The thermal deformation behavior of FV520B stainless steel is investigated.Isothermal compression tests were conducted at temperatures ranging from 600 to 900℃ and strain rates from 0.001 to 10 s^(−1).The true stress...The thermal deformation behavior of FV520B stainless steel is investigated.Isothermal compression tests were conducted at temperatures ranging from 600 to 900℃ and strain rates from 0.001 to 10 s^(−1).The true stress–strain curves were corrected for friction and temperature due to the drum shape and adiabatic heating.The comparison shows that there is a large difference between the stress before and after the correction,which proves that the correction is necessary.Five constitutive models were developed:the original Arrhenius model,the strain correction Arrhenius model,a new modified Arrhenius model,the back propagation neural network model(BPNN)and the dandelion optimization BPNN model(DO-BPNN).The DO-BPNN model showed the highest prediction accuracy though it was more computationally intensive than the other models.The new modified Arrhenius model performed a better predictive capacity than the strain correction version,while it showed a negligible increase in the number of parameters and computational time.Although artificial neural network-based models exhibit superior accuracy compared to the Arrhenius models,their application in finite element simulations still faces notable challenges.展开更多
Objective This study aimed to examine the role of long non-coding RNA PCED1B antisense RNA 1(PCED1B-AS1)in the development of hepatocellular carcinoma(HCC).Methods A total of 62 pairs of HCC tissues and adjacent non-t...Objective This study aimed to examine the role of long non-coding RNA PCED1B antisense RNA 1(PCED1B-AS1)in the development of hepatocellular carcinoma(HCC).Methods A total of 62 pairs of HCC tissues and adjacent non-tumor tissues were obtained from 62 HCC patients.The interactions of PCED1B-AS1 and microRNA-34a(miR-34a)were detected by dual luciferase activity assay and RNA pull-down assay.The RNA expression levels of PCED1B-AS1,miR-34a and CD44 were detected by RT-qPCR,and the protein expression level of CD44 was determined by Western blotting.The cell proliferation was detected by cell proliferation assay,and the cell invasion and migration by transwell invasion assay.The HCC tumor growth after PCED1B-AS1 was downregulated was determined by in vivo animal study.Results PCED1B-AS1 was highly expressed in HCC tissues,which was associated with poor survival of HCC patients.Furthermore,PCED1B-AS1 interacted with miR-34a in HCC cells,but they did not regulate the expression of each other.Additionally,PCED1B-AS1 increased the expression level of CD44,which was targeted by miR-34a.The cell proliferation and invasion assay revealed that miR-34a inhibited the proliferation and invasion of HCC in vitro,while CD44 exhibited the opposite effects.Furthermore,PCED1B-AS1 suppressed the role of miR-34a.Moreover,the knockdown of PCED1B-AS1 repressed the HCC tumor growth in nude mice in vivo.Conclusion PCED1B-AS1 may play an oncogenic role by regulating the miR-34a/CD44 axis in HCC.展开更多
Background:Aortic dissection(AD)is a fatal cardiovascular disease for which the key involved genes are largely unknown.Here,we aimed to identify promising AD biomarkers from high-throughput RNA expressing data.Methods...Background:Aortic dissection(AD)is a fatal cardiovascular disease for which the key involved genes are largely unknown.Here,we aimed to identify promising AD biomarkers from high-throughput RNA expressing data.Methods:In the GSE98770 dataset,differentially expressed mRNAs(DE-mRNAs)and microRNAs(DE-microRNAs)were identified through differentially expressed gene analysis and gene set enrichment analysis.The regulatory network between DE-mRNAs and DE-microRNAs was established,and hub genes were identified with Cytoscape.Relationships between hub genes and AD were confirmed in the Comparative Toxicogenomics Database(CTD).Potential key transcription factors were discovered with Cytoscape.Hub gene verification was performed by qPCR and immunofluorescence analyses of human specimens.Results:DE-mRNAs and DE-microRNAs were identified.Four mRNAs and microRNA-1321(miR-1321)were found to have the most connections with other genes.CBL was connected to the most genes and interacted with miR-1321,which was also connected to the most genes among the DE-microRNAs.In addition,CBL was associated with AD in the CTD.Among the top five transcription factors potentially regulating CBL transcription,only HOXB13 was a DE-mRNA.The findings were further successfully verified in human specimens.Conclusion:CBL,which may be transcriptionally regulated by HOXB13 and post-transcriptionally regulated by miR-1321,was identified as the most promising potential biomarker for AD.展开更多
Acute mitochondrial damage and the energy crisis following axonal injury highlight mitochondrial transport as an important target for axonal regeneration.Syntaphilin(Snph),known for its potent mitochondrial anchoring ...Acute mitochondrial damage and the energy crisis following axonal injury highlight mitochondrial transport as an important target for axonal regeneration.Syntaphilin(Snph),known for its potent mitochondrial anchoring action,has emerged as a significant inhibitor of both mitochondrial transport and axonal regeneration.Therefore,investigating the molecular mechanisms that influence the expression levels of the snph gene can provide a viable strategy to regulate mitochondrial trafficking and enhance axonal regeneration.Here,we reveal the inhibitory effect of microRNA-146b(miR-146b)on the expression of the homologous zebrafish gene syntaphilin b(snphb).Through CRISPR/Cas9 and single-cell electroporation,we elucidated the positive regulatory effect of the miR-146b-snphb axis on Mauthner cell(M-cell)axon regeneration at the global and single-cell levels.Through escape response tests,we show that miR-146b-snphb signaling positively regulates functional recovery after M-cell axon injury.In addition,continuous dynamic imaging in vivo showed that reprogramming miR-146b significantly promotes axonal mitochondrial trafficking in the pre-injury and early stages of regeneration.Our study reveals an intrinsic axonal regeneration regulatory axis that promotes axonal regeneration by reprogramming mitochondrial transport and anchoring.This regulation involves noncoding RNA,and mitochondria-associated genes may provide a potential opportunity for the repair of central nervous system injury.展开更多
基金supported by the National Natural Science Foundation of China(Grant No.52275373)the National Natural Science Foundation of China(Grant No.52105397)the Open Foundation of National Key Laboratory of Metal Forming Technology and Heavy Equipment(Grant No.S2308100.W08).
文摘The thermal deformation behavior of FV520B stainless steel is investigated.Isothermal compression tests were conducted at temperatures ranging from 600 to 900℃ and strain rates from 0.001 to 10 s^(−1).The true stress–strain curves were corrected for friction and temperature due to the drum shape and adiabatic heating.The comparison shows that there is a large difference between the stress before and after the correction,which proves that the correction is necessary.Five constitutive models were developed:the original Arrhenius model,the strain correction Arrhenius model,a new modified Arrhenius model,the back propagation neural network model(BPNN)and the dandelion optimization BPNN model(DO-BPNN).The DO-BPNN model showed the highest prediction accuracy though it was more computationally intensive than the other models.The new modified Arrhenius model performed a better predictive capacity than the strain correction version,while it showed a negligible increase in the number of parameters and computational time.Although artificial neural network-based models exhibit superior accuracy compared to the Arrhenius models,their application in finite element simulations still faces notable challenges.
基金supported by the Medical Science and Technology Research Foundation of Guangdong Province(No.A2020559).
文摘Objective This study aimed to examine the role of long non-coding RNA PCED1B antisense RNA 1(PCED1B-AS1)in the development of hepatocellular carcinoma(HCC).Methods A total of 62 pairs of HCC tissues and adjacent non-tumor tissues were obtained from 62 HCC patients.The interactions of PCED1B-AS1 and microRNA-34a(miR-34a)were detected by dual luciferase activity assay and RNA pull-down assay.The RNA expression levels of PCED1B-AS1,miR-34a and CD44 were detected by RT-qPCR,and the protein expression level of CD44 was determined by Western blotting.The cell proliferation was detected by cell proliferation assay,and the cell invasion and migration by transwell invasion assay.The HCC tumor growth after PCED1B-AS1 was downregulated was determined by in vivo animal study.Results PCED1B-AS1 was highly expressed in HCC tissues,which was associated with poor survival of HCC patients.Furthermore,PCED1B-AS1 interacted with miR-34a in HCC cells,but they did not regulate the expression of each other.Additionally,PCED1B-AS1 increased the expression level of CD44,which was targeted by miR-34a.The cell proliferation and invasion assay revealed that miR-34a inhibited the proliferation and invasion of HCC in vitro,while CD44 exhibited the opposite effects.Furthermore,PCED1B-AS1 suppressed the role of miR-34a.Moreover,the knockdown of PCED1B-AS1 repressed the HCC tumor growth in nude mice in vivo.Conclusion PCED1B-AS1 may play an oncogenic role by regulating the miR-34a/CD44 axis in HCC.
基金supported by grants from the Guangzhou Basic and Applied Basic Research Foundation(202201010940)National Natural Science Foundation of China(82200306)Guangdong Basic and Applied Basic Research Foundation(2021A1515111092).
文摘Background:Aortic dissection(AD)is a fatal cardiovascular disease for which the key involved genes are largely unknown.Here,we aimed to identify promising AD biomarkers from high-throughput RNA expressing data.Methods:In the GSE98770 dataset,differentially expressed mRNAs(DE-mRNAs)and microRNAs(DE-microRNAs)were identified through differentially expressed gene analysis and gene set enrichment analysis.The regulatory network between DE-mRNAs and DE-microRNAs was established,and hub genes were identified with Cytoscape.Relationships between hub genes and AD were confirmed in the Comparative Toxicogenomics Database(CTD).Potential key transcription factors were discovered with Cytoscape.Hub gene verification was performed by qPCR and immunofluorescence analyses of human specimens.Results:DE-mRNAs and DE-microRNAs were identified.Four mRNAs and microRNA-1321(miR-1321)were found to have the most connections with other genes.CBL was connected to the most genes and interacted with miR-1321,which was also connected to the most genes among the DE-microRNAs.In addition,CBL was associated with AD in the CTD.Among the top five transcription factors potentially regulating CBL transcription,only HOXB13 was a DE-mRNA.The findings were further successfully verified in human specimens.Conclusion:CBL,which may be transcriptionally regulated by HOXB13 and post-transcriptionally regulated by miR-1321,was identified as the most promising potential biomarker for AD.
基金supported by the core facility Center for Life Sciences,University of Science and Technology of China,Research Funds of the Center for Advanced Interdisciplinary Science and Biomedicine of IHM(QYZD20220002)the National Natural Science Foundation of China(82071357)the Ministry of Science and Technology of China(2019YFA0405600).
文摘Acute mitochondrial damage and the energy crisis following axonal injury highlight mitochondrial transport as an important target for axonal regeneration.Syntaphilin(Snph),known for its potent mitochondrial anchoring action,has emerged as a significant inhibitor of both mitochondrial transport and axonal regeneration.Therefore,investigating the molecular mechanisms that influence the expression levels of the snph gene can provide a viable strategy to regulate mitochondrial trafficking and enhance axonal regeneration.Here,we reveal the inhibitory effect of microRNA-146b(miR-146b)on the expression of the homologous zebrafish gene syntaphilin b(snphb).Through CRISPR/Cas9 and single-cell electroporation,we elucidated the positive regulatory effect of the miR-146b-snphb axis on Mauthner cell(M-cell)axon regeneration at the global and single-cell levels.Through escape response tests,we show that miR-146b-snphb signaling positively regulates functional recovery after M-cell axon injury.In addition,continuous dynamic imaging in vivo showed that reprogramming miR-146b significantly promotes axonal mitochondrial trafficking in the pre-injury and early stages of regeneration.Our study reveals an intrinsic axonal regeneration regulatory axis that promotes axonal regeneration by reprogramming mitochondrial transport and anchoring.This regulation involves noncoding RNA,and mitochondria-associated genes may provide a potential opportunity for the repair of central nervous system injury.
