Image Registration Methode in Radar Interferometry

This article presents a methodology for the determination of the registration of an Interferometric Synthetic radar (InSAR) pair images with half pixel precision. Using the two superposed radar images Single Look complexes (SLC) [1-4], we developed an iterative process to superpose these two images according to their correlation coefficient with a high coherence area. This work concerns the exploitation of ERS Tandem pair of radar images SLC of the Algiers area acquired on 03 January and 04 January 1994. The former is taken as a master image and the latter as a slave image

Condition-Based Maintenance Strategy for Production Systems Generating Environmental Damage

We consider production systems which generate damage to environment as they get older and degrade. The system is submitted to inspections to assess the generated environmental damage. The inspections can be periodic or nonperiodic. In case an inspection reveals that the environmental degradation level has exceeded the critical level U, the system is considered in an advanced deterioration state and will have generated significant environmental damage. A corrective maintenance action is then performed to renew the system and clean the environment and a penalty has to be paid. In order to prevent such an undesirable situation, a lower threshold level L is considered to trigger a preventive maintenance action to bring back the system to a state as good as new at a lower cost and without paying the penalty. Two inspection policies are considered (periodic and nonperiodic). For each one of them, a mathematical model and a numerical procedure are developed to determine simultaneously the preventive maintenance (PM) threshold L∗ and the inspection sequence which minimize the average long-run cost per time unit. Numerical calculations are performed to illustrate the proposed maintenance policies and highlight their main characteristics with respect to relevant input parameters

Kyste hydatique du masséter: a propos d’un cas

La localisation cervico faciale et particulièrement musculaire massétérine est exceptionnelle même en zone d’endémie. Le kyste hydatique au niveau de cette localisation pose un problème de diagnostic et des difficultés thérapeutiques du fait de la présence de filets nerveux du VII. Les auteurs rapportent un cas rare de localisation primaire d’un kyste hydatique au niveau du muscle masséter.Mots clès : Kyste hydatique, face, masséter, imagerie, chirurgie

Mucormycose rhinosinusienne a extension palatine

Les mucormycoses sont des infections fongiques, aigues, rares et souvent fatales. Elles touchent avec prédilection les sujets  immunodéprimés. La forme rhinocérébrale est la plus fréquente. Le diagnostic repose sur l’examen clinique, anatomopathologique et mycologique. L’approche thérapeutique doit être multidisciplinaire. Les auteurs rapportent l’histoire clinique d’un patient, ayant présenté une mucormycose rhinosinusienne avec atteinte du palais au décours d’une infection dentaire. A travers cette observation, ils discutent les différents aspects cliniques, les moyens du diagnostic et les modalités thérapeutiques de la mucormycose rhinocérébrale.Mots clés : Infection fongique, mucormycose rhinocérébrale, zygomycètes, pronostic, traitement

Impairment of both IRE1 expression and XBP1 activation is a hallmark of GCB DLBCL and contributes to tumor growth.

The endoplasmic reticulum kinase inositol-requiring enzyme 1 (IRE1) and its downstream target X-box-binding protein 1 (XBP1) drive B-cell differentiation toward plasma cells and have been shown to contribute to multiple myeloma development; yet, little is known of the role of this pathway in diffuse large B-cell lymphoma (DLBCL). Here, we show that in the germinal center B-cell-like (GCB) DLBCL subtype, IRE1 expression is reduced to a level that prevents XBP1 activation. Gene expression profiles indicated that, in GCB DLBCL cancer samples, expression of IRE1 messenger RNA was inversely correlated with the levels and activity of the epigenetic repressor, histone methyltransferase enhancer of zeste homolog 2 (EZH2). Correspondingly, in GCB-derived cell lines, the IRE1 promoter carried increased levels of the repressive epigenetic mark histone 3 lysine 27 trimethylation. Pharmacological inhibition of EZH2 erased those marks and restored IRE1 expression and function in vitro and in vivo. Moreover, reconstitution of the IRE1-signaling pathway, by expression of the XBP1-active form, compromised GCB DLBCL tumor growth in a mouse xenograft cancer model. These findings indicate that IRE1-XBP1 downregulation distinguishes GCB DLBCL from other DLBCL subtypes and contributes to tumor growth

The helicase HAGE prevents interferon-a-induced PML expression in ABCB5+ malignant melanoma-initiating cells by promoting the expression of SOCS1

The tumour suppressor PML (promyelocytic leukaemia protein) regulates several cellular pathways involving cell growth, apoptosis, differentiation and senescence. PML also has an important role in the regulation of stem cell proliferation and differentiation. Here, we show the involvement of the helicase HAGE in the transcriptional repression of PML expression in ABCB5 + malignant melanoma-initiating cells (ABCB5 + MMICs), a population of cancer stem cells which are responsible for melanoma growth, progression and resistance to drug-based therapy. HAGE prevents PML gene expression by inhibiting the activation of the JAK-STAT (janus kinase-signal transducers and activators of transcription) pathway in a mechanism which implicates the suppressor of cytokine signalling 1 (SOCS1). Knockdown of HAGE led to a significant decrease in SOCS1 protein expression, activation of the JAK-STAT signalling cascade and a consequent increase of PML expression. To confirm that the reduction in SOCS1 expression was dependent on the HAGE helicase activity, we showed that SOCS1, effectively silenced by small interfering RNA, could be rescued by re-introduction of HAGE into cells lacking HAGE. Furthermore, we provide a mechanism by which HAGE promotes SOCS1 mRNA unwinding and protein expression in vitro

NLRC5 promotes transcription of BTN3A1-3 genes and Vγ9Vδ2 T cell-mediated killing

BTN3A molecules-BTN3A1 in particular-emerged as important mediators of Vγ9Vδ2 T cell activation by phosphoantigens. These metabolites can originate from infections, e.g. with Mycobacterium tuberculosis, or by alterations in cellular metabolism. Despite the growing interest in the BTN3A genes and their high expression in immune cells and various cancers, little is known about their transcriptional regulation. Here we show that these genes are induced by NLRC5, a regulator of MHC class I gene transcription, through an atypical regulatory motif found in their promoters. Accordingly, a robust correlation between NLRC5 and BTN3A gene expression was found in healthy, in M. tuberculosis-infected donors' blood cells, and in primary tumors. Moreover, forcing NLRC5 expression promoted Vγ9Vδ2 T-cell-mediated killing of tumor cells in a BTN3A-dependent manner. Altogether, these findings indicate that NLRC5 regulates the expression of BTN3A genes and hence open opportunities to modulate antimicrobial and anticancer immunity

Interferon-beta induces S phase slowing via up-regulated expression of PML in squamous carcinoma cells.

Interferon-β induces S phase slowing via up-regulated expression of PML in squamous carcinoma cell

The Intensity of IUGR-Induced Transcriptome Deregulations Is Inversely Correlated with the Onset of Organ Function in a Rat Model

A low-protein diet applied during pregnancy in the rat results in intrauterine growth restricted (IUGR) fetuses. In humans, IUGR is associated with increased perinatal morbidity, higher incidence of neuro-developmental defects and increased risk of adult metabolic anomalies, such as diabetes and cardiovascular disease. Development and function of many organs are affected by environmental conditions such as those inducing fetal and early postnatal growth restriction. This phenomenon, termed “fetal programming” has been studied unconnectedly in some organs, but very few studies (if any) have investigated at the same time several organs, on a more comparative basis. However, it is quite probable that IUGR affects differentially most organ systems, with possible persistent changes in gene expression. In this study we address transcriptional alterations induced by IUGR in a multi-organ perspective, by systematic analysis of 20-days rat fetuses. We show that (1) expressional alterations are apparently stronger in organs functioning late in foetal or postnatal life than in organs that are functioning early (2) hierarchical classification of the deregulations put together kidney and placenta in one cluster, liver, lungs and heart in another; (3) the epigenetic machinery is set up especially in the placenta, while its alterations are rather mild in other organs; (4) the genes appear deregulated in chromosome clusters; (5) the altered expression cascades varies from organ to organ, with noticeably a very significant modification of the complement and coagulation cascades in the kidney; (6) we found a significant increase in TF binding site for HNF4 proteins specifically for liver genes that are down-regulated in IUGR, suggesting that this decrease is achieved through the action of HNF transcription factors, that are themselves transcriptionnally induced in the liver by IUGR (x 1.84 fold). Altogether, our study suggests that a combination of tissue-specific mechanisms contributes to bring about tissue-driven modifications of gene cascades. The question of these cascades being activated to adapt the organ to harsh environmental condition, or as an endpoint consequence is still raised