Coopération entre processus guidés par les données et par les modèles pour la segmentation

Parmi les méthodes de segmentation existantes on peut distinguer deux grands types d'approches : les approches guidées par les données, utilisant l'information sur les niveaux de gris, et les approches à base de modèles, exploitant de la connaissance a priori. Cependant, les résultats obtenus par l'une ou l'autre de ces approches ne sont pas suffisamment satisfaisants (cas de mauvais contrastes pour les approches bas-niveau,trop grande variabilité morphologique pour les approches à base de modèles...) . Nous nous intéressons donc à l'étude et à la mise en oeuvre de techniques de coopération dans le but d'améliorer les résultats de la segmentation. Le travail est appliqué à l'IRM du cerveau

Stat3 controls tubolointerstitial communication during CKD

Functional Genomics of Systemic Disorder

180 Real-world treatment patterns and outcomes with first-line maintenance olaparib for BRCAm advanced ovarian cancer: a pan-European study (OVAL-1)

n/

Time Trends in the Incidence and Treatment of Extra-Abdominal and Abdominal Aggressive Fibromatosis: A Population-Based Study

BACKGROUND: Aggressive fibromatosis (AF) is a locally infiltrating soft-tissue tumor. In a population-based study in the Netherlands, we evaluated time trends for the incidence and treatment of AF. METHODS: In PALGA: Dutch Pathology Registry, all patients diagnosed between 1993 and 2013 as having extra-abdominal or abdominal wall aggressive fibromatosis were identified and available pathology data of the patients were evaluated. Epidemiological and treatment-related factors were analyzed with χ(2)and regression analysis. RESULTS: During the study period, 1134 patients were identified. The incidence increased from 2.10 to 5.36 per million people per year. Median age at the time of diagnosis increased annually by B 0.285 (P = 0.001). Female gender prevailed and increased over time [annual odds ratio (OR) 1.022; P = 0.058]. All anatomic localizations, but in particular truncal tumors, became more frequent. During the study period diagnostic histological biopsies were performed more often (annual OR 1.096; P < 0.001). The proportion of patients who underwent surgical treatment decreased (annual OR 0.928; P < 0.001). When resection was preceded by biopsy, 49.8 % of the patients had R0-resection versus 30.7 % in patients without biopsy (P < 0.001). CONCLUSIONS: In this population-based study, an increasing incidence of extra-abdominal and abdominal-wall aggressive fibromatosis was observed. The workup of patients improved and a trend towards a nonsurgical treatment policy was observed

Se-methylselenocysteine inhibits phosphatidylinositol 3-kinase activity of mouse mammary epithelial tumor cells in vitro

INTRODUCTION: Se-methylselenocysteine (MSC), a naturally occurring selenium compound, is a promising chemopreventive agent against in vivo and in vitro models of carcinogen-induced mouse and rat mammary tumorigenesis. We have demonstrated previously that MSC induces apoptosis after a cell growth arrest in S phase in a mouse mammary epithelial tumor cell model (TM6 cells) in vitro. The present study was designed to examine the involvement of the phosphatidylinositol 3-kinase (PI3-K) pathway in TM6 tumor model in vitro after treatment with MSC. METHODS: Synchronized TM6 cells treated with MSC and collected at different time points were examined for PI3-K activity and Akt phosphorylation along with phosphorylations of Raf, MAP kinase/ERK kinase (MEK), extracellular signal-related kinase (ERK) and p38 mitogen-activated protein kinase (MAPK). The growth inhibition was determined with a [(3)H]thymidine incorporation assay. Immunoblotting and a kinase assay were used to examine the molecules of the survival pathway. RESULTS: PI3-K activity was inhibited by MSC followed by dephosphorylation of Akt. The phosphorylation of p38 MAPK was also downregulated after these cells were treated with MSC. In parallel experiments MSC inhibited the Raf–MEK–ERK signaling pathway. CONCLUSION: These studies suggest that MSC blocks multiple signaling pathways in mouse mammary tumor cells. MSC inhibits cell growth by inhibiting the activity of PI3-K and its downstream effector molecules in mouse mammary tumor cells in vitro