http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Jia, Xiangling,Zhang, Chen,Liu, Juanjuan,Lv, Wei,Wang, Da-Wei,Tao, Ying,Li, Zhengjie,Zheng, Xiaoyu,Yu, Jong-Sung,Yang, Quan-Hong The Royal Society of Chemistry 2016 Nanoscale Vol.8 No.8
<P>A controllable drying strategy is proposed for the precise and non-destructive control over the structure of a 3D graphene assembly. Such an assembly is used as a model carbon material to investigate the pore structure-dependent shuttle effect and cycling performance of the cathode of a Li-S battery.</P>
Inhibition of Microcystis aeruginosa by the Extracellular Substances from an Aeromonas sp
( Yu Mei Liu ),( Ming Jun Chen ),( Meng Hui Wang1 ),( Rui Bao Jia ),( Li Li ) 한국미생물 · 생명공학회 2013 Journal of microbiology and biotechnology Vol.23 No.9
Growth of Microcystis aeruginosa could be inhibited significantly within 24 h by the extracellular substances prepared from Aeromonas sp. strain FM. During the treatment, the concentration of extracellular soluble carbohydrates increased significantly in algal culture. Morphological and ultrastructural changes in M. aeruginosa cells, including breakage of the cell surface, secretion of mucilage, and intracellular disorganization of thylakoids, were observed. HPLC-MS analysis showed that the extracellular substances of Aeromonas sp. strain FM were a mixture of free amino acids, tripeptides, and clavulanate. Among these, the algaelysis effects of lysine and clavulanate were confirmed.
Wang, Zehua,Yang, Bo,Zhang, Min,Guo, Weiwei,Wu, Zhiyuan,Wang, Yue,Jia, Lin,Li, Song,Caesar-Johnson, Samantha J.,Demchok, John A.,Felau, Ina,Kasapi, Melpomeni,Ferguson, Martin L.,Hutter, Carolyn M.,Sof Cell Press 2018 Cancer Cell Vol. No.
<P><B>Summary</B></P> <P>We characterized the epigenetic landscape of genes encoding long noncoding RNAs (lncRNAs) across 6,475 tumors and 455 cancer cell lines. In stark contrast to the CpG island hypermethylation phenotype in cancer, we observed a recurrent hypomethylation of 1,006 lncRNA genes in cancer, including <I>EPIC1</I> (epigenetically-induced lncRNA1). Overexpression of <I>EPIC1</I> is associated with poor prognosis in luminal B breast cancer patients and enhances tumor growth <I>in vitro</I> and <I>in vivo.</I> Mechanistically, <I>EPIC1</I> promotes cell-cycle progression by interacting with MYC through <I>EPIC1</I>'s 129–283 nt region. <I>EPIC1</I> knockdown reduces the occupancy of MYC to its target genes (e.g., <I>CDKN1A</I>, <I>CCNA2</I>, <I>CDC20</I>, and <I>CDC45</I>). MYC depletion abolishes <I>EPIC1</I>'s regulation of MYC target and luminal breast cancer tumorigenesis <I>in vitro</I> and <I>in vivo</I>.</P> <P><B>Highlights</B></P> <P> <UL> <LI> LncRNAs show a hypomethylation phenotype, in contrast to a CIMP phenotype in cancer </LI> <LI> <I>EPIC1</I> promotes breast tumorigenesis through regulating cancer cell-cycle progression </LI> <LI> <I>EPIC1</I> directly interacts with MYC protein through <I>EPIC1</I>'s 129–283 nt region </LI> <LI> <I>EPIC1</I> regulates MYC targets by enhancing MYC occupancy on its target promoters </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
Bioremediation of Coastal Saline-Alkali Marshy Soil by the Irrigation with Pulp & Paper Wastewater
LI Jia-liang,LU Zhao-hua,TIAN Jia-yi,WANG Lin,LI Peng-hui,XIAO Zhong-feng 대전대학교 환경문제연구소 2009 환경문제연구소 논문집 Vol.13 No.-
Based on the importance of coastal saline-alkali soil remediation in Yellow River Delta, China, the Cl-、Na+ transferring tendency in soil and the saline-alkali soil eco-remediation effects were researched by measuring soil Cl-、Na+ 、soluble salt、soil respire rate and dry biomass weight of reed, etc. periodically. The results shows: the concentration of irrigated soil Cl-、Na+ and soluble salt were decreased 57.7-70%、45.7-47.1% and 53.2-59.7%, respectively, and soil salt decreasing level were little influenced by the hydraulic load, inundation depth varies in some degree, but it was influenced by dry-wet alternative irrigating mode The concentration of soil total nitrogen、organic mass、microbial respire rate, and the reed biomass above ground were increased averagely to 2.17、1.20、1.46 and 1.34 multiple respectively afterirrigation with wastewater, which have complex remediation effects on the coastal saline-alkali wetland, but there are some differences among the different irrigating crafts.
Expression of Endogenous Hypoxia Markers in Vulvar Squamous Cell Carcinoma
Li, Yu-Zhu,Li, Shu-Ling,Li, Xia,Wang, Li-Jie,Wang, Jiu-Ling,Xu, Jia-Wen,Wu, Zhi-Hong,Gong, Li,Zhang, Xiao-Dan Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8
Objective: To investigate the expression of endogenous hypoxia-related markers identified as being involved in vulvar squamous cell carcinoma (VSCC). Methods: We performed immunohistochemical staining of hypoxia-inducible factor-$1{\alpha}$ (HIF-$1{\alpha}$), glucose transporter-1 (GLUT-1), carbonic anhydrase 9 (CA-9) and vascular endothelial growth factor (VEGF), on tissue sections of 25 VSCC patients, 10 vulvar intraepithelial neoplasia (VIN) patients and 12 healthy controls. Results: HIF-$1{\alpha}$ expression was found in all sections, with no significant difference between controls, VIN and VSCC sections (all P<0.05). Glut-1 expression was found in 25% of control, 90% of VIN and 100% of VSCC sections. A significant difference between control and VIN or VSCC was observed (all P<0.05), while no difference was found between VIN and VSCC sections (P>0.05). CA-9 expression was negative in control sections, but it was found in 30% of VIN sections and 52% of VSCC sections with strong staining. Similarly, CA-9 expression also showed obvious differences between controls and VIN or VSCC sections (all P<0.05). However, there was no significant difference between VIN and VSCC (P>0.05). There were only 25% of control sections with weak VEGF expression, while strong staining was found in about 60% of VIN sections and 25% of VSCC sections (all P<0.05). In addition, a difference was also found between VIN and VSCC sections (P<0.05). Conclusion: Expression of endogenous hypoxia markers (HIF-$1{\alpha}$, GLUT-1, CA-9 and VEGF) might be involved in the malignant progression of VSCC.
Zhu, Jia-Ying,Li, Yuyao,Cao, Dong-Mei,Yang, Hongjuan,Oh, Eunkyoo,Bi, Yang,Zhu, Shengwei,Wang, Zhi-Yong Elsevier 2017 Molecular cell Vol.66 No.5
<P><B>Summary</B></P> <P>The glycogen synthase kinase-3 (GSK3) family kinases are central cellular regulators highly conserved in all eukaryotes. In <I>Arabidopsis</I>, the GSK3-like kinase BIN2 phosphorylates a range of proteins to control broad developmental processes, and BIN2 is degraded through unknown mechanism upon receptor kinase-mediated brassinosteroid (BR) signaling. Here we identify KIB1 as an F-box E3 ubiquitin ligase that promotes the degradation of BIN2 while blocking its substrate access. Loss-of-function mutations of KIB1 and its homologs abolished BR-induced BIN2 degradation and caused severe BR-insensitive phenotypes. KIB1 directly interacted with BIN2 in a BR-dependent manner and promoted BIN2 ubiquitination in vitro. Expression of an F-box-truncated KIB1 caused BIN2 accumulation but dephosphorylation of its substrate BZR1 and activation of BR responses because KIB1 blocked BIN2 binding to BZR1. Our study demonstrates that KIB1 plays an essential role in BR signaling by inhibiting BIN2 through dual mechanisms of blocking substrate access and promoting degradation.</P> <P><B>Highlights</B></P> <P> <UL> <LI> KIB1 is an essential positive regulator in brassinosteroid signaling </LI> <LI> KIB1 mediates BR-induced ubiquitination and degradation of GSK3 kinase BIN2 </LI> <LI> KIB1 binding to BIN2 prevents BIN2-substrate interaction and promotes BIN2 degradation </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
Li-Ying Wang,Xiu-Hua Wang,Jia-Lian Tan,Shuai Xia,Heng-Zhi Sun,Jin-Wen Shi,Ming-Dong Jiang,Liang Fang,Hua Zuo,Gautam Dupati,장기완,신동수 대한화학회 2012 Bulletin of the Korean Chemical Society Vol.33 No.11
A number of novel small molecules, safrole oxide derivatives 4a-c, 6a-c, 9a-h, were synthesized by the reaction of safrole oxide with anilines 3 and 5, or its alkyl allyl ether derivative 7 with alkyl bromide 8 in moderate yields. The antiproliferative effects of all the target molecules on A549 cell growth were investigated and it was found that the 14 novel compounds could suppress A549 lung cancer cell growth. Among them, compound 6b was the most effective compound in inhibiting the proliferation of A549 cells.
Jia-Wang Ding,Xiao-Hong Tong,Jun Yang,Zhao-Qi Liu,Yan Zhang,Jian Yang,Song Li,Li Li 대한의학회 2010 Journal of Korean medical science Vol.25 No.11
Activated protein C (APC) is known to be beneficial on ischemia reperfusion injury in myocardium. However, the protection mechanism of APC is not fully understood. The purpose of this study was to investigate the effects and possible mechanisms of APC on myocardial ischemic damage. Artificially ventilated anaesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 hr of reperfusion. Rats were randomly divided into four groups; Sham, I/R, APC preconditioning and postconditioning group. Myocardial infarct size, apoptosis index, the phosphorylation of ERK1/2, Bcl-2, Bax and cytochrome c genes and proteins were assessed. In APC-administrated rat hearts, regardless of the timing of administration, infarct size was consistently reduced compared to ischemia/reperfusion (I/R) rats. APC improved the expression of ERK1/2 and anti-apoptotic protein Bcl-2 which were significantly reduced in the I/R rats. APC reduced the expression of pro-apoptotic genes, Bax and cytochrome c. These findings suggest that APC produces cardioprotective effect by preserving the expression of proteins and genes involved in anti-apoptotic pathways, regardless of the timing of administration.
Staged Improvement in Awareness of Disease for Elderly Cancer Patients in Southern China
Li, Xing,Dong, Min,Wen, Jing-Yun,Wei, Li,Ma, Xiao-Kun,Xing, Yan-Fang,Deng, Yun,Chen, Zhan-Hong,Chen, Jie,Ruan, Dan-Yun,Lin, Ze-Xiao,Wang, Tian-Tian,Wu, Dong-Hao,Liu, Xu,Hu, Hai-Tao,Lin, Jia-Yu,Li, Zhu Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.15
Background: In mainland China, awareness of disease of elderly cancer patients largely relies on the patients' families. We developed a staged procedure to improve their awareness of disease. Materials and Methods: Participants were 224 elderly cancer patients from 9 leading hospitals across Southern China. A questionnaire was given to the oncologists in charge of each patient to evaluate the interaction between family and patients, patient awareness of their disease and participation in medical decision-making. After first cycles of treatment, increased information of disease was given to patients with cooperation of the family. Then patient awareness of their disease and participation in medical decision-making was documented. Results: Among the 224 cancer elderly patients, 26 (11.6%) made decisions by themselves and 125 (55.8%) delegated their rights of decision-making to their family. Subordinate family members tended to play a passive role in decision-making significantly. Patients participating more in medical decision-making tended to know more about their disease. However, in contrast to the awareness of disease, patient awareness of violation of medical recommendations was reversely associated with their participation in medical decision-making. Improvement in awareness of diagnosis, stages and prognosis was achieved in about 20% elderly cancer patients. About 5% participated more actively in medical decision-making. Conclusions: Chinese elderly cancer patient awareness of disease and participation in medical decision-making is limited and relies on their family status. The staged procedure we developed to improve patient awareness of disease proved effective.
Wang, Chao,Xiao, Qian,Li, Yu-Wen,Zhao, Chao,Jia, Na,Li, Rui-Li,Cao, Shan-Shan,Cui, Jia,Wang, Lu,Wu, Yin,Wen, Ai-Dong Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.7
Adenocarcinoma of lung has high incidence and a poor prognosis, woith chemotherapy as the main therapeutic tool, most commonly with cisplatin. However, chemotherapy resistance develops in the majority of patients during clinic treatment. Mechanisms of resistance are complex and still unclear. Although annexin play important roles in various tumor resistance mechanisms, their actions in cisplatin-resistant lung adenocarcinoma remain unclear. Preliminary studies by our group found that in cisplatin-resistant lung cancer A549 cells and lung adenocarcinoma tissues, both mRNA and protein expression of annexins A1, A2 and A3 is increased. Using a library of annexin A1, A2 and A3 targeting combined molecules already established by ourselves we found that specific targeting decreased cisplatin-resistance. Taken together, the underlined effects of annexins A1, A2 and A3 on drug resistance and suggest molecular mechanisms in cisplatin-resistant A549 cells both in vivo and in vitro. Furthermore, the study points to improved research on occurrence and development of lung adenocarcinoma, with provision of effective targets and programmes for lung adenocarcinoma therapy in the clinic.