Single-Crystalline Perovskite Nanowire Arrays for Stable X-ray Scintillators with Micrometer Spatial Resolution.

X-ray scintillation detectors based on metal halide perovskites have shown excellent light yield, but they mostly target applications with spatial resolution at the tens of micrometers level. Here, we use a one-step solution method to grow arrays of 15-µm-long single-crystalline CsPbBr3 nanowires (NWs) in an AAO (anodized aluminum oxide) membrane template, with nanowire diameters ranging from 30 to 360 nm. The CsPbBr3 nanowires in AAO (CsPbBr3 NW/AAO) show increasing X-ray scintillation efficiency with decreasing nanowire diameter, with a maximum photon yield of ∼5 300 ph/MeV at 30 nm diameter. The CsPbBr3 NW/AAO composites also display high radiation resistance, with a scintillation-intensity decrease of only ∼20-30% after 24 h of X-ray exposure (integrated dose 162 Gyair) and almost no change after ambient storage for 2 months. X-ray images can distinguish line pairs with a spacing of 2 µm for all nanowire diameters, while slanted edge measurements show a spatial resolution of ∼160 lp/mm at modulation transfer function (MTF) = 0.1. The combination of high spatial resolution, radiation stability, and easy fabrication makes these CsPbBr3 NW/AAO scintillators a promising candidate for high-resolution X-ray imaging applications.

Mouse Idh3a mutations cause retinal degeneration and reduced mitochondrial function.

Isocitrate dehydrogenase (IDH) is an enzyme required for the production of α-ketoglutarate from isocitrate. IDH3 generates the NADH used in the mitochondria for ATP production, and is a tetramer made up of two α, one ß and one γ subunit. Loss-of-function and missense mutations in both IDH3A and IDH3B have previously been implicated in families exhibiting retinal degeneration. Using mouse models, we investigated the role of IDH3 in retinal disease and mitochondrial function. We identified mice with late-onset retinal degeneration in a screen of ageing mice carrying an ENU-induced mutation, E229K, in Idh3a Mice homozygous for this mutation exhibit signs of retinal stress, indicated by GFAP staining, as early as 3 months, but no other tissues appear to be affected. We produced a knockout of Idh3a and found that homozygous mice do not survive past early embryogenesis. Idh3a-/E229K compound heterozygous mutants exhibit a more severe retinal degeneration compared with Idh3aE229K/E229K homozygous mutants. Analysis of mitochondrial function in mutant cell lines highlighted a reduction in mitochondrial maximal respiration and reserve capacity levels in both Idh3aE229K/E229K and Idh3a-/E229K cells. Loss-of-function Idh3b mutants do not exhibit the same retinal degeneration phenotype, with no signs of retinal stress or reduction in mitochondrial respiration. It has previously been reported that the retina operates with a limited mitochondrial reserve capacity and we suggest that this, in combination with the reduced reserve capacity in mutants, explains the degenerative phenotype observed in Idh3a mutant mice.This article has an associated First Person interview with the first author of the paper.