SGR J1550-5418 bursts detected with the Fermi Gamma-ray Burst Monitor during its most prolific activity

We have performed detailed temporal and time-integrated spectral analysis of 286 bursts from SGR J1550-5418 detected with the Fermi Gamma-ray Burst Monitor (GBM) in January 2009, resulting in the largest uniform sample of temporal and spectral properties of SGR J1550-5418 bursts. We have used the combination of broadband and high time-resolution data provided with GBM to perform statistical studies for the source properties. We determine the durations, emission times, duty cycles and rise times for all bursts, and find that they are typical of SGR bursts. We explore various models in our spectral analysis, and conclude that the spectra of SGR J1550-5418 bursts in the 8-200 keV band are equally well described by optically thin thermal bremsstrahlung (OTTB), a power law with an exponential cutoff (Comptonized model), and two black-body functions (BB+BB). In the spectral fits with the Comptonized model we find a mean power-law index of -0.92, close to the OTTB index of -1. We show that there is an anti-correlation between the Comptonized Epeak and the burst fluence and average flux. For the BB+BB fits we find that the fluences and emission areas of the two blackbody functions are correlated. The low-temperature BB has an emission area comparable to the neutron star surface area, independent of the temperature, while the high-temperature blackbody has a much smaller area and shows an anti-correlation between emission area and temperature. We compare the properties of these bursts with bursts observed from other SGR sources during extreme activations, and discuss the implications of our results in the context of magnetar burst models.Comment: 13 pages, 10 figures, 2 tables; minor changes, ApJ in pres

Relation between serum uric acid and carotid intima-media thickness in healthy postmenopausal women

OBJECTIVE: Serum uric acid (SUA) is associated with cardiovascular disease (CVD). However it is still disputed whether the relationship is mediated by other risk factors such as obesity, dyslipidaemia, hypertension and insulin resistance. We explored the association of the uric acid level with carotid intima-media thickness (IMT), a well known marker of CVD, in postmenopausal healthy women. METHODS: We consecutively enrolled postmenopausal women undergoing a screening for health evaluation. After an accurate clinical examination, and a biochemical evaluation, the enrolled subjects underwent B mode ultrasonography to assess common carotid intima media thickness. RESULTS: Among 234 women aged 45-70 years, the uric acid level is associated with carotid IMT independently of other prognostic factors (p=0.03). In particular, women in the highest tertiles of uric acid level have a greater IMT than women in the lowest tertile (p=0.007). CONCLUSIONS: Independently of other cardiovascular risk factors, SUA levels are associated with carotid IMT even in subjects without the metabolic syndrome. This confirms and expands the role of uric acid in the determinism of CVD. Prospective trials would be useful to evaluate interventions aimed at lowering the uric acid level

The Swift Deep Galactic Plane Survey (DGPS) Phase-I Catalog

The \textit{Swift} Deep Galactic Plane Survey is a \textit{Swift} Key Project consisting of 380 tiled pointings covering 40 deg$^{2}$ of the Galactic Plane between longitude $10$\,$<$\,$|l|$\,$<$\,$30$ deg and latitude $|b|$\,$<$\,$0.5$ deg. Each pointing has a $5$ ks exposure, yielding a total of 1.9 Ms spread across the entire survey footprint. Phase-I observations were carried out between March 2017 and May 2021. The Survey is complete to depth $L_X$\,$>$\,$10^{34}$ erg s$^{-1}$ to the edge of the Galaxy. The main Survey goal is to produce a rich sample of new X-ray sources and transients, while also covering a broad discovery space. Here, we introduce the Survey strategy and present a catalog of sources detected during Phase-I observations. In total, we identify 928 X-ray sources, of which 348 are unique to our X-ray catalog. We report on the characteristics of sources in our catalog and highlight sources newly classified and published by the DGPS team.Comment: Submitted to ApJ

Heterozygous Mutation of Drosophila Opa1 Causes the Development of Multiple Organ Abnormalities in an Age-Dependent and Organ-Specific Manner

Optic Atrophy 1 (OPA1) is a ubiquitously expressed dynamin-like GTPase in the inner mitochondrial membrane. It plays important roles in mitochondrial fusion, apoptosis, reactive oxygen species (ROS) and ATP production. Mutations of OPA1 result in autosomal dominant optic atrophy (DOA). The molecular mechanisms by which link OPA1 mutations and DOA are not fully understood. Recently, we created a Drosophila model to study the pathogenesis of optic atrophy. Heterozygous mutation of Drosophila OPA1 (dOpa1) by P-element insertion results in no obvious morphological abnormalities, whereas homozygous mutation is embryonic lethal. In eye-specific somatic clones, homozygous mutation of dOpa1 causes rough (mispatterning) and glossy (decreased lens deposition) eye phenotypes in adult Drosophila. In humans, heterozygous mutations in OPA1 have been associated with mitochondrial dysfunction, which is predicted to affect multiple organs. In this study, we demonstrated that heterozygous dOpa1 mutation perturbs the visual function and an ERG profile of the Drosophila compound eye. We independently showed that antioxidants delayed the onset of mutant phenotypes in ERG and improved larval vision function in phototaxis assay. Furthermore, heterozygous dOpa1 mutation also caused decreased heart rate, increased heart arrhythmia, and poor tolerance to stress induced by electrical pacing. However, antioxidants had no effects on the dysfunctional heart of heterozygous dOpa1 mutants. Under stress, heterozygous dOpa1 mutations caused reduced escape response, suggesting abnormal function of the skeletal muscles. Our results suggest that heterozygous mutation of dOpa1 shows organ-specific pathogenesis and is associated with multiple organ abnormalities in an age-dependent and organ-specific manner