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described in Table 17.4, and individual effects may be misdiagnosed as organ-speci c toxicity. Hypothyroidism can result from various causes other than chemical toxicity including diseases of the hypothalamic pituitary thyroidal axis, iodine de ciency, and heritable defects in thyroid hormone production. Chemical agents that have historically been recognized for their ability to cause hypothyroidism include phenylbutazone, resorcinol, lithium, and para-aminosalicylic acid. Disruptions in thyroid hormone levels can occur through chemical-induced increases in the metabolic inactivation and elimination of the hormone. Chemicals that are capable of increasing the metabolic clearance of thyroid hormone include the polycyclic halogenated hydrocarbons (i.e., dioxins, furans, polychlorinated biphenyls, polybrominated biphenyls). A study reported in the New England Journal of Medicine suggested that environmental or occupational exposure to such chemicals can result in hypothyroidism in humans. The study consisted of a comparison of thyroid status in workers who were occupationally exposed to polybrominated biphenyls as compared to workers who were not exposed to any polyhalogenated hydrocarbons. Four of 35 exposed workers and none of 89 unexposed workers exhibited signs of hypothyroidism that included increased plasma levels of thyrotropin and decreased plasma levels of thyroxine. Thyrotropin is secreted by the pituitary gland and stimulates the thyroid gland to produce thyroxine (see Figure 17.1). The increase in thyrotropin and decrease in thyroxine is consistent with hypothyroidism caused by increased clearance of the thyroxine. As discussed earlier in this chapter, perinatal exposure to PBBs during the Michigan milk contamination also produced symptoms characteristics of hypothyroidism.

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13 30,44 46 These intact cell studies have clearly demonstrated that mPEG grafting dramatically reduces cell cell (eg, T cell antigen presenting cell and erythrocyte Rouleaux formation) and receptor ligand interactions (eg, CD28 CD80 costimulatory pathway) consequent to the steric hindrance and cell surface charge occlusion by the heavily hydrated neutrally charged polymer More importantly, the grafted polymer does not affect either the function or viability of the modi ed cells This is most dramatically demonstrated by normal in vivo survival of pegylated murine erythrocytes and the establishment of normoglycemia in diabetic rats transplanted with pegylated pancreatic islets Based on these ndings, we proposed that immunocamou age of either the virus (direct viral inactivation) or host cell (indirect viral inactivation) would prevent viral entry and subsequent infection.

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The endocrine system possesses many targets at which toxicants can elicit either reversible or permanent effects on an individual. Effects of chemicals on endocrineregulated processes such as development, maturation, growth, and reproduction have been well documented in both laboratory and epidemiological studies. Less is know of the potential effects of endocrine toxicants on more generalized endocrine-regulated processes such as bone maintenance, general organ function, and metabolism. The US Environmental Protection Agency has been mandated by the US Congress to develop and implement a program for the screening and testing of chemicals for endocrinedisrupting toxicity. At this writing, the EPA is in the process of developing such a

Fig. 14.8 Traf c mixing effect for two le size distributions: Pareto a 1:05 and exponential at 100 second aggregation level. (a) Both servers are Pareto, (b) one server is Pareto, the other one is exponential; and (c) both servers are exponential.

program that will focus on the effects of chemicals on the androgen/estrogen and thyroid hormone regulated processes. Once implemented, this required testing will greatly expand our knowledge of the extent to which humans are exposed to chemicals that interfere with processes regulated by these hormones. However, it is important to recognize that chemicals have the potential ability to interfere with other hormone cascades, including those involving mineralcorticoids, glucocorticoids, retinoids, and perhaps some peptide hormones. Research is needed to increase our understanding of the susceptibility of endocrine signaling pathways involving these hormones to chemical toxicity and, ultimately, to our establishing chemical exposure limits that include these considerations.

shows the case when both servers have exponential le size distributions. Figure 14.8(b) is the combined case, where one server has a Pareto distribution with a 1:05 and the other server has an exponential distribution. Figure 14.8 shows that the mixed case is less ``bursty'' than the pure Pareto case but more bursty than the pure exponential case. Performance indicators such as packet drop rate and retransmission rate (not shown here) exhibit a smooth linear degradation when transiting from one extreme to the other. That is, the presence of less bursty crosstraf c does not drastically smooth out the more bursty one, nor does the latter swallow up the smooth traf c entirely. Traf c mixing was applied to all combination pairs for a 1:05, 1.35, 1.65, and 1.95, keeping one server xed at a 1:05. The H-values for the three cases shown are 0.86, 0.81, and 0.54, respectively. 14.4.5 Effect of Network Topology

Furthermore, because mPEG grafting results in the global immunocamou age of the virus or host cell, we hypothesized that mPEG derivatization should be capable of preventing infection by a broad spectrum of viruses including those that enter via receptor-mediated endocytosis or via membrane fusion To test the antiviral ef cacy of immunocamou age, multiple viral families were examined These families include Picornaviridae, Adenoviridae, and Coronaviridae (all representative of common human respiratory viruses), as well as Papovaviridae and Herpesviridae (Table 161) To experimentally test these hypotheses, mPEG derivatization of virus or host (target) cells (CV-1, BHK-21, L2, BALB/3T3, and MRC-5 cell lines) was preformed as previously described, with slight modi cations due to cell type13 30 Cells were split into either 35 or 60 mm petri dishes and were grown until 75 100% con uent The cells were brie y washed with phosphate buffered saline (PBS, pH 7.

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