Contributions au colloque La conciliation dans le ressort de la cour d'appel de Toulouse, Acte 2

Ce document contient une partie des contributions au colloque "La conciliation dans le ressort de la cour d'appel de Toulouse, Acte 2" organisé par la cour d'appel de Toulouse et l'Institut de Droit Privé de l'Université Toulouse 1 Capitole : - Plaquette de présentation du colloque - Propos introductifs de M. Defix - Table ronde "la tentative de conciliation obligatoire préalable à la saisine du juge", interventions de Mme Leclercq et Mr Brugel - Table ronde "la tentative de conciliation obligatoire devant le juge", interventions de Mme Bruggeman et Me Capéla - Table ronde "la conciliation devant le conseil de prud'hommes", interventions de Mme Dupouey-Dehan et Mr Made

Contributions au colloque La conciliation dans le ressort de la cour d'appel de Toulouse, Acte 2

Ce document contient une partie des contributions au colloque "La conciliation dans le ressort de la cour d'appel de Toulouse, Acte 2" organisé par la cour d'appel de Toulouse et l'Institut de Droit Privé de l'Université Toulouse 1 Capitole : - Plaquette de présentation du colloque - Propos introductifs de M. Defix - Table ronde "la tentative de conciliation obligatoire préalable à la saisine du juge", interventions de Mme Leclercq et Mr Brugel - Table ronde "la tentative de conciliation obligatoire devant le juge", interventions de Mme Bruggeman et Me Capéla - Table ronde "la conciliation devant le conseil de prud'hommes", interventions de Mme Dupouey-Dehan et Mr Made

The PRSS3P2 and TRY7 deletion copy number variant modifies risk for chronic pancreatitis

Background PRSS1 and PRSS2 constitute the only functional copies of a tandemly-arranged five-trypsinogen-gene cluster (i.e., PRSS1, PRSS3P1, PRSS3P2, TRY7 and PRSS2) on chromosome 7q35. Variants in PRSS1 and PRSS2, including missense and copy number variants (CNVs), have been reported to predispose to or protect against chronic pancreatitis (CP). We wondered whether a common trypsinogen pseudogene deletion CNV (that removes two of the three trypsinogen pseudogenes, PRSS3P2 and TRY7) might be associated with CP causation/predisposition. Methods We analyzed the common PRSS3P2 and TRY7 deletion CNV in a total of 1536 CP patients and 3506 controls from France, Germany, India and Japan by means of quantitative fluorescent multiplex polymerase chain reaction. Results We demonstrated that the deletion CNV variant was associated with a protective effect against CP in the French, German and Japanese cohorts whilst a trend toward the same association was noted in the Indian cohort. Meta-analysis under a dominant model yielded a pooled odds ratio (OR) of 0.68 (95% confidence interval (CI) 0.52–0.89; p = 0.005) whereas an allele-based meta-analysis yielded a pooled OR of 0.84 (95% CI 0.77–0.92; p = 0.0001). This protective effect is explicable by reference to the recent finding that the still functional PRSS3P2/TRY7 pseudogene enhancers upregulate pancreatic PRSS2 expression. Conclusions The common PRSS3P2 and TRY7 deletion CNV was associated with a reduced risk for CP. This finding provides additional support for the emerging view that dysregulated PRSS2 expression represents a discrete mechanism underlying CP predisposition or protection

The PRSS3P2 and TRY7 deletion copy number variant modifies risk for chronic pancreatitis

International audienc

Mucoepidermoid carcinoma of salivary glands: A French Network of Rare Head and Neck Tumors (REFCOR) prospective study of 292 cases

International audienc

Pancreatology

BACKGROUND: PRSS1 and PRSS2 constitute the only functional copies of a tandemly-arranged five-trypsinogen-gene cluster (i.e., PRSS1, PRSS3P1, PRSS3P2, TRY7 and PRSS2) on chromosome 7q35. Variants in PRSS1 and PRSS2, including missense and copy number variants (CNVs), have been reported to predispose to or protect against chronic pancreatitis (CP). We wondered whether a common trypsinogen pseudogene deletion CNV (that removes two of the three trypsinogen pseudogenes, PRSS3P2 and TRY7) might be associated with CP causation/predisposition. METHODS: We analyzed the common PRSS3P2 and TRY7 deletion CNV in a total of 1536 CP patients and 3506 controls from France, Germany, India and Japan by means of quantitative fluorescent multiplex polymerase chain reaction. RESULTS: We demonstrated that the deletion CNV variant was associated with a protective effect against CP in the French, German and Japanese cohorts whilst a trend toward the same association was noted in the Indian cohort. Meta-analysis under a dominant model yielded a pooled odds ratio (OR) of 0.68 (95% confidence interval (CI) 0.52-0.89; p = 0.005) whereas an allele-based meta-analysis yielded a pooled OR of 0.84 (95% CI 0.77-0.92; p = 0.0001). This protective effect is explicable by reference to the recent finding that the still functional PRSS3P2/TRY7 pseudogene enhancers upregulate pancreatic PRSS2 expression. CONCLUSIONS: The common PRSS3P2 and TRY7 deletion CNV was associated with a reduced risk for CP. This finding provides additional support for the emerging view that dysregulated PRSS2 expression represents a discrete mechanism underlying CP predisposition or protection