Displacement Damage dose and DLTS Analyses on Triple and Single Junction solar cells irradiated with electrons and protons

Space solar cells radiation hardness is of fundamental importance in view of the future missions towards harsh radiation environment (like e.g. missions to Jupiter) and for the new spacecraft using electrical propulsion. In this paper we report the radiation data for triple junction (TJ) solar cells and related component cells. Triple junction solar cells, InGaP top cells and GaAs middle cells degrade after electron radiation as expected. With proton irradiation, a high spread in the remaining factors was observed, especially for the TJ and bottom cells. Very surprising was the germanium bottom junction that showed very high degradation after protons whereas it is quite stable against electrons. Radiation results have been analyzed by means of the Displacement Damage Dose method and DLTS spectroscopy.Comment: Abstract accepted for poster session at 2017 IEEE Nuclear and Space Radiation Effects Conference, July 17-21, New Orlean

Progress on Low-Temperature Pulsed Electron Deposition of CuInGaSe2 Solar Cells

The quest for single-stage deposition of CuInGaSe2 (CIGS) is an open race to replace very effective but capital intensive thin film solar cell manufacturing processes like multiple-stage coevaporation or sputtering combined with high pressure selenisation treatments. In this paper the most recent achievements of Low Temperature Pulsed Electron Deposition (LTPED), a novel single stage deposition process by which CIGS can be deposited at 250 °C, are presented and discussed. We show that selenium loss during the film deposition is not a problem with LTPED as good crystalline films are formed very close to the melting temperature of selenium. The mechanism of formation of good ohmic contacts between CIGS and Mo in the absence of any MoSe2 transition layers is also illustrated, followed by a brief summary of the measured characteristics of test solar cells grown by LTPED. The 17% efficiency target achieved by lab-scale CIGS devices without bandgap modulation, antireflection coating or K-doping is considered to be a crucial milestone along the path to the industrial scale-up of LTPED. The paper ends with a brief review of the open scientific and technological issues related to the scale-up and the possible future applications of the new technology

Sterol-regulated transmembrane protein TMEM86a couples LXR signaling to regulation of lysoplasmalogens in macrophages

Lysoplasmalogens are a class of vinyl ether bioactive lipids that have a central role in plasmalogen metabolism and membrane fluidity. The liver X receptor (LXR) transcription factors are important determinants of cellular lipid homeostasis owing to their ability to regulate cholesterol and fatty acid metabolism. However, their role in governing the composition of lipid species such as lysoplasmalogens in cellular membranes is less well studied. Here, we mapped the lipidome of bone marrow–derived macrophages (BMDMs) following LXR activation. We found a marked reduction in the levels of lysoplasmalogen species in the absence of changes in the levels of plasmalogens themselves. Transcriptional profiling of LXR-activated macrophages identified the gene encoding transmembrane protein 86a (TMEM86a), an integral endoplasmic reticulum protein, as a previously uncharacterized sterol-regulated gene. We demonstrate that TMEM86a is a direct transcriptional target of LXR in macrophages and microglia and that it is highly expressed in TREM2þ/ lipid-associated macrophages in human atherosclerotic plaques, where its expression positively correlates with other LXR-regulated genes. We further show that both murine and human TMEM86a display active lysoplasmalogenase activity that can be abrogated by inactivating mutations in the predicted catalytic site. Consequently, we demonstrate that overexpression of Tmem86a in BMDM markedly reduces lysoplasmalogen abundance and membrane fluidity, while reciprocally, silencing of Tmem86a increases basal lysoplasmalogen levels and abrogates the LXR-dependent reduction of this lipid species. Collectively, our findings implicate TMEM86a as a sterol-regulated lysoplasmalogenase in macrophages that contributes to sterol-dependent membrane remodeling

Global deletion of the LXR-regulated gene EEPD1 reveals macrophage-specific changes in lipid metabolism and cholesterol efflux

Background and aims: We recently reported that Endonuclease/Exonuclease/Phosphatase family Domain containing 1 (EEPD1) is a transcriptional target of the sterol-responsive nuclear Liver X Receptors (LXR) in macrophages. The aim of this study is to clarify the in vivo role of EEPD1 in whole-body and macrophage lipid handling, and in the development of atherosclerosis. Methods: We developed mice with global deletion of Eepd1 and challenged them with a high-fat- and a Westerntype diet. Bone marrow-derived macrophages (BMDM) were used for profiling transcriptomic and lipidomic changes, and evaluating cholesterol efflux in the absence of Eepd1. We transplanted bone marrow from wildtype and Eepd1KO mice into LdlrKO recipients to assess the role of myeloid-specific EEPD1 in atherogenesis. Results: Eepd1KO mice were indistinguishable from wildtype controls when fed a low-fat diet. However, when challenged with a high-fat diet or a cholesterol-containing western diet, Eepd1KO displayed enhanced weight gain, with no evident changes in plasma and hepatic lipid levels observed. Consistent with our earlier report, BMDM isolated from Eepd1KO mice had attenuated LXR-stimulated cholesterol efflux to high density lipoprotein and Apolipoprotein A1 when compared to wildtype cells. The transcriptomic and lipidomic landscape of these cells revealed a small reduction in expression of cholesterol biosynthetic genes in LXR-stimulated Eepd1KO cells, and prominent changes in diacylglycerol and hexosylceramides level and species. Changes were also observed in triglyceride and cholesterol-ester species. Myeloid-specific loss of Eepd1 did not alter atherosclerotic plaque size and collagen content in bone marrow-transplanted LdlrKO recipients. Conclusions: Loss of Eepd1 results in an altered lipidomic landscape and reduced LXR-stimulated cholesterol efflux in BMDM, but myeloid-specific loss of Eepd1 does not influence atherogenesis in mice.Financial support N.Z. is an Established Investigator of the Dutch Heart Foundation (2013T111) and is supported by a Vici grant from the Netherlands Organization for Scientific Research (NWO; 016.176.643) and an NWO ENW grant (M.22.034; GENESIS). Acknowledgments We thank Ezra van der Wel for help with the atherosclerosis lesion analysis. We also thank Nienke van Loon for her assistance and all members of the Zelcer group, Irith Koster, and Jayron Habibe for their valuable feedback and recommendations. We acknowledge the Core Facility Metabolomics of the AMC (www.cfmetabolomics.nl) for executing the lipidomics analysis