF concentrations in the Wistar rat continued to fall significantly from 18 to 28 weeks of age, the levels were maintained between 18 and 28 weeks of age in GK rats. Levels were significantly different between the GK and Wistar rats at 28 weeks of age. Results of immunohistochemical studies of the eyes of Wistar and GK rats at 28 weeks of age suggest diffuse distribution of this cytokine in cells of neural origin. Weak to moderate VEGF immunoreactivity was exhibited mainly in the ganglion cell layer, inner plexiform layer and inner/outer nuclear layers in rats with and without diabetes. However, in the retinal optic nerve fiber layer, retinal pigment epithelium and choroid, strong VEGF immunoreactivity was noted only in the GK rat. In conclusion, increased VEGF production in certain ocular tissue, similar to that in humans, is observed quite early, at least before the appearance of observable retinal changes in the diabetic GK rat. This also suggests that the GK rat can be used as a model of initial or latent phase diabetic retinopathy. [Diabetologia (1997) 40: 726–730]
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Transgenic mice ; aldose reductase ; diabetic angiopathies ; diabetic retinopathy ; diabetic nephropathies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the role of human aldose reductase (hAR) in the pathogenesis of diabetic complications, we generated transgenic mice carrying hAR cDNA driven by the murine MHC class I molecule promoter (hAR-Tg). Northern and Western blot analyses and immunoassay of hAR revealed that both hAR mRNA and the protein were expressed in all tissues tested. Thrombosis in renal vessels and fibrinous deposits in Bowman's capsule were observed in 6-week-old hAR-Tg mice fed a normal diet. Ingestion of a 30% glucose diet for 5 days caused sorbitol concentrations in the liver, kidney, and muscle of hAR-Tg mice to be elevated significantly. Seven-week-old hAR-Tg mice fed a 20% galactose diet for 7 days developed cataracts and occlusion of the retinochoroidal vessels, in addition to pathological changes in the kidney. Despite an elevated aldose reductase level in hAR-Tg mice and their intake of an aldose diet, no histopathological changes were found in other tissues, including the brain, lungs, heart, thymus, spleen, intestine, liver, muscle, spinal cord, or sciatic nerve. Results suggest that target organs of diabetic complications, such as the kidney, lens, and retina are sensitive to damage associated with a high level of AR expression, but other organs are not; the susceptibility of each organ to diabetic complications is determined by not only hAR but also other factors.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Glucagon ; insulin secretion ; exendin (9–39) ; GLP-1 ; pancreas perfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since glucagon-like peptide-1 (7–36) amide (7–37) (GLP-1) has been found to be a potent insulinotropic hormone, it has been postulated that glucagon stimulates insulin secretion from islet beta cells through the GLP-1 receptor. We therefore examined the effects of a GLP-1 receptor antagonist, exendin (9–39) amide, on glucagon- or GLP-1-stimulated insulin release from isolated perfused rat pancreas. When infusion of 100 nmol/l exendin (9–39) amide was started 5 min before that of 1 nmol/l glucagon, the stimulation of insulin release by glucagon was similar to that found in the control situation (preinfusion with vehicle alone). By contrast, when 0.3 nmol/l GLP-1 was used in the same experimental setting, exendin (9–39) amide clearly inhibited insulin release. These results indicate that glucagon stimulates insulin release mainly through glucagon receptors but not GLP-1 receptors on islet beta cells.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 40 (1997), S. 1363-1364 
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 40 (1997), S. 1493-1494 
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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