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Background Resolvin D1 could reduce the inflammatory, catabolic response of OA chondrocyte, and promote the repair of various tissues.Our goal was to explore whether RvD1 could inhibit NLRP3/caspase-1 signaling pathway, slow down the occurrence of pyroptosis of OA chondrocytes, and then promote the proliferation of OA chondrocytes and repair of articular cartilage.Methods Animal care and use protocols comply with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.After the rat osteoarthritis model was established, RvD1 was injected and a control group trial was set up, Joint specimens were then collected.The micro-CT system was used to determine the acquisition of a 3D model of the rat knee joint. Chondrocytes were stained with toluidine blue, Then the cover slip was examined under a light microscope. EDU was used to detect the proliferation of chondrocytes.Western Blot,RT-qPCR and Immunofluorescence was used to detect markers in experiments.Results Compared with the control group, RvD1 can promote OA chondrocytes multiplication and inhibit chondrocytes pyrosis by regulating the cell cycle.Belnacasan is a specific inhibitor of caspase-1, Treatment of OA chondrocytes with Belnacasan and RvD1 showed that Belnacasan could specifically inhibit the conduction of pyroptosis pathway induced by caspase-1, and the synergistic inhibitory effect with RvD1 was more significant.Conclusion RvD1 promotes the proliferation of OA chondrocytes by inhibiting the expression of caspase-1 to regulate NLRP3/caspase-1 signaling − 8 pathway. At the same time, RvD1 promoted the repair of articular cartilage and retarded the progression of OA in rats.

To improve the hydrothermal durability of Cu-SSZ-13 selective catalytic reduction (SCR) catalyst, a thin Al2O3 modification layer was coated on the external surface of Cu-SSZ-13 by a chemical liquid deposition (CLD) method. The high-temperature SCR activity of the Al-modified Cu-SSZ-13 can be maintained upon 750-800 °C hydrothermal aging, and over-oxidation of NH3 is largely inhibited. Based on H2-TPR and EPR results, it is revealed that CuAl2O4-like species forms upon Al modification and converts further to CuAlO2-like species during aging. The high affinity of Al-containing species (i.e., Al2O3 and CuAl2O4-like species) with Cu(OH)2 is suggested by DFT calculations, indicating that Cu(OH)2 detached from ion-exchange sites are captured by Al to form CuAlO2-like species instead of CuO-like species. The passivation of aggregated Cu species by coated Al leads to somewhat weakened low-temperature SCR activity, but successfully preserves the high-temperature SCR performance upon aging, which can be applied to high-temperature SCR scenarios.

Degeneration of the cartilage endplate (CEP) induces intervertebral disc degeneration (IVDD). Nucleus pulposus cell (NPC) apoptosis is also an important exacerbating factor in IVDD, but the cascade mechanism in IVDD is not clear. We investigated the apoptosis of NPCs and IVDD when stimulated by normal cartilage endplate stem cell (CESC)‐derived exosomes (N‐Exos) and degenerated CESC‐derived exosomes (D‐Exos) in vitro and in vivo. Tert‐butyl hydroperoxide (TBHP) was used to induce inflammation of CESCs. The bioinformatics differences between N‐Exos and D‐Exos were analyzed using mass spectrometry, heat map, and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. NPC apoptosis was examined using TUNEL staining. The involvement of the AKT and autophagy signaling pathways was investigated using the signaling inhibitor LY294002. Magnetic resonance imaging, Western blotting, and immunofluorescence staining were used to evaluate the therapeutic effects of N‐Exos in rats with IVDD. TBHP effectively induced inflammation and the degeneration of CEP in rat. N‐Exos were more conducive to autophagy activation than D‐Exos. The apoptotic rate of NPCs decreased obviously after treatment with N‐Exos compared to D‐Exos. N‐Exos inhibited NPCs apoptosis and attenuated IVDD in rat via activation of the AKT and autophagy pathways. These results are the first findings to confirm that CEP delayed the progression of IVDD via exosomes. The therapeutic effects of N‐Exos on NPC apoptosis inhibition and the slowing of IVDD progression were more effective than D‐Exos due to activation of the PI3K/AKT/autophagy pathway, which explained the increase in the incidence of IVDD after inflammation of the CEP., Graphical abstract of the mechanism that cartilage endplate (CEP) inflammation accelerated the progression of intervertebral disc degeneration (IVDD). Normal cartilage endplate stem cell (CESC)‐derived exosomes (N‐Exos) can more effectively inhibit nucleus pulposus cell (NPC) apoptosis than degenerated CEPC‐derived exosomes (D‐Exos) due to the anti‐apoptotic protein carried by exosomes decreasing after the CEP degeneration. Furthermore, N‐Exos also activate the PI3K/AKT signaling pathway in NPC more conducively compared with D‐Exos, enhancing autophagy, alleviating NPC apoptosis in vitro and ameliorating IVDD in vivo

Intervertebral disc degeneration (IDD) is recognized as the major contributor to low back pain, which results in disability worldwide and heavy burdens on society and economy. Here we present evidence that the lower level of Nrf2 is closely associated with higher grade of IDD. The apoptosis and senescence of nucleus pulposus cells (NPCs) were exacerbated by Nrf2 knockdown, but suppressed by Nrf2 overexpression under oxidative stress. Based on findings that Kinsenoside could exert multiple pharmacological effects, we found that Kinsenoside rescued the NPC viability under oxidative stress and protected against apoptosis, senescence and mitochondrial dysfunction in a Nrf2-dependent way. Further experiments revealed that Kinsenoside activated a signaling pathway of AKT-ERK1/2-Nrf2 in NPCs. Moreover, in vivo study showed that Kinsenoside ameliorated IDD in a puncture-induced model. Together, the present work suggests that Nrf2 is involved in the pathogenesis of IDD and shows the protective effects as well as the underlying mechanism of Kinsenoside on Nrf2 activation in NPCs.

Cartilage endplate (CEP) calcification inhibits the transport of metabolites and nutrients in the intervertebral disk and is an important initiating factor of intervertebral disk degeneration. However, the mechanisms governing CEP degeneration have not been thoroughly elucidated. In this study, we established a mouse CEP degeneration model and showed that autophagy insufficiency caused the degeneration of CEP. We found that the inflammatory cytokine tumor necrosis factor-α (TNF-α) increased the level of intracellular reactive oxygen species (ROS) and caused cell senescence and osteogenic differentiation of cartilage endplate stem cells (CESCs), whereas rapamycin-induced autophagy protected CESCs from TNF-α-induced oxidative stress and cell senescence. Furthermore, rapamycin-induced autophagy helped CESCs maintain the chondrogenic properties and inhibited extracellular matrix protease expression and osteogenic differentiation. Further study revealed that autophagy activated by rapamycin or inhibited by chloroquine influenced the expression and nuclear translocation of Nrf2, thereby controlling the expression of antioxidant proteins and the scavenging of ROS. Taken together, the results indicate that rapamycin-induced autophagy enhances Nrf2/Keap1 signaling and promotes the expression of antioxidant proteins, thereby eliminating ROS, alleviating cell senescence, reducing the osteogenic differentiation of CESCs, and ultimately protecting CEPs from chronic inflammation-induced degeneration. Stem Cells 2019;37:828–840

Background Nucleus pulposus cells (NPCs) apoptosis is an important factor in exacerbating intervertebral disc degeneration (IVDD) that can be effectively suppressed by exosomes. The aim of this study was to reaearch whether normal cartilage endplate stem cells (CESCs) derived exosomes (N-Exos) were more conducive to activation of autophagy and inhibition of NPCs apoptosis and IVDD than degenerated CESCs derived exosomes (D-Exos) or not. Methods Rat CESCs were isolated and identified, and the exosomes produced by normal CESCs and degenerated CESCs were extracted. The bioinformatics differences between normal CESCs derived exosomes (N-Exos) and degenerated CESCs derived exosome (D-Exos) were analyzed by mass spectrometry, heat map and KEGG enrichment analysis biology. The effects of N-Exos and D-Exos on the inhibition of NPCs apoptosis were examined by TUNEL staining, flow cytometry and western blotting. The involvement of the AKT and autophagy signaling pathways was investigated using the signaling inhibitor LY294002. Magnetic resonance imaging, western blotting and immunofluorescence staining were used to evaluate the therapeutic effects of N-Exos in vivo. Results CESCs in the cartilage endplate (CEP) could secrete a large amount of exosomes. N-Exos were more conducive to activation of autophagy than D-Exos. The apoptotic rate of NPCs was decreased obviously after treatment with N-Exos than after D-Exos treatment. N-Exos inhibited NPCs apoptosis or attenuated IVDD in a rat tail model by activating the AKT and autophagy signaling pathways. Conclusions It was the first to confirm that CEP could delay the progression of IVDD through exosomes secreted by normal CESCs. The therapeutic effects of N-Exos on inhibiting NPCs apoptosis and slowing IVDD progression was more effective than D-Exos by activating the PI3K/AKT/autophagy pathway, which explained the reason that the incidence of IVDD was increased after inflammation of the CEP.

There are critical needs for platinum catalysts with high hydrothermal stability and tunable Pt–acid site proximity, which could not be achieved via traditional methods. Here, we describe a simple strategy (SiO2 alumination combined with controlled removal of the capping agent) through which Pt-based core–shell catalysts that tolerant both high-temperature steam and boiling water can be obtained. More importantly, this strategy allows precise control of the distance between acid sites and Pt; thus, the interfacial electronic interaction can be cut off without prohibiting the spillover of adsorbed species. This tunable structure not only helps to unravel the mechanism of C3H8 oxidation over acidic Pt catalyst but also increases the N2 selectivity for NOx selective catalytic reduction. Given that the component of both the “core” and “shell” can be changed easily, this strategy should have wide application in mechanism exploration as well as the development of catalysts for various reactions.

Previous studies have identified the association between cartilage endplate (CEP) degeneration and abnormal mechanical loading. Several studies have reported that intermittent cyclic mechanical tension (ICMT) regulates CEP degeneration via various biological processes and signaling pathways. However, the functions of microRNAs in regulating the cellular responses of CEP chondrocytes to ICMT remain to be elucidated. The current study determined the differentially expressed microRNAs in human CEP chondrocytes exposed to ICMT using microarray analysis. A total 21 significantly upregulated and 62 downregulated miRNAs were identified compared with the control. The findings were subsequently partially validated by reverse transcription‑quantitative polymerase chain reaction. Potential target genes of the significantly differentially expressed miRNAs were predicted using bioinformatics analysis and were used for Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis. The present study revealed that the significantly differentially expressed microRNAs were involved in various signaling pathways and biological processes that are crucial to regulating the responses of CEP chondrocytes to ICMT. The current study provided a global view of microRNA expression in CEP chondrocytes under mechanical stimulation, suggesting that microRNAs are important for regulating the mechanical response of CEP chondrocytes. Additionally, it provided a novel insight into the association between mechanical stress and the establishment and progression of intervertebral disc degeneration.

A series of Ag/CeO 2 catalysts was synthesized by the incipient wetness method. Compared with Ag/Al 2 O 3 and CeO 2 catalysts, Ag/CeO 2 catalysts are more promising candidates for naphthalene oxidation, in which Ce x + act as the main active sites and are efficiently promoted by Ag species. By characterizing the solid properties and the redox ability, the mechanism of ceria catalysis by the Ag-modified catalysts was investigated. It was found that Ag species can work as an oxygen pump to enhance the oxygen availability in the ceria bulk. They also promote the oxygen regeneration capacity by the oxygen spillover effect. However, such an effect would also decrease the ability for active oxygen regeneration at higher Ag loading, which arises from the lower surface oxygen vacancy concentration. Because of the balance between these two factors, the Ag/CeO 2 catalyst with 1 wt.% Ag shows the best performance for isothermal catalytic oxidation of naphthalene.

A series of experiments were carried out in linked vessels with two spherical vessels of 600 mm and 350 mm diameter respectively and pipe of 60 mm diameter to investigate the influential factors on H2-air mixtures explosion. This research is focused on the effects of ignition position, initial pressure and pipe length on H2-air mixtures explosion in linked vessels. The experimental results show that the different ignition position has less impact on the maximum hydrogen explosion pressure in big vessel, however, the impact on the maximum hydrogen explosion pressure in small vessel and the maximum hydrogen explosion pressure rising rate in linked vessels is obvious. The initial pressure has a distinct effect on the maximum hydrogen explosion pressure in linked vessels. In big vessel, the maximum hydrogen explosion pressure increases with the increasing of initial pressure nearly linear relationship. In small vessel, the maximum hydrogen explosion pressure also increases with the increasing of initial pressure. Moreover, the maximum hydrogen explosion pressure has a sharp increase from 0.02 MPa to 0.03 MPa. When the ignition in big vessel, the maximum hydrogen explosion pressures are all increased with the pipe length. Meanwhile, the change of the maximum hydrogen explosion pressure in small vessel is more severe than in big vessel. The maximum hydrogen explosion pressure in the big vessel increases with pipe length when the ignition is located in the small vessel. However, the maximum hydrogen explosion pressure in small vessel increases first then decreases. The maximum hydrogen explosion pressure, the maximum rates of pressure rise and the time delay between ignition in the big and small vessel are discussed.

Intervertebral disc degeneration (IDD) is typically accompanied by a reduced nutrient supply, which is thought to be a contributor to the apoptosis of nucleus pulposus cells (NPCs). Here, we explored whether Forkhead box O3 (FOXO3), a key transcription factor involved in cellular quality control, could protect NPCs against apoptosis under nutrient deficiency. Firstly, we found that FOXO3 knockdown aggravated nutrient deficiency-induced mitochondrial dysfunction, apoptosis and matrix degradation in NPCs. In addition, the siRNA-mediated downregulation of FOXO3 suppressed mitophagy in starved NPCs. However, when we overexpressed FOXO3 in NPCs by lentivirus transfection, the observed detrimental effects induced by nutrient deprivation were significantly reversed by the FOXO3-activated autophagy. Moreover, by analyzing the human NP samples from different age groups as well as degenerated groups, we found that the FOXO3 protein level decreased with aging and degeneration. Together, our data suggest that FOXO3 plays a vital role in disc degeneration and can be a novel therapeutic target for IDD.

Different Ag/CeO2 catalysts with uniform structures and diverse surface oxygen vacancy (VO-s) contents were synthesized via a modified solution combustion method. Based on the results of Raman spectroscopy, H2-TPR and isothermal soot oxidation, it was suggested that even with gaseous O2 participating in the reaction, ceria surface sites around the catalyst–soot contact points can still be reduced by soot gradually. This interfacial reduction led to the generation of extra VO-s without changing the oxygen vacancies in the bulk of CeO2. Notably, this VO-s dynamic change and the insufficient O2− regeneration/delivery further resulted in the activation and deactivation of Ag/CeO2 during reaction with soot. This means that both the existence of ceria VO-s and its dynamic change during reaction may have a crucial influence on catalyst behavior. By further exploring these activity variations, the VO-s content, catalyst–soot contact condition and extra oxygen supplier were proved to be the three most important structural factors behind the soot oxidation activity of all the ceria-based catalysts. In this sense, Ag/CeO2 catalysts with appropriate morphology and moderate initial VO-s content may exhibit good activity for soot oxidation.

Soot oxidation was conducted over Ag/Al2O3 and Ag/SO42−/Al2O3 catalysts. Spent catalysts were found to exhibit higher activities than fresh ones for soot oxidation in oxygen. Environmental transmission electron microscopy (ETEM) was performed for the catalytic oxidation of soot over fresh and spent catalysts. Aggregation of silver nanoparticles occurred significantly on the alumina support under very low oxygen pressure. On increasing the oxygen pressure, redispersion of large Ag particles was observed on both supports, which explains the superior activities of the spent catalysts. Sulphated alumina was found to anchor the silver species effectively and deter the migration of silver to soot particles. Hence, the aggregation of silver was alleviated over Ag/SO42−/Al2O3, leading to higher activity than the Ag/Al2O3 catalyst.

Transplantation of mesenchymal stem cells (MSCs) into the degenerated intervertebral disc (IVD) has shown promise for decelerating or arresting IVD degeneration. Cellular mechanical properties play crucial roles in regulating cell-matrix interactions, potentially reflecting specific changes that occur based on cellular phenotype and behavior. However, the effect of co-culturing of MSCs with nucleus pulposus cells (NPCs) on the mechanical properties of NPCs remains unknown. In our study, we demonstrated that co-culture of degenerated NPCs with MSCs resulted in significantly decreased mechanical moduli (elastic modulus, relaxed modulus, and instantaneous modulus) and increased biological activity (proliferation and expression of matrix genes) in degenerated NPCs, but not normal NPCs. SDF-1, CXCR4 ligand, was highly expressed in MSCs when co-cultured with degenerated NPCs. Inhibition of SDF-1 using CXCR4 antagonist AMD3100 or knocking-down CXCR4 in degenerated NPCs abolished the MSCs-induced decrease in the mechanical moduli and increased biological activity of degenerated NPCs, suggesting a crucial role for SDF-1/CXCR4 signaling. AKT and FAK inhibition attenuated the MSCs- or SDF-1-induced decrease in the mechanical moduli of degenerated NPCs. In conclusion, it was demonstrated in vitro that MSCs regulate the mechanical properties of degenerated NPCs through SDF-1/CXCR4/AKT signaling. These findings highlight a possible mechanical mechanism for MSCs-induced modulation with degenerated NPCs, which may be applicable to MSCs-based therapy for disc degeneration.

Glucose is the major energy supply and a critical metabolite for most cells and is especially important when cell is differentiating. High or low concentrations of glucose enhances or inhibits the osteogenic, chondrogenic and adipogenic differentiation of cell via the insulin, transforming growth factor‐β and peroxisome proliferator‐activated receptor γ pathways, among others. New evidence implicates the hexosamine biosynthetic pathway as a mediator of crosstalk between glucose flux, cellular signalling and epigenetic regulation of cell differentiation. Extracellular glucose flux alters intracellular O‐GlcNAcylation levels through the hexosamine biosynthetic pathway. Signalling molecules that are important for cell differentiation, including protein kinase C, extracellular signal‐regulated kinase, Runx2, CCAAT/enhancer‐binding proteins, are modified by O‐GlcNAcylation. Thus, O‐GlcNAcylation markedly alters cell fate during differentiation via the post‐transcriptional modification of proteins. Furthermore, O‐GlcNAcylation and phosphorylation show complex interactions during cell differentiation: they can either non‐competitively occupy different sites on a substrate or competitively occupy a single site or proximal sites. Therefore, the influence of glucose on cell differentiation via O‐GlcNAcylation offers a potential target for controlling tissue homoeostasis and regeneration in ageing and disease. Here, we review recent progress establishing an emerging relationship among glucose concentration, O‐GlcNAcylation levels and cell differentiation.

Background Adult stem cells exist in a quiescent state (G0) within the in vivo niche; the loss of quiescence often leads to a decrease in the number and function of adult stem cells, impairing tissue regeneration and repair. Endogenous repair by nucleus pulposus-derived stem cells has recently shown promising regenerative potential for the treatment of intervertebral disc degeneration (IDD). However, the number and function of nucleus pulposus stem cells (NPSCs) declined throughout the process of IDD. This effect may have a specific relationship with quiescence. However, the biology of the quiescent NPSCs has not been reported. Methods First, we established an in vitro model for NPSC quiescence with serum starvation. The induction of G0 was confirmed by flow cytometry analyses of dual staining with Hoechst 33342 and Pyronin Y, immunofluorescent staining with Ki67 and Western blot analysis of P27 expression. NPSCs were cultured under serum starvation conditions for a long time period (21 days). To examine the functional phenotype of quiescent NPSCs, the cells were reactivated with 10% serum and differentiated into osteogenic and chondrogenic lineages in vitro. The number of colony-forming units was also estimated. To elucidate the role of autophagy in the quiescence of NPSCs, we activated and inhibited autophagy in starved cells with rapamycin and chloroquine, respectively. Then, the expression of P27 was evaluated by Western blot analysis, and the immunofluorescence of Ki67 was assessed. Finally, we assessed the role of P27 siRNA in NPSC quiescence by flow cytometry analyses and 5-ethynyl-20-deoxyuridine incorporation assays under normal and serum-starved conditions. Results NPSC quiescence was induced by 48 h of serum starvation, and they maintained quiescence for up to 21 days. Upon reactivation with serum, the quiescent NPSCs re-entered the cell cycle and exhibited enhanced clonogenic self-renewal, osteogenic differentiation and chondrogenic differentiation potentials compared to control NPSCs under normal culture conditions. We also found that autophagy underlay serum starvation-induced NPSC quiescence. Further study demonstrated that autophagy mediated the quiescence of NPSCs by regulating P27. Conclusions Serum starvation efficiently induces quiescence in NPSCs. Quiescent NPSCs maintain stem cell properties. Our study reveals that autophagy plays a role in maintaining NPSC quiescence and that autophagy mediates the quiescence of NPSCs by regulating P27. We conclude that the induction of quiescence in cultured NPSCs provides a useful model for the analysis of mechanisms that might be relevant to the biology of NPSCs in vivo.

Background Radiotherapy to cancer patients is inevitably accompanied by normal tissue injury, and the bone is one of the most commonly damaged tissues. Damage to bone marrow mesenchymal stem cells (BM-MSCs) induced by radiation is thought to be a major cause of radiation-induced bone loss. Exosomes exhibit great therapeutic potential in the treatment of osteoporosis, but whether exosomes are involved in radiation-induced bone loss has not been thoroughly elucidated to date. The main purpose of this study is to investigate the role of exosomes derived from BM-MSCs in restoring recipient BM-MSC function and alleviating radiation-induced bone loss. Methods BM-MSC-derived exosomes were intravenously injected to rats immediately after irradiation. After 28 days, the left tibiae were harvested for micro-CT and histomorphometric analysis. The effects of exosomes on antioxidant capacity, DNA damage repair, proliferation, and cell senescence of recipient BM-MSCs were determined. Osteogenic and adipogenic differentiation assays were used to detect the effects of exosomes on the differentiation potential of recipient BM-MSCs, and related genes were measured by qRT-PCR and Western blot analysis. β-Catenin expression was detected at histological and cytological levels. Results BM-MSC-derived exosomes can attenuate radiation-induced bone loss in a rat model that is similar to mesenchymal stem cell transplantation. Exosome-treated BM-MSCs exhibit reduced oxidative stress, accelerated DNA damage repair, and reduced proliferation inhibition and cell senescence-associate protein expression compared with BM-MSCs that exclusively received irradiation. Following irradiation, exosomes promote β-catenin expression in BM-MSCs and restore the balance between adipogenic and osteogenic differentiation. Conclusions Our findings indicate that BM-MSC-derived exosomes take effects by restoring the function of recipient BM-MSCs. Therefore, exosomes may represent a promising cell-free therapeutic approach for the treatment of radiation-induced bone loss. Electronic supplementary material The online version of this article (10.1186/s13287-018-1121-9) contains supplementary material, which is available to authorized users.

Additional file 1: Figure S1. CESCs Shared Features with BM-MSCs Regarding Morphology, Stem Cell Surface Markers, and Differentiation Ability.

The study was aimed at evaluating the effect of electrospun scaffold containing TGF-β1 on promoting human mesenchymal stem cells (MSCs) differentiation towards a nucleus pulposus-like phenotype under hypoxia. Two kinds of nanofibrous scaffolds containing TGF-β1 were fabricated using uniaxial electrospinning (Group I) and coaxial electrospinning (Group II). Human MSCs were seeded on both kinds of scaffolds and cultured in a hypoxia chamber (2% O2), and then the scaffolds were characterised. Cell proliferation and differentiation were also evaluated after 3 weeks of cell culture. Results showed that both kinds of scaffolds shared similar diameter distributions and protein release. However, Group I scaffolds were more hydrophilic than that of Group II. Both kinds of scaffolds induced the MSCs to differentiate towards the nucleus pulposus-type phenotype in vitro. In addition, the expression of nucleus pulposus-associated genes (aggrecan, type II collagen, HIF-1α and Sox-9) in Group I increased more than that of Group II. These results indicate that electrospinning nanofibrous scaffolds containing TGF-β1 supports the differentiation of MSCs towards the pulposus-like phenotype in a hypoxia chamber, which would be a more appropriate choice for nucleus pulposus regeneration.

An efficient scheme of component retrieval can significantly reduce the cost of software reuse. For this purpose, a method of successfully retrieving of specified components from the component repository is a crucial consideration. However, neither the retrieval efficiency, nor the query-matching rate of the traditional method, which is based on a faceted classification scheme, satisfies the requirements of component retrieval. In this paper a novel component retrieval method combining the features of the faceted classification scheme and the theory of tree matching is proposed. This method not only accurately retrieves components that match queries, but also considers any incomplete descriptions of the retrieval component to completely ensure the relaxation ability of the component retrieval. The experimental results show that the retrieval matching method proposed is highly efficient, and it retrieves feasibly and efficiently the components.

We herein report the construction of a novel azo-linked conjugated microporous polymers (Ag@Azo

Thoracic spinal tuberculosis (TST) is a dangerous disease. Besides antituberculosis chemotherapy, surgery is also necessary for treating TST. To date, no study has focused on the prognostic factors for recovery of patients after surgery for TST.From 2001-2016, 237 patients who underwent surgery for TST in our department were included in this study. Japanese Orthopedic Association score was used to assess recovery after surgery. Kaplan-Meier method and Cox regression analysis were employed to identify the significant prognostic factors.Univariate analysis demonstrated that diabetes, paralysis, kyphosis, duration of symptoms (≥3/3 months), and number of involved vertebrae (2/≤2) were identified as potential prognostic factors responsible for recovery after surgery for TST. Multivariate analysis suggested that paralysis, duration of symptoms (≥3/3 months), and number of involved vertebrae (2/≤2) were identified as the significant prognostic factors responsible for recovery after surgery for TST.This study supports the previously published evidence that nonparalysis, shorter duration of symptoms, and fewer involved vertebrae are favorable prognostic factors for recovery after surgery for TST. For a better recovery effect, the key points for treating TST were timely diagnosis and treatment. It is urgent for government to arouse attention and popularize the knowledge of spinal tuberculosis.

Summary Degenerative cartilage endplate (CEP) shows decreased chondrification and increased ossification. Cartilage endplate stem cells (CESCs), with the capacity for chondro-osteogenic differentiation, are responsible for CEP restoration. CEP is avascular and hypoxic, while the physiological hypoxia is disrupted in the degenerated CEP. Hypoxia promoted chondrogenesis but inhibited osteogenesis in CESCs. This tissue-specific differentiation fate of CESCs in response to hypoxia was physiologically significant with regard to CEP maintaining chondrification and refusing ossification. MIF, a downstream target of HIF1A, is involved in cartilage and bone metabolisms, although little is known about its regulatory role in differentiation. In CESCs, MIF was identified as a key point through which HIF1A regulated the chondro-osteogenic differentiation. Unexpectedly, unlike the traditionally recognized mode, increased nuclear-expressed MIF under hypoxia was identified to act as a transcriptional regulator by interacting with the promoter of SOX9 and RUNX2. This mode of HIF1A/MIF function may represent a target for CEP degeneration therapy., Graphical Abstract, Highlights • The hypoxic microenvironment is disrupted in degenerative CEP • Hypoxia promotes chondrogenesis but inhibits osteogenesis in CESCs • Hypoxia regulates chondro-osteogenesis through HIF1A/MIF pathway • MIF acts as a transcriptional regulator under hypoxia, In this article, Zhou, Huang, Liu, and colleagues show how the HIF1A/MIF pathway regulated the chondro-osteogenic differentiation of CESCs and suggest the role of MIF as a transcriptional regulator under hypoxia.