The global estimation of microplastic afloat in the ocean is only approximately 1% of annual global plastic inputs. This reflects fundamental knowledge gaps in the transformation, fragmentation, and fates of microplastics in the ocean. In order to better understand microplastic fragmentation we proceeded to a thorough physicochemical characterization of samples collected from the North Artlantic subtropical gyre during the sea campaign Expedition seventh Continent in May 2014. The results were confronted with a mathematical approach. The introduction of mass distribution in opposition to the size distribution commonly proposed in this area clarify the fragmentation pattern. The mathematical analysis of the mass distribution points out a lack of debris with mass lighter than 1 mg. Characterization by means of microscopy, microtomography, and infrared microscopy gives a better understanding of the behavior of microplastic at sea. Flat pieces of debris (2 to 5 mm in length) typically have one face that is more photodegraded (due to exposure to the sun) and the other with more biofilm, suggesting that they float in a preferred orientation. Smaller debris, with a cubic shape (below 2 mm), seems to roll at sea. All faces are evenly photodegraded and they are less colonized. The breakpoint in the mathematical model and the experimental observation around 2 mm leads to the conclusion that there is a discontinuity in the rate of fragmentation: we hypothesized that the smaller microplastics, the cubic ones mostly, are fragmented much faster than the parallelepipeds.

The microsomal antiestrogen-binding site (AEBS) is a highaffinity membranous binding site for the antitumor drug tamoxifen that selectively binds diphenylmethane derivatives of tamoxifen such as PBPE and mediates their antiproliferative properties. The AEBS is a hetero-oligomeric complex consisting of 3B-hydroxysterol-# 8 -# 7 -isomerase and 3B-hydroxysterol-# 7 -reductase. High-affinity AEBS ligands inhibit these enzymes leading to the massive intracellular accumulation of zymostenol or 7-dehydrocholesterol (DHC), thus linking AEBS binding to the modulation of cholesterol metabolism and growth control. The aim of the present study was to gain more insight into the control of breast cancer cell growth by AEBS ligands. We report that PBPE and tamoxifen treatment induced differentiation in human breast adenocarcinoma cells MCF-7 as indicated by the arrest of cells in the G 0 -G 1 phase of the cell cycle, the increase in the cell volume, the accumulation and secretion of lipids, and a milk fat globule protein found in milk. These effects were observed with other AEBS ligands and with zymostenol and DHC. Vitamin E abrogates the induction of differentiation and reverses the control of cell growth produced by AEBS ligands, zymostenol, and DHC, showing the importance of the oxidative processes in this effect. AEBS ligands induced differentiation in estrogen receptor-negative mammary tumor cell lines SKBr-3 and MDA-MB-468 but with a lower efficiency than observed with MCF-7. Together, these data show that AEBS ligands exert an antiproliferative effect on mammary cancer cells by inducing cell differentiation and growth arrest and highlight the importance of cholesterol metabolism in these effects.

The ability to self-assemble was evaluated for a large variety of amphiphilic block copolymers, including poly(ethyleneoxide-b-ε-caprolactone), poly(ethyleneoxide-b-d,l-lactide), poly(ethyleneoxide-b-styrene), poly(ethyleneoxide-b-butadiene) and poly(ethyleneoxide-b-methylmethacrylate). Different methods of formation are discussed, such as cosolvent addition, film hydration or electroformation. The influence of experimental parameters and macromolecular structures on the size and morphology of the final self-assembled structures is investigated and critically compared with the literature. The same process is carried out regarding the characterization of these structures. This analysis demonstrates the great care that should be taken when dealing with such polymeric assemblies. If the morphology of such assemblies can be predicted to some extent by macromolecular parameters like the hydrophilic/hydrophobic balance, those parameters cannot be considered as universal. In addition, external experimental parameters (methods of preparation, use of co-solvent, …) appeared as critical key parameters to obtain a good control over the final structure of such objects, which are very often not at thermodynamic equilibrium but kinetically frozen. A principal component analysis is also proposed, in order to examine the important parameters for forming the self-assemblies. Here again, the hydrophilic/hydrophobic fraction is identified as an important parameter.

Abstract-Little is known regarding the molecular mechanisms of atherogenicity of triglyceride-rich lipoproteins such as very low-density lipoproteins (VLDLs). We examined the effect of VLDL on proliferation of rat aortic smooth muscle cells, intracellular Ca 2ϩ handling, and activity of cAMP-responsive element binding protein (CREB) and nuclear factor of activated T cells (NFAT) transcription factors. VLDL, isolated from human serum, dose-and time-dependently promoted proliferation. After 4 hours of exposure to VLDL (0.15 g/L proteins), the caffeine-induced Ca 2ϩ release was inhibited and the IP3-sensitive Ca 2ϩ release induced by ATP (10 mol/L) was markedly prolonged. In quiescent cells, CREB was phosphorylated (pCREB) and NFAT was present in the cytosol, whereas in cells exposed to VLDL for 4 to 24 hours, pCREB disappeared and NFAT was translocated to the nucleus. VLDL-induced NFAT translocation and proliferation were blocked by cyclosporin A and LY294002 involving calcineurin and phosphatidylinositol 3-kinase (PI3K) pathways. Indeed, VLDLs rapidly phosphorylate protein kinase B and glycogen synthase kinase-3␤ in a PI3K-dependent way. These results provide the first evidence that VLDLs induce smooth muscle cell proliferation by activating the PI3K pathway and nuclear NFAT translocation. Blockade of the Ca 2ϩ -induced Ca 2ϩ release mechanism and dephosphorylation of pCREB contribute but were not sufficient to induce a proliferating phenotype. (Circ Res. 2003;92:1115-1122.)Key Words: vascular disease Ⅲ smooth muscle Ⅲ calcium signaling Ⅲ transcription factors Ⅲ lipoproteins H ypertriglyceridemia is considered an independent risk factor of atherosclerosis and coronary disease, 1,2 but the mechanisms of atherogenicity are not clearly defined. An increasing body of evidence supports multiple roles for very low-density lipoproteins (VLDLs), the main carriers of triglycerides, in the development of atherosclerosis and cardiovascular diseases. The VLDLs may have an indirect role because of the strong relationship between elevated triglycerides and other atherogenic metabolic changes, including decreased levels of high-density lipoprotein (HDL) and a predominance of atherogenic small and dense low-density lipoprotein (LDL) particles. They may also have a direct influence on atherosclerosis by altering physiological functions of arterial wall cells. 2,3 A potential relationship between hypertriglyceridemia and disease progression has been suggested in studies showing that atherogenic lipoproteins induce smooth muscle cell (SMC) proliferation, a phenomenon of primary importance in atherosclerosis, restenosis after balloon injury, or neointimal occlusion of grafts. How hypertriglyceridemia alters vascular cells toward the atherosclerotic phenotype is still under intense investigation. Previous studies showed that VLDL stimulated SMC DNA replication and growth by themselves 4,5 via activation of the mitogenactivated protein kinase (MAPK) extracellular signal-regulated kinase (ERK1) and ERK2. 5 ␤VLDL, a cholesteryl ester-r...

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