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1.
Figure 6.

Figure 6. From: Postexposure Administration of a ?2-Agonist Decreases Chlorine-Induced Airway Hyperreactivity in Mice.

Airway hyperreactivity of inducible nitric oxide synthase (iNOS)−/− mice exposed to Cl2. iNOS−/− mice were exposed to 400 ppm Cl2 for 30 minutes; respiratory system resistance was measured at 24 hours after exposure. Air-breathing iNOS−/− mice served as control. Values of respiratory resistance of wild-type (iNOS+/+) mice at 24 hours after Cl2 exposure are also shown for comparison (*P < 0.05, compared with control; n = 8 for each group of knockout mice; n = 10 for wild-type mice).

Weifeng Song, et al. Am J Respir Cell Mol Biol. 2011 July;45(1):88-94.
2.
Figure 4.

Figure 4. From: Postexposure Administration of a ?2-Agonist Decreases Chlorine-Induced Airway Hyperreactivity in Mice.

Cl2 exposure induced lung injury and inflammation. (A) Protein concentration in bronchoalveolar lavage (BAL) fluid at different time points after Cl2 exposure and treatment with Arfor. (B) Total live cell counts and (C) cell differentials for lymphocytes, macrophages, and neutrophils in BAL fluid at different time points after Cl2 exposure and treatment with Arfor (*P < 0.05, compared with control; n = 6 from two independent experiments for each time point).

Weifeng Song, et al. Am J Respir Cell Mol Biol. 2011 July;45(1):88-94.
3.
Figure 2.

Figure 2. From: Postexposure Administration of a ?2-Agonist Decreases Chlorine-Induced Airway Hyperreactivity in Mice.

Lung histology after Cl2 exposure and treatment of Arfor: Airway cross-sections of mice breathing air (A), or exposed to Cl2 treated with saline (B) or Arfor (C), and killed at 24 hours after exposure. Significant injury to both groups of Cl2-exposed mice is present. Cross-sections of alveolar compartments from mice breathing air (D), or exposed to Cl2 treated with saline (E) or Arfor (F), and killed at 24 hours after Cl2. Sections from Cl2-exposed mice show increased granularity, but no overt injury. Sections are representatives of three control, five Cl2/saline–, and six Cl2/Arfor–treated mice. Stain used was hematoxylin and eosin. Scale bars, 50 μm.

Weifeng Song, et al. Am J Respir Cell Mol Biol. 2011 July;45(1):88-94.
4.
Figure 3.

Figure 3. From: Postexposure Administration of a ?2-Agonist Decreases Chlorine-Induced Airway Hyperreactivity in Mice.

Changes in lung cAMP levels in mice exposed to Cl2 and instilled with saline or Arfor. (A) Lung cAMP concentration in total lung homogenate was measured by ELISA at the indicated time points after Cl2 exposure with or without treatment with Arfor (*P < 0.05, compared with corresponding Cl2-exposed group; #P < 0.05, compared with control; n = 4–8 for each group). (B) Alveolar fluid clearance (AFC) was measured in control air-breathing, saline-treated mice; air-breathing mice treated with Arfor for 1 hour; mice exposed to 400 ppm Cl2 for 30 minutes, then returned to room air and treated with vehicle (saline) for 1 hour; or mice exposed to Cl2, and then returned to room air and treated with Arfor for 1 hour (*P < 0.05, compared with Cl2/saline; #P < 0.05, compared with control; n = 18, 5, 7, and 10 for air/saline, air/Arfor, Cl2/saline, and Cl2/Arfor groups, respectively).

Weifeng Song, et al. Am J Respir Cell Mol Biol. 2011 July;45(1):88-94.
5.
Figure 1.

Figure 1. From: Postexposure Administration of a ?2-Agonist Decreases Chlorine-Induced Airway Hyperreactivity in Mice.

Chlorine (Cl2) exposure increases respiratory resistance and elastance, which are mitigated by arformoterol (Arfor). (AC) Cl2 significantly increased both baseline resistance and airway responsiveness to methacholine at 1 hour, 24 hours, and 6 days after exposure as compared with that of the air-breathing, saline control animals. Arfor significantly decreased resistance at the corresponding time points after exposure. (DF) Cl2 exposure significantly increased elastance as compared with air-breathing, saline control mice. Arfor decreased elastance at 6 days after exposure. Squares, Cl2/saline (n = 10); circles, Cl2/Arfor (n = 10); triangles, air/saline (n = 6). Mice were exposed to 400 ppm Cl2 for 30 minutes, then intranasally administered either saline or Arfor as described in Materials and Methods (*P < 0.05, compared with Cl2/Arfor group; #P < 0.05, compared with saline control). Values are means (±SEM) for the indicated number of mice. E, elastance; R, resistance.

Weifeng Song, et al. Am J Respir Cell Mol Biol. 2011 July;45(1):88-94.
6.
Figure 5.

Figure 5. From: Postexposure Administration of a ?2-Agonist Decreases Chlorine-Induced Airway Hyperreactivity in Mice.

Cytokine levels and lung NF-κB activity of Cl2-exposed mice. (A) IL-6 and (B) TNF-α in BAL fluid measured by ELISA at different time points after Cl2 exposure and treatment with Arfor (*P < 0.05, compared with control; n = 6 from two independent experiments for each time point). (C) Nuclear extract from lung homogenate of control, Cl2-exposed, and Cl2-exposed mice treated with Arfor were subjected to electrophoretic mobility shift assay at 30 minutes, 2 hours, and 24 hours after Cl2 exposure. Mice with intranasally instilled LPS (2 μg/g body weight) for 24 hours served as positive control. Densitometric analysis of the gel is shown in Figures E3. Results are gel images of typical experiments that were repeated at least twice. Con, control.

Weifeng Song, et al. Am J Respir Cell Mol Biol. 2011 July;45(1):88-94.

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