Tasavallan Presidentti Urho Kekkosen vierailu Tshekkoslovakiaan 1.-4.10.1969 (Tasavallan Presidentin Tshekkoslovakiaan saapumispuhe 1.10.1969)

Puhe

Berlin 1/4 -32

Kirje 1.4.1932

Kapteeni Artturi Vuorimaa 1/4 1958

Kirje 1.4.1958

Tasavallan Presidentti Urho Kekkosen vierailu Tshekkoslovakiaan 1.-4.10.1969 (Tasavallan Presidentin radio- ja TV-haastattelu Romanian, Unkarin ja Tshekkoslovakian matkojen jälkeen 6.10.1969)

Haastattelu

n=1/4 domain-growth universality class: Crossover to the n=1/2 class

The kinetic domain-growth exponent is studied by Monte Carlo simulation as a function of temperature for a nonconserved order-parameter model. In the limit of zero temperature, the model belongs to the n=(1/4 slow-growth unversality class. This is indicative of a temporal pinning in the domain-boundary network of mixed-, zero-, and finite-curvature boundaries. At finite temperature the growth kinetics is found to cross over to the Allen-Cahn exponent n=(1/2. We obtain that the pinning time of the zero-curvature boundary decreases rapidly with increasing temperature.

Les médias et le politique : actes du colloque Le français parlé dans les médias, Lausanne, 1-4 septembre 2009

Voir site éditeur.

Paschase, Ratbert sur S. Matthieu, livres 1-4.

A la fin, lettre de A., archevêque de Hambourg, à l'abbé de Corbie.

Glucagon-like peptide-1 increases beta-cell glucose competence and proliferation by translational induction of insulin-like growth factor-1 receptor expression.

Glucagon-like peptide-1 (GLP-1) protects beta-cells against apoptosis, increases their glucose competence, and induces their proliferation. We previously demonstrated that the anti-apoptotic effect was mediated by an increase in insulin-like growth factor-1 receptor (IGF-1R) expression and signaling, which was dependent on autocrine secretion of insulin-like growth factor 2 (IGF-2). Here, we further investigated how GLP-1 induces IGF-1R expression and whether the IGF-2/IGF-1R autocrine loop is also involved in mediating GLP-1-increase in glucose competence and proliferation. We show that GLP-1 up-regulated IGF-1R expression by a protein kinase A-dependent translational control mechanism, whereas isobutylmethylxanthine, which led to higher intracellular accumulation of cAMP than GLP-1, increased both IGF-1R transcription and translation. We then demonstrated, using MIN6 cells and primary islets, that the glucose competence of these cells was dependent on the level of IGF-1R expression and on IGF-2 secretion. We showed that GLP-1-induced primary beta-cell proliferation was suppressed by Igf-1r gene inactivation and by IGF-2 immunoneutralization or knockdown. Together our data show that regulation of beta-cell number and function by GLP-1 depends on the cAMP/protein kinase A mediated-induction of IGF-1R expression and the increased activity of an IGF-2/IGF-1R autocrine loop.