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In vivo exposure

Andersen ME, Kirshnan K. 1994. Relating in vitro to in vivo exposures with physiologically based tissue dosimetry and tissue response models. In Salem H,ed. Animal test alternatives Refinement, reduction, replacement. New York, NY Marcel Dekker, Inc., 9-25. [Pg.192]

Exposure to UVB radiation has a profound effect on the corneal endothelium. Following exposure to UV radiation, the cornea swells, the extent and duration of which is directly related to the magnitude and duration of the exposure (Riley etal., 1987). At very high in vivo exposures, these authors reported a decrease in ascorbate concentration and an increase in protein content, which they suggested resulted from a breakdown of the blood-aqueous barrier. They concluded that UV radiation may cause or promote changes in the endothelium associated with ageing. [Pg.129]

Canli, M. and R.M. Stagg. 1996. The effects of in vivo exposure to cadmium, copper and zinc on the activities of gill ATPases in the Norway lobster, Nephmps norvegicus.Arch. Environ. Contam. Toxicol. 31 494-501. [Pg.70]

Rice, C.D. and B.A. Weeks. 1990. The influence of in vivo exposure to tributyltin on reactive oxygen formation in oyster toadfish macrophages. Arch. Environ. Contam. Toxicol. 19 854-857. [Pg.631]

Blossom, S.J., Pumford, N.R., and Gilbert, K.M., Activation and attenuation of apoptosis of CD4+ T cells following in vivo exposure to two common environmental toxicants, trichloroacetaldehyde hydrate and trichloroacetic acid, J. Autoimmun., 23, 211, 2004. [Pg.451]

There are different ways to use exposure with clients. The first method, called in vivo exposure, means that you expose the client under real-life conditions. In vivo exposure allows clients to practice for experiences they will likely face regularly in the real world under the controlled conditions of therapy. Let me present an example of how in vivo exposure would work with a client. Suppose your client has chronic pain and a history of abusing prescription pain-controlling medicines. Chronic pain in this instance represents a cue for drug use. You would most certainly want your client to learn how to confront his or her chronic pain directly without resorting to use of the pain medicines. In vivo cue exposure to pain in session would encourage the client to face his or her pain in real life without responding in the old way. [Pg.187]

Chatteijee et al., 1984 Sens et al., 1988), and cyclosporine (TrifiUis et al., 1984). Studies reported by Tay et al. (1988) in rabbit proximal tubule cultures with cisplatin revealed biochemical effects upon DNA synthetic activty that correlated with in vivo histochemical effects of this antitumor agent in animals. With respect to studies involving mercuric chloride and aminoglycoside antibiotics in primary renal cultures, light and electron microscopy revealed similar patterns of cellular pathology in vitro as compared to in vivo exposure in animals (Chatteijee et al., 1984 Aleo et al., 1987). [Pg.672]

Hits on individual assays can be analyzed in a couple of different ways. First, drugs can be identified that have similar strength hits and then the ADR profiles of these drugs can be examined to identify ADRs that maybe associated with these hits. Also, contained in BioPrint are extensive collections of ADR associations [2], which have been identified by querying the database for statistically significant correlations between individual assays and individual ADRs. These ADRs are stored in the database and can be accessed by searching assay or the ADR. It is also useful to consult the pharmacokinetic data to confirm that the strength of the in vitro hit is consistent with in vivo exposure levels. [Pg.43]

Tujimori K, Benet H, Mehendale HM, et al. 1986. In vivo and in vitro synthesis, release, and uptake of [3-H]-dopamine in mouse striatal slices after in vivo exposure to chlordecone. J Biochem Toxicol 1 (4) 1-12. [Pg.255]

In Vivo exposure of trout to piperonyl butoxide also affected the disposition and metabolism of l C-DEHP. The results in Table IX show that piperonyl butoxide reduced biliary but increased ll+C in muscle and blood. Because the bile contains mostly DEHP metabolites, this represents decreased metabolism. [Pg.89]

In Vivo Exposures. Aldrin (200 yg/200 yl DMSO or methanol) was administered by injection into the posterior adductor muscle or slowly released from a syringe (27 gauge, 1/2 inch) directly onto viscera. Mussels in situ in their natural habitat and others contained in small cheesecloth bags were also treated. After... [Pg.260]

The extent of upregulation varies with nAChR subtype and is typically much greater in cell lines than in native tissues after in vivo exposure to nicotine. The P2-containing nAChRs display the highest level of upregulation (Xiao and Kellar 2004), reflecting differences in the interface between adjacent a and p subunits, with respect to p2 versus p4 subunits (Sallette et al. 2004). Interestingly, inclusion of the... [Pg.194]

Buell, G. C., Y. Tokiwa, and P. K. Mueller. Potential crosslinking agents in lung tissue. Formation and isolation after in vivo exposure to ozone. Arch. Environ. Health 10 213-219, 1%5. [Pg.378]

Crofton KM, Paul KB, De Vito MJ, Hedge JM (2007) Short-term in vivo exposure to the water contaminant triclosan evidence for disruption of thyroxine. Environ Toxicol Pharmacol 24 194-197... [Pg.298]

Lizasa T, Moniki S, Bauer B, et al. 1993. Invasive tumors derived from xenotransplanted, immortalized human cells after in vivo exposure to chemical carcinogens. Carcinogenesis 14(9) 1789-1794. [Pg.184]


See other pages where In vivo exposure is mentioned: [Pg.419]    [Pg.165]    [Pg.165]    [Pg.127]    [Pg.205]    [Pg.38]    [Pg.56]    [Pg.200]    [Pg.24]    [Pg.70]    [Pg.241]    [Pg.280]    [Pg.536]    [Pg.187]    [Pg.205]    [Pg.564]    [Pg.147]    [Pg.158]    [Pg.180]    [Pg.277]    [Pg.457]   
See also in sourсe #XX -- [ Pg.187 ]




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In vivo Tests of Animal Exposure

In vivo Tests of Human Exposure

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