硫系玻璃具有独特的红外光学性能和极高的光学非线性等特点,使得硫系光纤成为中红外超连续谱产生的优选材料。基于二次挤压法制备了单模As-S光纤,并利用飞秒脉冲和光参量放大器作为泵浦源研究了该光纤的中红外超连续谱的产生特性,包括...硫系玻璃具有独特的红外光学性能和极高的光学非线性等特点,使得硫系光纤成为中红外超连续谱产生的优选材料。基于二次挤压法制备了单模As-S光纤,并利用飞秒脉冲和光参量放大器作为泵浦源研究了该光纤的中红外超连续谱的产生特性,包括光纤长度、泵浦波长、泵浦功率对超连续谱产生的影响。结果表明该单模光纤具有较低的传输损耗和较小的材料色散分布;相比于传统零色散点波长附近泵浦,在正常色散区且杂质吸收峰附近泵浦也可获得脉冲的极大展宽(泵浦参数:4.5μm,1 k Hz,150 fs,光纤长度23 cm,输出谱宽为1.5~8.7μm@60 d B带宽);较短长度的硫系光纤便可产生超宽频谱输出,相反,光纤长度越长输出频谱越窄且平坦性变差。展开更多
Background:Vasculogenic mimicry(VM)is a novel tumor blood supply in some highly aggressive malignant tumors.Recently,we reported VM existed in gallbladder carcinomas(GBCs)and the formation of the special passage throu...Background:Vasculogenic mimicry(VM)is a novel tumor blood supply in some highly aggressive malignant tumors.Recently,we reported VM existed in gallbladder carcinomas(GBCs)and the formation of the special passage through the activation of the PI3K/MMPs/Ln-5γ2 signaling pathway.GBC is a highly aggressive malignant tumor with disappointing treatments and a poor prognosis.Norcantharidin(NCTD)has shown to have multiple antitumor activities against GBCs,etc;however the exact mechanism is not thoroughly elucidated.In this study,we firstly investigated the anti-VM activity of NCTD as a VM inhibitor for GBCs and its underlying mechanisms.Methods:In vitro and in vivo experiments to determine the effects of NCTD on proliferation,invasion,migration,VM formation,hemodynamic and tumor growth of GBC-SD cells and xenografts were respectively done by proliferation,invasion,migration assays,HE staining and CD31-PAS double staining,optic/electron microscopy,tumor assay,and dynamic microMRA.Further,immunohistochemistry,immunofluorescence,Western blotting and RT-PCR were respectively used to examine expression of VM signaling-related markers PI3-K,MMP-2,MT1-MMP and Ln-5γ2 in GBC-SD cells and xenografts in vitro and in vivo.Results:After treatment with NCTD,proliferation,invasion,migration of GBC-SD cells were inhibited;GBC-SD cells and xenografts were unable to form VM-like structures;tumor center-VM region of the xenografts exhibited a decreased signal in intensity;then cell or xenograft growth was inhibited.Whereas all of untreated GBC-SD cells and xenografts formed VM-like structures with the same conditions;the xenograft center-VM region exhibited a gradually increased signal;and facilitated cell or xenograft growth(Figure 1-6).Furthermore,expression of MMP-2 and MT1-MMP products from sections/supernates of 3-D matrices and the xenografts,and expression of PI3-K,MMP-2,MM1-MMP and Ln-5γ2 proteins/mRNAs of the xenografts were all decreased in NCTD or TIMP-2 group(Figure 7-10;all P<0.01,vs.control group);NCTD down-regulated expression of these VM signaling-related markers in vitro and in vivo.Conclusions:NCTD inhibited tumor growth and VM formation of human gallbladder carcinoma GBC-SD cells and xenografts by suppression of the PI3-K/MMPs/Ln-5γ2 signaling pathway.It is firstly concluded that NCTD may be a potential anti-VM agent for human GBCs.展开更多
文摘硫系玻璃具有独特的红外光学性能和极高的光学非线性等特点,使得硫系光纤成为中红外超连续谱产生的优选材料。基于二次挤压法制备了单模As-S光纤,并利用飞秒脉冲和光参量放大器作为泵浦源研究了该光纤的中红外超连续谱的产生特性,包括光纤长度、泵浦波长、泵浦功率对超连续谱产生的影响。结果表明该单模光纤具有较低的传输损耗和较小的材料色散分布;相比于传统零色散点波长附近泵浦,在正常色散区且杂质吸收峰附近泵浦也可获得脉冲的极大展宽(泵浦参数:4.5μm,1 k Hz,150 fs,光纤长度23 cm,输出谱宽为1.5~8.7μm@60 d B带宽);较短长度的硫系光纤便可产生超宽频谱输出,相反,光纤长度越长输出频谱越窄且平坦性变差。
文摘Background:Vasculogenic mimicry(VM)is a novel tumor blood supply in some highly aggressive malignant tumors.Recently,we reported VM existed in gallbladder carcinomas(GBCs)and the formation of the special passage through the activation of the PI3K/MMPs/Ln-5γ2 signaling pathway.GBC is a highly aggressive malignant tumor with disappointing treatments and a poor prognosis.Norcantharidin(NCTD)has shown to have multiple antitumor activities against GBCs,etc;however the exact mechanism is not thoroughly elucidated.In this study,we firstly investigated the anti-VM activity of NCTD as a VM inhibitor for GBCs and its underlying mechanisms.Methods:In vitro and in vivo experiments to determine the effects of NCTD on proliferation,invasion,migration,VM formation,hemodynamic and tumor growth of GBC-SD cells and xenografts were respectively done by proliferation,invasion,migration assays,HE staining and CD31-PAS double staining,optic/electron microscopy,tumor assay,and dynamic microMRA.Further,immunohistochemistry,immunofluorescence,Western blotting and RT-PCR were respectively used to examine expression of VM signaling-related markers PI3-K,MMP-2,MT1-MMP and Ln-5γ2 in GBC-SD cells and xenografts in vitro and in vivo.Results:After treatment with NCTD,proliferation,invasion,migration of GBC-SD cells were inhibited;GBC-SD cells and xenografts were unable to form VM-like structures;tumor center-VM region of the xenografts exhibited a decreased signal in intensity;then cell or xenograft growth was inhibited.Whereas all of untreated GBC-SD cells and xenografts formed VM-like structures with the same conditions;the xenograft center-VM region exhibited a gradually increased signal;and facilitated cell or xenograft growth(Figure 1-6).Furthermore,expression of MMP-2 and MT1-MMP products from sections/supernates of 3-D matrices and the xenografts,and expression of PI3-K,MMP-2,MM1-MMP and Ln-5γ2 proteins/mRNAs of the xenografts were all decreased in NCTD or TIMP-2 group(Figure 7-10;all P<0.01,vs.control group);NCTD down-regulated expression of these VM signaling-related markers in vitro and in vivo.Conclusions:NCTD inhibited tumor growth and VM formation of human gallbladder carcinoma GBC-SD cells and xenografts by suppression of the PI3-K/MMPs/Ln-5γ2 signaling pathway.It is firstly concluded that NCTD may be a potential anti-VM agent for human GBCs.
