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1.
Fig. 6.

Fig. 6. From: Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease.

Current and former smokers, ≥65 yr of age (n = 72) mean and 95% confidence limits. Results adjusted for age (years), sex (M/F), smoking history (former, current, never), and race (white, nonwhite). COPD, chronic obstructive pulmonary disease.

Maor Sauler, et al. Am J Physiol Lung Cell Mol Physiol. 2014 Mar 15;306(6):L487-L496.
2.
Fig. 4.

Fig. 4. From: Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease.

A: box plot with minimum and maximum lung volumes in 2- and 6-mo-old WT and Cd74−/− mice; n = 4–6 mice in WT groups, 7–9 mice in Cd74−/− group. *P < 0.0001; Wilcoxon rank-sum. B: box plot of mean linear intercept in 2- and 6-mo-old WT and Cd74−/− mice; n = 3–5 mice in WT group, 4 in Cd74−/− group. *P < 0.05; Wilcoxon rank-sum. C: H&E lung histology of WT and Cd74−/− mice. Original magnification ×10.

Maor Sauler, et al. Am J Physiol Lung Cell Mol Physiol. 2014 Mar 15;306(6):L487-L496.
3.
Fig. 3.

Fig. 3. From: Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease.

A: densitometry and representative Western blots of p21, phosphorylated-p53 (Ser15), total p53, and β-actin in 6-mo-old WT and Mif−/− mice. Data represent means ± SE; n = 4 mice/group; Wilcoxon rank-sum. B: relative mRNA of p16 and p19 in 2- and 6-mo-old WT and Mif−/− lung tissue. Data are means ± SE; n = 4–5 in WT group and n = 5–6 in Mif−/− group. *P < 0.05; Wilcoxon rank-sum. C: representative immunohistochemistry of p16 in 6-mo-old WT and Mif−/− mice. Arrows denote p16-positive staining. Original magnification ×10.

Maor Sauler, et al. Am J Physiol Lung Cell Mol Physiol. 2014 Mar 15;306(6):L487-L496.
4.
Fig. 2.

Fig. 2. From: Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease.

A: box plot with minimum and maximum lung volumes in 2- and 6-mo-old WT and Mif−/− mice; n = 6 mice in WT groups, 6–9 mice in Mif−/− group. *P < 0.0005; Wilcoxon rank-sum. B: box plot of mean linear intercept in 2- and 6-mo-old WT and Mif−/− mice; n = 3–5 mice in WT group, 4 in Mif−/− group. *P < 0.05; Wilcoxon rank-sum. C: representative hematoxylin and eosin (H&E) lung histology of WT and Mif−/− mice. Original magnification ×10. D: box plot with minimum and maximum BAL macrophages in 2- and 6-mo-old WT and Mif−/− mice; n = 6 mice in WT groups, 6–9 mice in Mif−/− groups. *P < 0.05; Wilcoxon rank-sum.

Maor Sauler, et al. Am J Physiol Lung Cell Mol Physiol. 2014 Mar 15;306(6):L487-L496.
5.
Fig. 1.

Fig. 1. From: Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease.

A: box plot with minimum and maximum macrophage migration inhibitory factor (MIF) concentrations (ng/ml) in wild-type (WT) mice at 2 mo, 6 mo, and 12 mo of age; n = 10 in 2 mo group, n = 8 in 6 mo and 12 mo group. Data represent means ± SE. *P < 0.05 between 12 mo and 6 mo group; Wilcoxon rank-sum. B: Western blot of MIF in homogenized lung tissue from WT mice at 4, 12, 24, and 32 mo of age with densitometry analysis. *P < 0.05 between groups; Wilcoxon rank-sum. C: box plot with minimum and maximum bronchoalveolar lavage (BAL) MIF concentrations (ng/ml) in WT mice following 3 or 6 mo of cigarette smoke (CS) exposure compared with control; n = 9–11 for control group; n = 8–10 for CS group. *P < 0.0003 between 3-mo control and 6-mo CS group; Wilcoxon rank-sum. *P < 0.05 between 6-mo control and 6-mo CS group; Wilcoxon rank-sum.

Maor Sauler, et al. Am J Physiol Lung Cell Mol Physiol. 2014 Mar 15;306(6):L487-L496.
6.
Fig. 5.

Fig. 5. From: Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease.

A: box plot with minimum and maximum lung volumes in room air (RA)- and CS-exposed WT and Mif−/− mice; n = 4/group. *P < 0.05 Mif−/− CS vs. WT CS, P < 0.05 WT RA vs. WT CS; Wilcoxon rank-sum. B: box plot with minimum and maximum mean linear intercept in RA- and CS-exposed WT and Mif−/− mice; n = 4/group. *P < 0.05 WT RA vs. Mif−/− RA; *P < 0.05 WT CS vs. Mif−/− CS; Wilcoxon rank-sum. C: H&E lung histology of WT and Mif−/− mice with and without CS exposure. Original magnification ×10. D: H&E lung histology of WT and Mif−/− mice with and without CS exposure, apical and basal regions. Original magnification ×4. E: total BAL cell count in RA- and CS-exposed WT and Mif−/− mice; n = 4/group. *P < 0.05 Mif−/− CS compared with WT RA control; Wilcoxon rank-sum. F: BAL cell type distribution in WT and Mif−/− exposed to CS; n = 4/group. *P < 0.05 Mif−/− mice vs. WT; Wilcoxon rank-sum. G: densitometry and representative Western blot of homogenized lung tissue for pro- and cleaved caspase 3 in CS-exposed mice; n = 4/group. *P < 0.05 Mif−/− mice exposed to CS compared with WT mice exposed to CS; Wilcoxon rank-sum. H and I: cleaved caspase 3-positive cells as a percentage of total cells with representative immunofluorescence images. Arrows represent cleaved caspase 3-positive cells; n = 4/group. *P < 0.05 compared with WT CS; Wilcoxon rank-sum).

Maor Sauler, et al. Am J Physiol Lung Cell Mol Physiol. 2014 Mar 15;306(6):L487-L496.

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