Networks are composed with servers and rather larger amounts of terminals and most menace of attack and virus come from terminals. Eliminating malicious code and ac cess or breaking the conditions only under witch att...Networks are composed with servers and rather larger amounts of terminals and most menace of attack and virus come from terminals. Eliminating malicious code and ac cess or breaking the conditions only under witch attack or virus can be invoked in those terminals would be the most effec tive way to protect information systems. The concept of trusted computing was first introduced into terminal virus immunity. Then a model of security domain mechanism based on trusted computing to protect computers from proposed from abstracting the general information systems. The principle of attack resistant and venture limitation of the model was demonstrated by means of mathematical analysis, and the realization of the model was proposed.展开更多
The histological hallmark of autoimmune hepatitis（AIH） is a dense portal mononuclear cell infiltrate that invades the surrounding parenchyma and comprises T and B lymphocytes,macrophages,and plasma cells.An unknown ...The histological hallmark of autoimmune hepatitis（AIH） is a dense portal mononuclear cell infiltrate that invades the surrounding parenchyma and comprises T and B lymphocytes,macrophages,and plasma cells.An unknown but powerful stimulus must be promoting the formation of this massive inflammatory cellular reaction that is likely to initiate and perpetuate liver damage.An autoimmune attack can follow different pathways to inflict damage on hepatocytes.Liver damage is likely to be orchestrated by CD4^＋ T lymphocytes recognizing an autoantigenic liver peptide.To trigger an autoimmune response,the peptide must be embraced by an HLA class Ⅱ molecule and presented to naive CD4^＋ T helper（Th0） cells by professional antigen presenting cells,with the co-stimulation of ligand-ligand fostering interaction between the two cells.Th0 cells become activated,differentiate into functional phenotypes according to the cytokines prevailing in the microenvironment and the nature of the antigen,and initiate a cascade of immune reactions determined by the cytokines produced by the activated T cells.Th1 cells,arising in the presence of the macrophage-derived interleukin（IL） -12,secrete mainly IL-2 and interferon-gamma（IFN-γ）,which activate macrophages,enhance expression of HLA classⅠ（increasing liver cell vulnerability to a CD8^＋ T cell cytotoxic attack）,and induce expression of HLA class Ⅱ molecules on hepatocytes.Th2 cells,which differentiate from Th0 if the microenvironment is rich in IL-4,produce mainly IL-4,IL-10,and IL-13 which favour autoantibody production by B lymphocytes.Physiologically,Th1 and Th2 antagonize each other.Th17 cells,a recently described population,arise in the presence of transforming growth factor beta（TGF-β） and IL-6 and appear to have an important effector role in inflammation and autoimmunity.Theprocess of autoantigen recognition is strictly controlled by regulatory mechanisms,such as those exerted by CD4^＋CD25^＋ regulatory T cells,which derive from Th0 in the presence of TGF-β,but in the absence of IL-6.If regulatory mechanisms fail,the autoimmune attack is perpetuated.Over the past three decades different aspects of the above pathogenic scenario have been investigated.In particular,a defect in immunoregulation affecting CD4^＋CD25^＋ regulatory T cells（T-regs） has been demonstrated in AIH,particularly at diagnosis or during relapse.Advances in the study of autoreactive T cells have occurred mostly in AIH type 2,since the knowledge that CYP2D6 is the main autoantigen has enabled the characterization of both CD4 and CD8 T cells targeting this cytochrome.CD4 T cells from patients with type 2 AIH positive for the predisposing HLA allele DRB10701 recognize seven regions of CYP2D6,five of which are also recognized by CD8 T cells.High numbers of IFN-γ producing CD4 T cells and CD8 T cells are associated with biochemical evidence of liver damage,suggesting a combined cellular immune attack.展开更多
The trace inverse functions Tr(λx^(-1)) over the finite field F_(2~n) are a class of very important Boolean functions and are used in many stream ciphers such as SFINKS,RAKAPOSHI,the simple counter stream cipher(SCSC...The trace inverse functions Tr(λx^(-1)) over the finite field F_(2~n) are a class of very important Boolean functions and are used in many stream ciphers such as SFINKS,RAKAPOSHI,the simple counter stream cipher(SCSC) presented by Si W and Ding C(2012),etc.In order to evaluate the security of those ciphers in resistance to(fast) algebraic attacks,the authors need to characterize algebraic properties of Tr(λx^(-1)).However,currently only some bounds on algebraic immunity of Tr(λx^(-1)) are given in the public literature,for example,the NGG upper bound and the Bayev lower bound,etc.This paper gives the exact value of the algebraic immunity of Tr(λx^(-1)) over F_(2~n),that is,AI(Tr(λx^(-1))) =[2n^(1/2)]- 2,where n ≥ 2,A ∈ F_(2~n) and λ≠ 0,which shows that Dalai's conjecture on the algebraic immunity of Tr(λx^(-1)) is correct.What is more,the authors demonstrate some weak properties of Tr(λx^(-1)) against fast algebraic attacks.展开更多
基金Supported by the National High-TechnologyResearch and Development Programof China (2002AA1Z2101)
文摘Networks are composed with servers and rather larger amounts of terminals and most menace of attack and virus come from terminals. Eliminating malicious code and ac cess or breaking the conditions only under witch attack or virus can be invoked in those terminals would be the most effec tive way to protect information systems. The concept of trusted computing was first introduced into terminal virus immunity. Then a model of security domain mechanism based on trusted computing to protect computers from proposed from abstracting the general information systems. The principle of attack resistant and venture limitation of the model was demonstrated by means of mathematical analysis, and the realization of the model was proposed.
文摘The histological hallmark of autoimmune hepatitis（AIH） is a dense portal mononuclear cell infiltrate that invades the surrounding parenchyma and comprises T and B lymphocytes,macrophages,and plasma cells.An unknown but powerful stimulus must be promoting the formation of this massive inflammatory cellular reaction that is likely to initiate and perpetuate liver damage.An autoimmune attack can follow different pathways to inflict damage on hepatocytes.Liver damage is likely to be orchestrated by CD4^＋ T lymphocytes recognizing an autoantigenic liver peptide.To trigger an autoimmune response,the peptide must be embraced by an HLA class Ⅱ molecule and presented to naive CD4^＋ T helper（Th0） cells by professional antigen presenting cells,with the co-stimulation of ligand-ligand fostering interaction between the two cells.Th0 cells become activated,differentiate into functional phenotypes according to the cytokines prevailing in the microenvironment and the nature of the antigen,and initiate a cascade of immune reactions determined by the cytokines produced by the activated T cells.Th1 cells,arising in the presence of the macrophage-derived interleukin（IL） -12,secrete mainly IL-2 and interferon-gamma（IFN-γ）,which activate macrophages,enhance expression of HLA classⅠ（increasing liver cell vulnerability to a CD8^＋ T cell cytotoxic attack）,and induce expression of HLA class Ⅱ molecules on hepatocytes.Th2 cells,which differentiate from Th0 if the microenvironment is rich in IL-4,produce mainly IL-4,IL-10,and IL-13 which favour autoantibody production by B lymphocytes.Physiologically,Th1 and Th2 antagonize each other.Th17 cells,a recently described population,arise in the presence of transforming growth factor beta（TGF-β） and IL-6 and appear to have an important effector role in inflammation and autoimmunity.Theprocess of autoantigen recognition is strictly controlled by regulatory mechanisms,such as those exerted by CD4^＋CD25^＋ regulatory T cells,which derive from Th0 in the presence of TGF-β,but in the absence of IL-6.If regulatory mechanisms fail,the autoimmune attack is perpetuated.Over the past three decades different aspects of the above pathogenic scenario have been investigated.In particular,a defect in immunoregulation affecting CD4^＋CD25^＋ regulatory T cells（T-regs） has been demonstrated in AIH,particularly at diagnosis or during relapse.Advances in the study of autoreactive T cells have occurred mostly in AIH type 2,since the knowledge that CYP2D6 is the main autoantigen has enabled the characterization of both CD4 and CD8 T cells targeting this cytochrome.CD4 T cells from patients with type 2 AIH positive for the predisposing HLA allele DRB10701 recognize seven regions of CYP2D6,five of which are also recognized by CD8 T cells.High numbers of IFN-γ producing CD4 T cells and CD8 T cells are associated with biochemical evidence of liver damage,suggesting a combined cellular immune attack.
基金supported by the National Natural Science Foundation of China under Grant No.61572491the 973 Program under Grant No.2011CB302401the open project of the SKLOIS in Institute of Information Engineering,Chinese Academy of Sciences under Grant No.2015-MS-03
文摘The trace inverse functions Tr(λx^(-1)) over the finite field F_(2~n) are a class of very important Boolean functions and are used in many stream ciphers such as SFINKS,RAKAPOSHI,the simple counter stream cipher(SCSC) presented by Si W and Ding C(2012),etc.In order to evaluate the security of those ciphers in resistance to(fast) algebraic attacks,the authors need to characterize algebraic properties of Tr(λx^(-1)).However,currently only some bounds on algebraic immunity of Tr(λx^(-1)) are given in the public literature,for example,the NGG upper bound and the Bayev lower bound,etc.This paper gives the exact value of the algebraic immunity of Tr(λx^(-1)) over F_(2~n),that is,AI(Tr(λx^(-1))) =[2n^(1/2)]- 2,where n ≥ 2,A ∈ F_(2~n) and λ≠ 0,which shows that Dalai's conjecture on the algebraic immunity of Tr(λx^(-1)) is correct.What is more,the authors demonstrate some weak properties of Tr(λx^(-1)) against fast algebraic attacks.
