Minnesota Indian Resources Directory, Second Edition.

Training Center for Community Programs and Minnesota Indian Affairs Commission

Looking at the distant universe with the MeerKAT array: discovery of a luminous OH megamaser at z > 0.5

In the local universe, OH megamasers (OHMs) are detected almost exclusively in infrared-luminous galaxies, with a prevalence that increases with IR luminosity, suggesting that they trace gas-rich galaxy mergers. Given the proximity of the rest frequencies of OH and the hyperfine transition of neutral atomic hydrogen (H i), radio surveys to probe the cosmic evolution of H i in galaxies also offer exciting prospects for exploiting OHMs to probe the cosmic history of gas-rich mergers. Using observations for the Looking At the Distant Universe with the MeerKAT Array (LADUMA) deep H i survey, we report the first untargeted detection of an OHM at z > 0.5, LADUMA J033046.20-275518.1 (nicknamed "Nkalakatha"). The host system, WISEA J033046.26-275518.3, is an infrared-luminous radio galaxy whose optical redshift z ≈ 0.52 confirms the MeerKAT emission-line detection as OH at a redshift z OH = 0.5225 ± 0.0001 rather than H i at lower redshift. The detected spectral line has 18.4σ peak significance, a width of 459 ± 59 km s-1, and an integrated luminosity of (6.31 ± 0.18 [statistical] ± 0.31 [systematic]) × 103 L ⊙, placing it among the most luminous OHMs known. The galaxy's far-infrared luminosity L FIR = (1.576 ±0.013) × 1012 L ⊙ marks it as an ultraluminous infrared galaxy; its ratio of OH and infrared luminosities is similar to those for lower-redshift OHMs. A comparison between optical and OH redshifts offers a slight indication of an OH outflow. This detection represents the first step toward a systematic exploitation of OHMs as a tracer of galaxy growth at high redshifts

Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis

To elucidate the genetic architecture of amyotrophic lateral sclerosis (ALS) and find associated loci, we assembled a custom imputation reference panel from whole-genome-sequenced patients with ALS and matched controls (n = 1,861). Through imputation and mixed-model association analysis in 12,577 cases and 23,475 controls, combined with 2,579 cases and 2,767 controls in an independent replication cohort, we fine-mapped a new risk locus on chromosome 21 and identified C21orf2 as a gene associated with ALS risk. In addition, we identified MOBP and SCFD1 as new associated risk loci. We established evidence of ALS being a complex genetic trait with a polygenic architecture. Furthermore, we estimated the SNP-based heritability at 8.5%, with a distinct and important role for low-frequency variants (frequency 1–10%). This study motivates the interrogation of larger samples with full genome coverage to identify rare causal variants that underpin ALS risk