The interfacial enhanced ferromagnetism in maganite/ruthenate system is regarded as a promising path to broaden the potential of oxide-based electronic device applications.Here,we systematically studied the physical p...The interfacial enhanced ferromagnetism in maganite/ruthenate system is regarded as a promising path to broaden the potential of oxide-based electronic device applications.Here,we systematically studied the physical properties of La_(1-x)Ca_(x)MnO_(3)/SrRuO_(3)superlattices and compared them with the La1-x Cax MnO_(3)thin films and bulk compounds.The La_(1-x)Ca_(x)MnO_(3)/SrRuO_(3)superlattices exhibit significant enhancement of Curie temperature(TC)beyond the corresponding thin films and bulks.Based on these results,we constructed an extended phase diagram of La_(1-x)Ca_(x)MnO_(3)under interfacial engineering.We considered the interfacial charge transfer and structural proximity effects as the origin of the interfaceinduced high TC.The structural characterizations revealed a pronounced increase of B-O-B bond angle,which could be the main driving force for the high TCin the superlattices.Our work inspires a deeper understanding of the collective effects of interfacial charge transfer and structural proximity on the physical properties of oxide heterostructures.展开更多
目的观察丙泊酚（propofol，P）对大鼠急性心肌缺血／再灌注（ischemia／reperfusion，I／R）损伤中微管相关蛋白1轻链3（micmtubule-associated protein 1 light3，LC3）的影响，探讨P心肌保护的可能机制。方法采用大鼠在体心肌I／R损...目的观察丙泊酚（propofol，P）对大鼠急性心肌缺血／再灌注（ischemia／reperfusion，I／R）损伤中微管相关蛋白1轻链3（micmtubule-associated protein 1 light3，LC3）的影响，探讨P心肌保护的可能机制。方法采用大鼠在体心肌I／R损伤模型，84只雄性sD大鼠采用随机数字表法分为6组：假手术组（Sham组）、I／R组、脂肪乳组（Int组）、P低剂量组（P1组）、P中剂量组（P2组）、P高剂量组（P3组）。除Sham组外，其余各组均缺血30min，再灌注2h。Int、P1、P2、P3组分别依次经股静脉输注脂肪乳2．4ml·kg^-1·h^-1、P6、12、24mg·kg^-1·h^-1。连续记录功能学指标；2，3，5氯化三苯基四氮唑（2，3，5-trigIhenyhetrazoliumchloride，TYC）染色法检测心肌梗死面积，酶标仪法测定乳酸脱氢酶（1actatedehydrogenase，LDH）的活性，Westemblot分析LC3、磷酸化蛋白激酶B（p-Akt）和蛋白激酶B（Akt）的表达水平。结果与YR组比较，P1、P2、P3组心功能明显改善，心肌梗死面积[（33．8±2．7）％、（27．1±1．9）％和（36．2±312）％VS（50．3±4．2）％，P〈O．05]和血浆LDH水平都显著降低，心肌损伤减轻，LC3II／LC3I比率[（0．97±0．03）、（0．76±0．08）和（0．93±0．04）VS（1．15±0．07），P〈0．05]减低，P-Akt表达[（1．69±0．43）、（2．51±0．15）和（1．95±0．41）vs（1．00±0．13），P〈0．05]增加，而Int组则差异无统计学意义（P〉0．05）；与P1组比较，P2组心功能明显改善，心肌梗死面积[（27．1±1．9）％VS（33．8±2．7）％，P〈0．05]和血浆LDH水平均显著降低，心肌损伤更轻，LC311／LC3I比率[（0．76±0．08）vs（0．97±0．03），P〈0．05]减低，p-Akt表达[（2．51±0．15）vs（1．69±0．43），P〈0．05]增加，而P3组差异没有统计学意义（P〉0．05）。结论P通过抑制LC3的表达，对心肌发挥保护作用，且可能与磷脂酰肌醇-3激酶／蛋白激酶B（phosphatid3rlinositol3kinase／Akt。P13l（／Akt）信号通路有关。展开更多
基金Project supported by the National Key Research and Development Program of China(Grant Nos.2016YFA0401003,2017YFA0403502,and2020YFA0309100)the National Natural Science Foundation of China(Grant Nos.11974326,12074365,11804342,U2032218,and 51872278)+1 种基金the Fundamental Research Funds for the Central Universities,China(Grant Nos.WK2030000035 and WK2340000102)Hefei Science Center of Chinese Academy of Sciences(Grant No.2020HSC-UE014)。
文摘The interfacial enhanced ferromagnetism in maganite/ruthenate system is regarded as a promising path to broaden the potential of oxide-based electronic device applications.Here,we systematically studied the physical properties of La_(1-x)Ca_(x)MnO_(3)/SrRuO_(3)superlattices and compared them with the La1-x Cax MnO_(3)thin films and bulk compounds.The La_(1-x)Ca_(x)MnO_(3)/SrRuO_(3)superlattices exhibit significant enhancement of Curie temperature(TC)beyond the corresponding thin films and bulks.Based on these results,we constructed an extended phase diagram of La_(1-x)Ca_(x)MnO_(3)under interfacial engineering.We considered the interfacial charge transfer and structural proximity effects as the origin of the interfaceinduced high TC.The structural characterizations revealed a pronounced increase of B-O-B bond angle,which could be the main driving force for the high TCin the superlattices.Our work inspires a deeper understanding of the collective effects of interfacial charge transfer and structural proximity on the physical properties of oxide heterostructures.
文摘目的观察丙泊酚（propofol，P）对大鼠急性心肌缺血／再灌注（ischemia／reperfusion，I／R）损伤中微管相关蛋白1轻链3（micmtubule-associated protein 1 light3，LC3）的影响，探讨P心肌保护的可能机制。方法采用大鼠在体心肌I／R损伤模型，84只雄性sD大鼠采用随机数字表法分为6组：假手术组（Sham组）、I／R组、脂肪乳组（Int组）、P低剂量组（P1组）、P中剂量组（P2组）、P高剂量组（P3组）。除Sham组外，其余各组均缺血30min，再灌注2h。Int、P1、P2、P3组分别依次经股静脉输注脂肪乳2．4ml·kg^-1·h^-1、P6、12、24mg·kg^-1·h^-1。连续记录功能学指标；2，3，5氯化三苯基四氮唑（2，3，5-trigIhenyhetrazoliumchloride，TYC）染色法检测心肌梗死面积，酶标仪法测定乳酸脱氢酶（1actatedehydrogenase，LDH）的活性，Westemblot分析LC3、磷酸化蛋白激酶B（p-Akt）和蛋白激酶B（Akt）的表达水平。结果与YR组比较，P1、P2、P3组心功能明显改善，心肌梗死面积[（33．8±2．7）％、（27．1±1．9）％和（36．2±312）％VS（50．3±4．2）％，P〈O．05]和血浆LDH水平都显著降低，心肌损伤减轻，LC3II／LC3I比率[（0．97±0．03）、（0．76±0．08）和（0．93±0．04）VS（1．15±0．07），P〈0．05]减低，P-Akt表达[（1．69±0．43）、（2．51±0．15）和（1．95±0．41）vs（1．00±0．13），P〈0．05]增加，而Int组则差异无统计学意义（P〉0．05）；与P1组比较，P2组心功能明显改善，心肌梗死面积[（27．1±1．9）％VS（33．8±2．7）％，P〈0．05]和血浆LDH水平均显著降低，心肌损伤更轻，LC311／LC3I比率[（0．76±0．08）vs（0．97±0．03），P〈0．05]减低，p-Akt表达[（2．51±0．15）vs（1．69±0．43），P〈0．05]增加，而P3组差异没有统计学意义（P〉0．05）。结论P通过抑制LC3的表达，对心肌发挥保护作用，且可能与磷脂酰肌醇-3激酶／蛋白激酶B（phosphatid3rlinositol3kinase／Akt。P13l（／Akt）信号通路有关。
