Avian Ecology During Oak Savanna and Woodland Restoration in the Mid-South

Disturbance-dependent ecosystems in the eastern United States have been declining since European settlement, and, in recent years, early-successional species have followed. My objective for this research was to determine if oak savanna and woodland restoration (i.e., overstory thinning and prescribed fire) was a viable method of recovering declining earlysuccessional species to the landscape of the Mid-South. At 3 sites, Catoosa Wildlife Management Area (CWMA; Tennessee), Green River Game Lands (GRGL; North Carolina), and Land Between the Lakes National Recreation Area (LBL; Tennessee), oak savanna and woodland restoration projects were established and maintained. Closed-canopy stands were thinned and a 2-year burn schedule was implemented. In Chapter One, I present on nest- and stand-level vegetation metrics associated with Prairie Warbler (Setophaga discolor) nest survival and nest-site selection at CWMA 7 years after canopy disturbance and consistent burning. In 2015 and 2016, Prairie Warblers had average nest success (0.937 ± 0.007) compared with other studies and selected for increased herbaceous groundcover around the nest compared with available habitat. Nest survival in 2015 was lower than in 2016. A positive trend between groundcover and nest survival was found. In Chapter Two, I describe nest- and stand-level vegetation metrics associated with Red-headed Woodpecker (Melanerpes erythrocephalus) nest survival and nest-site selection at CWMA 7 years after canopy disturbance and consistent burning. Red-headed Woodpeckers had very high nest success (84.1%) compared with other studies and selected nest sites with greater herbaceous groundcover, dead basal area, and midstory density (in 2016) compared with available habitat. A negative trend was found between nest survival and live basal area. In Chapter Three, I describe vegetation metrics (herbaceous groundcover, live and dead basal area, and midstory density) influencing 28 bird species’ abundances at CWMA, GRGL, and LBL 2010–2012 and 2014–2016. Moderate to high amounts of disturbance were associated with increased populations of early-successional species while low to moderate amounts of disturbance either did not affect or were positively associated with populations of most mature forest species. Oak savanna and woodland restoration is a viable method to increase populations of early-successional bird species while retaining most mature forest species

Prediction Of Runaway Episodes From Community-Based Treatment Facilities

No abstract available

A study on prescriptions contributing to the risk of high anticholinergic burden in adults with intellectual disabilities: retrospective record linkage study

Background: People with intellectual disabilities may face a disproportionate risk of experiencing high anticholinergic burden, and its negative sequalae, from a range of medications, and at younger ages than the general population, but there has been little previous study. Our aim was to determine the source of anticholinergic burden from prescribed medication. Methods: Retrospective matched observational study using record linkage. Adults with (n = 4,305), and without (n = 12,915), intellectual disabilities matched by age-, sex- and neighbourhood deprivation. The main outcome measure was the prescription of long-term (approximately 12 months use) anticholinergic medications overall (classified according to the Anticholinergic Risk Scale [ARS]), by drug class, individual drugs, and polypharmacy. Results: Adults with n = 1,654 (38.4%), and without n = 3,047 (23.6%), intellectual disabilities were prescribed medications long-term with anticholinergic effects. Of those on such drugs, adults with intellectual disabilities were most likely to be on central nervous system (62.6%), gastrointestinal (46.7%), and cardiovascular (28.4%) medications. They were prescribed more central nervous system, gynaecological/urinary tract, musculoskeletal, and respiratory medications, and less cardiovascular, infection, and endocrine medications than their matched comparators. Regardless of age, sex, or neighbourhood deprivation, adults with intellectual disabilities had greater odds of being prescribed antipsychotics (OR = 5.37 [4.40–6.57], p < 0.001), antiepileptics (OR = 2.57 [2.22–2.99], p < 0.001), and anxiolytics/hypnotics (OR = 1.28 [1.06–1.56], p = 0.012). Compared to the general population, adults with intellectual disabilities were more likely to be exposed to overall anticholinergic polypharmacy (OR = 1.48 [1.33–1.66], p < 0.001), and to psychotropic polypharmacy (OR = 2.79 [2.41–3.23], p < 0.001). Conclusions: Adults with intellectual disabilities are exposed to a greater risk of having very high anticholinergic burden through polypharmacy from several classes of medications, which may be prescribed by several different prescribers. There is a need for evidence-based recommendations specifically about people with intellectual disabilities with multiple physical and mental ill-health conditions to optimise medication use, reduce inappropriate prescribing and adverse anticholinergic effects

Genome-wide scan of 29,141 African Americans finds no evidence of directional selection since admixture.

The extent of recent selection in admixed populations is currently an unresolved question. We scanned the genomes of 29,141 African Americans and failed to find any genome-wide-significant deviations in local ancestry, indicating no evidence of selection influencing ancestry after admixture. A recent analysis of data from 1,890 African Americans reported that there was evidence of selection in African Americans after their ancestors left Africa, both before and after admixture. Selection after admixture was reported on the basis of deviations in local ancestry, and selection before admixture was reported on the basis of allele-frequency differences between African Americans and African populations. The local-ancestry deviations reported by the previous study did not replicate in our very large sample, and we show that such deviations were expected purely by chance, given the number of hypotheses tested. We further show that the previous studys conclusion of selection in African Americans before admixture is also subject to doubt. This is because the FST statistics they used were inflated and because true signals of unusual allele-frequency differences between African Americans and African populations would be best explained by selection that occurred in Africa prior to migration to the Americas

Global Patterns of Prostate Cancer Incidence, Aggressiveness, and Mortality in Men of African Descent

Prostate cancer (CaP) is the leading cancer among men of African descent in the USA, Caribbean, and Sub-Saharan Africa (SSA). The estimated number of CaP deaths in SSA during 2008 was more than five times that among African Americans and is expected to double in Africa by 2030. We summarize publicly available CaP data and collected data from the men of African descent and Carcinoma of the Prostate (MADCaP) Consortium and the African Caribbean Cancer Consortium (AC3) to evaluate CaP incidence and mortality in men of African descent worldwide. CaP incidence and mortality are highest in men of African descent in the USA and the Caribbean. Tumor stage and grade were highest in SSA. We report a higher proportion of T1 stage prostate tumors in countries with greater percent gross domestic product spent on health care and physicians per 100,000 persons. We also observed that regions with a higher proportion of advanced tumors reported lower mortality rates. This finding suggests that CaP is underdiagnosed and/or underreported in SSA men. Nonetheless, CaP incidence and mortality represent a significant public health problem in men of African descent around the world

Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation.

Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa.This work was supported by NIH fellowship F32 GM106584 (AG), NIH grants R01 MH101244(A.G.), R01 CA188392 (B.P.), U01 CA194393(B.P.), R01 GM107427 (M.L.F.), R01 CA193910 (M.L.F./M.P.) and Prostate Cancer Foundation Challenge Award (M.L.F./M.P.). This study makes use of data generated by the Wellcome Trust Case Control Consortium and the Wellcome Trust Sanger Institute. A full list of the investigators who contributed to the generation of the Wellcome Trust Case Control Consortium data is available on www.wtccc.org.uk. Funding for the Wellcome Trust Case Control Consortium project was provided by the Wellcome Trust under award 076113. This study makes use of data generated by the UK10K Consortium. A full list of the investigators who contributed to the generation of the data is available online (http://www.UK10K.org). The PRACTICAL consortium was supported by the following grants: European Commission's Seventh Framework Programme grant agreement n° 223175 (HEALTH-F2-2009-223175), Cancer Research UK Grants C5047/A7357, C1287/A10118, C5047/A3354, C5047/A10692, C16913/A6135 and The National Institute of Health (NIH) Cancer Post-Cancer GWAS initiative Grant: no. 1 U19 CA 148537-01 (the GAME-ON initiative); Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007 and C5047/A10692), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065 and 1U19 CA148112—the GAME-ON initiative), the Department of Defense (W81XWH-10-1-0341), A Linneus Centre (Contract ID 70867902), Swedish Research Council (grant no K2010-70X-20430-04-3), the Swedish Cancer Foundation (grant no 09-0677), grants RO1CA056678, RO1CA082664 and RO1CA092579 from the US National Cancer Institute, National Institutes of Health; US National Cancer Institute (R01CA72818); support from The National Health and Medical Research Council, Australia (126402, 209057, 251533, 396414, 450104, 504700, 504702, 504715, 623204, 940394 and 614296); NIH grants CA63464, CA54281 and CA098758; US National Cancer Institute (R01CA128813, PI: J.Y. Park); Bulgarian National Science Fund, Ministry of Education and Science (contract DOO-119/2009; DUNK01/2–2009; DFNI-B01/28/2012); Cancer Research UK grants [C8197/A10123] and [C8197/A10865]; grant code G0500966/75466; NIHR Health Technology Assessment Programme (projects 96/20/06 and 96/20/99); Cancer Research UK grant number C522/A8649, Medical Research Council of England grant number G0500966, ID 75466 and The NCRI, UK; The US Dept of Defense award W81XWH-04-1-0280; Australia Project Grant [390130, 1009458] and Enabling Grant [614296 to APCB]; the Prostate Cancer Foundation of Australia (Project Grant [PG7] and Research infrastructure grant [to APCB]); NIH grant R01 CA092447; Vanderbilt-Ingram Cancer Center (P30 CA68485); Cancer Research UK [C490/A10124] and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge; Competitive Research Funding of the Tampere University Hospital (9N069 and X51003); Award Number P30CA042014 from the National Cancer Institute.This is the final version of the article. It first appeared from Nature Publishing Group via http://dx.doi.org/0.1038/ncomms1097

Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer

We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 x 10(-12)), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 x 10(-10)), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 x 10(-9)) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 x 10(-8)). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 x 10(-14)). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 x 10(-7)) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies