Curie temperature of amorphous alloys Co_(90-x)Cr_x Zr_(10) decreases linearly with increas- ing x.Average magnetic moment per magnetic atom Co or Cr is 1.51 μB or -3.62 μB respectively.The temperature dependence of...Curie temperature of amorphous alloys Co_(90-x)Cr_x Zr_(10) decreases linearly with increas- ing x.Average magnetic moment per magnetic atom Co or Cr is 1.51 μB or -3.62 μB respectively.The temperature dependence of spontaneous magnetization at low temper- atures is in agreement with Bloch's T^(3/2) law.The spin wave stiffness constant decreases with increasing x from 4 to 20.The range of interaction is 2—3 atoms for x=4 and nearest neighbour atom for x=20.The crystallization temperature increases mono- tonically with increasing x.It may relate to the average number of outer electrons per atom.The crystalline phase components of heat-treated alloys were analyzed by X-ray diffration and thermomagnetic measurement.展开更多
文摘Curie temperature of amorphous alloys Co_(90-x)Cr_x Zr_(10) decreases linearly with increas- ing x.Average magnetic moment per magnetic atom Co or Cr is 1.51 μB or -3.62 μB respectively.The temperature dependence of spontaneous magnetization at low temper- atures is in agreement with Bloch's T^(3/2) law.The spin wave stiffness constant decreases with increasing x from 4 to 20.The range of interaction is 2—3 atoms for x=4 and nearest neighbour atom for x=20.The crystallization temperature increases mono- tonically with increasing x.It may relate to the average number of outer electrons per atom.The crystalline phase components of heat-treated alloys were analyzed by X-ray diffration and thermomagnetic measurement.
基金Supported by National Natural Science Foundation of China(No. 81773618)Shanghai Jiao Tong University Medical-Industrial Crossover Research Program (No. ZH2018QNA13)。
文摘趋化因子及其受体信号通路是肿瘤细胞转移的主要调控因素之一,趋化因子受体CXCR4和XCR1都被证明参与了乳腺癌的进展。本文基于膜蛋白酵母双杂交发现了XCR1-CXCR4这一尚未报道过的相互作用对,进一步通过生物发光共振能量转移技术(bioluminescence resonance energy transfer,BRET)验证并发现XCR1可以竞争性地结合CXCR4受体(P<0.01),形成异源二聚体。在功能方面,首先通过XCR1和CXCR4瞬时转染HEK293细胞进行划痕实验,加入30 nmol/L SDF-1β后,共转组41.55%的伤口愈合率低于单转CXCR4组的58.75%,说明XCR1的共表达抑制了基质细胞衍生因子-1β(SDF-1β)/CXC趋化因子受体4型(CXCR4)信号通路介导的细胞运动性(P<0.05);其次,利用CXCR4-EGFP转基因HEK293细胞系,共表达XCR1后,流式细胞术检测细胞表面CXCR4受体荧光。结果显示,在30 nmol/L SDF-1β的诱导下,XCR1能够加速异源二聚体中CXCR4的内化(P<0.05),使得内化率从14.38%上升到64.10%;最后,分别检测了控制细胞增殖的Akt和控制细胞迁移的ERK信号通路的变化。结果发现,在SDF-1β刺激10 min后,单转CXCR4组的ERK磷酸化为3.59倍,而共转染XCR1/CXCR4组ERK的磷酸化水平仅为2.08倍,二聚化使得ERK磷酸化水平下降,且激活时间缩短;而Akt的磷酸化水平几乎不受影响。本研究揭示了CXCR4和XCR1二聚化现象,以及该二聚体对CXCR4介导的细胞运动性、受体内化和ERK磷酸化的影响。提示靶向XCR1的药物可以成为CXCR4交叉脱敏的候选药物,对于抑制乳腺癌转移提供了一个可供选择的思路。
