1,652 research outputs found
275 Candidates and 149 Validated Planets Orbiting Bright Stars in K2 Campaigns 0-10
Since 2014, NASA's K2 mission has observed large portions of the ecliptic
plane in search of transiting planets and has detected hundreds of planet
candidates. With observations planned until at least early 2018, K2 will
continue to identify more planet candidates. We present here 275 planet
candidates observed during Campaigns 0-10 of the K2 mission that are orbiting
stars brighter than 13 mag (in Kepler band) and for which we have obtained
high-resolution spectra (R = 44,000). These candidates are analyzed using the
VESPA package (Morton 2012, 2015b) in order to calculate their false-positive
probabilities (FPP). We find that 149 candidates are validated with an FPP
lower than 0.1%, 39 of which were previously only candidates and 56 of which
were previously undetected. The processes of data reduction, candidate
identification, and statistical validation are described, and the demographics
of the candidates and newly validated planets are explored. We show tentative
evidence of a gap in the planet radius distribution of our candidate sample.
Comparing our sample to the Kepler candidate sample investigated by Fulton et
al. (2017), we conclude that more planets are required to quantitatively
confirm the gap with K2 candidates or validated planets. This work, in addition
to increasing the population of validated K2 planets by nearly 50% and
providing new targets for follow-up observations, will also serve as a
framework for validating candidates from upcoming K2 campaigns and the
Transiting Exoplanet Survey Satellite, expected to launch in 2018.Comment: Published in AJ, 47 pages, 18 figures, 7 tables, associated
supplementary dataset available at https://zenodo.org/record/116479
New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.
Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes
Hundreds of variants clustered in genomic loci and biological pathways affect human height
Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (Pâ<â0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.
Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial
Background
Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy
Zodiacal Exoplanets in Time (ZEIT). VII. A Temperate Candidate Super-Earth in the Hyades Cluster
Transiting exoplanets in young open clusters present opportunities to study
how exoplanets evolve over their lifetimes. Recently, significant progress
detecting transiting planets in young open clusters has been made with the K2
mission, but so far all of these transiting cluster planets orbit close to
their host stars, so planet evolution can only be studied in a high-irradiation
regime. Here, we report the discovery of a long-period planet candidate, called
HD 283869 b, orbiting a member of the Hyades cluster. Using data from the K2
mission, we detected a single transit of a super-Earth-sized (1.96 +/- 0.12
R_earth) planet candidate orbiting the K-dwarf HD 283869 with a period longer
than 72 days. Since we only detected a single transit event, we cannot validate
HD 283869 b with high confidence, but our analysis of the K2 images, archival
data, and follow-up observations suggests that the source of the event is
indeed a transiting planet. We estimated the candidate's orbital parameters and
find that if real, it has a period P~100 days and receives approximately
Earth-like incident flux, giving the candidate a 71% chance of falling within
the circumstellar habitable zone. If confirmed, HD 283869 b would have the
longest orbital period, lowest incident flux, and brightest host star of any
known transiting planet in an open cluster, making it uniquely important to
future studies of how stellar irradiation affects planetary evolution.Comment: 13 pages, 9 figures, 1 table. Accepted in A
Localization of type 1 diabetes susceptibility to the MHC class I genes HLA-B and HLA-A
The major histocompatibility complex (MHC) on chromosome 6 is associated with susceptibility to more common diseases than any other region of the human genome, including almost all disorders classified as autoimmune. In type 1 diabetes the major genetic susceptibility determinants have been mapped to the MHC class II genes HLA-DQB1 and HLA-DRB1 (refs 1-3), but these genes cannot completely explain the association between type 1 diabetes and the MHC region. Owing to the region's extreme gene density, the multiplicity of disease-associated alleles, strong associations between alleles, limited genotyping capability, and inadequate statistical approaches and sample sizes, which, and how many, loci within the MHC determine susceptibility remains unclear. Here, in several large type 1 diabetes data sets, we analyse a combined total of 1,729 polymorphisms, and apply statistical methods - recursive partitioning and regression - to pinpoint disease susceptibility to the MHC class I genes HLA-B and HLA-A (risk ratios >1.5; Pcombined = 2.01 à 10-19 and 2.35 à 10-13, respectively) in addition to the established associations of the MHC class II genes. Other loci with smaller and/or rarer effects might also be involved, but to find these, future searches must take into account both the HLA class II and class I genes and use even larger samples. Taken together with previous studies, we conclude that MHC-class-I-mediated events, principally involving HLA-B*39, contribute to the aetiology of type 1 diabetes. ©2007 Nature Publishing Group
275 Candidates and 149 Validated Planets Orbiting Bright Stars in K2 Campaigns 0â10
Since 2014, NASA's K2 mission has observed large portions of the ecliptic plane in search of transiting planets and has detected hundreds of planet candidates. With observations planned until at least early 2018, K2 will continue to identify more planet candidates. We present here 275 planet candidates observed during Campaigns 0â10 of the K2 mission that are orbiting stars brighter than 13 mag (in Kepler band) and for which we have obtained high-resolution spectra (R = 44,000). These candidates are analyzed using the vespa package in order to calculate their false-positive probabilities (FPP). We find that 149 candidates are validated with an FPP lower than 0.1%, 39 of which were previously only candidates and 56 of which were previously undetected. The processes of data reduction, candidate identification, and statistical validation are described, and the demographics of the candidates and newly validated planets are explored. We show tentative evidence of a gap in the planet radius distribution of our candidate sample. Comparing our sample to the Kepler candidate sample investigated by Fulton et al., we conclude that more planets are required to quantitatively confirm the gap with K2 candidates or validated planets. This work, in addition to increasing the population of validated K2 planets by nearly 50% and providing new targets for follow-up observations, will also serve as a framework for validating candidates from upcoming K2 campaigns and the Transiting Exoplanet Survey Satellite, expected to launch in 2018
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