25 research outputs found
Detecting the Companions and Ellipsoidal Variations of RS CVn Primaries: I. sigma Geminorum
To measure the properties of both components of the RS CVn binary sigma
Geminorum (sigma Gem), we directly detect the faint companion, measure the
orbit, obtain model-independent masses and evolutionary histories, detect
ellipsoidal variations of the primary caused by the gravity of the companion,
and measure gravity darkening. We detect the companion with interferometric
observations obtained with the Michigan InfraRed Combiner (MIRC) at Georgia
State University's Center for High Angular Resolution Astronomy (CHARA) Array
with a primary-to-secondary H-band flux ratio of 270+/-70. A radial velocity
curve of the companion was obtained with spectra from the Tillinghast Reflector
Echelle Spectrograph (TRES) on the 1.5-m Tillinghast Reflector at Fred Lawrence
Whipple Observatory (FLWO). We additionally use new observations from the
Tennessee State University Automated Spectroscopic and Photometric Telescopes
(AST and APT, respectively). From our orbit, we determine model-independent
masses of the components (M_1 = 1.28 +/- 0.07 M_Sun, M_2 = 0.73 +/- 0.03
M_Sun), and estimate a system age of 5 -/+ 1 Gyr. An average of the 27-year APT
light curve of sigma Gem folded over the orbital period (P = 19.6027 +/- 0.0005
days) reveals a quasi-sinusoidal signature, which has previously been
attributed to active longitudes 180 deg apart on the surface of sigma Gem. With
the component masses, diameters, and orbit, we find that the predicted light
curve for ellipsoidal variations due to the primary star partially filling its
Roche lobe potential matches well with the observed average light curve,
offering a compelling alternative explanation to the active longitudes
hypothesis. Measuring gravity darkening from the light curve gives beta < 0.1,
a value slightly lower than that expected from recent theory.Comment: Accepted to ApJ, 11 pages, 6 figures, 8 table
TOI-836 : a super-Earth and mini-Neptune transiting a nearby K-dwarf
Funding: TGW, ACC, and KH acknowledge support from STFC consolidated grant numbers ST/R000824/1 and ST/V000861/1, and UKSA grant ST/R003203/1.We present the discovery of two exoplanets transiting TOI-836 (TIC 440887364) using data from TESS Sector 11 and Sector 38. TOI-836 is a bright (T = 8.5 mag), high proper motion (∼200 mas yr−1), low metallicity ([Fe/H]≈−0.28) K-dwarf with a mass of 0.68 ± 0.05 M⊙ and a radius of 0.67 ± 0.01 R⊙. We obtain photometric follow-up observations with a variety of facilities, and we use these data-sets to determine that the inner planet, TOI-836 b, is a 1.70 ± 0.07 R⊕ super-Earth in a 3.82 day orbit, placing it directly within the so-called ‘radius valley’. The outer planet, TOI-836 c, is a 2.59 ± 0.09 R⊕ mini-Neptune in an 8.60 day orbit. Radial velocity measurements reveal that TOI-836 b has a mass of 4.5 ± 0.9 M⊕, while TOI-836 c has a mass of 9.6 ± 2.6 M⊕. Photometric observations show Transit Timing Variations (TTVs) on the order of 20 minutes for TOI-836 c, although there are no detectable TTVs for TOI-836 b. The TTVs of planet TOI-836 c may be caused by an undetected exterior planet.Publisher PDFPeer reviewe
TOI-836: A super-Earth and mini-Neptune transiting a nearby K-dwarf
We present the discovery of two exoplanets transiting TOI-836 (TIC 440887364)
using data from TESS Sector 11 and Sector 38. TOI-836 is a bright (
mag), high proper motion ( mas yr), low metallicity
([Fe/H]) K-dwarf with a mass of M and a
radius of R. We obtain photometric follow-up
observations with a variety of facilities, and we use these data-sets to
determine that the inner planet, TOI-836 b, is a R
super-Earth in a 3.82 day orbit, placing it directly within the so-called
'radius valley'. The outer planet, TOI-836 c, is a R
mini-Neptune in an 8.60 day orbit. Radial velocity measurements reveal that
TOI-836 b has a mass of M , while TOI-836 c has a mass
of M. Photometric observations show Transit Timing
Variations (TTVs) on the order of 20 minutes for TOI-836 c, although there are
no detectable TTVs for TOI-836 b. The TTVs of planet TOI-836 c may be caused by
an undetected exterior planet
Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19
IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19.
Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19.
DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022).
INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days.
MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes.
RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively).
CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes.
TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570
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Characterization of a germline variant MSH6 c.4001G > C in a Lynch syndrome family
BackgroundGermline variants in the DNA mismatch repair (MMR) genes (MLH1, MSH2, MSH6, and PMS2) cause Lynch syndrome, an autosomal dominant hereditary cancer susceptibility syndrome. The risk for endometrial cancer is significantly higher in women with MSH6 pathogenic/likely pathogenic (P/LP) variants compared with that for MLH1 or MSH2 variants.MethodsThe proband was tested via a clinical testing, Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets (MSK-IMPACT). RT-PCR was performed using patient's blood DNA and cDNA was analyzed by DNA sequencing and a cloning approach.ResultsWe report a 56-year-old female with endometrial cancer who carries a germline variant, MSH6 c.4001G > C, located at the last nucleotide of exon 9. While the pathogenicity of this variant was previously unknown, functional studies demonstrated that this variant completely abolished normal splicing and caused exon 9 skipping, which is expected to lead to a prematurely truncated or abnormal protein.ConclusionOur results indicate that this variant likely contributes to cancer predisposition through disruption of normal splicing, and is classified as likely pathogenic
‘Not to Be Harsh but Try Less to Relate to ‘the Teens’ and You’ll Relate to Them More’: Co-Designing Obesity Prevention Text Messages with Adolescents
Novel Somatic Mutations to PI3K Pathway Genes in Metastatic Melanoma
<div><h3>Background</h3><p>BRAF<sup>V600</sup> inhibitors have offered a new gateway for better treatment of metastatic melanoma. However, the overall efficacy of BRAF<sup>V600</sup> inhibitors has been lower than expected in clinical trials, and many patients have shown resistance to the drug’s effect. We hypothesized that somatic mutations in the Phosphoinositide 3-Kinase (PI3K) pathway, which promotes proliferation and survival, may coincide with BRAF<sup>V600</sup> mutations and contribute to chemotherapeutic resistance.</p> <h3>Methods</h3><p>We performed a somatic mutation profiling study using the 454 FLX pyrosequencing platform in order to identify candidate cancer genes within the MAPK and PI3K pathways of melanoma patients. Somatic mutations of theses candidate cancer genes were then confirmed using Sanger sequencing.</p> <h3>Results</h3><p>As expected, BRAF<sup>V600</sup> mutations were seen in 51% of the melanomas, whereas NRAS mutations were seen in 19% of the melanomas. However, PI3K pathway mutations, though more heterogeneous, were present in 41% of the melanoma, with PTEN being the highest mutated PI3K gene in melanomas (22%). Interestingly, several novel PI3K pathway mutations were discovered in MTOR, IRS4, PIK3R1, PIK3R4, PIK3R5, and NFKB1. PI3K pathway mutations co-occurred with BRAF<sup>V600</sup> mutations in 17% of the tumors and co-occurred with 9% of NRAS mutant tumors, implying cooperativity between these pathways in terms of melanoma progression.</p> <h3>Conclusions</h3><p>These novel PI3K pathway somatic mutations could provide alternative survival and proliferative pathways for metastatic melanoma cells. They therefore may be potential chemotherapeutic targets for melanoma patients who exhibit resistance to BRAF<sup>V600</sup> inhibitors.</p> </div
List of PI3K and MAPK pathway genes sequenced.
<p>List of PI3K and MAPK pathway genes sequenced.</p
Distribution of melanoma patients according to pathway somatic mutations.
<p>(a) Percentages of melanomas that have: a BRAF<sup>V600</sup> mutation without a PI3K pathway mutation, a BRAF<sup>V600</sup> mutation with a PI3K pathway mutation, a NRAS mutation without a PI3K pathway mutation, a NRAS mutations with a PI3K pathway mutation, and a PI3K pathway mutation with wild-type BRAF<sup>V600</sup> and NRAS. (b) Number of patients who carried the somatic mutations identified by Sanger sequencing.</p