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This finding, that a gaseous molecule produced endogenously by cells can exert anti-inflammatory effects, opened new avenues of research in both experimental models of clinical disease and in human disease.
Most strikingly, the KCC2-NTD was neuroprotective in both experimental models of neurodegeneration.
RAS blockade with angiotensin-converting enzyme (ACE) inhibitors improves cardiac remodeling and outcomes in both experimental models of MI as well as in humans [ 1].
Both experimental models of infection (19 – 22 ) and clinical studies (23 – 27 ) have shown that bactericidal activity predicts therapeutic efficacy and results in improved clinical outcome.
Further, TGFβ isoforms and their receptors were upregulated in both experimental models of DN, as well as in human DN [ 5, 6].
In both experimental models of IBD and in humans the mucus layer becomes more permeable to bacteria and is therefore considered critical etiological factors in this disease and possibly other intestinal disorders [ 28].
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The sequence Dox→Pacl→48-h washout→5-FU produced a synergistic and highly schedule-dependent interaction (combination index < 1), resulting in an induction of apoptosis in both experimental models regardless of hormonal, p53, bcl-2 or bax status.
In both experimental models, the positive loading of the second eigensystem was significantly associated with overlapping GO terms describing the inflammatory response to the brain injury.
Finally, we discuss the interactions between lung infection and periodic application of high intrathoracic pressure, both in experimental models of ALI and in patients with ARDS.
More insight is needed regarding the pathophysiological conditions associated with presepsin release, both in experimental models of sepsis and in well-characterized patients.
Antibody-mediated immunity has been shown to be crucial in both experimental models and in human cases of pyelonephritis [ 30].
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