Scanning Capacitance Spectroscopy on n\u3csup\u3e+\u3c/sup\u3e-p Asymmetrical Junctions in Multicrystalline Si Solar Cells

We report on a scanning capacitance spectroscopy (SCS) study on the n+-p junction of multicrystalline silicon solar cells. We found that the spectra taken at space intervals of ∼10 nm exhibit characteristic features that depend strongly on the location relative to the junction. The capacitance-voltage spectra exhibit a local minimum capacitance value at the electrical junction, which allows the junction to be identified with ∼10-nm resolution. The spectra also show complicated transitions from the junction to the n-region with two local capacitance minima on the capacitance-voltage curves; similar spectra to that have not been previously reported in the literature. These distinctive spectra are due to uneven carrier-flow from both the n- and p-sides. Our results contribute significantly to the SCS study on asymmetrical junctions

On the Security of Millimeter Wave Vehicular Communication Systems using Random Antenna Subsets

Millimeter wave (mmWave) vehicular communica tion systems have the potential to improve traffic efficiency and safety. Lack of secure communication links, however, may lead to a formidable set of abuses and attacks. To secure communication links, a physical layer precoding technique for mmWave vehicular communication systems is proposed in this paper. The proposed technique exploits the large dimensional antenna arrays available at mmWave systems to produce direction dependent transmission. This results in coherent transmission to the legitimate receiver and artificial noise that jams eavesdroppers with sensitive receivers. Theoretical and numerical results demonstrate the validity and effectiveness of the proposed technique and show that the proposed technique provides high secrecy throughput when compared to conventional array and switched array transmission techniques

Enhancing discovery of genetic variants for posttraumatic stress disorder through integration of quantitative phenotypes and trauma exposure information

BACKGROUND: Posttraumatic stress disorder (PTSD) is heritable and a potential consequence of exposure to traumatic stress. Evidence suggests that a quantitative approach to PTSD phenotype measurement and incorporation of lifetime trauma exposure (LTE) information could enhance the discovery power of PTSD genome-wide association studies (GWASs). METHODS: A GWAS on PTSD symptoms was performed in 51 cohorts followed by a fixed-effects meta-analysis (N = 182,199 European ancestry participants). A GWAS of LTE burden was performed in the UK Biobank cohort (N = 132,988). Genetic correlations were evaluated with linkage disequilibrium score regression. Multivariate analysis was performed using Multi-Trait Analysis of GWAS. Functional mapping and annotation of leading loci was performed with FUMA. Replication was evaluated using the Million Veteran Program GWAS of PTSD total symptoms. RESULTS: GWASs of PTSD symptoms and LTE burden identified 5 and 6 independent genome-wide significant loci, respectively. There was a 72% genetic correlation between PTSD and LTE. PTSD and LTE showed largely similar patterns of genetic correlation with other traits, albeit with some distinctions. Adjusting PTSD for LTE reduced PTSD heritability by 31%. Multivariate analysis of PTSD and LTE increased the effective sample size of the PTSD GWAS by 20% and identified 4 additional loci. Four of these 9 PTSD loci were independently replicated in the Million Veteran Program. CONCLUSIONS: Through using a quantitative trait measure of PTSD, we identified novel risk loci not previously identified using prior case-control analyses. PTSD and LTE have a high genetic overlap that can be leveraged to increase discovery power through multivariate methods

The Genetics of Amyotrophic Lateral Sclerosis: Current Insights

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that results in loss of the upper and lower motor neurons from motor cortex, brainstem and spinal cord. Whilst the majority of cases are sporadic, around 10% show familial inheritance. ALS is usually inherited in an autosomal dominant manner, though autosomal recessive and X-linked inheritance do occur. To date, 24 of the genes at 26 loci have been identified; these include loci linked to ALS as well as to FTD-ALS, where family pedigrees contain individuals with frontotemporal dementia with/without ALS. The most commonly established genetic causes of FALS to date are the presence of a hexanucleotide repeat expansion in the C9ORF72 gene (39.3% FALS) and mutation of SOD1, TARDBP and FUS, with frequencies of 12-23.5%, 5% and 4.1% respectively. However, with the increasing use of next generation sequencing of small family pedigrees, this has led to an increasing number of genes associated with ALS. This review provides a comprehensive review on the genetics of ALS and an update of the pathogenic mechanisms associated with these genes. Commonly implicated pathways have been established, including RNA processing, the protein degradation pathways of autophagy and ubiquitin-proteasome-system as well as protein trafficking and cytoskeletal function. Elucidating the role genetics plays in both FALS and SALS is essential for understanding the subsequent cellular dysregulation that leads to motor neuron loss, in order to develop future effective therapeutic strategies