Publications by authors named "Chaochang Li"

A composite scaffold composed of a porous scaffold and hydrogel filling can facilitate engraftment, survival, and retention in cell transplantation processes. This study presents a composite scaffold made of poly(ε-caprolactone) (PCL) and methacrylated hyaluronic acid (MeHA) hydrogel and describes the corresponding physical properties (surface area, porosity, and mechanical strength) and host response (angiogenesis and fibrosis) after subcutaneous transplantation. Specifically, we synthesise MeHA with different degrees of substitution and fabricate a PCL scaffold with different porosities.

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Objectives: Progressive pseudorheumatoid arthropathy of childhood (PPAC), caused by deficiency of (), has been challenging to study because no animal model of the disease exists and cartilage recovered from affected patients is indistinguishable from common end-stage osteoarthritis. Therefore, to gain insights into why precocious articular cartilage failure occurs in this disease, we made in vitro derived articular cartilage using isogenic -deficient and -sufficient human pluripotent stem cells (hPSCs).

Methods: We generated articular cartilage-like tissues from induced-(i) PSCs from two patients with PPAC and one wild-type human embryonic stem cell line in which we knocked out WISP3.

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Objectives: Progressive Pseudorheumatoid Arthropathy of Childhood (PPAC), caused by deficiency of ( ), has been challenging to study because no animal model of the disease exists and cartilage recovered from affected patients is indistinguishable from common end-stage osteoarthritis. Therefore, to gain insights into why precocious articular cartilage failure occurs in this disease, we made derived articular cartilage using isogenic -deficient and -sufficient human pluripotent stem cells (hPSCs).

Methods: We generated articular cartilage-like tissues from induced-(i)PSCs from 2 patients with PPAC and 1 wild-type human embryonic stem cell line in which we knocked out WISP3.

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Heterozygous deletion of Six2, which encodes a member of sine oculis homeobox family transcription factors, has recently been associated with the frontonasal dysplasia syndrome FND4. Previous studies showed that Six2 is expressed in multiple tissues during craniofacial development in mice, including embryonic head mesoderm, postmigratory frontonasal neural crest cells, and epithelial and mesenchymal cells of the developing palate and nasal structures. Whereas Six2 mice exhibited cranial base defects but did not recapitulate frontonasal phenotypes of FND4 patients, Six1 Six2 double mutant mice showed severe craniofacial defects including midline facial clefting.

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