60 research outputs found
The Internal Energy for Molecular Hydrogen in Gravitationally Unstable Protoplanetary Disks
The gas equation of state may be one of the critical factors for the disk
instability theory of gas giant planet formation. This letter addresses the
treatment of H in hydrodynamical simulations of gravitationally unstable
disks. In our discussion, we point out possible consequences of erroneous
specific internal energy relations, approximate specific internal energy
relations with discontinuities, and assumptions of constant . In
addition, we consider whether the ortho/para ratio for H in protoplanetary
disks should be treated dynamically as if the species are in equilibrium.
Preliminary simulations indicate that the correct treatment is particularly
critical for the study of gravitational instability when -50 K.Comment: 13 pages, 3 figures. To appear in ApJ
A Critical Examination of the X-Wind Model for Chondrule and Calcium-rich, Aluminum-rich Inclusion Formation and Radionuclide Production
Meteoritic data, especially regarding chondrules and calcium-rich,
aluminum-rich inclusions (CAIs), and isotopic evidence for short-lived
radionuclides (SLRs) in the solar nebula, potentially can constrain how
planetary systems form. Intepretation of these data demands an astrophysical
model, and the "X-wind" model of Shu et al. (1996) and collaborators has been
advanced to explain the origin of chondrules, CAIs and SLRs. It posits that
chondrules and CAIs were thermally processed < 0.1 AU from the protostar, then
flung by a magnetocentrifugal outflow to the 2-3 AU region to be incorporated
into chondrites. Here we critically examine key assumptions and predictions of
the X-wind model. We find a number of internal inconsistencies: theory and
observation show no solid material exists at 0.1 AU; particles at 0.1 AU cannot
escape being accreted into the star; particles at 0.1 AU will collide at speeds
high enough to destroy them; thermal sputtering will prevent growth of
particles; and launching of particles in magnetocentrifugal outflows is not
modeled, and may not be possible. We also identify a number of incorrect
predictions of the X-wind model: the oxygen fugacity where CAIs form is orders
of magnitude too oxidizing; chondrule cooling rates are orders of magnitude
lower than those experienced by barred olivine chondrules; chondrule-matrix
complementarity is not predicted; and the SLRs are not produced in their
observed proportions. We conclude that the X-wind model is not relevant to
chondrule and CAI formation and SLR production. We discuss more plausible
models for chondrule and CAI formation and SLR production.Comment: Accepted for publication in The Astrophysical Journa
Planet Populations as a Function of Stellar Properties
Exoplanets around different types of stars provide a window into the diverse
environments in which planets form. This chapter describes the observed
relations between exoplanet populations and stellar properties and how they
connect to planet formation in protoplanetary disks. Giant planets occur more
frequently around more metal-rich and more massive stars. These findings
support the core accretion theory of planet formation, in which the cores of
giant planets form more rapidly in more metal-rich and more massive
protoplanetary disks. Smaller planets, those with sizes roughly between Earth
and Neptune, exhibit different scaling relations with stellar properties. These
planets are found around stars with a wide range of metallicities and occur
more frequently around lower mass stars. This indicates that planet formation
takes place in a wide range of environments, yet it is not clear why planets
form more efficiently around low mass stars. Going forward, exoplanet surveys
targeting M dwarfs will characterize the exoplanet population around the lowest
mass stars. In combination with ongoing stellar characterization, this will
help us understand the formation of planets in a large range of environments.Comment: Accepted for Publication in the Handbook of Exoplanet
Exome sequencing identifies novel AD-associated genes
The genetic component of Alzheimer’s disease (AD) has been mainly assessed using Genome Wide Association Studies (GWAS), which do not capture the risk contributed by rare variants. Here, we compared the gene-based burden of rare damaging variants in exome sequencing data from 32,558 individuals —16,036 AD cases and 16,522 controls— in a two-stage analysis. Next to known genes TREM2, SORL1 and ABCA7, we observed a significant association of rare, predicted damaging variants in ATP8B4 and ABCA1 with AD risk, and a suggestive signal in ADAM10. Next to these genes, the rare variant burden in RIN3, CLU, ZCWPW1 and ACE highlighted these genes as potential driver genes in AD-GWAS loci. Rare damaging variants in these genes, and in particular loss-of-function variants, have a large effect on AD-risk, and they are enriched in early onset AD cases. The newly identified AD-associated genes provide additional evidence for a major role for APP-processing, Aβ-aggregation, lipid metabolism and microglial function in AD
A SUB-ARCSECOND SURVEY TOWARD CLASS 0 PROTOSTARS IN PERSEUS: SEARCHING FOR SIGNATURES OF PROTOSTELLAR DISKS
Assessment of facial profile changes in patients treated with maxillary premolar extractions
Lawson criterion for ignition exceeded in an inertial fusion experiment
For more than half a century, researchers around the world have been engaged in attempts to achieve fusion ignition as a proof of principle of various fusion concepts. Following the Lawson criterion, an ignited plasma is one where the fusion heating power is high enough to overcome all the physical processes that cool the fusion plasma, creating a positive thermodynamic feedback loop with rapidly increasing temperature. In inertially confined fusion, ignition is a state where the fusion plasma can begin "burn propagation" into surrounding cold fuel, enabling the possibility of high energy gain. While "scientific breakeven" (i.e., unity target gain) has not yet been achieved (here target gain is 0.72, 1.37 MJ of fusion for 1.92 MJ of laser energy), this Letter reports the first controlled fusion experiment, using laser indirect drive, on the National Ignition Facility to produce capsule gain (here 5.8) and reach ignition by nine different formulations of the Lawson criterion
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
Analysis of shared heritability in common disorders of the brain
ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders
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