Publications by authors named "Kaiqi Qin"

Repairing osteochondral (OC) defect presents a significant challenge due to the intricate structural requirements and the unpredictable differentiation pathways of bone marrow mesenchymal stem cells (BMSCs). To address this challenge, a novel biomimetic OC hydrogel scaffold is developed that features a structure of soft and hard components. This scaffold incorporates bilayer metal-organic frameworks (MOFs), specifically ZIF-67 in the upper layer and ZIF-8 in the lower layer, achieved through an in situ printing process.

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Background: The permanent canine usually has a single root and a single root canal. A one-rooted canine with two canals or a canine with two roots and two separate canals may also occur at a lower incidence in the permanent dentition. However, bilateral symmetrical mandibular canines with two roots and two separate canals are less common.

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Muscle atrophy resulting from peripheral nerve injury (PNI) poses a threat to a patient's mobility and sensitivity. However, an effective method to inhibit muscle atrophy following PNI remains elusive. Drawing inspiration from the sea cucumber, we have integrated microneedles (MNs) and microchannel technology into nerve guidance conduits (NGCs) to develop bionic microneedle NGCs (MNGCs) that emulate the structure and piezoelectric function of sea cucumbers.

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Bone defects are a common complication of bone diseases, which often affect the quality of life and mental health of patients. The use of biomimetic bone scaffolds loaded with bioactive substances has become a focal point in the research on bone defect repair. In this study, composite scaffolds resembling bone tissue were created using nacre powder (NP) and sodium alginate (SA) through 3D printing.

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The breakdown of all-trans-retinal (atRAL) clearance is closely associated with photoreceptor cell death in dry age-related macular degeneration (AMD) and autosomal recessive Stargardt's disease (STGD1), but its mechanisms remain elusive. Here, we demonstrate that activation of gasdermin E (GSDME) but not gasdermin D promotes atRAL-induced photoreceptor damage by activating pyroptosis and aggravating apoptosis through a mitochondria-mediated caspase-3-dependent signaling pathway. Activation of c-Jun N-terminal kinase was identified as one of the major causes of mitochondrial membrane rupture in atRAL-loaded photoreceptor cells, resulting in the release of cytochrome c from mitochondria to the cytosol, where it stimulated caspase-3 activation required for cleavage of GSDME.

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