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FIGURE 16.1 Effects of immunocamou age on viral pathogenesis. (A) Virus recognizes, binds to cell receptor , is internalized undergoes multiple rounds of replication , 1 2 3 progeny virus is packaged and shed into the extracellular environment , whereupon it 4 5 infects new host cells . mPEG grafting to either the free virus (B) or host cells 1 (C) interrupts the disease cycle.

Estrogenic Pharmaceuticals. Administration of estrogenic pharmaceuticals to children or adults can result in a variety of abnormalities associated largely with secondary sex characteristics that are reversible upon cessation of drug treatment. Gynecomastia, the development of breast tissue in males, is often the consequence of perturbations in the normal androgen/estrogen ratio. As discussed earlier in this chapter, prolonged administration of drugs with estrogenic or antiandrogenic activity can cause gynecomastia. Gynecomastia had been reported in the medical literature

where B is the buffer size. We assume that the queueing process is in its stationary regime. The loss rate is de ned as lB E QB An 1 Cn 1 B : n loss Theorem 10.3.2. EA < EC, then Let G1 be the integrated tail distribution of A. If G1 P s and lB E A B 1 o 1 loss

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to occur as a result of frequent intercourse when an estrogen-containing cream was used as a vaginal lubricant and among morticans who applied estrogen-containing skin creams to corpses without the use of gloves. Similar to gynecomastia in adult males, activational toxicity from estrogenic drugs has been reported to cause pseudoprecocious puberty in children. Pseudoprecocious puberty is characterized by the development of some indicators of puberty (pubic or facial hair, morphological changes in sex organs, breast development, etc.) in preadolescent individuals. An outbreak of pseudoprecocious puberty was reported among a group of children ranging in age from 4 months to 2 years of age following application of a skin cream to treat dermatitis. Symptoms included pigmentation of the nipples, breast development, the presence of pubic hair, and vaginal discharge and bleeding among the females. Breast development also was reported in prepubertal boys following use of an estrogen-containing hair cream. These reports highlight the fact that dermal exposure can be adequate to attain a suf cient dose of endocrine-active compound to elicit adverse responses. In all of these cases the symptoms of endocrine toxicity resolved following cessation of exposure to the causative agent.

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Over the last several years, our laboratory has focused on the prevention of allorecognition of donor tissues (erythrocytes, lymphocytes, endothelial cells, and pancreatic islets) by the application of cellular immunocamou age.13 30 The immunocamou age of cells is mediated by the covalent grafting of cell surfaces with poly(ethylene glycol) [PEG; HO (CH2CH2O)n CH2CH2OH]. To chemically graft the PEG to proteins, a chemical linker compound is attached to one of the terminal hydroxyl ( OH) residues. Chemical linkers commonly employed include cyanuric chloride, succinimidyl proprionate, and benzotriazolylcarbonate. To further diminish any residual reactivity of the grafted PEG, the remaining OH group is substituted with a methyl ( CH3) group to produce activated methoxypoly(ethylene glycol) [mPEG; CH3 (CH2CH2O)n CH2CH2 linker chemistry]. Biophysically, the grafted mPEG confers its immunoprotective effects due to the rapid mobility and intramolecular exibility of the heavily hydrated PEG chains. As shown in Figure 16.2, rigid linear molecules lack any signi cant radius of gyration (Rg), resulting in poor or absent camou aging of membrane antigens. In contrast, mPEG, while a linear molecule, exhibits a high degree of intrachain exibility due to the repeating, highly mobile, ethoxy units. Based on this intrachain mobility, its Rg is very close to its linear length (L). As a result of this intrachain mobility, as

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