Graphene has excellent theoretical properties and a wide range of applications in metal-based composites. However, because of defects on the graphene surface, the actual performance of the material is far below theore...Graphene has excellent theoretical properties and a wide range of applications in metal-based composites. However, because of defects on the graphene surface, the actual performance of the material is far below theoretical expectations. In addition, graphene containing defects could easily react with a matrix alloy, such as Al, to generate brittle and hydrolyzed phases that could further reduce the performance of the resulting composite. Therefore, defect repair is an important area of graphene research. The repair methods reported in the present paper include chemical vapor deposition, doping, liquid-phase repair, external energy graphitization, and alloying. Detailed analyses and comparisons of these methods are carried out, and the characterization methods of graphene are introduced. The mechanism, research value, and future outlook of graphene repair are also discussed at length. Graphene defect repair mainly relies on the spontaneous movement of C atoms or heteroatoms to the pore defects under the condition of applied energy. The repair degree and mechanism of graphene repair are also different according to different preparations. The current research on graphene defect repair is still in its infancy, and it is believed that the problem of defect evolution will be explained in more depth in the future.展开更多
BACKGROUND Spinal cord injury(SCI)is a destructive disease that incurs huge personal and social costs,and there is no effective treatment.Although the pathogenesis and treatment mechanism of SCI has always been a stro...BACKGROUND Spinal cord injury(SCI)is a destructive disease that incurs huge personal and social costs,and there is no effective treatment.Although the pathogenesis and treatment mechanism of SCI has always been a strong scientific focus,the pathogenesis of SCI is still under investigation.AIM To determine the key genes based on the modularization of in-depth analysis,in order to identify the repair mechanism of astrocytes and non-astrocytes in SCI.METHODS Firstly,the differences between injured and non-injured spinal cord of astrocyte(HA),injured and non-injured spinal cord of non-astrocyte(FLOW),injured spinal cord of non-injured astrocyte(HA)and non-injured spinal cord of nonastrocyte(FLOW),and non-injured spinal cord of astrocyte(HA)and nonastrocyte(FLOW)were analyzed.The total number of differentially expressed genes was obtained by merging the four groups of differential results.Secondly,the genes were co-expressed and clustered.Then,the enrichment of GO function and KEGG pathway of module genes was analyzed.Finally,non-coding RNA,transcription factors and drugs that regulate module genes were predicted using hypergeometric tests.RESULTS In summary,we obtained 19 expression modules involving 5216 differentially expressed genes.Among them,miR-494,XIST and other genes were differentially expressed in SCI patients,and played an active regulatory role in dysfunction module,and these genes were recognized as the driving genes of SCI.Enrichment results showed that module genes were significantly involved in the biological processes of inflammation,oxidation and apoptosis.Signal pathways such as NF-kappa B/A20,AMPK and MAPK were significantly regulated.In addition,non-coding RNA pivot(including miR-136-5p and let-7d-5p,etc.)and transcription factor pivot(including NFKB1,MYC,etc.)were identified as significant regulatory dysfunction modules.CONCLUSION Overall,this study uncovered a co-expression network of key genes involved in astrocyte and non-astrocyte regulation in SCI.These findings helped to reveal the core dysfunction modules,potential regulatory factors and driving genes of the disease,and to improve our understanding of its pathogenesis.展开更多
To study the mechanism of repair of pancreas following acute pancreatitis (AP).Methods NIH Swiss mice were randomized into the saline control group and AP group.AP was induced by intraperitoneal injection of 50 ug/kg ...To study the mechanism of repair of pancreas following acute pancreatitis (AP).Methods NIH Swiss mice were randomized into the saline control group and AP group.AP was induced by intraperitoneal injection of 50 ug/kg body weight cearulein for 4 times,once per hour.The cellular proliferation was detected using flow cytometry.Collagen Ⅰ was detected with immunohistochemistry.Protein zymography was used to evaluate the expression of matrix metalloproteinase-3 (MMP-3).Results In the AP group,the pancreatic lesions were the severest in 8 h and then recovered on the 7th d after induction of AP.Flow cytometry showed that there were three stages of cell proliferation after AP:the active proliferation in early stage,inhibition of proliferation in middle stage and high proliferation in the late stage.The expression level of collage Ⅰ and MMP-3 was markedly higher in the AP group than in the saline control group.Conclusion The pancreas can be repaired after AP.The regeneration mechanism includes intersitial fibrosis and acinar cell replication.7 refs,4 figs.展开更多
The urban transit routing problem (UTRP) involves the construction of route sets on existing road networks to cater for the transit demand efficiently. This is an NP-hard problem, where the generation of candidate rou...The urban transit routing problem (UTRP) involves the construction of route sets on existing road networks to cater for the transit demand efficiently. This is an NP-hard problem, where the generation of candidate route sets can lead to a number of potential routes being discarded on the grounds of infeasibility. This paper presents a new repair mechanism to complement the existing terminal repair and the make-small-change operators in dealing with the infeasibility of the candidate route set. When solving the UTRP, the general aim is to determine a set of transit route networks that achieves a minimum total cost for both the passenger and the operator. With this in mind, we propose a differential evolution (DE) algorithm for solving the UTRP with a specific objective of minimizing the average travel time of all served passengers. Computational experiments are performed on the basis of benchmark Mandl’s Swiss network. Computational results from the proposed repair mechanism are comparable with the existing repair mechanisms. Furthermore, the combined repair mechanisms of all three operators produced very promising results. In addition, the proposed DE algorithm outperformed most of the published results in the literature.展开更多
This paper presents practical research on repair mechanismand its four repair trajectories in FL classroom interaction. Thisshows that it is effective and efficient in assisting FL learners todevelop their communicati...This paper presents practical research on repair mechanismand its four repair trajectories in FL classroom interaction. Thisshows that it is effective and efficient in assisting FL learners todevelop their communicative competence and understand theprocess of language acquisition. Repair strategies that are ofgreat value to FL teachers in FL classroom teaching are also ex-pounded.展开更多
Ever since gene targeting or specific modification of genome sequences in mice was achieved in the early 1980s,the reverse genetic approach of precise editing of any genomic locus has greatly accelerated biomedical re...Ever since gene targeting or specific modification of genome sequences in mice was achieved in the early 1980s,the reverse genetic approach of precise editing of any genomic locus has greatly accelerated biomedical research and biotechnology development.In particular,the recent development of the CRISPR/Cas9 system has greatly expedited genetic dissection of 3D genomes.CRISPR gene-editing outcomes result from targeted genome cleavage by ectopic bacterial Cas9 nuclease followed by presumed random ligations via the host double-strand break repair machineries.Recent studies revealed,however,that the CRISPR genomeediting system is precise and predictable because of cohesive Cas9 cleavage of targeting DNA.Here,we synthesize the current understanding of CRISPR DNA fragment-editing mechanisms and recent progress in predictable outcomes from precise genetic engineering of 3D genomes.Specifically,we first briefly describe historical genetic studies leading to CRISPR and 3D genome engineering.We then summarize different types of chromosomal rearrangements by DNA fragment editing.Finally,we review significant progress from precise ID gene editing toward predictable 3D genome engineering and synthetic biology.The exciting and rapid advances in this emerging field provide new opportunities and challenges to understand or digest 3D genomes.展开更多
The optical properties of polymethyl methacrylate(PMMA)with varying degrees of artificial scratches have been studied with the aim of reproducing the change of visibility of an aircraft’s PMMA optical windows after b...The optical properties of polymethyl methacrylate(PMMA)with varying degrees of artificial scratches have been studied with the aim of reproducing the change of visibility of an aircraft’s PMMA optical windows after being damaged in their service environment.A novel maintenance method that can perfectly restore the optical property of PMMA has been identified and employed in the repair of the scratches that are formed on the surface of PMMA.This convenient and low-cost method entails polishing PMMA with different types of sandpaper to remove the scratches,and then spin-coating the repair solution in order to restore the optical properties of PMMA.The effect of this repair mechanism and parameters of the repair process were studied.The results indicated that the optical performance of PMMA is closely related to the mesh size of sandpaper,and improper parameter selection destroys the general effect of the repair.When the number of sandpaper mesh is low,the size of the abrasive particle is relatively larger,which can cause deeper friction marks on the surface of PMMA optical windows.Surface treatment using 5000 mesh sandpaper lowers surface roughness(R——a=0.566 nm),and optical transmittance in visible range can be restored to more than 88%.展开更多
基金This work was financially supported by the National Natural Science Foundation of China(Nos.51871073,51871072,51771063,61604086,and U1637201)China Postdoctoral Science Foundation(Nos.2016M590280 and 2017T100240)+1 种基金Heilongjiang Postdoctoral Foundation(No.LBH-Z16075)the Fundamental Research Funds for the Central Universities(Nos.HIT.NSRIF.20161 and HIT.MKSTISP.201615).
文摘Graphene has excellent theoretical properties and a wide range of applications in metal-based composites. However, because of defects on the graphene surface, the actual performance of the material is far below theoretical expectations. In addition, graphene containing defects could easily react with a matrix alloy, such as Al, to generate brittle and hydrolyzed phases that could further reduce the performance of the resulting composite. Therefore, defect repair is an important area of graphene research. The repair methods reported in the present paper include chemical vapor deposition, doping, liquid-phase repair, external energy graphitization, and alloying. Detailed analyses and comparisons of these methods are carried out, and the characterization methods of graphene are introduced. The mechanism, research value, and future outlook of graphene repair are also discussed at length. Graphene defect repair mainly relies on the spontaneous movement of C atoms or heteroatoms to the pore defects under the condition of applied energy. The repair degree and mechanism of graphene repair are also different according to different preparations. The current research on graphene defect repair is still in its infancy, and it is believed that the problem of defect evolution will be explained in more depth in the future.
文摘BACKGROUND Spinal cord injury(SCI)is a destructive disease that incurs huge personal and social costs,and there is no effective treatment.Although the pathogenesis and treatment mechanism of SCI has always been a strong scientific focus,the pathogenesis of SCI is still under investigation.AIM To determine the key genes based on the modularization of in-depth analysis,in order to identify the repair mechanism of astrocytes and non-astrocytes in SCI.METHODS Firstly,the differences between injured and non-injured spinal cord of astrocyte(HA),injured and non-injured spinal cord of non-astrocyte(FLOW),injured spinal cord of non-injured astrocyte(HA)and non-injured spinal cord of nonastrocyte(FLOW),and non-injured spinal cord of astrocyte(HA)and nonastrocyte(FLOW)were analyzed.The total number of differentially expressed genes was obtained by merging the four groups of differential results.Secondly,the genes were co-expressed and clustered.Then,the enrichment of GO function and KEGG pathway of module genes was analyzed.Finally,non-coding RNA,transcription factors and drugs that regulate module genes were predicted using hypergeometric tests.RESULTS In summary,we obtained 19 expression modules involving 5216 differentially expressed genes.Among them,miR-494,XIST and other genes were differentially expressed in SCI patients,and played an active regulatory role in dysfunction module,and these genes were recognized as the driving genes of SCI.Enrichment results showed that module genes were significantly involved in the biological processes of inflammation,oxidation and apoptosis.Signal pathways such as NF-kappa B/A20,AMPK and MAPK were significantly regulated.In addition,non-coding RNA pivot(including miR-136-5p and let-7d-5p,etc.)and transcription factor pivot(including NFKB1,MYC,etc.)were identified as significant regulatory dysfunction modules.CONCLUSION Overall,this study uncovered a co-expression network of key genes involved in astrocyte and non-astrocyte regulation in SCI.These findings helped to reveal the core dysfunction modules,potential regulatory factors and driving genes of the disease,and to improve our understanding of its pathogenesis.
文摘To study the mechanism of repair of pancreas following acute pancreatitis (AP).Methods NIH Swiss mice were randomized into the saline control group and AP group.AP was induced by intraperitoneal injection of 50 ug/kg body weight cearulein for 4 times,once per hour.The cellular proliferation was detected using flow cytometry.Collagen Ⅰ was detected with immunohistochemistry.Protein zymography was used to evaluate the expression of matrix metalloproteinase-3 (MMP-3).Results In the AP group,the pancreatic lesions were the severest in 8 h and then recovered on the 7th d after induction of AP.Flow cytometry showed that there were three stages of cell proliferation after AP:the active proliferation in early stage,inhibition of proliferation in middle stage and high proliferation in the late stage.The expression level of collage Ⅰ and MMP-3 was markedly higher in the AP group than in the saline control group.Conclusion The pancreas can be repaired after AP.The regeneration mechanism includes intersitial fibrosis and acinar cell replication.7 refs,4 figs.
文摘The urban transit routing problem (UTRP) involves the construction of route sets on existing road networks to cater for the transit demand efficiently. This is an NP-hard problem, where the generation of candidate route sets can lead to a number of potential routes being discarded on the grounds of infeasibility. This paper presents a new repair mechanism to complement the existing terminal repair and the make-small-change operators in dealing with the infeasibility of the candidate route set. When solving the UTRP, the general aim is to determine a set of transit route networks that achieves a minimum total cost for both the passenger and the operator. With this in mind, we propose a differential evolution (DE) algorithm for solving the UTRP with a specific objective of minimizing the average travel time of all served passengers. Computational experiments are performed on the basis of benchmark Mandl’s Swiss network. Computational results from the proposed repair mechanism are comparable with the existing repair mechanisms. Furthermore, the combined repair mechanisms of all three operators produced very promising results. In addition, the proposed DE algorithm outperformed most of the published results in the literature.
文摘This paper presents practical research on repair mechanismand its four repair trajectories in FL classroom interaction. Thisshows that it is effective and efficient in assisting FL learners todevelop their communicative competence and understand theprocess of language acquisition. Repair strategies that are ofgreat value to FL teachers in FL classroom teaching are also ex-pounded.
基金This work was supported by grants from the National Natural Science Foundation of China(31630039 and 32000425)the Ministry of Science and Technology of China(2017YFA0504203 and 2018YFC1004504)the Science and Technology Commission of Shanghai Municipality(19JC1412500).
文摘Ever since gene targeting or specific modification of genome sequences in mice was achieved in the early 1980s,the reverse genetic approach of precise editing of any genomic locus has greatly accelerated biomedical research and biotechnology development.In particular,the recent development of the CRISPR/Cas9 system has greatly expedited genetic dissection of 3D genomes.CRISPR gene-editing outcomes result from targeted genome cleavage by ectopic bacterial Cas9 nuclease followed by presumed random ligations via the host double-strand break repair machineries.Recent studies revealed,however,that the CRISPR genomeediting system is precise and predictable because of cohesive Cas9 cleavage of targeting DNA.Here,we synthesize the current understanding of CRISPR DNA fragment-editing mechanisms and recent progress in predictable outcomes from precise genetic engineering of 3D genomes.Specifically,we first briefly describe historical genetic studies leading to CRISPR and 3D genome engineering.We then summarize different types of chromosomal rearrangements by DNA fragment editing.Finally,we review significant progress from precise ID gene editing toward predictable 3D genome engineering and synthetic biology.The exciting and rapid advances in this emerging field provide new opportunities and challenges to understand or digest 3D genomes.
基金supported by the National Science Fund for Distinguished Young Scholars(Grant No.51625201)the National Key Research and Development Program of China(Grant No.2016YFE0201600)+2 种基金the National Natural Science Foundation of China(Grant No.51702066)the Open Fund of Key Laboratory of Micro-systems and Micro-structures Manufacturing,Ministry of Education(Grant No.2016KM001)the Major State Basic Search Program(Grant No.2014CB46505)。
文摘The optical properties of polymethyl methacrylate(PMMA)with varying degrees of artificial scratches have been studied with the aim of reproducing the change of visibility of an aircraft’s PMMA optical windows after being damaged in their service environment.A novel maintenance method that can perfectly restore the optical property of PMMA has been identified and employed in the repair of the scratches that are formed on the surface of PMMA.This convenient and low-cost method entails polishing PMMA with different types of sandpaper to remove the scratches,and then spin-coating the repair solution in order to restore the optical properties of PMMA.The effect of this repair mechanism and parameters of the repair process were studied.The results indicated that the optical performance of PMMA is closely related to the mesh size of sandpaper,and improper parameter selection destroys the general effect of the repair.When the number of sandpaper mesh is low,the size of the abrasive particle is relatively larger,which can cause deeper friction marks on the surface of PMMA optical windows.Surface treatment using 5000 mesh sandpaper lowers surface roughness(R——a=0.566 nm),and optical transmittance in visible range can be restored to more than 88%.