Variability in the measured parameters in one female patient with sporadic pseudo bulbar paresis, the samples were collected over 11 months with one time-point in duplicate.

<p>Variability in the measured parameters in one female patient with sporadic pseudo bulbar paresis, the samples were collected over 11 months with one time-point in duplicate.</p

Female subjects Average values ± standard deviation for parameters measured for female controls and ALS patients, fold change (ALS/controls), and p-values for females.

<p>Female subjects Average values ± standard deviation for parameters measured for female controls and ALS patients, fold change (ALS/controls), and p-values for females.</p

Male subjects Average values ± standard deviation for parameters measured for male controls, ALS patients, fold change (ALS/controls), and p-values for males.

<p>Male subjects Average values ± standard deviation for parameters measured for male controls, ALS patients, fold change (ALS/controls), and p-values for males.</p

Correlation to survival Pearson's correlation for the parameters plotted against survival from time of sampling for all subjects and Spearman's correlation for the parameters plotted against survival from time of sampling for females and males.

<p>Correlation to survival Pearson's correlation for the parameters plotted against survival from time of sampling for all subjects and Spearman's correlation for the parameters plotted against survival from time of sampling for females and males.</p

Multivariate analysis using PCA of the parameters in tables 1 and 2 (with BMI and age excluded) using two significant principal components based on eigenvalue criteria (>2).

<p>A. Females with ALS overlapped with female controls in the measured parameters. (t <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113619#pone.0113619-Andersen1" target="_blank">[1]</a>, 34% of variation vs. t <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113619#pone.0113619-Desport1" target="_blank">[2]</a>, 20% of variation; R2 = 0.67; Q2 = .25). B) The male ALS group was shifted from the male controls in the measured parameters. (t <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113619#pone.0113619-Andersen1" target="_blank">[1]</a>, 36% of variation vs. t <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113619#pone.0113619-Desport1" target="_blank">[2]</a>, 15% of variation; R2 = 0.51; Q2 = 0.22).</p

OPLS model predicting survival from the time of sampling for diet-matched ALS cases (p = 0.003).

<p>A. Survival predicted by model plotted against time of survival from sampling. B. Long survival from sampling correlated with higher levels of LDL cholesterol, total cholesterol, coenzyme Q, and VLDL cholesterol.</p

Correlation between HDL triglycerides and time of survival in female patients (A); HDL triglycerides and time of survival in female patients (B) after exclusion of one long-surviving patient (shown in A).

<p>Correlation between HDL triglycerides and time of survival in female patients (A); HDL triglycerides and time of survival in female patients (B) after exclusion of one long-surviving patient (shown in A).</p

VLDL-R expression is increased in clear-cell RCC.

<p>(<b>A</b>) Oil Red O staining of human tissue sections from normal kidney tissue (upper) and clear-cell RCC tissue (CCRCC; lower). (<b>B</b>) VLDL-R immunostaining (left) and quantification of immunostaining (right) of human tissue sections from normal kidney tissue (upper) and clear-cell RCC tissue (lower) (<i>n</i> = 6, *<i>p</i> = 0.0022). (<b>C</b>) Oil Red O staining (left) and quantification of staining (right) of cultured human cells isolated from healthy kidney tissue (upper) and clear-cell RCC tissue (lower) (<i>n</i> = 10, *<i>p</i> = 0.0058). (<b>D</b>) Quantification of VLDL-R mRNA normalized to 18S mRNA from cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue (<i>n</i> = 6, *<i>p</i> = 0.004). (<b>E</b>) Quantification of immunoblot against VLDL-R with β-actin as loading control from cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue (<i>n</i> = 6, *<i>p</i> = 0.0002). Data are shown as mean ± SEM.</p

Lipid classes in human tissue sections from normal kidney tissue and clear-cell RCC tissue (CCRCC).

<p>All values are nmol/mg. Data are mean ± SEM.</p

VLDL-R overexpression in clear-cell RCC cells is mediated by HIF-1α, and promotes increased lipid accumulation through increased lipid uptake.

<p>(<b>A</b>) Quantification of VLDL-R mRNA normalized to 18S mRNA from cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue treated with siRNA against HIF-1α or VLDL-R (<i>n</i> = 10, *<i>p</i>≤0.05 vs. control siRNA normal cells, †<i>p</i>≤0.05 vs. control siRNA clear-cell RCC cells). (<b>B</b>) Quantification of immunoblot against VLDL-R with β-actin as loading control from cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue treated with siRNA against HIF-1α or VLDL-R (<i>n</i> = 10, *<i>p</i>≤0.05 vs. control siRNA normal cells, †<i>p</i>≤0.05 vs. control siRNA clear-cell RCC cells). (<b>C</b>) Quantification of Oil Red O staining of cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue treated with siRNA against HIF-1α or VLDL-R (<i>n</i> = 10, *<i>p</i>≤0.001 vs. control siRNA normal cells, †<i>p</i>≤0.05 vs. control siRNA clear-cell RCC cells). (<b>D</b>) Quantification of fluorescently internalized DiI-labeled lipoproteins in cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue treated with siRNA against HIF-1α or VLDL-R (<i>n</i> = 5, *<i>p</i>≤0.05 vs. control siRNA normal cells, †<i>p</i>≤0.05 vs. control siRNA clear-cell RCC cells). Data are shown as mean ± SEM.</p