SSRs distribution in the leaf transcriptome of <i>Q.pubescens</i>.

<p>SSRs distribution in the leaf transcriptome of <i>Q.pubescens</i>.</p

Summary of RNA-Seq and <i>de novo</i> sequence assembly for <i>Q. pubescens</i>.

<p>N75 length is defined as the length N for which 75% of all bases in the sequences are in a sequence of length L </p><p>N50 length is defined as the length N for which 50% of all bases in the sequences are in a sequence of length L </p><p>N25 length is defined as the length N for which 25% of all bases in the sequences are in a sequence of length L </p><p>Summary of RNA-Seq and <i>de novo</i> sequence assembly for <i>Q. pubescens</i>.</p

Histogram of the 30 most abundant InterPro domains revealed by the InterProScan annotation of the high quality <i>Quercus pubescens</i> transcript set.

<p>Histogram of the 30 most abundant InterPro domains revealed by the InterProScan annotation of the high quality <i>Quercus pubescens</i> transcript set.</p

Histogram of GO classifications of assembled <i>Quercus pubescens</i> transcripts.

<p>Results are summarized for three main GO categories: biological process, cellular component and molecular function.</p

<i>Q. pubescens</i> contigs related to genes involved in drought avoidance in <i>Arabidopsis Thaliana.</i>

<p><i>Q. pubescens</i> contigs related to genes involved in drought avoidance in <i>Arabidopsis Thaliana.</i></p

KOG functional classification of all <i>Q. pubescens</i> transcripts.

<p>KOG functional classification of all <i>Q. pubescens</i> transcripts.</p

Top 30 metabolic pathways in <i>Q. pubescens</i>.

<p>This table shows the KEGG metabolic pathways of plants that were well represented by unique sequences of <i>Quercus pubescens</i>. The number of sequences and enzymes involved are described</p

Representative lung micrographs of <i>p66</i>^{<i>Shc−/−</i>} and WT mice at 7 months after CS or air exposure.

<p>(A) Representative lung parenchyma from an air-control <i>p66</i>^{<i>Shc−/−</i>} mouse showing a normal architecture. (B) Smoking <i>p66</i>^{<i>Shc−/−</i>} mice show patchy changes with a bronchiolocentric distribution characterized by peribronchiolar inflammatory infiltrates (black rectangles). (C) Alveolar parenchyma from a smoking WT mouse showing areas of emphysema (*) with a patchy distribution. (D) is higher magnifications of (B) showing in peribronchiolar areas a large number of macrophages within the adjacent alveoli. H&E stain. Scale bars = 200 μm.</p

Immunohistochemical analysis of caspase 3-, ceramide-, and 8-HG- positive cells, as well as BAL cell counts in smoking mice.

<p>Quantification of caspase 3- positive cells in lungs after 5 months of CS exposure. Increased number of caspase 3- positive cells was detected in the lungs of CS-exposed WT mice. Few 8-HG-positive cells were detected in the lung tissues of air-exposed mice from both groups and in smoking <i>p66</i>^{<i>Shc−/−</i>} mice. Values [positive cells/10 fields] are represented as means ± SD, *p < 0.05 compared with air-control values of the same genotype. ^<b>†</b>p< 0.05 <i>vs</i> smoking WT mice. (B-C) Immunohistochemistry for ceramide in WT (B) and p66Shc KO mice (C) at 5 months after CS exposure. A positive reaction is evident on macrophages and alveolar epithelial cells in lungs from WT mice (arrowheads). Scale bars = 25 μm. (D-E) Immunohistochemistry for 8-hydroxyguanosine (8-HG). A strong 8-HG staining is present on lung tissue of WT mice at 3 months after CS exposure (D). A faint 8-HG reaction is found on lung slides from <i>p66</i>^{<i>Shc−/−</i>} smoking mice at the same time point (E). (D, E): Scale bars = 40 μm. (F) Quantification of 8-HG-positive cells in lungs after 3 months of CS exposure. Increased number of 8-HG-positive cells was detected in the lungs of CS-exposed WT mice. Few 8-HG-positive cells were detected in the lung tissues of air-exposed mice from both groups and in smoking <i>p66</i>^{<i>Shc−/−</i>} mice. Values [positive cells/10 fields] are represented as means ± SD, *p < 0.05 compared with air-control values of the same genotype. ^<b>†</b>p< 0.05 <i>vs</i> smoking WT mice. (G-H) Macrophage (G) and Neutrophil (H) counts in bronchoalveolar lavage [BAL] fluids of mice immediately sacrificed after smoking at 7months of treatment. Values reported in are means ± SD. *p< 0.05 <i>vs</i> air controls of the same genotype; n = 5 animal/group. ^†p< 0.05 <i>vs</i> smoking WT mice.</p

Representative lung micrographs and TGF- mRNA expression of p66Shc−/− mice and WT mice exposed to CS for 7 months.

<p>(A) and (D) are lung micrographs of a p66Shc−/− mouse at 7 months after CS exposure. (B) and (D) show morphologic appearance of peribronchiolar fibrosis, characterized by a progressive deposition of collagen expanding into contiguous alveolar septa. (B) and (C) represent higher magnifications of (A). These micrographs show intraseptal collagen accumulation (“sea green”) (arrowheads) and alveolar lumens, which are lined by hyperplastic epithelial cells and filled with macrophages. These macrophages are often multinucleated. (E) is representative lung parenchyma from an air-control p66Shc−/− mouse showing a normal appearance. (F) is a lung parenchyma from a WT mouse exposed to CS for 7 months, showing air space enlargements (emphysema) (*). Masson’s trichrome stain. Scale bars = 40 μm. Immunohistochemical staining for transforming growth factor-beta (TGF-) on lung sections of WT (G) and p66Shc−/− (H) mice at 7 months. (I) Real-time PCR analysis of mRNA for TGF-β carried out on lungs from six mice for each experimental group at 7 month after CS exposure. Values are corrected for 18S rRNA and normalised to a median control value of 1.0. Data are presented as meanSD. * P< 0.05 with air-control values of the same genotype.</p