These direct measurements (not based on MRI) have established that substantial edema only occurs in infarcted myocardium.
This approach is designed to account for continued tumor growth during the time required for an immune response to develop, or for a tumor volume increase due to transient T-cell infiltration (with or without edema) into established, radiographically undetectable tumor deposits [ 72, 74].
The diagnosis of pulmonary edema was established on the basis of the following criteria: (1) the presence of bilateral infiltrates on chest radiographs; (2) a P/F ratio of ≤300 mm Hg; and (3) an increase in the EVLW indexed to the predicted body weight (EVLWi) of ≥10 mL/kg.
In this study, the diagnosis of pulmonary edema was established on the basis of: the presence of bilateral infiltrates on chest radiography; P/F ratio ≤ 300 mmHg; and an increase in the EVLW indexed to the predicted body weight (extravascular lung water index (EVLWI)) ≥ 10 ml/kg.
The score-based evaluation of the radiographs to establish whether pulmonary edema were present took 23 ± 12 seconds and, thus, significantly longer than the standard approach (7 ± 3 seconds).
For differentiation between cardiac renal origin of the observed edema and we established eye assay models for indirect measuring of the integrity of the glomerular filtration barrier.
Interestingly, however, inhibition of p38 MAPK did not affect the resolution of the pulmonary edema in previously established inflammation in rats [ 117].
However, anti-angiogenic therapies may have only anti-edema effects and the role of ADC as a sensitive biomarker of tumor edema is less well established.
Carrageenan-induced paw edema is a well established animal model to assess the anti-inflammatory effect of natural products as well as synthetic chemical compounds.
In order to analyze morbidity and mortality associated with pulmonary acute edema, a protocol was established with a prospective data collection.
