Tolerance of the fetus by the maternal immune system: role of inflammatory mediators at the feto-maternal interface

The adaptive immune system of placental mammals has evolved to tolerate the fetus. Rejection of the fetus by adaptive immune responses is therefore a rare event, with abortion being caused more frequently by inflammation in the placenta. This review will cover recent aspects of immune privilege and the innate immune system at the feto-maternal interface, citing examples of the role played by microbial infections in fetal demise

ITTACA: a new database for integrated tumor transcriptome array and clinical data analysis

Transcriptome microarrays have become one of the tools of choice for investigating the genes involved in tumorigenesis and tumor progression, as well as finding new biomarkers and gene expression signatures for the diagnosis and prognosis of cancer. Here, we describe a new database for Integrated Tumor Transcriptome Array and Clinical data Analysis (ITTACA). ITTACA centralizes public datasets containing both gene expression and clinical data. ITTACA currently focuses on the types of cancer that are of particular interest to research teams at Institut Curie: breast carcinoma, bladder carcinoma and uveal melanoma. A web interface allows users to carry out different class comparison analyses, including the comparison of expression distribution profiles, tests for differential expression and patient survival analyses. ITTACA is complementary to other databases, such as GEO and SMD, because it offers a better integration of clinical data and different functionalities. It also offers more options for class comparison analyses when compared with similar projects such as Oncomine. For example, users can define their own patient groups according to clinical data or gene expression levels. This added flexibility and the user-friendly web interface makes ITTACA especially useful for comparing personal results with the results in the existing literature. ITTACA is accessible online at

Recruitment of BAD by the Chlamydia trachomatis Vacuole Correlates with Host-Cell Survival.

Chlamydiae replicate intracellularly in a vacuole called an inclusion. Chlamydial-infected host cells are protected from mitochondrion-dependent apoptosis, partly due to degradation of BH3-only proteins. The host-cell adapter protein 14-3-3β can interact with host-cell apoptotic signaling pathways in a phosphorylation-dependent manner. In Chlamydia trachomatis-infected cells, 14-3-3β co-localizes to the inclusion via direct interaction with a C. trachomatis-encoded inclusion membrane protein. We therefore explored the possibility that the phosphatidylinositol-3 kinase (PI3K) pathway may contribute to resistance of infected cells to apoptosis. We found that inhibition of PI3K renders C. trachomatis-infected cells sensitive to staurosporine-induced apoptosis, which is accompanied by mitochondrial cytochrome c release. 14-3-3β does not associate with the Chlamydia pneumoniae inclusion, and inhibition of PI3K does not affect protection against apoptosis of C. pneumoniae-infected cells. In C. trachomatis-infected cells, the PI3K pathway activates AKT/protein kinase B, which leads to maintenance of the pro-apoptotic protein BAD in a phosphorylated state. Phosphorylated BAD is sequestered via 14-3-3β to the inclusion, but it is released when PI3K is inhibited. Depletion of AKT through short-interfering RNA reverses the resistance to apoptosis of C. trachomatis-infected cells. BAD phosphorylation is not maintained and it is not recruited to the inclusion of Chlamydia muridarum, which protects poorly against apoptosis. Thus, sequestration of BAD away from mitochondria provides C. trachomatis with a mechanism to protect the host cell from apoptosis via the interaction of a C. trachomatis-encoded inclusion protein with a host-cell phosphoserine-binding protein

Recruitment of BAD by the Chlamydia trachomatis vacuole correlates with host-cell survival

Chlamydiae replicate intracellularly in a vacuole called an inclusion. Chlamydial-infected host cells are protected from mitochondrion-dependent apoptosis, partly due to degradation of BH3-only proteins. The host-cell adapter protein 14-3-3β can interact with host-cell apoptotic signaling pathways in a phosphorylation-dependent manner. In Chlamydia trachomatis-infected cells, 14-3-3β co-localizes to the inclusion via direct interaction with a C. trachomatis-encoded inclusion membrane protein. We therefore explored the possibility that the phosphatidylinositol-3 kinase (PI3K) pathway may contribute to resistance of infected cells to apoptosis. We found that inhibition of PI3K renders C. trachomatis-infected cells sensitive to staurosporine-induced apoptosis, which is accompanied by mitochondrial cytochrome c release. 14-3-3β does not associate with the Chlamydia pneumoniae inclusion, and inhibition of PI3K does not affect protection against apoptosis of C. pneumoniae-infected cells. In C. trachomatis-infected cells, the PI3K pathway activates AKT/protein kinase B, which leads to maintenance of the pro-apoptotic protein BAD in a phosphorylated state. Phosphorylated BAD is sequestered via 14-3-3β to the inclusion, but it is released when PI3K is inhibited. Depletion of AKT through short-interfering RNA reverses the resistance to apoptosis of C. trachomatis-infected cells. BAD phosphorylation is not maintained and it is not recruited to the inclusion of Chlamydia muridarum, which protects poorly against apoptosis. Thus, sequestration of BAD away from mitochondria provides C. trachomatis with a mechanism to protect the host cell from apoptosis via the interaction of a C. trachomatis-encoded inclusion protein with a host-cell phosphoserine-binding protein

Performantiemaatstaven voor ontslagmanagement. Een aanzet tot kwaliteitsmeting

peer reviewe

A POSSIBLE ROLE OF GUT MICROBIOTA IN THE BEHAVORIAL CONTROL OF ALCOHOL-DEPENDENT SUBJECTS

These observations suggest that alterations at the level of the gut microbiota influence the gut permeability and activate specific inflammation pathways that are related to psychological symptoms of alcoholdependence. Altogether these observations are consistent with a role of inflammation as one mediator of a gut-brain communication in AD patients

Claudine Drame, Des films pour le dire, reflets de la Shoah au cinéma 1945-1985

L’année 2007 a été marquée par la sortie de deux ouvrages relatifs à la représentation au cinéma du génocide des Juifs d’Europe : celui de Claudine Drame et Le cinéma et la Shoah, un art à l’épreuve de la tragédie du XXe siècle, coordonné par Jean-Michel Frodon aux éditions Cahiers du Cinéma. Ces deux livres partent du même principe : jeter un regard rétrospectif sur des dizaines d’années de représentation des crimes génocidaires nazis au cinéma, en concluant sur la suprématie du film Shoah d..

IsoGeneGUI: Multiple Approaches for Dose-Response Analysis of Microarray Data Using R

The analysis of transcriptomic experiments with ordered covariates, such as dose-response data, has become a central topic in bioinformatics, in particular in omics studies. Consequently, multiple R packages on CRAN and Bioconductor are designed to analyse microarray data from various perspectives under the assumption of order restriction. We introduce the new R package IsoGene Graphical User Interface (IsoGeneGUI), an extension of the original IsoGene package that includes methods from most of available R packages designed for the analysis of order restricted microarray data, namely orQA, ORIClust, goric and ORCME. The methods included in the new IsoGeneGUI range from inference and estimation to model selection and clustering tools. The IsoGeneGUI is not only the most complete tool for the analysis of order restricted microarray experiments available in R but also it can be used to analyse other types of dose-response data. The package provides all the methods in a user friendly fashion, so analyses can be implemented by users with limited knowledge of R programming

Integrated cleanroom process for the vapor-phase deposition of large-area zeolitic imidazolate framework thin films

Robust and scalable thin-film deposition methods are key to realize the potential of metal-organic frameworks (MOFs) in electronic devices. Here, we report the first integration of the chemical vapor deposition (CVD) of MOF coatings in a custom reactor within a cleanroom setting. As a test case, the MOF-CVD conditions for the zeolitic imidazolate framework-8 are optimized to enable smooth, pinhole-free, and uniform thin films on full 200 mm wafers under mild conditions. The single-chamber MOF-CVD process and the impact of the deposition parameters are elucidated via a combination of in situ monitoring and ex situ characterization. The resulting process guidelines will pave the way for new MOF-CVD formulations and a plethora of MOF-based devices