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  • 1
    Electronic Resource
    Electronic Resource
    Production of tissue factor in CD14-expressing human umbilical vein endothelial cells by lipopolysaccharide (1999)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 178 (1999), S. 0 
    Details
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Production of tissue factor (TF) in response to lipopolysaccharide (LPS) was examined in human umbilical vein endothelial cells (HUVECs) transfected with human CD14 DNA. The expression of CD14 on HUVECs dramatically enhanced the production of TF at a low concentration of LPS in the absence of fetal calf serum (FCS). On the other hand, mock-transfected HUVECs did not respond to even a high concentration of LPS. TF production in CD14-expressing HUVECs was significantly inhibited by anti-CD14 monoclonal antibody. Addition of FCS to the culture of CD14-expressing HUVECs markedly augmented the LPS-induced TF production, whereas only a marginal effect was observed in mock-transfected HUVECs. The findings suggested that the integration of membrane CD14 rendered HUVECs highly sensitive to LPS in the production of TF irrespective of the presence of FCS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-6968.1999.tb08682.x
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  • 2
    Electronic Resource
    Electronic Resource
    Lipopolysaccharide induces apoptotic cell death of B memory cells and regulates B cell memory in antigen-nonspecific manner (1996)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 15 (1996), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Abstract Lipopolysaccharide (LPS) was administered into sheep red blood cells (SRBC)-primed mice, and the effect of LPS on SRBC-specific memory cells was investigated. Spleen cells from SRBC-primed mice which were injected with LPS exhibited much lower in vitro secondary plaque-forming cells (PFC) responses to SRBC than those from untreated SRBC-primed mice. The in vitro anti-SRBC response of the spleen cells to LPS was also reduced. The combination experiments of B cells and T cells from SRBC-primed mice which were injected with or without LPS demonstrated that the reduction of immune responses to SRBC after administration of LPS was caused by the defect of SRBC-specific B memory cells, but not T memory cells. B cell type rosette-forming cells (RFC) for SRBC markedly decreased after injection of LPS, while PFC as antibody-forming cells did not increase subsequently. Therefore, the reduction of RFC was not due to their differentiation into PFC. The lymphoid follicles in the spleens from mice injected with LPS were stained positively by in situ nick end labeling specific for fragmented DNA. A large percentage of Ig+ spleen cells from SRBC-primed mice which were injected with LPS was also stained positively. The injection of glucocorticoids into SRBC-primed mice induced similar reduction of B memory cells. It was suggested that LPS might induce apoptosis of B memory cells and regulate B cell memory in antigen-nonspecific manner.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1996.tb00351.x
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  • 3
    Electronic Resource
    Electronic Resource
    Anisotropy due to plastic deformation of initially isotropic mild steel and its analytical formulation
    Amsterdam : Elsevier
    Journal of the Mechanics and Physics of Solids 23 (1975), S. 277-294 
    Details
    ISSN: 0022-5096
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0022-5096(75)90029-0
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  • 4
    Electronic Resource
    Electronic Resource
    A synthetic study of (-)-dihydroedulan II and related compounds
    Amsterdam : Elsevier
    Tetrahedron 47 (1991), S. 7227-7236 
    Details
    ISSN: 0040-4020
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0040-4020(01)89725-8
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  • 5
    Electronic Resource
    Electronic Resource
    Premature apoptosis of keratinocytes and the dysregulation of keratinization in porokeratosis (2002)
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 147 (2002), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Porokeratosis is a dyskeratotic disorder of the skin characterized by cornoid lamella with parakeratosis, hyperkeratosis and loss of granular layers. The pathogenesis of porokeratosis and the mechanism(s) of its abnormal keratinization are still unknown. Objective To elucidate the mechanism(s) of abnormal keratinization that leads to the formation of cornoid lamellae in porokeratosis. Methods Apoptosis of keratinocytes was assessed in the skin of seven patients by an in situ apoptosis assay based on the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) reaction. Patterns of loricrin and involucrin expression were examined by immunohistochemistry. Results TUNEL-positive keratinocytes were observed in the epidermis underlying the cornoid lamella in all cases examined. Furthermore, loricrin expression was interrupted there, in contrast to involucrin, which was expressed diffusely in the lesional epidermis. Conclusions These results suggest that an abnormal early keratinocyte apoptosis accompanied by dysregulation of terminal differentiation of those cells may be involved in the pathogenesis of porokeratosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.2002.04853.x
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  • 6
    Electronic Resource
    Electronic Resource
    Strong adjuvant action of Klebsiella O3 lipopolysaccharide and its inhibition of systemic anaphylaxis (1995)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 10 (1995), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Abstract Immunization with lipopolysaccharide from Klebsiella O3 as an immunological adjuvant did not cause the death of mice in systemic anaphylaxis to bovine serum albumin. On the other hand, most mice immunized with lipopolysaccharide from Escherichia coli O111, Klebsiella O4 and Salmonella minnesota did die. Klebsiella O3 lipopolysaccharide enhanced IgM and IgG antibody response to BSA more markedly than Escherichia coli O111 lipopolysaccharide, while it affected the production of IgE antibody only slightly. Therefore, it is suggested that the inhibition of systemic anaphylaxis by Klebsiella O3 lipopolysaccharide adjuvant might be related to its strong adjuvant action on IgM and IgG class antibody production, and that high levels of circulating IgM and IgG antibodies might act as blocking antibodies in the development of IgE-mediated systemic anaphylaxis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1995.tb00031.x
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  • 7
    Electronic Resource
    Electronic Resource
    Expression of intercellular adhesion molecule-1 (ICAM-1) on vascular endothelial cells and renal tubular cells in the generalized Shwartzman reaction as an experimental disseminated intravascular coagulation model (1997)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 18 (1997), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The participation of adhesion molecules in systemic vascular injuries of the generalized Shwartzman reaction was studied. The generalized Shwartzman reaction was induced in mice by two consecutive injections of lipopolysaccharide. Intercellular adhesion molecule-1 (ICAM-1) was expressed on vascular endothelial cells, renal tubular cells and alveolar wall in generalized Shwartzman reaction-induced mice. The preparative injection of lipopolysaccharides induced ICAM-1 expression in those cells, and the provocative injection of lipopolysaccharides for the generalized Shwartzman reaction augmented it further. The simultaneous administration of anti-gamma interferon antibody with the preparative injection of lipopolysaccharides completely inhibited ICAM-1 expression on vascular endothelial cells. The injection of recombinant gamma interferon in replacement of lipopolysaccharides resulted in ICAM-1 expression. The administration of anti-ICAM-1 antibody together with the provocative injection of lipopolysaccharides significantly blocked the apoptosis of vascular endothelial cells in generalized Shwartzman reaction-induced mice. It was suggested that ICAM-1 expression on vascular endothelial cells might be involved in systemic vascular injuries of the generalized Shwartzman reaction, and that it might be regulated by gamma interferon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1997.tb01029.x
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  • 8
    Electronic Resource
    Electronic Resource
    Flavonoids protect mice from two types of lethal shock induced by endotoxin (2001)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 31 (2001), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The protective effect of flavonoids on two types of lethal endotoxic shock was studied. A lethal endotoxic shock was induced by administration of lipopolysaccharide (LPS) into d-galactosamine (d-GalN)-sensitized mice and another one was done by administration of a high dose of LPS into normal mice. Pretreatment with a series of flavonoids protected mice from two types of endotoxin lethality. Flavonoid pretreatment reduced the serum tumor necrosis factor-α (TNF-α) level in mice injected with d-GalN and LPS, but not in mice injected with a high dose of LPS. TNF-α-induced lethal shock in d-GalN-sensitized mice was also protected by pretreatment with flavonoids, suggesting that flavonoids augmented the resistance to TNF-α lethality. On the other hand, flavonoids reduced the plasma level of lipid peroxides in mice injected with a high dose of LPS, but not in d-GalN-sensitized mice. Taken together, these results indicated that flavonoids might protect mice from two types of endotoxin lethality. The protective mechanism of flavonoids in each endotoxin lethality is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.2001.tb01582.x
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  • 9
    Electronic Resource
    Electronic Resource
    Altered expression of constitutive type and inducible type heat shock proteins in response of d-galactosamine-sensitized mice to lipopolysaccharide as an experimental endotoxic shock model (1998)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 21 (1998), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The expression of heat shock proteins (HSPs) as stress-induced proteins was studied in mice injected with d-galactosamine (D-GalN) and lipopolysaccharide (LPS) as an experimental endotoxic shock model. The expression of constitutive type heat shock protein 70 (HSC70) was significantly reduced in livers of mice injected with d-galactosamine and lipopolysaccharide, while its expression was unaffected in livers of mice injected with d-galactosamine or lipopolysaccharide alone. The expression of other constitutive type heat shock proteins, namely HSP60, HSP32 and HSP25 was also reduced in mice injected with d-galactosamine and lipopolysaccharide. On the other hand, inducible type HSP70 was detected in livers from mice injected with d-galactosamine and lipopolysaccharide, but not in livers from mice injected with d-galactosamine or lipopolysaccharide alone. Simultaneous injection of anti-tumor necrosis factor (TNF)-α antibody prevented the liver from reduced expression of constitutive type HSC70, and lead to marked expression of inducible type HSP70 in the liver. Reduced expression of constitutive type HSC70 was also found when d-galactosamine and recombinant TNF-α was injected. Therefore, TNF-α was suggested to play a critical role on altered expression of constitutive HSC70 and inducible type HSP70 in response of d-galactosamine-sensitized mice to lipopolysaccharide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1998.tb01147.x
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  • 10
    Electronic Resource
    Electronic Resource
    Role of CD86 (B7–2) in triggering of antigen-specific IgE antibody response by lipopolysaccharide (1998)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 21 (1998), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The role of CD86 in triggering of ascaris extract-specific IgE antibody response by lipopolysaccharide was studied. The simultaneous administration of anti-CD86 antibody with ascaris extract and lipopolysaccharide prevented the production of IgE antibody response to ascaris extract. CD86+ cells were detected in peritoneal cavities and spleens of mice injected intraperitoneally with lipopolysaccharide. CD86+ cells appeared in peritoneal cavities and spleens eight hours after lipopolysaccharide injection, and they were detectable for a week. CD86+ cells in peritoneal cavities and spleens were mainly surface Ig-positive B-cells and some Ig-negative cells. It was suggested that lipopolysaccharide induced the expression of CD86 mainly on B-cells, and that CD86+ cells induced by lipopolysaccharide injection might play an important role as antigen-presenting cells on triggering of ascaris extract-specific IgE antibody response by lipopolysaccharide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1998.tb01178.x
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