Abstract: The disclosure pertains to the field of molecular means capable of binding calcium, in particular peptides which are calcium chelators, appropriate for use in vitro or in vivo and preferably capable of targeting specific cellular compartments. Polypeptide comprising a first calcium-binding domain, a peptide linker and a second calcium binding domain, wherein the first and second binding domains are linked through the peptide linker, and wherein: the first calcium-binding domain and the second calcium binding domain each comprise at least one calcium-binding site derived from a EF-hand motif; and, the first calcium-binding domain and the second calcium binding domain differ in at least one calcium-binding site.

Abstract: A system for automatic evaluation of cognition and consciousness of a subject, the system including a micro-controller, a digital-to-analog converter and at least one sensory stimulation element, wherein the system is configured to receive as input an information concerning a stimulation paradigm and to generate as output a sensory stimulation according to the stimulation paradigm and transmit at least one synchronization signal determined by the stimulation paradigm to a device for the acquisition of a physiological signal so as to synchronize the system for stimulation with the device for the acquisition of a physiological signal during an acquisition.

Abstract: The invention relates to an in vitro method to generate T cell progenitors, comprising the step of culturing CD34+ cells in a medium containing TNF-alpha and/or an antagonist of the Aryl hydrocarbon/Dioxin receptor, in particular StemRegenin 1 (SR1), in presence of a Notch ligand and optionally a fibronectin fragment.

Abstract: The present invention relates to the Compound of following formula (I): or a pharmaceutically acceptable salt thereof. The present invention also relates to a pharmaceutical composition containing such a compound and a method for preparing such a compound.

Abstract: The present invention relates to methods and pharmaceutical compositions for the treatment of diseases mediated by the NRP-1/OBR complex signaling pathway. In particular, the present invention relates to a method for treating a disease selected from the group consisting of cancers, obesity and obesity related diseases, anorexia, autoimmune diseases and infectious diseases in a subject in need thereof comprising administering the subject with a therapeutically effective amount of an antagonist of the NRP-1/OBR signaling pathway.

Abstract: The invention concerns a multicistronic nucleic acid, in particular an isolated multicistronic nucleic acid, comprising: A) a sequence comprising successively: A1) a sequence encoding the light chain variable domain of an antibody of interest, fused in the frame with A2) a sequence encoding the constant region of the light chain of an immunoglobulin Ig; and B) a sequence comprising successively: B1) a sequence encoding the heavy chain variable domain of said antibody of interest, fused in the frame with B2) a sequence encoding the constant regions of the heavy chain of an immunoglobulin Ig? in secretory form; B3) an intronic sequence of the gene of the heavy chain of said immunoglobulin Ig?, said intronic sequence comprising an internal 5? splice site enabling the splicing of said intronic sequence B3) and a secretory-specific poly(A) (p AS) signal from the 3? terminal exon of said gene; B4) a sequence, in frame with sequence B1), encoding the transmembrane and cytoplasmic domains M1 and M2 of the immunoglobu

Abstract: Vaccines for preventing or treating diabetes, obesity and complications thereof are provided. The vaccines comprise at least one active agent such as attenuated Porphyromonas gingivalis, inactivated Porphyromonas gingivalis, a subunit of Porphyromonas gingivalis, a recombinant or isolated immunogenic polypeptide or peptide from Porphyromonas gingivalis or a cDNA from Porphyromonas gingivalis.

Abstract: The present invention relates to an engineered immune cell defective for Suv39h1. Preferably, said engineered immune cell further comprises a genetically engineered antigen receptor that specifically binds a target antigen. The present invention also relates to a method for obtaining a genetically engineered immune cell comprising a step consisting in inhibiting the expression and/or activity of Suv39h1 in the immune cell; and further optionally comprising a step consisting in introducing in the said immune cell a genetically engineered antigen receptor that specifically binds to a target antigen. The invention also encompasses said engineered immune cell for their use in adoptive therapy, notably for the treatment of cancer.

Abstract: The present invention relates to regulatory T cell and uses thereof. By their immunosuppressive and anti-inflammatory activities, regulatory T cells play a central role in peripheral tolerance and thus critically prevent the development of autoimmune and inflammatory disorders. The inventors showed that Foxp3+CD4+ Tregs express high levels of LT?, which negatively regulates their immunosuppressive signature. They demonstrated that the adoptive transfer of LT??/? Tregs in mice protects from dextran sodium sulfate (DSS)-induced colitis and attenuates inflammatory bowel disease (IBD), multi-organ autoimmunity and the development of CAC. The inventors also showed that by mixed bone marrow chimeras that LT? expression specifically in hematopoietic cells negatively controls the immunosuppressive signature of Tregs. In particular, the present invention relates to regulatory T cell characterized in that it does not express or expresses reduced levels of lymphotoxin alpha.

Abstract: The present invention aims at improving the Doppler imaging of a biological sample comprising blood. For this, it is proposed a method for imaging a biological sample (10), the sample (10) comprising blood (14) comprising diffusors and solid tissue (16), the method comprising obtaining observation, each observation being characterized by a different point spread function associating a signal to each location of the region of interest, the signal comprising a first contribution representative of the diffusors of blood vessels within the location, a second contribution representative of the tissue diffusors and a third contribution representative of blood signal associated to blood diffusors outside of the location, and estimating, for each location, the blood flow by using a statistical analysis.

Abstract: The present invention relates to methods and devices to consolidate memory and/or cognitive functions by monitoring brain rhythms and delivering a stimulus at an appropriate stage of sleep cycle.

Abstract: Using chemical proteomics with a potent unique irreversible inhibitor, inventors found that major brain tubulin carboxypeptidase (TCP) is a complex of vasohibin-1 (VASH1) with the Small Vasohibin-Binding Protein (SVBP). VASH1 and its homologue vasohibin-2 (VASH2), when complexed with SVBP, exhibit robust and specific Tyr/Phe carboxypeptidase activity on microtubules. Accordingly inventors are the first to identify the enzymatic activity of vasohibin and vasohibin/SVBP complex. Knock down of vasohibins or SVBP in cultured neurons results in a marked reduction of tyrosinated ?-tubulin levels and onset of severe differentiation defects. Furthermore, knock down of vasohibins disrupts neuronal migration in developing mouse neocortex. These results establish vasohibin/SVBP complexes as TCP enzymes.

Abstract: The present invention relates to pseudotyped retrovirus-like particles or retroviral vectors comprising both engineered envelope glycoproteins derived from a virus of the Paramyxoviridae family fused to a cell targeting domain and fused to a functional domain. The present invention also relates to the use of said pseudotyped retrovirus-like particles or retroviral vectors to selectively modulate the activity of specific subsets of cells, in particular of specific immune cells. These pseudotyped retrovirus-like particles or retroviral vectors are particularly useful for gene therapy, immune therapy and/or vaccination.

Abstract: The present invention concerns a compound having the following formula (I): wherein: —A is in particular —N(R?a)—C(?O)—R, R?a being H or a (C1-C6)alkyl group, and R being preferably a group having the following formula (II): —X is in particular chosen from the group consisting of: —SO2—N(R?b)—, R?b being H or a (C1-C6)alkyl group, —N(R?b)—SO2—, R?b being H or a (C1-C6)alkyl group, —CO—NH—, and —NH—CO—, for use for the treatment of pathologies characterized by bronchoconstriction, such as asthma.

Abstract: Compositions containing micropeptides capable of modulating the accumulation of miRs involved in certain pathologies, and the use of these micropeptides for treating the certain pathologies. Also, methods of identifying these micropeptides modulating the accumulation of miRs involved in pathologies. Further, nuclei acids encoding those micropeptides that modulate the accumulation of miRs involved in pathologies.

Abstract: A method for determining wavefront shapes of N angular channels CL of different propagation directions PL, said propagation directions PL being determined by a mean propagation direction vector , from a single signal image acquisition I(x,y) of a multi-angular signal light beam containing said angular channels, each angular channel Ci being separated from other angular channels Cj by an angular separation ??ij defined by ??ij=arccos, where “·” stands for the inner product between and .

Abstract: The present invention concerns a polyelectrolyte coating comprising at least one polycationic layer consisting of at least one polycation consisting of n repetitive units having the formula (1) and at least one polyanionic layer consisting of hyaluronic acid. The polyelectrolyte coating has a biocidal activity and the invention thus further refers to the use of said polyelectrolyte coating for producing a device, in particular a bacteriostatic medical device, more particularly an implantable device, comprising said polyelectrolyte coating, and a method for preparing said device and a kit.

Abstract: Method and system for localizing a region of interest in a medium in which cavitation occurs. Method for localizing a region of interest (R) in a medium (M) in which cavitation occurs, the method comprising the steps consisting in: producing cavitation in the region of interest (R), the cavitation generating an acoustic signal, at each of at least three separate positions, detecting a cavitation signal representative of the acoustic signal of the cavitation, for at least two pairs of cavitation signals, determining a delay between the cavitation signals of each pair of cavitation signals, calculating a localization of the region of interest (R) based on the delays and the positions.

Abstract: The invention relates to an isolated monoclonal antibody that specifically binds to the D4 domain of VWF, competes for binding to VWF D4 domain with ADAMTS13 and partially inhibits ADAMTS 13-mediated degradation of VWF. More particularly, the invention relates to an isolated monoclonal antibody comprising a heavy chain wherein the variable domain comprises at least one CDR having a sequence selected from the group consisting of SEQ ID NO: 3 for H-CDR1, SEQ ID NO: 4 for H-CDR2 and SEQ ID NO: 5 for H-CDR3 and a light chain wherein the variable domain comprises at least one CDR having a sequence selected from the group consisting of SEQ ID NO: 7 for L-CDR1, SEQ ID NO: 8 for L-CDR2 and SEQ ID NO: 9 for L-CDR3. Antibodies of the invention are presented to be useful in for the prevention or the treatment of bleeding episodes, such as bleeding episodes occurring in patients with aortic stenosis or patients with ventricular assist devices (VAD).

Abstract: The present invention concerns synthetic polynucleotides encoding a human fukutin-related protein (FKRP) wherein the synthetic polynucleotides contain at least a mutation avoiding supplementary transcript(s) generated from frameshift start codon(s). The synthetic polynucleotides are useful, especially for treating a pathology linked to a FKRP deficiency or induced by a defect in ?-dystroglycan (?-DG) glycosylation, such as LGMD2I.