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Pu Su Zhao,Yu Feng Li,Huan Mei Guo,Fang Fang Jian*,Xian Wang 대한화학회 2007 Bulletin of the Korean Chemical Society Vol.28 No.9
1-Phenyl-3-p-fluorophenyl-5-p-chlorophenyl-2-pyrazoline has been synthesized and characterized by elemental analysis, IR, UV-Vis and X-ray single crystal diffraction. Density functional calculations show that B3LYP/6-311G** method can reproduce the structural parameters. The electronic absorption spectra have been predicted based on the optimized structure by using 6-311G** and 6-311++G** basis sets and compared with the experimental values. The results indicate that TD-DFT method can only predict the electronic absorption spectra of the system studied here approximately. On the basis of vibrational analyses, the thermodynamic properties of the title compound at different temperatures have been calculated, revealing the correlations between , , and temperature.
Preparation and characterization of Mn doped copper nitride films with high photocurrent response
Aiai Yu,Ruiyuan Hu,Wei Liu,Rui Zhang,Jian Zhang,Yong Pu,Liang Chu,Jianping Yang,Xingao Li 한국물리학회 2018 Current Applied Physics Vol.18 No.11
The Mn-doped copper nitride (Cu3N) films with Mn concentration of 2.0 at. % have high crystallinity and uniform surface morphology. We found that the as-synthesized Mn-doped Cu3N films show suitable optical absorption in the visible region and the band gap is ∼1.48 eV. A simple photodetector based on Mn doped Cu3N films was firstly fabricated via magnetron sputtering method. The fabricated device with doping of Mn demonstrated high photocurrent response and fast response shorter than 0.1 s both for rise and decay time superior to the pure Cu3N. Furthermore, the energy levels of Mn-doped Cu3N matched well with ITO and Ag electrode. The excellent photoelectric properties reflect a good balance between sensitivities and response rate. Our investigation reveals the excellent potential of Mn-doped Cu3N films for application of photodetectors.
Zhao, Pu Su,Li, Yu Feng,Guo, Huan Mei,Jian, Fang Fang,Wang, Xian Korean Chemical Society 2007 Bulletin of the Korean Chemical Society Vol.28 No.9
1-Phenyl-3-p-fluorophenyl-5-p-chlorophenyl-2-pyrazoline has been synthesized and characterized by elemental analysis, IR, UV-Vis and X-ray single crystal diffraction. Density functional calculations show that B3LYP/6-311G** method can reproduce the structural parameters. The electronic absorption spectra have been predicted based on the optimized structure by using 6-311G** and 6-311++G** basis sets and compared with the experimental values. The results indicate that TD-DFT method can only predict the electronic absorption spectra of the system studied here approximately. On the basis of vibrational analyses, the thermodynamic properties of the title compound at different temperatures have been calculated, revealing the correlations between ,C0p,m,S0m,H0m and temperature.
Yong-Xiao Cao,Jian-Pu Zheng,Jian-Yu He,Jie Li,Cang-Bao Xu,Lars Edvinsson 대한약학회 2005 Archives of Pharmacal Research Vol.28 No.6
The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1 µM, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the α1-adrenoreceptor. The β- adrenoreceptor and ATP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and CaCl2 in Ca2+-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular Ca2+ influx through the receptoroperated calcium channels and intracellular Ca2+ release from the Ca2+ store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular Ca2+ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated Ca2+-influx and Ca2+- release, and partly from the endothelium mediated by EDHF.
Cao Yong-Xiao,Zheng Jian-Pu,He Jian-Yu,Li Jie,Xu Cang-Bao,Edvinsson Lars The Pharmaceutical Society of Korea 2005 Archives of Pharmacal Research Vol.28 No.6
The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1$\mu$M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the ${\alpha}_1$-adrenoreceptor. The $\beta$-adrenoreceptor and ATP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and $CaCl_2$ in $Ca^{2+}$-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular $Ca^{2+}$ influx through the receptor-operated calcium channels and intracellular $Ca^{2+}$ release from the $Ca^{2+}$ store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular $Ca^{2+}$ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated $Ca^{2+}$-influx and $Ca^{2+}$-release, and partly from the endothelium mediated by EDHF.
Variants on ESR1 and their Association with Prostate Cancer Risk: A Meta-analysis
Ding, Xiang,Cui, Feng-Mei,Xu, Song-Tao,Pu, Jin-Xian,Huang, Yu-Hua,Zhang, Jiang-Lei,Wei, Xue-Dong,Hou, Jian-Quan,Yan, Chun-Yin Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8
Background: Epidemiological studies evaluating the association of two variants rs9340799 and rs2234693 on estrogen receptor 1 (ESR1) with prostate risk have generated inconsistent results. Methods: A meta-analysis was here conducted to systematically evaluate the relationship of these two variants with prostate cancer susceptibility. Results: For rs9340799, heterozygosity of T/C carriers showed a significant increased prostate cancer risk with a pooled odds ratio (OR) of 1.34 (95% CI = 1.06-1.69) while homozygote C/C carriers showed an increased but not statistically significant association with prostate cancer risk (pooled OR = 1.29, 95% CI = 0.94-1.79). Compared to the homozygous TT carriers, the allele C carriers showed a 31% increased risk for prostate cancer (pooled OR = 1.31, 95% CI = 1.06-1.63). No significant association between the rs2234693 and prostate cancer risk was found with the pooled OR of 1.15 (95% CI = 0.97-1.39, T/C and C/C vs. T/T) under the dominant genetic model. Compared to the homozygote T/T carriers, the heterozygous T/C carriers did not show any significantly different risk of prostate cancer (pooled OR = 1.13, 95% CI = 0.94-1.36) and the homozygous C/C carriers also did not show a significant change for prostate cancer risk compared to the wide-type T/T carriers (pooled OR = 1.26, 95% CI = 0.98-1.62). Conclusion: These data suggested that variant rs9340799, but not rs2234693, on ESR1 confers an elevated risk of prostate cancer.