Å fôra eller ikkje? Ei litteraturoversikt om fôring av storvilt

Ettersom storviltbestandane i Europa og Nord-Amerika har auka, ser folk ogso ulemper med tette bestandar. For å minska ulempene utan å redusera viltbestandane, har mange byrja å fôra. 2. Me har gått gjennom all tilgjengeleg litteratur for å sjå om forvaltarane nådde måla med fôringa og om fôringa hadde andre, ikkje planlagde fylgjer. 3. Me fann klare bevis for at fôring i periodar med lite anna fôr førde til større bestandar der kvart individ reproduserte betre. Haustvektene vart ikkje høgare ved fôring, haustvektene vart bestemt av sumarfôret. Me fann ikkje bevis for at forvaltarane klarte ved hjelp av fôring å trekkja beitinga bort frå innmark, ung furuskog eller andre attraktive matkjelder, truleg fordi det tilførde fôret ikkje tilfredsstilte nærings- og oppførselsbehova til viltet og fordi fôringa førde til tettare bestandar. Undersøkjingar viser at fôring har minska talet på påkøyrsler, men fleire undersøkjingar trengst for å få full visse. 4. Samling av mykje storvilt rundt fôringsplassar påverkar omgjevnadene. Effektane kan vera komplekse endringar i vegetasjonssamansetning og struktur. Dette kan påverka andre arter i systemet. Nokre sjukdomar vert lettare overførte når dyr samlar seg som rundt fôringsplassar. Ikkje planlagde fylgjer av fôring er lite studert, noko som gjer det vanskeleg å føreseia fylgjene. 5. Det er vanskeleg å rekna på økonomien for den einskilde jaktrettshavar då storviltbestandar gjerne kryssar eigedomsgrenser frå jakttid til fôringstid og ein ofte ikkje kjenner alle fylgjene. Fôringa fører gjerne til høgare og meir reproduktive bestandar og det kan vera vanskeleg å skilja negative verknader av det å fôra og det å ha tette bestandar. Tette bestandar kan ha langtidsverknader som folk kan oppfatta som bra eller dårlege. Før nokon set i gang større program med fôring av storvilt, bør dei grundig vurdera alle sider ved fôring og ha solid stønad frå grunneigarane i viltbestanden sitt heiltårsleveområde. Dersom dei vil slutta fôringa, må dei fyrst redusera viltbestanden. 6. Me har laga ei liste (kapittel 4.3) med punkt som forvaltarar bør gå gjennom og drøfta om dei vurderer å byrja fôra vilt.English: There are costs and benefits associated with large herbivore populations. As populations have grown, conflicts have arisen between stakeholders who benefit from high numbers and those faced with the costs. Feeding may potentially mitigate conflicts while maintaining harvest yields. 2. We created a series of hypotheses associated with the intended management goals of large herbivore feeding programmes and the commonly perceived unintended consequences. We quantified the empirical evidence in support of each hypothesis and established which factors determined the effectiveness of feeding and under what conditions unintended effects may occur. 3. We found clear and consistent evidence of demographic consequences of supplementary feeding. Reproduction and population size were enhanced in food-limited populations, where a high proportion of females had access to feed throughout the limiting season. By contrast, we found limited evidence of the effectiveness of diversionary feeding to protect crops, forestry and natural habitats, largely because any positive effects were undermined by high herbivore densities. The use of diversionary feeding to reduce traffic collisions requires further investigation. 4. Evidence indicates that unintended effects of feeding are likely when feeding causes aggregation and high densities, and when feed type does not match the foraging strategy of the target species. Unintended effects can be complex, involving habitat impacts, such as changes to vegetation composition and structure, with consequent cascading effects through the trophic levels. Disease transmission risks are also often increased. Unintended effects are generally less well studied, making clear predictions difficult. 5. The economic costs and benefits of feeding are typically borne by different stakeholder groups and may occur over different time-frames. Ethical views of feeding also vary between groups, ranging from obligation to undesirable step towards domestication. The risks of unintended consequences are likely to increase with longevity of feeding and should be considered at the outset. 6. We have written a list (chapter 4.3) with points that managers should discuss if they consider feeding wildlife

To feed or not to feed? Evidence of the intended and unintended effects of feeding wild ungulates

Ungulate populations are important natural resources, associated with both costs and benefits. Conflicts have arisen between stakeholders who benefit from high ungulate numbers and those faced with the costs. Supplementary or diversionary feeding may potentially mitigate conflicts while maintaining harvest yields but can have conservation implications. We quantified the empirical evidence for whether the intended effects, and hence management goals, of feeding are met. We also examined whether any potential unintended consequences of feeding occur and under what conditions. We found clear evidence that supplementary feeding enhanced reproduction and population growth under certain conditions. By contrast, we found limited evidence of the effectiveness of diversionary feeding to protect crops, forestry, and natural habitats, with positive effects often undermined by increases in ungulate density. However, the use of diversionary feeding to reduce traffic collisions seems promising but requires further investigation. The unintended effects of feeding are typically complex, involving changes to demography, behavior, and vegetation with consequent cascading effects on other trophic levels, as well as exacerbated risks of disease transmission. Increased ungulate density is the primary driver behind these unintended effects, the consequences of which tend to increase with longevity of feeding and affect a range of stakeholders. We urge managers to take seriously the risks as well as the economic and ethical issues before deciding to feed ungulate

The JWST Resolved Stellar Populations Early Release Science Program. II. Survey Overview

We present the JWST Resolved Stellar Populations Early Release Science (ERS) program. We obtained 27.5 hr of NIRCam and NIRISS imaging of three targets in the Local Group (Milky Way globular cluster M92, ultrafaint dwarf galaxy Draco II, and star-forming dwarf galaxy WLM), which span factors of similar to 10(5) in luminosity, similar to 10(4) in distance, and similar to 10(5) in surface brightness. We describe the survey strategy, scientific and technical goals, implementation details, present select NIRCam color-magnitude diagrams (CMDs), and validate the NIRCam exposure time calculator (ETC). Our CMDs are among the deepest in existence for each class of target. They touch the theoretical hydrogen-burning limit in M92 (<0.08 M-circle dot; M-F090W similar to +13.6), include the lowest-mass stars observed outside the Milky Way in Draco II (0.09M(circle dot); M-F090W similar to +12.1), and reach similar to 1.5 mag below the oldest main-sequence turnoff in WLM (M-F090W similar to +4.6). The PARSEC stellar models provide a good qualitative match to the NIRCam CMDs, though they are similar to 0.05 mag too blue compared to M92 F090W - F150W data. Our CMDs show detector-dependent color offsets ranging from similar to 0.02 mag in F090W - F150W to similar to 0.1 mag in F277W - F444W; these appear to be due to differences in the zero-point calibrations among the detectors. The NIRCam ETC (v2.0) matches the signal-to-noise ratios based on photon noise in uncrowded fields, but the ETC may not be accurate in more crowded fields, similar to what is known for the Hubble Space Telescope. We release the point-source photometry package DOLPHOT, optimized for NIRCam and NIRISS, for the community

Identification of a BRCA2-Specific modifier locus at 6p24 related to breast cancer risk

Common genetic variants contribute to the observed variation in breast cancer risk for BRCA2 mutation carriers; those known to date have all been found through population-based genome-wide association studies (GWAS). To comprehensively identify breast cancer risk modifying loci for BRCA2 mutation carriers, we conducted a deep replication of an ongoing GWAS discovery study. Using the ranked P-values of the breast cancer associations with the imputed genotype of 1.4 M SNPs, 19,029 SNPs were selected and designed for inclusion on a custom Illumina array that included a total of 211,155 SNPs as part of a multi-consortial project. DNA samples from 3,881 breast cancer affected and 4,330 unaffected BRCA2 mutation carriers from 47 studies belonging to the Consortium of Investigators of Modifiers of BRCA1/2 were genotyped and available for analysis. We replicated previously reported breast cancer susceptibility alleles in these BRCA2 mutation carriers and for several regions (including FGFR2, MAP3K1, CDKN2A/B, and PTHLH) identified SNPs that have stronger evidence of association than those previously published. We also identified a novel susceptibility allele at 6p24 that was inversely associated with risk in BRCA2 mutation carriers (rs9348512; per allele HR = 0.85, 95% CI 0.80-0.90, P = 3.9×10−8). This SNP was not associated with breast cancer risk either in the general population or in BRCA1 mutation carriers. The locus lies within a region containing TFAP2A, which encodes a transcriptional activation protein that interacts with several tumor suppressor genes. This report identifies the first breast cancer risk locus specific to a BRCA2 mutation background. This comprehensive update of novel and previously reported breast cancer susceptibility loci contributes to the establishment of a panel of SNPs that modify breast cancer risk in BRCA2 mutation carriers. This panel may have clinical utility for women with BRCA2 mutations weighing options for medical prevention of breast cancer

Associations of common breast cancer susceptibility alleles with risk of breast cancer subtypes in BRCA1 and BRCA2 mutation carriers

Introduction: More than 70 common alleles are known to be involved in breast cancer (BC) susceptibility, and several exhibit significant heterogeneity in their associations with different BC subtypes. Although there are differences in the association patterns between BRCA1 and BRCA2 mutation carriers and the general population for several loci, no study has comprehensively evaluated the associations of all known BC susceptibility alleles with risk of BC subtypes in BRCA1 and BRCA2 carriers. Methods: We used data from 15,252 BRCA1 and 8,211 BRCA2 carriers to analyze the associations between approximately 200,000 genetic variants on the iCOGS array and risk of BC subtypes defined by estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and triple-negative- (TN) status; morphologic subtypes; histological grade; and nodal involvement. Results: The estimated BC hazard ratios (HRs) for the 74 known BC alleles in BRCA1 carriers exhibited moderate correlations with the corresponding odds ratios from the general population. However, their associations with ER-positive BC in BRCA1 carriers were more consistent with the ER-positive as

Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3′-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk

Shared heritability and functional enrichment across six solid cancers

Correction: Nature Communications 10 (2019): art. 4386 DOI: 10.1038/s41467-019-12095-8Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (r(g) = 0.57, p = 4.6 x 10(-8)), breast and ovarian cancer (r(g) = 0.24, p = 7 x 10(-5)), breast and lung cancer (r(g) = 0.18, p = 1.5 x 10(-6)) and breast and colorectal cancer (r(g) = 0.15, p = 1.1 x 10(-4)). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis.Peer reviewe

A framework for human microbiome research

A variety of microbial communities and their genes (the microbiome) exist throughout the human body, with fundamental roles in human health and disease. The National Institutes of Health (NIH)-funded Human Microbiome Project Consortium has established a population-scale framework to develop metagenomic protocols, resulting in a broad range of quality-controlled resources and data including standardized methods for creating, processing and interpreting distinct types of high-throughput metagenomic data available to the scientific community. Here we present resources from a population of 242 healthy adults sampled at 15 or 18 body sites up to three times, which have generated 5,177 microbial taxonomic profiles from 16S ribosomal RNA genes and over 3.5 terabases of metagenomic sequence so far. In parallel, approximately 800 reference strains isolated from the human body have been sequenced. Collectively, these data represent the largest resource describing the abundance and variety of the human microbiome, while providing a framework for current and future studies