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  • Articles: DFG German National Licenses  (3)
  • Glucose tolerance  (2)
  • 02.70.-c  (1)
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  • Articles: DFG German National Licenses  (3)
Material
Years
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Applied physics 62 (1996), S. 389-397 
    ISSN: 1432-0649
    Keywords: 02.60.Cb ; 02.70.-c ; 42.10 ; 42.25.Bs ; 42.65
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract We describe and example the Beam Propagation Method (BPM) used to model and simulate nonlinear refractive and absorptive effects in materials with applications to optical limiting and switching. Various scenarios including laser-beam trapping and laser-beam division are investigated, in order to demonstrate the power of the BPM. A novel technique is also described for efficiently modelling the external far-field propagation from nonlinear media, including the propagation of non-Gaussian-shaped spatial profiles. The methods are finally combined with the phenomenon of nonlinear absorption to demonstrate enhanced power limiting in the presence of self-refraction. Optimal parameters for high-fluence power-limiting are subsequently discussed.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta diabetologica 33 (1996), S. 211-215 
    ISSN: 1432-5233
    Keywords: High sucrose diet ; Glucose tolerance ; Islet function ; Insulin release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We fed normal rats a high sucrose diet in order to test the hypothesis that mild hyperglycemia can induce defects in pancreatic beta-cell function and impair glucosestimulated insulin release. Rats provided with free access to a sucrose solution (35%) voluntarily consumed 50% more carbohydrate than control per day. After 7 days of sucrose feeding, glucose tolerance was significantly impaired; the area under the glucose tolerance test curve (GTT) was 683±61 mmol/120 min compared with 472±56 mmol/120 min in controls (P〈0.05). Impaired glucose tolerance was still present after a further 12 days (area under the GTT: 749±99 mmol/120 min). Sucrosefed rats were significantly (P〈0.05) hyperglycemic by 1.5 mmol/l over controls. When insulin secretion was assessed in vivo and in vitro in control and sucrose-fed rats, no significant differences were apparent in plasma samples collected over a 1-h period or in statically incubated or perifused isolated pancreatic islets. In addition, the rates of glucose utilisation and oxidation were normal in islets from sucrose-fed rats. These data do not support the hypothesis that minimal hyperglycemia is sufficient to impair glucose-stimulated insulin release.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta diabetologica 33 (1996), S. 211-215 
    ISSN: 1432-5233
    Keywords: Key words High sucrose diet ; Glucose tolerance ; Islet function ; Insulin release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We fed normal rats a high sucrose diet in order to test the hypothesis that mild hyperglycemia can induce defects in pancreatic beta-cell function and impair glucose-stimulated insulin release. Rats provided with free access to a sucrose solution (35%) voluntarily consumed 50% more carbohydrate than control per day. After 7 days of sucrose feeding, glucose tolerance was significantly impaired; the area under the glucose tolerance test curve (GTT) was 683±61 mmol/120 min compared with 472±56 mmol/120 min in controls (P〈0.05). Impaired glucose tolerance was still present after a further 12 days (area under the GTT: 749±99 mmol/120 min). Sucrose-fed rats were significantly (P〈0.05) hyperglycemic by 1.5 mmol/l over controls. When insulin secretion was assessed in vivo and in vitro in control and sucrose-fed rats, no significant differences were apparent in plasma samples collected over a 1-h period or in statically incubated or perifused isolated pancreatic islets. In addition, the rates of glucose utilisation and oxidation were normal in islets from sucrose-fed rats. These data do not support the hypothesis that minimal hyperglycemia is sufficient to impair glucose-stimulated insulin release.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
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