Taking monocrystalline silicon to the ultimate lifetime limit

A central quantity to assess the high quality of monocrystalline silicon (on scales beyond mere purity) is the minority charge carrier lifetime. We demonstrate that the lifetime in high purity float zone material can be improved beyond existing observations, thanks to a deeper understanding of grown-in defects and how they can be permanently annihilated. In a first step we investigate the influence of several process sequences on the lifetime by applying a low temperature superacid passivation treatment. We find that a pre-treatment consisting of an oxidation at 1050 °C followed by a POCl3 diffusion at 900 °C can improve the lifetime by deactivating or eliminating grown-in defects. Then, pre-treated wafers of different float zone materials are passivated with three state-of-the-art layer stacks. Very high effective lifetime values are measured, thereby demonstrating the high quality of the surface passivation schemes and the pre-treated silicon wafers. The measured effective lifetimes exceed previous records, and we report an effective lifetime of 225 ms measured on a 200 µm thick 100 Ω cm n-type silicon wafer symmetrically passivated with a layer stack of a thin thermally grown oxide and a polycrystalline layer (the TOPCon layer stack)

Theory and simulation of quantum photovoltaic devices based on the non-equilibrium Green's function formalism

This article reviews the application of the non-equilibrium Green's function formalism to the simulation of novel photovoltaic devices utilizing quantum confinement effects in low dimensional absorber structures. It covers well-known aspects of the fundamental NEGF theory for a system of interacting electrons, photons and phonons with relevance for the simulation of optoelectronic devices and introduces at the same time new approaches to the theoretical description of the elementary processes of photovoltaic device operation, such as photogeneration via coherent excitonic absorption, phonon-mediated indirect optical transitions or non-radiative recombination via defect states. While the description of the theoretical framework is kept as general as possible, two specific prototypical quantum photovoltaic devices, a single quantum well photodiode and a silicon-oxide based superlattice absorber, are used to illustrated the kind of unique insight that numerical simulations based on the theory are able to provide.Comment: 20 pages, 10 figures; invited review pape

Impacts of zero tillage on soil enzyme activities, microbial characteristics and organic matter functional chemistry in temperate soils

Zero tillage management of agricultural soils has potential for enhancing soil carbon (C) storage and reducing greenhouse gas emissions. However, the mechanisms which control carbon (C) sequestration in soil in response to zero tillage are not well understood. The aim of this study was to investigate the links between zero tillage practices and the functioning of the soil microbial community with regards to C cycling, testing the hypothesis that zero tillage enhances biological functioning in soil with positive implications for C sequestration. Specifically, we determined microbial respiration rates, enzyme activities, carbon source utilization and the functional chemistry of the soil organic matter in temperate well drained soils that had been zero tilled for seven years against annually tilled soils. Zero tilled soils contained 9% more soil C, 30% higher microbial biomass C than tilled soil and an increased presence of aromatic functional groups indicating greater preservation of recalcitrant C. Greater CO2 emission and higher respirational quotients were observed from tilled soils compared to zero tilled soils while microbial biomass was 30% greater in zero tilled soils indicating a more efficient functioning of the microbial community under zero tillage practice. Furthermore, microbial enzyme activities of dehydrogenase, cellulase, xylanase, β-glucosidase, phenol oxidase and peroxidase were higher in zero tilled soils. Considering zero tillage enhanced both microbial functioning and C storage in soil, we suggest that it offers significant promise to improve soil health and support mitigation measures against climate change

Whole Exome Sequencing of Patients with Steroid-Resistant Nephrotic Syndrome

BACKGROUND AND OBJECTIVES: Steroid-resistant nephrotic syndrome overwhelmingly progresses to ESRD. More than 30 monogenic genes have been identified to cause steroid-resistant nephrotic syndrome. We previously detected causative mutations using targeted panel sequencing in 30% of patients with steroid-resistant nephrotic syndrome. Panel sequencing has a number of limitations when compared with whole exome sequencing. We employed whole exome sequencing to detect monogenic causes of steroid-resistant nephrotic syndrome in an international cohort of 300 families. DESIGN, SETTING, PARTIIPANTS AND MEASUREMENTS: Three hundred thirty-five individuals with steroid-resistant nephrotic syndrome from 300 families were recruited from April of 1998 to June of 2016. Age of onset was restricted to <25 years of age. Exome data were evaluated for 33 known monogenic steroid-resistant nephrotic syndrome genes. RESULTS: In 74 of 300 families (25%), we identified a causative mutation in one of 20 genes known to cause steroid-resistant nephrotic syndrome. In 11 families (3.7%), we detected a mutation in a gene that causes a phenocopy of steroid-resistant nephrotic syndrome. This is consistent with our previously published identification of mutations using a panel approach. We detected a causative mutation in a known steroid-resistant nephrotic syndrome gene in 38% of consanguineous families and in 13% of nonconsanguineous families, and 48% of children with congenital nephrotic syndrome. A total of 68 different mutations were detected in 20 of 33 steroid-resistant nephrotic syndrome genes. Fifteen of these mutations were novel. NPHS1, PLCE1, NPHS2, and SMARCAL1 were the most common genes in which we detected a mutation. In another 28% of families, we detected mutations in one or more candidate genes for steroid-resistant nephrotic syndrome. CONCLUSIONS: Whole exome sequencing is a sensitive approach toward diagnosis of monogenic causes of steroid-resistant nephrotic syndrome. A molecular genetic diagnosis of steroid-resistant nephrotic syndrome may have important consequences for the management of treatment and kidney transplantation in steroid-resistant nephrotic syndrome

Mourning and melancholia revisited: correspondences between principles of Freudian metapsychology and empirical findings in neuropsychiatry

Freud began his career as a neurologist studying the anatomy and physiology of the nervous system, but it was his later work in psychology that would secure his place in history. This paper draws attention to consistencies between physiological processes identified by modern clinical research and psychological processes described by Freud, with a special emphasis on his famous paper on depression entitled 'Mourning and melancholia'. Inspired by neuroimaging findings in depression and deep brain stimulation for treatment resistant depression, some preliminary physiological correlates are proposed for a number of key psychoanalytic processes. Specifically, activation of the subgenual cingulate is discussed in relation to repression and the default mode network is discussed in relation to the ego. If these correlates are found to be reliable, this may have implications for the manner in which psychoanalysis is viewed by the wider psychological and psychiatric communities

Mutations in KEOPS-Complex Genes Cause Nephrotic Syndrome with Primary Microcephaly

Galloway-Mowat syndrome (GAMOS) is an autosomal-recessive disease characterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain anomalies. Here we identified recessive mutations in OSGEP, TP53RK, TPRKB, and LAGE3, genes encoding the four subunits of the KEOPS complex, in 37 individuals from 32 families with GAMOS. CRISPR-Cas9 knockout in zebrafish and mice recapitulated the human phenotype of primary microcephaly and resulted in early lethality. Knockdown of OSGEP, TP53RK, or TPRKB inhibited cell proliferation, which human mutations did not rescue. Furthermore, knockdown of these genes impaired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-response signaling, and ultimately induced apoptosis. Knockdown of OSGEP or TP53RK induced defects in the actin cytoskeleton and decreased the migration rate of human podocytes, an established intermediate phenotype of SRNS. We thus identified four new monogenic causes of GAMOS, describe a link between KEOPS function and human disease, and delineate potential pathogenic mechanisms