磷酸盐纤维的性能和应用

这种制造水泥的方法是,可以利用工业废渣作为生料的一种组分,并且制得的熟料的化学组成与用粘土、石灰石等原料时相同,生料在窑中进行高温分解时不会释放出污染环境的有害物质。将不含金属成分的工业废渣和方解石(CaO 含量51.5%)分别磨细。

全降解玻璃纤维增强复合材料的制备及其性能

为开发高性能全降解聚乳酸复合材料,以连续磷酸盐玻璃纤维通过无捻合股与加捻合股工艺构建的无捻与有捻纱线为增强体,利用模压成型工艺制备单向纤维增强聚乳酸复合材料,并基于弯曲性能分析、扫描电子显微镜(SEM)、降解失重与pH检测等方法,表征不同纱线结构、纤维体积含量对复合材料降解过程中力学性能与降解行为的影响。研究表明:连续磷酸盐玻璃纤维纱线可有效提升复合材料的力学性能,但其弯曲强度与模量受有捻纤维结构影响分别下降22%与10%。然而,降解过程中可见复合材料的力学性能随磷酸盐玻璃纤维的降解而衰减,降解28天后磷酸盐玻璃纤维完全降解,复合材料弯曲强度与模量分别下降85%与90%。

Surface plasmon resonance analysis to evaluate the importance of heparin sulfate groups＇ binding with human aFGF and bFGF

Human acidic and basic fibroblast growth factors (aFGF and bFGF) are classic and well characterized members of the heparin binding growth factor family. Heparin is generally thought to play an extremely important role in regulating aFGF and bFGF bioactivities through its strong binding with them. In order to unravel the mechanism of the interactions between heparin and FGFs, and evaluate the importance of heparin sulfate groups' binding with FGFs, surface plasmon resonance analyses were performed using IAsys Cuvettes System. Heparin and its regioselectively desulfated derivatives were immobilized on the cuvettes. aFGF and bFGF solutions with different concentrations were pipetted into the cuvettes and the progress of the interaction was monitored in real\|time by Windows based software, yielding kinetic and equilibrium constants for these interactions. In addition, in order to reduce the delicate difference among the cuvettes, inhibition analyses of mixture of FGFs and immobilized native heparin by modified heparins were also done. The data from these two methods were similar, indicating that all sulfate groups at 2 O, 6 O and N in heparin were required for the binding to aFGF; and that their contribution to the binding was in the order 2 O, N and 6 O sulfate group. In contrast, definite contribution of the 6 O sulfate group to the binding with bFGF was most apparent, while the other two sulfate groups appeared to be necessary in the order 2 O and N sulfate group. These methods established here can be used for analysing the effect of sulfate groups in heparin on the binding with other human FGF members or other heparin binding proteins.

TypeⅠinositol 1, 4, 5-triphosphate receptors increase in kidney of mice with fulminant hepatic failure

AIM： To delineate the mechanisms of renal vasoconstriction in hepatorenal syndrome （HRS）, we investigated the expression of type I inositol 1, 4, 5-triphosphate receptors （IP3R I） of kidney in mice with fulminant hepatic failure （FHF）. METHODS： FHF was induced by lipopolysaccharide （LPS） in D-galactosamine （GAIN） sensitized BALB/c mice. There were 20 mice in normal saline （NS）-treated group, 20 mice in LPS-treated group, 20 mice in GaIN- treated group, and 60 mice in GalN/LPS-treated group （FHF group）. Liver and kidney tissues were obtained at 2, 6, and 9 h after administration. The liver and kidney specimens were stained with hematoxylin-eosin for studying morphological changes under light microscope. The expression of IP3R I in kidney tissue was tested by immunohistochemistry, Western blot and reverse transcription （RT）-PCR. RESULTS： Kidney tissues were morphologically normal at all time points in all groups. IP3R I proteins were found localized in the plasma region of glomerular mesangial cells （GMC） and vascular smooth muscle cells （VSMC） in kidney by immunohistochemical staining. In kidney of mice with FHF at 6 h and 9 h IP3R I staining was upregulated. Results from Western blot demonstrated consistent and significant increment of IP3R I expression in mice with FHF at 6 h and 9 h （t = 3.16, P 〈 0.05; t = 5.43, P 〈 0.01）. Furthermore, we evaluated IP3R I mRNA expression by RT-PCR and observed marked upregulation of IP3R I mRNA in FHF samples at 2 h, 6 h and 9 h compared to controls （t = 2.97, P 〈 0.05; t = 4.42, P 〈 0.01; t = 3.81, P 〈 0.01）. CONCLUSION： The expression of IP3R I protein increased in GMC and renal VSMC of mice with FHF, possibly caused by up-regulation of IP3R I mRNA.