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Yang Jiashu,Zhang Ming,Yang Dawei,Ma Yunfei,Tang Yuting,Xing Mengying,Li Lingyun,Chen Li,Jin Yucui,Ma Changyan 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
Long noncoding RNAs (lncRNAs) have emerged as important regulators of osteoarthritis (OA), but the biological roles and clinical significance of most lncRNAs in OA are not fully understood. Microarray analysis was performed to identify differentially expressed lncRNAs, mRNAs, and miRNAs between normal and osteoarthritic cartilage. We found that AC008440.5 (abbreviated AC008), as well as AQP1 and ANKH, were highly expressed in osteoarthritic cartilage, whereas miR-328-3p was expressed at a low level in osteoarthritic cartilage. Functional assays showed that ectopic expression of AC008, AQP1, and ANKH significantly decreased chondrocyte viability and promoted chondrocyte apoptosis and extracellular matrix (ECM) degradation, whereas knockdown of AC008, AQP1, and ANKH resulted in the opposite effects. Moreover, miR-328-3p overexpression increased chondrocyte viability and attenuated chondrocyte apoptosis and ECM degradation, whereas inhibition of miR-328-3p resulted in the opposite effects. Bioinformatics analysis, RNA immunoprecipitation (RIP), and luciferase assays revealed that AC008 functioned as a competing endogenous RNA (ceRNA) to regulate miR-328-3p, which specifically targeted the AQP1 and ANKH genes. In addition, miR-328-3p significantly ameliorated MIA-induced OA, whereas AC008 accelerated OA progression in vivo. Furthermore, fat mass and obesity-associated (FTO)-mediated N6-methyladenosine demethylation downregulated AC008 transcription, while lower FTO expression led to upregulation of AC008 transcription in OA. In conclusion, our data reveal that AC008 plays a critical role in OA pathogenesis via the miR-328-3p‒AQP1/ANKH pathway, suggesting that AC008 may be a potential therapeutic target for OA.
Huanhuan Sun,Haiqing Ma,Guangyao He,Jiashu Chen,Pengxin Qiu,Guangmei Yan 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.7
FIa, a factor X activator, was isolated from the venom of Daboia russellii siamensis (Myanmar) after a series of chromatographic separations. FIa displayed procoagulant activity by shortening plasma recalcification time and converted human factor X (FX) to activated human factor X (FXa) by cleaving the heavy FX chain, possibly at the Arg51-Ile52 peptide. FIa was positive in a glycoprotein staining test, demonstrating that it is a glycoprotein. Optimal temperature and pH values were important for FIa procoagulant activity. Procoagulant activity was maintained above 85% of the initial activity at pH 7.0~8.0, and showed equally maximum activity at temperatures ranging from 30 to 50oC. In addition, FIa procoagulant activity was completely inhibited by EDTA (5 mM), but not by PMSF (10 mM), suggesting that it is a metalloproteinase.
The Correlation between Thyrotropin and Dyslipidemia in a Population-based Study
Li Lu,Beibei Wang,Zhongyan Shan,Fengwei Jiang,Xiaochun Teng,Yanyan Chen,Yaxin Lai,Jiani Wang,Haibo Xue,Sen Wang,Chenyan Li,He Liu,Ningna Li,Jiashu Yu,Liangfeng Shi,Xin Hou,Qian Xing,Xue Bai,Weiping Te 대한의학회 2011 Journal of Korean medical science Vol.26 No.2
This study investigated the relationship between serum thyrotrophin levels and dyslipidemia in subclinical hypothyroid and euthyroid subjects. A total of 110 subjects with subclinical hypothyroidism and 1,240 euthyroid subjects enrolled in this study. Patients with subclinical hypothyroidism had significantly lower high density lipoprotein cholesterol (HDL-C) levels than those who were euthyroid. The lipid profiles were each categorized and mean thyrotrophin levels were higher in subjects in the dyslipidemia subclasses than subjects in the normal subclasses. Thyrotrophin was positively associated with serum triglyceride and negatively associated with serum HDL-C in women. Thyrotrophin was also positively associated with total cholesterol (TC) in the overweight population along with TC and LDL-C in overweight women. In the euthyroid population, thyrotrophin was positively associated with TC in the overweight population. In conclusion, serum thyrotrophin was correlated with dyslipidemia in subclinical hypothyroid and euthyroid subjects; the correlation was independent of insulin sensitivity.