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Cell provoked

Dearman, R.J. et al., Inducible interleukin-4-secreting cells provoked in mice during chemical sensitization. Immunology, 81, 551, 1994. [Pg.604]

There is conflicting evidence concerning the mutagenicity of 1,2-dimethylhydrazine to bacteria. In a single study, it induced recombination in Saccharomyces cerevisiae. In vitro, 1,2-dimcthylhydrazine formed DNA adducts in human bronchial cells, provoked unscheduled DNA synthesis in rat hepatocytes and induced gene mutation in mammalian cells. It gave positive results in rodents in microbial host-mediated assays. [Pg.975]

Percupo CM, Hooks JJ, Sliinohai a T, Caspi R (1990) Detiick B Cytokine-mediated acdvadon of a neui onal rednal resident cell provokes andgen presentadon. J Immunol 145 4101 107. [Pg.57]

Decreased free cholesterol in the cell provokes cleavage of SREBP from its tether (cholesteryl esters do not influence the activation of SREBF). [Pg.368]

Effect on ROS-mediated events Leucocyte adhesion to endothelial cells provoked by oxLDL FO Hamster Reference (38)... [Pg.76]

Figure 8.2. Liposome-cell interaction. Drug-loaded liposomes can adsorb on the cell surface specifically (1) or non-specifically (2). Liposome can also fuse with the cell membrane releasing its contents inside cell cytoplasm (3). It can also be destabilized by certain cell membrane components when adsorbed on the surface so that the released drug can enter cell via micropinocytosis (4). Liposome can undergo the direct or transfer protein-mediated exchange of lipid components with the cell membrane (5). It can also be subjected to a specific or non-specific endocytosis (6). In this case, a liposome can be delivered by the endosome into the lyso-some (6a) or, on the route to lysosome, liposome can provoke endosome destabilization, which results in drug liberation into the cell cytoplasm (6b). Drug-loaded Upxjsome modified with certain viral components can specifically interact with cells, provoke endocytosis, and, via the interaction of viral components with the irmer membrane of the endosome, allow for the drug efflux into the cell cytoplasm (7). Figure 8.2. Liposome-cell interaction. Drug-loaded liposomes can adsorb on the cell surface specifically (1) or non-specifically (2). Liposome can also fuse with the cell membrane releasing its contents inside cell cytoplasm (3). It can also be destabilized by certain cell membrane components when adsorbed on the surface so that the released drug can enter cell via micropinocytosis (4). Liposome can undergo the direct or transfer protein-mediated exchange of lipid components with the cell membrane (5). It can also be subjected to a specific or non-specific endocytosis (6). In this case, a liposome can be delivered by the endosome into the lyso-some (6a) or, on the route to lysosome, liposome can provoke endosome destabilization, which results in drug liberation into the cell cytoplasm (6b). Drug-loaded Upxjsome modified with certain viral components can specifically interact with cells, provoke endocytosis, and, via the interaction of viral components with the irmer membrane of the endosome, allow for the drug efflux into the cell cytoplasm (7).
Non-solvent processes have been developed in answer to the high cost of large-scale solvent extraction. Holmes and Lim [61] described the enzymatic process used at Zeneca for the recovery of PHB and PHBV. First, a high-temperature (100 to 150 °C) treatment of the cells provokes cell lysis and denaturation of nucleic acids, which could otherwise interfere with the subsequent steps. Non-PHA biomass is then solubilized with proteolytic enzymes (pepsin, trypsin, papain, others, and mixtures thereof) and anionic surfactants. Concentration of PHA by centrifugation is finally followed by bleaching with H2O2. [Pg.279]

The viruses responsible for AIDS are human immunodeficiency virus 1 and 2 (HIV 1 and HIV 2) Both are retroviruses, meaning that their genetic material is RNA rather than DNA HI Vs require a host cell to reproduce and the hosts m humans are the T4 lymphocytes which are the cells primarily responsible for inducing the immune system to respond when provoked The HIV penetrates the cell wall of a T4 lymphocyte and deposits both its RNA and an enzyme called reverse transcriptase inside There the reverse transcriptase catalyzes the formation of a DNA strand that is complementary to the viral RNA The transcribed DNA then serves as the template from which the host lymphocyte produces copies of the virus which then leave the host to infect other T4 cells In the course of HIV reproduction the ability of the T4 lymphocyte to reproduce Itself IS compromised As the number of T4 cells decrease so does the body s ability to combat infections... [Pg.1179]

Mansueto et al. suggested that the susceptibility of embryos to toxicants could be first related to their interaction with egg membrane where they could provoke changes of permeability, of transmembrane potential, and of receptors distribution which could in turn drastically interfere with normal cell physiology. Cima et al. observed that TBT alters, immediately after the entry of... [Pg.421]

A molecular variation of plasma membrane has been reported by Puccia et al. Reduction of total lipids (XL) content and significant variations of triglyceride (TG) and phospholipids (PL) fractions were observed as a consequence of exposure of C. intestinalis ovaries to TBTCl solutions. In particular, an evident TG decrease and a PL increase were observed, which probably provoked an increment in membrane fluidity, because of the high concentration of long chain fatty acids and, as a consequence, PL. This could be a cell-adaptive standing mechanism toward the pollutants, as observed in Saccharomyces cerevisiae. Also the increase in the content of the polyunsaturated fatty acids (PUPA), important in the synthesis of compounds such as prostaglandin which are present in the ovary in a stress situation, was probably a consequence of a defense mechanism to the stress provoked by the presence of TBTCl. [Pg.422]

Physical factors, such as heat, mechanical stimulation and exercise, may sometimes lead to mast cell degranulation and whealing in the skin, but rarely provoke systemic anaphylaxis [4, 26]. Patients do report that these and other factors in combination (such as exercise, heat and alcohol) may elicit anaphylaxis in summation. [Pg.117]

The human pancreas secretes about 40—50 units of insulin daily, which represents about 15—20% of the hormone stored in the B cells. Insidin and the C-peptide (see Figure 42—12) are normally secreted in equimolar amounts. Stimuh such as glucose, which provokes insidin secretion, therefore trigger the processing of proinsidin to insidin as an essential part of the secretory response. [Pg.453]

Organic peroxides such as cumene hydroperoxide and t-butyl hydroperoxide have extensively been used as experimental agents. They provoke lipid peroxidation in hepatocytes, probably by the generation of alkoxyl and peroxyl radical intermediates after reaction with cytochrome P450. Other cytotoxic mechanisms are probably involved including protein thiol and non-protein thiol oxidation and deranged calcium homeostasis (Jewell et al., 1986). In fact, the addition of cumene hydroperoxide to isolated bUe duct cells, devoid of cytochrome P450 activity, still results in cell death but lipid peroxidation is not detectable (Parola et al., 1990). [Pg.241]

But there are those in my lab who believe that the excitation is being seen by a bias toward large cells and that they represent a large cell population in the neostriatum. I don t necessarily believe that. I don t know why, in the anesthetized animal, you can flip a nerve cell that is inhibited by amphetamine by increasing the dose. It has been postulated that the excitation is related to the occurrence of both the stereotyped behaviors, and that this may be provoked at doses that produce neurotoxicity. We have also done a number of studies looking at the neurotoxicity of amphetamine administration in animals, most of which replicate Lou Seiden s work. [Pg.139]

Kouskoff V, Korganow AS, Duchatelle V, Degott C, Benoist C, Mathis D. Organ-specific disease provoked by systemic autoimmunity. Cell 1996 87(5) 811—822. [Pg.187]


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See also in sourсe #XX -- [ Pg.400 ]




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