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Cycle-to-cycle variations in respiratory motion can cause significant geometric and dosimetric errors in the administration of lung cancer radiation therapy.
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In experiment 1 the effects of exogenous surfactant administration on lung and systemic inflammation during MV of otherwise normal lungs were determined.
Lung tumors were experimentally induced by tail vein administration of Lewis lung carcinoma (LLC) cells derived from the lung of C57BL/6 mouse.
The criteria for other heath conditions were imposed to allow administration of a lung function test on the same individuals.
Previously a report has suggested that administration of a lung-protective strategy for one-lung ventilation (OLV) results in oxygen desaturation of the brain parenchyma.
RCNV treatment also prolonged survival in treatment-resistant models of brain tumors and decreased tumor burden by systemic administration in models of lung metastasis.
Our experimental model demonstrated that intrapulmonary administration of SPA caused lung injury consistent with injury characteristic of ARDS of pulmonary origin, possibly due to direct alveolar epithelial injury.
In addition, therapeutic administration of Z3G1 reduced lung viral titers in mice infected with different viral strains, including amantadine and oseltamivir-resistant strains.
Previous animal studies revealed that administration of statins ameliorates lung injury following endotoxin exposure or ischemia-reperfusion.
Müller and colleagues [ 28] showed, in a mouse model of VILI, that the administration of simvastatin mitigated lung injury caused by large-tidal volume MV.
Generally, the administration of surfactant after lung transplantation is based on experimental findings that indicate an alteration in surfactant composition and function after transplantation [ 1].
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