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Cells deficient

The in vivo relevance and biological importance of in vitro observations about mast cell function, as well as the contributions of mast cells towards the expression of particular biological responses (such as various models of anaphylaxis) in vivo, can be assessed using c-kit mutant mice (e.g., WBB6Fi-FCit or mice) that virtually lack mast cell populations. Mice with mutations of c-kit [6,11] or mutations that affect KIT expression [12-14] have other abnormalities of phenotype besides a mast cell deficiency. However, the mast cell deficiency of these mice can be selectively repaired by the adoptive transfer of genetically compatible, in vitro-derived... [Pg.46]

Kitamura Y, Go S, Hatanaka K Decrease of mast cells in W/W" mice and their increase by bone marrow transplantation. Blood 1978 52 447-452. Grimbaldeston MA, Chen CC. Piliponsky AM, Tsai M. Tam SY, Galh SJ Mast cell-deficient W-sash c-kit mutant mice as a model for investigating... [Pg.63]

Nigrovic PA, Gray DH. Jones T. Hallgren J, Kuo EC, Chaletzky B, Gurish M. Mathis D. Benoist C, Lee DM genetic inversion in mast cell-deficient W mice interrupts Cortn and manifests as hematopoietic and cardiac aberrancy. Am J Pathol 2008 173 1693-16701. [Pg.63]

Wolters PJ, Mallen-St Clair J, Lewis CC, Villalta SA, 27 Baluk P, Erie DJ, Caughey GH Tissue-selective mast cell reconstitution and differential lung gene expression in mast cell-deficient sash mice. [Pg.64]

Jacoby W Cammarata PV, Findlay S, Pincus SH Anaphylaxis in mast cell-deficient mice. J Invest Dermatol 1984 83 302-304. [Pg.96]

Arimura A, Nagata M, Takeuchi M, Watanabe A, Nakamura K, Harada M Active and passive cutaneous anaphylaxis in WBB6F1 mouse, a mast cell-deficient strain. Immunol Invest 1990 19 227-233. [Pg.96]

Numerous lectins have been purified and are commercially available three plant lectins that have been widely used experimentally are listed in Table 47-7. Among many uses, lectins have been employed to purify specific glycoproteins, as tools for probing the glycoprotein profiles of cell surfaces, and as reagents for generating mutant cells deficient in certain enzymes involved in the biosynthesis of oligosaccharide chains. [Pg.518]

Crowle, P.K. and Reed, N.D. (1981) Rejection of the parasite Nippostrongylus brasiliensis by mast cell deficient W/Wv anaemic mice. Infection and Immunity 33, 54-58. [Pg.367]

Infection of W/W mast-cell-deficient mice with T. muris showed that although mast cells were not important for protection they appeared to be important for the generation of the Th2 responses (Koyama and I to, 2000). [Pg.389]

Fig. 18.3. Burdens of adult T. spiralis and development of intestinal pathology in mast-cell-deficient N/W mice. W/W mice and their normal littermates were infected with 400 T. spiralis muscle larvae. (A) Adult worm burdens are represented as mean + sem, five mice per group (, significantly different from day 6 p.i., P< 0.05). (B) Crypt and villus lengths were measured at day 0 and day 13 p.i. Results are expressed as mean + sem for five mice per group (, significantly different from uninfected animals (day 0), P< 0.05). Unpublished data. Fig. 18.3. Burdens of adult T. spiralis and development of intestinal pathology in mast-cell-deficient N/W mice. W/W mice and their normal littermates were infected with 400 T. spiralis muscle larvae. (A) Adult worm burdens are represented as mean + sem, five mice per group (, significantly different from day 6 p.i., P< 0.05). (B) Crypt and villus lengths were measured at day 0 and day 13 p.i. Results are expressed as mean + sem for five mice per group (, significantly different from uninfected animals (day 0), P< 0.05). Unpublished data.
B-cell deficient mice are resistant to intraperitoneal inoculation with prions probably because of their involvement with FDC maturation and maintenance. The interface between FDCs and sympathetic nerves represents a critical site for the transfer of lymphoid prions into the nervous system however, the mechanism by which this is achieved remains unknown. Distinct forms of prion disease show differences in lymphoreticular involvement that may be related to the etiology of the disease or to divergent properties of distinct prion strains. For a review of prion disease peripheral pathogenesis see [18]. [Pg.795]

T-cell-deficient mice do not lose bone after OVX (Cenci et al. 2000). [Pg.179]

Orange, J.S., Human natural killer cell deficiencies and susceptibility to infection, Microbes Infect., 4, 1545, 2002. [Pg.45]

Dziedzic, D. and White, H.J., Response of T-cell-deficient mice to ozone exposure, J. Toxicol. Environ. Health. 21, 1-2, 57, 1987. [Pg.322]

Boyer O, Saadoun D, Abriol J, Dodille M, Piette JC, Cacoub P, Klatzmann D CD4+CD25+ regulatory T-cell deficiency in patients with hepatitis C-mixed cryoglobulinemia vasculitis. Blood 2004 103 3428-3430. [Pg.38]

Ghosh AK, Hirasawa N, Ohtsu H, Watanabe T, Ohuchi K Defective angiogenesis in the inflammatory granulation tissue in histidine decarboxylase-deficient mice but not in mast cell-deficient mice. J Exp Med 2002 195 973-982. [Pg.80]

Tnfrsfll RANK Deletion in exon 8 Osteopetrosis without osteoclasts unknown Deficiency of lymph nodes, T and B cell deficiency... [Pg.90]

Kandell and Bernstein published one of the earliest reports to suggest that bile acids also demonstrate DNA-damaging effects in eukaryotic cells. They showed that human foreskin fibroblasts underwent unscheduled DNA synthesis (indicating DNA repair), as measured by tritiated thymidine incorporation when cells were treated with increasing concentrations of sodium deoxycholate or chenodeoxycholate. Utilising mutant Chinese hamster ovary cells deficient in strand rejoining (EM9), the authors were able to demonstrate that the repair of deoxycholate-induced DNA damage was dependent on strand break repair capacity. [Pg.75]


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See also in sourсe #XX -- [ Pg.298 , Pg.299 , Pg.303 , Pg.304 ]




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Anemias blood cell deficiencies causing

Blood cell deficiencies, anemias

Blood cell deficiencies, anemias caused

Hereditary Hemolytic Anemia Associated with Red Blood Cell Enzyme Deficiency

Hereditary Nonhemolytic Disorders Associated with Red Blood Cell Enzyme Deficiency

Intestinal goblet cells, vitamin A deficiency mucosal cell proliferation

Thiamine neuronal cell death, deficiency

Vitamin deficient cells

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