Floating plastics in Adriatic waters (Mediterranean Sea): From the macro- to the micro-scale.

Macro- and microplastics abundances were determined in the Adriatic Sea following the MSFD TG10 protocol. The studied areas included populated gulfs, river outlets and offshore waters in five Adriatic countries. The use of small ships enabled us to detect small sized plastics (2.5-5 cm) and record average macroplastics densities of 251 ±â€¯601 items km-2, one order of magnitude higher than previously considered. Results from manta net tows for microplastics revealed an average abundance of 315,009 ±â€¯568,578 items km-2 (217 ±â€¯575 g km-2). We found significantly higher microplastics abundances in nearshore (≤4 km) than in offshore waters (>4 km) and this trend seems to affect also the small sized macro plastic fragments (2.5-5 cm). The dominant polymers were polyethylene and polypropylene while the presence of some rare polymers and waxes used in food and dentistry indicated waste water treatment plants as potential sources of microplastics.

Impaired control of the tissue factor pathway of blood coagulation in systemic lupus erythematosus.

Thrombosis is a frequent manifestation in patients with systemic lupus erythematosus (SLE), although precise mechanisms remain unclear. This study investigated whether the major physiological trigger of blood coagulation, the tissue factor (TF) pathway, was altered in SLE patients. Furthermore, we investigated potential associations between the TF pathway, the presence of antiphospholipid (APL) antibodies and other abnormalities present in SLE. A total of 101 participants (40 SLE patients and 61 age- and sex-matched controls) were recruited from Tasmania, Australia. Markers of the TF pathway, hypercoagulability, inflammation and endothelial cell damage were measured in plasma. Serum levels of APL antibodies (anti-cardiolipin antibodies [ACL], lupus anticoagulants [LAC], anti-beta2-glycoprotein-1 [anti-ß2GP1] and anti-prothrombin antibodies) were also determined. Despite similar TF and TF pathway inhibitor (TFPI) total antigen levels, SLE patients had significantly increased levels of TFPI free antigen (patients vs controls; mean ± SD) (11.6 ± 0.9 ng/mL vs 6.4 ± 0.4 ng/mL; p < 0.001) but significantly reduced TFPI activity (0.66 ± 0.07 U/mL vs 1.22 ± 0.03 U/mL; p < 0.001), compared with healthy controls. Anti-TFPI activity, designated as the ability of isolated IgG fractions to inhibit TFPI activity in normal plasma, was detected in 19/40 (47.5%) of SLE patients and 3/40 (7.5%) of healthy controls. The significant reduction in TFPI activity in SLE patients reflects impaired functional control of the TF pathway. Moreover, SLE patients with a history of thrombosis demonstrated higher levels of TFPI activity compared with patients without a previous thrombotic event (0.97 ± 0.07 U/mL vs 0.53 ± 0.14 U/mL; p = 0.0026). Changes to the TF pathway were not associated with manifestations of SLE such as inflammation or endothelial cell damage. The results from this study suggest hypercoagulability in SLE may (in part) be due to reduced TFPI activity, a mechanism that appears to be independent of other abnormalities in SLE.