Planted Grasslands and Native Sod Prairie: Equivalent Habitat for Grassland Birds

Little is known about how avian relationships to tracts of native sod prairie compare with avian relationships to single and multiple species of cool- and warm-season grassland plantings. We compared grassland bird species richness and density in 5 grassland cover types (n = 97) in the tallgrass prairie region of eastern South Dakota and western Minnesota, 2001–2004. Grassland bird species richness was significantly higher in native sod prairies than it was in all planted cover types except warm-season mixes. Grasslands dominated by exotic species did not support as many grassland bird species or have species densities as high as grasslands containing native species. Intermediate wheatgrass monotypes and cool-season mixes comprised of exotic species contained 40%–60% fewer grassland bird species than native sod prairie. Bobolink (Dolichonyx oryzivorus) density was 68% and 51% lower in intermediate wheatgrass monotypes and cool-season mixes, respectively, than it was in switchgrass monotypes. Clay-colored Sparrow (Spizella pallida) density was 75%–91% higher in native sod prairies than it was in any other cover type. Savannah Sparrow (Passerculus sandwichensis) density was 72% higher in native prairie than it was in grasslands dominated by exotic species. We recommend incorporating a diversity of native plant species into grassland plantings for biomass fuels or wildlife, rather than using monotypes or exotic species, to provide habitat for grassland birds. Although replacing croplands with planted grasslands would benefit grassland bird populations, we caution that replacing existing native sod tracts with planted grasslands would be detrimental to populations of several grassland bird species

Birds of the Oak Lake Field Station

A preliminary check-off list of avian species was compiled using regional field guides shortly after the establishment of the field station (Northern Plains Biological Field Station Committee 1987). While this list has been a useful reference, little observational data have been available to establish accuracy. Field observation data were collected to verify this checklist and establish a baseline inventory of resident and migratory avifauna for the station. Obse1vations were collected Janua1y 1994 through August 1996 during bird watching expeditions and research activities. In addition, formal bird counts were conducted at eight sites along 100 m transects of 30 m fixed width from 16 May to 23 June 23 1995. Birds were tallied, based upon sight and call, along each transect on twelve dates

Patterns in Avian Community Structure and Non-Point Source Disturbance Potential Along the Land-Water Interface of a Prairie Pothole Lake

This study was conducted to test the hypothesis that bird community structure varies significantly between areas which are prone versus not prone to disturbance within the land-water interface of a prairie lake. On-site assessment of land cover and a Geographic Information System (GIS) with coverages of slope, soil erodability, soil hydrologic group and drainages were used to delineate sites prone and not prone to non-point source disturbance. Habitat and community attributes were examined within these site classes during the summer of 1995. While habitat differences between classes (prone and not prone) were inconclusive, results of avian community analyses indicated that sites prone to disturbance had significantly higher average densities (69 individuals/ha vs. 56), species richness (10.9 vs. 8.1 species) and diversity (H’=2.05 vs. 1.72) than sites not prone to disturbance. These results are consistent with observations of other ecological communities exposed to intermediate levels of disturbance. Furthermore, these results suggest a relationship between GIS generated nonpoint source disturbance potential and ecological communities within the landwater interface

Tree Cover in the Surrounding Landscape Reduces Burrowing Owl (Athene cunicularia) Occupancy of Black-Tailed Prairie Dog Colonies in South Dakota

Burrowing Owl (Athene cunicularia) population declines have led to the owl’s designation as a species of conservation concern in South Dakota. Burrowing Owls nest primarily in black-tailed prairie dog (Cynomys ludovicianus) colonies, but a significant proportion of colonies in South Dakota are not occupied by owls. We studied the influence of landscape-level habitat variables on colony selection by Burrowing Owls. We used call-playback surveys to document presence or absence of Burrowing Owls at 613 prairie dog colonies throughout western and central South Dakota. We used a geographic information system to calculate the percent cover of prairie dog colonies, grassland, cropland, and tree canopy in the surrounding landscape at four buffer sizes. We modeled Burrowing Owl occupancy of prairie dog colonies using logistic regression, and ranked models using Akaike’s Information Criterion. All competitive models contained a tree-canopy-cover variable. Increasing tree canopy cover within 800 m and 1200 m of colony centers was associated with decreasing likelihood of occupancy by Burrowing Owls. Grassland, cropland, and prairie dog colony cover variables did not influence occupancy by Burrowing Owls, and these variables did not improve model fit or discrimination. In landscapes where the presence of nesting burrows is not a limiting factor, as in central and western South Dakota, Burrowing Owls occupied colonies based on the absence of trees. Trees provide habitat for avian and mammalian predators and reduce the available foraging area for Burrowing Owls around prairie dog colonies. Management for Burrowing Owls should include conserving prairie dog colonies in landscapes with few trees and preventing the establishment of trees near occupied colonies

Association of Risk Variants in the <i>CFH </i>Gene With Elevated Levels of Coagulation and Complement Factors in Idiopathic Multifocal Choroiditis

Importance: Idiopathic multifocal choroiditis (MFC) is poorly understood, thereby hindering optimal treatment and monitoring of patients. Objective: To identify the genes and pathways associated with idiopathic MFC. Design, Setting, and Participants: This was a case-control genome-wide association study (GWAS) and protein study of blood plasma samples conducted from March 2006 to February 2022. This was a multicenter study involving 6 Dutch universities. Participants were grouped into 2 cohorts: cohort 1 consisted of Dutch patients with idiopathic MFC and controls, and cohort 2 consisted of patients with MFC and controls. Plasma samples from patients with idiopathic MFC who had not received treatment were subjected to targeted proteomics. Idiopathic MFC was diagnosed according to the Standardization of Uveitis Nomenclature (SUN) Working Group guidelines for punctate inner choroidopathy and multifocal choroiditis with panuveitis. Data were analyzed from July 2021 to October 2022. Main outcomes and measures: Genetic variants associated with idiopathic MFC and risk variants associated with plasma protein concentrations in patients. Results: This study included a total of 4437 participants in cohort 1 (170 [3.8%] Dutch patients with idiopathic MFC and 4267 [96.2%] controls; mean [SD] age, 55 [18] years; 2443 female [55%]) and 1344 participants in cohort 2 (52 [3.9%] patients with MFC and 1292 [96.1%] controls; 737 male [55%]). The primary GWAS association mapped to the CFH gene with genome-wide significance (lead variant the A allele of rs7535263; odds ratio [OR], 0.52; 95% CI, 0.41-0.64; P = 9.3 × 10-9). There was no genome-wide significant association with classical human leukocyte antigen (HLA) alleles (lead classical allele, HLA-A*31:01; P = .002). The association with rs7535263 showed consistent direction of effect in an independent cohort of 52 cases and 1292 control samples (combined meta-analysis OR, 0.58; 95% CI, 0.38-0.77; P = 3.0 × 10-8). In proteomic analysis of 87 patients, the risk allele G of rs7535263 in the CFH gene was strongly associated with increased plasma concentrations of factor H-related (FHR) proteins (eg, FHR-2, likelihood ratio test, adjusted P = 1.1 × 10-3) and proteins involved in platelet activation and the complement cascade. Conclusions and relevance: Results suggest that CFH gene variants increase systemic concentrations of key factors of the complement and coagulation cascades, thereby conferring susceptibility to idiopathic MFC. These findings suggest that the complement and coagulation pathways may be key targets for the treatment of idiopathic MFC.</p

Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons

Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons. A cross-ancestry genome-wide association meta-analysis of amyotrophic lateral sclerosis (ALS) including 29,612 patients with ALS and 122,656 controls identifies 15 risk loci with distinct genetic architectures and neuron-specific biology

Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons. A cross-ancestry genome-wide association meta-analysis of amyotrophic lateral sclerosis (ALS) including 29,612 patients with ALS and 122,656 controls identifies 15 risk loci with distinct genetic architectures and neuron-specific biology

Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

A cross-ancestry genome-wide association meta-analysis of amyotrophic lateral sclerosis (ALS) including 29,612 patients with ALS and 122,656 controls identifies 15 risk loci with distinct genetic architectures and neuron-specific biology. Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons