The phytoextraction and analysis of tonalide in water solutions

<p><b>Copyright information:</b></p><p>Taken from "Invasive and noninvasive methods for studying pulmonary function in mice"</p><p>http://respiratory-research.com/content/8/1/63</p><p>Respiratory Research 2007;8(1):63-63.</p><p>Published online 14 Sep 2007</p><p>PMCID:PMC2039738.</p><p></p>hamber ensured a body temperature of 34–35°C as measured by rectal thermometer. Defined aerosol concentrations of methacholine, as measured by an aerosol photometer, were delivered into the airways via the orotracheal tube. For calculation of pulmonary resistance (R), transpulmonary pressure (P) was recorded via an esophageal tube, and tidal flow was determined by a pneumotachograph attached directly to the orotracheal tube. PT, pressure transducer. Taken from [10] with permission

Additional file 4: of Physical activity in the morning and afternoon is lower in patients with chronic obstructive pulmonary disease with morning symptoms

Figure S3. Steps during the course of the day, Few morning symptoms: morning symptom score < 15; severe morning symptoms: morning symptom score ≥ 15. (JPEG 203 kb

Additional file 2: of Physical activity in the morning and afternoon is lower in patients with chronic obstructive pulmonary disease with morning symptoms

Figure S2. Steps during each hour of the day, Low mMRC < 2 (N = 27); high mMRC ≥2 (N = 52). (JPEG 195 kb

Additional file 1: of Physical activity in the morning and afternoon is lower in patients with chronic obstructive pulmonary disease with morning symptoms

Figure S1. Number of steps in the morning, Error bars present 95% confidence intervals. Low morning symptom score: score < 17.0; high morning symptom score: score ≥ 17.0. (JPEG 192 kb

Additional file 1 of Cough suppression and HRQoL in adult people with cystic fibrosis: an unexplored correlation

Additional file 1: Testing of the assumptions regarding the respective statistical procedure

Cigarette Smoke Modulates Repair and Innate Immunity following Injury to Airway Epithelial Cells

<div><p>Cigarette smoking is the main risk factor associated with chronic obstructive pulmonary disease (COPD), and contributes to COPD development and progression by causing epithelial injury and inflammation. Whereas it is known that cigarette smoke (CS) may affect the innate immune function of airway epithelial cells and epithelial repair, this has so far not been explored in an integrated design using mucociliary differentiated airway epithelial cells. In this study, we examined the effect of whole CS exposure on wound repair and the innate immune activity of mucociliary differentiated primary bronchial epithelial cells, upon injury induced by disruption of epithelial barrier integrity or by mechanical wounding. Upon mechanical injury CS caused a delayed recovery in the epithelial barrier integrity and wound closure. Furthermore CS enhanced innate immune responses, as demonstrated by increased expression of the antimicrobial protein RNase 7. These differential effects on epithelial repair and innate immunity were both mediated by CS-induced oxidative stress. Overall, our findings demonstrate modulation of wound repair and innate immune responses of injured airway epithelial cells that may contribute to COPD development and progression.</p></div

EGFR and ERK1/2 signaling in wounded ALI-PBEC.

<p>(A) Intrinsic wound healing of ALI-PBEC was determined in the presence of the EGFR tyrosine kinase inhibitor AG1478 (1 μM) or the MEK1/2 inhibitor U0126 (25 μM) at 6 h after exposure with either air or CS. Data are shown as percentage wound closure compared to t = 0 h. (B) mRNA expression of <i>RNASE7</i> was determined by qPCR. Data are shown as normalized mRNA expression compared to <i>RPL13A</i> and <i>ATP5B</i>. (C) Western blot analysis of EGFR and ERK1/2 phosphorylation of wounded ALI-PBEC exposed to air or CS in the presence of AG1478, U0126, and NAC, at 6 h after exposure. (D) Bands were quantified by densitometry for analysis of EGFR and (E) ERK1/2 phosphorylation and corrected for total-EGFR and total-ERK1/2, respectively. For all graphs data are shown as mean; error bars represent SEM; experiments were conducted in duplicate; n = 3 independent donors; * p < 0.05.</p

Proposed model.

<p>EGFR signaling is activated by CS and injury, and this leads to MEK1/2-mediated phosphorylation of downstream ERK1/2. CS furthermore directly causes phosphorylation and activation of ERK1/2 via oxidative stress, which is independent of EGFR signaling. EGFR/ERK1/2-mediated wound repair is suppressed by CS via oxidative stress. In contrast, activation of ERK1/2 due to a combined effect of CS-induced oxidative stress and injury, results in an enhanced innate immune response. Solid lines represent the effect of CS, dashed lines the effect of injury. NAC, AG1478 and U0126 were used to inhibit oxidative stress, EGFR phosphorylation, and ERK/12 phosphorylation respectively.</p

Effect of CS on airway epithelial wound healing and innate immunity.

<p>ALI-PBEC were mechanically injured and subsequently exposed to air (control) or whole cigarette smoke (CS). (A) Phase-contrast light microscopy images were made of air- and CS-exposed ALI-PBEC at 0, 6, 24 and 48 h after exposure. (B) Wound closure is shown in percentage in air- versus CS-exposed cells and (C) wound closure rate in percentage per hour at different time intervals was calculated. n = 8 independent donors. (D) Wound closure rates per hour in air- and CS-exposed ALI-PBEC up to 12 h after exposure were determined using live imaging. n = 7 independent donors. (E) <i>RNASE7</i> mRNA expression was determined in intact or wounded ALI-PBEC exposed to air or CS, at 6 h after exposure. Values shown represent normalized mRNA expression compared to <i>RPL13A</i> and <i>ATP5B</i>. n = 7 independent donors. (F) IL-8 secretion was determined in the basal culture medium. n = 9 independent donors. Data are shown as mean; error bars represent SEM; experiments were conducted in duplicate i, * p < 0.05.</p

p63⁺ cells at the wound edge of ALI-PBEC.

<p>(A) Immunofluorescence staining for p63 (green) and nuclei (blue (DAPI)) of mechanically injured ALI-PBEC. (B) Percentage of p63⁺ cells at the first line of cells directly at the wound edge or in intact areas, in air- versus CS-exposed cells. (C) Number of p63⁺ cells and p63^- cells at the wound edge per 400 μm length of wound edge, in air- versus CS-exposed cells. (D) Internuclear distance in μm between p63⁺ cells located directly at the leading wound edge and the first adjacent p63⁺ cell. All graphs: data are shown as mean; error bars represent SEM, experiments were conducted in duplicate, n = 3 independent donors, * p < 0.05.</p