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Wang, Xia,Wang, Hong,Li, Qiang,Li, Hongsen,Xu, Jie,Zhao, Guoxia,Li, Hongliang,Guo, Peizhi,Li, Shandong,Sun, Yang-kook The Electrochemical Society 2017 Journal of the Electrochemical Society Vol.164 No.13
<P>A promising anode material for lithium-ion batteries (LIBs) consisting of Sb2Se3 nanorods and reduced graphene oxide (rGO) sheets has been prepared by an effective solvothermal approach. The synergetic effect between Sb2Se3 nanorods and rGO matrix provides not only high conductivity paths and strong electron contact interface, but also alleviates the volume change of Sb2Se3 nanorods, resulting in excellent lithium-storage performance. When tested as an anode material for LIBs, a high capacity of 868.30 mAh g(-1) can be retained after 100 cycles at 200 mA g(-1). Even at 2000 mA g(-1), a satisfactory capacity of 430.40 mAh g(-1) after long 550 cycles can be delivered. Ex situ X-ray diffraction study suggests that the Sb2Se3/rGO composite follows the combined Li+ intercalation, conversion reaction and alloying reaction mechanism. These features suggest the Sb2Se3/rGO composite a viable choice for application as an anode material in high-performance LIBs. (C) 2017 The Electrochemical Society. All rights reserved.</P>
Effects of Ga-doping on the microstructure and magnetic properties of MnBi alloys
Yang, Yang,Kim, Jong-Woo,Si, Ping-Zhan,Qian, Hui-Dong,Shin, Yongho,Wang, Xinyou,Park, Jihoon,Li, Oi Lun,Wu, Qiong,Ge, Hongliang,Choi, Chul-Jin Elsevier 2018 JOURNAL OF ALLOYS AND COMPOUNDS Vol.769 No.-
<P><B>Abstract</B></P> <P>The low temperature phase Mn<SUB>55</SUB>Bi<SUB>45-<I>x</I> </SUB>Ga<SUB> <I>x</I> </SUB> (<I>x</I> = 0, 1, 3, 5, and 10) alloys were prepared by induction melting process with subsequent low temperature annealing. The effects of Ga-doping on the crystal structure and magnetic properties of the alloys were systematically studied. The room temperature coercivities of Mn<SUB>55</SUB>Bi<SUB>45-<I>x</I> </SUB>Ga<SUB> <I>x</I> </SUB> after ball milling increased from 1.43 T for <I>x</I> = 0 to 1.66 T for <I>x</I> = 5, while the saturation magnetization decreased from 60.7 Am<SUP>2</SUP>/kg (<I>x</I> = 0) to 45.1 Am<SUP>2</SUP>/kg (<I>x</I> = 5). The maximum energy product (<I>BH</I>)<SUB>max</SUB> of Mn<SUB>55</SUB>Bi<SUB>44</SUB>Ga powders reached 7.87 MGOe. The Curie temperature of the Mn<SUB>55</SUB>Bi<SUB>45-<I>x</I> </SUB>Ga<SUB> <I>x</I> </SUB> alloys increased from 633 K to 658 K with increasing Ga concentration in the range of 0 ≤ <I>x</I> ≤ 5.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Effects of doping Ga on the microstructural and magnetic properties of MnBi alloy. </LI> <LI> The MnBi-Ga powders are achieved by surfactant assisted high energy ball milling. </LI> <LI> The maximum energy produce (<I>BH</I>)<SUB>max</SUB> shows 7.87 MGOe for Mn<SUB>55</SUB>Bi<SUB>44</SUB>Ga sample. </LI> <LI> The coercivity of Mn<SUB>55</SUB>Bi<SUB>40</SUB>Ga<SUB>5</SUB> after ball milling reached 1.66 T at room temperature. </LI> <LI> The elevated curie temperature (<I>T</I> <SUB>c</SUB>) by doping Ga makes it a possible candidate for high temperature applications. </LI> </UL> </P>
The anti-diabetic drug dapagliflozin induces vasodilation via activation of PKG and Kv channels
Li, Hongliang,Shin, Sung Eun,Seo, Mi Seon,An, Jin Ryeol,Choi, Il-Whan,Jung, Won-Kyo,Firth, Amy L.,Lee, Dae-Sung,Yim, Mi-Jin,Choi, Grace,Lee, Jeong Min,Na, Sung Hun,Park, Won Sun Elsevier 2018 Life sciences Vol.197 No.-
<P><B>Abstract</B></P> <P><B>Aim</B></P> <P>Considering the clinical efficacy of dapagliflozin in patients with type 2 DM and the pathophysiological relevance of Kv channels for vascular reactivity. We investigate the vasodilatory effect of dapagliflozin and related mechanisms using phenylephrine (Phe)-induced contracted aortic rings.</P> <P><B>Material and methods</B></P> <P>Arterial tone measurement was performed in aortic smooth muscle.</P> <P><B>Key findings</B></P> <P>Application of dapagliflozin induced vasodilation in a concentration-dependent manner. Pre-treatment with the BK<SUB>Ca</SUB> channel inhibitor paxilline, the K<SUB>ATP</SUB> channel inhibitor glibenclamide, and the Kir channel inhibitor Ba<SUP>2+</SUP> did not change dapagliflozin-induced vasodilation. However, application of the Kv channels inhibitor 4-AP effectively inhibited dapagliflozin-induced vasodilation. Application of the Ca<SUP>2+</SUP> channel inhibitor nifedipine and the sarcoplasmic/endoplasmic reticulum Ca<SUP>2+</SUP>-ATPase (SERCA) pump inhibitor thapsigargin did not alter the vasodilatory effect of dapagliflozin. Moreover, the adenylyl cyclase inhibitor SQ 22536 and the protein kinase A (PKA) inhibitor KT 5720 had no effect on dapagliflozin-induced vasodilation. Although guanylyl cyclase inhibitors, NS 2028 and ODQ, did not reduce the vasodilatory effect of dapagliflozin, the protein kinase G (PKG) inhibitor KT 5823 effectively inhibited dapagliflozin-induced vasodilation. The vasodilatory effect of dapagliflozin was not affected by elimination of the endothelium. Furthermore, pretreatment with the nitric oxide synthase inhibitor L-NAME or the small-conductance Ca<SUP>2+</SUP>-activated K (SKCa) channel inhibitor apamin did not change the vasodilatory effect of dapagliflozin.</P> <P><B>Significance</B></P> <P>We concluded that dapagliflozin induced vasodilation via the activation of Kv channels and PKG, and was independent of other K<SUP>+</SUP> channels, Ca<SUP>2+</SUP> channels, intracellular Ca<SUP>2+</SUP>, and the endothelium.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Hongliang Li,Yue Zhou,Yongqi Yang,Yiwen Zha,Bingqian Ye,Seo-Yeong Mun,Wenwen Zhuang,Jingyan Liang,Won Sun Park The Korean Society of Pharmacology 2023 The Korean Journal of Physiology & Pharmacology Vol.27 No.4
Voltage-dependent K<sup>+</sup> (Kv) channels are widely expressed on vascular smooth muscle cells and regulate vascular tone. Here, we explored the inhibitory effect of encainide, a class Ic anti-arrhythmic agent, on Kv channels of vascular smooth muscle from rabbit coronary arteries. Encainide inhibited Kv channels in a concentration-dependent manner with an IC<sub>50</sub> value of 8.91 ± 1.75 μM and Hill coefficient of 0.72 ± 0.06. The application of encainide shifted the activation curve toward a more positive potential without modifying the inactivation curve, suggesting that encainide inhibited Kv channels by altering the gating property of channel activation. The inhibition by encainide was not significantly affected by train pulses (1 and 2 Hz), indicating that the inhibition is not use (state)-dependent. The inhibitory effect of encainide was reduced by pretreatment with the Kv1.5 subtype inhibitor. However, pretreatment with the Kv2.1 subtype inhibitor did not alter the inhibitory effects of encainide on Kv currents. Based on these results, encainide inhibits vascular Kv channels in a concentration-dependent and use (state)-independent manner by altering the voltage sensor of the channels. Furthermore, Kv1.5 is the main Kv subtype involved in the effect of encainide.
Li, Hongliang,An, Jin Ryeol,Seo, Mi Seon,Ha, Kwon-Soo,Han, Eun-Taek,Hong, Seok-Ho,Jung, Won-Kyo,Lee, Dae-Sung,Yim, Mi-Jin,Choi, Grace,Lee, Jeong Min,Bae, Young Min,Choi, Il-Whan,Park, Won Sun Elsevier 2019 european journal of pharmacology Vol.849 No.-
<P><B>Abstract</B></P> <P>In the present study, we investigated the inhibitory effect of tacrolimus, a macrolide immunosuppressive drug that acts through calcineurin inhibition, on voltage-gated K<SUP>+</SUP> (Kv) channels expressed in native smooth muscle cells isolated from the coronary arteries of rabbits. Tacrolimus reduced the amplitude of Kv currents in a dose-dependent manner with an IC<SUB>50</SUB> value and Hill coefficient of 7.80 ± 3.01 μM and 1.07 ± 0.25, respectively. Tacrolimus caused a shift in the activation curve toward a more positive potential and in the inactivation curve toward a more negative potential. Tacrolimus-induced inhibition of Kv current was increased by the application of train pulses (1 or 2 Hz). Furthermore, the recovery time constant of inactivation was extended in the presence of tacrolimus, suggesting that tacrolimus inhibited Kv channels in a use-dependent manner. Two kinds of Kv subtype inhibitors, DPO-1 and guangxitoxin did not affect the degree of tacrolimus-induced inhibition of Kv current. Furthermore, pretreatment with another calcineurin inhibitor, cyclosporine A, did not affect the Kv current, and did not alter the inhibitory effect of tacrolimus. Using perforated-patch clamp experiments, inhibition of Kv channels by tacrolimus caused membrane depolarization. From these results, we concluded that tacrolimus inhibited the vascular Kv currents in a dose, state (open and closed)-dependent manner.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Li, Jinjie,Li, Yang,Yin, Zhigang,Jiang, Jihong,Zhang, Minghui,Guo, Xiao,Ye, Zhujia,Zhao, Yan,Xiong, Haiyan,Zhang, Zhanying,Shao, Yujie,Jiang, Conghui,Zhang, Hongliang,An, Gynheung,Paek, Nam‐,Cho John Wiley and Sons Inc. 2017 Plant biotechnology journal Vol.15 No.2
<P><B>Summary</B></P><P>Drought is one of the major abiotic stresses that directly implicate plant growth and crop productivity. Although many genes in response to drought stress have been identified, genetic improvement to drought resistance especially in food crops is showing relatively slow progress worldwide. Here, we reported the isolation of <I>abscisic acid</I>,<I> stress</I> and <I>ripening</I> (<I>ASR</I>) genes from upland rice variety, IRAT109 (<I>Oryza sativa</I> L. ssp. <I>japonica</I>), and demonstrated that overexpression of <I>OsASR5</I> enhanced osmotic tolerance in <I>Escherichia coli</I> and drought tolerance in <I>Arabidopsis</I> and rice by regulating leaf water status under drought stress conditions. Moreover, overexpression of <I>OsASR5</I> in rice increased endogenous ABA level and showed hypersensitive to exogenous ABA treatment at both germination and postgermination stages. The production of H<SUB>2</SUB>O<SUB>2</SUB>, a second messenger for the induction of stomatal closure in response to ABA, was activated in overexpression plants under drought stress conditions, consequently, increased stomatal closure and decreased stomatal conductance. In contrast, the loss‐of‐function mutant, <I>osasr5</I>, showed sensitivity to drought stress with lower relative water content under drought stress conditions. Further studies demonstrated that OsASR5 functioned as chaperone‐like protein and interacted with stress‐related HSP40 and 2OG‐Fe (II) oxygenase domain containing proteins in yeast and plants. Taken together, we suggest that <I>OsASR5</I> plays multiple roles in response to drought stress by regulating ABA biosynthesis, promoting stomatal closure, as well as acting as chaperone‐like protein that possibly prevents drought stress‐related proteins from inactivation.</P>
Hongliang Li,Shenglan Ji,Yang Jiang,Jiangwei Chu 대한기계학회 2021 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.35 No.8
Active deicing technologies, such as conductive asphalt concrete and heating cable, are not applicable to the existing roads, and passive deicing based on mechanical methods damage the roads. A novel scraping deicing system for thin ice using end-of-life wire ropes was proposed, and the scraping deicing mechanism was given to optimizing the inclination angle for minimal external deicing force. The prototype was developed and fabricated, and a laboratory deicing experiment was designed to evaluate the deicing performance for a prefabricate frozen asphalt concrete block (ACB). The results showed that the deicing brush could naturally clean with the thickness of the ice layer of 10 mm. There was good stability when the deicing brush's rotation speed reached 500 r/min, and the removal rate can get 92 %. No apparent scratches occurred on the upper body of the ACB, which will not cause severe damage to the pavement surface.
Li, Hongliang,Kim, Hye Won,Shin, Sung Eun,Seo, Mi Seon,An, Jin Ryeol,Ha, Kwon-Soo,Han, Eun-Taek,Hong, Seok-Ho,Firth, Amy L.,Choi, Il-Whan,Han, Il Yong,Lee, Dae-Sung,Yim, Mi-Jin,Park, Won Sun Elsevier 2017 Life sciences Vol.188 No.-
<P><B>Abstract</B></P> <P><B>Aims</B></P> <P>The vasorelaxant effects of the anti-diabetic drug, mitiglinide in phenylephrine (Phe)-pre-contracted aortic rings were examined.</P> <P><B>Materials and methods</B></P> <P>Arterial tone measurement was performed in aortic smooth muscle cells.</P> <P><B>Key findings</B></P> <P>Mitiglinide dose-dependently induced vasorelaxation. Application of the large-conductance Ca<SUP>2+</SUP>-activated K<SUP>+</SUP> (BK<SUB>Ca</SUB>) channel blocker paxilline, inwardly rectifying K<SUP>+</SUP> (Kir) channel blocker Ba<SUP>2+</SUP>, and ATP-sensitive K<SUP>+</SUP> (K<SUB>ATP</SUB>) channel blocker glibenclamide did not affect the vasorelaxant effect of mitiglinide. However, application of the voltage-dependent K<SUP>+</SUP> (Kv) channel blocker 4-AP, effectively inhibited mitiglinide-induced vasorelaxation. Although pretreatment with the Ca<SUP>2+</SUP> channel blocker nifedipine did not alter the mitiglinide-induced vasorelaxation, pretreatment with the sarcoplasmic/endoplasmic reticulum Ca<SUP>2+</SUP>-ATPase (SERCA) pump inhibitor thapsigargin and cyclopiazonic acid reduced the vasorelaxant effect of mitiglinide. In addition, the vasorelaxant effect of mitiglinide was not affected by the inhibitors of adenylyl cyclase, protein kinase A, guanylyl cyclase, or protein kinase G. Elimination of the endothelium and inhibition of endothelium-dependent vasorelaxant mechanisms also did not change the vasorelaxant effect of mitiglinide.</P> <P><B>Significance</B></P> <P>We proposed that mitiglinide induces vasorelaxation via activation of Kv channels and SERCA pump. However, the vasorelaxant effects of mitiglinide did not involve other K<SUP>+</SUP> channels, Ca<SUP>2+</SUP> channels, PKA/PKG signaling pathways, or the endothelium.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>