Lettres du cardinal Mazarin pendant son ministère. Tome 1 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 3 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 6 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 9 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 5 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 7 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 6 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 8 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 2 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Lettres du cardinal Mazarin pendant son ministère. Tome 5 / recueillies et publ. par M. A. Chéruel [puis, pour le t. IX] par M. le Vte G. d'Avenel

Collection : Collection de documents inédits sur l'histoire de France

Tissue transglutaminase (TG2) acting as G protein protects hepatocytes against Fas-mediated cell death in mice.

Tissue transglutaminase (TG2) is a protein cross-linking enzyme known to be expressed by hepatocytes and to be induced during the in vivo hepatic apoptosis program. TG2 is also a G protein that mediates intracellular signaling by the alpha-1b-adrenergic receptor (AR) in liver cells. Fas/Fas ligand interaction plays a crucial role in various liver diseases, and administration of agonistic anti-Fas antibodies to mice causes both disseminated endothelial cell apoptosis and fulminant hepatic failure. Here we report that an intraperitoneal dose of anti-Fas antibodies, which is sublethal for wild-type mice, kills all the TG2 knock-out mice within 20 hours. Although TG2-/- thymocytes exposed to anti-Fas antibodies die at the same rate as wild-type mice, TG2-/- hepatocytes show increased sensitivity toward anti-Fas treatment both in vivo and in vitro, with no change in their cell surface expression of Fas, levels of FLIP(L) (FLICE-inhibitory protein), or the rate of I-kappaBalpha degradation, but a decrease in the Bcl-xL expression. We provide evidence that this is the consequence of the impaired AR signaling that normally regulates the levels of Bcl-xL in the liver. In conclusion, our data suggest the involvement of adrenergic signaling pathways in the hepatic regeneration program, in which Fas ligand-induced hepatocyte proliferation with a simultaneous inhibition of the Fas-death pathway plays a determinant role.

A genome-wide approach accounting for body mass index identifies genetic variants influencing fasting glycemic traits and insulin resistance.

Recent genome-wide association studies have described many loci implicated in type 2 diabetes (T2D) pathophysiology and β-cell dysfunction but have contributed little to the understanding of the genetic basis of insulin resistance. We hypothesized that genes implicated in insulin resistance pathways might be uncovered by accounting for differences in body mass index (BMI) and potential interactions between BMI and genetic variants. We applied a joint meta-analysis approach to test associations with fasting insulin and glucose on a genome-wide scale. We present six previously unknown loci associated with fasting insulin at P < 5 × 10(-8) in combined discovery and follow-up analyses of 52 studies comprising up to 96,496 non-diabetic individuals. Risk variants were associated with higher triglyceride and lower high-density lipoprotein (HDL) cholesterol levels, suggesting a role for these loci in insulin resistance pathways. The discovery of these loci will aid further characterization of the role of insulin resistance in T2D pathophysiology.

G-1 Appeal Activity in the Public Assistance Programs, August 2007

G-1 - Appeal Activity in the Public Assistance Programs - August 2007