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- 저자 : Xiaoling Qu (검색결과 2 건)
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Xiaoling Qu,Guangyuan Zhou,Rui Wang,Haiyan Zhang,Zhipeng Wang,Min Jiang,Jun Tang 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.99 No.-
In pursuit of poly(ethylene 2,5-furandicarboxylate) PEF materials with high molecular weight,satisfactory appearance and faster crystallization rate, its preparation from dimethyl furan-2,5-dicarboxylate (DMFD) with ethylene glycol (EG) in the trace presence of metal zinc was performed viatransesterification method. Optimization of the main polymerization parameters enabled Zn-catalyzedPEF to gain high molecular weight (Mn, 5.40 104 g mol 1) and low content of diethylene glycolfurandicarboxylate unit (DEGF, 2.91%). On the basis of experimental phenomena and high performanceliquid chromatography (HPLC), the actual catalytic active species of metal zinc in the polymerization wasspeculated to be a salt of 2, 5-furandicarboxylate derivative (Zn(II)). The in-stiu catalyst can efficaciouslyinhibit the influence of by-product FDCA on the color of PEF, which displayed quite better appearance(close to white). Differential Scanning Calorimetry (DSC) showed that the in-stiu catalytic system acted asnucleating agent (NA) and the crystallization half-time (t1/2) of PEFs-Zn was only 1/4 of that of PEF-tin. Additionally, series of high molecular weight furan-based polyesters from DMFD and diols with differentmethylene (3, 5, 6 and 8) were obtained by zinc powder as in-stiu catalyst, which further evidenced it tobe efficiency and universality.
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Abrin Induces HeLa Cell Apoptosis by Cytochrome c Release and Caspase Activation
Qu, Xiaoling,Qing, Liuting Korean Society for Biochemistry and Molecular Biol 2004 Journal of biochemistry and molecular biology Vol.37 No.4
We identified apoptosis as being a significant mechanism of toxicity following the exposure of HeLa cell cultures to abrin holotoxin, which is in addition to its inhibition of protein biosynthesis by N-glycosidase activity. The treatment of HeLa cell cultures with abrin resulted in apoptotic cell death, as characterized by morphological and biochemical changes, i.e., cell shrinkage, internucleosomal DNA fragmentation, the occurrence of hypodiploid DNA, chromatin condensation, nuclear breakdown, DNA single strand breaks by TUNEL assay, and phosphatidylserine (PS) externalization. This apoptotic cell death was accompanied by caspase-9 and caspase-3 activation, as indicated by the cleavage of caspase substrates, which was preceded by mitochondrial cytochrome c release. The broad-spectrum caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk), prevented abrin-triggered caspase activation and partially abolished apoptotic cell death, but did not affect mitochondrial cytochrome c release. These results suggest that the release of mitochondrial cytochrome c, and the sequential caspase-9 and caspase-3 activations are important events in the signal transduction pathway of abrin-induced apoptotic cell death in the HeLa cell line.
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