These mice also exhibited higher endothelial barrier dysfunction levels, total protein, malondialdehyde (an aldehydic secondary product of lipid peroxidation), IL-6, and MMP-9 protein production and lower sodium dismutase production than mice without endotoxemia subjected to VT = 30 mL/kg and the nonventilated control mice (Figure 1 and Figure 2A–D). The gene discussed is IL6; the disease is serum lipopolysaccharide activity.