Le Courier de l'Europe

24 décembre 17841784/12/24 (VOL16,N51)-1784/12/24.Appartient à l’ensemble documentaire : NordPdeC

Clinical characteristics of the study population.

<p>Clinical characteristics of the study population.</p

Odds ratios for type 2 diabetes according to HDL endothelial protective functions and selected dyslipidemia and common risk factors.

<p>Multivariate logistic regression models included the listed dyslipidemia and other cardiovascular risk factors and odds ratios for continuous variables are presented per 1-SD increase for <b>(A)</b> HDL ability to stimulate eNOS activation, and <b>(B)</b> for the suppression of NFκB activation.</p

Vaisar et al, Type 2 Diabetes is Associated with Loss of HDL Endothelium Protective Functions

Targeted proteomics analysis of HDL from people with and without T2D. Attached files contain Skyline documents with relevant SRM-LCMS data. Data is directly accessible at PanoramaWeb Public, https://panoramaweb.org/labkey/VaisarHDL_T2D.url.<br>Original publication - Vaisar et al, PlosOne 2018.<br

Protein quantified in the targeted proteomics analysis.

<p>Protein quantified in the targeted proteomics analysis.</p

Protective effects of HDL on endothelial cells are impaired in diabetes, correlate with S1P and negatively associate with <i>in vivo</i> measure of endothelial dysfunction.

<p><b>(A)</b> The ability of HDL to suppress NFκB activation was measured as phosphorylation of p65 in HMEC after 16 h incubation with HDL (50 μg/mL) followed by 4 h stimulation with TNFα (n = 41 per group). <b>(B)</b> The ability of HDL to stimulate eNOS Ser1179 phosphorylation was measured in BAEC after 30 min incubation with HDL (50 μg/mL) (n = 38 non-diabetic, n = 41 diabetic subjects). (Data is expressed relative to cells not treated with HDL). <b>(C)</b> Sphigosine-1-phosphate concentration measured by LC-MS is reduced in patients with diabetes and <b>(D)</b> correlates positively with HDL ability to stimulate eNOS phosphorylation (n = 40 non-diabetic, n = 39 diabetic subjects; *excluded outlier and <i>P</i>-value after exclusion). <b>(E)</b> The ability of HDL to stimulate eNOS is inversely correlated negatively with level of P-selectin in plasma, an <i>in vivo</i> measure of endothelial dysfunction (Pearson correlation coefficient; n = 81 after an outlier exclusion).</p

More Than Just Nickels and Dimes: A Cross-National Analysis of Working Poverty in Affluent Democracies

Despite its centrality to contemporary inequality, working poverty is often popularly discussed but rarely studied by sociologists. Using the Luxembourg Income Study, we analyze whether an individual is working poor across 18 affluent democracies circa 2000. We demonstrate that working poverty does not simply mirror overall poverty and that there is greater cross-national variation in working than overall poverty. We then examine four explanations for working poverty: demographic characteristics, economic performance, unified theory, and welfare generosity. We utilize Heckman probit models to jointly model the likelihood of employment and poverty among the employed. Our analyses provide the least support for the economic performance explanation. There is modest support for unified theory as unionization reduces working poverty in some models. However, most of these effects appear to be mediated by welfare generosity. More substantial evidence exists for the demographic characteristics and welfare generosity explanations. An individual's likelihood of being working poor can be explained by a) a lack of multiple earners or other adults in one's household, low education, single motherhood, having children and youth; and b) the generosity of the welfare state in which he or she resides. Also, welfare generosity does not undermine employment and reduces working poverty even among demographically vulnerable groups. Ultimately, we encourage a greater role for the welfare state in debates about working poverty