The KELT Follow-Up Network And Transit False-Positive Catalog: Pre-Vetted False Positives For TESS

The Kilodegree Extremely Little Telescope (KELT) project has been conducting a photometric survey of transiting planets orbiting bright stars for over 10 years. The KELT images have a pixel scale of ~23\u27\u27 pixel⁻¹—very similar to that of NASA\u27s Transiting Exoplanet Survey Satellite (TESS)—as well as a large point-spread function, and the KELT reduction pipeline uses a weighted photometric aperture with radius 3\u27. At this angular scale, multiple stars are typically blended in the photometric apertures. In order to identify false positives and confirm transiting exoplanets, we have assembled a follow-up network (KELT-FUN) to conduct imaging with spatial resolution, cadence, and photometric precision higher than the KELT telescopes, as well as spectroscopic observations of the candidate host stars. The KELT-FUN team has followed-up over 1600 planet candidates since 2011, resulting in more than 20 planet discoveries. Excluding ~450 false alarms of non-astrophysical origin (i.e., instrumental noise or systematics), we present an all-sky catalog of the 1128 bright stars (6 \u3c V \u3c 13) that show transit-like features in the KELT light curves, but which were subsequently determined to be astrophysical false positives (FPs) after photometric and/or spectroscopic follow-up observations. The KELT-FUN team continues to pursue KELT and other planet candidates and will eventually follow up certain classes of TESS candidates. The KELT FP catalog will help minimize the duplication of follow-up observations by current and future transit surveys such as TESS

KELT-22Ab: A Massive, Short-Period Hot Jupiter Transiting A Near-Solar Twin

We present the discovery of KELT-22Ab, a hot Jupiter from the KELT-South survey. KELT-22Ab transits the moderately bright (V ~ 11.1) Sun-like G2V star TYC 7518-468-1. The planet has an orbital period of P = 1.3866529 ± 0.0000027 days, a radius of RP = 1.285 ((+0.12)/(=0.071)) RJ, and a relatively large mass of MP = 3.47 ((+0.15)/(=0.14)) MJ. The star has R★ = 1.099 ((+0.079)/(=0.046)) R⊙, M★ = 1.092 ((+0.045)/(-0.041) M⊙, Teff = 5767 ((+50)/(-49) K, log g★ = 4.393 ((+0.039)/(-0.060)) (cgs), and [m/H] = +0.259 ((+0.085)/(-0.083)); thus other than its slightly super-solar metallicity, it appears to be a near-solar twin. Surprisingly, KELT-22A exhibits kinematics and a Galactic orbit that are somewhat atypical for thin-disk stars. Nevertheless, the star is rotating rapidly for its estimated age, and shows evidence of chromospheric activity. Imaging reveals a slightly fainter companion to KELT-22A that is likely bound, with a projected separation of 6\u27\u27 (~1400 au). In addition to the orbital motion caused by the transiting planet, we detect a possible linear trend in the radial velocity of KELT-22A, suggesting the presence of another relatively nearby body that is perhaps non-stellar. KELT-22Ab is highly irradiated (as a consequence of the small semimajor axis of a/R★ = 4.97), and is mildly inflated. At such small separations, tidal forces become significant. The configuration of this system is optimal for measuring the rate of tidal dissipation within the host star. Our models predict that, due to tidal forces, the semimajor axis is decreasing rapidly, and KELT-22Ab is predicted to spiral into the star within the next Gyr

KELT-24b: A 5M\u3csub\u3eJ\u3c/sub\u3e Planet on a 5.6 day Well-aligned Orbit around the Young V = 8.3 F-star HD 93148

We present the discovery of KELT-24 b, a massive hot Jupiter orbiting a bright (V = 8.3 mag, K = 7.2 mag) young F-star with a period of 5.6 days. The host star, KELT-24 (HD 93148), has a T eff = ${6509}_{-49}^{+50}$ K, a mass of M * = ${1.460}_{-0.059}^{+0.055}$ M ⊙, a radius of R * = 1.506 ± 0.022 R ⊙, and an age of ${0.78}_{-0.42}^{+0.61}$ Gyr. Its planetary companion (KELT-24 b) has a radius of R P = 1.272 ± 0.021 R J and a mass of M P = ${5.18}_{-0.22}^{+0.21}$ M J, and from Doppler tomographic observations, we find that the planet\u27s orbit is well-aligned to its host star\u27s projected spin axis ($\lambda ={2.6}_{-3.6}^{+5.1}$). The young age estimated for KELT-24 suggests that it only recently started to evolve from the zero-age main sequence. KELT-24 is the brightest star known to host a transiting giant planet with a period between 5 and 10 days. Although the circularization timescale is much longer than the age of the system, we do not detect a large eccentricity or significant misalignment that is expected from dynamical migration. The brightness of its host star and its moderate surface gravity make KELT-24b an intriguing target for detailed atmospheric characterization through spectroscopic emission measurements since it would bridge the current literature results that have primarily focused on lower mass hot Jupiters and a few brown dwarfs

KELT-25 B And KELT-26 B: A Hot Jupiter And A Substellar Companion Transiting Young A Stars Observed By TESS

We present the discoveries of KELT-25 b (TIC 65412605, TOI-626.01) and KELT-26 b (TIC 160708862, TOI-1337.01), two transiting companions orbiting relatively bright, early A stars. The transit signals were initially detected by the KELT survey and subsequently confirmed by Transiting Exoplanet Survey Satellite (TESS) photometry. KELT-25 b is on a 4.40 day orbit around the V = 9.66 star CD-24 5016 (${T}_{\mathrm{eff}}={8280}_{-180}^{+440}$ K, Msstarf = ${2.18}_{-0.11}^{+0.12}$ M⊙), while KELT-26 b is on a 3.34 day orbit around the V = 9.95 star HD 134004 (${T}_{\mathrm{eff}}$ = ${8640}_{-240}^{+500}$K, Msstarf = ${1.93}_{-0.16}^{+0.14}$M⊙), which is likely an Am star. We have confirmed the substellar nature of both companions through detailed characterization of each system using ground-based and TESS photometry, radial velocity measurements, Doppler tomography, and high-resolution imaging. For KELT-25, we determine a companion radius of RP = ${1.64}_{-0.043}^{+0.039}$RJ and a 3σ upper limit on the companion\u27s mass of ~64 MJ. For KELT-26 b, we infer a planetary mass and radius of MP = ${1.41}_{-0.51}^{+0.43}$${M}_{{\rm{J}}}$and RP = ${1.94}_{-0.058}^{+0.060}$RJ. From Doppler tomographic observations, we find KELT-26 b to reside in a highly misaligned orbit. This conclusion is weakly corroborated by a subtle asymmetry in the transit light curve from the TESS data. KELT-25 b appears to be in a well-aligned, prograde orbit, and the system is likely a member of the cluster Theia 449

Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets

Importance Substantial genome-wide association study (GWAS) work in Parkinson disease (PD) has led to the discovery of an increasing number of loci shown reliably to be associated with increased risk of disease. Improved understanding of the underlying genes and mechanisms at these loci will be key to understanding the pathogenesis of PD. / Objective To investigate what genes and genomic processes underlie the risk of sporadic PD. / Design and Setting This genetic association study used the bioinformatic tools Coloc and transcriptome-wide association study (TWAS) to integrate PD case-control GWAS data published in 2017 with expression data (from Braineac, the Genotype-Tissue Expression [GTEx], and CommonMind) and methylation data (derived from UK Parkinson brain samples) to uncover putative gene expression and splicing mechanisms associated with PD GWAS signals. Candidate genes were further characterized using cell-type specificity, weighted gene coexpression networks, and weighted protein-protein interaction networks. / Main Outcomes and Measures It was hypothesized a priori that some genes underlying PD loci would alter PD risk through changes to expression, splicing, or methylation. Candidate genes are presented whose change in expression, splicing, or methylation are associated with risk of PD as well as the functional pathways and cell types in which these genes have an important role. / Results Gene-level analysis of expression revealed 5 genes (WDR6 [OMIM 606031], CD38 [OMIM 107270], GPNMB [OMIM 604368], RAB29 [OMIM 603949], and TMEM163 [OMIM 618978]) that replicated using both Coloc and TWAS analyses in both the GTEx and Braineac expression data sets. A further 6 genes (ZRANB3 [OMIM 615655], PCGF3 [OMIM 617543], NEK1 [OMIM 604588], NUPL2 [NCBI 11097], GALC [OMIM 606890], and CTSB [OMIM 116810]) showed evidence of disease-associated splicing effects. Cell-type specificity analysis revealed that gene expression was overall more prevalent in glial cell types compared with neurons. The weighted gene coexpression performed on the GTEx data set showed that NUPL2 is a key gene in 3 modules implicated in catabolic processes associated with protein ubiquitination and in the ubiquitin-dependent protein catabolic process in the nucleus accumbens, caudate, and putamen. TMEM163 and ZRANB3 were both important in modules in the frontal cortex and caudate, respectively, indicating regulation of signaling and cell communication. Protein interactor analysis and simulations using random networks demonstrated that the candidate genes interact significantly more with known mendelian PD and parkinsonism proteins than would be expected by chance. / Conclusions and Relevance Together, these results suggest that several candidate genes and pathways are associated with the findings observed in PD GWAS studies

Identification of sixteen novel candidate genes for late onset Parkinson’s disease

Background Parkinson’s disease (PD) is a neurodegenerative movement disorder affecting 1–5% of the general population for which neither effective cure nor early diagnostic tools are available that could tackle the pathology in the early phase. Here we report a multi-stage procedure to identify candidate genes likely involved in the etiopathogenesis of PD. Methods The study includes a discovery stage based on the analysis of whole exome data from 26 dominant late onset PD families, a validation analysis performed on 1542 independent PD patients and 706 controls from different cohorts and the assessment of polygenic variants load in the Italian cohort (394 unrelated patients and 203 controls). Results Family-based approach identified 28 disrupting variants in 26 candidate genes for PD including PARK2, PINK1, DJ-1(PARK7), LRRK2, HTRA2, FBXO7, EIF4G1, DNAJC6, DNAJC13, SNCAIP, AIMP2, CHMP1A, GIPC1, HMOX2, HSPA8, IMMT, KIF21B, KIF24, MAN2C1, RHOT2, SLC25A39, SPTBN1, TMEM175, TOMM22, TVP23A and ZSCAN21. Sixteen of them have not been associated to PD before, were expressed in mesencephalon and were involved in pathways potentially deregulated in PD. Mutation analysis in independent cohorts disclosed a significant excess of highly deleterious variants in cases (p = 0.0001), supporting their role in PD. Moreover, we demonstrated that the co-inheritance of multiple rare variants (≥ 2) in the 26 genes may predict PD occurrence in about 20% of patients, both familial and sporadic cases, with high specificity (> 93%; p = 4.4 × 10− 5). Moreover, our data highlight the fact that the genetic landmarks of late onset PD does not systematically differ between sporadic and familial forms, especially in the case of small nuclear families and underline the importance of rare variants in the genetics of sporadic PD. Furthermore, patients carrying multiple rare variants showed higher risk of manifesting dyskinesia induced by levodopa treatment. Conclusions Besides confirming the extreme genetic heterogeneity of PD, these data provide novel insights into the genetic of the disease and may be relevant for its prediction, diagnosis and treatment