Electrospun triple-layered PLLA/gelatin. PRGF/PLLA scaffold induces fibroblast migration

The function of fibroblast cells in wounded areas results in reconstruction of the extra cellular matrix and consequently resolution of granulation tissue. It is suggested that the use of platelet-rich plasma can accelerate the healing process in nonhealing or slow-healing wounds. In this study, a simple and novel method has been used to fabricate an electrospun three-layered scaffold containing plasma rich in growth factor with the aim of increasing the proliferation and migration of fibroblast cells in vitro. First, plasma rich in growth factor was derived from platelet rich plasma, and then a three-layered scaffold was fabricated using PLLA nanofibers as the outer layers and plasma rich in growth factor-containing gelatin fibers as the internal layer. The growth morphology of cells seeded on this scaffold was compared to those seeded on one layered PLLA scaffold. The study of the cell growth rate on different substrates and the migration of cells in response to the drug release of multilayered scaffold was investigated by the cell quantification assay and a modified under agarose assay. Scanning electron microscopy and fluorescence images showed that cells seeded on multilayered scaffold were completely oriented 72 hours after seeding compared to those seeded on PLLA scaffold. The cell quantification assay also indicated significant increase in proliferation rate of cells seeded on three-layered scaffold compared to those seeded on PLLA scaffold and finally, monitoring cell migration proved that cells migrate significantly toward the three-layered scaffold up to 48 to 72 hours and afterwards start to show a diminished migration rate toward this scaffold.     

The oxidation hypothesis of atherogenesis: the role of oxidized phospholipids and HDL

For more than two decades, there has been continuing evidence of lipid oxidation playing a central role in atherogenesis. The oxidation hypothesis of atherogenesis has evolved to focus on specific proinflammatory oxidized phospholipids that result from the oxidation of LDL phospholipids containing arachidonic acid and that are recognized by the innate immune system in animals and humans. These oxidized phospholipids are largely generated by potent oxidants produced by the lipoxygenase and myeloperoxidase pathways. The failure of antioxidant vitamins to influence clinical outcomes may have many explanations, including the inability of vitamin E to prevent the formation of these oxidized phospholipids and other lipid oxidation products of the myeloperoxidase pathway. Preliminary data suggest that the oxidation hypothesis of atherogenesis and the reverse cholesterol transport hypothesis of atherogenesis may have a common biological basis. The levels of specific oxidized lipids in plasma and lipoproteins, the levels of antibodies to these lipids, and the inflammatory/anti-inflammatory properties of HDL may be useful markers of susceptibility to atherogenesis. Apolipoprotein A-I (apoA-I) and apoA-I mimetic peptides may both promote a reduction in oxidized lipids and enhance reverse cholesterol transport and therefore may have therapeutic potential.     

Mapping the Interactions between the Alzheimer’s Aβ-Peptide and Human Serum Albumin beyond Domain Resolution

Human serum albumin (HSA) is a potent inhibitor of Aβ self-association and this novel, to our knowledge, function of HSA is of potential therapeutic interest for the treatment of Alzheimer’s disease. It is known that HSA interacts with Aβ oligomers through binding sites evenly partitioned across the three albumin domains and with comparable affinities. However, as of this writing, no information is available on the HSA-Aβ interactions beyond domain resolution. Here, we map the HSA-Aβ interactions at subdomain and peptide resolution. We show that each separate subdomain of HSA domain 3 inhibits Aβ self-association. We also show that fatty acids (FAs) compete with Aβ oligomers for binding to domain 3, but the determinant of the HSA/Aβ oligomer interactions are markedly distinct from those of FAs. Although salt bridges with the FA carboxylate determine the FA binding affinities, hydrophobic contacts are pivotal for Aβ oligomer recognition. Specifically, we identified a site of Aβ oligomer recognition that spans the HSA (494–515) region and aligns with the central hydrophobic core of Aβ. The HSA (495–515) segment includes residues affected by FA binding and this segment is prone to self-associate into β-amyloids, suggesting that sites involved in fibrilization may provide a lead to develop inhibitors of Aβ self-association.Abbreviations: AD, Alzheimer’s Disease, BBB, Blood Brain Barrier, CNS, Central Nervous System, CSF, Cerebrospinal Fluid, FA, Fatty Acid, HSA, Human Serum Albumin, ICP, Inductively Coupled Plasma, MA, Myristic Acid, SL, Spin-Lock, RC, Random Coil, STD, Saturation Transfer Difference, STR, Saturation Transfer Reference, WG, Watergate water-suppression NMR technique     

High Efficiency Perovskite‐Silicon Tandem Solar Cells: Effect of Surface Coating versus Bulk Incorporation of 2D Perovskite

Mixed‐dimensional perovskite solar cells combining 3D and 2D perovskites have recently attracted wide interest owing to improved device efficiency and stability. Yet, it remains unclear which method of combining 3D and 2D perovskites works best to obtain a mixed‐dimensional system with the advantages of both types. To address this, different strategies of combining 2D perovskites with a 3D perovskite are investigated, namely surface coating and bulk incorporation. It is found that through surface coating with different aliphatic alkylammonium bulky cations, a Ruddlesden–Popper “quasi‐2D” perovskite phase is formed on the surface of the 3D perovskite that passivates the surface defects and significantly improves the device performance. In contrast, incorporating those bulky cations into the bulk induces the formation of the pure 2D perovskite phase throughout the bulk of the 3D perovskite, which negatively affects the crystallinity and electronic structure of the 3D perovskite framework and reduces the device performance. Using the surface‐coating strategy with n‐butylammonium bromide to fabricate semitransparent perovskite cells and combining with silicon cells in four‐terminal tandem configuration, 27.7% tandem efficiency with interdigitated back contact silicon bottom cells (size‐unmatched) and 26.2% with passivated emitter with rear locally diffused silicon bottom cells is achieved in a 1 cm² size‐matched tandem.