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Complete conversion of cellulose to water soluble substances by pretreatment with ionic liquids
Weina Liu,Weize Wu,Yucui Hou,Shuhang Ren,Wenhua Wang 한국화학공학회 2012 Korean Journal of Chemical Engineering Vol.29 No.10
Pretreatment of cellulose to water soluble substances (WSS) can enhance its efficient conversion in water solvent, such as ethanol fermentation. In this work, we found ionic liquid (IL), 1-methyl-3-methylimidazolium dimethylphosphate ([Mmim][DMP]), could convert efficiently cellulose to obtain WSS, and the product WSS and IL mixture could be separated by ethanol anti-solvent way. Effects of ILs, time, temperature and water on cellulose conversion were investigated. NMR, FTIR, XRD and SEM were employed to study the mechanism of cellulose conversion with ILs. The results indicate that [Mmim][DMP] has a greater ability to interact with cellulose than [Bmim][Cl] under the same conditions. Cellulose can be completely converted into WSS in [Mmim][DMP] under all the investigated temperatures from 140 to 160 oC. Increasing temperature is beneficial to the conversion rate of cellulose. But the presence of water can decrease the conversion rate of cellulose. During the treatment by [Mmim][DMP], the hydroxyls of cellulose can form hydrogen bonds with both anion and cation of [Mmim][DMP], and after the treatment the inter- and intramolecular hydrogen bonds of cellulose and the compact structure of cellulose are collapsed.
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Illuminating the hepatotoxic mechanism of norcantharidin in rats using metabolomics analysis
Cheng Weina,Chen Qihong,Wang Xiaoning,Liu Liu,Li Xiaofei,Duan Cancan,Zhang Jianyong 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.3
Norcantharidin (NCTD) has multiple antitumor effects. However, NCTD can induce significant hepatotoxicity and the mechanism of hepatotoxicity is not clear for now.This study aimed to explore the hepatotoxicity of NCTD in rat by ultra-performance liquid chromatography (UPLC) quadrupole time-of-flight (Q-TOF)-MS (UPLC/Q-TOF-MS) metabolomics.Serum biochemical indices including alanine aminotransferase (ALT) and total bilirubin (T-BIL) were significantly increased. Histopathological and ultrastructure results revealed that hepatocytes were damaged. Furthermore, the metabolomics results showed that 11 metabolites in serum and 8 metabolites in liver were differential metabolites for NCTD hepatotoxicity. Four metabolic pathways including the sphingolipid metabolism, purine metabolism, arachidonic acid metabolism, and glycerophospholipid metabolism were the key metabolic pathways related to NCTD hepatotoxicity.The metabolomics analysis in this study reveal new clues on the hepatotoxicity mechanism of NCTD in rats. These findings have potential applications in the toxicity study of NCTD.
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A Metadata-based Method for Sharing Multiply Heterogeneous Information
Xiaotao Li,Xiaohui Hu,Weina Lu,Xi Liu 보안공학연구지원센터 2015 International Journal of Database Theory and Appli Vol.8 No.3
As users’ requirements for information integration enhance increasingly, how to integrate multiply heterogeneous data in a global sharing system has especially been a challenge for its large scale and diverse formats. To address the above problem, this paper proposes an information sharing approach for multiply heterogeneous data based on a two-layer metadata. Firstly, the architecture of the two-layer metadata is introduced. Secondly, the synchronization between different users for distributed heterogeneous data is realized by sharing table structures. Finally, Lucene search engine combined with the element GM-description of the two-layer metadata is presented to retrieve metadata, which reduces the response time compared to other retrieval methods. The experiment results illustrate the effectiveness of our approach and the conclusion is given.
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Inhibition of mouse SP2/0 myeloma cell growth by the B7-H4 protein vaccine
( Nan Mu ),( Nannan Liu ),( Qiang Hao ),( Yujin Xu ),( Jialin Li ),( Weina Li ),( Shouzhen Wu ),( Cun Zhang ),( Haichuan Su ) 생화학분자생물학회 2014 BMB Reports Vol.47 No.7
B7-H4 is a member of B7 family of co-inhibitory molecules and B7-H4 protein is found to be overexpressed in many human cancers and which is usually associated with poor survival. In this study, we developed a therapeutic vaccine made from a fusion protein composed of a tetanus toxoid (TT) T-helper cell epitope and human B7-H4IgV domain (TT-rhB7-H4IgV). We investigated the anti-tumor effect of the TT-rhB7-H4IgV vaccine in BALB/c mice and SP2/0 myeloma growth was significantly suppressed in mice. The TT-rhB7-H4IgV vaccine induced high-titer specific antibodies in mice. Further, the antibodies induced by TT-rhB7-H4IgV vaccine were capable of depleting SP2/0 cells through complement-dependent cytotoxicity (CDC) in vitro. On the other hand, the poor cellular immune response was irrelevant to the therapeutic efficacy. These results indicate that the recombinant TT-rhB7-H4IgV vaccine might be a useful candidate of immunotherapy for the treatment of some tumors associated with abnormal expression of B7-H4. [BMB Reports 2014; 47(7): 399-404]
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Peng Chen,Dengming Zhou,Yongsheng Liu,Ping Wang,Weina Wang 대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.2
Myocardial infarction promotes cardiac remodeling and myocardial fibrosis, thus leading to cardiac dysfunction or heart failure. Peiminine has been regarded as a traditional anti-fibrotic Chinese medicine in pulmonary fibrosis. However, the role of peiminine in myocardial infarction-induced myocardial injury and fibrosis remained elusive. Firstly, rat model of myocardial infarction was established using ligation of the left coronary artery, which were then intraperitoneally injected with 2 or 5 mg/kg peiminine once a day for 4 weeks. Echocardiography and haemodynamic evaluation results showed that peiminine treatment reduced left ventricular end-diastolic pressure, and enhanced maximum rate of increase/decrease of left ventricle pressure (± dP/dt max) and left ventricular systolic pressure, which ameliorate the cardiac function. Secondly, myocardial infarction-induced myocardial injury and infarct size were also attenuated by peiminine. Moreover, peiminine inhibited myocardial infarction-induced increase of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α production, as well as the myocardial cell apoptosis, in the rats. Thirdly, peiminine also decreased the myocardial fibrosis related protein expression including collagen I and collagen III. Lastly, peiminine reduced the expression of p38 and phosphorylation of extracellular signal-regulated kinase 1/2 in rat model of myocardial infarction. In conclusion, peiminine has a cardioprotective effect against myocardial infarction-induced myocardial injury and fibrosis, which can be attributed to the inactivation of mitogen-activated protein kinase pathway.
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