Décorrélation de sources large bande en traitement d'antenne actif à haute résolution

Les méthodes de localisation à haute résolution basées sur l'exploitation de la matrice spectrale des signaux reçus sont mises en défaut lorsque les sources observées sont trop fortement corrélées. Les traitements actifs y sont d'autant plus sensibles que, dans ce cas précis, le signal reçu est constitué de copies atténuées et retardées d'un unique signal, celui qui est émis. Afin de s'affranchir de ces restrictions, une méthode de décorrélation adaptée au formalisme des méthodes de localisation actives large bande est présentée ici

Geneviève Jourdain : Sa carrière et son oeuvre

Geneviève Jourdain, comment décrire simplement et complètement sa carrière et son œuvre si riches, si larges et si diverses? Chercheur de renom, elle a bâti une œuvre considérable et diverse. Enseignante de talent et de conviction, elle a formé plusieurs générations d'ingénieurs. Femme de communication et d'action, elle a marqué de son empreinte la communauté de recherche en lui apportant sa connaissance du terrain et sa vision prospective de l'évolution de la recherche et de l'enseignement. Guide sûr et bienveillant, elle a été un maître au sens classique. Elle a formé de nombreux élèves, stagiaires, thésards, qu'elle a pris sous son aile et qui lui ont été chers. Elle les a guidés, conseillés, leur a ouvert des portes. Ils sont venus enrichir la famille, selon la belle image du Professeur Blanc-Lapierre, du GRETSI, contribuant ainsi à la vie de l'École française de traitement du signal

Acadesine Kills Chronic Myelogenous Leukemia (CML) Cells through PKC-Dependent Induction of Autophagic Cell Death

CML is an hematopoietic stem cell disease characterized by the t(9;22) (q34;q11) translocation encoding the oncoprotein p210BCR-ABL. The effect of acadesine (AICAR, 5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside) a compound with known antileukemic effect on B cell chronic lymphoblastic leukemia (B-CLL) was investigated in different CML cell lines. Acadesine triggered loss of cell metabolism in K562, LAMA-84 and JURL-MK1 and was also effective in killing imatinib-resistant K562 cells and Ba/F3 cells carrying the T315I-BCR-ABL mutation. The anti-leukemic effect of acadesine did not involve apoptosis but required rather induction of autophagic cell death. AMPK knock-down by Sh-RNA failed to prevent the effect of acadesine, indicating an AMPK-independent mechanism. The effect of acadesine was abrogated by GF109203X and Ro-32-0432, both inhibitor of classical and new PKCs and accordingly, acadesine triggered relocation and activation of several PKC isoforms in K562 cells. In addition, this compound exhibited a potent anti-leukemic effect in clonogenic assays of CML cells in methyl cellulose and in a xenograft model of K562 cells in nude mice. In conclusion, our work identifies an original and unexpected mechanism by which acadesine triggers autophagic cell death through PKC activation. Therefore, in addition to its promising effects in B-CLL, acadesine might also be beneficial for Imatinib-resistant CML patients

Prise en compte de l'environnement en sonar actif

GRENOBLE1-BU Sciences (384212103) / SudocSudocFranceF

Wideband spectral matrix filtering for multicomponent sensors array

International audienc

Wideband spectral matrix filtering for multicomponent sensors array

International audienc

Estimation des correlations spatiales du bruit recu sur une antenne de grande dimension

SIGLEINIST T 74942 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc

Identification of Ebola virus sequences present as RNA or DNA in organs of terrestrial small mammals of the Central African Republic

WOS:000084213200007International audienceThe life cycle of the Ebola (EBO) virus remains enigmatic. We tested for EBO virus in the organs of 242 small mammals captured during ecological studies in the Central African Republic. EBO virus glycoprotein or polymerase gene sequences were detected by reverse transcription PCR in RNA extracts of the organs of seven animals and by PCR in DNA extract of one animal. Neither live virus nor virus antigen was detected in any organ sample. Direct sequencing of amplicons identified the virus as being of the Zaire/Gabon subtype. Virus-like nucleocapsids were observed by electron microscopy in the cytoplasm of the spleen cells of one animal. The animals belonged to two genera of rodents (Muridae; Mus setulosus, Praomys sp1 and P. sp2) and one species of shrew (Soricidae; Sylvisorex ollula). These preliminary results provide evidence that common terrestrial small mammals living in peripheral forest areas have been in contact with the EBO virus and demonstrate the persistence of EBO virus RNA and DNA in the organs of the animals. Our findings should lead to better targeting of research into the life cycle of the EBO virus. (C) 1999 Editions scientifiques et medicales Elsevier SAS

Induction of transient macroapertures in endothelial cells through RhoA inhibition by Staphylococcus aureus factors.

The GTPase RhoA is a major regulator of the assembly of actin stress fibers and the contractility of the actomyosin cytoskeleton. The epidermal cell differentiation inhibitor (EDIN) and EDIN-like ADP-ribosyltransferases of Staphylococcus aureus catalyze the inactivation of RhoA, producing actin cable disruption. We report that purified recombinant EDIN and EDIN-producing S. aureus provoke large transcellular tunnels in endothelial cells that we have named macroapertures (MAs). These structures open transiently, followed by the appearance of actin-containing membrane waves extending over the aperture. Disruption of actin cables, either directly or indirectly, through rhoA RNAi knockdown also triggers the formation of MAs. Intoxication of endothelial monolayers by EDIN produces a loss of barrier function and provides direct access of the endothelium basement membrane to S. aureus