Ultrastructural alterations of intracellular stages and effects on blood forms of Trypanosoma cruzi induced in vivo by 2-amino-5-(1-methyil-5-nitro-2-imidazolyl)-1,3,4 - Thiadiazole

An electron microscopy study shows that the administration of a single dose (500 mg/kg, p.o.) of 2-amino-5-(1-methyl-5-nitro-2-imidazolyl)-1, 3, 4-thiadiazole induces in mice infected with Trypanosoma cruzi results in degenerative lesions of the intracellular stages. Ultrastructural alterations are detected as early as 6 hours after the drug administration and destruction of the parasites occurs within 18 - 36 hours. Trypomastigotes are cleared from the bloodstream 4 to 6 hours after treatment. The combined effect on both developmental stages is apparently responsible for the in vivo ejfects of this drug which is the most active drug ever tested in our laboratory in experimental Chagas' disease.

Bedeutung der Expression der G-Protein-gekoppelten-Rezeptoren BRS 3, CCKA, CXCR 4, GHRH, GRPR, NK 1, NMBR, NT 2, PAC 1, VPAC 1 und VPAC 2 bei kolorektalen Tumoren in Abhängigkeit von Tumorstadium und Differenzierungsgrad

Magdeburg, Univ., Med. Fak., Diss., 2012

Paul et la Loi : le retournement (Philippiens 3,2-4,1)

(Résumé de l'ouvrage) L'apôtre Paul est au centre d'une intense interrogation aujourd'hui. Quel fut son rapport au judaïsme ? Que sait-il de Jésus ? Comment s'est construite sa théologie, d'une épître à l'autre ? Dix-huit biblistes suisses, français, italiens, allemands et américains ont été invités à explorer la question. Leurs analyses sont précises, rigoureuses et documentées. On trouvera ici une synthèse unique en français des plus récentes avancées de la recherche paulinienne.

GLP-1 protects beta-cells against apoptosis by enhancing the activity of an IGF-2/IGF-1 receptor autocrine loop

GLP-1 protects β-cells against apoptosis by still incompletely understood mechanisms. In a recent study, we searched for novel anti-apoptotic pathways by performing comparative transcriptomic analysis of islets from Gipr-/-;Glp-1r-/- mice, which show increased susceptibility to cytokine-induced apoptosis. We observed a strong reduction in IGF-1R expression in the knockout islets suggesting a link between the gluco-incretin and IGF-1R signaling pathways. Using MIN6 and primary islet cells, we demonstrated that GLP-1 strongly stimulates IGF-1R expression and that activation of the IGF-1R/Akt signaling pathway required active secretion of IGF-2 by the β-cells. We showed that inactivation of the IGF-1 receptor gene in β-cells or preventing its up-regulation by GLP-1, as well as suppressing IGF-2 expression or action, blocked the protective effect of GLP-1 against cytokine-induced apoptosis. Thus, an IGF-2/IGF-1 receptor autocrine loop operates in β-cells and GLP-1 increases its activity by enhancing IGF-1R expression and by stimulating IGF-2 secretion. This mechanism is required for GLP-1 to protect β-cells against apoptosis.