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1.发明公开公开(公告)号：US20230162860A1
公开(公告)日：2023-05-25
申请号：US17996848
申请日：2021-04-21
申请人： NSERM (Institut National de la Santé et de la Recherche Médicale) , Centre National de la Recherche Scientifique (CNRS) , Université Paris Cité , Assistance Publique-Hôpitaux de Paris (APHP)
发明人： Dany ANGLICHEAU , Claire TINEL
CPC分类号： G16H50/20 , G01N33/6863 , C12Q1/701 , G16H50/30 , G01N2800/245 , G01N2800/52 , G01N2333/522
摘要： By using a fully phenotyped cohort of kidney transplant recipients (KTRs), inventors have clearly established the clinical conditions that should be considered when using urinary chemokine levels to noninvasively identify patients at risk of acute rejection (AR). They have developed and validated (in two external validation cohorts) a multiparametric model that predicts individual risk of AR with high accuracy. Accordingly, the invention relates to a method for calculating a probability (p) to have a risk of an acute rejection (AR) in a kidney transplant recipient by using the following equation: (I)
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公开(公告)号：US20210010030A1
公开(公告)日：2021-01-14
申请号：US17040246
申请日：2019-03-22
申请人： NSERM (INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE) , ECOLE NORMALE SUPÉRIEURE DE LYON , CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE - CNRS , INSTITUT NATIONAL DE LA RECHERCHE POUR L'AGRICULTURE, L'ALIMENTATION ET L'ENVIRONNEMNT , UNIVERSITE CLAUDE BERNARD LYON 1
发明人： Bertrand PAIN , Noémie AURINE , Camille BAQUERRE , Branka HORVAT
摘要： The disclosure relates to a method for reprogramming somatic cells from mammalian cells including human, bat and equine cells. The inventors have identified an original combination of reprogramming factors for use in methods for reprogramming somatic cells into stem cells from various species, such as bat, bovine, equine and human species. In particular, the disclosure relates to an in vitro method for preparing stem cells reprogrammed from mammalian somatic cells, said method comprising culturing mammalian somatic cells and expressing at least the following combination of reprogramming factors: (i) a reprogramming factor encoded by ESRRB gene, (ii) a reprogramming factor encoded by CDX-2 gene, and, (iii) a reprogramming factor encoded by c-MYC gene, under appropriate conditions for reprogramming said mammalian somatic cells into stem cells.
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公开(公告)号：US20210275543A1
公开(公告)日：2021-09-09
申请号：US16497704
申请日：2018-03-29
申请人： NSERM (INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE) , CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE (CNRS) , UNIVERSITÉ PARIS DESCARTES , ASSISTANCE PUBLIQUE-HÔPITAUX DE PARIS (APHP)
发明人： Guillaume CANAUD
IPC分类号： A61K31/553 , A61K31/4439 , A61P25/28 , C12Q1/48
摘要： The invention relates to a method for treating mitochondrial genetic diseases. The inventors have worked with primary fibroblasts from patients and control individuals and collected protein lysates for western blotting. Importantly, they observed that the genetic mitochondrial disorders, show a significant increase in phosphorylation of ribosomal protein S6 (pS6) compared to control fibroblasts, indicative of hyperactivated mTOR signaling. Patients with mitochondrial disorders and controls cells were treated for 48 hours with DMSO or BYL719. All lines from patients with mitochondrial diseases show reduced membrane potential, determined by TMRE staining intensity, and abnormal morphology, fragmentation and the presence of depolarized (low TMRE staining) mitochondria. Treatment with BYL719 attenuated these phenotypes in all MELAS fibroblasts while having no overt impact on the control cells. Similar experiments using flow cytometry confirmed membrane potential (TMRE) rescue by BYL719 treatment in MELAS fibroblasts.
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4.发明申请公开(公告)号：US20190119652A1
公开(公告)日：2019-04-25
申请号：US16093361
申请日：2017-04-12
申请人： NSERM (INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE) , ASSISTANCE PUBLIQUE-HÔPITAUX DE PARIS (APHP) , UNIVERSITÉ PARIS DIDEROT - PARIS 7 , INSTITUT PASTEUR , UNIVERSITÉ PARIS XIII PARIS-NORD
IPC分类号： C12N7/00 , A61K35/76 , C07K14/005 , A61P31/00
摘要： The present invention relates to a bacteriophage strain capable of producing a lytic infection in the Escherichia coli ST131-025b:H4 clone. The burden of STl31-025b:H4 Escherichia coli clonal complex in human community and hospital-acquired infections is increasing worldwide, going along with a worrying and growing resistance to betalactams and fluoroquinolones. Bacteriophage LM33_P1 infects exclusively (100% specificity) 025b E. coli strains with 70% coverage on the two major antibiotic resistant pandemic clonal complexes STI31-025b:H4 and ST69-025b. The inventors evaluated the in vivo activity of bacteriophage LM33_P1 using three different extraintestinal virulence murine models and showed that it infects bacteria in several organs. In particular, the invention relates to a bacteriophage capable of producing a lytic infection in the Escherichia coli ST131-025b:H4 clone comprising a polypeptide corresponding to the bacteriophage tail fiber protein and responsible for the attachment of the bacteriophage to the Escherichia coli ST131-025b:H4 clone.
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公开(公告)号：US20220000893A1
公开(公告)日：2022-01-06
申请号：US17289413
申请日：2019-10-30
申请人： |NSERM (INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE) , UNIVERSITÉ PAUL SABATIER TOULOUSE III , CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE (CNRS)
IPC分类号： A61K31/704 , A61K31/437 , A61K31/337 , A61K39/39 , A61P37/08
摘要： The present invention relates to the treatment of T-helper type 2 (Th2)-mediated disease. Here, the inventors set out to investigate at the genome level the effects of SETDB1-dependent H3K9me3 deposition on CD4 T cell activation, differentiation and commitment. By using conditional Setdb1−/− mice, they show that SETDB1 restricts Th1 cell priming and ensures Th2 cell integrity. Unlike their wild-type counterparts, SETDB1-deficient Th2 cells readily express the entire Th1 gene network when exposed to the Th1-instructing cytokine IL-12. More, SETDB1 methylates H3K9 at a subset of ERVs that flank and repress Th1 enhancers or behave themselves as cis-regulatory elements of a large network of Th1 genes, including Ifng, Stat4, Runx3 and Tbx21. Therefore, H3K9me3 deposition by SETDB1 locks the Th1 gene expression program and thus ensures T cell lineage integrity by repressing a repertoire of ERVs that have been co-opted to behave as Th1 lineage-specific cis-regulatory modules. Thus, the invention relates to a SETDB1 inhibitor for use in a method for increasing the Th1/Th2 ratio of an immune response in a subject in need thereof.
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公开(公告)号：US20210322418A1
公开(公告)日：2021-10-21
申请号：US17258894
申请日：2019-07-15
申请人： |NSERM (INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE) , UNIVERSITÉ DE PARIS , ASSISTANCE PUBLIQUE-HÔPITAUX DE PARIS (APHP)
IPC分类号： A61K31/517 , A61K31/439 , A61P17/02
摘要： The present invention relates to a method for promoting wound healing in a subject suffering from Ectodermal dysplasia in need thereof comprising a step of administering subcutaneously, intradermally or topically to said subject a therapeutically effective amount of a compound which restores the activity of p63. Inventors have performed a primary culture of patient keratinocytes suffering from ectodermal dysplasias with two compounds which restore the activity of p63 (e.g. STIMA-1 and/or PRIMA-1Met). They have shown that there is an important differentiation of the keratinocytes of said patient compared to the cells not treated with these compounds. They observed that the activity of p63 mutated is restored, thus the proliferation and differentiation of keratinocytes from the patient are activated. Moreover, inventors have used PRIMA-1Met by topical application on a young patient suffering from ectodermal dysplasias and shown that said patient presents an improvement on her hand. Typically, severe skin erosions (on hands and feet) are healing when PRIMA-1Met is administered topically on the hand.
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