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To study ischemia reperfusion injury in a clinically relevant setting, models of warm ischemia have been extensively used in rodents.
Specifically, it has been shown that neutralization of CXC chemokines significantly attenuated neutrophil infiltration and liver injury in rat and mouse models of warm hepatic IR [ 12, 13].
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We also discuss other simple models that are in agreement with the Planck data within a renormalizable model of warm inflation.
This study demonstrates that IPC improves the intestinal microvascular perfusion and tissue oxygenation in a model of warm IR injury of the intestine.
Objective: This study was designed to compare the effect of lung preservation with low-potassium dextran solution and Euro-Collins solution on reperfusion injury and surfactant function by using an in situ model of warm ischemia.
We utilised a model of warm in vitro hypoxia and H R that we have described previously [14].
Therefore, a model of warm ischemia reperfusion injury was applied to differentiate cellular infiltrates and to quantify tissue damage.
Laffey et al. [ 9] focused on the effects of hypercapnia vs acidosis per se in an ex-vivo model of warm ischemia-reperfusion rabbit lung injury.
Laffey et al evaluated the effects of metabolic acidosis vs hypercapnic acidosis on an isolated ex vivo rabbit lung model of warm ischemia-reperfusion injury [ 9].
Shibata et al. [ 6] demonstrated that hypercapnic acidosis exerts protective effects to a certain extent in an isolated and perfused rabbit lung model of warm ischemia-reperfusion lung injury.
Behavior of subjects not choosing the dominant or Pareto-efficient contributions is well-organized by a model of warm-glow giving with a logit decision error.
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