Using the transit of Venus to probe the upper planetary atmosphere

The atmosphere of a transiting planet shields the stellar radiation providing us with a powerful method to estimate its size and density. In particular, because of their high ionization energy, atoms with high atomic number (Z) absorb short-wavelength radiation in the upper atmosphere, undetectable with observations in visible light. One implication is that the planet should appear larger during a primary transit observed in high energy bands than in the optical band. The last Venus transit in 2012 offered a unique opportunity to study this effect. The transit has been monitored by solar space observations from Hinode and Solar Dynamics Observatory (SDO). We measure the radius of Venus during the transit in three different bands with subpixel accuracy: optical (4500A), UV (1600A, 1700A), Extreme UltraViolet (EUV, 171-335A) and soft X-rays (about 10A). We find that, while the Venus optical radius is about 80 km larger than the solid body radius (the expected opacity mainly due to clouds and haze), the radius increases further by more than 70 km in the EUV and soft X-rays. These measurements mark the densest ion layers of Venus' ionosphere, providing information about the column density of CO2 and CO. They are useful for planning missions in situ to estimate the dynamical pressure from the environment, and can be employed as a benchmark case for observations with future missions, such as the ESA Athena, which will be sensitive enough to detect transits of exoplanets in high-energy bands.Comment: 13 pages, 2 figures; published in Nature Communications; the full and copy-edited version is open access at http://www.nature.com/ncomms/2015/150623/ncomms8563/full/ncomms8563.htm

NIVEAUX DE L'EUROPIUM-155

Le spectre d'électrons et le spectre [γ de 155Sm [MATH] 155Eu (22 min) ont été observés à haute résolution. Un schéma de niveaux est proposé

World-leading science with SPIRou - the nIR spectropolarimeter / high-precision velocimeter for CFHT

SPIRou is a near-infrared (nIR) spectropolarimeter / velocimeter proposed as a new-generation instrument for CFHT. SPIRou aims in particular at becoming world-leader on two forefront science topics, (i) the quest for habitable Earth-like planets around very- low-mass stars, and (ii) the study of low-mass star and planet formation in the presence of magnetic fields. In addition to these two main goals, SPIRou will be able to tackle many key programs, from weather patterns on brown dwarf to solar-system planet atmospheres, to dynamo processes in fully-convective bodies and planet habitability. The science programs that SPIRou proposes to tackle are forefront (identified as first priorities by most research agencies worldwide), ambitious (competitive and complementary with science programs carried out on much larger facilities, such as ALMA and JWST) and timely (ideally phased with complementary space missions like TESS and CHEOPS). SPIRou is designed to carry out its science mission with maximum efficiency and optimum precision. More specifically, SPIRou will be able to cover a very wide single-shot nIR spectral domain (0.98-2.35 \mu m) at a resolving power of 73.5K, providing unpolarized and polarized spectra of low-mass stars with a ~15% average throughput and a radial velocity (RV) precision of 1 m/s.Comment: 12 pages, 5 figures, conference proceedings of the French Society of Astronomy and Astrophysics meeting 201

Carboxypeptidase G2 rescue in patients with methotrexate intoxication and renal failure

The methotrexate (MTX) rescue agent carboxypeptidase G2 (CPDG2) rapidly hydrolyses MTX to the inactive metabolite DAMPA (4-[[2,4-diamino-6-(pteridinyl)methyl]-methylamino]-benzoic acid) and glutamate in patients with MTX-induced renal failure and delayed MTX excretion. DAMPA is thought to be an inactive metabolite of MTX because it is not an effective inhibitor of the MTX target enzyme dihydrofolate reductase. DAMPA is eliminated more rapidly than MTX in these patients, which suggests a nonrenal route of elimination. In a phase II study (May 1997–March 2002), CPDG2 was administered intravenously to 82 patients at a median dose of 50 U kg−1 (range 33–60 U kg−1). Eligible patients for this study had serum MTX concentrations of >10 μM at 36 h or >5 μM at 42 h after start of MTX infusion and documented renal failure (serum creatinine ⩾1.5 times the upper limit of normal). Immediately before CPDG2 administration, a median MTX serum level of 11.93 μM (range 0.52–901 μM) was documented. Carboxypeptidase G2 was given at a median of 52 h (range 25–178 h) following the start of an MTX infusion of 1–12 g m−2 4–36 h−1 and resulted in a rapid 97% (range 73–99%) reduction of the MTX serum level. Toxicity related to CPDG2 was not observed. Toxicity related to MTX was documented in about half the patients; four patients died despite CPDG2 administration due to severe myelosuppression and septic complications. In conclusion, administration of CPDG2 is a well-tolerated, safe and a very effective way of MTX elimination in delayed excretion due to renal failure

Genetically engineered minipigs model the major clinical features of human neurofibromatosis type 1.

Neurofibromatosis Type 1 (NF1) is a genetic disease caused by mutations in Neurofibromin 1 (NF1). NF1 patients present with a variety of clinical manifestations and are predisposed to cancer development. Many NF1 animal models have been developed, yet none display the spectrum of disease seen in patients and the translational impact of these models has been limited. We describe a minipig model that exhibits clinical hallmarks of NF1, including café au lait macules, neurofibromas, and optic pathway glioma. Spontaneous loss of heterozygosity is observed in this model, a phenomenon also described in NF1 patients. Oral administration of a mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor suppresses Ras signaling. To our knowledge, this model provides an unprecedented opportunity to study the complex biology and natural history of NF1 and could prove indispensable for development of imaging methods, biomarkers, and evaluation of safety and efficacy of NF1-targeted therapies

Study of the plutino object (208996) 2003 AZ84 from stellar occultations: size, shape and topographic features

We present results derived from four stellar occultations by the plutino object (208996) 2003~AZ$_{84}$, detected at January 8, 2011 (single-chord event), February 3, 2012 (multi-chord), December 2, 2013 (single-chord) and November 15, 2014 (multi-chord). Our observations rule out an oblate spheroid solution for 2003~AZ$_{84}$'s shape. Instead, assuming hydrostatic equilibrium, we find that a Jacobi triaxial solution with semi axes $(470 \pm 20) \times (383 \pm 10) \times (245 \pm 8)$~km % axis ratios $b/a= 0.82 \pm 0.05$ and $c/a= 0.52 \pm 0.02$, can better account for all our occultation observations. Combining these dimensions with the rotation period of the body (6.75~h) and the amplitude of its rotation light curve, we derive a density $\rho=0.87 \pm 0.01$~g~cm$^{-3}$ a geometric albedo $p_V= 0.097 \pm 0.009$. A grazing chord observed during the 2014 occultation reveals a topographic feature along 2003~AZ$_{84}$'s limb, that can be interpreted as an abrupt chasm of width $\sim 23$~km and depth $> 8$~km or a smooth depression of width $\sim 80$~km and depth $\sim 13$~km (or an intermediate feature between those two extremes)

The stellar occultation by Makemake on 2011 April 23

We have taken advantage of a stellar occultation by the dwarf planet Makemake on 2011 April 23, to determine several of its main physical properties. We present results from a multisite campaign with 8 positive occultation detections from 5 different sites, including data from the 8-m VLT and 3.5-m NTT telescopes in Chile, which have very high temporal resolution. Because the star was significantly fainter than Makemake (setting a record in the magnitude of a star whose occultation has been detected), the occultation resulted in a drop of just ~0.3 mag in the lightcurves. From the lightcurves we have been able to determine the size and shape of the body, its geometric albedo and constraints on its atmosphere

Cell-free DNA ultra-low-pass whole genome sequencing to distinguish malignant peripheral nerve sheath tumor (MPNST) from its benign precursor lesion: A cross-sectional study

BACKGROUND: The leading cause of mortality for patients with the neurofibromatosis type 1 (NF1) cancer predisposition syndrome is the development of malignant peripheral nerve sheath tumor (MPNST), an aggressive soft tissue sarcoma. In the setting of NF1, this cancer type frequently arises from within its common and benign precursor, plexiform neurofibroma (PN). Transformation from PN to MPNST is challenging to diagnose due to difficulties in distinguishing cross-sectional imaging results and intralesional heterogeneity resulting in biopsy sampling errors. METHODS AND FINDINGS: This multi-institutional study from the National Cancer Institute and Washington University in St. Louis used fragment size analysis and ultra-low-pass whole genome sequencing (ULP-WGS) of plasma cell-free DNA (cfDNA) to distinguish between MPNST and PN in patients with NF1. Following in silico enrichment for short cfDNA fragments and copy number analysis to estimate the fraction of plasma cfDNA originating from tumor (tumor fraction), we developed a noninvasive classifier that differentiates MPNST from PN with 86% pretreatment accuracy (91% specificity, 75% sensitivity) and 89% accuracy on serial analysis (91% specificity, 83% sensitivity). Healthy controls without NF1 (participants = 16, plasma samples = 16), PN (participants = 23, plasma samples = 23), and MPNST (participants = 14, plasma samples = 46) cohorts showed significant differences in tumor fraction in plasma (P = 0.001) as well as cfDNA fragment length (P \u3c 0.001) with MPNST samples harboring shorter fragments and being enriched for tumor-derived cfDNA relative to PN and healthy controls. No other covariates were significant on multivariate logistic regression. Mutational analysis demonstrated focal NF1 copy number loss in PN and MPNST patient plasma but not in healthy controls. Greater genomic instability including alterations associated with malignant transformation (focal copy number gains in chromosome arms 1q, 7p, 8q, 9q, and 17q; focal copy number losses in SUZ12, SMARCA2, CDKN2A/B, and chromosome arms 6p and 9p) was more prominently observed in MPNST plasma. Furthermore, the sum of longest tumor diameters (SLD) visualized by cross-sectional imaging correlated significantly with paired tumor fractions in plasma from MPNST patients (r = 0.39, P = 0.024). On serial analysis, tumor fraction levels in plasma dynamically correlated with treatment response to therapy and minimal residual disease (MRD) detection before relapse. Study limitations include a modest MPNST sample size despite accrual from 2 major referral centers for this rare malignancy, and lack of uniform treatment and imaging protocols representing a real-world cohort. CONCLUSIONS: Tumor fraction levels derived from cfDNA fragment size and copy number alteration analysis of plasma cfDNA using ULP-WGS significantly correlated with MPNST tumor burden, accurately distinguished MPNST from its benign PN precursor, and dynamically correlated with treatment response. In the future, our findings could form the basis for improved early cancer detection and monitoring in high-risk cancer-predisposed populations

Constraints on Charon's Orbital Elements from the Double Stellar Occultation of 2008 June 22

The original publication is available at http://iopscience.iop.org/1538-3881/International audiencePluto and its main satellite, Charon, occulted the same star on 2008 June 22. This event was observed from Australia and La Réunion Island, providing the east and north Charon Plutocentric offset in the sky plane (J2000): X= + 12,070.5 ± 4 km (+ 546.2 ± 0.2 mas), Y= + 4,576.3 ± 24 km (+ 207.1 ± 1.1 mas) at 19:20:33.82 UT on Earth, corresponding to JD 2454640.129964 at Pluto. This yields Charon's true longitude L= 153.483 ± 0fdg071 in the satellite orbital plane (counted from the ascending node on J2000 mean equator) and orbital radius r= 19,564 ± 14 km at that time. We compare this position to that predicted by (1) the orbital solution of Tholen & Buie (the "TB97" solution), (2) the PLU017 Charon ephemeris, and (3) the solution of Tholen et al. (the "T08" solution). We conclude that (1) our result rules out solution TB97, (2) our position agrees with PLU017, with differences of ΔL= + 0.073 ± 0fdg071 in longitude, and Δr= + 0.6 ± 14 km in radius, and (3) while the difference with the T08 ephemeris amounts to only ΔL= 0.033 ± 0fdg071 in longitude, it exhibits a significant radial discrepancy of Δr= 61.3 ± 14 km. We discuss this difference in terms of a possible image scale relative error of 3.35 × 10-3in the 2002-2003 Hubble Space Telescope images upon which the T08 solution is mostly based. Rescaling the T08 Charon semi-major axis, a = 19, 570.45 km, to the TB97 value, a = 19636 km, all other orbital elements remaining the same ("T08/TB97" solution), we reconcile our position with the re-scaled solution by better than 12 km (or 0.55 mas) for Charon's position in its orbital plane, thus making T08/TB97 our preferred solution

Circulating endothelial cell count: a reliable marker of endothelial damage in patients undergoing hematopoietic stem cell transplantation

The physio-pathologic interrelationships between endothelium and GvHD have been better elucidated and have led to definition of the entity 'endothelial GvHD' as an essential early phase prior to the clinical presentation of acute GvHD. Using the CellSearch system, we analyzed circulating endothelial cells (CEC) in 90 allogeneic hematopoietic stem cell transplantation (allo-HSCT) patients at the following time-points: T1 (pre-conditioning), T2 (pre-transplant), T3 (engraftment), T4 (onset of GvHD) and T5 (1 week after steroid treatment). Although CEC changes in allo-HSCT represent a dynamic phenomenon influenced by many variables (that is, conditioning, immunosuppressive treatments, engraftment syndrome and infections), we showed that CEC peaks were constantly seen at onset of acute GvHD and invariably returned to pre-transplant values after treatment response. Since we showed that CEC changes during allo-HSCT has rapid kinetics that may be easily missed if blood samples are drawn at pre-fixed time-points, we rather suggest an 'on demand' evaluation of CEC counts right at onset of GvHD clinical symptoms to possibly help differentiate GvHD from other non-endothelial complications. We confirm that CEC changes are a suitable biomarker to monitor endothelial damage in patients undergoing allo-transplantation and hold the potential to become a useful tool to support GvHD diagnosis (ClinicalTrials.gov NCT02064972).Bone Marrow Transplantation advance online publication, 11 September 2017; doi:10.1038/bmt.2017.194