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Articles by Jia Li
Total Records ( 6 ) for Jia Li
  Jianguo Zhao and Jia Li
  This study selects the top ten heavily held by stock of National Social Security Funds (NSSF) as the research samples, then uses the VAR model and stress tests to analyze the macroeconomic factors of NSSF and the investment security. The results show that short-term effects of the price factors, the money supply and fixed asset investment are more significant but the mechanism is different significantly. And the interest rate is once again proved that the impact is not significant. The constructed of three macroeconomic scenarios of extreme stress test studies in this study have shown the social security fund to pay equity portfolio will have a certain risk. These conclusions will contribute to improve the investment income of NSSF and reduce the affects of adverse systemic risk of macroeconomic factors, which will provide an important theoretical and empirical basis.
  Jia Li , Ya-Guang Chen and Chun-Jing Zhang
  Two supramolecular compounds based on tungstoferrate [FeW12O40]5-, [FeII(2,2’-bipy)3]2[HFeW12O40] · 5H2O (1), and [Hpy]2[4,4’-H2bipy]6(H3O)[FeW12O40]3 · 11H2O (2) (py = pyridine, bipy = bipyridine) were synthesized hydrothermally and characterized structurally. The hydrogen bonds between polyoxoanions and water and the edge-to-face π-π interaction between [FeII(2,2’-bipy)3]2+ with a shortest C-C distance of 3.513 Å are the main forces to construct the 3-D architecture of 1. In 2, a 3-D supramolecular architecture is assembled by the tungstoferrate anions, protonated 4,4’-bipy cations, and water through hydrogen bonding. The variable-temperature magnetic susceptibilities indicate that 1 is paramagnetic with μeff corresponding to one Fe(III) with spin-only contribution, showing that Fe in the coordination cations has a +II oxidation number and low spin state.
  Ze-Hou Liu , Yong Zhou , Jia Li , Yu-Jiao Liu and Ya-Xi Liu
  Alpha-amylase enzyme is the important member in physiological metabolism of high plant, especially during seed germination stage. The current study identified 19 amy1 genes from 19 hexaploid wheat (Triticum aestivum L.) accessions. The nucleotide and deduced amino acid sequences of amy1 genes were analyzed in detail, respectively. It showed that two main variation types were characterized due to the base substitution and/or indel mutations in genomic nucleotide sequences and the exon and intron domains were presented different variation degree. This study identified 8 clustered haplotypes from hexaploid wheat accessions through characterization of exon domains. The haplotype 8 was the major variation types and the others were low relative frequency. The haplotype 7 was a special kind of haplotypes among amy1 genes in wheat accession PI243793 because of the variation of amino acid sequences at 155-161 sites. These results would contribute to the understanding in functional aspects and efficient utilization of amy1 genes in hexaploid wheat cultivars.
  Yi Zang , Li-Fang Yu , Tao Pang , Lei-Ping Fang , Xu Feng , Tie-Qiao Wen , Fa-Jun Nan , Lin-Yin Feng and Jia Li
  Neural stem cell differentiation and the determination of lineage decision between neuronal and glial fates have important implications in the study of developmental, pathological, and regenerative processes. Although small molecule chemicals with the ability to control neural stem cell fate are considered extremely useful tools in this field, few were reported. AICAR is an adenosine analog and extensively used to activate AMP-activated protein kinase (AMPK), a metabolic "fuel gauge" of the biological system. In the present study, we found an unrecognized astrogliogenic activity of AICAR on not only immortalized neural stem cell line C17.2 (C17.2-NSC), but also primary neural stem cells (NSCs) derived from post-natal (P0) rat hippocampus (P0-NSC) and embryonic day 14 (E14) rat embryonic cortex (E14-NSC). However, another AMPK activator, Metformin, did not alter either the C17.2-NSC or E14-NSC undifferentiated state although both Metformin and AICAR can activate the AMPK pathway in NSC. Furthermore, overexpression of dominant-negative mutants of AMPK in C17.2-NSC was unable to block the gliogenic effects of AICAR. We also found AICAR could activate the Janus kinase (JAK) STAT3 pathway in both C17.2-NSC and E14-NSC but Metformin fails. JAK inhibitor I abolished the gliogenic effects of AICAR. Taken together, these results suggest that the astroglial differentiation effect of AICAR on neural stem cells was acting independently of AMPK and that the JAK-STAT3 pathway is essential for the gliogenic effect of AICAR.
  Tao Pang , Zhen-Shan Zhang , Min Gu , Bei-Ying Qiu , Li-Fang Yu , Peng-Rong Cao , Wei Shao , Ming-Bo Su , Jing-Ya Li , Fa-Jun Nan and Jia Li
  AMP-activated protein kinase (AMPK) serves as an energy sensor and is considered a promising drug target for treatment of type II diabetes and obesity. A previous report has shown that mammalian AMPK α1 catalytic subunit including autoinhibitory domain was inactive. To test the hypothesis that small molecules can activate AMPK through antagonizing the autoinhibition in α subunits, we screened a chemical library with inactive human α1394 (α1, residues 1-394) and found a novel small-molecule activator, PT1, which dose-dependently activated AMPK α1394, α1335, α2398, and even heterotrimer α1β1γ1. Based on PT1-docked AMPK α1 subunit structure model and different mutations, we found PT1 might interact with Glu-96 and Lys-156 residues near the autoinhibitory domain and directly relieve autoinhibition. Further studies using L6 myotubes showed that the phosphorylation of AMPK and its downstream substrate, acetyl-CoA carboxylase, were dose-dependently and time-dependently increased by PT1 with-out an increase in cellular AMP:ATP ratio. Moreover, in HeLa cells deficient in LKB1, PT1 enhanced AMPK phosphorylation, which can be inhibited by the calcium/calmodulin-dependent protein kinase kinases inhibitor STO-609 and AMPK inhibitor compound C. PT1 also lowered hepatic lipid content in a dose-dependent manner through AMPK activation in HepG2 cells, and this effect was diminished by compound C. Taken together, these data indicate that this small-molecule activator may directly activate AMPK via antagonizing the autoinhibition in vitro and in cells. This compound highlights the effort to discover novel AMPK activators and can be a useful tool for elucidating the mechanism responsible for conformational change and autoinhibitory regulation of AMPK.
  Jun- Qing Du , Jian Wu , Hua- Jie Zhang , Ya- Hui Zhang , Bei- Ying Qiu , Fang Wu , Yi-Hua Chen , Jing- Ya Li , Fa -Jun Nan , Jian -Ping Ding and Jia Li
  Caspase-3 is an attractive therapeutic target for treatment of diseases involving disregulated apoptosis. We report here the mechanism of caspase-3 inactivation by isoquinoline-1,3,4-trione derivatives. Kinetic analysis indicates the compounds can irreversibly inactivate caspase-3 in a 1,4-dithiothreitol (DTT)- and oxygen-dependent manner, implying that a redox cycle might take place in the inactivation process. Reactive oxygen species detection experiments using a chemical indicator, together with electron spin resonance measurement, suggest that ROS can be generated by reaction of isoquinoline-1,3,4-trione derivatives with DTT. Oxygen-free radical scavenger catalase and superoxide dismutase eliciting the inactivation of caspase-3 by the inhibitors confirm that ROS mediates the inactivation process. Crystal structures of caspase-3 in complexes with isoquinoline-1,3,4-trione derivatives show that the catalytic cysteine is oxidized to sulfonic acid (-SO3H) and isoquinoline-1,3,4-trione derivatives are bound at the dimer interface of caspase-3. Further mutagenesis study shows that the binding of the inhibitors with caspase-3 appears to be nonspecific. Isoquinoline-1,3,4-trione derivative-catalyzed caspase-3 inactivation could also be observed when DTT is substituted with dihydrolipoic acid, which exists widely in cells and might play an important role in the in vivo inactivation process in which the inhibitors inactivate caspase-3 in cells and then prevent the cells from apoptosis. These results provide valuable information for further development of small molecular inhibitors against caspase-3 or other oxidation-sensitive proteins.
 
 
 
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