The invention relates to the prophylaxis and/or treatment of fibrosis and/or fibrotic diseases by means of antibodies. Above all, the invention relates to the administration of an anti-alpha-v integrin (receptor) antibody to patients suffering from fibrosis and/or fibrotic diseases, including but not limited to systemic sclerosis (SSc). More specifically, the instant invention relates to the treatment of fibrotic diseases of the skin, lung, heart, liver and/or kidney by means of said antibody. Even more specifically, the instant invention relates to the administration of a recombinant, de-immunized monoclonal antibody targeting αv-integrins patients suffering from systemic sclerosis, including, but not limited to systemic sclerosis of the skin, lung, heart and/or kidney by means of the anti-alpha-v integrin antibody DI17E6 and structural mutants or modifications thereof.

A method and a kit for detecting one or more analytes in a sample is disclosed. In one aspect, the method includes introducing the sample to a surface bound to at least one portion of a first antibody to form a first antibody-analyte complex. The method further includes incubating the first antibody-analyte complex with a set of second antibodies to form a first antibody-analyte-second antibody complex, wherein one second antibody is conjugated with a nucleic acid fragment comprising an exposed 3′ hydroxyl group and another second antibody is conjugated with an exposed 5′ phosphate group. Additionally, the method includes ligating the nucleic acid fragment comprising the exposed 3′ hydroxyl group and the nucleic acid fragment comprising the exposed 5′ phosphate group. Furthermore, the method includes separating the ligated nucleic acid fragments from the first antibody-analyte-second antibody complex.

A method and a kit for detecting one or more analytes in a sample is disclosed. In one aspect, the method includes introducing the sample to a surface bound to at least one portion of a first antibody to form a first antibody-analyte complex. The method further includes incubating the first antibody-analyte complex with a set of second antibodies to form a first antibody-analyte-second antibody complex, wherein one second antibody is conjugated with a nucleic acid fragment comprising an exposed 3′ hydroxyl group and another second antibody is conjugated with an exposed 5′ phosphate group. Additionally, the method includes ligating the nucleic acid fragment comprising the exposed 3′ hydroxyl group and the nucleic acid fragment comprising the exposed 5′ phosphate group. Furthermore, the method includes separating the ligated nucleic acid fragments from the first antibody-analyte-second antibody complex.

The present invention relates to the treatment of AML. The inventors previously discovered a new epigenetic biomarker in a cohort of CN-AML patients; this consists in a strong enrichment in the H3K27me3 histone mark located on a 70 Kb part of the major histone cluster 1 (HIST1) that separates patients into two distinguishable groups defined as H3K27me3HIST1.sup.low and H3K27me3HIST1.sup.high. Patients harboring the H3K27me3 HIST1 epigenetic mark had a better event free survival. This first observation suggests that H3K27me3HIST1.sup.high patients may develop a less aggressive disease. Molecular characterisation of H3K27me3HIST1.sup.high patients showed that the linker histone H1d, but not the other histone H1 subtypes, was down-regulated in the H3K27me3 HIST1high group of patients. H1d knockdown primed ATRA differentiation, as assessed on CD11b/CD11c markers, morphological and gene expression analyses. These results suggested that targeting H1d could help to reverse the adverse immature phenotype of the H3K27me3 HIST1low group into the more favourable one of the H3K27me3 HIST1.sup.high group of patients and thus could be a good target in AML. Thus the invention relates to an H1d inhibitor for use in the treatment of acute myeloid leukemia (AML) in a patient in need thereof.

The present invention relates to the treatment of AML. The inventors previously discovered a new epigenetic biomarker in a cohort of CN-AML patients; this consists in a strong enrichment in the H3K27me3 histone mark located on a 70 Kb part of the major histone cluster 1 (HIST1) that separates patients into two distinguishable groups defined as H3K27me3HIST1.sup.low and H3K27me3HIST1.sup.high. Patients harboring the H3K27me3 HIST1 epigenetic mark had a better event free survival. This first observation suggests that H3K27me3HIST1.sup.high patients may develop a less aggressive disease. Molecular characterisation of H3K27me3HIST1.sup.high patients showed that the linker histone H1d, but not the other histone H1 subtypes, was down-regulated in the H3K27me3 HIST1high group of patients. H1d knockdown primed ATRA differentiation, as assessed on CD11b/CD11c markers, morphological and gene expression analyses. These results suggested that targeting H1d could help to reverse the adverse immature phenotype of the H3K27me3 HIST1low group into the more favourable one of the H3K27me3 HIST1.sup.high group of patients and thus could be a good target in AML. Thus the invention relates to an H1d inhibitor for use in the treatment of acute myeloid leukemia (AML) in a patient in need thereof.

The present disclosure provides markers specific for pluripotent stem cells. In particular, the present disclosure relates to nucleic acid and polypeptide markers that are selectively expressed by pluripotent stem cells; and to methods for detecting the presence and/or absence of one or a plurality of pluripotent stem cells, by detecting such markers.

Provided herein are methods of detecting an analyte of interest to interrogate spatial gene expression in a sample using RNA-templated ligation.

Provided herein are methods of detecting an analyte of interest to interrogate spatial gene expression in a sample using RNA-templated ligation.

A microfluidic device includes a substrate having an electromagnetic wave transmission property, a lid member facing the substrate and being separated from the substrate such that a flow channel is formed between the substrate and the lid member, a light absorption layer which is placed in the flow channel and absorbs an electromagnetic wave, and a microwell array formed on the substrate and having plural microwells that are open to the flow channel to receive a target of analysis.

A microfluidic device includes a substrate having an electromagnetic wave transmission property, a lid member facing the substrate and being separated from the substrate such that a flow channel is formed between the substrate and the lid member, a light absorption layer which is placed in the flow channel and absorbs an electromagnetic wave, and a microwell array formed on the substrate and having plural microwells that are open to the flow channel to receive a target of analysis.