Nanopublications LDF server

Matches in Nanopublications for { ?s ?p "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." ?g. }

• _5 value "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." provenance.
• _5 value "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." provenance.
• _5 value "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." provenance.
• _5 value "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." provenance.
• _5 value "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." provenance.
• _5 value "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." provenance.
• _5 value "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." provenance.
• _5 value "ecause smoke exposure in vivo affects a variety of cell types in the lung, and because cell culture studies cannot mimic the complexity of animal physiology, we performed in vivo studies to examine the signaling pathways activated in murine lung after exposure to cigarette smoke. Western blotting of normal mouse lung homogenates showed increased p-ERK at 10 days of smoke exposure compared with lungs from control (unexposed) mice (Fig. 4A). Immunohistochemistry of lung tissue sections revealed nominal p-ERK staining in airway lining cells and red blood cells in control mice, with no staining in alveolar cells (Figs. 4, B and C). Robust expression of p-ERK is observed in airway lining cells, as well as in macrophages in the alveolar spaces at 10 days of smoke exposure (Figs. 4, D and E).Strong airway and alveolar p-ERK staining was still present at 6 months of exposure (Fig. 4, F and G)." provenance.