Caspase-3 and RasGAP: a stress-sensing survival/demise switch.

The final decision on cell fate, survival versus cell death, relies on complex and tightly regulated checkpoint mechanisms. The caspase-3 protease is a predominant player in the execution of apoptosis. However, recent progress has shown that this protease paradoxically can also protect cells from death. Here, we discuss the underappreciated, protective, and prosurvival role of caspase-3 and detail the evidence showing that caspase-3, through differential processing of p120 Ras GTPase-activating protein (RasGAP), can modulate a given set of proteins to generate, depending on the intensity of the input signals, opposite outcomes (survival vs death).

The G0/G1 switch gene 2 is a novel PPAR target gene.

PPARs (peroxisome-proliferator-activated receptors) alpha, beta/delta and gamma are a group of transcription factors that are involved in numerous processes, including lipid metabolism and adipogenesis. By comparing liver mRNAs of wild-type and PPARalpha-null mice using microarrays, a novel putative target gene of PPARalpha, G0S2 (G0/G1 switch gene 2), was identified. Hepatic expression of G0S2 was up-regulated by fasting and by the PPARalpha agonist Wy14643 in a PPARalpha-dependent manner. Surprisingly, the G0S2 mRNA level was highest in brown and white adipose tissue and was greatly up-regulated during mouse 3T3-L1 and human SGBS (Simpson-Golabi-Behmel syndrome) adipogenesis. Transactivation, gel shift and chromatin immunoprecipitation assays indicated that G0S2 is a direct PPARgamma and probable PPARalpha target gene with a functional PPRE (PPAR-responsive element) in its promoter. Up-regulation of G0S2 mRNA seemed to be specific for adipogenesis, and was not observed during osteogenesis or myogenesis. In 3T3-L1 fibroblasts, expression of G0S2 was associated with growth arrest, which is required for 3T3-L1 adipogenesis. Together, these data indicate that G0S2 is a novel target gene of PPARs that may be involved in adipocyte differentiation.

Transposition of great arteries and single coronary artery: a new surgical technique for the arterial switch operation.

A single coronary artery can complicate the surgical technique of arterial switch operations, impairing early and late outcomes. We propose a new surgical approach, successfully applied in a 2.1 kg neonate, aimed at reducing the risk of early and late compression and/or distortion of the newly constructed coronary artery system.

Single amino acid charge switch defines clinically distinct proline-serine-threonine phosphatase-interacting protein 1 (PSTPIP1)-associated inflammatory diseases.

BACKGROUND: Hyperzincemia and hypercalprotectinemia (Hz/Hc) is a distinct autoinflammatory entity involving extremely high serum concentrations of the proinflammatory alarmin myeloid-related protein (MRP) 8/14 (S100A8/S100A9 and calprotectin). OBJECTIVE: We sought to characterize the genetic cause and clinical spectrum of Hz/Hc. METHODS: Proline-serine-threonine phosphatase-interacting protein 1 (PSTPIP1) gene sequencing was performed in 14 patients with Hz/Hc, and their clinical phenotype was compared with that of 11 patients with pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) syndrome. PSTPIP1-pyrin interactions were analyzed by means of immunoprecipitation and Western blotting. A structural model of the PSTPIP1 dimer was generated. Cytokine profiles were analyzed by using the multiplex immunoassay, and MRP8/14 serum concentrations were analyzed by using an ELISA. RESULTS: Thirteen patients were heterozygous for a missense mutation in the PSTPIP1 gene, resulting in a p.E250K mutation, and 1 carried a mutation resulting in p.E257K. Both mutations substantially alter the electrostatic potential of the PSTPIP1 dimer model in a region critical for protein-protein interaction. Patients with Hz/Hc have extremely high MRP8/14 concentrations (2045 ± 1300 μg/mL) compared with those with PAPA syndrome (116 ± 74 μg/mL) and have a distinct clinical phenotype. A specific cytokine profile is associated with Hz/Hc. Hz/Hc mutations altered protein binding of PSTPIP1, increasing interaction with pyrin through phosphorylation of PSTPIP1. CONCLUSION: Mutations resulting in charge reversal in the y-domain of PSTPIP1 (E→K) and increased interaction with pyrin cause a distinct autoinflammatory disorder defined by clinical and biochemical features not found in patients with PAPA syndrome, indicating a unique genotype-phenotype correlation for mutations in the PSTPIP1 gene. This is the first inborn autoinflammatory syndrome in which inflammation is driven by uncontrolled release of members of the alarmin family.

[Tracteur] Exelsior 35/40 HP [tractant une herse à] Rocquencourt, Versailles, 13/3/20 : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 58493

Agro 10 HP [motoculteur en démonstration à] Rocquencourt, Versailles, 13/3/20 : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 58495

Racer Sunbeam 1800 HP [bateau de course, vue sur le moteur] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 60370

Racer Sunbeam 1800 HP [bateau de course, vue sur le moteur] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 60371

新刻全像批評西遊記Xin ke quan xiang pi ping xi you ji.Le Xi you ji, nouvelle édition illustrée.

Livre 18 seulement (hui 86 à 91).

新鐫批評秘本玉支磯小傳Xin juan pi ping bi ben yu zhi ji xiao zhuan.Histoire du rocher aux veines de jade.

Par Yin shui shan ren et par l'homme du Tian hua zang. Édition du pavillon Zui hua.20 hui.

新鐫批評繡像賽紅絲小說Xin juan pi ping xiu xiang sai hong si xiao shuo.Histoire de l'offrande du fil rouge, édition illustrée.

Préface du maître du Tian hua zang. Ancienne impression.16 hui.

新鐫古本批評三世報. 隔簾花影Xin juan gu ben pi ping san shi bao. — Ge lian hua ying.Rétribution pendant trois générations : l'ombre des fleurs à travers la jalousie ; nouvelle édition.

A la fin des Song. Préface non datée.48 hui.

新鐫繡像西廂琵琶合刻Xin juan xiu xiang xi xiang pi pa he ke.Histoire du pavillon occidental et Histoire du luth, nouvelle édition collective illustrée.

Contient : I園林午夢Yuan lin wu meng.Songe de midi dans le bosquet ; II圍棋馬局Wei qi ma ju.L'échiquier ; III西廂摘句骰譜Xi xiang zhe ju tou pu.Tableaux explicatifs des parties de dés du Xi xiang ji ; IV錢塘夢Qian tang meng.Songe de Qian tang ; V會眞記Hui zhen ji.Histoire du portrait ; VI李卓吾先生（alias 卓老）批㸃西廂記眞本Li zhuo wu xian sheng (alias tcho lao) pi dian xi xiang ji zhen ben.Le Xi xiang ji (Histoire du pavillon occidental), ponctué par Li Zhuo wu ; VII新校琵琶記始末Xin jiao pi pa ji shi mo.Le Pi pa ji (Histoire du luth), édition revue