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  • 1
    Book
    Book
    Polytopes: abstract, convex and computational. Proceedings of the NATO Advanced Study Institute, Scarborough, Ontario, Canada, August 20 - September 3, 1993; 440 (1994)
    Dordrecht, Netherlands :Kluwer,
    Details
    Title: Polytopes: abstract, convex and computational. Proceedings of the NATO Advanced Study Institute, Scarborough, Ontario, Canada, August 20 - September 3, 1993; 440
    Contributer: Bisztriczky, Tibor , McMullen, Peter , Weiss, A. Ivic , Schneider, Rolf
    Publisher: Dordrecht, Netherlands :Kluwer,
    Year of publication: 1994
    Pages: 507 S.
    Series Statement: NATO ASI series C: Mathematical and physical sciences 440
    Type of Medium: Book
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  • 2
    Electronic Resource
    Electronic Resource
    Positron Annihilation Induced Auger Electron Spectroscopy (1992)
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 105-110 (Jan. 1992), p. 511-520 
    Details
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/01/59/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.105-110.511.pdf
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Aminoguanidine does not inhibit the initial phase of experimental diabetic retinopathy in rats (1995)
    Springer
    Diabetologia 38 (1995), S. 269-273 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; retinal basement membrane.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have previously shown that long-term administration of aminoguanidine, an inhibitor of advanced glycosylation product formation, reduces the extent of experimental diabetic retinopathy in the rat by 85 %. In order to determine whether the residual retinopathy that developed despite aminoguanidine was attributable to advanced glycation endproduct formation, a time-course study was performed in three different groups of male Wistar rats: non-diabetic controls (NC), streptozotocin-diabetic controls (DC) and streptozotocin-diabetic rats treated with aminoguanidine HCL, 50 mg/100 ml drinking water (D-AG). Eyes were obtained at 24, 32, 44 and 56 weeks of diabetes/treatment duration and morphologic evaluation was done on retinal digest preparations. At 56 weeks, retinal basement membrane thickness was additionally measured. After 24 weeks of diabetes, the number of acellular capillaries was significantly elevated in DC (44.6 ± 5.7/mm2 of retinal area, NC 19.6 ± 4.9; p 〈 0.001) and increased continuously over time (DC 56 weeks 87.4 ± 15.1; p 〈 0.001 vs DC 24 weeks). In contrast, acellular capillaries in D-AG increased over the first 24 weeks and then remained constant for the rest of the study (D-AG 24 weeks 35.7 ± 5.18; p 〈 0.01 vs NC 24 weeks and NS vs DC 24 weeks; D-AG 56 weeks 42.0 ± 6.20; p NS vs D-AG 24 weeks). Diabetes-associated pericyte loss (DC 24 weeks 2310 ± 170/mm2 of capillary area; NC 24 weeks 3120 ± 190; p 〈 0.001; DC 56 weeks 1570 ± 230; NC 56 weeks 2960 ± 50; p 〈 0.001) was significantly prevented by aminoguanidine after diabetic-like changes over the initial 24 weeks (D-AG 24 weeks 2450 ± 75; p NS vs DC 24 weeks; D-AG 56 weeks 2350 ± 90; p 〈 0.001 vs DC 56 weeks). At 56 weeks, aminoguanidine treatment was associated with a 67.4 % reduction in retinal basement membrane thickening. This time-course study demonstrates that aminoguanidine prevents the progression of experimental diabetic retinopathy, and suggests that non AG-inhibitable mechanisms are involved in the initial phase of diabetic retinopathy. [Diabetologia (1995) 38: 269–273]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400629
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  • 4
    Electronic Resource
    Electronic Resource
    Realizations of Regular Toroidal Maps of Type {4,4} (2000)
    Springer
    Discrete & computational geometry 24 (2000), S. 453-466 
    Details
    ISSN: 1432-0444
    Source: Springer Online Journal Archives 1860-2000
    Topics: Computer Science , Mathematics
    Notes: Abstract. We determine and completely describe all pure realizations of the finite toroidal maps of types {4,4} (b,0) and {4,4} (b,b) , b \geq; 2 . For large values of b , most such realizations are eight-dimensional.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004540010048
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Aminoguanidine does not inhibit the initial phase of experimental diabetic retinopathy in rats (1995)
    Springer
    Diabetologia 38 (1995), S. 269-273 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; retinal basement membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have previously shown that long-term administration of aminoguanidine, an inhibitor of advanced glycosylation product formation, reduces the extent of experimental diabetic retinopathy in the rat by 85%. In order to determine whether the residual retinopathy that developed despite aminoguanidine was attributable to advanced glycation endproduct formation, a time-course study was performed in three different groups of male Wistar rats: non-diabetic controls (NC), streptozotocin-diabetic controls (DC) and streptozotocin-diabetic rats treated with aminoguanidine HCL, 50 mg/100 ml drinking water (D-AG). Eyes were obtained at 24, 32, 44 and 56 weeks of diabetes/treatment duration and morphologic evaluation was done on retinal digest preparations. At 56 weeks, retinal basement membrane thickness was additionally measured. After 24 weeks of diabetes, the number of acellular capillaries was significantly elevated in DC (44.6±5.7/mm2 of retinal area, NC 19.6±4.9; p〈0.001) and increased continuously over time (DC 56 weeks 87.4±15.1; p〈0.001 vs DC 24 weeks). In contrast, acellular capillaries in D-AG increased over the first 24 weeks and then remained constant for the rest of the study (D-AG 24 weeks 35.7±5.18; p〈0.01 vs NC 24 weeks and NS vs DC 24 weeks; D-AG 56 weeks 42.0±6.20; p NS vs D-AG 24 weeks). Diabetes-associated pericyte loss (DC 24 weeks 2310±170/mm2 of capillary area; NC 24 weeks 3120±190; p〈0.001; DC 56 weeks 1570±230; NC 56 weeks 2960±50; p〈0.001) was significantly prevented by aminoguanidine after diabetic-like changes over the initial 24 weeks (D-AG 24 weeks 2450±75; p NS vs DC 24 weeks; D-AG 56 weeks 2350±90; p〈0.001 vs DC 56 weeks). At 56 weeks, aminoguanidine treatment was associated with a 67.4% reduction in retinal basement membrane thickening. This time-course study demonstrates that aminoguanidine prevents the progression of experimental diabetic retinopathy, and suggests that non AG-inhibitable mechanisms are involved in the initial phase of diabetic retinopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400629
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    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Secondary intervention with aminoguanidine retards the progression of diabetic retinopathy in the rat model (1995)
    Springer
    Diabetologia 38 (1995), S. 656-660 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; secondary intervention ; islet transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Primary prevention with aminoguanidine — an inhibitor of advanced glycation end product (AGE) formation — has been successfully employed to prevent diabetic retinopathy in the rat. However, it is unknown whether inhibition of AGE formation is still effective in a secondary intervention strategy. The present study addresses this question by comparing secondary intervention with aminoguanidine with syngeneic islet transplantation in the rat model. After 6 months of diabetes, one group was treated with aminoguanidine (50 mg/100 ml drinking water; D-AG) while another group received syngeneic transplantation of collagenase-ficoll isolated islets by intraportal injection (Tx). After an additional 4 months, both groups were compared to a normal (NC 10) and diabetic (DC 10) control group. Retinal autofluorescence was increased 2.5-fold after 6 months and increased 3.7-fold after 10 months of diabetes (p〈0.001). Aminoguanidine and islet Tx retarded the further accumulation of autofluorescence equally (p〈0.001 vs DC 10), although the values were higher than those observed in DC at 6 months (p〈0.001). Diabetes was associated with a 2.7-fold increase in acellular capillaries after 6 months and a 4.1-fold increase after 10 months. Treatment with aminoguanidine or islet Tx reduced but did not completely attenuate the progression of vascular occlusion (p〈0.001 vs DC 10; D-AG vs DC 6, p〈0.05; Tx vs DC 6, p〈0.01). Both treatments reduced endothelial proliferation (22.4% after 10 months; p〈0.001) and completely arrested pericyte dropout (40% after 10 months; p〈0.001). These data demonstrate that aminoguanidine is as effective as islet transplantation in retarding the progression of diabetic retinopathy in a secondary prevention setting.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401835
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Acceleration of experimental diabetic retinopathy in the rat by omega-3 fatty acids (1996)
    Springer
    Diabetologia 39 (1996), S. 251-255 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic retinopathy ; rat model ; omega-3 fatty acids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Omega-3 fatty acids exert several important biological effects on factors that may predispose to diabetic retinopathy. Potential pathogenetic mechanisms include platelet dysfunction, altered eicosanoid production, increased blood viscosity in association with impaired cell deformability and pathologic leucocyte/endothelium interaction. Therefore, we tested whether a 6-month administration of fish oil (750 mg Maxepa, 5 times per week), containing 14% eicosapentaenoic acid (EPA) and 10% docosahexaenic acid, could inhibit the development of experimental retinopathy of the streptozotocin-diabetic rat. The efficiency of fish oil supplementation was evaluated by measuring EPA concentrations in total, plasma and membrane fatty acids and by measuring the generation of lipid mediators (leukotrienes and thromboxanes). Retinal digest preparations were quantitatively analysed for pericyte loss, and the formation of acellular capillaries. Omega-3 fatty acid administration to diabetic rats resulted in a twofold increase of EPA 20∶5 in total fatty acids, and a reduction of the thromboxane2/3 ratio from 600 (untreated diabetic rats) to 50 (treated diabetic rats). Despite these biochemical changes, diabetes-associated pericyte loss remained unaffected and the formation of acellular, occluded capillaries was increased by 75% in the fish oil treated diabetic group (115.1±26.8; untreated diabetic 65.2±15.0 acellular capillary segments/mm2 of retinal area). We conclude from this study that dietary fish oil supplementation may be harmful for the diabetic microvasculature in the retina.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418338
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    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Secondary intervention with aminoguanidine retards the progression of diabetic retinopathy in the rat model (1995)
    Springer
    Diabetologia 38 (1995), S. 656-660 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; secondary intervention ; islet transplantation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Primary prevention with aminoguanidine – an inhibitor of advanced glycation end product (AGE) formation – has been successfully employed to prevent diabetic retinopathy in the rat. However, it is unknown whether inhibition of AGE formation is still effective in a secondary intervention strategy. The present study addresses this question by comparing secondary intervention with aminoguanidine with syngeneic islet transplantation in the rat model. After 6 months of diabetes, one group was treated with aminoguanidine (50 mg/100 ml drinking water; D-AG) while another group received syngeneic transplantation of collagenase-ficoll isolated islets by intraportal injection (Tx). After an additional 4 months, both groups were compared to a normal (NC 10) and diabetic (DC 10) control group. Retinal autofluorescence was increased 2.5-fold after 6 months and increased 3.7-fold after 10 months of diabetes (p 〈 0.001). Aminoguanidine and islet Tx retarded the further accumulation of autofluorescence equally (p 〈 0.001 vs DC 10), although the values were higher than those observed in DC at 6 months (p 〈 0.001). Diabetes was associated with a 2.7-fold increase in acellular capillaries after 6 months and a 4.1-fold increase after 10 months. Treatment with aminoguanidine or islet Tx reduced but did not completely attenuate the progression of vascular occlusion (p 〈 0.001 vs DC 10; D-AG vs DC 6, p 〈 0.05; Tx vs DC 6, p 〈 0.01). Both treatments reduced endothelial proliferation (22.4 % after 10 months; p 〈 0.001) and completely arrested pericyte dropout (40 % after 10 months; p 〈 0.001). These data demonstrate that aminoguanidine is as effective as islet transplantation in retarding the progression of diabetic retinopathy in a secondary prevention setting. [Diabetologia (1995) 38: 656–660]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401835
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Acceleration of experimental diabetic retinopathy in the rat by omega-3 fatty acids (1996)
    Springer
    Diabetologia 39 (1996), S. 251-255 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic retinopathy ; rat model ; omega-3 fatty acids.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Omega-3 fatty acids exert several important biological effects on factors that may predispose to diabetic retinopathy. Potential pathogenetic mechanisms include platelet dysfunction, altered eicosanoid production, increased blood viscosity in association with impaired cell deformability and pathologic leucocyte/endothelium interaction. Therefore, we tested whether a 6-month administration of fish oil (750 mg Maxepa, 5 times per week), containing 14 % eicosapentaenoic acid (EPA) and 10 % docosahexaenic acid, could inhibit the development of experimental retinopathy of the streptozotocin-diabetic rat. The efficiency of fish oil supplementation was evaluated by measuring EPA concentrations in total, plasma and membrane fatty acids and by measuring the generation of lipid mediators (leukotrienes and thromboxanes). Retinal digest preparations were quantitatively analysed for pericyte loss, and the formation of acellular capillaries. Omega-3 fatty acid administration to diabetic rats resulted in a twofold increase of EPA 20:5 in total fatty acids, and a reduction of the thromboxane2/3 ratio from 600 (untreated diabetic rats) to 50 (treated diabetic rats). Despite these biochemical changes, diabetes-associated pericyte loss remained unaffected and the formation of acellular, occluded capillaries was increased by 75 % in the fish oil treated diabetic group (115.1 ± 26.8; untreated diabetic 65.2 ± 15.0 acellular capillary segments/mm2 of retinal area). We conclude from this study that dietary fish oil supplementation may be harmful for the diabetic microvasculature in the retina. [Diabetologia (1996) 39: 251–255]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418338
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    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    SV 40 related Papova-viruses in human meningiomas (1976)
    Springer
    Acta neuropathologica 34 (1976), S. 171-174 
    Details
    ISSN: 1432-0533
    Keywords: Brain tumor ; Meningiomas ; Papova-Virus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Human meningiomas show characteristic chromosome aberrations very similar to those reported in human cell cultures experimentally transformed by Simian virus 40 (SV 40). Three out of eight meningiomas tested showed SV 40 specific tumor antigen but no virus capsid antigen. Experiments to rescue virus were successfully performed. Electron microscopic studies of these cell cultures revealed cytoplasmic inclusions containing virus particles which corresponded in size and morphology to Papova viruses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00684667
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