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( Wan Xing Yong ),( Xu Cheng Fu ),( Lu Chao ),( Yu Wei Lai ),( Zhu Hua Tuo ),( Yu Chao Hui ),( Li You Ming ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Serum uric acid is strongly associated with nonalcoholic fatty liver disease (NAFLD) and insulin resistance in patients. However, whether this association is causally or coincidentally with NAFLD and insulin resistance remains uncertain, neither the mechanisms behind this association are unclear so far. Methods: We first analyzed the impact of uric acid on development of hepatic steatosis in mice and two cell models (HepG2 and HL7702), and then explored the effect of uric acid on insulin signaling, including phosphorylation of insulin receptor substrate 1 (IRS1) and Akt in HepG2 and HL7702 cells. Further, we studied the role of NLRP3 inflammasome in regulation of hepatic steatosis and insulin signaling. Results: Uric acid directly induced hepatocyte fat accumulation both in vivo and in vitro. Further, uric acid treatment decreased insulin-induced phospho-Akt (ser437) and enhanced the phospho-IRS1(ser307) in HepG2 and HL7702 cells. Then, we found significant increases of NLRP3 inflammasome-related molecules, both mRNA and protein levels, including NLPR3, caspase-1, IL-1ß, and IL-18, in HepG2 and HL7702 cells stimulated with uric acid. We also found that uric acid induced significant elevations of IL-1ß and IL-18 levels in culture supernatants of HepG2 and HL7702 cells. Consistent with in vitro results, mice fed 8 weeks of hyperuricemia-inducing diet resulted in significant up-regulation of hepatic mRNA and protein expressions of NLPR3, caspase-1, IL-1ß and IL-18, and elevation of serum IL-1ß and IL-18 levels. Further experiments indicated that silencing NLRP3 expression significantly alleviated uric acid-induced fat accumulation in vitro. Moreover, inhibition of NLRP3 expression ameliorated uric acid induced insulin signaling impairing, confirmed by increased insulin- induced phospho-Akt (ser437) and reduced the phospho-IRS1(ser307) in vitro. Conclusions: Our results suggest that uric acid contributes to hepatic steatosis and impairs insulin signaling through the NLRP3 inflammasome dependent mechanism.
A Mixed Co-clustering Algorithm Based on Information Bottleneck
Yongli Liu,Tianyi Duan,Xing Wan,Hao Chao 한국정보처리학회 2017 Journal of information processing systems Vol.13 No.6
Fuzzy co-clustering is sensitive to noise data. To overcome this noise sensitivity defect, possibilistic clusteringrelaxes the constraints in FCM-type fuzzy (co-)clustering. In this paper, we introduce a new possibilistic fuzzyco-clustering algorithm based on information bottleneck (ibPFCC). This algorithm combines fuzzy coclusteringand possibilistic clustering, and formulates an objective function which includes a distance functionthat employs information bottleneck theory to measure the distance between feature data point and featurecluster centroid. Many experiments were conducted on three datasets and one artificial dataset. Experimentalresults show that ibPFCC is better than such prominent fuzzy (co-)clustering algorithms as FCM, FCCM,RFCC and FCCI, in terms of accuracy and robustness.
( Xing Ai Gao ),( Wan Taek Ju ),( Yong Feng Zhang ),( Rong De Jin ),( Si Yan Liu ),( Ro Dong Park ) 한국키틴키토산학회 2012 한국키틴키토산학회지 Vol.17 No.1
A chitosanase-producing bacterium, Bacillus cereus D-11, was isolated from an environmental soil sample. The optimal culture condition for chitosanase production by B. cereus D-11 was 3 days of cultivation at 30 o C in a medium composed of 0.5% inoculation concentration (1.4×10 8 CFU/mL), 0.7% colloidal chitosan, 1% yeast extract and 1% NaCl at initial pH 7.0. The highest activity achieved was 7.8 U/mL. The crude enzyme preparation from Bacillus cereus D-11 degraded the chitooligomers pentamer, hexamer, and heptamer into (GlcN)2-4, but not degraded the chitooligomers less than (GlcN)4. These results indicate that B. cereus D-11 chitosanase cleaves the oligomeric chains in the endo-splitting manner and the catalytic domain of D-11 chitosanase recognizes and needs at least 5 glucosamine units for hydrolytic catalysis of the glycosidic linkages.
A Mixed Co-clustering Algorithm Based on Information Bottleneck
Liu, Yongli,Duan, Tianyi,Wan, Xing,Chao, Hao Korea Information Processing Society 2017 Journal of information processing systems Vol.13 No.6
Fuzzy co-clustering is sensitive to noise data. To overcome this noise sensitivity defect, possibilistic clustering relaxes the constraints in FCM-type fuzzy (co-)clustering. In this paper, we introduce a new possibilistic fuzzy co-clustering algorithm based on information bottleneck (ibPFCC). This algorithm combines fuzzy co-clustering and possibilistic clustering, and formulates an objective function which includes a distance function that employs information bottleneck theory to measure the distance between feature data point and feature cluster centroid. Many experiments were conducted on three datasets and one artificial dataset. Experimental results show that ibPFCC is better than such prominent fuzzy (co-)clustering algorithms as FCM, FCCM, RFCC and FCCI, in terms of accuracy and robustness.
Na Han,Xing-xiang Zhang,Wan-yong Yu,Xi-yin Gao 한국고분자학회 2010 Macromolecular Research Vol.18 No.11
A series of 85/15 AN/MA copolymers (acrylonitrile-methyl acrylate copolymers with feed ratio of 85/15 mol%) were synthesized by aqueous precipitation polymerization at 20, 30, and 40 oC, and the copolymers were used to produce a series of fibers by melt spinning. The copolymers and fibers were characterized by element analysis (EA), nuclear magnetic resonance (1H NMR and 13C NMR), capillary rheometry, differential scanning calorimetry (DSC), X-ray diffraction (XRD), and scanning electronic microscopy (SEM). The average length of the contiguous AN units synthesized at 30 oC had a maximum value of 10.53. Aqueous polymerization at 30 oC resulted the lowest glass transition temperature (Tg) of 87.1 oC, the lowest melting point (Tm) of 154.5 oC,and the highest decomposition temperature (Td) of 325.0 oC. 85/15 AN/MA prepared at 20 and 30 oC exhibited a better fluidity at 210 oC. The ideal reaction temperatures for melt processing of the AN/MA copolymers were found to be 20 and 30 oC.
( Jie Xia Ding ),( Meng Li ),( Xing Yong Wan ),( Xi Jin ),( Shao Hua Chen ),( Chao Hui Yu ),( You Ming Li ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: The mechanisms of pathogenesis underlying nonalcoholic fatty liver disease (NAFLD) remain unclear at present and the depth study of HADHA in the development of NAFLD has never been investigated. Methods: The NAFLD cell model was established by treating L02 cells with free fatty acid (FFA) overload. Small interfering RNA (siRNA) was used to knock down HADHA level. The expression of HADHA and key enzymes associated with fatty acid beta- oxidation in L02 cells were determined by q-PCR. Key protein associated in energy metabolism, endoplasmic reticulum(ER) stress and infl ammatory were determined by western blotting. ATP, hydroperoxide (H2O2), catalase (CAT) and mitochondrial membrane potential (MMP) were measured. The prediction of HADHA upstream regulation of miRNA was carried out and luciferase reporter assays were implemented to validate the prediction. Results: After culturing L02 cells by FFA for 48h, we detect the increased protein level of HADHA. HADHA knockdown in L02 cells resulted in an increased of lipid accumulation and downregulation of gene expression involved in fatty acid beta-oxidation, including PPARa, ACOX1, CPT2, EHHADH, ECHS1, HADHB and HADH. Additionally, administering HADHA siRNA exhibited improvement of oxidative stress, embodied in decreased level of H2O2 and MDA, meanwhile, increased levels of ATP, CAT and MMP. Furthermore, HADHA knockdown demonstrated weakened AMPK pathway, activation of MAPK and MKK3 pathway, and improve ER stress by downregulation of C/EBPa and C/EBPß. Moreover, HADHA was regulated directly by upstream gene of miR-124. Conclusions: Our results show that HADHA may plays a role of double-edged sword in hepatic steatosis and cell injury in NAFLD, and provide a new insight into the pathogenic mechanisms of NAFLD, may becoming a potential new therapeutic target for NAFLD.