AIM: To investigate the killing efficiency of a recombinant plasmid containing a thymidine kinase (TK) domain insert driven by the vascular endothelial growth factor receptor 2 (VEGFR2) promoter (KDR) on vascular endo...AIM: To investigate the killing efficiency of a recombinant plasmid containing a thymidine kinase (TK) domain insert driven by the vascular endothelial growth factor receptor 2 (VEGFR2) promoter (KDR) on vascular endothelial cells.METHODS: The KDR-TK fragment was extracted from pBluescript Ⅱ KDR-TK plasmid by enzymatic digestion with Xho I and Sal I. The enhanced green fluorescence protein (EGFP) carrier was extracted from pEGFP by the same procedure. The KDR-TK was inserted into the pEGFP carrier to construct pEGFP-KDR-TK. Using ultrasound irradiation and microbubble, pEGFP-KDR-TK was transferred into human umbilical vein endothelial cells (HUVECs). The transient infection rate was estimated by green fluorescent protein (GFP) expression. Transfected HUVECs, non-transfected HUVECs, and HepG2 cells were cultured in the presence of different concentrations of ganciclovir (GCV), and the killing efficacy of HSV-TK/GCV was analyzed by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide (MTT) assay. RESULTS: The recombinant pEGFP-KDR-TK was successfully constructed by inserting the KDR-TK fragment into the pEGFP carrier. Transfected HUVECs showed cytoplasmic green fluorescence, and the transient transfection rate was about 20.3%. Pools of G418-resistant cells exhibited a higher sensitivity to theprodrug/GCV compared to non-transfected HUVECs or non-transfected HepG2 cells, respectively. CONCLUSION: KDR promoter and the suicide gene/prodrug system mediated by diagnostic ultrasound combined with microbubble can significantly kill HUVECs. Such therapy may present a novel and attractive approach to target gene therapy on tumor vessels.展开更多
Non-HFE hereditary haemochromatosis （HH） refers to a genetically heterogeneous group of iron overload disorders that are unlinked to mutations in the HFE gene. The four main types of non-HFE HH are caused by mutatio...Non-HFE hereditary haemochromatosis （HH） refers to a genetically heterogeneous group of iron overload disorders that are unlinked to mutations in the HFE gene. The four main types of non-HFE HH are caused by mutations in the hemojuvelin, hepcidin, transferrin receptor 2 and ferroportin genes. Juvenile haemochromatosis is an autosomal recessive disorder and can be caused by mutations in either hemojuvelin or hepcidin. Ar~ adult onset form of HH similar to HFE-HH is caused by homozygosity for mutations in transferrin receptor 2. The autosomal dominant iron overload disorder ferroportin disease is caused by mutations in the iron exporter ferroportin. The clinical characteristics and molecular basis of the various types of non-HFE haemochromatosis are reviewed. The study of these disorders and the molecules involved has been invaluable in improving our understanding of the mechanisms involved in the regulation of iron metabolism.展开更多
In this work,we study environment-assisted excitation energy transfer(EET) through calculating energy transfer efficiency(ETE) in LH1-RC-type and LH2-type trimers,which can be used to mimic energy transfer behaviors i...In this work,we study environment-assisted excitation energy transfer(EET) through calculating energy transfer efficiency(ETE) in LH1-RC-type and LH2-type trimers,which can be used to mimic energy transfer behaviors in the basic unit cells of LH1-RC and LH2 light-harvesting complexes.Quantum state evolution of the trimers is described by a non-Hermitian quantum master equation.ETE in these trimer systems is investigated by the use of numerical solutions at finite temperatures for the non-Hermitian master equation.We theoretically reveal the temperature-assisted ETE enhancement.It is found that highly efficient EET with nearly unit efficiency may occur in the nearby regime of the critical point of quantum phase transition.展开更多
基金supported by National Natural Science Foundation of the People’s Republic of China“On the symmetries and local properties of graphs with square-free order”(11601005)Anhui Provincial Science Fund for Excellent Young Scholars“On the symmetries of edge-primitive graphs with square-free order”(gxyq2020011).
基金New Century Distinguished Scholar Supporting Program of Ministry of Education (80000-3171404) The National Natural Science Foundation of China, No. 30300082, No. 30470467
文摘AIM: To investigate the killing efficiency of a recombinant plasmid containing a thymidine kinase (TK) domain insert driven by the vascular endothelial growth factor receptor 2 (VEGFR2) promoter (KDR) on vascular endothelial cells.METHODS: The KDR-TK fragment was extracted from pBluescript Ⅱ KDR-TK plasmid by enzymatic digestion with Xho I and Sal I. The enhanced green fluorescence protein (EGFP) carrier was extracted from pEGFP by the same procedure. The KDR-TK was inserted into the pEGFP carrier to construct pEGFP-KDR-TK. Using ultrasound irradiation and microbubble, pEGFP-KDR-TK was transferred into human umbilical vein endothelial cells (HUVECs). The transient infection rate was estimated by green fluorescent protein (GFP) expression. Transfected HUVECs, non-transfected HUVECs, and HepG2 cells were cultured in the presence of different concentrations of ganciclovir (GCV), and the killing efficacy of HSV-TK/GCV was analyzed by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide (MTT) assay. RESULTS: The recombinant pEGFP-KDR-TK was successfully constructed by inserting the KDR-TK fragment into the pEGFP carrier. Transfected HUVECs showed cytoplasmic green fluorescence, and the transient transfection rate was about 20.3%. Pools of G418-resistant cells exhibited a higher sensitivity to theprodrug/GCV compared to non-transfected HUVECs or non-transfected HepG2 cells, respectively. CONCLUSION: KDR promoter and the suicide gene/prodrug system mediated by diagnostic ultrasound combined with microbubble can significantly kill HUVECs. Such therapy may present a novel and attractive approach to target gene therapy on tumor vessels.
文摘Non-HFE hereditary haemochromatosis （HH） refers to a genetically heterogeneous group of iron overload disorders that are unlinked to mutations in the HFE gene. The four main types of non-HFE HH are caused by mutations in the hemojuvelin, hepcidin, transferrin receptor 2 and ferroportin genes. Juvenile haemochromatosis is an autosomal recessive disorder and can be caused by mutations in either hemojuvelin or hepcidin. Ar~ adult onset form of HH similar to HFE-HH is caused by homozygosity for mutations in transferrin receptor 2. The autosomal dominant iron overload disorder ferroportin disease is caused by mutations in the iron exporter ferroportin. The clinical characteristics and molecular basis of the various types of non-HFE haemochromatosis are reviewed. The study of these disorders and the molecules involved has been invaluable in improving our understanding of the mechanisms involved in the regulation of iron metabolism.
基金supported by the National Fundamental Research Program (Grant No. 2007CB925204)the National Natural Science Foundation of China (Grant Nos. 11075050 and 10775048)+1 种基金the Program for Changjiang Scholars and Innovative Research Team in University (Grant No. IRT0964)the Hunan Provincial Natural Science Foundation (Grant No. 11JJ7001)
文摘In this work,we study environment-assisted excitation energy transfer(EET) through calculating energy transfer efficiency(ETE) in LH1-RC-type and LH2-type trimers,which can be used to mimic energy transfer behaviors in the basic unit cells of LH1-RC and LH2 light-harvesting complexes.Quantum state evolution of the trimers is described by a non-Hermitian quantum master equation.ETE in these trimer systems is investigated by the use of numerical solutions at finite temperatures for the non-Hermitian master equation.We theoretically reveal the temperature-assisted ETE enhancement.It is found that highly efficient EET with nearly unit efficiency may occur in the nearby regime of the critical point of quantum phase transition.
