Very Low-mass Stellar and Substellar Companions to Solar-like Stars from MARVELS II: A Short-period Companion Orbiting an F Star with Evidence of a Stellar Tertiary And Significant Mutual Inclination

We report the discovery via radial velocity of a short-period (P = 2.430420 \pm 0.000006 days) companion to the F-type main sequence star TYC 2930-00872-1. A long-term trend in the radial velocities indicates the presence of a tertiary stellar companion with $P > 2000$ days. High-resolution spectroscopy of the host star yields T_eff = 6427 +/- 33 K, log(g) = 4.52 +/- 0.14, and [Fe/H]=-0.04 +/- 0.05. These parameters, combined with the broad-band spectral energy distribution and parallax, allow us to infer a mass and radius of the host star of M_1=1.21 +/- 0.08 M_\odot and R_1=1.09_{-0.13}^{+0.15} R_\odot. We are able to exclude transits of the inner companion with high confidence. The host star's spectrum exhibits clear Ca H and K core emission indicating stellar activity, but a lack of photometric variability and small v*sin(I) suggest the primary's spin axis is oriented in a pole-on configuration. The rotational period of the primary from an activity-rotation relation matches the orbital period of the inner companion to within 1.5 \sigma, suggesting they are tidally locked. If the inner companion's orbital angular momentum vector is aligned with the stellar spin axis, as expected through tidal evolution, then it has a stellar mass of M_2 ~ 0.3-0.4 M_\odot. Direct imaging limits the existence of stellar companions to projected separations < 30 AU. No set of spectral lines and no significant flux contribution to the spectral energy distribution from either companion are detected, which places individual upper mass limits of M < 1.0 M_\odot, provided they are not stellar remnants. If the tertiary is not a stellar remnant, then it likely has a mass of ~0.5-0.6 M_\odot, and its orbit is likely significantly inclined from that of the secondary, suggesting that the Kozai-Lidov mechanism may have driven the dynamical evolution of this system.Comment: 37 pages, 7 tables, 21 figures, Accepted in A

The Relationship Between Intelligence Mindset and Test Anxiety as Mediated by Effort Regulation

Test anxiety affects a sizable proportion of college students, especially in competitive STEM fields. Prior research has proposed interventions aimed at changing students’ implicit beliefs about intelligence (intelligence mindset) to help reduce students’ test anxiety, but results have been mixed and the mechanisms underlying this relationship are unclear. We propose that students’ beliefs about effort regulation may partially mediate the relationship between intelligence mindsets and test anxiety. We tested our model as an exploratory post-hoc analysis in a small sample of introductory physics students reporting psychological threat in a laboratory study. Effort regulation was measured as self-reported judgements of persistence in the face of difficulty and test anxiety was measured on a problem by problem basis during a laboratory physics assessment. Students’ intelligence mindset at pretest was a significant predictor of test anxiety at posttest, and this relationship was mediated by self-reported effort regulation. We discuss potential implications of these findings for mindset-based interventions aimed at reducing test anxiety

The Relationship Between Intelligence Mindset and Test Anxiety as Mediated by Effort Regulation

Test anxiety affects a sizable proportion of college students, especially in competitive STEM fields. Prior research has proposed interventions aimed at changing students’ implicit beliefs about intelligence (intelligence mindset) to help reduce students’ test anxiety, but results have been mixed and the mechanisms underlying this relationship are unclear. We propose that students’ beliefs about effort regulation may partially mediate the relationship between intelligence mindsets and test anxiety. We tested our model as an exploratory post-hoc analysis in a small sample of introductory physics students reporting psychological threat in a laboratory study. Effort regulation was measured as self-reported judgements of persistence in the face of difficulty and test anxiety was measured on a problem by problem basis during a laboratory physics assessment. Students’ intelligence mindset at pretest was a significant predictor of test anxiety at posttest, and this relationship was mediated by self-reported effort regulation. We discuss potential implications of these findings for mindset-based interventions aimed at reducing test anxiety

Very low mass stellar and substellar companions to solar-like stars from MARVELS. II. A short-period companios orbiting an F star with evidence of a stellar tertiary and significant mutual inclination

We report the discovery via radial velocity (RV) measurements of a short-period (P = 2.430420±0.000006 days) companion to the F-type main-sequence star TYC 2930-00872-1. A long-term trend in the RV data also suggests the presence of a tertiary stellar companion with P > 2000 days. High-resolution spectroscopy of the host star yields Teff = 6427 ± 33 K, log g = 4.52 ± 0.14, and [Fe/H] = −0.04 ± 0.05. These parameters, combined with the broadband spectral energy distribution (SED) and a parallax, allow us to infer a mass and radius of the host star of M1 = 1.21 ± 0.08 M and R1 = 1.09+0.15 −0.13 R . The minimum mass of the inner companion is below the hydrogen-burning limit; however, the true mass is likely to be substantially higher. We are able to exclude transits of the inner companion with high confidence. Further, the host star spectrum exhibits a clear signature of Ca H and K core emission, indicating stellar activity, but a lack of photometric variability and small v sin I suggest that the primary’s spin axis is oriented in a pole-on configuration. The rotational period of the primary estimated through an activity–rotation relation matches the orbital period of the inner companion to within 1.5 σ, suggesting that the primary and inner companion are tidally locked. If the inner companion’s orbital angular momentum vector is aligned with the stellar spin axis as expected through tidal evolution, then it has a stellar mass of ∼0.3–0.4 M . Direct imaging limits the existence of stellar companions to projected separations <30 AU. No set of spectral lines and no significant flux contribution to the SED from either companion are detected, which places individual upper mass limits of M{2,3} 1.0 M , provided they are not stellar remnants. If the tertiary is not a stellar remnant, then it likely has a mass of ∼0.5–0.6M , and its orbit is likely significantly inclined from that of the secondary, suggesting that the Kozai–Lidov mechanism may have driven the dynamical evolution of this system

Naive and memory human B cells have distinct requirements for STAT3 activation to differentiate into antibody-secreting plasma cells

Long-lived antibody memory is mediated by the combined effects of long-lived plasma cells (PCs) and memory B cells generated in response to T cell–dependent antigens (Ags). IL-10 and IL-21 can activate multiple signaling pathways, including STAT1, STAT3, and STAT5; ERK; PI3K/Akt, and potently promote human B cell differentiation. We previously showed that loss-of-function mutations in STAT3, but not STAT1, abrogate IL-10– and IL-21–mediated differentiation of human naive B cells into plasmablasts. We report here that, in contrast to naive B cells, STAT3-deficient memory B cells responded to these STAT3-activating cytokines, differentiating into plasmablasts and secreting high levels of IgM, IgG, and IgA, as well as Ag-specific IgG. This was associated with the induction of the molecular machinery necessary for PC formation. Mutations in IL21R, however, abolished IL-21–induced responses of both naive and memory human B cells and compromised memory B cell formation in vivo. These findings reveal a key role for IL-21R/STAT3 signaling in regulating human B cell function. Furthermore, our results indicate that the threshold of STAT3 activation required for differentiation is lower in memory compared with naive B cells, thereby identifying an intrinsic difference in the mechanism underlying differentiation of naive versus memory B cells

Dissolved organic carbon reduces uranium toxicity to the unicellular eukaryote Euglena gracilis

The influence of dissolved organic carbon (DOC), in the form of Suwannee River fulvic acid (SRFA), on uranium (U) toxicity to the unicellular eukaryote, Euglena gracilis (Z strain), was investigated at pH 6. In a background medium without SRFA, exposure of E. gracilis to 57 μg L U resulted in a 50% reduction in growth (IC50). The addition of 20 mg L DOC (as SRFA), reduced U toxicity 4 to 5-fold (IC increased to 254 μg L U). This reduction in toxicity was also evident at more sensitive effect levels with a 10% reduction in growth (IC ) occurring at 5 μg L U in the background medium and at 17 μg L U in the SRFA medium, respectively. This amelioration of toxicity with the addition of SRFA was linked to a decrease in the bioavailability of U, with geochemical speciation modelling predicting 84% of U would be complexed by SRFA. The decrease in bioavailability of U in the presence of SRFA was also evident from the 11-14 fold reduction in the cellular concentration of U compared to that of E. gracilis in the background medium. Stepwise multiple linear regression analyses indicated that UO alone explained 51% of the variation in measured U toxicity to E. gracilis. Preliminary U exposures to E. gracilis in the presence of a reactive oxygen species probe, suggest exposure to ≥60 μg L U may induce oxidative stress, but this endpoint was not considered to be a sensitive biological indicator

De Novo Nonsense Mutations in KAT6A, a Lysine Acetyl-Transferase Gene, Cause a Syndrome Including Microcephaly and Global Developmental Delay

Chromatin remodeling through histone acetyltransferase (HAT) and histone deactylase (HDAC) enzymes affects fundamental cellular processes including the cell-cycle, cell differentiation, metabolism, and apoptosis. Nonsense mutations in genes that are involved in histone acetylation and deacetylation result in multiple congenital anomalies with most individuals displaying significant developmental delay, microcephaly and dysmorphism. Here, we report a syndrome caused by de novo heterozygous nonsense mutations in KAT6A (a.k.a., MOZ, MYST3) identified by clinical exome sequencing (CES) in four independent families. The same de novo nonsense mutation (c.3385C>T [p.Arg1129∗]) was observed in three individuals, and the fourth individual had a nearby de novo nonsense mutation (c.3070C>T [p.Arg1024∗]). Neither of these variants was present in 1,815 in-house exomes or in public databases. Common features among all four probands include primary microcephaly, global developmental delay including profound speech delay, and craniofacial dysmorphism, as well as more varied features such as feeding difficulties, cardiac defects, and ocular anomalies. We further demonstrate that KAT6A mutations result in dysregulation of H3K9 and H3K18 acetylation and altered P53 signaling. Through histone and non-histone acetylation, KAT6A affects multiple cellular processes and illustrates the complex role of acetylation in regulating development and disease