Sentence examples for model the inflammatory from inspiring English sources

In the proposed model, the inflammatory response is activated when endotoxin is recognized by pathogen recognition receptors [50].

In the model, the inflammatory response targets pathogens while simultaneously causing increased damage to the intestinal wall.

To examine this, we exposed emphysematous rats (the pre-existing emphysema was formed through smoke exposure for 16 weeks) to hypoxia during sleep in a custom-made chamber therefore developing a novo rat model of SH in emphysema (SHE); with this model the inflammatory cytokines of the liver was studied and the four important coagulant/anticoagulant factors just mentioned above were measured.

We thus used TNFα to model the inflammatory milieu of obese adipose tissue in cell culture to determine whether the cytokine might also regulate β-adrenergic signaling in this context.

In vivo, rats were injected with endotoxin to model systemic inflammation, whereas isolated rat cardiomyocytes were treated with tumor necrosis factor-alpha to model the inflammatory environment seen following exposure to bacterial products such as lipopolysaccharide.

We combined a literature survey with a computational analysis of multiple transcriptomic data sets to construct a computable causal network model (the Inflammatory Process Network (IPN)) of the main pulmonary inflammatory processes.

EAE reliably models the inflammatory phase of MS and BBB alterations observed in EAE resemble those observed in MS [ 1].

It is now generally accepted that in CS models the inflammatory response driving the pathophysiological changes is characterized by two phases: the acute reaction during the first week of CS exposure, which shows a strong neutrophilic influx, and the progressive inflammation after 1 month of exposure consisting of neutrophils, macrophages and lymphocytes [ 12– 12].

The first is simple direct model without any mediators, while the second model includes the inflammatory markers score as potential mediator between childhood social position and type 2 diabetes, and the third model uses all three possible pathways.

Second, our model identifies the inflammatory pathways of the innate immune system as targets for modulating Aβ generation/accumulation.

CCR2 and CX3CR1 have been implicated as disease modifiers in EAE, a model for the inflammatory aspects of multiple sclerosis.