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Han Lian,Baohua Wang,Quan Lu,Bin Chen,Hui Yang 한국유전학회 2021 Genes & Genomics Vol.43 No.7
Background Parkinson’s disease (PD) is a common neurodegenerative movement disorder, but the pathogenesis is still unclear. Long non-coding RNAs (lncRNAs) have been reported to play a prominent role in PD. Objective This study is designed to explore the role and mechanism of long intergenic non-coding RNA 00943 (LINC00943) in the N-methyl-4-phenylpyridine (MPP+)-inducted PD model. Methods LINC00943, microRNA-7-5p (miR-7-5p), and the chemokine (C-X-C motif) ligand 12 (CXCL12, also referred to as SDF-1) level were examined by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability and apoptosis were analyzed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), and fow cytometry assays, severally. Protein levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and CXCL12 were assessed by western blot assay. The ROS generation and SOD activity were detected by the corresponding kits. The binding relationship between miR-7-5p and LINC00943 or CXCL12 was predicted by Starbase and then verifed by a dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. Results LINC00943 and CXCL12 were increased, and miR-7-5p was decreased in MPP+-inducted SK-N-SH cells. LINC00943 silencing promoted cell viability, and repressed apoptosis and the infammatory response in MPP+-treated SK-N-SH cells. The mechanical analysis discovered that LINC00943 acted as a sponge of miR-7-5p to regulate CXCL12 expression. Conclusions LINC00943 knockdown could attenuate MPP+-triggered neuron injury by regulating the miR-7-5p/CXCL12 axis, hinting at a promising therapeutic target for PD treatment.
Han-li Lian,Rui-xue Cheng 한양대학교 세라믹연구소 2019 Journal of Ceramic Processing Research Vol.20 No.5
The ZnO-added (Bi0.5Na0.5)0.94Ba0.06TiO3 (denoted as BNBTZ) ceramics were prepared by means of a solid-state reaction method. The ceramics were sintered at 0.5 oC/min and 9 oC/min. Their microstructure, phase structure, piezoelectric, and dielectric properties were investigated. Both the ceramics exhibit dense microstructures. Compared to the ceramics sintered at 0.5 oC/min, those sintered at 9 oC/min have smaller grains. The X-ray diffraction (XRD) and energy-dispersive spectrum reveal that the ceramics exhibit two phases, i.e., BNBTZ phase with perovskite structure and ZnO phase. The movement of the peak position implies enlargement of the crystallite lattice due to the entrance of Zn2+ ions into the lattice. The effect of sintering rates on depolarization behavior was discussed.
Han-li Lian 한양대학교 세라믹연구소 2016 Journal of Ceramic Processing Research Vol.17 No.7
The BaTiO3 and BaTi0.99Fe0.01O3-δ ceramics were prepared via a solid state reaction method. The crystallite structure,microstructure, dielectric and ferroelectric properties of the ceramics were studied. The Fe3+ ions were soluble into BaTiO3lattice with the given concentration. The crystallite structure was investigated by using Rietveld refinement and the resultsshow a decrease in the tetragonality due to the doping of Fe3+. Both ceramics have dense microstructures. The mean grain sizeof BaTi0.99Fe0.01O3-δ is larger than that of BaTiO3. Compared with BaTiO3, BaTi0.99Fe0.01O3-δ demonstrates decreased dielectricconstant, Curie temperature and ferroelectric properties. A diffuse phase transition behavior was observed on the dielectricconstant-temperature curves of BaTi0.99Fe0.01O3-δ. The differences in dielectric and ferroelectric properties between the twoceramics were discussed.
Proteomic analysis of pulmonary sclerosing hemangioma
Jin, Lian-Jin,Shin, Bong Kyung,Jung, Woon Yong,Lee, Hyun-Juu,Cho, Su Jin,Han, Joung-Ho,Ha, Seong-Yeon,Kim, Ae-Ree,Sik Kim, Young,Sun Kim, In,Uhm, Chang-Sub,Kim, Han Kyeom WILEY-VCH 2006 Proteomics Vol. No.
<P>Sclerosing hemangioma (SH) is a rare benign pulmonary tumor derived from the primitive respiratory epithelium. However, the pathogenesis of SH has not yet been clear. Surfactant protein, thyroid transcription factor-1, epithelial membrane antigen, cytokeratin, and vimentin have been identified in SH by immunohistochemistry and electron microscopy. To identify proteins specifically regulated in SH, 2-D PAGE was performed using SH and paired normal tissues. Ten selected differentially expressed protein spots were identified by PMF, MALDI-TOF-MS, and database searching. Apolipoprotein A-1, antizyme inhibitor, heat shock 27-kDa protein 1, and antioxidant proteins, such as peroxiredoxin II (Prx II) and GST, were identified among the down-regulated proteins in SH. Western blot and immunohistochemistry confirmed reduced expressions of Prx II and GST in SH versus normal lung tissue. This study is the first report on the reduced expressions of Prx II and GST in SH.</P>
나노초 레이저 접합이 폴리프로필렌의 물리적 및 화학적 특성에 미치는 영향
한시은(S. Han),서영진(Y. Seo),Trinh Ngoc Lanh(N. L. Trinh),박동규(D. Park),Mang Muan Lian(M. M. Lian),Mulugeta Gebrekiros Berhe(M. G. Berhe),백승은(S. Baek),김준기(J. Kim),전수빈(S. Jeon),이동경(D. Lee) Korean Society for Precision Engineering 2021 한국정밀공학회 학술발표대회 논문집 Vol.2021 No.5월
Lian Shen,Yan Han,C.S. Cai,Guochao Dong,Jianren Zhang,Peng Hu 한국풍공학회 2017 Wind and Structures, An International Journal (WAS Vol.24 No.1
Wind environment in urban residential areas is an important index to consider when evaluating the living environment. However, due to the complexity of the flow field in residential areas, it is difficult to specify the correct inflow boundary conditions in the large eddy simulation (LES). In this paper, the weighted amplitude wave superposition (WAWS) is adopted to simulate the fluctuating velocity data, which satisfies the desired target wind field. The fluctuating velocity data are given to the inlet boundary of the LES by developing an UDF script, which is implemented into the FLUENT. Then, two numerical models - the empty numerical wind tunnel model and the numerical wind tunnel model with spires and roughness elements are established based on the wind tunnel experiment to verify the present method. Finally, the turbulence generation approach presented in this paper is used to carry out a numerical simulation on the wind environment in an urban residential area in Lisbon. The computational results are compared with the wind tunnel experimental data, showing that the numerical results in the LES have a good agreement with the experimental results, and the simulated flow field with the inlet fluctuations can generate a reasonable turbulent wind field. It also shows that strong wind velocities and turbulent kinetic energy occur at the passageways, which may affect the comfort of people in the residential neighborhood, and the small wind velocities and vortexes appear at the leeward corners of buildings, which may affect the spreading of the pollutants.
Han, Min-Su,Kim, Hyo-Jin,Wee, Hee-Jun,Lim, Kyung-Eun,Park, Na-Rae,Bae, Suk-Chul,van Wijnen, Andre J.,Stein, Janet L.,Lian, Jane B.,Stein, Gary S.,Choi, Je-Yong Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of cellular biochemistry Vol.110 No.1
<P>Cleidocranial dysplasia (CCD) is caused by haploinsufficiency in RUNX2 function. We have previously identified a series of RUNX2 mutations in Korean CCD patients, including a novel R131G missense mutation in the Runt-homology domain. Here, we examine the functional consequences of the RUNX2<SUP>R131G</SUP> mutation, which could potentially affect DNA binding, nuclear localization signal, and/or heterodimerization with core-binding factor-β (CBF-β). Immunofluorescence microscopy and western blot analysis with subcellular fractions show that RUNX2<SUP>R131G</SUP> is localized in the nucleus. Immunoprecipitation analysis reveals that heterodimerization with CBF-β is retained. However, precipitation assays with biotinylated oligonucleotides and reporter gene assays with RUNX2 responsive promoters together reveal that DNA-binding activity and consequently the transactivation of potential of RUNX2<SUP>R131G</SUP> is abrogated. We conclude that loss of DNA binding, but not nuclear localization or CBF-β heterodimerization, causes RUNX2 haploinsufficiency in patients with the RUNX2<SUP>R131G</SUP> mutation. Retention of specific functions including nuclear localization and binding to CBF-β of the RUNX2<SUP>R131G</SUP> mutation may render the mutant protein an effective competitor that interferes with wild-type function. J. Cell. Biochem. 110: 97–103, 2010. © 2010 Wiley-Liss, Inc.</P>