Synthesis of magnetic Co1−xNixFe2O4/carbon nanotubes with controlled microstructure for adsorption of pentachlorophenol

Chunyue Cui,Mengyuan Sun,Qingzhu Zheng 한국화학공학회 2016 Korean Journal of Chemical Engineering Vol.33 No.5

Magnetic Co1−xNixFe2O4/Carbon nanotube (CNTs) nanocomposite was successfully prepared by hydrothermal method and used for the adsorption of pentachlorophenol. The properties of Co1−xNxFe2O4/CNTs were characterized by scanning and transmission electron microscopy, energy dispersive X-ray spectroscopy, X-ray diffractometry, Brunauer-Emmett-Teller surface area determination, and magnetic measurement. Results showed that the Co1−xNixFe2O4 nanoparticles with amorphous structure are dispersed uniformly on the CNTs, which enhanced the adsorption capacity. The Co1−xNixFe2O4/CNTs as a magnetic material are easy to separate from the aqueous solution in magnetic field. The adsorption capacity and magnetization were improved by controlling the Ni content and calcination temperature. In addition, the Co1−xNixFe2O4/CNTs loaded with pentachlorophenol (PCP) could be regenerated by microwave radiation and the regeneration efficiency reached 110% after six regeneration cycles.

Highly stable palladium-loaded TiO2 nanotube array electrode for the electrocatalytic hydrodehalogenation of polychlorinated biphenyls

Chunyue Cui,Juan Wu,Yanjun Xin,Yanhe Han 한국화학공학회 2015 Korean Journal of Chemical Engineering Vol.32 No.6

Palladized TiO2 nanotube array electrode was prepared for the electrocatalytic hydrodehalogenation (HDH) of 2,4,5-trichlorobiphenyl (2,4,5-PCB). The TiO2 nanotube array electrode was successfully fabricated by anodic oxidation method, and Pd was loaded onto the TiO2 nanotubes by electrochemical deposition. The morphology and structure of the nanotube array electrodes with and without Pd catalysts were evaluated by scanning electron microscopy (SEM), X-ray diffraction (XRD), and X-ray photoelectron spectroscopy (XPS). The results showed that the diameters and lengths of the TiO2 nanotubes were 30-50 nm and 200-400 nm, respectively. The particle size of the Pd was about 12 nm. Electrocatalytic HDH of 2,4,5-PCB with the Pd/TiO2 nanotube array electrode was performed in H-cell reactor. Under a constant potential of −1.0 V, the HDH efficiency of 2,4,5-PCB was 90% and the biphenyl yield was 83% (15% current efficiency) within 180min at the Pd/TiO2 nanotube array electrode. Compared with the Pd/Ti electrode, the Pd/TiO2 nanotube array electrode exhibited higher HDH efficiency and stability. Additionally, the effect of the primary HDH factors was also investigated.

A GROUNDED THEORY APPROACH TO EXPLORING THE PHENOMENON OF SELLER MANIPULATIONS OF ONLINE PRODUCT REVIEWS

Chunyu Li,Ling Peng,Geng Cui 글로벌지식마케팅경영학회 2016 Global Marketing Conference Vol.2016 No.7

We adopt a semi-grounded theory approach to investigate the impact of different review manipulation tactics. Shoppers take a negative view toward seller manipulations, but the degree of negativity varies across different tactics. Moreover, different manipulations tactics vary in the ease of detection, perceived unethicality, and the effect on consumer perceptions.

The bifunctional effect of propofol on thromboxane agonist (U46619)-induced vasoconstriction in isolated human pulmonary artery

Jianxiu Cui,Zhaojun Wang,Sujuan Kuang,Guangyan Zhang,Chunyu Deng,Jue Ma,Jianxiu Cui 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.6

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from 10-300 μM). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations (10-100 μM) followed by secondary relaxation (at 100-300 μM). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed CaCl2-induced constriction in the 60 mM K+-containing Ca2+-free solution in a dose-dependent manner. Fluorescent imaging of Ca2+ using fluo- 4 showed that a 10 min incubation with propofol (10-300 μM) inhibited the Ca2+ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM K+- containing Ca2+-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.

Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase

Lidan Nong,Jue Ma,Guangyan Zhang,Chunyu Deng,Songsong Mao,Haifeng Li,Jianxiu Cui 대한생리학회-대한약리학회 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.5

Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (α₂-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of 10^–8~10^–6 mol/L, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or 3×10^–9 mmol/L) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial α₂- adrenoceptor and nitric oxide synthase.

Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase

Nong, Lidan,Ma, Jue,Zhang, Guangyan,Deng, Chunyu,Mao, Songsong,Li, Haifeng,Cui, Jianxiu The Korean Society of Pharmacology 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.5

Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (${\alpha}_2$-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of $10^{-8}{\sim}10^{-6}mol/L$, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or $3{\times}10^{-9}mmol/L$) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial ${\alpha}_2$-adrenoceptor and nitric oxide synthase.

The bifunctional effect of propofol on thromboxane agonist (U46619)-induced vasoconstriction in isolated human pulmonary artery

Hao, Ning,Wang, Zhaojun,Kuang, Sujuan,Zhang, Guangyan,Deng, Chunyu,Ma, Jue,Cui, Jianxiu The Korean Society of Pharmacology 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.6

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from $10-300{\mu}m$). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations ($10-100{\mu}m$) followed by secondary relaxation (at $100-300{\mu}m$). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed $CaCl_2$-induced constriction in the 60 mM $K^+$-containing $Ca^{2+}$-free solution in a dose-dependent manner. Fluorescent imaging of $Ca^{2+}$ using fluo-4 showed that a 10 min incubation with propofol ($10-300{\mu}m$) inhibited the $Ca^{2+}$ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM $K^+$-containing $Ca^{2+}$-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.

The bifunctional effect of propofol on thromboxane agonist (U46619)-induced vasoconstriction in isolated human pulmonary artery

Ning Hao,Zhaojun Wang,Sujuan Kuang,Guangyan Zhang,Chunyu Deng,Jue Ma,Jianxiu Cui 대한생리학회-대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.13 No.3

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from 10-300 μM). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations (10-100 μM) followed by secondary relaxation (at 100-300 μM). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed CaCl₂-induced constriction in the 60 mM K⁺-containing Ca²⁺-free solution in a dose-dependent manner. Fluorescent imaging of Ca²⁺ using fluo-4 showed that a 10 min incubation with propofol (10-300 μM) inhibited the Ca²⁺ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM K⁺-containing Ca²⁺-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.

IL-17A Secreted by Th17 Cells Is Essential for the Host against Streptococcus agalactiae Infections

( Jing Chen ),( Siyu Yang ),( Wanyu Li ),( Wei Yu ),( Zhaowei Fan ),( Mengyao Wang ),( Zhenyue Feng ),( Chunyu Tong ),( Baifen Song ),( Jinzhu Ma ),( Yudong Cui ) 한국미생물생명공학회(구 한국산업미생물학회) 2021 Journal of microbiology and biotechnology Vol.31 No.5

Streptococcus agalactiae is an important bacterial pathogen and causative agent of diseases including neonatal sepsis and meningitis, as well as infections in healthy adults and pregnant women. Although antibiotic treatments effectively relieve symptoms, the emergence and transmission of multidrug-resistant strains indicate the need for an effective immunotherapy. Effector T helper (Th) 17 cells are a relatively newly discovered subpopulation of helper CD4⁺ T lymphocytes, and which, by expressing interleukin (IL)-17A, play crucial roles in host defenses against a variety of pathogens, including bacteria and viruses. However, whether S. agalactiae infection can induce the differentiation of CD4⁺ T cells into Th17 cells, and whether IL-17A can play an effective role against S. agalactiae infections, are still unclear. In this study, we analyzed the responses of CD4⁺ T cells and their defensive effects after S. agalactiae infection. The results showed that S. agalactiae infection induces not only the formation of Th1 cells expressing interferon (IFN)-γ, but also the differentiation of mouse splenic CD4⁺ T cells into Th17 cells, which highly express IL-17A. In addition, the bacterial load of S. agalactiae was significantly increased and decreased in organs as determined by antibody neutralization and IL-17A addition experiments, respectively. The results confirmed that IL-17A is required by the host to defend against S. agalactiae and that it plays an important role in effectively eliminating S. agalactiae. Our findings therefore prompt us to adopt effective methods to regulate the expression of IL-17A as a potent strategy for the prevention and treatment of S. agalactiae infection.