Additional file 1: of General and disease-specific pain trajectories as predictors of social and political outcomes in arthritis and cancer

Table S1. Baseline health and socio-demographic characteristics of the sample. Comparisons are between the cancer and arthritis subsamples. Table S2. Binary logistic regression models modelling the relationship between pain and dropout or death in the Wave 1 ELSA respondents and the cancer and arthritis subsamples. Table S3. Model characteristics of each identified trajectory. Table S4. Uncorrected post hoc 2 × 2 χ2 tests on dropout by Wave 7 between classes. Table S5. Growth models for social and civic engagement variables (unstandardised). Table S6. Regression coefficients for age and trajectory on the intercept and slope for growth models for each index of social and civic engagement for respondents in the whole sample. Table S7. Regression coefficients for age and trajectory on the intercept and slope for growth models for each index of social and civic engagement for respondents with arthritis. Table S8. Regression coefficients for age and trajectory on the intercept and slope for growth models for each index of social and civic engagement for respondents with cancer. Figure S1. Histogram of the chronic pain measurement at Wave 1 for all Wave 1 ELSA respondents. Figure S2. Histogram of the chronic pain measurement at Wave 1 for respondents included in the arthritis subsample. Figure S3. Histogram of the chronic pain measurement at Wave 1 for respondents included in the cancer subsample. (DOCX 3796 kb

Percentage quenching of nuclease Trp fluorescence by brominated lipids.

<p>Nucleases were incubated with LUVs at P∶L of 1∶150 in 10 mM Kpi pH 7.5. Standard errors are derived from the averaging of a minimum of three independent experiments. N.Q. denotes no quenching.</p

Extent of lipid mixing induced by nuclease membrane binding.

<p>Nuclease colicins were added at P∶L of 0.02 (black bars) and 0.002 (grey bars) to DOPC∶DOPG (3∶1, solid bars) or <i>E. coli</i> lipid (striped bars) LUVs. Lipid mixing was deduced from the loss of FRET efficiency after addition of the nucleases to a LUVs suspension containing NBD-PE- and Rh-PE-labelled (0.6 mol % each) LUVs with a four-fold excess of unlabelled LUVs. The standard errors are derived from the averaging of a minimum of three independent experiments.</p

Effect of nuclease addition on LUV aggregation.

<p>Nuclease domains were added to a LUV suspension (100 µM lipid concentration) at a range of P∶L and the aggregation was monitored via measuring the OD at 436 nm. Nuclease addition to DOPC∶DOPG (3∶1) and <i>E. coli</i> lipid LUVs are depicted by closed and open symbols respectively. DNases: E7 (◊) and E9 (o), rRNase E3 (Δ). The DNases JB10 and E8 gave similar results to E9 and are omitted for clarity. The standard errors are derived from the averaging of a minimum of three independent experiments.</p

Social heterogeneity of calves, measured at the group level, during barn grouping.

<p>Social heterogeneity of calves, measured at the group level, during barn grouping.</p

Heterogeneity of social interactions.

<p>The coefficient of variation (CV) in association strength for calves in each rearing treatment during week one (a) and week four (b). Dark grey boxes show all data; light grey boxes show data when associations between previously paired calves was omitted.</p

Additional file 1: Figure S1. of Association between ethnicity and obesity with high-density lipoprotein (HDL) function and subclass distribution

Paraoxonase protein expression in white and black women. Isolated HDL (a–c) and serum (d–f) from each participant was randomly loaded and run on reducing 12.5 % SDS-PAGE gels and transferred to nitrocellulose membrane. Ponceau S staining was used to confirm equal loading. Blots were probed with mouse anti-PON-1 antibody. WN = White normal-weight. WO = White obese. BN = Black normal weight. BO = Black obese. Figure S2. PAF-AH protein expression in white and black women. Isolated HDL (a–c) and serum (d–f) from each participant was randomly loaded and run on reducing 12.5 % SDS-PAGE gels and transferred to nitrocellulose membrane. Ponceau S staining was used to confirm equal loading. Blots were probed with rabbit anti-PAF-AH antibody. WN = White normal-weight. WO = White obese. BN = Black normal weight. BO = Black obese. Figure S3. Vascular Cell Adhesion Molecule (VCAM) expression in endothelial cells treated with HDL. HUVEC cells were treated overnight with 10 μg/ml subject HDL. Cells were exposed to 20 ng/ml tumour necrosis factor (TNF) for 8 h. Cell lysates were harvested and stored in RNAprotect reagent prior to RNA extraction, followed by cDNA synthesis and quantitative real time PCR. Results are presented relative to a no-HDL treatment control. Results are means of 3 independent experiments ± SEM. Figure S4. Antioxidant capacity of isolated HDL. Isolated subject HDL was diluted in phosphate buffer and measured using the Oxygen Radical Absorbance Capacity (ORAC) assay. (PDF 403 kb

Damsel Data for Am Nat

Damsel Data for Am Na