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| http://dx.doi.org/10.1002/hep.28700 | DOI Listing |
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Enhancing Fat Transplantation Efficiency in a Mouse Model through Pretreatment of Adipose-Derived Stem Cells with RIP3 Inhibitors.
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Chinese Academy of Medical Sciences & Peking Union Medical College Plastic Surgery Hospital and Institute, 33 Badachu Road, Shijingshan District, Beijing, 100144, China.
Background: Autologous fat transplantation, widely used in cosmetic and reparative surgery for volumetric enhancements, faces challenges with its inconsistent long-term survival rates. The technique's efficacy, crucial for its development, is hindered by unpredictable outcomes. Enriching fat grafts with adipose-derived stem cells (ADSCs) shows promise in improving survival efficiency.
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April 2023
School of Geographic and Biological Information, Nanjing University of Posts and Telecommunications, Nanjing 210023, China.
Modern drug discovery typically faces large virtual screens from huge compound databases where multiple docking tools are involved for meeting various real scenes or improving the precision of virtual screens. Among these tools, AutoDock Vina and its numerous derivatives are the most popular and have become the standard pipeline for molecular docking in modern drug discovery. Our recent Vina-GPU method realized 14-fold acceleration against AutoDock Vina on a piece of NVIDIA RTX 3090 GPU in one virtual screening case.
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University of Ottawa Heart Institute, Canada (D.K., M.-A.N., M.G., Z.L., H.W., J.W.K., R.J., A.M., A.R., P.L., K.J.R.).
Background: Chronic activation of the innate immune system drives inflammation and contributes directly to atherosclerosis. We previously showed that macrophages in the atherogenic plaque undergo RIPK3 (receptor-interacting serine/threonine-protein kinase 3)-MLKL (mixed lineage kinase domain-like protein)-dependent programmed necroptosis in response to sterile ligands such as oxidized low-density lipoprotein and damage-associated molecular patterns and that necroptosis is active in advanced atherosclerotic plaques. Upstream of the RIPK3-MLKL necroptotic machinery lies RIPK1 (receptor-interacting serine/threonine-protein kinase 1), which acts as a master switch that controls whether the cell undergoes NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells)-dependent inflammation, caspase-dependent apoptosis, or necroptosis in response to extracellular stimuli.
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Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
Receptor-interacting protein kinase 3 (RIPK3) was recently implicated in promoting atherosclerosis progression through a proposed role in macrophage necroptosis. However, RIPK3 has been connected to numerous other cellular pathways, which raises questions about its actual role in atherosclerosis. Furthermore, RIPK3 is expressed in a multitude of cell types, suggesting that it may be physiologically relevant to more than just macrophages in atherosclerosis.
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