7 research outputs found
Apparent Molar Mass of a Polyelectrolyte in an Organic Solvent in the Low Ionic Strength Limit As Revealed by Light Scattering
The
apparent molar mass of a partially quaternized poly-2-vinylpyridines
(degree of quaternization 4.3% < <i>Q</i> < 35%) in
1-propanol is measured by light scattering at low ionic strength (10<sup>–6</sup> M < <i>c</i><sub>s</sub> < 10<sup>–3</sup> M) as a function of polyion repeat unit concentration
(7 × 10<sup>–5</sup> monomol/L < <i>c</i><sub>m,p</sub> < 4 × 10<sup>–2</sup> monomol/L). No
dialysis was applied prior to measurements. The apparent molar mass
under “salt-free” conditions is smaller than the true
molar mass by an order of magnitude, while approaching the true value
at higher ionic strength. Concomitant data on the dependence of scattering
intensity on scattering wave vector show that the dilute polyelectrolyte
solutions are strongly correlated. A recent theory by Muthukumar for
light scattering of dilute polyelectrolyte solutions, developed for
correlated multicomponent systems, accounts for interchain electrostatic
correlations and regularization of polymer charge by counterion binding
isotherm. The experimental results on the relation between the apparent
and true molar masses as a function of salt concentration are compared
with the predictions of Muthukumar’s counterion adsorption
theory. Taking binding equilibrium constant as a single fitting parameter,
this theory is demonstrated to describe the experimental data as long
as the chains do not interact significantly
Distribution of difficulty and relevance in n = 77 PwMS participating in the 197-item bank survey.
<p>Data as mean (SD).</p><p>Distribution of difficulty and relevance in n = 77 PwMS participating in the 197-item bank survey.</p
Characteristics associated to MS knowledge (RIKNO 1.0 total score) in 192 PwMS, (PEPADIP RCT sub-sample, baseline data) in linear regression analysis.
<p>HADS = Hospital anxiety and depression scale (19), UNDS = UK Disability Scale (17), CPS = Control Preference Scale (21), KKĂś = KontrollĂĽberzeugungen zu Gesundheit und Krankheit (20).</p><p>* corrected R<sup>2</sup></p><p>Characteristics associated to MS knowledge (RIKNO 1.0 total score) in 192 PwMS, (PEPADIP RCT sub-sample, baseline data) in linear regression analysis.</p
Characteristics of the three patient groups who participated in RIKNO 1.0 validation.
<p>*Mean (range).</p><p>** RRMS = relapsing remitting multiple sclerosis; SPMS = secondary progressive multiple sclerosis; PPMS = primary progressive multiple sclerosis.</p><p>***secondary school or higher.</p><p>Characteristics of the three patient groups who participated in RIKNO 1.0 validation.</p
The Role of Adiposity in Cardiometabolic Traits: A Mendelian Randomization Analysis
BACKGROUND: The association between adiposity and cardiometabolic traits is well known from epidemiological studies. Whilst the causal relationship is clear for some of these traits, for others it is not. We aimed to determine whether adiposity is causally related to various cardiometabolic traits using the Mendelian randomization approach. METHODS AND FINDINGS: We used the adiposity-associated variant rs9939609 at the FTO locus as an instrumental variable (IV) for body mass index (BMI) in a Mendelian randomization design. Thirty-six population-based studies of individuals of European descent contributed to the analyses. Age- and sex-adjusted regression models were fitted to test for association between (i) rs9939609 and BMI (n  =  198,502), (ii) rs9939609 and 24 traits, and (iii) BMI and 24 traits. The causal effect of BMI on the outcome measures was quantified by IV estimators. The estimators were compared to the BMI-trait associations derived from the same individuals. In the IV analysis, we demonstrated novel evidence for a causal relationship between adiposity and incident heart failure (hazard ratio, 1.19 per BMI-unit increase; 95% CI, 1.03-1.39) and replicated earlier reports of a causal association with type 2 diabetes, metabolic syndrome, dyslipidemia, and hypertension (odds ratio for IV estimator, 1.1-1.4; all p < 0.05). For quantitative traits, our results provide novel evidence for a causal effect of adiposity on the liver enzymes alanine aminotransferase and gamma-glutamyl transferase and confirm previous reports of a causal effect of adiposity on systolic and diastolic blood pressure, fasting insulin, 2-h post-load glucose from the oral glucose tolerance test, C-reactive protein, triglycerides, and high-density lipoprotein cholesterol levels (all p < 0.05). The estimated causal effects were in agreement with traditional observational measures in all instances except for type 2 diabetes, where the causal estimate was larger than the observational estimate (p  =  0.001). CONCLUSIONS: We provide novel evidence for a causal relationship between adiposity and heart failure as well as between adiposity and increased liver enzymes
Sex-stratified genoSex-stratified Genome-wide Association Studies Including 270,000 Individuals Show Sexual Dimorphism in Genetic Loci for Anthropometric Traits
Given the anthropometric differences between men and women and previous evidence of sex-difference in genetic effects, we conducted a genome-wide search for sexually dimorphic associations with height, weight, body mass index, waist circumference, hip circumference, and waist-to-hip-ratio (133,723 individuals) and took forward 348 SNPs into follow-up (additional 137,052 individuals) in a total of 94 studies. Seven loci displayed significant sex-difference (FDR<5%), including four previously established (near GRB14/COBLL1, LYPLAL1/SLC30A10, VEGFA, ADAMTS9) and three novel anthropometric trait loci (near MAP3K1, HSD17B4, PPARG), all of which were genome-wide significant in women (P<5Ă—10(-8)), but not in men. Sex-differences were apparent only for waist phenotypes, not for height, weight, BMI, or hip circumference. Moreover, we found no evidence for genetic effects with opposite directions in men versus women. The PPARG locus is of specific interest due to its role in diabetes genetics and therapy. Our results demonstrate the value of sex-specific GWAS to unravel the sexually dimorphic genetic underpinning of complex traits
Correction: The Influence of Age and Sex on Genetic Associations with Adult Body Size and Shape: A Large-Scale Genome-Wide Interaction Study.
The arcOGEN Consortium should be listed as an author of this article. They contributed to the genome-wide association study results presented in this work. They should be listed in the author byline at position 292 and affiliated with The Arthritis Research UK Osteoarthritis Genetics Consortium. They should also be included in the footnote designating consortia which is underneath the author affiliation list in the PDF version of the article, and in the S2 Text. Please view the correct S2 Text below, containing correct consortia members. S2 Text. Consortia members and extended acknowledgments.
https://doi.org/10.1371/journal.pgen.1006166.s001
(DOCX) [This corrects the article DOI: 10.1371/journal.pgen.1005378.]