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Yue Li,WanWan Li,Minhua Fang,XiaoLin Yao,Chao Chen,Miao Shui,Jie Shu,Yuanlong Ren 한국물리학회 2017 Current Applied Physics Vol.17 No.8
Zn1-xCoxO (0 x 0.15) anode material was prepared by an easy polyacrylamide assisted sol-gel route. The successful replacement of Zinc by Cobalt within Cobalt content x 0.09 was confirmed by structural characterization. The introduction of Cobalt element greatly improved the electro-chemical performances of the matrix Zinc oxide. Without carbon coating, at the 20th cycle, Zn0.91Co0.09O anode still preserved a capacity a little bit more than 1000 mA h g1 and a capacity more than 600 mA h g1 was retained at the end of the 50th cycle. Better rate capability was also witnessed. The SEM, EIS at OCV, CV and in situ XRD were further carried out to elucidate the lithiation mechanism. The role Cobalt doping played can be summarized as follows: the stabilization of the Li2Zn phase, the minimization of charge transfer resistance and the enhanced reversibility of the reduction from metal oxide to metal.
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Clinicopathological Features of Low-Grade Thyroid-like Nasopharyngeal Papillary Adenocarcinoma
Minhua Li,Jiangguo Wei,Xiaofei Yao,Cheng Wang 대한암학회 2017 Cancer Research and Treatment Vol.49 No.1
Purpose Primary low-grade thyroid-like papillary adenocarcinomas are extremely rare neoplasms that generally originate in the nasopharynx. Here, we describe a novel case of a 15-year-old Chinese girl who was diagnosed with low-grade thyroid-like papillary adenocarcinoma, including a brief review of the literature to reveal the clinicopathological features of lowgrade thyroid-like nasopharyngeal papillary adenocarcinoma. Materials and Methods Immunohistochemistry was used to evaluate the expression of pan-cytokeratin (CKpan), cytokeratin (CK) 7, thyroid transcription factor 1 (TTF-1), vimentin, epithelial membrane antigen (EMA), thyroglobulin, CD15, S100, P40, CK20, CDX-2, glial fibrillary acidic protein (GFAP), and Ki-67. Additionally, in situ hybridization investigation was utilized to identify the presence of small Epstein-Barr virus (EBV)–encoded RNA. Results Histopathological analysis revealed florid proliferation of papillary structures lined by columnar epithelial cells with fibrovascular cores. Immunohistochemically, the neoplastic cells were positive for CKpan, CK7, TTF-1, vimentin, and EMA, but negative for thyroglobulin, CD15, S100, P40, CK20, CDX-2, and GFAP. The Ki-67–labeling index reached 5% in the most concentrated spot. In situ hybridization for EBV was negative. Conclusion Due to the distinct rarity of low-grade thyroid-like papillary adenocarcinomas with a favorable clinical outcome, a nationwide effort to raise public awareness of this neoplasm is required.
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Huang Jingyan,Huang Siyun,Li Jinhong,Li Minhua,Gong Lin,Li Tongshun,Gu Lian 한국유전학회 2022 Genes & Genomics Vol.44 No.4
Background: Calmodulin 1 (CALM1) mutations are involved in the development of coronary artery disease (CAD). However, the relationship of CALM1 rs3179089 polymorphism with CAD is unknown. Objective: This study aimed to identify the relationship of CALM1 rs3179089 polymorphism with CAD susceptibility, CALM1 expression, blood pressure, blood glucose, blood coagulation and serum lipid levels of CAD patients. Methods: 550 CAD patients and 550 control subjects were genotyped for CALM1 using Sequenom MassARRAY technology. CALM1 expression level was measured by quantitative real time polymerase chain reaction (qRT-PCR). Results: CALM1 mRNA expression was higher in CAD patients than that in control subjects (P < 0.001). CAD patients with CC genotype had higher CALM1 mRNA expression level than control subjects with CC genotype (P = 0.006). Genotypic frequency of rs3179089 was different between male patients of CAD and control subjects (P = 0.045). Rs3179089 polymorphism was related to CAD risk of males in recessive model (P = 0.039). Moreover, rs3179089 polymorphism was associated with systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting plasma glucose (FPG), and D-Dimer (D-D) level of patients with CAD in recessive model (P = 0.013 for SBP; P = 0.034 for DBP; P = 0.004 for FPG; P = 0.046 for D-D). In addition, rs3179089 polymorphism was correlated with low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) serum levels of patients with CAD in both addictive (P = 0.025 for LDL-C; P = 0.001 for TC) and recessive models (P = 0.001 for LDL-C; P = 0.001 for TC). Conclusion: CALM1 expression is associated with development of CAD. CALM1 rs3179089 polymorphism affects CAD susceptibility in males, and blood pressure, blood glucose, blood coagulation and serum lipid of CAD patients.
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Potential Antitumor Activity of SIM-89 in Non-Small Cell Lung Cancer Cells
Jun Pei,Baohui Han,Tianqing Chu,Minhua Shao,Jiajun Teng,Huifang Sha,Aiqing Gu,Rong Li,Jialin Qian,Weifeng Mao,Ying Li 연세대학교의과대학 2017 Yonsei medical journal Vol.58 No.3
Purpose: c-Met and its ligand, hepatocyte growth factor (HGF), play a critical role in oncogenesis and metastatic progression. The aim of this study was to identify inhibited enzymogram and to test the antitumor activity of SIM-89 (a c-Met receptor tyrosine kinaseinhibitor) in non-small cell lung cancer. Materials and Methods: Z’-LYTE kinase assay was employed to screen the kinase enzymogram, and mechanism of action (MOA) analysis was used to identify the inhibited kinases. Cell proliferation was then analyzed by CCK8 assay, and cell migration was determinedby transwell assay. The gene expression and the phosphorylation of c-Met were examined by realtime-PCR and western blotting, respectively. Finally, the secretion of HGF was detected by ELISA assay. Results: c-Met, activated protein kinase (AMPK), and tyrosine kinase A (TRKA) were inhibited by SIM-89 with the IC50 values of 297 nmol/L, 1.31 μmol/L, and 150.2 nmol/L, respectively. SIM-89 exerted adenosine triphosphate (ATP) competitive inhibition on c-Met. Moreover, the expressions of STAT1, JAK1, and c-Met in H460 cells were decreased by SIM-89 treatment, and c-Met phosphorylationwas suppressed in A549, H441, H1299, and B16F10 cells by the treatment. In addition, SIM-89 treatment significantly decreased the level of HGF, which accounted for the activation of c-Met receptor tyrosine kinase. Finally, we showed cell proliferationinhibition and cell migration suppression in H460 and H1299 cells after SIM-89 treatment. Conclusion: In conclusion, SIM-89 inhibits tumor cell proliferation, migration and HGF autocrine, suggesting it’s potential antitumoractivity.
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