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Articles by Yong Xia
Total Records ( 4 ) for Yong Xia
  Liang-Cai Yu , Lan Lai , Sheng-Li Liu and Yong Xia
  Two complexes with enoxacin and ciprofloxacin were synthesized and the crystal structures are reported. Compound 1, [Cu(H-Eno) · Cl2] · 3H2O (H-Eno = Enoxacin), crystallizes in the triclinic system, space group P 1, with lattice parameters a = 8.7731(12) Aring, b = 9.4976(14) Aring, c = 13.2033(19) Aring, agr = 86.319(7)°, β = 71.912(7)°, γ = 80.604(7)°, V = 1031.6(3) Aring3, Z = 2, Dc = 1.625 mgm-3. 2, [Mn(Cip)2] · 2H2O (Cip = mono-anion of ciprofloxacin), crystallizes in the monoclinic, space group P2(1)/c, with lattice parameters a = 5.85690(10), b = 21.9490(6), c = 13.4443(3) Aring, β = 100.9700(10)°, V = 1696.72(7) Aring3, Z = 2, Dc = 1.459 mgm-3.
  Liang-Cai Yu , Lan Lai , Sheng-Li Liu and Yong Xia
  Two zinc complexes of enoxacin were synthesized and their crystal structures were determined. Compound 1, [Zn(H-Eno) · Cl2] · 3H2O (H-Eno = Enoxacin), crystallizes in the triclinic system, space group P 1, with lattice parameters a = 8.7731(12), b = 9.4976(14), and c = 13.2033(19) Aring, agr = 86.319(7)°, β = 71.912(7)°, and γ = 80.604(7)°, V = 1031.6(3) Aring3, Z = 2, DCalcd = 1.631 Mg m-3; compound 2, [Zn(H-Eno) · (H2O)2] · 2NO3, also crystallizes in the triclinic system, space group P 1, with lattice parameters a = 8.751(2), b = 9.014(2), and c = 12.594(3) Aring, agr = 92.277(14)°, β = 109.867(12)°, and γ = 111.469(12)°, V = 854.1(3) Aring3, Z = 1, DCalcd = 1.684 Mg m-3.
  C. Wetzel , Yufeng Li , J. Senawiratne , Mingwei Zhu , Yong Xia , S. Tomasulo , P.D. Persans , Lianghong Liu , D. Hanser and T. Detchprohm
 

An enhancement of radiative recombination in GaInN/GaN heterostructures is being pursued by a reduction of defects associated with threading dislocations and a structural control of piezoelectric polarization in the active light-emitting regions. First, in conventional heteroepitaxy on sapphire substrate along the polar c-axis of GaN, green and deep green emitting light-emitting diode (LED) wafers are being developed. By means of photoluminescence at variable low temperature and excitation density, internal quantum efficiencies of 0.18 for LEDs emitting at 530 nm and 0.08 for those emitting at 555 nm are determined. Those values hold for the high current density of 50 A/cm2 of high-power LED lamps. In bare epi dies, we obtain efficacies of 16 lm/W. At 780 A/cm2 we obtain 22 lm when measured through the substrate only. The 555 nm LED epi material under pulsed photoexcitation shows stimulated emission up to a wavelength of 485 nm. This strong blue shift of the emission wavelength can be avoided in homoepitaxial multiple quantum well (MQW) and LED structures grown along the non-polar a- and m-axes of low-dislocation-density bulk GaN. Here, wavelength-stable emission is obtained at 500 and 488 nm, respectively, independent on excitation power density opening perspectives for visible laser diodes.

  Zhuangli Hu , Juan Chen , Qin Wei and Yong Xia
  Endothelial NO synthase (eNOS) is critically modulated by kinases via the phosphorylation of its Ser1179 (bovine) or Ser1177 (human) residue. Reactive oxygen species such as H2O2 was reported to activate Akt, leading to increased eNOS Ser1179 phosphorylation and activity. But reactive oxygen species are also known to attenuate eNOS function in cardiovascular diseases. Prior studies showing H2O2-stimulated eNOS phosphorylation were performed on serum-starved cells, and only the short term effect of H2O2 was examined. Here we found that the effects of H2O2 on eNOS Ser1179 phosphorylation and function were bidirectional. With endothelial cells cultured with serum, H2O2 initially raised eNOS Ser1179 phosphorylation and activity. However, after the peak increase at 30 min, eNOS Ser1179 phosphorylation dramatically declined. Parallel to the alterations of eNOS Ser1179 phosphorylation, Akt was transiently activated by H2O2 and subsequently became dormant. In contrast, AMP-activated protein kinase (AMPK) was progressively activated in H2O2-treated cells. Blocking Akt activation abolished the initial rise of eNOS Ser1179 phosphorylation after H2O2 treatment. In long term H2O2-treated cells where Akt was deactivated, significant amounts of Ser1179-phosphorylated eNOS remained. AMPK inhibition eradicated the remaining eNOS Ser1179 phosphorylation. Taken together, these studies revealed that Akt and AMPK orchestrated a bidirectional action on eNOS Ser1179 phosphorylation in H2O2-treated cells. Long term H2O2 exposure decreased eNOS Ser1179 phosphorylation, and this might account for the loss of eNOS function in cardiovascular diseases where chronic oxidative injury occurs.
 
 
 
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