3D bioprinted functional scaffold based on synergistic induction of iprf and laponite exerts efficient and personalised bone regeneration via MiRNA-mediated TGF-β/Smads signaling.

Background: Limited stem cells, low vascularization efficiency and weak osteoinductive activity plague the repair and reconstruction of bone defects with cell-free scaffolds.

Methods: Herein, injectable platelet-rich fibrin (i-PRF) was loaded into a methacrylated alginate/gelatin-methylcellulose (AGM) bioink system and constructed a porous hydrogel scaffold by three-dimensional bioprinting. The addition of nanosilicate-laponite (Lap) further enhanced this scaffold and synergized with i-PRF to promote efficient and personalized cranial regeneration.

3D-printed biodegradable magnesium alloy scaffolds with zoledronic acid-loaded ceramic composite coating promote osteoporotic bone defect repair.

Osteoporotic fracture is one of the most serious complications of osteoporosis. Most fracture sites have bone defects, and restoring the balance between local osteogenesis and bone destruction is difficult during the repair of osteoporotic bone defects. In this study, we successfully fabricated three-dimensional (3D)-printed biodegradable magnesium alloy (Mg-Nd-Zn-Zr) scaffolds and prepared a zoledronic acid-loaded ceramic composite coating on the surface of the scaffolds.

3D-printed vascularized biofunctional scaffold for bone regeneration.

3D-printed biofunctional scaffolds have promising applications in bone tissue regeneration. However, the development of bioinks with rapid internal vascularization capabilities and relatively sustained osteoinductive bioactivity is the primary technical challenge. In this work, we added rat platelet-rich plasma (PRP) to a methacrylated gelatin (GelMA)/methacrylated alginate (AlgMA) system, which was further modified by a nanoclay, laponite (Lap).

Effects of astragaloside IV on glucocorticoid-induced avascular necrosis of the femoral head via regulating Akt-related pathways.

We investigated the role of astragaloside IV (AS-IV) in preventing glucocorticoid-induced avascular necrosis of the femoral head (ANFH) and the underlying molecular mechanisms. Network pharmacology was used to predict the molecular targets of AS-IV. Molecular dynamic simulations were performed to explore the binding mechanism and interaction mode between AS-IV and Akt.

The first 3D-bioprinted personalized active bone to repair bone defects: A case report.

The repair and reconstruction of bone defects are still major problems to be solved in the field of orthopedics. Meanwhile, 3D-bioprinted active bone implants may provide a new and effective solution. In this case, we used bioink prepared from the patient's autologous platelet-rich plasma (PRP) combined with polycaprolactone/β-tricalcium phosphate (PCL/β-TCP) composite scaffold material to print personalized PCL/β-TCP/PRP active scaffolds layer by layer through 3D bioprinting technology.

Mechanosensitive miR-99b mediates the regulatory effect of matrix stiffness on bone marrow mesenchymal stem cell fate both and .

Mechanical signals from extracellular matrix stiffness are important cues that regulate the proliferation and differentiation of bone marrow mesenchymal stem cells (BMSCs). However, the incorporation of BMSCs into soft hydrogels and the dominance of soft matrices for BMSC growth and differentiation limit the directed differentiation of BMSCs incorporated into hydrogels for tissue engineering, especially osteogenesis. Here, we found that the expression of miR-99b increased with increasing hydrogel stiffness and that miR-99b regulated the proliferation and differentiation of BMSCs seeded on the surface of substrates with different stiffnesses.

Niobium promotes fracture healing in rats by regulating the PI3K-Akt signalling pathway: An and study.

Background: Stable fixation is crucial in fracture treatment. Currently, optimal fracture fixation devices with osteoinductivity, mechanical compatibility, and corrosion resistance are urgently needed for clinical practice. Niobium (Nb), whose mechanical properties are similar to those of bone tissue, has excellent biocompatibility and corrosion resistance, so it has the potential to be the most appropriate fixation material for internal fracture treatment.

Comprehensive Analysis of Regulatory Networks of m6A Regulators and Reveals Prognosis Biomarkers in Sarcoma.

Sarcomas are rare malignant tumors that may arise from anywhere of the body, such as bone, adipose, muscle and vascular. However, the conventional pathogenesis of sarcomas has not been found. Therefore, there is an urgent need to identify novel therapeutic strategies and improve prognosis effects for sarcomas.

MicroRNA-365 promotes the contractile phenotype of venous smooth muscle cells and inhibits neointimal formation in rat vein grafts.

The high rate of autologous vein graft failure caused by neointimal hyperplasia remains an unresolved issue in the field of cardiovascular surgery; therefore, it is important to explore new methods for protecting against neointimal hyperplasia. MicroRNA-365 has been reported to inhibit the proliferation of vascular smooth muscle cells (SMCs). This study aimed to test whether adenovirus-mediated miR-365 was able to attenuate neointimal formation in rat vein grafts.

Dedicator of cytokinesis 2 silencing therapy inhibits neointima formation and improves blood flow in rat vein grafts.

Objective: The high rate of vein graft failure due to neointimal hyperplasia is a major challenge for cardiovascular surgery. Finding novel approaches to prevent neointimal hyperplasia is important. Thus, the purpose of this study was to investigate whether dedicator of cytokinesis 2 (DOCK2) plays a role in the development of neointima formation in the vein grafts.

MicroRNA-146a sponge therapy suppresses neointimal formation in rat vein grafts.

The long-term failure of vein grafts due to neointimal hyperplasia remains a difficult problem in cardiovascular surgery. Exploring novel approaches to prevent neointimal hyperplasia is important. MicroRNA-146a (miR-146a) plays an essential role in promoting vascular smooth muscle cell (VSMC) proliferation.