The authors acknowledge the financial support from the National Natural Science Foundation of China(project No.31971247).

Mineralized tissue regeneration is an important and challenging part of the field of tissue engineering and regeneration.At present,autograft harvest procedures may cause secondary trauma to patients,while bone scaffold materials lack osteogenic activity,resulting in a limited application.Loaded with osteogenic induction growth factor can improve the osteoinductive performance of bone graft,but the explosive release of growth factor may also cause side effects.In this study,we innovatively used platelet-rich fibrin(PRF)-modified bone scaffolds(Bio-Oss®)to replace autograft,and used cytokine(BMP-2)to enhance osteogenesis.Encouragingly,this mixture,which we named“Autograft Mimic(AGM)”,has multiple functions and advantages.(1)The fiber network provided by PRF binds the entire bone scaffold together,thereby shaping the bone grafts and maintaining the space of the defect area.(2)The sustained release of BMP-2 from bone graft promoted bone regeneration continuously.(3)AGM recruited bone marrow mesenchymal stem cells(BMSCs)and promote their proliferation,migration,and osteogenic differentiation.Thus,AGM developed in this study can improve osteogenesis,and provide new guidance for the development of clinical bone grafts.

Serum Iron Overload Activates the SMAD Pathway and Hepcidin Expression of Hepatocytes via SMURF1

Background and Aims:Liver iron overload can induce hepatic expression of bone morphogenic protein(BMP)6 and activate the BMP/SMAD pathway.However,serum iron overload can also activate SMAD but does not induce BMP6 expression.Therefore,the mechanisms through which serum iron overload activates the BMP/SMAD pathway remain unclear.This study aimed to clarify the role of SMURF1 in serum iron overload and the BMP/SMAD pathway.Methods:A cell model of serum iron overload was established by treating hepatocytes with 2 mg/mL of holo-transferrin(Holo-Tf).A serum iron overload mouse model and a liver iron overload mouse model were established by intraperitoneally injecting 10 mg of Holo-Tf into C57BL/6 mice and administering a high-iron diet for 1 week followed by a low-iron diet for 2 days.Western blotting and real-time PCR were performed to evaluate the activation of the BMP/SMAD pathway and the expression of hepcidin.Results:Holo-Tf augmented the sensitivity and responsiveness of hepatocytes to BMP6.The E3 ubiquitin-protein ligase SMURF1 mediated Holo-Tf-induced SMAD1/5 activation and hepcidin expression;specifically,SMURF1 expression dramatically decreased when the serum iron concentration was increased.Additionally,the expression of SMURF1 substrates,which are important molecules involved in the transduction of BMP/SMAD signaling,was significantly upregulated.Furthermore,in vivo analyses confirmed that SMURF1 specifically regulated the BMP/SMAD pathway during serum iron overload.Conclusions:SMURF1 can specifically regulate the BMP/SMAD pathway by augmenting the responsiveness of hepatocytes to BMPs during serum iron overload.

Dual effects of disorder on the strongly-coupled system composed of a single quantum dot and a photonic crystal L3 cavity

Light-matter interaction in the strong coupling regime enables light control at the single-photon level. We develop numerical method and analytical expressions to calculate the decay kinetics of an initially excited two-level quantum emitter in dielectric nanostructure and single-mode cavity, respectively. We use these methods to discover the dual effects of disorder on the stronglycoupled system composed of a single quantum dot and a photonic crystal L3 cavity. The quality factor is sensitive to disorder,while the g factor and vacuum Rabi splitting are robust against disorder. A small amount of disorder may either decrease or increase the light localization and the light-matter interaction. Our methods offer flexible and efficient theoretical tools for the investigation of light-matter interaction, especially cavity quantum electrodynamics. Our findings significantly lower the requirements for optimization effort and fabrication precision and open up many promising practical possibilities.

A Long Type of TBCK Is a Novel Cytoplasmic and Mitotic Apparatus-Associated Protein Likely Suppressing Cell Proliferation

Autoantibodies from patients with various connective tissue diseases have been shown to be specific probes that can detect cellular structures, including centrosome, centromere/kineto- chore, spliceosome, Golgi complex and the rough endoplasmic reticulum （Louvard et al., 1982; Rattner et al., 1998;