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  • 1
    ISSN: 1420-9071
    Keywords: Key words. Amphibian inductive interactions; anuran embryonic induction; urodele inductive interactions; activin action; mesoderm induction.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. As a first step towards providing a conceptual approach to understanding similarities and differences in the mechanisms which guide inductive interactions among related organisms (e.g. various amphibia), a set of five principles is offered here. These principles were formulated by analyzing literature examples of classical embryological phenomena and by performing experiments with activin, a peptide growth factor which is currently suspected to play for a role in mesoderm induction. Mechanisms which account, at least in part, for the observed differences between anuran and urodele inductive processes can be derived from these principles.
    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
    ISSN: 1432-1920
    Keywords: Key words Single photon emission tomography ; Acetazolamide ; Cerebral ischaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Reduced vasodilatory capacity resulting from occlusive lesions of the major cerebral arteries may return to normal without surgical revascularisation. We aimed to determine prospectively the frequency and predictors of recovery of impaired haemodynamics as demonstrated by acetazolamide (ACZ) reactivity on single-photon emission computed tomography (SPECT). Vasoreactivity was measured by 123I-IMP SPECT with an ACZ challenge, in 37 medically treated patients with unilateral occlusive disease of the internal carotid or middle cerebral artery at an interval of 1–2 years. Each ACZ challenge test was analysed semiquantitatively by calculating the degree of increase in cerebral blood flow (CBF) asymmetry after ACZ administration (ΔAI). Vasodilatory capacity was abnormal initially in 20 patients (65 %); eight of whom (40 %) exhibited spontaneous normalisation on follow-up. Although the baseline characteristics did not differ significantly between patients with or without increase in reactivity, logistic regression analysis revealed that the initial ΔAI (P 〈 0.05) and the type of vascular lesion (stenosis or occlusion) (P 〈 0.05) correlated significantly with a return towards normal of reduced ACZ reactivity. Spontaneous improvement of impaired vasodilatory capacity may not be a rare phenomenon. We found that mild reduction in the initial ACZ reactivity and a stenosis, but not complete occlusion, were independent factors contributing to normalisation of impaired cerebral haemodynamics.
    Type of Medium: Electronic Resource
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