Sentence examples for adaptation of inflammatory from inspiring English sources

There is considerable literature on adaptation of inflammatory and pulmonary responses to ozone; the association of ozone with daily deaths in the summer is also well established.

Despite the ample literature on adaptation of inflammatory and pulmonary responses to ozone, and the link, in cohort studies, between lung function and mortality risk there has been little done to date to examine the question of adaptation in the acute mortality risk associated with ambient ozone.

This temporal pattern of effect would be anticipated for O3, which produces acute inflammatory responses in the lung; adaptation of this inflammatory response with several days of repeated exposure has been demonstrated (Folinsbee et al. 1994; Frank et al. 2001).

To the extent that systemic inflammation is driven by inflammation in the lung, and such lung inflammation is involved in stimulation of irritant receptors, and hence the parasympathetic responses, it is possible that the adaptation seen in previous studies of inflammatory changes could result in an attenuation of the mortality risk over the ozone season.

SUMMARY Insufficient cellular stress adaptation may underpin the persistent activation of inflammatory and fibrogenic signaling in damaged kidneys.

Despite this considerable literature on adaptation [ 12, 16, 17] of inflammatory and pulmonary responses to ozone, and the link, in cohort studies, between lung function and mortality risk [ 18- 20] there has been little done to date to examine the question of adaptation in the acute mortality risk associated with ambient ozone.

However, in our rat model the serum inflammatory cytokine response can resolve to baseline levels in HRLF and LRHF rats, despite continued task performance for as long as 24 weeks, presumably due to down regulation by anti-inflammatory cytokines or adaptation of tissues to task demands [ 55, 59, 67].

At a molecular level, de novo lipogenesis, primed mitochondrial and ER dysfunction, and the activation of inflammatory response are the main pathways that are most likely to have long lasting adaptations under different early life environments.

After MI, cardiac adaptation to excess body fat could significantly affect cardiac function directly or through increased the risk of diabetes, hypertension and release of inflammatory cytokines, leading to cardiac failure.

Immunopathology of inflammatory bowel disease.

Experimental models of inflammatory bowel disease.