The Stars of the HETDEX Survey. I. Radial Velocities and Metal-Poor Stars from Low-Resolution Stellar Spectra

The Hobby-Eberly Telescope Dark Energy Experiment (HETDEX) is an unbiased, massively multiplexed spectroscopic survey, designed to measure the expansion history of the universe through low-resolution (R∼750) spectra of Lyman-Alpha Emitters. In its search for these galaxies, HETDEX will also observe a few 105 stars. In this paper, we present the first stellar value-added catalog within the internal second data release of the HETDEX Survey (HDR2). The new catalog contains 120,571 low-resolution spectra for 98,736 unique stars between 10∘) Galactic latitudes. With these spectra, we measure radial velocities (RVs) for ∼42,000 unique FGK-type stars in the catalog and show that the HETDEX spectra are sufficient to constrain these RVs with a 1σ precision of 28.0 km/s and bias of 3.5 km/s with respect to the LAMOST surveys and 1σ precision of 27.5 km/s and bias of 14.0 km/s compared to the SEGUE survey. Since these RVs are for faint (G≥16) stars, they will be complementary to Gaia. Using t-Distributed Stochastic Neighbor Embedding (t-SNE), we also demonstrate that the HETDEX spectra can be used to determine a star's Teff, and log g and its [Fe/H]. With the t-SNE projection of the FGK-type stars with HETDEX spectra we also identify 416 new candidate metal-poor ([Fe/H] <−1~dex) stars for future study. These encouraging results illustrate the utility of future low-resolution stellar spectroscopic surveys

The HETDEX Survey: Emission Line Exploration and Source Classification

The Hobby-Eberly Telescope Dark Energy Experiment (HETDEX) is an untargeted spectroscopic survey that aims to measure the expansion rate of the Universe at $z \sim 2.4$ to 1% precision for both $H(z)$ and $D_A(z)$. HETDEX is in the process of mapping in excess of one million Lyman Alpha emitting (LAE) galaxies and a similar number of lower-z galaxies as a tracer of the large-scale structure. The success of the measurement is predicated on the post-observation separation of galaxies with Ly$\alpha$ emission from the lower-$z$ interloping galaxies, primarily [OII], with low contamination and high recovery rates. The Emission Line eXplorer (ELiXer) is the principal classification tool for HETDEX, providing a tunable balance between contamination and completeness as dictated by science needs. By combining multiple selection criteria, ELiXer improves upon the 20 Angstrom rest-frame equivalent width cut commonly used to distinguish LAEs from lower-$z$ [OII] emitting galaxies. Despite a spectral resolving power, R $\sim800$, that cannot resolve the [OII] doublet, we demonstrate the ability to distinguish LAEs from foreground galaxies with 98.1% accuracy. We estimate a contamination rate of Ly$\alpha$ by [OII] of 1.2% and a Ly$\alpha$ recovery rate of 99.1% using the default ELiXer configuration. These rates meet the HETDEX science requirements.Comment: 38 pages, 11 figure

The Hobby–Eberly Telescope Dark Energy Experiment (HETDEX) Survey Design, Reductions, and Detections

We describe the survey design, calibration, commissioning, and emission-line detection algorithms for the Hobby–Eberly Telescope Dark Energy Experiment (HETDEX). The goal of HETDEX is to measure the redshifts of over a million Lyα emitting galaxies between 1.88 < z < 3.52, in a 540 deg2 area encompassing a comoving volume of 10.9 Gpc3. No preselection of targets is involved; instead the HETDEX measurements are accomplished via a spectroscopic survey using a suite of wide-field integral field units distributed over the focal plane of the telescope. This survey measures the Hubble expansion parameter and angular diameter distance, with a final expected accuracy of better than 1%. We detail the project’s observational strategy, reduction pipeline, source detection, and catalog generation, and present initial results for science verification in the Cosmological Evolution Survey, Extended Groth Strip, and Great Observatories Origins Deep Survey North fields. We demonstrate that our data reach the required specifications in throughput, astrometric accuracy, flux limit, and object detection, with the end products being a catalog of emission-line sources, their object classifications, and flux-calibrated spectra

Novel Common Genetic Susceptibility Loci for Colorectal Cancer

BACKGROUND: Previous genome-wide association studies (GWAS) have identified 42 loci (P < 5 × 10-8) associated with risk of colorectal cancer (CRC). Expanded consortium efforts facilitating the discovery of additional susceptibility loci may capture unexplained familial risk. METHODS: We conducted a GWAS in European descent CRC cases and control subjects using a discovery-replication design, followed by examination of novel findings in a multiethnic sample (cumulative n = 163 315). In the discovery stage (36 948 case subjects/30 864 control subjects), we identified genetic variants with a minor allele frequency of 1% or greater associated with risk of CRC using logistic regression followed by a fixed-effects inverse variance weighted meta-analysis. All novel independent variants reaching genome-wide statistical significance (two-sided P < 5 × 10-8) were tested for replication in separate European ancestry samples (12 952 case subjects/48 383 control subjects). Next, we examined the generalizability of discovered variants in East Asians, African Americans, and Hispanics (12 085 case subjects/22 083 control subjects). Finally, we examined the contributions of novel risk variants to familial relative risk and examined the prediction capabilities of a polygenic risk score. All statistical tests were two-sided. RESULTS: The discovery GWAS identified 11 variants associated with CRC at P < 5 × 10-8, of which nine (at 4q22.2/5p15.33/5p13.1/6p21.31/6p12.1/10q11.23/12q24.21/16q24.1/20q13.13) independently replicated at a P value of less than .05. Multiethnic follow-up supported the generalizability of discovery findings. These results demonstrated a 14.7% increase in familial relative risk explained by common risk alleles from 10.3% (95% confidence interval [CI] = 7.9% to 13.7%; known variants) to 11.9% (95% CI = 9.2% to 15.5%; known and novel variants). A polygenic risk score identified 4.3% of the population at an odds ratio for developing CRC of at least 2.0. CONCLUSIONS: This study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screenin

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals &lt;1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

Genetic variant predictors of gene expression provide new insight into risk of colorectal cancer.

Genome-wide association studies have reported 56 independently associated colorectal cancer (CRC) risk variants, most of which are non-coding and believed to exert their effects by modulating gene expression. The computational method PrediXcan uses cis-regulatory variant predictors to impute expression and perform gene-level association tests in GWAS without directly measured transcriptomes. In this study, we used reference datasets from colon (n = 169) and whole blood (n = 922) transcriptomes to test CRC association with genetically determined expression levels in a genome-wide analysis of 12,186 cases and 14,718 controls. Three novel associations were discovered from colon transverse models at FDR ≤ 0.2 and further evaluated in an independent replication including 32,825 cases and 39,933 controls. After adjusting for multiple comparisons, we found statistically significant associations using colon transcriptome models with TRIM4 (discovery P = 2.2 × 10- 4, replication P = 0.01), and PYGL (discovery P = 2.3 × 10- 4, replication P = 6.7 × 10- 4). Interestingly, both genes encode proteins that influence redox homeostasis and are related to cellular metabolic reprogramming in tumors, implicating a novel CRC pathway linked to cell growth and proliferation. Defining CRC risk regions as one megabase up- and downstream of one of the 56 independent risk variants, we defined 44 non-overlapping CRC-risk regions. Among these risk regions, we identified genes associated with CRC (P < 0.05) in 34/44 CRC-risk regions. Importantly, CRC association was found for two genes in the previously reported 2q25 locus, CXCR1 and CXCR2, which are potential cancer therapeutic targets. These findings provide strong candidate genes to prioritize for subsequent laboratory follow-up of GWAS loci. This study is the first to implement PrediXcan in a large colorectal cancer study and findings highlight the utility of integrating transcriptome data in GWAS for discovery of, and biological insight into, risk loci

Fine-mapping analysis including over 254,000 East Asian and European descendants identifies 136 putative colorectal cancer susceptibility genes

Genome-wide association studies (GWAS) have identified more than 200 common genetic variants independently associated with colorectal cancer (CRC) risk, but the causal variants and target genes are mostly unknown. We sought to fine-map all known CRC risk loci using GWAS data from 100,204 cases and 154,587 controls of East Asian and European ancestry. Our stepwise conditional analyses revealed 238 independent association signals of CRC risk, each with a set of credible causal variants (CCVs), of which 28 signals had a single CCV. Our cis-eQTL/mQTL and colocalization analyses using colorectal tissue-specific transcriptome and methylome data separately from 1299 and 321 individuals, along with functional genomic investigation, uncovered 136 putative CRC susceptibility genes, including 56 genes not previously reported. Analyses of single-cell RNA-seq data from colorectal tissues revealed 17 putative CRC susceptibility genes with distinct expression patterns in specific cell types. Analyses of whole exome sequencing data provided additional support for several target genes identified in this study as CRC susceptibility genes. Enrichment analyses of the 136 genes uncover pathways not previously linked to CRC risk. Our study substantially expanded association signals for CRC and provided additional insight into the biological mechanisms underlying CRC development

Selective <i>ortho</i>-C–H Activation in Arenes without Functional Groups

Aromatic C-H activation in alkylarenes is a key step for the synthesis of functionalised organic molecules from simple hydrocarbon precursors. Known examples of such C-H activations often yield mixtures of products resulting from activation of least-hindered C-H bonds. Here we report highly selective ortho-C-H activation in alkylarenes by simple iridium complexes. We demon-strate that the capacity of the alkyl substituent to override the typical preference of metal-mediated C-H activation for least hindered aromatic C-H bonds results from transient insertion of iridium into the benzylic C-H bond. This enables fast iridium insertion into the ortho-C-H bond, followed by regeneration of the benzylic C-H bond by reductive elimination. Bulkier alkyl substituents increase ortho-selectivity. The described chemistry comprises a conceptually new alternative to existing approaches to aromatic C-H bond activation