Suzaku and Chandra observations of the galaxy cluster RXC J1053.7+5453 with a radio relic

We present the results of Suzaku and Chandra observations of the galaxy cluster RXC J1053.7+5453 ($z=0.0704$), which contains a radio relic. The radio relic is located at the distance of $\sim 540$ kpc from the X-ray peak toward the west. We measured the temperature of this cluster for the first time. The resultant temperature in the center is $\sim 1.3$ keV, which is lower than the value expected from the X-ray luminosity - temperature and the velocity dispersion - temperature relation. Though we did not find a significant temperature jump at the outer edge of the relic, our results suggest that the temperature decreases outward across the relic. Assuming the existence of the shock at the relic, its Mach number becomes $M \simeq 1.4$. A possible spatial variation of Mach number along the relic is suggested. Additionally, a sharp surface brightness edge is found at the distance of $\sim 160$ kpc from the X-ray peak toward the west in the Chandra image. We performed X-ray spectral and surface brightness analyses around the edge with Suzaku and Chandra data, respectively. The obtained surface brightness and temperature profiles suggest that this edge is not a shock but likely a cold front. Alternatively, it cannot be ruled out that thermal pressure is really discontinuous across the edge. In this case, if the pressure across the surface brightness edge is in equilibrium, other forms of pressure sources, such as cosmic-rays, are necessary. We searched for the non-thermal inverse Compton component in the relic region. Assuming the photon index $\Gamma = 2.0$, the resultant upper limit of the flux is $1.9 \times 10^{-14} {\rm erg \ s^{-1} \ cm^{-2}}$ for $4.50 \times 10^{-3} {\rm \ deg^{2}}$ area in the 0.3-10 keV band, which implies that the lower limit of magnetic field strength becomes $ 0.7 {\rm \ \mu G}$.Comment: 13page, 8 figures, accepted for publication in PASJ. arXiv admin note: text overlap with arXiv:1508.0584

All is nice and well unless she outshines him: Higher social status benefits women's well‐being and relationship quality but not if they surpass their male partner

In two studies, we find that climbing the societal ladder has positive associations with women's well-being and relationship outcomes but can also have negative consequences when women surpass their male partners in status. In Study 1 (N = 314), we found that women who reported having higher personal status also reported several positive relationship outcomes (e.g., higher relationship quality than women with lower personal status). However, these associations reversed for women who surpassed their partners in social status. In Study 2, a diary study (N = 112), we show how women's implicit endorsement of gender stereotypes qualifies the negative associations of surpassing one's partner in status. Among women with higher status than their partner, traditional women intend to adjust their behavior to fit the gender norm (e.g., thinking about reducing work hours in favor of their time at home), whereas egalitarian women did not, but felt guilty toward their partner. We show how the relationship dynamics of women who have surpassed their partners in social status should be considered when attempting to tackle structural discrimination and advance women's careers

Lithium carbonate in amyotrophic lateral sclerosis patients homozygous for the C-allele at SNP rs12608932 in UNC13A: protocol for a confirmatory, randomized, group-sequential, event-driven, double-blind, placebo-controlled trial

BackgroundGiven the large genetic heterogeneity in amyotrophic lateral sclerosis (ALS), it seems likely that genetic subgroups may benefit differently from treatment. An exploratory meta-analysis identified that patients homozygous for the C-allele at SNP rs12608932, a single nucleotide polymorphism in the gene UNC13A, had a statistically significant survival benefit when treated with lithium carbonate. We aim to confirm the efficacy of lithium carbonate on the time to death or respiratory insufficiency in patients with ALS homozygous for the C-allele at SNP rs12608932 in UNC13A. MethodsA randomized, group-sequential, event-driven, double-blind, placebo-controlled trial will be conducted in 15 sites across Europe and Australia. Patients will be genotyped for UNC13A; those homozygous for the C-allele at SNP rs12608932 will be eligible. Patients must have a diagnosis of ALS according to the revised El Escorial criteria, and a TRICALS risk-profile score between -6.0 and -2.0. An expected number of 1200 patients will be screened in order to enroll a target sample size of 171 patients. Patients will be randomly allocated in a 2:1 ratio to lithium carbonate or matching placebo, and treated for a maximum duration of 24 months. The primary endpoint is the time to death or respiratory insufficiency, whichever occurs first. Key secondary endpoints include functional decline, respiratory function, quality of life, tolerability, and safety. An interim analysis for futility and efficacy will be conducted after the occurrence of 41 events. DiscussionLithium carbonate has been proven to be safe and well-tolerated in patients with ALS. Given the favorable safety profile, the potential benefits are considered to outweigh the burden and risks associated with study participation. This study may provide conclusive evidence about the life-prolonging potential of lithium carbonate in a genetic ALS subgroup

Distinct Loci in the CHRNA5 / CHRNA3 / CHRNB4 Gene Cluster Are Associated With Onset of Regular Smoking

Neuronal nicotinic acetylcholine receptor (nAChR) genes (CHRNA5/CHRNA3/CHRNB4) have been reproducibly associated with nicotine dependence, smoking behaviors, and lung cancer risk. Of the few reports that have focused on early smoking behaviors, association results have been mixed. This meta-analysis examines early smoking phenotypes and SNPs in the gene cluster to determine: (1) whether the most robust association signal in this region (rs16969968) for other smoking behaviors is also associated with early behaviors, and/or (2) if additional statistically independent signals are important in early smoking. We focused on two phenotypes: age of tobacco initiation (AOI) and age of first regular tobacco use (AOS). This study included 56,034 subjects (41 groups) spanning nine countries and evaluated five SNPs including rs1948, rs16969968, rs578776, rs588765, and rs684513. Each dataset was analyzed using a centrally generated script. Meta-analyses were conducted from summary statistics. AOS yielded significant associations with SNPs rs578776 (beta = 0.02, P = 0.004), rs1948 (beta = 0.023, P = 0.018), and rs684513 (beta = 0.032, P = 0.017), indicating protective effects. There were no significant associations for the AOI phenotype. Importantly, rs16969968, the most replicated signal in this region for nicotine dependence, cigarettes per day, and cotinine levels, was not associated with AOI (P = 0.59) or AOS (P = 0.92). These results provide important insight into the complexity of smoking behavior phenotypes, and suggest that association signals in the CHRNA5/A3/B4 gene cluster affecting early smoking behaviors may be different from those affecting the mature nicotine dependence phenotype

Viral coinfections in hospitalized coronavirus disease 2019 patients recruited to the international severe acute respiratory and emerging infections consortium WHO clinical characterisation protocol UK study

Background We conducted this study to assess the prevalence of viral coinfection in a well characterized cohort of hospitalized coronavirus disease 2019 (COVID-19) patients and to investigate the impact of coinfection on disease severity. Methods Multiplex real-time polymerase chain reaction testing for endemic respiratory viruses was performed on upper respiratory tract samples from 1002 patients with COVID-19, aged <1 year to 102 years old, recruited to the International Severe Acute Respiratory and Emerging Infections Consortium WHO Clinical Characterisation Protocol UK study. Comprehensive demographic, clinical, and outcome data were collected prospectively up to 28 days post discharge. Results A coinfecting virus was detected in 20 (2.0%) participants. Multivariable analysis revealed no significant risk factors for coinfection, although this may be due to rarity of coinfection. Likewise, ordinal logistic regression analysis did not demonstrate a significant association between coinfection and increased disease severity. Conclusions Viral coinfection was rare among hospitalized COVID-19 patients in the United Kingdom during the first 18 months of the pandemic. With unbiased prospective sampling, we found no evidence of an association between viral coinfection and disease severity. Public health interventions disrupted normal seasonal transmission of respiratory viruses; relaxation of these measures mean it will be important to monitor the prevalence and impact of respiratory viral coinfections going forward

SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway

Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant