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  • Electronic Resource  (4)
  • 1995-1999  (4)
  • GLP-1  (2)
  • Chemistry  (1)
  • Glioma  (1)
  • (2Z,4E)-5-(1',2'-epoxy-2',6',6'-trimethylcyclohexyl)-3-methyl-2,4-pentadieno
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  • Electronic Resource  (4)
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 96 (1998), S. 351-356 
    ISSN: 1432-0533
    Keywords: Key words Apoptosis ; Hyperthermia ; Glioma ; Rat ; c-Jun
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hyperthermia has been shown to inhibit glioma growth both in vitro and in vivo, and has been reported to induce apoptosis of a variety of cells. We investigated the role of apoptosis in tumor cell death following hyperthermia in a rat glioma model representing human glioblastoma. Apoptotic cell death was evaluated by terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) and hematoxylin and eosin (H & E) staining. We also examined c-Jun expression immunohistochemically. Apoptotic cell death in rat brain tumors that grew after implantation of C6 glioma cells showed regional differences. In all rats, apoptotic cells, characterized by extreme chromatin condensation and fragmented nuclei with apoptotic bodies in H & E-stained sections, were observed in the gliomas’ necrotic cores. TUNEL-positive cells were observed in the border zones between necrotic and vital tumor cells. Before hyperthermia, TUNEL-positive cells were sporadically distributed in the vital tumor tissue. After hyperthermia, the number of TUNEL-positive cells in the peripheral region of the tumor mass increased significantly, reached a peak after 6 h and returned to the basal level within 24 h (P 〈 0.01). C-Jun protein immunoreactivity was not observed in the cells at the tumor periphery. These data indicate that significantly apoptotic cell death unrelated to c-Jun expression occurs after hyperthermia, and that this form of cell death may be the mechanism of tumor regression following hyperthermia treatment of intracranial gliomas.
    Type of Medium: Electronic Resource
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  • 2
    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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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Applied Polymer Science 62 (1996), S. 1877-1885 
    ISSN: 0021-8995
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: A new three component photoinitiator system consisting of a dye, an iron arene complex, and a phenylglycine derivative was investigated by fluorescence quenching experiments and laser flash photolysis. The efficiency of a three-component system in photopolymerization reactions is higher by a two-fold factor compared to that of the two-component system. The first step of the photoreaction occurs between the dye and the iron arene complex. The iron arene complex reacts either with the singlet excited dye or with the triplet excited dye according to the nature of the dye. An electron transfer occurs in these systems. The mechanism was discussed in terms of the absence of the formation of a terminating radical in the three-component system. © 1996 John Wiley & Sons, Inc.
    Additional Material: 12 Ill.
    Type of Medium: Electronic Resource
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