Abstract: SARS-CoV-2 vaccines will be essential to reduce morbidity and mortality. The inventors produced an antibody that is directed against a surface antigen (i.e. CD40) of an antigen presenting cell (i.e. dendritic cell) wherein the heavy chain was conjugated to the receptor-binding domain of the Sars-Cov-2 spike protein for its use as vaccine. In particular, the inventors show that said vaccine induces circulating Ab-secreting hu-B cells, elicits S-specific IgG+ hu-B cells, elicits the expansion of central memory CD4+ hu-T cells and the emergence of effector memory CD4+ T cells, elicits the expansion of central memory CD8+ hu-T cells at and the emergence of effector memory CD8+ T cells at and finally induces Stem-cell like memory hu-CD8+ T cells.

Abstract: Friedreich ataxia (FRDA) is caused by a GAA repeat expansion in FXN gene that encodes a mitochondrial protein, frataxin, involved in iron sulfur complex (ISC) assembly. Frataxin deficiency results in abnormal ISC containing proteins, namely respiratory chain complex I-III and aconitases and accumulation of iron in brain and heart of patients. Here, the inventors show that FRDA fibroblasts are unable to limit iron uptake inducing a massive cytosolic iron accumulation and to a lesser extent in mitochondria. The inventors also observed increased transferrin receptor (TfR1) steady state levels and membrane TfR1 accumulation that they ascribed to impaired post-translational modification by palmitoylation as well as delayed transferrin recycling. Finally, the inventors showed that artesunate, dichloroacetate and Coenzyme-A improved TfR1 palmitoylation and thus represent candidate molecules for the treatment of patients with Friedreich ataxia.

Abstract: The present invention relates to compounds of formula (I); for use as peripheral NMDA receptor antagonists.

Abstract: The use of recombinant AAV vectors expressing a molecule of interest in a method for treating diseases or conditions affecting the nervous system in a subject in need thereof, or in a method for increasing or inducing expression of the molecule of interest in the nervous system of a subject.

Abstract: The invention is in the field of therapy of antibody deficiencies. Inventors demonstrate for the first time in both controls and IgA-deficient patients, systemic anti-microbiota IgG responses correlate with reduced inflammation suggesting that systemic IgG responses contribute to the gut microbiota confinement. Furthermore, SIgAd-associated inflammation is inversely correlated with systemic anti-commensal IgG responses, which may thus serve as a second line of defense. Altogether, these data suggest that systemic IgG and intestinal IgA cooperate in different body compartments to limit systemic pro-inflammatory pathways. As selective IgA deficient patients harbour elevated seric anti-commensal IgG levels, these findings suggest that in selective IgA deficiency, microbiota confinement is obtained at the price of a strong inflammatory response.

Abstract: The present disclosure provides polypeptides derived from SARS-CoV-2 which have therapeutic use. One such polypeptide is a polypeptide, referred to as “Npep2,” is derived from the SARS-CoV-2 protein N and has at least 50 consecutive amino acids of the amino acid sequence having at least 90% identity with the amino acid sequence that ranges from the residue at position 276 to the residue at position 411 of SEQ ID NO:2. Further described are conjugates wherein a heterologous polypeptide is conjugated or fused to Npep2. The present disclosure further provides vaccines employing the polypeptides, polynucleotides encoding the polypeptides, and methods of vaccinating subjects against SARS-CoV-2 by administering a therapeutically effective amount of one or more of the polypeptides.

Abstract: A computer-implemented method for detecting pathological brain activity patterns from a scalp electroencephalographic signal, the method including the steps of obtaining (A) an electroencephalographic signal as a function of multiple channels and time; identifying (C), for each channel, the zero-crossings of the electroencephalographic signal over a fixed threshold; generating a zero-crossing representation of at least a segment of the obtained electroencephalographic signal with the identified zero-crossings; obtaining (D) a reference family of real functions of time and channels from a zero-crossing statistical analysis of zero-crossing representation of pre-recorded electroencephalographic signals; calculating (E) a matching score by comparing the zero-crossing representation of a segment of the electroencephalographic signal with at least one reference function from the reference family of functions; and computing the matching score as a function of time by sliding the at least one reference function from

Abstract: The present invention relates to methods for performing antisense oligonucleotide-mediated exon skipping in the retina of a subject in need thereof. In particular, the present invention relates to a method for performing antisense oligonucleotide-mediated exon skipping in a retina cell of a subject comprising the step of injecting into the vitreous of the subject an amount of the antisense oligonucleotide.

Abstract: A topical composition including erlotinib and a pharmaceutically acceptable excipient for use in the treatment of a keratoderma in a child, preferably a palmoplantar keratoderma (PPK), wherein the composition is topically administered. The composition may further include a penetration enhancer. The treated subject may be younger than three years old. Also, woven or non-woven fabric support including erlotinib and to dressings, patches, gloves and socks having the support useful in the treatment of a PPK.

Abstract: A method for predicting the return to functional autonomy in a subject suffering from an acute event, including the steps of i) determining neopterin level in a biological sample obtained from the subject; ii) comparing the level with its predetermined reference neopterin level and iii) predicting that the subject will have a long time to return to functional autonomy when the level of neopterin is higher than its predetermined reference neopterin level or predicting that the subject will have a short time to return to functional autonomy when the level of neopterin is lower than its predetermined reference neopterin level.

Abstract: A system for calculating an indicator associated to a brain activity of a subject, the system including an acquisition module configured to acquire at least an epoch of electroencephalographic signal of a subject from a plurality of electrodes and a data processing module configured to carry out the steps of: calculating an average vector (VA) using as input of an autoencoder neural network (aNN) an electroencephalographic signals (ES) of a subject acquired from a plurality of electrodes; detecting (DET) the presence of at least a predefined pattern in the consecutive average values of the average vector (VA); and generating an indicator of brain activity (Idx) of the subject when detecting the predefined pattern.

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 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 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: Disclosed is a method for the generation of a consciousness indicator for a non-communicating subject, including the steps of generating an auditory stimulation, receiving an electrocardiographic signal of the subject obtained from a recording during the generation of the auditory stimulation, extracting at least one feature from the electrocardiographic signal and deducing a consciousness indicator from an analysis of the electrocardiographic feature.

Abstract: The inventors initially participated to the identification of LPIN1 mutations as a cause for massive rhabdomyolysis episodes in children, triggered by febrile illness. The inventors have suggested that TLR9 antagonists would be suitable for the treatment of rhabdomyolysis (WO2017085115). The inventors thus treated 2 patients with lipin-1 disease by a TRL9 antagonist (hydroxychloroquine). They showed that the accumulation of mtDNA in plasma of the two patients before treatment decreases under treatment. When the treatment was stopped, the accumulation of mtDNA reappeared, then normalized when treatment was resumed. Accordingly, the present invention relates to a method for determining whether a patient suffering from rhabdomyolysis achieves a response with a TLR9 antagonist comprising determining the amount of mitochondrial DNA (mtDNA) in a blood sample obtained from the patient (e.g. by PCR).

Abstract: The inventors have developed a metastatic 4T1 breast tumor model in BALB/c mice. They have shown that the vaccination with xenogeneic embryonic stem cells in combination with valproic acid (VPA) generates a higher anti-tumoral response against breast cancer and inhibits metastasis development. They established that these responses are achieved only by the addition of valproic acid in the therapeutic regimen in comparison to the use ESCs or iPSCs alone. Thus, the inventors provide a new therapeutic strategy to treat cancers expressing embryonic antigens. Accordingly, the present invention relates to i) a population of pluripotent cells and ii) a compound selected from a group which activates MHC expression, as a combined preparation for use in a method for treating a subject suffering from a cancer, comprising a step of administering simultaneously, separately or sequentially to said subject a therapeutically amount thereof.

Abstract: The present invention relates to compounds of formula (I): for use as peripheral NMDA receptor antagonists.

Abstract: A method for providing cardioprotection in a subject who experienced a myocardial infarction, including administering a therapeutically effective amount of a Granzyme B inhibitor. Following acute MI in mice, CD8+ T lymphocytes are quickly recruited and activated in ischemic heart tissue, and release Granzyme B, leading to cardiomyocyte apoptosis and deterioration of myocardial function. Antibody-mediated depletion of CD8+ T lymphocytes decreases Granzyme B content and apoptotic within the myocardium and inflammatory response. mAb mediated-CD8 depletion limits myocardial injury and improves heart function. These effects are recapitulated in mice with CD8+ T cell selective Granzyme B deficiency in mice. Granzyme B is produced by other cell types (e.g., NK cells). Global Granzyme B deletion (GzmB-/- mice) decreases apoptotic within the myocardium, reduces local pro-inflammatory signature and ultimately limits infarct size after MI.

Abstract: The present invention relates to methods and pharmaceutical compositions for the treatment of tissue lesions. The inventors showed that CCR2 is expressed on FMCs, especially on a subpopulation of progenitor cells, that they call “fetal myeloid progenitor cells” (FMPCs), and mediates the recruitment of these cells to maternal wound tissue. Moreover, the inventors reported that recruited FMCs/FMPCs improve maternal skin wound healing by organizing blood vessel endothelium and secreting pro-angiogenesis peptides, particularly chemokine CXCL1, to enhance angiogenesis in wound. In particular, the present invention relates to CCR2 agonists for use in the treatment of tissue lesions in a subject in need thereof.