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Mice, immunodeficient

Kino, T., Inamura, N., Nakahara, K., Kiyoto, S., Goto, T., Terano, H., Kohsaka, M., Aoki, H., and Imanaka, H. (1985). Studies of an immunomodulator, swainsonine. II. Effect of swainsonine on mouse immunodeficient system and experimental murine tumor. J. [Pg.147]

Similarly, under certain disease conditions, altered NA innervation and/or AR signaling capacity impairs sympathetic communication with cells of the immune system, influencing disease progression. Altered catecholamine communication with the immune system is evident in autoimmune diseases such as arthritis and multiple sclerosis [5-7] and in infectious diseases, such as leprosy and a mouse model of acquired immunodeficiency syndrome [15, 43, 44], The impact of altered NA innervation of... [Pg.498]

Jackobsen H, Yasargil K, Winslow JC, Craig JC, Krohn A, Duncan IB, Mous J. Characterization of human immunodeficiency virus type 1 mutants with decreased sensitivity to proteinase inhibitor RO 31-8959. Virology, 1995 206 527-534. [Pg.39]

The beta phase clearance kinetics of human IgG and therapeutic antibodies is typically monophasic and abides to a log-linear relationship of serum concentration with time after administration. However, in rare cases we have found that certain administered mAbs are immunogenic to the mouse and elicit mouse-anti-human antibodies. In this case, there is a bi-phasic kinetic, typically appearing at days 5-6 after antibody administration and resulting in a precipitous antibody loss. This complication can be overcome by the use of immunodeficient hFcRn transgenic mice, described in Section 3.7. [Pg.102]

Previous attempts to measure immune function of human cells following PBMC engraftment of immunodeficient mice have been met with limited success (34). The lack of a vigorous primary immune response mediated by human PBMC engrafted into earlier humanized mouse models was associated with host murine NK cell activity and other innate immune function as well as an overwhelming xenogeneic GVHD response of the... [Pg.113]

Banuelos, S. J. Shultz, L. D., Greiner, D. L., Burzenski, L. M., Gott, B., Lyons, B. L., Rossini, A. A. and Appel, M. C. (2004). Rejection of human islets and human HLA-A2.1 transgenic mouse islets by alloreac-tive human lymphocytes in immunodeficient NOD-rcz d and NOD-Raff I nuU Prfl nuU mice. Clin. Immunol. 112 273-283. [Pg.118]

Nickoloff, B. J. (2000) The search for pathogenic T cells and the genetic basis of psoriasis using a severe combined immunodeficient mouse model. Cutis 65, 110-114. [Pg.211]

This immunodeficient nude mouse was originally thought to be a BALB/c congenic. It was later determined that it was not inbred and is maintained as an outbred. It is expected that other strains of Nu/Nu mice could be used for this model (12). [Pg.250]

Uckun EM. Severe combined immunodeficient mouse models of human leukemia. Blood 1996 88 1135-46. [Pg.461]

Nakaoke R, Ryerse JS, Niwa M, Banks WA (2005) Human immunodeficiency virus type 1 ti ansport across tire in viti o mouse brain endotlrelial cell monolayer. Exp Neurol 193 101—109. [Pg.40]

Mous, J., Heimer, E. P., and Le Grice, S. F.(1988). Processing protease and reverse transcriptase from human immunodeficiency virus type I polyprotein in Escherichia coli. J. Virol. 62, 1433-1436. [Pg.653]

Myasaka M, Kobayashi T, Kumazawa Y Yamamoto N (1997) Primary human immunodeficiency virus type 1 viremia and central nervous system invasion in a novel hu-PBL-immunodeficient mouse strain. J Virol 71 2417-2424. [Pg.39]


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