This work develops a bioactive basic fibroblast growth factor (bFGF)/heparin and FeO nanoparticles (NPs) trifunctionalized degradable construct with the potential of using as a vascular tissue engineering scaffold with the aim of improving vascular repair and regeneration therapy. The covalent modification of heparin onto the poly(lactic acid) (PLA)-gelatin (Gel)-FeO (PGF) scaffold improves the hydrophilicity of the scaffold. Furthermore, the electrostatic adsorption of bFGF on heparin allows for a more consistent and prolonged release of bFGF in situ, hence increasing the stability and effectiveness of bFGF around the surrounding vascular tissues.
View Article and Find Full Text PDFVascular defects caused by trauma or vascular diseases can significantly impact normal blood circulation, resulting in serious health complications. Vascular grafts have evolved as a popular approach for vascular reconstruction with promising outcomes. However, four of the greatest challenges for successful application of small-diameter vascular grafts are (1) postoperative anti-infection, (2) preventing thrombosis formation, (3) utilizing the inflammatory response to the graft to induce tissue regeneration and repair, and (4) noninvasive monitoring of the scaffold and integration.
View Article and Find Full Text PDFSevere acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which causes coronavirus disease-2019 (COVID-19), interacts with the host cell receptor angiotensin-converting enzyme 2 (hACE2) via its spike 1 protein during infection. After the virus sequence was published, we identified two potent antibodies against the SARS-CoV-2 receptor binding domain (RBD) from antibody libraries using a phage-to-yeast (PtY) display platform in only 10 days. Our lead antibody JMB2002, now in a Phase 1 clinical trial (ChiCTR2100042150), showed broad-spectrum blocking activity against hACE2 binding to the RBD of multiple SARS-CoV-2 variants, including B.
View Article and Find Full Text PDFOsteochondroma is a benign autosomal dominant hereditary disease characterized by abnormal proliferation of cartilage in the long bone. It is divided into solitary osteochondroma and hereditary multiple exostoses (HMEs). The exostosin-1 (EXT-1) and exostosin-2 (EXT-2) gene mutations are well-defined molecular mechanisms in the pathogenesis of HME.
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