Flexible n-i-p thin film silicon solar cells on polyimide foils with textured ZnO:Ga back reflector

In thin film silicon solar cells on opaque substrates in n-i-p deposition sequence where the textured transparent conductive oxide (TCO) layer serves as a back reflector, one can independently optimize the morphology of the TCO layer without compromise on transparency and conductivity of this layer and further adjust the electro-optical properties of the back contact by using additional layers on top of the textured TCO. In the present work, we use this strategy to obtain textured back reflectors for solar cells in n-i-p deposition sequence on non-transparent flexible plastic foils. Gallium doped ZnO (ZnO:Ga) films were deposited on polyimide substrates by DC magnetron sputtering at a temperature of 200 °C. A wet-chemical etching step was performed by dipping the ZnO:Ga covered foil into a diluted HCl solution. The textured ZnO:Ga is then coated with a highly reflective Ag/ZnO double layer. On this back reflector, we develop thin film silicon solar cells with a microcrystalline silicon absorber layer. The current density for the cell with the textured ZnO:Ga layer is ~ 23 mA/cm2, 4 mA/cm2 higher than the one without such layer, and a maximum efficiency of 7.5% is obtained for a 1 cm2 cell.Fundação para a Ciência e a Tecnologia (FCT

Auto-aggressive CXCR6+ CD8 T cells cause liver immune pathology in NASH.

Nonalcoholic steatohepatitis (NASH) is a manifestation of systemic metabolic disease related to obesity, and causes liver disease and cancer1,2. The accumulation of metabolites leads to cell stress and inflammation in the liver3, but mechanistic understandings of liver damage in NASH are incomplete. Here, using a preclinical mouse model that displays key features of human NASH (hereafter, NASH mice), we found an indispensable role for T cells in liver immunopathology. We detected the hepatic accumulation of CD8 T cells with phenotypes that combined tissue residency (CXCR6) with effector (granzyme) and exhaustion (PD1) characteristics. Liver CXCR6+ CD8 T cells were characterized by low activity of the FOXO1 transcription factor, and were abundant in NASH mice and in patients with NASH. Mechanistically, IL-15 induced FOXO1 downregulation and CXCR6 upregulation, which together rendered liver-resident CXCR6+ CD8 T cells susceptible to metabolic stimuli (including acetate and extracellular ATP) and collectively triggered auto-aggression. CXCR6+ CD8 T cells from the livers of NASH mice or of patients with NASH had similar transcriptional signatures, and showed auto-aggressive killing of cells in an MHC-class-I-independent fashion after signalling through P2X7 purinergic receptors. This killing by auto-aggressive CD8 T cells fundamentally differed from that by antigen-specific cells, which mechanistically distinguishes auto-aggressive and protective T cell immunity