Anti-Factor V monoclonal antibody, clone BIW-5103

Soil is an important sink for perfluorooctane sulfonate (PFOS) that is a typical persistent organic pollutant with high toxicity. Understanding of PFOS sorption to various particle-size fractions of soil provides an insight into the mobility and bioavailability of PFOS in soil. This study evaluated kinetics, isotherms, and mechanisms of PFOS sorption to six soil particle-size fractions of paddy soil at environmentally relevant concentrations (0.01-1 mu g/mL). The used soil particle-size fractions included coarse sand (120.4-724.4 mm), fine sand (45.7-316.2 mm), coarse silt (17.3-79.4 mm), fine silt (1.9-39.8 mm), clay (0.5-4.4 mm), and humic acid fractions (8.2-83.7 mm) labeled as F1 similar to F6, respectively. PFOS sorption followed pseudo-second-order kinetics related to film diffusion and intraparticle diffusion, with speed-limiting phase acted by the latter. PFOS sorption isotherm data followed Freundlich model, with generally convex isotherms in larger size fractions (F1 similar to F3) but concave isotherms in smaller size fractions (F4 and F5) and humic acid fraction (F6). Increasing organic matter content, Brunner-Emmet-Teller surface area, and smaller size fractions were conducive to PFOS sorption. Hydrophobic force, divalent metal ion-bridging effect, ligand exchange, hydrogen bonding, and protein-like interaction played roles in PFOS sorption. But hydrophobic force controlled the PFOS sorption, because its relevant organic matter governed the contribution of the soil fractions to the overall PFOS sorption. The larger size fractions dominated the PFOS sorption to the original soil because of their high mass percentages (similar to 80%). This likely caused greater potential risks of PFOS migration into groundwater and bioaccumulation in crops at higher temperatures and c(e) values, based on their convex isotherms with an exothermic physical process.

Peripheral artery disease (PAD) is a leading cause of cardiovascular morbidity and mortality; however, the extent to which genetic factors increase risk for PAD is largely unknown. Using electronic health record data, we performed a genome-wide association study in the Million Veteran Program testing similar to 32 million DNA sequence variants with PAD (31,307 cases and 211,753 controls) across veterans of European, African and Hispanic ancestry. The results were replicated in an independent sample of 5,117 PAD cases and 389,291 controls from the UK Biobank. We identified 19 PAD loci, 18 of which have not been previously reported. Eleven of the 19 loci were associated with disease in three vascular beds (coronary, cerebral, peripheral), including LDLR, LPL and LPA, suggesting that therapeutic modulation of low-density lipoprotein cholesterol, the lipoprotein lipase pathway or circulating lipoprotein(a) may be efficacious for multiple atherosclerotic disease phenotypes. Conversely, four of the variants appeared to be specific for PAD, including F5 p.R506Q, highlighting the pathogenic role of thrombosis in the peripheral vascular bed and providing genetic support for Factor Xa inhibition as a therapeutic strategy for PAD. Our results highlight mechanistic similarities and differences among coronary, cerebral and peripheral atherosclerosis and provide therapeutic insights.