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      • SCIESCOPUSKCI등재

        Removal of Chromium (Ⅵ) by Escherichia coli Cells Expressing Cytoplasmic or Surface-Displayed ChrB: a Comparative Study

        ( Xiaofeng Zhou ),( Jianghui Li ),( Weilong Wang ),( Fan Yang ),( Bingqian Fan ),( Chenlu Zhang ),( Xiaojun Ren ),( Feng Liang ),( Rong Cheng ),( Fengying Jiang ),( Huaibin Zhou ),( Juanjuan Yang ),( 한국미생물 · 생명공학회 2020 Journal of microbiology and biotechnology Vol.30 No.7

        Various genetically engineered microorganisms have been developed for the removal of heavy metal contaminants. Metal biosorption by whole-cell biosorbents can be enhanced by overproduction of metal-binding proteins/peptides in the cytoplasm or on the cell surface. However, few studies have compared the biosorption capacity of whole cells expressing intracellular or surface-displayed metal-adsorbing proteins. In this study, several constructs were prepared for expressing intracellular and surface-displayed Ochrobactrum tritici 5bvl1 ChrB in Escherichia coli BL21(DE3) cells. E. coli cells expressing surface-displayed ChrB removed more Cr(VI) from aqueous solutions than cells with cytoplasmic ChrB under the same conditions. However, intracellular ChrB was less susceptible to variation in extracellular conditions (pH and ionic strength), and more effectively removed Cr(VI) from industrial wastewater than the surface-displayed ChrB at low pH (<3). An adsorptiondesorption experiment demonstrated that compared with intracellular accumulation, cell-surface adsorption is reversible, which allows easy desorption of the adsorbed metal ions and regeneration of the bioadsorbent. In addition, an intrinsic ChrB protein fluorescence assay suggested that pH and salinity may influence the Cr(VI) adsorption capacity of ChrB-expressing E. coli cells by modulating the ChrB protein conformation. Although the characteristics of ChrB may not be universal for all metal-binding proteins, our study provides new insights into different engineering strategies for whole-cell biosorbents for removing heavy metals from industrial effluents.

      • KCI등재

        3D Printing of Bioinspired Structural Materials with Fibers Induced by Doctor Blading Process

        Luquan Ren,Bingqian Li,Zhengyi Song,Qingping Liu,Lei Ren,Xueli Zhou 한국정밀공학회 2019 International Journal of Precision Engineering and Vol.6 No.1

        Fiber is a crucial element in biological micro-structural materials. Replication of fiber-reinforced composites with analogous architectures of their natural counterparts has caused widespread academic concern. Recent researches indicate 3D printing technology has the potential to produce biomimetic structural materials. The aim of this study is to develop a process to fabricate fiber-reinforced composites with ordered yet spatially tunable fiber arrangement. Specifically, we present a method to align fibers during the 3D printing of fiber-reinforced composites. A modified slurry-based stereolithography process was developed, and the fibers in the fiber–resin mixture were aligned by Shear force produced during the spreading of slurry. We investigated the influence of relative factors on fiber orientation, and two models were used to uncover the internal mechanism. By controlling the speed and the direction of the moving blade, the patterns that fibers were arranged can be freely programmed. Therefore, we have extracted bioinspired sinusoidal and zigzag design motifs to analyze their mechanical properties compared with non-bioinspired motifs. The proposed method is relatively material agnostic, more efficient and more facile. It thus provides a promising route to fabricate fiber-reinforced composites, and has potential to be adopted in biological structures researches and industrial applications.

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        Encainide, a class Ic anti-arrhythmic agent, blocks voltage-dependent potassium channels in coronary artery smooth muscle cells

        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.

      • KCI등재

        Incomplete autophagy promotes the replication of Mycoplasma hyopneumoniae

        Wang Zhaodi,Wen Yukang,Zhou Bingqian,Tian Yaqin,Ning Yaru,Ding Honglei 한국미생물학회 2021 The journal of microbiology Vol.59 No.8

        Autophagy is an important cellular homeostatic mechanism for recycling of degradative proteins and damaged organelles. Autophagy has been shown to play an important role in cellular responses to bacteria and bacterial replication. However, the role of autophagy in Mycoplasma hyopneumoniae infection and the pathogenic mechanism is not well characterized. In this study, we showed that M. hyopneumoniae infection significantly increases the number of autophagic vacuoles in host cells. Further, we found significantly enhanced expressions of autophagy marker proteins (LC3-II, ATG5, and Beclin 1) in M. hyopneumoniae-infected cells. Moreover, immunofluorescence analysis showed colocalization of P97 protein with LC3 during M. hyopneumoniae infection. Interestingly, autophagic flux marker, p62, accumulated with the induction of infection. Conversely, the levels of p62 and LC3-II were decreased after treatment with 3-MA, inhibiting the formation of autophagosomes, during infection. In addition, accumulation of autophagosomes promoted the expression of P97 protein and the survival of M. hyopneumoniae in PK- 15 cells, as the replication of M. hyopneumoniae was downregulated by adding 3-MA. Collectively, these findings provide strong evidence that M. hyopneumoniae induces incomplete autophagy, which in turn enhances its reproduction in host cells. These findings provide novel insights into the interaction of M. hyopneumoniae and host.

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