The imaging properties of the Gas Pixel Detector as a focal plane polarimeter

X-rays are particularly suited to probe the physics of extreme objects. However, despite the enormous improvements of X-ray Astronomy in imaging, spectroscopy and timing, polarimetry remains largely unexplored. We propose the photoelectric polarimeter Gas Pixel Detector (GPD) as an instrument candidate to fill the gap of more than thirty years of lack of measurements. The GPD, in the focus of a telescope, will increase the sensitivity of orders of magnitude. Moreover, since it can measure the energy, the position, the arrival time and the polarization angle of every single photon, allows to perform polarimetry of subsets of data singled out from the spectrum, the light curve or the image of source. The GPD has an intrinsic very fine imaging capability and in this work we report on the calibration campaign carried out in 2012 at the PANTER X-ray test facility of the Max-Planck-Institut f\"ur extraterrestrische Physik of Garching (Germany) in which, for the first time, we coupled it to a JET-X optics module with a focal length of 3.5 m and an angular resolution of 18 arcsec at 4.5 keV. This configuration was proposed in 2012 aboard the X-ray Imaging Polarimetry Explorer (XIPE) in response to the ESA call for a small mission. We derived the imaging and polarimetric performance for extended sources like Pulsar Wind Nebulae and Supernova Remnants as case studies for the XIPE configuration, discussing also possible improvements by coupling the detector with advanced optics, having finer angular resolution and larger effective area, to study with more details extended objects.Comment: Accepted for publication in The Astrophysical Journal Supplemen

USP15 deubiquitinase safeguards hematopoiesis and genome integrity in hematopoietic stem cells and leukemia cells

Altering ubiquitination by disruption of individual deubiquitinating enzymes (DUBs) has proven to affect hematopoietic stem cell (HSC) maintenance. However, comprehensive knowledge of DUB function during hematopoiesis in vivo is lacking. To accomplish this goal, we systematically inactivated DUBs in mouse hematopoietic progenitors using in vivo small hairpin RNAs (shRNAs) screens. We found that multiple DUBs may be individually required for hematopoiesis and that the ubiquitin-specific protease 15 (USP15) is particularly important for the maintenance of murine hematopoietic stem and progenitor cells in vitro and in vivo. Consistently, Usp15 knockout mice exhibited a reduced HSC pool. The defect was intrinsic to HSCs, as demonstrated by competitive repopulation assays. Importantly, USP15 is highly expressed in normal human hematopoietic cells and leukemias, and USP15 depletion in murine early progenitors and myeloid leukemia cells impaired in vitro expansion and increased genotoxic stress. Our study underscores the importance of DUBs in preserving normal hematopoiesis and uncovers USP15 as a critical DUB in safeguarding genome integrity in HSC and in leukemia cells

Final performances of the X-ray Mirrors of the JET-X telescope

The Joint European Telesscope (JET-X) is one of the core scientific instruments of the SPECTRUM-X-Gamma mission. JET-X was designed to study X-ray emissions in the band 0.3-10 KeV. Its angular resolution is better than 20 arcsec; the values of the effective areas are 161 cm2 at 1.5 KeV and 69 cm2 at 8 Kev (for one telescope). The value of the HEW circle in function of the off-axis angle is presented; it is found to be below 20 arcsec at 1.5 Kev and around 23 arcsec at 8 KeV up to an off-axis angle of 12 arcmin.Comment: 2 pages, 1 ps figure. To be published in the Proceedings of the IAU Symposium 188 THE HOT UNIVERSE, held in Kyoto (August 26-30, 1997) in occasion of the XXIII IAU General Assembl

An extension of the SHARC survey

We report on our search for distant clusters of galaxies based on optical and X-ray follow up observations of X-ray candidates from the SHARC survey. Based on the assumption that the absence of bright optical or radio counterparts to possibly extended X-ray sources could be distant clusters. We have obtained deep optical images and redshifts for several of these objects and analyzed archive XMM-Newton or Chandra data where applicable. In our list of candidate clusters, two are probably galaxy structures at redshifts of z$\sim$0.51 and 0.28. Seven other structures are possibly galaxy clusters between z$\sim$0.3 and 1. Three sources are identified with QSOs and are thus likely to be X-ray point sources, and six more also probably fall in this category. One X-ray source is spurious or variable. For 17 other sources, the data are too sparse at this time to put forward any hypothesis on their nature. We also serendipitously detected a cluster at z=0.53 and another galaxy concentration which is probably a structure with a redshift in the [0.15-0.6] range. We discuss these results within the context of future space missions to demonstrate the necessity of a wide field of view telescope optimized for the 0.5-2 keV range.Comment: Accepted in A&

The in-flight spectroscopic performance of the Swift XRT CCD camera during 2006-2007

The Swift X-ray Telescope focal plane camera is a front-illuminated MOS CCD, providing a spectral response kernel of 135 eV FWHM at 5.9 keV as measured before launch. We describe the CCD calibration program based on celestial and on-board calibration sources, relevant in-flight experiences, and developments in the CCD response model. We illustrate how the revised response model describes the calibration sources well. Comparison of observed spectra with models folded through the instrument response produces negative residuals around and below the Oxygen edge. We discuss several possible causes for such residuals. Traps created by proton damage on the CCD increase the charge transfer inefficiency (CTI) over time. We describe the evolution of the CTI since the launch and its effect on the CCD spectral resolution and the gain.Comment: 8 pages, 5 colour figures, submitted to SPI

Is Brain-Derived Neurotropic Factor Methylation Involved in the Association Between Prenatal Stress and Maternal Postnatal Anxiety During the COVID-19 Pandemic?

BackgroundThe COVID-19 pandemic is a collective trauma that may expose susceptible individuals to high levels of stress. Pregnant women represent a high-risk population, considering that pregnancy is a period of heightened neuroplasticity and susceptibility to stress through epigenetic mechanisms. Previous studies showed that the methylation status of the BDNF gene is linked with prenatal stress exposure. The goals of this study were (a) to assess the association between pandemic-related stress and postnatal anxiety and (b) to investigate the potential role of maternal BDNF methylation as a significant mediator of this association. MethodsIn the present study, we report data on the association among pandemic-related stress during pregnancy, maternal BDNF methylation, and postnatal anxiety symptoms. Pandemic-related stress and postnatal anxiety were assessed through self-report instruments. BDNF methylation was estimated in 11 CpG sites in DNA from mothers' buccal cells. Complete data were available from 108 mothers. ResultsResults showed that pandemic-related stress was associated with an increased risk of postnatal anxiety, r = 0.20, p < 0.05. CpG-specific BDNF methylation was significantly associated with both prenatal pandemic-related stress, r = 0.21, p < 0.05, and postnatal maternal anxious symptoms, r = 0.25, p = 0.01. Moreover, a complete mediation by the BDNF CpG6 methylation emerged between pandemic-related stress during pregnancy and postnatal maternal anxiety, ACME = 0.66, p < 0.05. ConclusionThese findings suggest that BDNF epigenetic regulation by pandemic-related stress might contribute to increase the risk of anxiety in mothers. Policymakers should prioritize the promotion of health and wellbeing in pregnant women and mothers during the present healthcare emergency

Movement disorder and neuronal migration disorder due to ARFGEF2 mutation

We report a child with a severe choreadystonic movement disorder, bilateral periventricular nodular heterotopia (BPNH), and secondary microcephaly based on compound heterozygosity for two new ARFGEF2 mutations (c.2031_2038dup and c.3798_3802del), changing the limited knowledge about the phenotype. The brain MRI shows bilateral hyperintensity of the putamen, BPNH, and generalized atrophy. Loss of ARFGEF2 function affects vesicle trafficking, proliferation/apoptosis, and neurotransmitter receptor function. This can explain BPNH and microcephaly. We hypothesize that the movement disorder and the preferential damage to the basal ganglia, specifically to the putamen, may be caused by an increased sensitivity to degeneration, a dynamic dysfunction due to neurotransmitter receptor mislocalization or a combination of both

Tight regulation of ubiquitin-mediated DNA damage response by USP3 preserves the functional integrity of hematopoietic stem cells

Histone ubiquitination at DNA breaks is required for activation of the DNA damage response (DDR) and DNA repair. How the dynamic removal of this modification by deubiquitinating enzymes (DUBs) impacts genome maintenance in vivo is largely unknown. To address this question, we generated mice deficient for Ub-specific protease 3 (USP3; Usp3{delta}/{delta}), a histone H2A DUB which negatively regulates ubiquitin-dependent DDR signaling. Notably, USP3 deletion increased the levels of histone ubiquitination in adult tissues, reduced the hematopoietic stem cell (HSC) reserves over time, and shortened animal life span. Mechanistically, our data show that USP3 is important in HSC homeostasis, preserving HSC self-renewal, and repopulation potential in vivo and proliferation in vitro. A defective DDR and unresolved spontaneous DNA damage contribute to cell cycle restriction of Usp3{delta}/{delta} HSCs. Beyond the hematopoietic system, Usp3{delta}/{delta} animals spontaneously developed tumors, and primary Usp3{delta}/{delta} cells failed to preserve chromosomal integrity. These findings broadly support the regulation of chromatin ubiquitination as a key pathway in preserving tissue function through modulation of the response to genotoxic stress