The Relationship Between General Anxiety, Social Physique Anxiety, and Body Image in Collegiate Athletes and Non-Athletes

Context: Due to the clinical significance, it is important that anxiety is identified early in collegiate athletes. Unlike the extensive amount of research done conducted on mental health in the general population, there is minimal research examining the mental health of athletes. The relationship between general anxiety (GAD), social physique anxiety (SPA), and body image (BI) in this population has not been studied. Objective: To examine the relationship between general anxiety, social physique anxiety, and body image in collegiate athletes and non-athletes. Design: Cross-sectional quantitative study. Setting: One NCAA Division II University. Participants: Three hundred and eleven students participated in this study. Interventions: Participants completed surveys electronically during the fall semester of the 2019-2020 academic year. Measures included the Generalized Anxiety Disorder 7-item (GAD-7) scale, Social Physique Anxiety Scale (SPAS), Multidimensional Body-Self Relations Questionnaire (Appearance Evaluation; MBSRQ-AE), and Weight Pressures in Sport (WPS) questionnaire. Main Outcome Measures: GAD-7, SPAS, MBSRQ-AE, and WPS mean scores. Results: A significant, negative relationship was found between SPA and BI satisfaction in all groups. There was no significant difference in mean WPS scores (p=.067) between male and female athletes, but males did have a higher mean score (p=2.15) than females (p=1.84). Conclusion: These findings support previous research on the topics discussed and assist in filling a gap in research being these relationships have never been studied before in this population. These findings may provide medical professionals in the fields of sports medicine and sports psychology a better understanding of the relationship between these constructs. Word Count: 249

Gravitational Microlensing Event Statistics for the Zwicky Transient Facility

Microlensing surveys have discovered thousands of events with almost all events discovered within the Galactic bulge or toward the Magellanic clouds. The Zwicky Transient Facility (ZTF), while not designed to be a microlensing campaign, is an optical time-domain survey that observes the entire northern sky every few nights including the Galactic plane. ZTF observes $\sim10^9$ stars in g-band and r-band and can significantly contribute to the observed microlensing population. We predict that ZTF will observe $\sim$1100 microlensing events in three years of observing within $10^\circ$ degrees latitude of the Galactic plane, with $\sim$500 events in the outer Galaxy ($\ell \geq 10^\circ$). This yield increases to $\sim$1400 ($\sim$800) events by combining every three ZTF exposures, $\sim$1800 ($\sim$900) events if ZTF observes for a total of five years, and $\sim$2400 ($\sim$1300) events for a five year survey with post-processing image stacking. Using the microlensing modeling software PopSyCLE, we compare the microlensing populations in the Galactic bulge and the outer Galaxy. We also present an analysis of the microlensing event ZTF18abhxjmj to demonstrate how to leverage these population statistics in event modeling. ZTF will constrain Galactic structure, stellar populations, and primordial black holes through photometric microlensing.Comment: 19 pages, 13 figures, 5 tables, accepted to ApJ (6/4/2020), microlensing simulation catalogs available at https://portal.nersc.gov/project/uLens/Galactic_Microlensing_Distribution

Ketamine and Attentional Bias Toward Emotional Faces: Dynamic Causal Modeling of Magnetoencephalographic Connectivity in Treatment-Resistant Depression

The glutamatergic modulator ketamine rapidly reduces depressive symptoms in individuals with treatment-resistant major depressive disorder (TRD) and bipolar disorder. While its underlying mechanism of antidepressant action is not fully understood, modulating glutamatergically-mediated connectivity appears to be a critical component moderating antidepressant response. This double-blind, crossover, placebo-controlled study analyzed data from 19 drug-free individuals with TRD and 15 healthy volunteers who received a single intravenous infusion of ketamine hydrochloride (0.5 mg/kg) as well as an intravenous infusion of saline placebo. Magnetoencephalographic recordings were collected prior to the first infusion and 6–9 h after both drug and placebo infusions. During scanning, participants completed an attentional dot probe task that included emotional faces. Antidepressant response was measured across time points using the Montgomery-Asberg Depression Rating Scale (MADRS). Dynamic causal modeling (DCM) was used to measure changes in parameter estimates of connectivity via a biophysical model that included realistic local neuronal architecture and receptor channel signaling, modeling connectivity between the early visual cortex, fusiform cortex, amygdala, and inferior frontal gyrus. Clinically, ketamine administration significantly reduced depressive symptoms in TRD participants. Within the model, ketamine administration led to faster gamma aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA) transmission in the early visual cortex, faster NMDA transmission in the fusiform cortex, and slower NMDA transmission in the amygdala. Ketamine administration also led to direct and indirect changes in local inhibition in the early visual cortex and inferior frontal gyrus and to indirect increases in cortical excitability within the amygdala. Finally, reductions in depressive symptoms in TRD participants post-ketamine were associated with faster α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) transmission and increases in gain control of spiny stellate cells in the early visual cortex. These findings provide additional support for the GABA and NMDA inhibition and disinhibition hypotheses of depression and support the role of AMPA throughput in ketamine's antidepressant effects.Clinical Trial Registration:https://clinicaltrials.gov/ct2/show/NCT00088699?term=NCT00088699&draw=2&rank=1, identifier NCT00088699

Discovery of Precursor LBV Outbursts in Two Recent Optical Transients: The Fitfully Variable Missing Links UGC 2773-OT and SN 2009ip

We present progenitor-star detections, light curves, and optical spectra of SN2009ip and the 2009 optical transient in UGC2773 (U2773-OT), which were not genuine SNe. Precursor variability in the decade before outburst indicates that both of the progenitor stars were LBVs. Their pre-outburst light curves resemble the S Doradus phases that preceded giant eruptions of eta Carinae and SN1954J (V12 in NGC2403), with intermediate progenitor luminosities. HST detections a decade before discovery indicate that the SN2009ip and U2773-OT progenitors were supergiants with likely initial masses of 50-80 Msun and \ga20 Msun, respectively. Both outbursts had spectra befitting known LBVs, although in different physical states. SN 2009ip exhibited a hot LBV spectrum with characteristic speeds of 550 km/s, plus faster material up to 5000 km/s, resembling the slow Homunculus and fast blast wave of eta Carinae. U2773-OT shows a forest of narrow absorption and emission lines comparable to that of S Dor in its cool state, plus [CaII] emission and an IR excess indicative of dust, similar to SN2008S and N300-OT. [CaII] emission is probably tied to a dusty pre-outburst environment, and not the outburst mechanism. SN2009ip and U2773-OT may provide a critical link between historical LBV eruptions, while U2773-OT may provide a link between LBVs and SN2008S and N300-OT. Future searches will uncover more examples of precursor LBV variability of this kind, providing key clues that may help unravel the instability driving LBVs.Comment: 18 pages, 13 Figures, accepted AJ. added significant material while revising after referee repor

Structure-function studies of the bHLH phosphorylation domain of TWIST1 in prostate cancer cells

The TWIST1 gene has diverse roles in development and pathologic diseases such as cancer. TWIST1 is a dimeric basic helix-loop-helix (bHLH) transcription factor existing as TWIST1-TWIST1 or TWIST1-E12/47. TWIST1 partner choice and DNA binding can be influenced during development by phosphorylation of Thr125 and Ser127 of the Thr-Gln-Ser (TQS) motif within the bHLH of TWIST1. The significance of these TWIST1 phosphorylation sites for metastasis is unknown. We created stable isogenic prostate cancer cell lines overexpressing TWIST1 wild-type, phospho-mutants, and tethered versions. We assessed these isogenic lines using assays that mimic stages of cancer metastasis. In vitro assays suggested the phospho-mimetic Twist1-DQD mutation could confer cellular properties associated with pro-metastatic behavior. The hypo-phosphorylation mimic Twist1-AQA mutation displayed reduced pro-metastatic activity compared to wild-type TWIST1 in vitro, suggesting that phosphorylation of the TWIST1 TQS motif was necessary for pro-metastatic functions. In vivo analysis demonstrates that the Twist1-AQA mutation exhibits reduced capacity to contribute to metastasis, whereas the expression of the Twist1-DQD mutation exhibits proficient metastatic potential. Tethered TWIST1-E12 heterodimers phenocopied the Twist1-DQD mutation for many in vitro assays, suggesting that TWIST1 phosphorylation may result in heterodimerization in prostate cancer cells. Lastly, the dual phosphatidylinositide 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) inhibitor BEZ235 strongly attenuated TWIST1-induced migration that was dependent on the TQS motif. TWIST1 TQS phosphorylation state determines the intensity of TWIST1-induced pro-metastatic ability in prostate cancer cells, which may be partly explained mechanistically by TWIST1 dimeric partner choice

Centaurs and Scattered Disk Objects in the Thermal Infrared: Analysis of WISE/NEOWISE Observations

The Wide-field Infrared Survey Explorer (WISE) observed 52 Centaurs and scattered disk objects (SDOs) in the thermal infrared, including 15 new discoveries. We present analyses of these observations to estimate sizes and mean optical albedos. We find mean albedos of 0.08 ± 0.04 for the entire data set. Thermal fits yield average beaming parameters of 0.9 ± 0.2 that are similar for both SDO and Centaur sub-classes. Biased cumulative size distributions yield size-frequency distribution power law indices of ~–1.7 ± 0.3. The data also reveal a relation between albedo and color at the 3σ level. No significant relation between diameter and albedos is found

Phenotypic and molecular characterisation of CDK13-related congenital heart defects, dysmorphic facial features and intellectual developmental disorders

Background: De novo missense variants in CDK13 have been described as the cause of syndromic congenital heart defects in seven individuals ascertained from a large congenital cardiovascular malformations cohort. We aimed to further define the phenotypic and molecular spectrum of this newly described disorder. Methods: To minimise ascertainment bias, we recruited nine additional individuals with CDK13 pathogenic variants from clinical and research exome laboratory sequencing cohorts. Each individual underwent dysmorphology exam and comprehensive medical history review. Results: We demonstrate greater than expected phenotypic heterogeneity, including 33% (3/9) of individuals without structural heart disease on echocardiogram. There was a high penetrance for a unique constellation of facial dysmorphism and global developmental delay, as well as less frequently seen renal and sacral anomalies. Two individuals had novel CDK13 variants (p.Asn842Asp, p.Lys734Glu), while the remaining seven unrelated individuals had a recurrent, previously published p.Asn842Ser variant. Summary of all variants published to date demonstrates apparent restriction of pathogenic variants to the protein kinase domain with clustering in the ATP and magnesium binding sites. Conclusions: Here we provide detailed phenotypic and molecular characterisation of individuals with pathogenic variants in CDK13 and propose management guidelines based upon the estimated prevalence of anomalies identified. Keywords: CDK13, CHDFIDD, De novo variant, Neurodevelopmental disorders, Agenesis of the corpus callosum, Hypertelorism, Developmental delay, Cyclin-dependent kinase, Undiagnosed Diseases Networ

The Global Nutrition Report 2014: Actions and Accountability to Accelerate the World’s Progress on Nutrition

In 2013, the Nutrition for Growth Summit called for a Global Nutrition Report (GNR) to strengthen accountability in nutrition so that progress in reducing malnutrition could be accelerated. This article summarizes the results of the first GNR. By focusing on undernutrition and overweight, the GNR puts malnutrition in a new light. Nearly every country in the world is affected by malnutrition, and multiple malnutrition burdens are the ‘‘new normal.’’ Unfortunately, the world is off track to meet the 2025 World Health Assembly (WHA) targets for nutrition. Many countries are, however, making good progress on WHA indicators, providing inspiration and guidance for others. Beyond the WHA goals, nutrition needs to be more strongly represented in the Sustainable Development Goal (SDG) framework. At present, it is only explicitly mentioned in 1 of 169 SDG targets despite the many contributions improved nutritional status will make to their attainment. To achieve improvements in nutrition status, it is vital to scale up nutrition programs. We identify bottlenecks in the scale-up of nutrition-specific and nutrition-sensitive approaches and highlight actions to accelerate coverage and reach. Holding stakeholders to account for delivery on nutrition actions requires a well-functioning accountability infrastructure, which is lacking in nutrition. New accountability mechanisms need piloting and evaluation, financial resource flows to nutrition need to be made explicit, nutrition spending targets should be established, and some key data gaps need to be filled. For example, many UN member states cannot report on their WHA progress and those that can often rely on data >5 y old. The world can accelerate malnutrition reduction substantially, but this will require stronger accountability mechanisms to hold all stakeholders to account. J Nutr doi: 10.3945/jn.114.206078

Novel genetic loci underlying human intracranial volume identified through genome-wide association

Intracranial volume reflects the maximally attained brain size during development, and remains stable with loss of tissue in late life. It is highly heritable, but the underlying genes remain largely undetermined. In a genome-wide association study of 32,438 adults, we discovered five novel loci for intracranial volume and confirmed two known signals. Four of the loci are also associated with adult human stature, but these remained associated with intracranial volume after adjusting for height. We found a high genetic correlation with child head circumference (ρgenetic=0.748), which indicated a similar genetic background and allowed for the identification of four additional loci through meta-analysis (Ncombined = 37,345). Variants for intracranial volume were also related to childhood and adult cognitive function, Parkinson’s disease, and enriched near genes involved in growth pathways including PI3K–AKT signaling. These findings identify biological underpinnings of intracranial volume and provide genetic support for theories on brain reserve and brain overgrowth