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• High performance ZrB 2 thin films were obtained by magnetron sputtering. • The infrared emissivity of samples decreases with increasing film thickness. • Hagen-Rubens relation is suitable for ZrB 2 thin films. Surface oxidation and deterioration of mechanical properties in high-temperature environment have hamperd application of low infrared emissivity materials. Zirconium diboride (ZrB 2) exhibits excellent thermal stability and electrical conductivity due to the combination of properties of ceramics and metallic materials, which is promising for application as low infrared emissivity material in high-temperature environment. In this work, we demonstrate the deposition of ZrB 2 thin films with different thicknesses, varying from 20 nm to 600 nm, on Si (111) and ZnS substrates by direct current magnetron sputtering method. Infrared emissivity characterization is carried out in the range of 3 to 14 μm, whereas thickness dependence is elaborated in terms of crystal structure, surface roughness and electrical conductivity. Experimental results reveal that normal infrared emissivity of ZrB 2 films decreases with an increase in film thickness, from 100 nm to 400 nm, due to influence of substrate, surface roughness and electrical conductivity. The relationship among surface roughness, electrical conductivity and infrared emissivity is theoretically illustrated in detail. [ABSTRACT FROM AUTHOR]

The intervertebral disc (IVD) is the largest avascular tissue. Hypoxia-inducible factors (HIFs) play essential roles in regulating cellular adaptation in the IVD under physiological conditions. Disc degeneration disease (DDD) is one of the leading causes of disability, and current therapies are ineffective. This study sought to explore the role of HIFs in DDD pathogenesis in mice. The findings of this study showed that among HIF family members, Hif1α was significantly upregulated in cartilaginous endplate (EP) and annulus fibrosus (AF) tissues from human DDD patients and two mouse models of DDD compared with controls. Conditional deletion of the E3 ubiquitin ligase Vhl in EP and AF tissues of adult mice resulted in upregulated Hif1α expression and age-dependent IVD degeneration. Aberrant Hif1α activation enhanced glycolytic metabolism and suppressed mitochondrial function. On the other hand, genetic ablation of the Hif1α gene delayed DDD pathogenesis in Vhl-deficient mice. Administration of 2-methoxyestradiol (2ME2), a selective Hif1α inhibitor, attenuated experimental IVD degeneration in mice. The findings of this study show that aberrant Hif1α activation in EP and AF tissues induces pathological changes in DDD, implying that inhibition of aberrant Hif1α activity is a potential therapeutic strategy for DDD., (© 2022. The Author(s).)

Acquired heterotopic ossification (HO) is the extraskeletal bone formation after trauma. Various mesenchymal progenitors are reported to participate in ectopic bone formation. Here we induce acquired HO in mice by Achilles tenotomy and observe that conditional knockout (cKO) of fibroblast growth factor receptor 3 (FGFR3) in Col2 + cells promote acquired HO development. Lineage tracing studies reveal that Col2 + cells adopt fate of lymphatic endothelial cells (LECs) instead of chondrocytes or osteoblasts during HO development. FGFR3 cKO in Prox1 + LECs causes even more aggravated HO formation. We further demonstrate that FGFR3 deficiency in LECs leads to decreased local lymphatic formation in a BMPR1a-pSmad1/5-dependent manner, which exacerbates inflammatory levels in the repaired tendon. Local administration of FGF9 in Matrigel inhibits heterotopic bone formation, which is dependent on FGFR3 expression in LECs. Here we uncover Col2 + lineage cells as an origin of lymphatic endothelium, which regulates local inflammatory microenvironment after trauma and thus influences HO development via FGFR3-BMPR1a pathway. Activation of FGFR3 in LECs may be a therapeutic strategy to inhibit acquired HO formation via increasing local lymphangiogenesis., (© 2021. The Author(s).)

Objectives: The role of Paeoniflorin on hepatic fibrosis and the specific mechanisms has not yet been elucidated. Therefore, we explored whether Paeoniflorin exerted protective effects on carbon tetrachloride (CCl4)-induced hepatic fibrosis and the underlying mechanisms., Methods: A model of hepatic fibrosis was induced by intraperitoneally injecting with CCl4 (10% 5 μl/g) twice a week for 7 weeks. To explore the effects of Paeoniflorin, mice were treated with Paeoniflorin (100 mg/kg) by gavage once a day at 1 week after modeling until they were sacrificed., Key Findings: Paeoniflorin remarkably improved liver function and histopathological changes of hepatic tissues in CCl4-induced liver injury. Besides, the serum MAO enzyme activity and hydroxyproline contents were notably decreased following the intervention of Paeoniflorin. The decreased expression of Vimentin, α-SMA, Col1a and Desmin manifested the inhibition of the hepatic stellate cells (HSCs) activation. Interestingly, Paeoniflorin intervention significantly upregulated the expression of heme oxygenase-1, and attenuated the inflammatory cytokines production as well as the CCl4-induced oxidative stress imbalance., Conclusions: Paeoniflorin could effectively alleviate CCl4-induced hepatic fibrosis by upregulation of heme oxygenase-1, and it might be a new effective option for the comprehensive treatment of hepatic fibrosis., (© The Author(s) 2020. Published by Oxford University Press on behalf of Royal Pharmaceutical Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Congenital scoliosis (CS) is a complex genetic disorder characterized by vertebral malformations. The precise etiology of CS is not fully defined. Here, we identify that mutation in dual serine/threonine and tyrosine protein kinase (dstyk) lead to CS-like vertebral malformations in zebrafish. We demonstrate that the scoliosis in dstyk mutants is related to the wavy and malformed notochord sheath formation and abnormal axial skeleton segmentation due to dysregulated biogenesis of notochord vacuoles and notochord function. Further studies show that DSTYK is located in late endosomal/lysosomal compartments and is involved in the lysosome biogenesis in mammalian cells. Dstyk knockdown inhibits notochord vacuole and lysosome biogenesis through mTORC1-dependent repression of TFEB nuclear translocation. Inhibition of mTORC1 activity can rescue the defect in notochord vacuole biogenesis and scoliosis in dstyk mutants. Together, our findings reveal a key role of DSTYK in notochord vacuole biogenesis, notochord morphogenesis and spine development through mTORC1/TFEB pathway.

Objectives: This study aims to investigate the role and mechanism of FGFR3 in macrophages and their biological effects on the pathology of arthritis., Methods: Mice with conditional knockout of FGFR3 in myeloid cells (R3cKO) were generated. Gait behaviours of the mice were monitored at different ages. Spontaneous synovial joint destruction was evaluated by digital radiographic imaging and μCT analysis; changes of articular cartilage and synovitis were determined by histological analysis. The recruitment of macrophages in the synovium was examined by immunostaining and monocyte trafficking assay. RNA-seq analysis, Western blotting and chemotaxis experiment were performed on control and FGFR3-deficient macrophages. The peripheral blood from non-osteoarthritis (OA) donors and patients with OA were analysed. Mice were treated with neutralising antibody against CXCR7 to investigate the role of CXCR7 in arthritis., Results: R3cKO mice but not control mice developed spontaneous cartilage destruction in multiple synovial joints at the age of 13 months. Moreover, the synovitis and macrophage accumulation were observed in the joints of 9-month-old R3cKO mice when the articular cartilage was not grossly destructed. FGFR3 deficiency in myeloid cells also aggravated joint destruction in DMM mouse model. Mechanically, FGFR3 deficiency promoted macrophage chemotaxis partly through activation of NF-κB/CXCR7 pathway. Inhibition of CXCR7 could significantly reverse FGFR3-deficiency-enhanced macrophage chemotaxis and the arthritic phenotype in R3cKO mice., Conclusions: Our study identifies the role of FGFR3 in synovial macrophage recruitment and synovitis, which provides a new insight into the pathological mechanisms of inflammation-related arthritis., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Objective: To compare the biomechanical properties of two ultra-strong sutures and suturing methods in panda rope bridge technique (PRBT) application, and provide guidance for clinical selection of suture threads and suture methods., Methods: Forty Achilles tendons from bulls were randomly divided into 4 groups ( n =10) and transected at the 4 cm proximal to the tendon insertion. Groups A and B used Ethibond sutures (USP 5), the proximal end was fixed at the myotendious junction with Krackow sutures and the distal end was fixed through a calcaneus canal. Groups A and B had 4 and 8 threads through the stump plane, respectively. Groups C and D used Ultrabraid sutures (USP 2), the proximal end was fixed at the myotendious junction with Krackow sutures and the distal end was fixed in the calcaneus with two anchors. Groups C and D had 4 and 8 threads through the stump plane, respectively. The dynamic tensile forces of 20-100, 20-200, 20-300, and 20-400 N were tested respectively by using a dynamic tensile testing machine at 0.5 Hz for 250 cycles. After each stage of testing, the gap between stumps was measured with a caliper and the type of suture failure was recorded., Results: After dynamic tensile forces of 20-100 N and 20-200 N, the gaps of the four groups arranged from small to large were groups D, B, C, and A. The differences between groups A and B and groups C and D were significant ( P <0.05). But after dynamic tensile forces of 20-300 N and 20-400 N, the gaps were more than 5 mm in all groups. The suture retention rates of the four groups after dynamic tensile forces of 20-100 N and 20-200 N were all 100%. The suture retention rates of groups A, B, C, and D were 0, 80%, 60%, and 100%, respectively after dynamic tensile forces of 20-300 N. The differences of suture retention rates between group A and groups B and D were significant ( P <0.05). There was no significant difference between groups B, C, and D ( P >0.05). After dynamic tensile forces of 20-400 N, the suture retention rates of groups A, B, C, and D were 0, 50%, 0, and 70%, respectively. There were significant differences between groups A and B and groups C and D ( P <0.05)., Conclusion: Repairing Achilles tendon rupture via PRBT with 8 ultra-strong sutures through the stump plane can meet the mechanical requirements for walking by using ankle boots and heel pads in the early accelerated rehabilitation after operation.

Synovitis, a common clinical symptom for osteoarthritis (OA) patients, is highly related to OA pathological progression and pain manifestation. The activated synovial macrophages have been demonstrated to play an important role in synovitis, but the mechanisms about macrophage activation are still not clear. In this study, we found that the exosome-like vesicles from osteoarthritic chondrocytes could be a new biological factor to stimulate inflammasome activation and increase mature IL-1β production in macrophages. The degraded cartilage explants produced more exosome-like vesicles than the nondegraded ones, while the exosome-like vesicles from chondrocytes could enter into joint synovium tissue and macrophages. Moreover, the exosome-like vesicles from osteoarthritic chondrocytes enhanced the production of mature IL-1β in macrophages. These vesicles could inhibit ATG4B expression via miR-449a-5p, leading to inhibition of autophagy in LPS-primed macrophages. The decreased autophagy promoted the production of mitoROS, which further enhanced the inflammasome activation and subsequent IL-1β processing. Ultimately, the increase of mature IL-1β may aggravate synovial inflammation and promote the progression of OA disease. Our study provides a new perspective to understand the activation of synovial macrophages and synovitis in OA patients, which may be beneficial for therapeutic intervention in synovitis-related OA patients.

Most microwave absorbers lose their function under harsh working conditions, such as a high temperature and an oxidative environment. Here, we developed a heterogeneous ZrN 0.4 B 0.6 /SiC nanohybrid via combined catalytic chemical vapor deposition (CCVD) and chemical vapor infiltration (CVI) processes using ZrB 2 as the starting material. The composition and structure of the ZrN 0.4 B 0.6 /SiC nanohybrid were controlled by tuning the CCVD and CVI parameters, such as reaction temperature, time, and reactant concentration. The optimal heterogeneous ZrN 0.4 B 0.6 /SiC nanohybrids were obtained initially by preparing ZrB 2 @C via the CCVD process at 650 °C for 30 min and the subsequent CVI at 1500 °C, where the ZrB 2 @C reacted with Si under N 2 . The ZrN 0.4 B 0.6 /SiC nanohybrid exhibited enhanced microwave absorption ability with a minimum reflection loss value of approximately -50.8 dB at 7.7 GHz, a thickness of ∼3.05 mm, and antioxidation features at a high temperature of 600 °C. The heterogeneous ZrN 0.4 B 0.6 /SiC nanohybrid possessed reasonable conductivity, leading to dielectric loss, whereas SiC nanofibers formed a three-dimensional network that brought higher dipole moments, whereas a small part of the ZrN 0.4 B 0.6 /SiC nanohybrid structure generated an effective interface for higher attenuation of microwaves. Therefore, these material features synergistically resulted in a well-defined Debye relaxation, Maxwell-Wagner relaxation, dipole polarization, and the quarter-wavelength cancellation, which accounted for the enhanced microwave absorption.

A novel green-yellow emitting Ca1.5Mg0.5Si1-xLixO4-δ:Ce3+ phosphor with high quantum efficiency and thermal stability was discovered for applications in near ultraviolet pumped white light-emitting diodes. Its crystal structure was determined with a single-particle diagnosis approach. The Si sites in the SiO4 tetrahedra are reported for the first time to accommodate Li+ ions. This substitution, confirmed by 6Li solid-state NMR and T.O.F. neutron powder diffraction, causes a disordered occupation of Ca/Mg in the Ca3MgSi2O8 host and favors a phase transformation at ∼330 °C, which results in the formation of the novel phosphor. The produced phosphor was efficiently excited by near UV light peaking at 365 and 410 nm and produced broad green-yellow emission with peaks at 500 and 560 nm, respectively. Its quantum efficiency reached 88.4% (internal) and 55.7% (external) under excitation at 365 nm, and 80.5% (internal) and 42.7% (external) under excitation at 410 nm, while the decrease of luminescence intensity at 200 °C was small (∼26%). A WLED lamp with a high color rendering index of Ra = 92.8 was produced with the combination of a 365 nm emitting chip with blue emitting BaMgAl10O17:Eu2+, green-yellow emitting CMSL:0.01Ce, and red emitting Sr2Si5N8:Eu2+ phosphors.

Bone morphogenetic proteins (BMPs) are members of the TGF-β superfamily and play a critical role in skeletal development, bone formation and stem cell differentiation. Disruptions in BMP signaling result in a variety of skeletal and extraskeletal anomalies. BMP9 is a poorly characterized member of the BMP family and is among the most osteogenic BMPs, promoting osteoblastic differentiation of mesenchymal stem cells (MSCs) both in vitro and in vivo. Recent findings from various in vivo and molecular studies strongly suggest that the mechanisms governing BMP9-mediated osteoinduction differ from other osteogenic BMPs. Many signaling pathways with diverse functions have been found to play a role in BMP9-mediated osteogenesis. Several of these pathways are also critical in the differentiation of other cell lineages, including adipocytes and chondrocytes. While BMP9 is known to be a potent osteogenic factor, it also influences several other pathways including cancer development, angiogenesis and myogenesis. Although BMP9 has been demonstrated as one of the most osteogenic BMPs, relatively little is known about the specific mechanisms responsible for these effects. BMP9 has demonstrated efficacy in promoting spinal fusion and bony non-union repair in animal models, demonstrating great translational promise. This review aims to summarize our current knowledge of BMP9-mediated osteogenesis by presenting recently completed work which may help us to further elucidate these pathways.

Objective: The biological effects of fibroblast growth factor (FGF) may be different under different intensities and durations. To investigate the impact of sustained increasing FGF signal upon the development of epiphyseal plate., Methods: Epiphyseal plates cultured in vitro were obtained from embryonic C57BL/6J mice, and were divided into control group (0.1% DMSO), basic FGF (bFGF) group (100 microg/L bFGF and 0.1% DMSO), and PD98059 group (100 microg/L bFGF and 50 micromol/L PD98059 with 0.1% DMSO). The total length (TL) and ossified tissue length (OSL) of the cultured bones were measured with Calcein staining 6 days after culture. The expressions of Indian hedgehog (Ihh), collagen type II (Col II), and Col X genes were detected by real-time fluorescent quantitative PCR 7 days after culture., Results: The embryonic bones cultured in vitro continued growth. At 6 days after culture, there was no significant difference in increased percentage of TL between bFGF group and control group (P > 0.05), the increased percentage of OSL in bFGF group was significantly less than that in control group (P < 0.05). There was no significant difference in the increased percentage of TL and OSL between PD98059 group and control group (P > 0.05), but they were significantly higher than those of bFGF group (P < 0.05). At 7 days after culture, the gene expressions of Ihh, Col II, and Col X in bFGF group significantly decreased when compared with those in control group (P < 0.05). There was no significant difference in the gene expressions of Col II and Col X between PD98059 group and control group (P > 0.05), but the gene expressions were significantly higher than those of bFGF group (P < 0.05); the expression of Ihh in PD98059 group was significantly higher than that in control group and bFGF group (P < 0.05)., Conclusion: Sustained increasing FGF signal may affect the Col II and Col X expressions by down-regulating Ihh, which may lead to the development retardation of epiphyseal plate cultured in vitro. The external signal regulated kinase pathway may play an important role in the process.