A5075283363- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Kruppel-like factors research
- Acute Myeloid Leukemia Research
- Chronic Myeloid Leukemia Treatments
- Bone Metabolism and Diseases
- Eosinophilic Disorders and Syndromes
- Bone health and treatments
- Bone health and osteoporosis research
- Cytokine Signaling Pathways and Interactions
- Wnt/β-catenin signaling in development and cancer
- Osteoarthritis Treatment and Mechanisms
- Platelet Disorders and Treatments
- Linguistics and Discourse Analysis
- Connective tissue disorders research
- Cancer-related gene regulation
- Fibroblast Growth Factor Research
- Cystic Fibrosis Research Advances
- Neonatal Respiratory Health Research
- Chronic Lymphocytic Leukemia Research
- linguistics and terminology studies
- Bone and Joint Diseases
- Cell Adhesion Molecules Research
- Renal Diseases and Glomerulopathies
- Parathyroid Disorders and Treatments
- Blood disorders and treatments
Sorbonne Paris Cité
2012-2024
Sorbonne Université
2017-2024
Inserm
2015-2024
Université Paris-Saclay
2015-2024
Institut Gustave Roussy
2015-2024
Centre de linguistique en Sorbonne
2017-2024
Laboratory of Excellence GR-Ex
2013-2022
Université Paris Cité
2012-2022
Assistance Publique – Hôpitaux de Paris
2011-2022
Hôpital Lariboisière
2009-2021
Arterial calcification (AC) is a common complication of end-stage renal disease (ESRD). The mechanisms responsible are complex, including disturbances mineral metabolism and active expression various mineral-regulating proteins. An inverse relationship between AC bone density has been documented in uremic patients. In the study presented here, which included 58 patients with ESRD on hemodialysis (HD), bone-histomorphometry characteristics were compared scores (0 to 4) determined according...
<ns4:p>JAK inhibitors have been developed following the discovery of the<ns4:italic>JAK2</ns4:italic>V617F in 2005 as driver mutation majority non-<ns4:italic>BCR-ABL1</ns4:italic>myeloproliferative neoplasms (MPNs). Subsequently, search for JAK2 continued with that other mutations (<ns4:italic>CALR</ns4:italic>and<ns4:italic>MPL</ns4:italic>) also exhibited persistent activation. Several type I ATP-competitive JAK different specificities were assessed clinical trials and minimal hematologic...
Objective Wnt signaling is a master regulator of joint homeostasis, but its role in osteoarthritis (OA) remains unclear. This study was undertaken to characterize the activation Wnt/β‐catenin knee joints mice with OA and assess how inhibiting this pathway bone could affect cartilage. Methods induced by partial meniscectomy Topgal transgenic overexpressing Dkk‐1 under control 2.3‐kb Col1a1 promoter (Col1a1‐Dkk‐1–Tg mice). assessed X‐Gal staining at baseline weeks 4, 6, 9. Cartilage damage...
During normal megakaryocyte development, in response to thrombopoetin, mature cells enter a senescence-like state which they shed platelets; this state, characterized by cell cycle arrest, is defective malignant megakaryocytes.
With aging, bone marrow mesenchymal stromal cell (MSC) osteoblast differentiation decreases whereas MSC into adipocytes increases, resulting in increased adipogenesis and loss. Here, we investigated whether activation of signaling by strontium ranelate (SrRan) can reverse the excessive adipogenic associated with aging. In murine cultures, SrRan Runx2 expression matrix mineralization decreased PPARγ2 adipogenesis. This effect was Wnt noncanonical representative Wnt5a modulator Maf abrogated...
Background Osteoarthritis (OA) is characterised by cartilage degradation and bone lesions. Subchondral may be involved in the pathogenesis of matrix breakdown. Objective To assess role remodelling OA studying effect bisphosphonate on development mice with high remodelling. Methods Mice overexpressing Runx2 (Runx2-Tg) under control collagen type I that displayed were used. Joint instability was performed partial medial meniscectomy to induce OA. Results Six weeks after surgery, tibial...
Stimulating bone formation is an important challenge for anabolism in osteoporotic patients or to repair defects. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions GAGs at surface bone-forming cells are less documented. Syndecan-2 a membrane heparan sulfate proteoglycan that associated with osteoblastic differentiation. We used transgenic mouse model high syndecan-2 expression osteoblasts enrich cellular GAGs. Bone mass was increased...