Tensile testing showed that the porogens can significantly alter the mechanical properties.

<p>The PHEMA-PEGDA made with water porogen was significantly stiffer than samples made with benzyl alcohol porogen. Low damping factors (tan (δ)) show that the PHEMA-PEGDA samples are viscoelastic with dominant elastic properties (B; n = 3). Tension was applied until rupture to determine the ductility and overall strength of the scaffolds (C). “X” marks the failure or rupture point of each sample. Horizontal bars identify samples with a statistically significant difference (p<0.05).</p

Porogens used to generate pores in the PHEMA-PEGDA include water (W), sucrose solution (S), and benzyl alcohol (BOH).

<p>This table shows the % v/v quantity of components used to create the PHEMA-PEGDA structures. The deionized water content (% v/v) listed shows the total aqueous content of the final pre-polymerized mix of monomers and other agents. As porogen types and volumes were adjusted, the quantities of PHEMA and PEGDA monomers remained constant.</p

Collagen type I coating the PHEMA-PEGDA scaffolds was immunostained using collagen antibody.

<p>Scaffolds were removed from the tissue culture wells and rinsed with PBS. (A) Collagen gelled within the micron sized surface pores of PHEMA-PEGDA using the water porogen. Collagen fibers were evident in the sucrose and benzyl alcohol PHEMA-PEGDA scaffolds (B and C, respectively). At week 2, HCFs were detected in the three different PHEMA-PEDGA scaffold types, and average DNA contents were quantitatively measured (D; n = 6). “*” indicates p<0.05, and error bars represent standard error. Cell viability staining at day 7 shows both live (green) and a significant number of dead (red) HCFs in the benzyl alcohol PHEMA-PEGDA scaffold (E).</p

SEM images of PHEMA-PEGDA scaffolds in low (A) and high (B) magnification.

<p>By increasing the content of the total deionized water content by 7%, average pore area was substantially increased. Data from alamarBlue shows that HCFs proliferated significantly in this structure from day 4 to 20 (C, p<0.05, n = 3). Fluorescent images show that, at day 8, live HCFs were clearly visible in this scaffold with essentially minimal cell death (D).</p

SEM images show dehydrated PHEMA-PEGDA.

<p>Water (A), sucrose (B), and benzyl alcohol (C) were used as porogens. Low magnification SEM images are displayed in the top row. Corresponding SEM images with higher magnification are shown in the bottom row. Image analysis was used to measure pore areas. Histograms display pore areas for the scaffolds made with water (D, n = 558), sucrose (E, n = 12,533), or benzyl alcohol (F, n = 11,485) porogens.</p

NMR spectroscopy results indicate that PEG chains appear to have leached out of the PHEMA-PEGDA scaffold following 3 days soaking in PBS.

<p>The signal for the middle O-CH2 group of PEGDA (A) and the middle O-CH2 group of PEG (B) were both found at approximately 70 ppm. Signals that represent the repeating side groups in PHEMA were not observed in PBS, however, indicating neither HEMA nor PHEMA leached out.</p

Additional file 1: of Ensemble genomic analysis in human lung tissue identifies novel genes for chronic obstructive pulmonary disease

Supplemental Data. Supplemental supporting figures (Figures S1–S10) and tables (Tables S1-S8). (PDF 4193 kb

Additional file 2: of Ensemble genomic analysis in human lung tissue identifies novel genes for chronic obstructive pulmonary disease

Supplemental Table S5. Table containing Sherlock results. (PDF 68 kb

Additional file 2: of The value of blood cytokines and chemokines in assessing COPD

Cross Sectional Associations by Subgroup Heat Map. (PDF 156 kb

Chronic obstructive pulmonary disease and related phenotypes: polygenic risk scores in population-based and case-control cohorts

Background: Genetic factors influence chronic obstructive pulmonary disease (COPD) risk, but the individual variants that have been identified have small effects. We hypothesised that a polygenic risk score using additional variants would predict COPD and associated phenotypes.Methods: We constructed a polygenic risk score using a genome wide association study of lung function (FEV1 and FEV1/forced vital capacity [FVC]) from the UK Biobank and SpiroMeta. We tested this polygenic risk score in nine cohorts of multiple ethnicities for an association with moderate-to-severe COPD (defined as FEV1/FVC Findings: The polygenic risk score was associated with COPD in European (odds ratio [OR] per SD 1·81 [95% CI 1·74–1·88] and non-European (1·42 [1·34–1·51]) populations. Compared with the first decile, the tenth decile of the polygenic risk score was associated with COPD, with an OR of 7·99 (6·56–9·72) in European ancestry and 4·83 (3·45–6·77) in non-European ancestry cohorts. The polygenic risk score was superior to previously described genetic risk scores and, when combined with clinical risk factors (ie, age, sex, and smoking pack-years), showed improved prediction for COPD compared with a model comprising clinical risk factors alone (AUC 0·80 [0·79–0·81] vs 0·76 [0·75 0·76]). The polygenic risk score was associated with CT imaging phenotypes, including wall area percent, quantitative and qualitative measures of emphysema, local histogram emphysema patterns, and destructive emphysema subtypes. The polygenic risk score was associated with a reduced lung growth pattern. Interpretation: A risk score comprised of genetic variants can identify a small subset of individuals at markedly increased risk for moderate-to-severe COPD, emphysema subtypes associated with cigarette smoking, and patterns of reduced lung growth.</div