The RadFxSat-2 Mission to Measure SEU Rates in FinFET Microelectronics

The RadFxSat-2 mission was launched January 17, 2021 with Virgin Orbit\u27s LauncherOne under the NASA ELaNa-20 initiative. RadFxSat-2 carries a radiation effects payload designed to investigate single event upsets (SEUs) in sub-65 nm commercial memories, including a FinFET-based memory. Sub-65 nm technologies have demonstrated enhanced sensitivity to low-energy protons, but current models have not considered low-energy protons as a source of SEUs. Missions utilizing the latest commercial technologies could experience a higher error rate than predicted. RadFxSat-2 was designed to assess SEU rates for FinFET SRAMs operated in low-Earth orbit (LEO), a proton-heavy environment. Details of the mission and data collected over the previous two years are presented. Results from RadFxSat-2 suggest that FinFET-based microelectronic technologies are suitable for high-performance, high-density storage in LEO

PINT: A Modern Software Package for Pulsar Timing

Over the past few decades, the measurement precision of some pulsar-timing experiments has advanced from ~10 us to ~10 ns, revealing many subtle phenomena. Such high precision demands both careful data handling and sophisticated timing models to avoid systematic error. To achieve these goals, we present PINT (PINT Is Not Tempo3), a high-precision Python pulsar timing data analysis package, which is hosted on GitHub and available on Python Package Index (PyPI) as pint-pulsar. PINT is well-tested, validated, object-oriented, and modular, enabling interactive data analysis and providing an extensible and flexible development platform for timing applications. It utilizes well-debugged public Python packages (e.g., the NumPy and Astropy libraries) and modern software development schemes (e.g., version control and efficient development with git and GitHub) and a continually expanding test suite for improved reliability, accuracy, and reproducibility. PINT is developed and implemented without referring to, copying, or transcribing the code from other traditional pulsar timing software packages (e.g., TEMPO and TEMPO2) and therefore provides a robust tool for cross-checking timing analyses and simulating pulse arrival times. In this paper, we describe the design, usage, and validation of PINT, and we compare timing results between it and TEMPO and TEMPO2.Comment: Re-submitted to the Astrophysical Journal at December 31st, 202

Cross-ancestry atlas of gene, isoform, and splicing regulation in the developing human brain

INTRODUCTION Genome-wide association studies (GWASs) have identified thousands of loci associated with neurodevelopmental and psychiatric disorders, yet our lack of understanding of the target genes and biological mechanisms underlying these associations remains a major challenge. GWAS signals for many neuropsychiatric disorders, including autism spectrum disorder, schizophrenia, and bipolar disorder, are particularly enriched for gene-regulatory elements active during human brain development. However, the lack of a unified population-scale, ancestrally diverse gene-regulatory atlas of human brain development has been a major obstacle for the functional assessment of top loci and post-GWAS integrative analyses. RATIONALE To address this critical gap in knowledge, we have uniformly processed and systematically characterized gene, isoform, and splicing quantitative trait loci (cumulatively referred to as xQTLs) in the developing human brain across 672 unique samples from 4 to 39 postconception weeks spanning European, African-American, and Latino/admixed American ancestries). With this expanded atlas, we sought to specifically localize the timing and molecular features mediating the greatest proportion of neuropsychiatric GWAS heritability, to prioritize candidate risk genes and mechanisms for top loci, and to compare with analogous results using larger adult brain functional genomic reference panels. RESULTS In total, we identified 15,752 genes harboring a gene, isoform and/or splicing cis-xQTL, including 49 genes associated with four large, recurrent inversions. Highly concordant effect sizes were observed across populations, and our diverse reference panel improved resolution to fine-map underlying candidate causal regulatory variants. Substantially more genes were found to harbor QTLs in the first versus second trimester of brain development, with a notable drop in gene expression and splicing heritability observed from 10 to 18 weeks coinciding with a period of rapidly increasing cellular heterogeneity in the developing brain. Isoform-level regulation, particularly in the second trimester, mediated a greater proportion of heritability across multiple psychiatric GWASs compared with gene expression regulation. Through colocalization and transcriptome-wide association studies, we prioritized biological mechanisms for ~60% of GWAS loci across five neuropsychiatric disorders, with >2-fold more colocalizations observed compared with larger adult brain functional genomic reference panels. We observed convergence between common and rare-variant associations, including a cryptic splicing event in the high-confidence schizophrenia risk gene SP4. Finally, we constructed a comprehensive set of developmentally regulated gene and isoform coexpression networks harboring unique cell-type specificity and genetic enrichments. Leveraging this cell-type specificity, we identified >8000 module interaction QTLs, many of which exhibited additional GWAS colocalizations. Overall, neuropsychiatric GWASs and rare variant signals localized more strongly within maturing excitatory- and interneuron-associated modules compared with those enriched for neural progenitor cell types. Results can be visualized at devbrainhub.gandallab.org. CONCLUSION We have generated a large-scale, cross-population resource of gene, isoform, and splicing regulation in the developing human brain, providing comprehensive developmental and cell-type-informed mechanistic insights into the genetic underpinnings of complex neurodevelopmental and psychiatric disorders