UNIVERSITÉ PARIS CITÉ

The present invention relates to a method for the treatment of FGFR-related bone repair and bone formation and quality impairment. The inventors provide data confirming that abnormal activation of the FGFR3 signaling impairs the bone formation and repair process in HCH mandible characterized by the presence of pseudarthrosis in many calluses and bone structure similar to osteoporotic bones. Interestingly, the treatment with an analog of peptide natriuretic C (e.g. BMN111) partially restore the defective bone reparation. The present invention thus relates to a method for the treatment of FGFR-related bone repair and bone formation impairment in a subject in need thereof comprising administering to the subject a therapeutically effective amount of at least one analog of C-type natriuretic peptide.

The present invention relates to a method for the treatment of FGFR-related bone repair and bone formation and quality impairment. The inventors provide data confirming that abnormal activation of the FGFR3 signaling impairs the bone formation and repair process in HCH mandible characterized by the presence of pseudarthrosis in many calluses and bone structure similar to osteoporotic bones. Interestingly, the treatment with (BGJ398) partially restore the defective bone formation and repair. The present invention thus relates to a method for the treatment of FGFR-related bone repair and bone formation impairment in a subject in need thereof comprising administering to the subject a therapeutically effective amount of at least one FGFR3 tyrosine kinase inhibitor.

A quantum computing device includes: a microwave cavity (CH) having an input port (PE) and an output port (PS) that are separate or coincident; a superconducting electronic device (DS) capacitively coupled to the microwave cavity and configured to support a chain of 2N Majorana modes (MM 1 -MM 4 , MM 2′ , MM 3′ ), N being a positive integer; and coupling means for applying microwave excitations between each pair of adjacent Majorana modes of the chain. It also relates to a method for producing a quantum braiding gate on a qubit by way of a quantum computing device.

The present invention relates to a bacterial strain of the species Limosilactobacillus mucosae , or a lysate or culture supernatant thereof, for use in the prevention and/or treatment of disorders requiring an increase in GLP-1 production in a subject in need of GLP-1, the disorders being selected from (i) a disorder related to dysregulation of insulin sensitivity and/or blood glucose concentration and (ii) loss of muscle mass and/or muscle function.

The present invention relates to a compound comprising a compound having formula (I) below: wherein R 1 , R 2 and R 3 are as defined, or a pharmaceutically acceptable salt thereof, for use in the prevention or in the treatment of an infection. The invention also relates to a pharmaceutical composition comprising the compound, for use in the prevention or in the treatment of an infection.

A novel method for obtaining NK cells, which includes culturing CD34+ cells in the presence of TNF-α or of a fragment thereof and of a Notch ligand or fragment thereof, thereby obtaining a first population of cells, and culturing the population of cells obtained in a cytokine-containing medium. Also, a NK cell population, and the use thereof for treating diseases, including cancer.

The present invention relates to methods and compositions for the care of breast cancer, from diagnosis to treatment management. The inventors show that LINC01087 downregulation contributes to a more aggressive phenotype of BC, and could represents a novel and promising specific biomarker for the diagnosis of triple-negative breast cancer. The inventors show that LINC01087 upregulation contributes to a less aggressive phenotype of BC, and could represents a novel and promising specific biomarker for the diagnosis of luminal BCs. The invention relates to a method comprising the steps of: i) determining the expression level of the long intergenic non-coding RNA 01087 (LINC01087) in a sample obtained from the subject, and ii) comparing the expression level determined at step i) with a predetermined reference value, wherein detecting difference between the expression level determined at step i) and the predetermined reference value is indicative of an aggressive TNBC or less aggressive luminal BCs.

A computer-implemented method includes identifying, in a set of previously aligned nucleotide and polypeptide sequences characteristic of a candidate protein, which can be referred to as target residues; identifying at least one candidate region consisting of at least one pair of target residues identified in the first step that include target residues located at a determined distance in space and being exposed at the surface of the candidate protein; determining the advantageous chemical interactions between each residue and/or between each pair of residues within the candidate protein, from the 2D and/or 3D structure of the candidate protein that are hydrophobic bonds and/or hydrogen bonds and/or saline bridges and/or negative-repulsion and/or positive-repulsion bonds; selecting the residues linked by said advantageous chemical interactions that are at a distance of at most 10 angstroms; and selecting at least one therapeutic target region from among the candidate regions that include the selected residues.

The clinical history of β-hemoglobinopathies shows that the severity is mitigated by the reduction of α-globin expression, resulting from co-inheritance of α-thalassemia. The inventors identified several mutations (T>C or A>G) that can disrupt binding motifs of transcription factors using CBE- and ABE-mediated base-editing approaches. In particular, the inventors designed gRNAs that, when combined with CBEs or ABEs, disrupt binding sites for transcriptional activators (GATA1 and NF-E2) in the MCS-R2 and recapitulate the beneficial α-globin reduction observed in patients presenting both β-hemoglobinopathies and α-thalassemia. Accordingly, the present invention relates to base editing approaches for the treatment of β-hemoglobinopathies.

The present invention relates to an isolated humanized protein binding to human Glycoprotein VI (hGPVI) for treating a GPVI-related condition in a subject in need thereof, wherein said isolated humanized protein is to be administered during at least 2 hours to the subject, preferably during at least 4 to 6 hours.