The thermodynamic properties of Ta metal under high pressure are studied by molecular dynamics simulation. For dislocation-free Ta crystal, all the thermodynamic properties considered are in good agreement with the re...The thermodynamic properties of Ta metal under high pressure are studied by molecular dynamics simulation. For dislocation-free Ta crystal, all the thermodynamic properties considered are in good agreement with the results from exper- iments or higher level calculations. If dislocations are included in the Ta crystal, it is found that as the dislocation density increases, the hydrostatic pressure at the phase transition point of bcc-＋hcp and hcp--＋fcc decreases, while the Hugoniot temperature increases. Meanwhile, the impact pressure at the elastic-plastic transition point is found to depend on the crys- tallographic orientation of the pressure. As the dislocation density increases, the pressure of the elastic-plastic transition point decreases rapidly at the initial stage, then gradually decreases with the increase of the dislocation density.展开更多
The canonical transient receptor potential channel(TRPC)proteins form Ca^(2+)-permeable cation channels that are involved in various heart diseases.However,the roles of specific TRPC proteins in myocardial ischemia/re...The canonical transient receptor potential channel(TRPC)proteins form Ca^(2+)-permeable cation channels that are involved in various heart diseases.However,the roles of specific TRPC proteins in myocardial ischemia/reperfusion(I/R)injury remain poorly understood.We observed that TRPC1 and TRPC6 were highly expressed in the area at risk(AAR)in a coronary artery ligation induced I/R model.Trpc1/mice exhibited improved cardiac function,lower serum Troponin T and serum creatine kinase level,smaller infarct volume,less fibrotic scars,and fewer apoptotic cells after myocardial-I/R than wild-type or Trpc6/mice.Cardiomyocyte-specific knockdown of Trpc1 using adeno-associated virus 9 mitigated myocardial I/R injury.Furthermore,Trpc1 deficiency protected adult mouse ventricular myocytes(AMVMs)and HL-1 cells from death during hypoxia/reoxygenation(H/R)injury.RNA-sequencing-based transcriptome analysis revealed differential expression of genes related to reactive oxygen species(ROS)generation in Trpc1/cardiomyocytes.Among these genes,oxoglutarate dehydrogenase-like(Ogdhl)was markedly downregulated.Moreover,Trpc1 deficiency impaired the calcineurin(CaN)/nuclear factorkappa B(NF-kB)signaling pathway in AMVMs.Suppression of this pathway inhibited Ogdhl upregulation and ROS generation in HL-1 cells under H/R conditions.Chromatin immunoprecipitation assays confirmed NF-kB binding to the Ogdhl promoter.The cardioprotective effect of Trpc1 deficiency was canceled out by overexpression of NF-kB and Ogdhl in cardiomyocytes.In conclusion,our findings reveal that TRPC1 is upregulated in the AAR following myocardial I/R,leading to increased Ca^(2+) influx into associated cardiomyocytes.Subsequently,this upregulates Ogdhl expression through the CaN/NF-kB signaling pathway,ultimately exacerbating ROS production and aggravating myocardial I/R injury.展开更多
The female ovaries are critical for follicle growth and development in the process known as"folliculogenesis".This complex process is regulated by various factors,among which the microenvironment around foll...The female ovaries are critical for follicle growth and development in the process known as"folliculogenesis".This complex process is regulated by various factors,among which the microenvironment around follicles appears to be crucial.According to previous studies,folliculogenesis is an energy-demanding process.In fact,well-balanced follicular energy metabolism is associated with ovarian function and female fertility.Consequently,glucose metabolism has been widely described as the main source of energy during folliculogenesis.Generally,the follicular glucose metabolism profiles change dynamically during follicular development.Metabolic abnormalities during folliculogenesis are associated with aging,primary ovarian insufficiency,and polycystic ovary syndrome,thereby leading to subfertility and infertility in females.The signaling pathways in follicles appear to form a link between glucose metabolism and folliculogenesis.Therefore,a better understanding of glucose metabolism dynamics at different stages of folliculogenesis and the associated signaling pathways will provide potential implications for follicle developmental competence.This review aimed to describe variations in glucose metabolism at different stages of folliculogenesis,provide new insights into glucose metabolic disorder-related diseases,and specifically discuss two major signaling pathways that regulate glucose metabolism during folliculogenesis:phosphatidylinositol 3-kinase,protein kinase B(PI3K-PKB/AKT),and AMP-activated protein kinase(AMPK)signaling pathways.展开更多
基金Project supported by the National Natural Science Foundation of China(Grant No.51231002)the Basic Scientific Research Projects in Central Colleges and Universities(Grant No.2018ZD10)
文摘The thermodynamic properties of Ta metal under high pressure are studied by molecular dynamics simulation. For dislocation-free Ta crystal, all the thermodynamic properties considered are in good agreement with the results from exper- iments or higher level calculations. If dislocations are included in the Ta crystal, it is found that as the dislocation density increases, the hydrostatic pressure at the phase transition point of bcc-＋hcp and hcp--＋fcc decreases, while the Hugoniot temperature increases. Meanwhile, the impact pressure at the elastic-plastic transition point is found to depend on the crys- tallographic orientation of the pressure. As the dislocation density increases, the pressure of the elastic-plastic transition point decreases rapidly at the initial stage, then gradually decreases with the increase of the dislocation density.
基金supported by the National Natural Science Foundation of China(Grant Nos.:81970245,82270357,and 81770432)the Scientific Research Project of Shaanxi Administration of Traditional Chinese Medicine,China(Grant Nos.:2021-04-ZZ-001,2021-QYPT-003,and 2022-SLRH-YQ-004)+1 种基金the Project of Science and Technology Department of Shaanxi Province in China(Project No.:2022YWZX-PG-01)the Natural Science Basic Research Program of Shaanxi Province in China(Grant No.:2023-JC-JQ-61).
文摘The canonical transient receptor potential channel(TRPC)proteins form Ca^(2+)-permeable cation channels that are involved in various heart diseases.However,the roles of specific TRPC proteins in myocardial ischemia/reperfusion(I/R)injury remain poorly understood.We observed that TRPC1 and TRPC6 were highly expressed in the area at risk(AAR)in a coronary artery ligation induced I/R model.Trpc1/mice exhibited improved cardiac function,lower serum Troponin T and serum creatine kinase level,smaller infarct volume,less fibrotic scars,and fewer apoptotic cells after myocardial-I/R than wild-type or Trpc6/mice.Cardiomyocyte-specific knockdown of Trpc1 using adeno-associated virus 9 mitigated myocardial I/R injury.Furthermore,Trpc1 deficiency protected adult mouse ventricular myocytes(AMVMs)and HL-1 cells from death during hypoxia/reoxygenation(H/R)injury.RNA-sequencing-based transcriptome analysis revealed differential expression of genes related to reactive oxygen species(ROS)generation in Trpc1/cardiomyocytes.Among these genes,oxoglutarate dehydrogenase-like(Ogdhl)was markedly downregulated.Moreover,Trpc1 deficiency impaired the calcineurin(CaN)/nuclear factorkappa B(NF-kB)signaling pathway in AMVMs.Suppression of this pathway inhibited Ogdhl upregulation and ROS generation in HL-1 cells under H/R conditions.Chromatin immunoprecipitation assays confirmed NF-kB binding to the Ogdhl promoter.The cardioprotective effect of Trpc1 deficiency was canceled out by overexpression of NF-kB and Ogdhl in cardiomyocytes.In conclusion,our findings reveal that TRPC1 is upregulated in the AAR following myocardial I/R,leading to increased Ca^(2+) influx into associated cardiomyocytes.Subsequently,this upregulates Ogdhl expression through the CaN/NF-kB signaling pathway,ultimately exacerbating ROS production and aggravating myocardial I/R injury.
基金financially supported by grants to Y.H.Y.from the Natural Science Foundation of Guangxi Zhuang Autonomous Region(2019GXNSFFA245013,2018GXNSFDA050017)the National Natural Science Foundation of China(81871172)the Guangxi Medical University Training Program for Distinguished Young Scholars.This review was also supported by Special Fund of the Female Fertility Preservation Innovation Team of the First Affiliated Hospital of Guangxi Medical University.
文摘The female ovaries are critical for follicle growth and development in the process known as"folliculogenesis".This complex process is regulated by various factors,among which the microenvironment around follicles appears to be crucial.According to previous studies,folliculogenesis is an energy-demanding process.In fact,well-balanced follicular energy metabolism is associated with ovarian function and female fertility.Consequently,glucose metabolism has been widely described as the main source of energy during folliculogenesis.Generally,the follicular glucose metabolism profiles change dynamically during follicular development.Metabolic abnormalities during folliculogenesis are associated with aging,primary ovarian insufficiency,and polycystic ovary syndrome,thereby leading to subfertility and infertility in females.The signaling pathways in follicles appear to form a link between glucose metabolism and folliculogenesis.Therefore,a better understanding of glucose metabolism dynamics at different stages of folliculogenesis and the associated signaling pathways will provide potential implications for follicle developmental competence.This review aimed to describe variations in glucose metabolism at different stages of folliculogenesis,provide new insights into glucose metabolic disorder-related diseases,and specifically discuss two major signaling pathways that regulate glucose metabolism during folliculogenesis:phosphatidylinositol 3-kinase,protein kinase B(PI3K-PKB/AKT),and AMP-activated protein kinase(AMPK)signaling pathways.
