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      • Exploiting Anti-T-shaped Graphene Architecture to Form Low Tortuosity, Sieve-like Interfaces for High-Performance Anodes for Li-Based Cells

        Wang, Dong,Zhang, Wei,Drewett, Nicholas E.,Liu, Xiaofei,Yoo, Seung Jo,Lee, Sang-Gil,Kim, Jin-Gyu,Deng, Ting,Zhang, Xiaoyu,Shi, Xiaoyuan,Zheng, Weitao American Chemical Society 2018 ACS central science Vol.4 No.1

        <▼1><P/><P>Graphitic carbon anodes have long been used in Li ion batteries due to their combination of attractive properties, such as low cost, high gravimetric energy density, and good rate capability. However, one significant challenge is controlling, and optimizing, the nature and formation of the solid electrolyte interphase (SEI). Here it is demonstrated that carbon coating via chemical vapor deposition (CVD) facilitates high electrochemical performance of carbon anodes. We examine and characterize the substrate/vertical graphene interface (multilayer graphene nanowalls coated onto carbon paper via plasma enhanced CVD), revealing that these low-tortuosity and high-selection graphene nanowalls act as fast Li ion transport channels. Moreover, we determine that the hitherto neglected parallel layer acts as a protective surface at the interface, enhancing the anode performance. In summary, these findings not only clarify the synergistic role of the parallel functional interface when combined with vertical graphene nanowalls but also have facilitated the development of design principles for future high rate, high performance batteries.</P></▼1><▼2><P>We explored an anti-T-shaped graphene surface-coating concept which offers a low-tortuosity, sieve-like interface that may be exploited for optimized Li-based anodes.</P></▼2>

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        The TL1A-DR3 Axis in Asthma: Membrane-Bound and Secreted TL1A Co-Determined the Development of Airway Remodeling

        Zhang Jintao,Zhang Dong,Pan Yun,Liu Xiaofei,Xu Jiawei,Qiao Xinrui,Cui Wenjing,Dong Liang 대한천식알레르기학회 2022 Allergy, Asthma & Immunology Research Vol.14 No.2

        Purpose: Tumor necrosis factor-like ligand 1A (TL1A), especially its secreted form, has been shown to contribute to eosinophilic inflammation and mucus production, cardinal features of asthma, through its receptor, death receptor 3 (DR3). However, the role of the TL1A-DR3 axis in asthma, especially in terms of airway remodeling, has not yet been fully understood. Methods: The present study investigated the expression and secretion of TL1A in the lung and human bronchial epithelial cells. DR3 small interfering RNA (siRNA), TL1A siRNA, and truncated plasmids were used respectively to identify the function of the TL1A-DR3 axis in vitro. To further validate the roles of the TL1A-DR3 axis in asthma, we collected airway biopsies and sputa from asthmatic patients and constructed a mouse model following rTL1A administration, DR3 knockdown, and TL1A knockout, the asthma-related inflammatory response and the pathological changes in airways were analyzed using various experimental methods. Associated signaling pathways downstream of TL1A knockout in the mouse model were analyzed using RNA sequencing. Results: TL1A, especially its non-secreted form (nsTL1A) was involved in the remodeling process in asthmatics’ airways. Knockdown of TL1A or its receptor DR3 decreased the expression of fibrosis-associated protein in BEAS-2B cells. Reversely, overexpression of nsTL1A in airway epithelial cells facilitated the transforming growth factor-β-induced remodeling progress. In the asthma mouse model, activating the TL1A-DR3 axis contributes to airway inflammation, remodeling, and tissue destruction. Reciprocally, DR3 knockdown or TL1A knockout partly reverses airway remodeling in the asthma model induced by ovalbumin. Conclusions: Our results confirm differential TL1A expression (including its secreted and non-secreted form) in asthma, which modulates remodeling. The shared mechanism of action by which nsTL1A and secreted TL1A exert their effects on asthma development might be mediated via the nuclear factor-κB pathway. The TL1A-DR3 axis presents a promising therapeutic target in asthma.

      • KCI등재

        Suppression of SPARC Ameliorates Ovalbumin-induced Airway Remodeling via TGFβ1/Smad2 in Chronic Asthma

        Pan Yun,Zhang Dong,Zhang Jintao,Liu Xiaofei,Xu Jiawei,Zeng Rong,Cui Wenjing,Liu Tian,Wang Junfei,Dong Liang 대한천식알레르기학회 2024 Allergy, Asthma & Immunology Research Vol.16 No.1

        Purpose: Airway remodeling is a critical feature of asthma. Secreted protein acidic and rich in cysteine (SPARC), which plays a cardinal role in regulating cell-matrix interactions, has been implicated in various fibrotic diseases. However, the effect of SPARC in asthma remains unknown. Methods: We studied the expression of SPARC in human bronchial epithelial cells and serum of asthmatics as well as in the lung tissues of chronic asthma mice. The role of SPARC was examined by using a Lentivirus-mediated SPARC knockdown method in the ovalbumin (OVA)-induced asthma mice. The biological processes regulated by SPARC were identified using RNA sequencing. The function of SPARC in the remodeling process induced by transforming growth factor β1 (TGFβ1) was conducted by using SPARC small interfering RNA (siRNA) or recombinant human SPARC protein in 16HBE cells. Results: We observed that SPARC was up-regulated in human bronchial epithelia of asthmatics and the asthmatic mice. The levels of serum SPARC in asthmatics were also elevated and negatively correlated with the forced expiratory volume in one second (FEV1) to forced vital capacity ratio (FVC) (r = −0.485, P < 0.01) and FEV1 (%predicted) (r = −0.425, P = 0.001). In the chronic asthmatic mice, Lentivirus-mediated SPARC knockdown significantly decreased airway remodeling and airway hyper-responsiveness. According to gene set enrichment analysis, negatively enriched pathways found in the OVA + short hairpin-SPARC group included ECM organization and collagen formation. In the lung function studies, knockdown of SPARC by siRNA reduced the expression of remodeling-associated biomarkers, cell migration, and contraction by blocking the TGFβ1/Smad2 pathway. Addition of human recombinant SPARC protein promoted the TGFβ1-induced remodeling process, cell migration, and contraction in 16HBE cells via the TGFβ1/Smad2 pathway. Conclusions: Our studies provided evidence for the involvement of SPARC in the airway remodeling of asthma via the TGFβ1/Smad2 pathway.

      • KCI등재

        Static and Seismic Experimental Study of Novel Prefabricated Beam-Column Joints with Elongated-Hole Brackets

        Zhang Zhiwei,Li Dong,Wang Huajie,Li Songling,Qian Hongliang,Bi Yanhua,Wang Guoxing,Jin Xiaofei,Fan Feng 한국강구조학회 2024 International Journal of Steel Structures Vol.24 No.1

        To enhance the structural connectivity of prefabricated steel frame systems and augment their construction effi ciency, this study introduces an innovative prefabricated joint design tailored for square steel columns and H-beams characterized by varying beam heights. This study includes both static loading tests and seismic tests performed on full-scale joints featuring two diff erent beam heights. This investigation involved a comprehensive analysis of the static and seismic performance of the joints, employing various performance metrics such as ultimate load capacities, ultimate rotation angles, hysteresis curves, skeleton curves, stiff ness degradation curves, and ductility coeffi cients, in alignment with established structural codes and standards. The results indicate that the plasticity of the H-beam is fully developed, exhibiting a relative slip phenomenon. Additionally, the joints demonstrate commendable rotational capacity, with hysteresis curves consistently manifesting an inverse S-shape and exhibiting noteworthy stiff ness degradation. Furthermore, the comparison with the unimproved joint shows that the novel joint, in addition to being easy to construct, has better ductility and energy dissipation capacity. The results of the study will provide a technical reference for further optimization and application of prefabricated beam-column joints.

      • KCI등재

        Characterization of a New Isolate of Chilli ringspot virus in Yunnan, China

        Md. Siddiqur Rahman,Xiaoxia Su,Kuanyu Zheng,Xiaofei Cheng,Ting Li,Lihua Zhao,Jiahong Dong,Zhongkai Zhang 한국작물학회 2020 Journal of crop science and biotechnology Vol.23 No.1

        Virus diseases are the major limiting factors of chilli production in China. A virus isolate of chilli ringspot virus-Yunnan (ChiRSV-YN) from chilli (Capsicum annuum L.) showing mild mosaic, leaf crinkling, ringspot, and vein banding symptoms was recently identified in Yunnan, China. The electron microscopy confirmed the virus as a typical potyvirus having flexuous filamentous particles ca. 780 nm in length. Several chilli and tobacco varieties were tested through mechanical inoculation and found to be susceptible to the virus isolate ChiRSV-YN. The viral genome was sequenced through RNA sequencing. The complete genomic RNA of the isolate (GenBank Acc. No. KX258620) consisted of 9,652 nucleotides (nt) excluding the poly (A) tail at the 3ʹ end. The isolate contains a large ORF which encodes a polyprotein of 3,086 amino acids (aa) with Mr. of 349.21 kDa. It had a typical genomic organization of potyviruses. The complete nucleotide and polyprotein sequences of ChiRSV-YN had 87.6 and 93.2% identities with the ChiRSV-HN/14, respectively. The result showed ChiRSV-YN is a new isolate of ChiRSV and it is the first full-length genome characterization of ChiRSV in Yunnan, China. Understanding of the characteristics of this virus isolate might provide the basis for disease diagnosis and control in the future.

      • KCI등재

        MiR-218-5p Suppresses the Killing Effect of Natural Killer Cell to Lung Adenocarcinoma by Targeting SHMT1

        Quanjun Yang,Jingjing Li,Yili Hu,Xiaofei Tang,Lili Yu,Lihua Dong,Diandian Chen 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.6

        Purpose: Lung adenocarcinoma (LA) is one of the major types of lung cancer. MicroRNAs (miRNAs) play an essential role in regulatingresponses of natural killer (NK) cells to cancer malignancy. However, the mechanism of miR-218-5p involved in the killingeffect of NK cells to LA cells remains poorly understood. Materials and Methods: The expression of miR-218-5p was examined by quantitative real-time polymerase chain reaction (qRTPCR). Serine hydroxymethyl transferase 1 (SHMT1) level was detected by qRT-PCR or western blots. Cytokines production ofinterferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) were detected by ELISA. The killing effect of NK cells to LA cells was investigatedusing lactate dehydrogenase cytotoxicity assay kit. The interaction of miR-218-5p and SHMT1 was probed by luciferaseactivity assay. Xenograft model was established to investigate the killing effect of NK cells in vivo. Results: miR-218-5p was enhanced and SHMT1 was inhibited in NK cells of LA patients, whereas stimulation of interleukin-2(IL-2) reversed their abundances. Addition of miR-218-5p reduced IL-2-induced cytokines expression and cytotoxicity in NK-92against LA cells. Moreover, SHMT1 was negatively regulated by miR-218-5p and attenuated miR-218-5p-mediated effect on cytotoxicity,IFN-γ and TNF-α secretion in IL-2-activated NK cells. In addition, miR-218-5p exhaustion inhibited tumor growth bypromoting killing effect of NK cells. Conclusion: miR-218-5p suppresses the killing effect of NK cells to LA cells by targeting SHMT1, providing a potential target forLA treatment by ameliorating NK cells function.

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