Thermodynamic Modeling of a Seawater-Cooled Foldable PV Panel System

Solar-powered systems can supply clean and sustainable energy for both service requirements and also for the propulsion of marine vessels. However, the restricted available area for photovoltaic panels and high setup costs inhibits the sufficient energy production for satisfying the whole needs of vessels. Due to the limited panel area that can be installed on the vessel, it is necessary to improve the system efficiency in order to obtain more power from the existing solar panel system. In this study, cooling solar panels from the back surface with seawater in an open loop cooling water circuit for a 527-W solar-powered system are investigated. In order to observe the effects of cooling the panels, thermodynamic modeling and analysis of a foldable photovoltaic panel set have been carried out. The result illustrates the potential of these systems as the power output difference of the panel set is more than the consumed power for cooling on above-specific irradiation conditions. The remaining power output, which would be up to 37% of the uncooled system, is high enough to be utilized to speed up the marine vessels or to increase their range

Inhibition of Proliferation and Epithelial Mesenchymal Transition in Retinal Pigment Epithelial Cells by Heavy Chain-Hyaluronan/Pentraxin 3

Proliferative vitreoretinopathy (PVR) is mediated by proliferation and epithelial mesenchymal transition (EMT) of retinal pigment epithelium (RPE). Because heavy chain-hyaluronic acid/pentraxin 3 (HC-HA/PTX3) purified from human amniotic membrane exerts anti-inflammatory and anti-scarring actions, we hypothesized that HC-HA/PTX3 could inhibit these PVR-related processes in vitro. In this study, we first optimized an ARPE-19 cell culture model to mimic PVR by defining cell density, growth factors, and cultivation time. Using this low cell density culture model and HA as a control, we tested effects of HC-HA/PTX3 on the cell viability (cytotoxicity), proliferation (EGF + FGF-2) and EMT (TGF-β1). Furthermore, we determined effects of HC-HA/PTX3 on cell migration (EGF + FGF-2 + TGF-β1) and collagen gel contraction (TGF-β1). We found both HA and HC-HA/PTX3 were not toxic to unstimulated RPE cells. Only HC-HA/PTX3 dose-dependently inhibited proliferation and EMT of stimulated RPE cells by down-regulating Wnt (β-catenin, LEF1) and TGF-β (Smad2/3, collagen type I, α-SMA) signaling, respectively. Additionally, HA and HC-HA/PTX3 inhibited migration but only HC-HA/PTX3 inhibited collagen gel contraction. These results suggest HC-HA/PTX3 is a non-toxic, potent inhibitor of proliferation and EMT of RPE in vitro, and HC-HA/PTX3’s ability to inhibit PVR formation warrants evaluation in an animal model