WASP-12b as a prolate, inflated and disrupting planet from tidal dissipation

The class of exotic Jupiter-mass planets that orbit very close to their parent stars were not explicitly expected before their discovery. The recently found transiting planet WASP-12b has a mass Mp = 1.4(+/-0.1) Jupiter masses (MJ), a mean orbital distance of only 3.1 stellar radii (meaning it is subject to intense tidal forces), and a period of 1.1 days. Its radius 1.79(+/- 0.09) RJ is unexpectedly large and its orbital eccentricity 0.049(+/-0:015) is even more surprising as such close orbits are in general quickly circularized. Here we report an analysis of its properties, which reveals that the planet is losing mass to its host star at a rate ~ 10^-7 MJ yr^-1. The planets surface is distorted by the stars gravity and the light curve produced by its prolate shape will differ by about ten per cent from that of a spherical planet. We conclude that dissipation of the stars tidal perturbation in the planets convective envelope provides the energy source for its large volume. We predict up to 10mJy CO band-head (2.292 micron) emission from a tenuous disk around the host star, made up of tidally stripped planetary gas. It may also contain a detectable resonant super-Earth, as a hypothetical perturber that continually stirs up WASP-12b's eccentricity.Comment: Accepted to Nature, 14 pages, 1 figur

Combined SIRT3 and SIRT5 deletion is associated with inner retinal dysfunction in a mouse model of type 1 diabetes

Abstract Diabetic retinopathy (DR) is a major cause of blindness in working adults in the industrialized world. In addition to vision loss caused by macular edema and pathological angiogenesis, DR patients often exhibit neuronal dysfunction on electrophysiological testing, suggesting that there may be an independent neuronal phase of disease that precedes vascular disease. Given the tremendous metabolic requirements of the retina and photoreceptors in particular, we hypothesized that derangements in metabolic regulation may accelerate retinal dysfunction in diabetes. As such, we induced hyperglycemia with streptozotocin in mice with monoallelic Nampt deletion from rod photoreceptors, mice lacking SIRT3, and mice lacking SIRT5 and tested multiple components of retinal function with electroretinography. None of these mice exhibited accelerated retinal dysfunction after induction of hyperglycemia, consistent with normal-appearing retinal morphology in hyperglycemic Sirt3 −/− or Sirt5 −/− mice. However, mice lacking both SIRT3 and SIRT5 (Sirt3 −/− Sirt5 −/− mice) exhibited significant evidence of inner retinal dysfunction after induction of hyperglycemia compared to hyperglycemic littermate controls, although this dysfunction was not accompanied by gross morphological changes in the retina. These results suggest that SIRT3 and SIRT5 may be involved in regulating neuronal dysfunction in DR and provide a foundation for future studies investigating sirtuin-based therapies

Asymmetric Lattice Disorder Induced at Oxide Interfaces

Control of order-disorder phase transitions is a fundamental materials science challenge, underpinning the development of energy storage technologies such as solid oxide fuel cells and batteries, ultra-high temperature ceramics, and durable nuclear waste forms. At present, the development of promising complex oxides for these applications is hindered by a poor understanding of how interfaces affect lattice disordering processes and defect transport. Here we explore the evolution of local disorder in ion-irradiated La$_2$Ti$_2$O$_7$ / SrTiO$_3$ thin film heterostructures using a combination of high-resolution scanning transmission electron microscopy (STEM), position-averaged convergent beam electron diffraction (PACBED), electron energy loss spectroscopy (STEM-EELS), and \textit{ab initio} theory calculations. We observe highly non-uniform lattice disordering driven by asymmetric oxygen vacancy formation across the interface. Our calculations indicate that this asymmetry results from differences in the polyhedral connectivity and vacancy formation energies of the two interface components, suggesting ways to manipulate lattice disorder in functional oxide heterostructures.Comment: 23 pages, 4 figure

Large area growth and electrical properties of p-type WSe2 atomic layers.

Transition metal dichacogenides represent a unique class of two-dimensional layered materials that can be exfoliated into single or few atomic layers. Tungsten diselenide (WSe(2)) is one typical example with p-type semiconductor characteristics. Bulk WSe(2) has an indirect band gap (∼ 1.2 eV), which transits into a direct band gap (∼ 1.65 eV) in monolayers. Monolayer WSe(2), therefore, is of considerable interest as a new electronic material for functional electronics and optoelectronics. However, the controllable synthesis of large-area WSe(2) atomic layers remains a challenge. The studies on WSe(2) are largely limited by relatively small lateral size of exfoliated flakes and poor yield, which has significantly restricted the large-scale applications of the WSe(2) atomic layers. Here, we report a systematic study of chemical vapor deposition approach for large area growth of atomically thin WSe(2) film with the lateral dimensions up to ∼ 1 cm(2). Microphotoluminescence mapping indicates distinct layer dependent efficiency. The monolayer area exhibits much stronger light emission than bilayer or multilayers, consistent with the expected transition to direct band gap in the monolayer limit. The transmission electron microscopy studies demonstrate excellent crystalline quality of the atomically thin WSe(2). Electrical transport studies further show that the p-type WSe(2) field-effect transistors exhibit excellent electronic characteristics with effective hole carrier mobility up to 100 cm(2) V(-1) s(-1) for monolayer and up to 350 cm(2) V(-1) s(-1) for few-layer materials at room temperature, comparable or well above that of previously reported mobility values for the synthetic WSe(2) and comparable to the best exfoliated materials

Modified Gravity and Dark Energy models Beyond w(z)w(z)CDM Testable by LSST

One of the main science goals of the Large Synoptic Survey Telescope (LSST) is to uncover the nature of cosmic acceleration. In the base analysis, possible deviations from the Lambda-Cold-Dark-Matter ($\Lambda$CDM) background evolution will be probed by fitting a $w(z)$CDM model, which allows for a redshift-dependent dark energy equation of state with $w(z)$, within general relativity (GR). A rich array of other phenomena can arise due to deviations from the standard $\Lambda$CDM+GR model though, including modifications to the growth rate of structure and lensing, and novel screening effects on non-linear scales. Concrete physical models are needed to provide consistent predictions for these (potentially small) effects, to give us the best chance of detecting them and separating them from astrophysical systematics. A complex plethora of possible models has been constructed over the past few decades, with none emerging as a particular favorite. This document prioritizes a subset of these models along with rationales for further study and inclusion into the LSST Dark Energy Science Collaboration (DESC) data analysis pipelines, based on their observational viability, theoretical plausibility, and level of theoretical development. We provide references and theoretical expressions to aid the integration of these models into DESC software and simulations, and give justifications for why other models were not prioritized. While DESC efforts are free to pursue other models, we provide here guidelines on which theories appear to have higher priority for collaboration efforts due to their perceived promise and greater instructional value.Comment: 61 pages. Some acknowledgments and references added. This is version-1.1 of an internal collaboration document of LSST-DESC that is being made public and is not planned for submission to a journa

Biological Consequences of Tightly Bent DNA: The Other Life of a Macromolecular Celebrity

The mechanical properties of DNA play a critical role in many biological functions. For example, DNA packing in viruses involves confining the viral genome in a volume (the viral capsid) with dimensions that are comparable to the DNA persistence length. Similarly, eukaryotic DNA is packed in DNA-protein complexes (nucleosomes) in which DNA is tightly bent around protein spools. DNA is also tightly bent by many proteins that regulate transcription, resulting in a variation in gene expression that is amenable to quantitative analysis. In these cases, DNA loops are formed with lengths that are comparable to or smaller than the DNA persistence length. The aim of this review is to describe the physical forces associated with tightly bent DNA in all of these settings and to explore the biological consequences of such bending, as increasingly accessible by single-molecule techniques.Comment: 24 pages, 9 figure

American Geriatrics Society and National Institute on Aging Bench-to-Bedside conference: sensory impairment and cognitive decline in older adults

This article summarizes the presentations and recommendations of the tenth annual American Geriatrics Society and National Institute on Aging Bench‐to‐Bedside research conference, “Sensory Impairment and Cognitive Decline,” on October 2–3, 2017, in Bethesda, Maryland. The risk of impairment in hearing, vision, and other senses increases with age, and almost 15% of individuals aged 70 and older have dementia. As the number of older adults increases, sensory and cognitive impairments will affect a growing proportion of the population. To limit its scope, this conference focused on sensory impairments affecting vision and hearing. Comorbid vision, hearing, and cognitive impairments in older adults are more common than would be expected by chance alone, suggesting that some common mechanisms might affect these neurological systems. This workshop explored the mechanisms and consequences of comorbid vision, hearing, and cognitive impairment in older adults; effects of sensory loss on the aging brain; and bench‐to‐bedside innovations and research opportunities. Presenters and participants identified many research gaps and questions; the top priorities fell into 3 themes: mechanisms, measurement, and interventions. The workshop delineated specific research questions that provide opportunities to improve outcomes in this growing population.Funding was provided by National Institutes of Health (NIH) Grant U13 AG054139-01. Dr. Whitson's efforts and contributions were supported by R01AG043438, R24AG045050, UH2AG056925, and 5P30AG028716. Dr. Lin's effort and contributions were also supported by R01AG055426, R01HL096812, and R33DC015062. (U13 AG054139-01 - National Institutes of Health (NIH); R01AG043438; R24AG045050; UH2AG056925; 5P30AG028716; R01AG055426; R01HL096812; R33DC015062)Accepted manuscrip

Subcutaneous nerve activity and mechanisms of sudden death in a rat model of chronic kidney disease

BACKGROUND: The mechanisms of sudden death in chronic kidney disease (CKD) remain unclear. OBJECTIVE: The purpose of this study was to test the hypotheses that subcutaneous nerve activity (SCNA) can be used to estimate sympathetic tone in ambulatory rats and that abrupt reduction of SCNA precedes the spontaneous arrhythmic death of Cy/+ rats. METHODS: Radiotransmitters were implanted in ambulatory normal (N = 6) and Cy/+ (CKD; N = 6) rats to record electrocardiogram and SCNA. Two additional rats were studied before and after chemical sympathectomy with 6-hydroxydopamine. RESULTS: In normal rats, the baseline heart rate (HR) and SCNA were 351 ± 29 bpm and 5.12 ± 2.97 mV·s, respectively. SCNA abruptly increased HR by 4.31% (95% confidence interval 4.15%-4.47%). In comparison, the CKD rats had reduced baseline HR (336 ± 21 bpm, P < .01) and SCNA (4.27 ± 3.19 mV·s, P < .01). When SCNA was observed, HR increased by only 2.48% (confidence interval 2.29%-2.67%, P < .01). All Cy/+ rats died suddenly, preceded by sinus bradycardia, advanced (second- and third-degree) AV block (N = 6), and/or ventricular tachycardia or fibrillation (N = 3). Sudden death was preceded by a further reduction of SCNA (3.22 ± 2.86 mV·s, P < .01) and sinus bradycardia (243 ± 55 bpm, P < .01). Histologic studies in CKD rats showed myocardial calcification that involved the conduction system. Chemical sympathectomy resulted in progressive reduction of SCNA over 7 days. CONCLUSION: SCNA can be used to estimate sympathetic tone in ambulatory rats. CKD is associated with reduced HR response to SCNA and conduction system diseases. Abrupt reduction of sympathetic tone precedes AV block, ventricular arrhythmia, and sudden death of CKD rats

Huntingtin exon 1 fibrils feature an interdigitated β-hairpin-based polyglutamine core

Polyglutamine expansion within the exon1 of huntingtin leads to protein misfolding, aggregation, and cytotoxicity in Huntington’s Disease. This incurable neurodegenerative disease is the most prevalent member of a family of CAG repeat expansion disorders. Although mature exon1 fibrils are viable candidates for the toxic species, their molecular structure and how they form have remained poorly understood. Using advanced magic angle spinning solid state NMR, we directly probe the structure of the rigid core that is at the heart of huntingtin exon1 fibrils and other polyglutamine aggregates, via measurements of long-range intra- and inter-molecular contacts, backbone and side chain torsion angles, relaxation measurements, and calculations of chemical shifts. These reveal the presence of β-hairpin-containing β-sheets that are connected through interdigitating extended side chains. Despite dramatic differences in aggregation behavior, huntingtin exon1 fibrils and other polyglutamine-based aggregates contain identical β-strand-based cores. Prior structural models, derived from X-ray fiber diffraction and computational analyses, are shown to be inconsistent with the solid-state NMR results. Internally, the polyglutamine amyloid fibrils are co-assembled from differently structured monomers, which we describe as a type of ‘intrinsic’ polymorphism. A stochastic polyglutamine-specific aggregation mechanism is introduced to explain this phenomenon. Weshow that the aggregation of mutant huntingtin exon1 proceeds via an intramolecular collapse of the expanded polyglutamine domain, and discuss the implications of this observation for our understanding of its misfolding and aggregation mechanisms