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Conservation translocations are frequently inhibited by extensive dispersal after release, which can expose animals to dispersal‐related mortality or Allee effects due to a lack of nearby conspecifics. However, translocation‐induced dispersals also provide opportunities to study how animals move across a novel landscape, and how their movements are influenced by landscape configuration and anthropogenic features. Translocation among populations is considered a potential conservation strategy for lesser prairie‐chickens (Tympanuchus pallidicinctus). We determined the influence of release area on dispersal frequency by translocated lesser prairie‐chickens and measured how lesser prairie‐chickens move through grassland landscapes through avoidance of anthropogenic features during their dispersal movements. We translocated 411 lesser prairie‐chickens from northwest Kansas to southeastern Colorado and southwestern Kansas in 2016–2019. We used satellite GPS transmitters to track 115 lesser prairie‐chickens throughout their post‐release dispersal movements. We found that almost all lesser prairie‐chickens that survived from their spring release date until June undergo post‐translocation dispersal, and there was little variation in dispersal frequency by release area (96% of all tracked birds, 100% in Baca County, Colorado, 94% in Morton County, Kansas, n = 55). Dispersal movements (male: 103 ± 73 km, female: 175 ± 108 km, n = 62) led to diffusion across landscapes, with 69% of birds settling >5 km from their release site. During dispersal movements, translocated lesser prairie‐chickens usually travel by a single 3.75 ± 4.95 km dispersal flight per day, selecting for steps that end far from roads and in Conservation Reserve Program (CRP) grasslands. Due to this “stepping stone” method of transit, landscape connectivity is optimized when <5 km separates grassland patches on the landscape. Future persistence of lesser prairie‐chicken populations can be aided through conservation of habitat and strategic placement of CRP to maximize habitat connectivity. Dispersal rates suggest that translocation is better suited to objectives for regional, rather than site‐specific, population augmentation for this species. Lesser prairie‐chickens translocated to southeastern Colorado and southwestern Kansas experienced almost universal dispersal away from the release site (96%). During dispersal movements, lesser prairie‐chickens selected for steps that ended far from roads and in Conservation Reserve Program grasslands. Dispersal rates suggest that translocation is better suited to regional, rather than site‐specific, population augmentation for this species.

Diets during critical brooding and winter periods likely influence the growth of Lesser Prairie-Chicken (Tympanuchus pallidicinctus) populations. During the brooding period, rapidly growing Lesser Prairie-Chicken chicks have high calorie demands and are restricted to foods within immediate surroundings. For adults and juveniles during cold winters, meeting thermoregulatory demands with available food items of limited nutrient content may be challenging. Our objective was to determine the primary animal and plant components of Lesser Prairie-Chicken diets among native prairie, cropland, and Conservation Reserve Program (CRP) fields in Kansas and Colorado, USA, during brooding and winter using a DNA metabarcoding approach. Lesser Prairie-Chicken fecal samples (n = 314) were collected during summer 2014 and winter 2014–2015, DNA was extracted, amplified, and sequenced. A region of the cytochrome oxidase I (COI) gene was sequenced to determine the arthropod component of the diet, and a portion of the trnL intron region was used to determine the plant component. Relying on fecal DNA to quantify dietary composition, as opposed to traditional visual identification of gut contents, revealed a greater proportion of soft-bodied arthropods than previously recorded. Among 80 fecal samples for which threshold arthropod DNA reads were obtained, 35% of the sequences were most likely from Lepidoptera, 26% from Orthoptera, 14% from Araneae, 13% from Hemiptera, and 12% from other orders. Plant sequences from 137 fecal samples were composed of species similar to Ambrosia (27%), followed by species similar to Lactuca or Taraxacum (10%), Medicago (6%), and Triticum (5%). Forbs were the predominant (>50% of reads) plant food consumed during both brood rearing and winter. The importance both of native forbs and of a broad array of arthropods that rely on forbs suggests that disturbance regimes that promote forbs may be crucial in providing food for Lesser Prairie-Chickens in the northern portion of their distribution.

Knowledge of landscape and regional circumstances where conservation programs are successful on working lands in agricultural production are needed. Converting marginal croplands to grasslands using conservation programs such as the United States Department of Agriculture Conservation Reserve Program (CRP) should be beneficial for many grassland-obligate wildlife species; however, addition of CRP grasslands may result in different population effects based on regional climate, characteristics of the surrounding landscape, or species planted or established. Within landscapes occupied by lesser prairie-chickens (Tympanuchus pallidicinctus), CRP may provide habitat only for specific life stages and habitat selection for CRP may vary between wet and dry years. Among all study sites, we captured and fitted 280 female lesser prairie-chickens with very high frequency (VHF)- and global positioning system (GPS) transmitters during the spring lekking seasons of 2013–2015 to monitor habitat selection for CRP in regions of varying climate. We also estimated vital rates and habitat selection for 148 individuals, using sites in northwest Kansas, USA. The greatest ecological services of CRP became apparent when examining habitat selection and densities. Nest densities were approximately 3 times greater in CRP grasslands than native working grasslands (i.e., grazed), demonstrating a population-level benefit (CRP = 6.0 nests/10 km² ± 1.29 [SE], native working grassland = 1.7 nests/10 km² ± 0.62). However, CRP supporting high nest density did not provide brood habitat; 85% of females with broods surviving to 7 days moved their young to other cover types. Regression analyses indicated lesser prairie-chickens were approximately 8 times more likely to use CRP when 5,000-ha landscapes were 70% rather than 20% grassland, indicating variation in the level of ecological services provided by CRP was dependent upon composition of the larger landscape. Further, CRP grasslands were 1.7 times more likely to be used by lesser prairie-chickens in regions receiving 40 cm compared to 70 cm of average annual precipitation and during years of greater drought intensity. Demographic and resource selection analyses revealed that establishing CRP grasslands in northwest Kansas can increase the amount nesting habitat in a region where it may have previously been limited, thereby providing refugia to sustain populations through periods of extreme drought. Nest survival, adult survival during breeding, and nonbreeding season survival did not vary between lesser prairie-chickens that used and did not use CRP grasslands. The finite rate of population growth was also similar for birds using CRP and using only native working grasslands, suggesting that CRP provides habitat similar to that of native working grassland in this region. Overall, lesser prairie-chickens may thrive in landscapes that are a mosaic of native working grassland, CRP grassland, with a minimal amount of cropland, particularly when nesting and brood habitat are in close proximity.

Regional populations of lesser prairie-chickens (Tympanuchus pallidicinctus) have been declining irregularly since the early 1900s (Jensen et al. 2000). Populations in the Sand Sagebrush Prairie Ecoregion of Kansas and Colorado, USA, have been experiencing declines during the last 2 decades. Ecoregion-wide declines included the Cimarron and Comanche National Grasslands in southwestern Kansas and southeastern Colorado, respectively, from which lesser prairie-chickens were nearly extirpated by 2016. In 2014, the United States Department of Agriculture (USDA)–Forest Service created a vegetation management plan to restore lesser prairie-chicken nesting habitat on the National Grasslands. We used management plan recommendations to evaluate available nesting habitat on National Grasslands and surrounding areas for 394 transmitter-marked lesser prairiechickens translocated to the Sand Sagebrush Prairie Ecoregion during 2016–2019. We found that a small proportion of vegetation measurements met the USDA–Forest Service's 100% visual obstruction guidelines of 25.4 to 38.1 cm (Cimarron: 5.3–21.8% of observations among cover types; Comanche: 1.5–3.0%), and grass species with a high value for nesting were rare (Cimarron: 0.5–20.1% of observations within each cover type; Comanche: 1.5–3.0%). Lesser prairie-chickens selected for 2 of the 10 National Grasslands' cover types (shrubland state and warm season shortgrass state) during breeding season movements, but only shrubland state was selected for during nesting. Our results indicate that nesting habitat for lesser prairie-chickens is limited on Cimarron and Comanche National Grasslands. As private grassland was also avoided during nesting, lesser prairie-chickens in Baca and Morton counties are currently primarily relying on Conservation Reserve Program (CRP) grasslands to meet nesting habitat thresholds (Morton, KS: 17.7% CRP; Baca, CO: 16.6% CRP), which may be insufficient to sustain a viable population. Due to the impermanence of CRP, efforts to sustain local populations are likely to depend on increased improved lesser prairie-chicken nesting habitat on National Grasslands. Grazing strategies such as rest-rotation and year-long deferments may provide opportunities to restore lesser prairie-chicken habitat on sand sagebrush prairie.

IntroductionAnnual influenza vaccination reduces disease burden but vaccination rates are suboptimal, with persistent disparities among subpopulations. The purpose of this trial is to evaluate multicomponent behavioural economic nudge interventions to clinicians and patients to increase influenza vaccination. This trial also includes an intensification nudge to reduce disparities in vaccination among older adult, primary care patients.MethodsThis is a two-part, multisite cluster randomised, pragmatic clinical trial. In the first part, a multicomponent nudge intervention will be tested over approximately 6 months (September 2023–February 2024). The second part consists of a replication trial conducted at an additional site during the following influenza season (September 2024–February 2025). Primary care clinics will be randomised to the nudge intervention or usual care. Eligible clinicians and patients at intervention clinics will receive the intervention, and patients deemed high risk for not receiving a vaccine will be further randomised to receive an intensification nudge. The primary outcome is vaccine completion during the eligible visit and the secondary outcome is vaccine completion within 3 months of the eligible visit.AnalysisThe effect of the clinic-level nudge intervention on the primary and secondary outcomes will be evaluated using generalised estimating equations (GEEs) with a clinic-level exchangeable working correlation to account for clustering of observations within the clinic. GEE models with an independent working correlation will be used to evaluate the impact of the additional intensification nudge on the primary and secondary outcomes.Ethics and disseminationThe University of Pennsylvania Institutional Review Board (IRB) approved this trial and serves as the single IRB of record (IRB #851838). Results will be disseminated via peer-reviewed publication and conference presentations.Trial registration numberNCT06057727.

Background Clinical and genetic studies have implicated lipid dysfunction in Alzheimer Disease (AD) pathogenesis. While the etiologic impact of lipid intake on individuals is receiving attention, the role of food systems in shaping community-level incidence remains uncharacterized. Methods Mean country-level lipid intakes were compared to Age-Standardized Alzheimer-and-other-Dementia Incidence Rates (ASAIR) in 183 countries across all inhabited continents. Free-knot penalized spline regression and multivariable-adjusted linear regression, including a lag between intake and incidence, were used to assess the relationships between five lipid intakes and ASAIR. Validation was conducted using longitudinal within-country changes between 1990 and 2019. Results Here we show that omega-6 Polyunsaturated-Fatty-Acid (omega-6) intake exhibits a positive linear relationship with ASAIR (multivariable-adjusted model: β  = 2.44; 95%CI: 1.70, 3.19; p  = 1.38 × 10 −9 ). ASAIR also increases with saturated-fat, trans-fat, and dietary-cholesterol up to a threshold. The association between omega6-PUFA and ASAIR is confirmed using longitudinal intake changes. The scale of predicted benefits varies by country but, our results predict a 2 standard deviation decrease (−3.8% as a percent of daily energy intake) in omega-6 intake would reduce ASAIR by 8% in the US. This level of consumption has already been achieved in 20 countries. If our other findings are validated in future work, decreasing all four lipids could potentially yield large ASAIR reductions (in the US: a 35% decrease). Conclusions Higher levels of omega-6 consumption associate with increased ASAIR. Thus, decreasing omega-6 consumption on the country-level may have substantial benefits in reducing the burden of dementia. Plain language summary Scientific evidence from several fields indicates that lipids (fats) play a role in Alzheimer Disease development. However, studies conducted on the individual-level are not well suited to inform population-level interventions. In other words, we need population-based approaches to study how fat intakes vary between people in different countries and food systems. Here we used statistical models to adjust for potential biases, and we observed that the incidence of Alzheimer Disease and other dementias increased with mean country-level intake of omega-6 polyunsaturated fatty acids (omega-6). It also increased with saturated-fat, trans-fat, and cholesterol intake up to a threshold. The country-level omega-6 finding was validated in a second set of analyses that evaluated changes in fat intake over time. If future research confirms these observations, they indicate that incidence of dementia could be reduced by lowering the mean intake of omega-6 globally. Ciesielski et al. address the weaknesses of individual-level studies for population-level inference on the role of lipid consumption in dementia. In cross-sectional and longitudinal analyses of 183 countries, they find that the age-standardized incidence of dementia increases with mean country-level intake of omega6 polyunsaturated fatty acids.

Alzheimer disease (AD) is a progressive dementia with high heritability. While genome-wide association studies have identified common variation associated with AD, most of these loci have effects too small to explain the segregation of disease within multiplex families. As such, these multiplex families likely harbor novel genetic variants with strong effects, and thus still play an important role in assessing the genetic etiology of AD. Linkage analyses were conducted on 670 individuals across 70 non-Hispanic white (NHW) multiplex families for AD or mild cognitive impairment (MCI). A combination of genome wide array data and imputed data was used for the analyses. Rare variants, and low-quality variants were excluded; remaining variants were LD pruned. Linkage analyses included both multipoint (MPT) and two-point (2PT) approaches, with non-parametric, parametric (affected only; AO), and parametric (age-penetrance; AP) models. Primary analyses included (1) all AD+MCI individuals and (2) all AD+MCI individuals with age at onset 65 or lower (early-onset AD). Sensitivity analyses included the same models but excluding MCI. We identified three primary linkage regions (HLOD > 3). For the MPT-parametric-AO model (AD+MCI) we identified chromosome 5q33 (HLOD = 3.017; 149MB-156MB). A region on 8p11-p21 (20MB-37MB) was identified using the MPT-parametric-AO model (AD and early-onset models; HLOD = 3.09, 3.27). Finally, chromosome 14q22-24 (57MB-70MB) was identified using the MPT-parametric-AP model (AD+MCI; HLOD = 3.56). The 5q33 region contains IL12B and ADAM19 genes. IL12B is an inflammatory cytokine that has been associated with amyloid burden and AD affection status. ADAM19 has been associated with AD progression and has functional links to APP. The 8p locus houses the CLU locus, first identified in large AD GWAS, while the 14q locus is near the PSEN1 gene. Further analyses of whole genome sequence data in these regions are ongoing. These analyses highlighted three regions and several genes connected with Alzheimer's disease. These new loci, along with the established loci identified, may give more insight into the causes of AD for multiplex families.

Blacks are disproportionately affected by Alzheimer's disease (AD), with rates twice as high as Whites. Etiological factors of AD include behavioral (e.g., sleep) and biological (i.e., genetics) contributors. Both short and long sleep durations are associated with worsened cognitive/functional impairments among older adults. A high prevalence of sleep disturbances has been found in African populations. Genetically, carriers of the APOE-ε4 allele, which are more abundant in Blacks compared to Whites, have a significantly greater risk for developing late-onset AD compared to non-carriers, especially for females. Although the APOE-ε4 allele has also been linked to sleep duration in prior work, results have been inconsistent. Hence, we investigated how the relationship between sleep duration and extent of cognitive/functional impairment differed between APOE-ε4 carriers METHOD: A subset of older adult participants residing throughout Africa with available APOE genotyping data (n =419, 51.3% female, aged 74.8±9.2 years) were included for analysis from a population-based DAWN Alzheimer's Research Study. Subjects self-reported sleep duration within a 24-hour timeframe in hour increments. Each participant was genotyped and categorized as APOE-ε4 carriers (50.4%) or non-carriers (49.6%). The extent of cognitive/functional impairments was measured by the Clinical Dementia Rating Scale Sum of Boxes (CDR-SB) scores. Zero-inflated negative binomial regression tested how self-reported sleep durations predicted CDR-SB scores when stratified by APOE-ε4 status and sex, controlling for age, years of education, and body mass index. Across the whole sample, sleep duration was not a significant predictor of CDR-SB scores (b=0.13, p >0.05), nor was there a two-way interaction between sleep duration and APOE-ε4 status alone (b=0.08, p >0.05) or sex alone (b=0.03, p >0.05). When stratified by APOE-ε4 status and sex, however, longer sleep duration was associated with more cognitive/functional impairments in (b=0.58, p <0.01). However, this group exhibited a U-shaped curve, with the lowest CDR-SB scores observed among those who reported sleeping 5-7 hours before increasing for those who reported sleeping >7 hours. This finding suggests that changes in sleep patterns - particularly, an uncharacteristic increase in sleep duration - may be indicative of emerging/exacerbating AD-associated pathology in older Black female APOE-ε4 non-carriers.

Background Blacks are disproportionately affected by Alzheimer’s disease (AD), with rates twice as high as Whites. Etiological factors of AD include behavioral (e.g., sleep) and biological (i.e., genetics) contributors. Both short and long sleep durations are associated with worsened cognitive/functional impairments among older adults. A high prevalence of sleep disturbances has been found in African populations. Genetically, carriers of the APOE‐ε4 allele, which are more abundant in Blacks compared to Whites, have a significantly greater risk for developing late‐onset AD compared to non‐carriers, especially for females. Although the APOE‐ε4 allele has also been linked to sleep duration in prior work, results have been inconsistent. Hence, we investigated how the relationship between sleep duration and extent of cognitive/functional impairment differed between APOE‐ε4 carriers Method A subset of older adult participants residing throughout Africa with available APOE genotyping data (n =419, 51.3% female, aged 74.8±9.2 years) were included for analysis from a population‐based DAWN Alzheimer's Research Study. Subjects self‐reported sleep duration within a 24‐hour timeframe in hour increments. Each participant was genotyped and categorized as APOE‐ε4 carriers (50.4%) or non‐carriers (49.6%). The extent of cognitive/functional impairments was measured by the Clinical Dementia Rating Scale Sum of Boxes (CDR‐SB) scores. Zero‐inflated negative binomial regression tested how self‐reported sleep durations predicted CDR‐SB scores when stratified by APOE‐ε4 status and sex, controlling for age, years of education, and body mass index. Result Across the whole sample, sleep duration was not a significant predictor of CDR‐SB scores (b=0.13, p >0.05), nor was there a two‐way interaction between sleep duration and APOE‐ε4 status alone (b=0.08, p >0.05) or sex alone (b=0.03, p >0.05). When stratified by APOE‐ε4 status and sex, however, longer sleep duration was associated with more cognitive/functional impairments in (b=0.58, p <0.01). However, this group exhibited a U‐shaped curve, with the lowest CDR‐SB scores observed among those who reported sleeping 5–7 hours before increasing for those who reported sleeping >7 hours. Conclusion This finding suggests that changes in sleep patterns — particularly, an uncharacteristic increase in sleep duration — may be indicative of emerging/exacerbating AD‐associated pathology in older Black female APOE‐ε4 non‐carriers

Background Alzheimer disease (AD) is a progressive dementia with high heritability. While genome‐wide association studies have identified common variation associated with AD, most of these loci have effects too small to explain the segregation of disease within multiplex families. As such, these multiplex families likely harbor novel genetic variants with strong effects, and thus still play an important role in assessing the genetic etiology of AD. Method Linkage analyses were conducted on 670 individuals across 70 non‐Hispanic white (NHW) multiplex families for AD or mild cognitive impairment (MCI). A combination of genome wide array data and imputed data was used for the analyses. Rare variants, and low‐quality variants were excluded; remaining variants were LD pruned. Linkage analyses included both multipoint (MPT) and two‐point (2PT) approaches, with non‐parametric, parametric (affected only; AO), and parametric (age‐penetrance; AP) models. Primary analyses included (1) all AD+MCI individuals and (2) all AD+MCI individuals with age at onset 65 or lower (early‐onset AD). Sensitivity analyses included the same models but excluding MCI. Result We identified three primary linkage regions (HLOD > 3). For the MPT‐parametric‐AO model (AD+MCI) we identified chromosome 5q33 (HLOD = 3.017; 149MB‐156MB). A region on 8p11‐p21 (20MB‐37MB) was identified using the MPT‐parametric‐AO model (AD and early‐onset models; HLOD = 3.09, 3.27). Finally, chromosome 14q22‐24 (57MB‐70MB) was identified using the MPT‐parametric‐AP model (AD+MCI; HLOD = 3.56). The 5q33 region contains IL12B and ADAM19 genes. IL12B is an inflammatory cytokine that has been associated with amyloid burden and AD affection status. ADAM19 has been associated with AD progression and has functional links to APP. The 8p locus houses the CLU locus, first identified in large AD GWAS, while the 14q locus is near the PSEN1 gene. Further analyses of whole genome sequence data in these regions are ongoing. Conclusion These analyses highlighted three regions and several genes connected with Alzheimer’s disease. These new loci, along with the established loci identified, may give more insight into the causes of AD for multiplex families.