Resistance modeling role

Further evidence to support the notion of a role for immunotoxic environmental contaminants in the 1988 outbreak came from two studies of laboratory rats carried out in tandem with the seal studies. PVG rats were fed the same two batches of herring used in the seal study, with a similar pattern of effects observed in the seals [63,64], However, there were additional indications of immunotoxicity that could not be evaluated in seals for ethical or technical reasons, including increased virus titers in a rat cytomegalovirus (RCMV) host resistance model, and reduced thymus cellularity in the rats fed Baltic Sea herring. A positive control group of rats in one of the studies was exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin, thereafter exhibiting an amplified pattern of the effects that had been observed in the Baltic group. The collective results from the captive seal studies and the laboratory animal studies were seen to implicate an AhR-mediated immunotoxicity, in which dioxin-like PCBs played a dominant role [64, 65],... 

The Listeria monocytogenes host resistance model is controlled primarily in the liver and spleen. The Listeria monocytogenes systemic infection assay is useful primarily to evaluate adverse effects on neutrophils and Kupffer cells of the liver and splenic macrophages and neutrophils. NK cells and T lymphocytes also play a role in bacterial clearance. The Listeria monocytogenes host... 

The resistivity of the composite, therefore, is determined by the contribution of metallic (crystalline) and non metallic (amorphous) resistivity. The role of each portion in the determination of DC conductivity is described by temperature functions which identify the contribution of each part in the total electrical transport mechanism. The metallic part is described by the quasi VRH one dimensional exponential model [2,17,18] and an expression describing the amorphous part of the resistivity which is based on the fluctuation-induced tuimeling between metallic islands[3]. 

The cumulative effects of these barriers and the resistance to flow they produce were computed, and it was demonstrated these macroscopically derived laws applied at molecular dimensions were able to provide semiquantitative agreement with the available data. While further tests of these models will undoubtedly provide refinements to our understanding, the agreement supports our understanding of the basic phenomena regulating transport of therapeutically active substances through these barriers and the role of disease states that impact hydrodynamic pressure on the efficacy of drug delivery. 

It is clear that the type 2 cytokines IL-4, IL-9 and IL-13 play an obligatory role in host resistance to nematode infection whereas type 1 responses promote host susceptibility. Therefore, given that susceptibility to nematode infection is not due to a lack of responsiveness perse, but rather the development of an inappropriate response, it is important to understand the factors that influence the induction and expansion of Th subset responses and so control infection outcome. Studies in nematode models and other systems have addressed these questions and identified the importance of host genetic factors, the nature of the antigen and the antigen presenting cell, co-stimulatory molecules on these cells, and the cytokine and chemokine environment immediately following induction of the response. 

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