OBJECTIVE Compound Kushen injection(CKI)is a bis-herbal formulation extracted from Kushen(Radix Sophorae Flavescentis)and Baituling(Rhizoma Heterosmilacis Japonicae).Clinically,it is used as the adjuvant treatment of ...OBJECTIVE Compound Kushen injection(CKI)is a bis-herbal formulation extracted from Kushen(Radix Sophorae Flavescentis)and Baituling(Rhizoma Heterosmilacis Japonicae).Clinically,it is used as the adjuvant treatment of cancer.However,with the increased application,the cases of immediate hypersensitivity reactions(IHRs)also gradually rise.In this study,we investigated the underlying mechanism(s)and active constituent(s)for CKI-induced IHRs in experimental models.METHODS T helper 2(Th2)immunity-amplified mice were prepared by aluminum adjuvant.Anaphylactic shock was detected by measuring rectal thermometry in propranolol pretreated mice.For evaluating microvascular permeability,Evans blue extravasation assay was used.Platelet-activating factor(PAF),serum total IgE(tIgE)and mouse mast cell protease 1(MMCP1)were measured by ELISA.RESULTS The obtained results showed that CKI did not elevate serum tIgE and MMCP1 after consecutive immunization for five weeks,but could induce Evans blue extravasation(local)and cause obvious hypothermia(systemic)after a single injection.Further study showed that alkaloids in Kushen,especially matrine,were responsible for CKI-induced IHRs.Mechanism study showed that various PAF receptor antagonists could significantly counter CKI-induced IHRs locally or systemically.In cell system,CKI was able to promote PAF production in a non-cell-selective manner.In cell lysate,the effect of CKI on PAF production became stronger and could be abolished by blocking de novo pathway.CONCLUSION In conclusion,our study identifies,for the first time,that CKI is a PAF inducer.It causes non-immunologic IHRs,rather than IgE-dependent IHRs,by promoting PAF production through de novo pathway.Alkaloids in Kushen,especially matrine,are the prime culprits for IHRs.Our findings may provide a potential approach for preventing and treating CKI-induced IHRs.展开更多
The frequency band between 5 010 MHz and 5 030 MHz allocated as C band has been used as a candidate in the global navigation satellite systems (GNSS) along with more and more naviga- tion services in L band. The pot...The frequency band between 5 010 MHz and 5 030 MHz allocated as C band has been used as a candidate in the global navigation satellite systems (GNSS) along with more and more naviga- tion services in L band. The potential benefits and technical requirements of C band for satellite navi- gation have been analyzed before. However the degradation of effective carrier-power-to-noise densi- ty ratio( A (C/No )eu) based on code tracking spectral sensitivity coefficient( CT_SSC ) as a compati- bility assessment methodology for potential GNSS radio frequency compatibility in C-Band has not been discussed clearly. So the compatibility of the signals in the C band between BeiDou (BD) B1 C and GPS L1C, L1C/A, Galileo E1Os as the interoperability or classical signals in L band is analyzed. Simulation results reveal the interference degree between BD III B1C and GPS L1C/A, L1C, Galileo E1OS. The results can also reveal that the multiplexed binary offset carrier (MBOC) and binary phase shift keying (BPSK) modulation is not appropriate for C band.展开更多
目的:探讨便秘型肠易激综合征(C-IBS)大鼠模型对直肠球囊扩张的内脏敏感性改变和脊髓背角5-羟色胺(5-HT)、c-fos的分布和异常表达.方法:C-IBS大鼠模型组应用冰水ig方法建立(A组,n=10),和正常对照大鼠(B组,n=10).所有大鼠给予直肠内球囊...目的:探讨便秘型肠易激综合征(C-IBS)大鼠模型对直肠球囊扩张的内脏敏感性改变和脊髓背角5-羟色胺(5-HT)、c-fos的分布和异常表达.方法:C-IBS大鼠模型组应用冰水ig方法建立(A组,n=10),和正常对照大鼠(B组,n=10).所有大鼠给予直肠内球囊扩张,检测球囊扩张引起腹部收缩反射的最小容量阈值及球囊不同容量扩张时腹部收缩反射的次数.腰骶段脊髓背角5-HT和c-fos表达应用免疫组织化学染色及计算机图像分析系统半定量进行分析.结果:直肠内球囊扩张时,A组引起腹部收缩的最小容量阈值略高于B组,无明显统计学差并(0.59±0.09 vs 0.57±0.13,P>0.05).直肠球囊扩张体积1.0mL时A组腹部收缩反射次数低于B组(10.3±3.3 vs 18.3±5.5,P<0.05);体积1.5和2.0mL高容量扩张时两组无明显差异(P>0.05).A组腰骶段脊髓背角5-HT、c-fos阳性神经组织的面积均明显高于B组(5-HT面积:146.5±15.1 vs 109.3±18.5;5-HT OD:45826±2563.2 vs 29358±8965.5:c-fos面积:125.4±23.3 vs 88.7±23.2;c-fos OD:46258±4642 vs 33238±4587;均P<0.05).结论:C-IBS大鼠模型存在对直肠球囊扩张的内脏敏感性异常,脊髓背角5-HT、c-fos的异常表达可能参与C-IBS大鼠内脏敏感性异常的调节.展开更多
文摘OBJECTIVE Compound Kushen injection(CKI)is a bis-herbal formulation extracted from Kushen(Radix Sophorae Flavescentis)and Baituling(Rhizoma Heterosmilacis Japonicae).Clinically,it is used as the adjuvant treatment of cancer.However,with the increased application,the cases of immediate hypersensitivity reactions(IHRs)also gradually rise.In this study,we investigated the underlying mechanism(s)and active constituent(s)for CKI-induced IHRs in experimental models.METHODS T helper 2(Th2)immunity-amplified mice were prepared by aluminum adjuvant.Anaphylactic shock was detected by measuring rectal thermometry in propranolol pretreated mice.For evaluating microvascular permeability,Evans blue extravasation assay was used.Platelet-activating factor(PAF),serum total IgE(tIgE)and mouse mast cell protease 1(MMCP1)were measured by ELISA.RESULTS The obtained results showed that CKI did not elevate serum tIgE and MMCP1 after consecutive immunization for five weeks,but could induce Evans blue extravasation(local)and cause obvious hypothermia(systemic)after a single injection.Further study showed that alkaloids in Kushen,especially matrine,were responsible for CKI-induced IHRs.Mechanism study showed that various PAF receptor antagonists could significantly counter CKI-induced IHRs locally or systemically.In cell system,CKI was able to promote PAF production in a non-cell-selective manner.In cell lysate,the effect of CKI on PAF production became stronger and could be abolished by blocking de novo pathway.CONCLUSION In conclusion,our study identifies,for the first time,that CKI is a PAF inducer.It causes non-immunologic IHRs,rather than IgE-dependent IHRs,by promoting PAF production through de novo pathway.Alkaloids in Kushen,especially matrine,are the prime culprits for IHRs.Our findings may provide a potential approach for preventing and treating CKI-induced IHRs.
基金Supported by the National High Technology Research and Development Program of China(863Program)(2011AA120502)
文摘The frequency band between 5 010 MHz and 5 030 MHz allocated as C band has been used as a candidate in the global navigation satellite systems (GNSS) along with more and more naviga- tion services in L band. The potential benefits and technical requirements of C band for satellite navi- gation have been analyzed before. However the degradation of effective carrier-power-to-noise densi- ty ratio( A (C/No )eu) based on code tracking spectral sensitivity coefficient( CT_SSC ) as a compati- bility assessment methodology for potential GNSS radio frequency compatibility in C-Band has not been discussed clearly. So the compatibility of the signals in the C band between BeiDou (BD) B1 C and GPS L1C, L1C/A, Galileo E1Os as the interoperability or classical signals in L band is analyzed. Simulation results reveal the interference degree between BD III B1C and GPS L1C/A, L1C, Galileo E1OS. The results can also reveal that the multiplexed binary offset carrier (MBOC) and binary phase shift keying (BPSK) modulation is not appropriate for C band.
文摘目的:探讨便秘型肠易激综合征(C-IBS)大鼠模型对直肠球囊扩张的内脏敏感性改变和脊髓背角5-羟色胺(5-HT)、c-fos的分布和异常表达.方法:C-IBS大鼠模型组应用冰水ig方法建立(A组,n=10),和正常对照大鼠(B组,n=10).所有大鼠给予直肠内球囊扩张,检测球囊扩张引起腹部收缩反射的最小容量阈值及球囊不同容量扩张时腹部收缩反射的次数.腰骶段脊髓背角5-HT和c-fos表达应用免疫组织化学染色及计算机图像分析系统半定量进行分析.结果:直肠内球囊扩张时,A组引起腹部收缩的最小容量阈值略高于B组,无明显统计学差并(0.59±0.09 vs 0.57±0.13,P>0.05).直肠球囊扩张体积1.0mL时A组腹部收缩反射次数低于B组(10.3±3.3 vs 18.3±5.5,P<0.05);体积1.5和2.0mL高容量扩张时两组无明显差异(P>0.05).A组腰骶段脊髓背角5-HT、c-fos阳性神经组织的面积均明显高于B组(5-HT面积:146.5±15.1 vs 109.3±18.5;5-HT OD:45826±2563.2 vs 29358±8965.5:c-fos面积:125.4±23.3 vs 88.7±23.2;c-fos OD:46258±4642 vs 33238±4587;均P<0.05).结论:C-IBS大鼠模型存在对直肠球囊扩张的内脏敏感性异常,脊髓背角5-HT、c-fos的异常表达可能参与C-IBS大鼠内脏敏感性异常的调节.