Theoretical investigation of topological ferrimagnetic intertwining double chain

In this paper, a novel trimeric chain approach to organometallic ferrimagnetics is proposed. The inter and intratrimer exchange interaction has been determined to be antiferromagnetic from a theoretical model magnetic susceptibility. The Curie law observed at very low temperature (q = 5.764 K l0) contrasts with significant ferromagnetic behaviour. The magnetic data were fitted with the IDC model. The compounds interestingly exhibit ferrimagnetic interactions with gCu1 =1.81, gCu2 =2.04 and gCu3 =2.43; J1 =-89.93K and J2= -2.68 KIn this paper, a novel trimeric chain approach to organometallic ferrimagnetics is proposed. The inter and intratrimer exchange interaction has been determined to be antiferromagnetic from a theoretical model magnetic susceptibility. The Curie law observed at very low temperature (q = 5.764 K l0) contrasts with significant ferromagnetic behaviour. The magnetic data were fitted with the IDC model. The compounds interestingly exhibit ferrimagnetic interactions with gCu1 =1.81, gCu2 =2.04 and gCu3 =2.43; J1 =-89.93K and J2= -2.68

Magnetic properties of M2P4O12 ( M = Ni, Co, Cu)

We have discussed thermodynamic properties from susceptibilities and specific heat mesurements of isostructural one-dimensional M2P4O12 system. The compounds show different magnetic behaviours, varied from ferromagnetic to antiferromagnetic ordering.We have discussed thermodynamic properties from susceptibilities and specific heat mesurements of isostructural one-dimensional M2P4O12 system. The compounds show different magnetic behaviours, varied from ferromagnetic to antiferromagnetic ordering

PTPN13 induces cell junction stabilization and inhibits mammary tumor invasiveness

International audienceClinical data suggest that the protein tyrosine phosphatase PTPN13 exerts an anti-oncogenic effect. Its exact role in tumorigenesis remains, however, unclear due to its negative impact on FAS receptor-induced apoptosis. Methods: We crossed transgenic mice deleted for PTPN13 phosphatase activity with mice that overexpress human HER2 to assess the exact role of PTPN13 in tumor development and aggressiveness. To determine the molecular mechanism underlying the PTPN13 tumor suppressor activity we developed isogenic clones of the aggressive human breast cancer cell line MDA-MB-231 overexpressing either wild type or a catalytically-inactive mutant PTPN13 and subjected these to phosphoproteomic and gene ontology analyses. We investigated the PTPN13 consequences on cell aggressiveness using wound healing and Boyden chamber assays, on intercellular adhesion using videomicroscopy, cell aggregation assay and immunofluorescence. Results: The development, growth and invasiveness of breast tumors were strongly increased by deletion of the PTPN13 phosphatase activity in transgenic mice. We observed that PTPN13 phosphatase activity is required to inhibit cell motility and invasion in the MDA-MB-231 cell line overexpressing PTPN13. In vivo, the negative PTPN13 effect on tumor invasiveness was associated with a mesenchymal-to-epithelial transition phenotype in athymic mice xenografted with PTPN13-overexpressing MDA-MB-231 cells, as well as in HER2-overexpressing mice with wild type PTPN13, compared to HER2-overexpressing mice that lack PTPN13 phosphatase activity. Phosphoproteomic and gene ontology analyses indicated a role of PTPN13 in the regulation of intercellular junction-related proteins. Finally, protein localization studies in MDA-MB-231 cells and HER2-overexpressing mice tumors confirmed that PTPN13 stabilizes intercellular adhesion and promotes desmosome formation. Conclusions: These data provide the first evidence for the negative role of PTPN13 in breast tumor invasiveness and highlight its involvement in cell junction stabilization

Bounding the Risk Probability

International audienceFor some safety–critical applications, it is important to calculate the probability that a discrete time autoregressive (AR) process leaves a given interval at least once during a certain period of time. For example, such AR process can be interpreted as a temporally correlated safety indicator and the interval as a target zone of the process. It is assumed that the safety of the system under surveillance is compromised if the above-mentioned probability becomes too important. This problem has been previously studied in the case of known distributions of the innovation process. Let us assume now that the distributions of the innovation and initial state are unknown but some special bounds for the cumulative distribution functions and/or for the probability density functions are available. Numerical methods to calculate the bounds for the above-mentioned probability are considered in the paper