Numerically Modeling the First Peak of the Type IIb SN 2016gkg

Many Type IIb supernovae (SNe) show a prominent additional early peak in their light curves, which is generally thought to be due to the shock cooling of extended hydrogen-rich material surrounding the helium core of the exploding star. The recent SN 2016gkg was a nearby Type IIb SN discovered shortly after explosion, which makes it an excellent candidate for studying this first peak. We numerically explode a large grid of extended envelope models and compare these to SN 2016gkg to investigate what constraints can be derived from its light curve. This includes exploring density profiles for both a convective envelope and an optically thick steady-state wind, the latter of which has not typically been considered for Type IIb SNe models. We find that roughly $\sim0.02\,M_\odot$ of extended material with a radius of $\approx180-260\,R_\odot$ reproduces the photometric light curve data, consistent with pre-explosion imaging. These values are independent of the assumed density profile of this material, although a convective profile provides a somewhat better fit. We infer from our modeling that the explosion must have occurred within $\approx2-3\,{\rm hrs}$ of the first observed data point, demonstrating that this event was caught very close to the moment of explosion. Nevertheless, our best-fitting one-dimensional models overpredict the earliest velocity measurements, which suggests that the hydrogen-rich material is not distributed in a spherically symmetric manner. We compare this to the asymmetries seen in the SN IIb remnant Cas A, and we discuss the implications of this for Type IIb SN progenitors and explosion models.Comment: 8 pages, 8 figures, updated version accepted for publication in The Astrophysical Journa

The Transatlantic Oarsmen Cooperative: Doubling Down on a Transatlantic Financial Regulatory Regime

This project argues that, in the wake of the 2007-09 financial crisis, the United States (US) and European Union (EU) are doubling down on finance-led domestic growth strategies and that this is their goal in constructing a transatlantic financial regulatory regime. The regime’s goal privileges the input of industry actors over other civil society actors. The construction of this regime is in response to pressure from emerging markets and to service domestic industry actors after the financial crisis. The regime is intended to allow the US and EU to maintain their dominance within the international financial regulatory regime and continue to enjoy finance-led growth. In the emergent transatlantic regulatory regime, there has been a new division of labor emerging between the state and civil society, best illustrated with a nautical analogy: civil society and industry are steering regulatory activity and the state is rowing by creating regulatory institutions to serve industry. I thus propose the term oarsman state to explain this division of labor and assert that the EU and US are operating a transatlantic oarsmen cooperative. Empirically this project demonstrates that the financial crisis was a critical juncture that caused institutional and functional changes in the (i) EU, (ii) US, (iii) international and (iv) transatlantic financial regulatory regimes. In order to address the first empirical dimension of institutional and functional change, the research method of process-tracing will be used to compare the regimes before and after the financial crisis. The second goal of this project is to explain how the changes in the EU, US and international regimes triggered an escalation in the creation of the transatlantic financial regulatory regime. This project applies an analytic framework that combines top-down and bottom-up approaches to explaining regulatory and institutional change to address the second question regarding causation. The changes in the EU, US, and international financial regulatory regimes are analyzed as causal factors that contribute to the emergence of the transatlantic financial regulatory regime

Policy analysis: A rich array of country and comparative insights

10.1080/23276665.2016.1217663Asia Pacific Journal of Public Administration383204-21

Commentary: Uterine Microbiota: Residents, Tourists, or Invaders?

The recently published review by Baker et al. summarizes the current status of uterine microbiota with the aim to promote research priorities and discussion on this novel research field (1). The authors are to be congratulated on this much anticipated review as microbiota in the uterus is one increasing research area, though poorly investigated microbial niche relative to other organs. However, emerging evidence is beginning to indicate that the uterine microbiota has important implications for female (reproductive) health and disease, and it is becoming evident that the concept of sterile uterus is outworn, although the true core uterine microbiota still needs to be assessed.SA is funded by grants RYC-2016-21199 and ENDORE SAF2017-87526 from the Spanish Ministry of Economy, Industry and Competitiveness (MINECO), and European Regional Development Fund (FEDER)

The 9p21.3 risk of childhood acute lymphoblastic leukaemia is explained by a rare high-impact variant in CDKN2A

Genome-wide association studies (GWAS) have provided strong evidence for inherited predisposition to childhood acute lymphoblastic leukaemia (ALL) identifying a number of risk loci. We have previously shown common SNPs at 9p21.3 influence ALL risk. These SNP associations are generally not themselves candidates for causality, but simply act as markers for functional variants. By means of imputation of GWAS data and subsequent validation SNP genotyping totalling 2,177 ALL cases and 8,240 controls, we have shown that the 9p21.3 association can be ascribed to the rare highimpact CDKN2A p.Ala148Thr variant (rs3731249; Odds ratio=2.42, P=3.45×10−19). The association between rs3731249 genotype and risk was not specific to particular subtype of B-cell ALL. The rs3731249 variant is associated with predominant nuclear localisation of the CDKN2A transcript suggesting the functional effect of p.Ala148Thr on ALL risk may be through compromised ability to inhibit cyclin D within the cytoplasm

A New Look at Family Migration and Women's Employment Status

Family migration has a negative impact on women’s employment status. Using longitudinal data from the British Household Panel Survey (3,617 women; 22,354 women/wave observations) we consider two neglected issues. First, instead of relying on the distance moved to distinguish employment-related migrations, we use information on the reason for moving, allowing us to separate employment-related moves, stimulated by the man or the woman, from other moves. Second, we consider selection effects and the role of state dependence in relation to women’s employment status prior to moving. Moving for the sake of the man’s job has a significant negative effect on subsequent employment status for previously employed women. Women who were not employed previously benefited only slightly from family migration

Suffering in long-term cancer survivors: An evaluation of the PRISM-R2 in a population-based cohort

The Pictorial Representation of Illness and Self Measure-Revised 2 (PRISM-R2) has been developed as generic measure to assess suffering. The aim of this study was to evaluate the ability of this instrument to identify long-term cancer survivors with high levels of suffering who may need additional support. 1299 cancer survivors completed the PRISM-R2, the Short Form Health Survey (SF-36), and the Quality of Life-Cancer Survivors questionnaire (QoL-CS). The PRISM-R2 distinguishes between the Self-Illness Separation (SIS) and Illness Perception Measure (IPM), both measuring aspects of suffering. 112 (9%) cancer survivors reported high suffering according to IPM. This group had a higher cancer stage at diagnosis, more cancer recurrences, more comorbidities, and were lower educated compared to people reporting less suffering. The PRISM-R2 could explain substantial amounts of variance (10-14%) in the psychological aspects of the SF-36 and QoL-CS. The IPM also discriminated statistically and clinically significant between high- and low-health status. The PRISM-R2 proved to be able to discriminate between individuals with good and deteriorated levels of QoL. Further evaluation of its validity and screening potential is recommended

Impact of a cis-associated gene expression SNP on chromosome 20q11.22 on bipolar disorder susceptibility, hippocampal structure and cognitive performance.

BackgroundBipolar disorder is a highly heritable polygenic disorder. Recent enrichment analyses suggest that there may be true risk variants for bipolar disorder in the expression quantitative trait loci (eQTL) in the brain.AimsWe sought to assess the impact of eQTL variants on bipolar disorder risk by combining data from both bipolar disorder genome-wide association studies (GWAS) and brain eQTL.MethodTo detect single nucleotide polymorphisms (SNPs) that influence expression levels of genes associated with bipolar disorder, we jointly analysed data from a bipolar disorder GWAS (7481 cases and 9250 controls) and a genome-wide brain (cortical) eQTL (193 healthy controls) using a Bayesian statistical method, with independent follow-up replications. The identified risk SNP was then further tested for association with hippocampal volume (n = 5775) and cognitive performance (n = 342) among healthy individuals.ResultsIntegrative analysis revealed a significant association between a brain eQTL rs6088662 on chromosome 20q11.22 and bipolar disorder (log Bayes factor = 5.48; bipolar disorder P = 5.85×10(-5)). Follow-up studies across multiple independent samples confirmed the association of the risk SNP (rs6088662) with gene expression and bipolar disorder susceptibility (P = 3.54×10(-8)). Further exploratory analysis revealed that rs6088662 is also associated with hippocampal volume and cognitive performance in healthy individuals.ConclusionsOur findings suggest that 20q11.22 is likely a risk region for bipolar disorder; they also highlight the informative value of integrating functional annotation of genetic variants for gene expression in advancing our understanding of the biological basis underlying complex disorders, such as bipolar disorder

Evidence For Genetic Heterogeneity Between Clinical Subtypes of Bipolar Disorder

We performed a genome-wide association study of 6447 bipolar disorder (BD) cases and 12 639 controls from the International Cohort Collection for Bipolar Disorder (ICCBD). Meta-analysis was performed with prior results from the Psychiatric Genomics Consortium Bipolar Group for a combined sample of 13 902 cases and 19 279 controls. We identified eight genome-wide significant, associated regions, including a novel associated region on chromosome 10 (rs10884920; P = 3.28 × 10 − 8) that includes the brain-enriched cytoskeleton protein adducin 3 (ADD3), a non-coding RNA, and a neuropeptide-specific aminopeptidase P (XPNPEP1). Our large sample size allowed us to test the heritability and genetic correlation of BD subtypes and investigate their genetic overlap with schizophrenia (SCZ) and major depressive disorder. We found a significant difference in heritability of the two most common forms of BD (BD I h2 = 0.35; BD II h2 = 0.25; P = 0.02) with a genetic correlation between BD I and BD II of 0.78,compared with a genetic correlation of 0.97 when BD cohorts containing both types were compared. In addition, we demonstrated a significantly greater load of polygenic risk alleles for SCZ and BD in patients with BD I compared with patients with BD II, and a greater load of SCZ risk alleles in the bipolar type of schizoaffective disorder (SAB) compared with both other BD subtypes. These results point to a partial difference in genetic architecture of BD subtypes, and are suggestive of a molecular correlate for the clinical division of BD into subtypes