The novel magnetic sepiolite/Fe_(3)O_(4)/zero-valent iron(nZVI)nanocomposite(nZVI@SepH-Mag)was prepared and used to achieve the removal of Cr(VI)in this work.The nZVI@SepH-Mag composites were characterized by XRD,FTIR...The novel magnetic sepiolite/Fe_(3)O_(4)/zero-valent iron(nZVI)nanocomposite(nZVI@SepH-Mag)was prepared and used to achieve the removal of Cr(VI)in this work.The nZVI@SepH-Mag composites were characterized by XRD,FTIR,BET,SEM and TEM.The characterization results indicated that the structure of the composite consisted of small nanoscale nZVI and magnetite(Mag)particles uniformly anchoring on the surface of acid-activated sepiolite(SepH).Batch experiments were used to analyze the effects of main factors on Cr(VI)removal.A 100%removal efficiency in 60 min and enhanced reaction ratio were reached by the composite comparing other existing materials.The kinetic of the adsorption and possible Cr(VI)removal mechanism of the hybrids were also evaluated and proposed.Based on the removal products identified by Raman,XRD and XPS,a reduction mechanism was proposed.The results indicated that the SepH and Mag can inhibit the agglomeration and enhance the dispersibility of nZVI,and Mag and nZVI displayed good synergetic effects.展开更多
Background:Most mutations in the COL6A3 gene lead to collagen VI-related myopathies.This is due to a reduced expression or mislocalization of the COL6A3 protein.Therefore,studying the consequence of knocking out the C...Background:Most mutations in the COL6A3 gene lead to collagen VI-related myopathies.This is due to a reduced expression or mislocalization of the COL6A3 protein.Therefore,studying the consequence of knocking out the Col6a3 gene in mouse models is relevant,but the Col6a3 mouse models reported so far do not entirely abolish COL6A3 protein expression.Methods:Here,we present the development,validation and preliminary phenotypic characterization of a novel CRISPR-based knockout mouse model targeting Col6a3 exon 3(Col6a3^(d3/d3)).Results:In this mouse model,Col6a3 mRNA is still expressed at a similar level to wild-type littermates,although the expected protein is undetectable by mass spectrometry.Histological analysis of Col6a3^(d3/d3)quadriceps revealed an abnormally high frequency of muscle cells with internally nucleated muscle cells,consistent with a myopathy phenotype.Interestingly,Col6a3^(d3/d3)mice are smaller in size,with their fat,muscle,and bone kept proportional compared to wild-type littermates.Conclusions:In summary,we performed the validation and preliminary phenotypic characterization of a novel Col6a3 knockout mouse model that could be further characterized and used to study COL6A3 biology and model collagen VI-associated diseases.展开更多
基金Projects(52474138,52104261,52525401)supported by the National Natural Science Foundation of ChinaProject supported by the New Cornerstone Science Foundation through the XPLORER PRIZE,ChinaProject supported by the Shanxi Key Laboratory Funds of Mine Rock Strata Control and Disaster Prevention,China。
文摘The novel magnetic sepiolite/Fe_(3)O_(4)/zero-valent iron(nZVI)nanocomposite(nZVI@SepH-Mag)was prepared and used to achieve the removal of Cr(VI)in this work.The nZVI@SepH-Mag composites were characterized by XRD,FTIR,BET,SEM and TEM.The characterization results indicated that the structure of the composite consisted of small nanoscale nZVI and magnetite(Mag)particles uniformly anchoring on the surface of acid-activated sepiolite(SepH).Batch experiments were used to analyze the effects of main factors on Cr(VI)removal.A 100%removal efficiency in 60 min and enhanced reaction ratio were reached by the composite comparing other existing materials.The kinetic of the adsorption and possible Cr(VI)removal mechanism of the hybrids were also evaluated and proposed.Based on the removal products identified by Raman,XRD and XPS,a reduction mechanism was proposed.The results indicated that the SepH and Mag can inhibit the agglomeration and enhance the dispersibility of nZVI,and Mag and nZVI displayed good synergetic effects.
文摘Background:Most mutations in the COL6A3 gene lead to collagen VI-related myopathies.This is due to a reduced expression or mislocalization of the COL6A3 protein.Therefore,studying the consequence of knocking out the Col6a3 gene in mouse models is relevant,but the Col6a3 mouse models reported so far do not entirely abolish COL6A3 protein expression.Methods:Here,we present the development,validation and preliminary phenotypic characterization of a novel CRISPR-based knockout mouse model targeting Col6a3 exon 3(Col6a3^(d3/d3)).Results:In this mouse model,Col6a3 mRNA is still expressed at a similar level to wild-type littermates,although the expected protein is undetectable by mass spectrometry.Histological analysis of Col6a3^(d3/d3)quadriceps revealed an abnormally high frequency of muscle cells with internally nucleated muscle cells,consistent with a myopathy phenotype.Interestingly,Col6a3^(d3/d3)mice are smaller in size,with their fat,muscle,and bone kept proportional compared to wild-type littermates.Conclusions:In summary,we performed the validation and preliminary phenotypic characterization of a novel Col6a3 knockout mouse model that could be further characterized and used to study COL6A3 biology and model collagen VI-associated diseases.
