4-7-19, stade Pershing, saut [en] hauteur avec élan [Robert Lyman "Dink" Templeton sautant, et Carl Rice en attente à gauche de l'aire de saut, Jeux interalliés] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 54707

Arrivée du 5000 mètres [vainqueur] Guillemot, Colombes 20/7/19 championnat de France d'athlétisme : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 55051

Arrivée du 100 mètres plat [vainqueur Hemmi, Colombes 20/7/19 championnat de France d'athlétisme : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 55052

Lemasson gagnant javelot [Colombes, 20/7/19 championnat de France d'athlétisme] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 55055

10-8-19, Deauville [promeneurs] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 55422

13-8-19, la vie chère aux halles [de Paris] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 55435

Parc des Princes, 9/11/19, rugby, équipe du Stade Français [qui a battu l'équipe de Nantes] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 56859

Lack of association between the protein tyrosine phosphatase non-receptor type 22 R263Q and R620W functional genetic variants and endogenous non-anterior uveitis.

OBJECTIVE Endogenous uveitis is a major cause of visual loss mediated by the immune system. The protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene encodes a lymphoid-specific phosphatase that plays a key role in T-cell receptor (TCR) signaling. Two independent functional missense single nucleotide polymorphisms (SNPs) located within the PTPN22 gene (R263Q and R620W) have been associated with different autoimmune disorders. We aimed to analyze for the first time the influence of these PTPN22 genetic variants on endogenous non-anterior uveitis susceptibility. METHODS We performed a case-control study of 217 patients with endogenous non-anterior uveitis and 718 healthy controls from a Spanish population. The PTPN22 polymorphisms (rs33996649 and rs2476601) were genotyped using TaqMan allelic discrimination assays. The allele, genotype, carriers, and allelic combination frequencies were compared between cases and controls with χ(2) analysis or Fisher's exact test. RESULTS Our results showed no influence of the studied SNPs in the global susceptibility analysis (rs33996649: allelic P- value=0.92, odds ratio=0.97, 95% confidence interval=0.54-1.75; rs2476601: allelic P- value=0.86, odds ratio=1.04, 95% confidence interval=0.68-1.59). Similarly, the allelic combination analysis did not provide additional information. CONCLUSIONS Our results suggest that the studied polymorphisms of the PTPN22 gene do not play an important role in the pathophysiology of endogenous non-anterior uveitis.

Claudin-19 mutations and clinical phenotype in Spanish patients with familial hypomagnesemia with hypercalciuria and nephrocalcinosis.

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis is an autosomal recessive tubular disorder characterized by excessive renal magnesium and calcium excretion and chronic kidney failure. This rare disease is caused by mutations in the CLDN16 and CLDN19 genes. These genes encode the tight junction proteins claudin-16 and claudin-19, respectively, which regulate the paracellular ion reabsorption in the kidney. Patients with mutations in the CLDN19 gene also present severe visual impairment. Our goals in this study were to examine the clinical characteristics of a large cohort of Spanish patients with this disorder and to identify the disease causing mutations. We included a total of 31 patients belonging to 27 unrelated families and studied renal and ocular manifestations. We then analyzed by direct DNA sequencing the coding regions of CLDN16 and CLDN19 genes in these patients. Bioinformatic tools were used to predict the consequences of mutations. Clinical evaluation showed ocular defects in 87% of patients, including mainly myopia, nystagmus and macular colobomata. Twenty two percent of patients underwent renal transplantation and impaired renal function was observed in another 61% of patients. Results of the genetic analysis revealed CLDN19 mutations in all patients confirming the clinical diagnosis. The majority of patients exhibited the previously described p.G20D mutation. Haplotype analysis using three microsatellite markers showed a founder effect for this recurrent mutation in our cohort. We also identified four new pathogenic mutations in CLDN19, p.G122R, p.I41T, p.G75C and p.G75S. A strategy based on microsequencing was designed to facilitate the genetic diagnosis of this disease. Our data indicate that patients with CLDN19 mutations have a high risk of progression to chronic renal disease.

2/6/19, remise du traité de paix aux Autrichiens [préliminaires du traité de Saint-Germain-en-Laye du 10 septembre, au château], MM. Clemenceau et Lloyd George : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 54216

Requête de conclusions du 19 février 1704. A Nosseigneurs de parlement en la chambre de la Tournelle. (Pour Jean-Baptiste Lorieul, sieur de la Noue, accusé de banqueroute frauduleuse, contre les nommés Passerat, Briand et autres / [Signé : Claude Berroyer].)

[Factum. Lorieul de la Noue, Jean-Baptiste. 1704?]