Enhancing Biodiversity and Multifunctionality of an Organic Farmscape in California’s Central Valley

Organic farmers in the USA increasingly manage the margins of previously monocultured farmed landscapes to increase biodiversity, e.g. they restore and protect riparian corridors, plant hedgerows and construct vegetated tailwater ponds. This study attempts to link habitat enhancements, biodiversity and changes in ecosystem functions by: 1. inventorying the existing biodiversity and the associated belowground community structure and composition in the various habitats of an organic farm in California’s Central Valley; and 2. monitoring key ecosystem functions of these habitats. Two years of inventories show greater native plant diversity in non-cropped areas. While nematode diversity did not differ between habitats, functional groups were clearly associated with particular habitats as were soil microbial communities (phospholipid fatty acid analysis). Earthworm diversity did not differ between habitats, but biomass was higher in non-cropped areas. Habitats with woody vegetation stored 20% of the farmscape’s total carbon (C), despite their relatively small size (only 5% of the total farm). Two years of monitoring data of farmscape C and nitrogen (N) through emissions, run-off and leaching showed distinct tradeoffs in function associated with each habitat. Clearly habitat restoration in field margins will increase both landscape biodiversity and the multifunctionality of the farmscape as a whole

Correlates of accelerometry non-adherence in an economically disadvantaged minority urban adult population

Objectives: The purpose of this study was to examine socio-demographic and psychosocial correlates of non-adherence to an accelerometry protocol in an economically disadvantaged urban population. Design: Cross-sectional study. Methods: We analyzed 985 New York City adult participants aged 18–81 years from the Physical Activity and Redesigned Community Spaces (PARCS) study. Participants were asked to wear a hip-worn ActiGraph GT3X-BT accelerometer for one week. Adherent accelerometer wear was defined as ≥3 days of ≥8 h/day of wear over a 7-day period and non-adherent accelerometry wear was defined as any wear less than adherent wear from returned accelerometers. Examined correlates of adherence included sociodemographic and psychosocial characteristics (e.g., general physical/mental health-related quality of life, self-efficacy for exercise, stress, sense of community/neighborhood well-being, and social cohesion). Results: From the total sample, 636 (64.6%) participants provided adherent wear and 349 (35.4%) provided non-adherent wear. In multivariable analysis, younger age (odds ratio [OR] = 0.63, 95% confidence interval [CI]: 0.53–0.75), poorer health-related quality of life (OR = 0.80, 95% CI: 0.65–0.98 for physical health and OR = 0.77, 95% CI: 0.62–0.94 for mental health), lower sense of community (OR = 0.79, 95% CI: 0.62–1.00) and current smoking status (OR = 1.97, 95% CI: 1.35–2.86) were associated with non-adherent wear. Conclusions: Non-adherent wear was associated with younger age, smoking, and lower self-reported physical/mental functioning and sense of community. This information can inform targeted adherence strategies to improve physical activity and sedentary behavior estimates from accelerometry data in future studies involving an urban minority population

The Role of the Physical and Social Environment in Observed and Self-Reported Park Use in Low-Income Neighborhoods in New York City

Physical and social environments of parks and neighborhoods influence park use, but the extent of their relative influence remains unclear. This cross-sectional study examined the relationship between the physical and social environment of parks and both observed and self-reported park use in low-income neighborhoods in New York City. We conducted community- (n = 54 parks) and individual-level (n = 904 residents) analyses. At the community level, observed park use was measured using a validated park audit tool and regressed on the number of facilities and programmed activities in parks, violent crime, stop-and-frisk incidents, and traffic accidents. At the individual level, self-reported park use was regressed on perceived park quality, crime, traffic-related walkability, park use by others, and social cohesion and trust. Data were collected in 2016–2018 and analyzed in 2019–2020. At the community level, observed park use was negatively associated with stop-and-frisk (β = −0.04; SE = 0.02; p < 0.05) and positively associated with the number of park facilities (β = 1.46; SE = 0.57; p < 0.05) and events (β = 0.16; SE = 0.16; p < 0.01). At the individual level, self-reported park use was positively associated with the social cohesion and trust scale (β = 0.02; SE = 0.01; p < 0.05). These results indicate that physical and social attributes of parks, but not perceptions of parks, were significantly associated with park use. The social environment of neighborhoods at both community and individual levels was significantly related to park use. Policies for increasing park use should focus on improving the social environment of parks and surrounding communities, not only parks' physical attributes. These findings can inform urban planning and public health interventions aimed at improving the well-being of residents in low-income communities

Genetic loci regulate Sarbecovirus pathogenesis: A comparison across mice and humans

Coronavirus (CoV) cause considerable morbidity and mortality in humans and other mammals, as evidenced by the emergence of Severe Acute Respiratory CoV (SARS-CoV) in 2003, Middle East Respiratory CoV (MERS-CoV) in 2012, and SARS-CoV-2 in 2019. Although poorly characterized, natural genetic variation in human and other mammals modulate virus pathogenesis, as reflected by the spectrum of clinical outcomes ranging from asymptomatic infections to lethal disease. Using multiple human epidemic and zoonotic Sarbecoviruses, coupled with murine Collaborative Cross genetic reference populations, we identify several dozen quantitative trait loci that regulate SARS-like group-2B CoV pathogenesis and replication. Under a Chr4 QTL, we deleted a candidate interferon stimulated gene, Trim14 which resulted in enhanced SARS-CoV titers and clinical disease, suggesting an antiviral role during infection. Importantly, about 60 % of the murine QTL encode susceptibility genes identified as priority candidates from human genome-wide association studies (GWAS) studies after SARS-CoV-2 infection, suggesting that similar selective forces have targeted analogous genes and pathways to regulate Sarbecovirus disease across diverse mammalian hosts. These studies provide an experimental platform in rodents to investigate the molecular-genetic mechanisms by which potential cross mammalian susceptibility loci and genes regulate type-specific and cross-SARS-like group 2B CoV replication, immunity, and pathogenesis in rodent models. Our study also provides a paradigm for identifying susceptibility loci for other highly heterogeneous and virulent viruses that sporadically emerge from zoonotic reservoirs to plague human and animal populations

A Multitrait Locus Regulates Sarbecovirus Pathogenesis

Infectious diseases have shaped the human population genetic structure, and genetic variation influences the susceptibility to many viral diseases. However, a variety of challenges have made the implementation of traditional human Genomewide Association Studies (GWAS) approaches to study these infectious outcomes challenging. In contrast, mouse models of infectious diseases provide an experimental control and precision, which facilitates analyses and mechanistic studies of the role of genetic variation on infection. Here we use a genetic mapping cross between two distinct Collaborative Cross mouse strains with respect to severe acute respiratory syndrome coronavirus (SARS-CoV) disease outcomes. We find several loci control differential disease outcome for a variety of traits in the context of SARS-CoV infection. Importantly, we identify a locus on mouse chromosome 9 that shows conserved synteny with a human GWAS locus for SARS-CoV-2 severe disease. We follow-up and confirm a role for this locus, and identify two candidate genes, CCR9 and CXCR6, that both play a key role in regulating the severity of SARS-CoV, SARS-CoV-2, and a distantly related bat sarbecovirus disease outcomes. As such we provide a template for using experimental mouse crosses to identify and characterize multitrait loci that regulate pathogenic infectious outcomes across species. IMPORTANCE Host genetic variation is an important determinant that predicts disease outcomes following infection. In the setting of highly pathogenic coronavirus infections genetic determinants underlying host susceptibility and mortality remain unclear. To elucidate the role of host genetic variation on sarbecovirus pathogenesis and disease outcomes, we utilized the Collaborative Cross (CC) mouse genetic reference population as a model to identify susceptibility alleles to SARS-CoV and SARS-CoV-2 infections. Our findings reveal that a multitrait loci found in chromosome 9 is an important regulator of sarbecovirus pathogenesis in mice. Within this locus, we identified and validated CCR9 and CXCR6 as important regulators of host disease outcomes. Specifically, both CCR9 and CXCR6 are protective against severe SARS-CoV, SARS-CoV-2, and SARS-related HKU3 virus disease in mice. This chromosome 9 multitrait locus may be important to help identify genes that regulate coronavirus disease outcomes in humans

Modeling Host Genetic Regulation of Influenza Pathogenesis in the Collaborative Cross

Genetic variation contributes to host responses and outcomes following infection by influenza A virus or other viral infections. Yet narrow windows of disease symptoms and confounding environmental factors have made it difficult to identify polymorphic genes that contribute to differential disease outcomes in human populations. Therefore, to control for these confounding environmental variables in a system that models the levels of genetic diversity found in outbred populations such as humans, we used incipient lines of the highly genetically diverse Collaborative Cross (CC) recombinant inbred (RI) panel (the pre-CC population) to study how genetic variation impacts influenza associated disease across a genetically diverse population. A wide range of variation in influenza disease related phenotypes including virus replication, virus-induced inflammation, and weight loss was observed. Many of the disease associated phenotypes were correlated, with viral replication and virus-induced inflammation being predictors of virus-induced weight loss. Despite these correlations, pre-CC mice with unique and novel disease phenotype combinations were observed. We also identified sets of transcripts (modules) that were correlated with aspects of disease. In order to identify how host genetic polymorphisms contribute to the observed variation in disease, we conducted quantitative trait loci (QTL) mapping. We identified several QTL contributing to specific aspects of the host response including virus-induced weight loss, titer, pulmonary edema, neutrophil recruitment to the airways, and transcriptional expression. Existing whole-genome sequence data was applied to identify high priority candidate genes within QTL regions. A key host response QTL was located at the site of the known anti-influenza Mx1 gene. We sequenced the coding regions of Mx1 in the eight CC founder strains, and identified a novel Mx1 allele that showed reduced ability to inhibit viral replication, while maintaining protection from weight loss

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

Plant and soil microfaunal biodiversity across the borders between arable and forest ecosystems in a Mediterranean landscape

International audienceThe distribution of organisms across ecosystem borders can be indicative of trophic interactions, food-web dynamics, and the potential for recovery after disturbance. Yet relatively little is known regarding patterns and ecology of belowground organisms across borders. Our hypothesis was that incremental zonation of vegetation and soil properties at the interface between cultivated fields and forests may facilitate the recolonization of a more complex soil faunal assemblage after disturbance ceases. Vegetation, soil characteristics, and soil nematodes (indicators of disturbance) were studied at the interface between arable and natural ecosystems (oak forest and maquis shrubland) in southwestern France. Sampling was along 23-m long transects, at six positions (center and edge of grain fields, both sides of field borders, and bands of shrub and forest vegetation) at four sites. Plant functional groups changed more markedly than species richness. Total soil carbon (C) and nematode biomass were 3.5 and 6 times higher in the forest than in the center of the cultivated fields. The nematode Structure Index gradually increased from fields to forests, along with higher total and labile soil C pools, litter, root C, and root C:N, and more negative root delta N-15. Microbivore nematodes were related to labile and total soil C. Structural equation modeling indicated that nematode predators and prey were both affected by total soil C, but proximity to the forest was important for predators, whereas plant community complexity was important for prey (i.e., microbivorous nematodes). The forested borders had minor effects on zonation of nematode assemblages and soil ecosystem services within the fields, yet woody vegetation may have facilitated recolonization by plants and soil fauna after tillage ceased and probably provided benefits for production of livestock (i.e., shade and erosion reduction) that were not measured. During plant succession, litter C and N apparently decomposed slowly into active forms in the soil, creating habitats for more K-selected, larger-bodied nematodes. Due to less cultivation and higher C inputs during the past 50 years, the more homogeneous landscape may promote more complex soil food webs, but less total agrobiodiversity, compared to the mosaic of diverse ecosystems that occurred in the ancient cultural landscape of the past