Radii, masses, and ages of 18 bright stars using interferometry and new estimations of exoplanetary parameters

Accurate stellar parameters are needed in numerous domains of astrophysics. The position of stars on the H-R diagram is an important indication of their structure and evolution, and it helps improve stellar models. Furthermore, the age and mass of stars hosting planets are required elements for studying exoplanetary systems. We aim at determining accurate parameters of a set of 18 bright exoplanet host and potential host stars from interferometric measurements, photometry, and stellar models. Using the VEGA/CHARA interferometer, we measured the angular diameters of 18 stars, ten of which host exoplanets. We combined them with their distances to estimate their radii. We used photometry to derive their bolometric flux and, then, their effective temperature and luminosity to place them on the H-R diagram. We then used the PARSEC models to derive their best fit ages and masses, with error bars derived from MC calculations. Our interferometric measurements lead to an average of 1.9% uncertainty on angular diameters and 3% on stellar radii. There is good agreement between measured and indirect estimations of angular diameters (from SED fitting or SB relations) for MS stars, but not as good for more evolved stars. For each star, we provide a likelihood map in the mass-age plane; typically, two distinct sets of solutions appear (an old and a young age). The errors on the ages and masses that we provide account for the metallicity uncertainties, which are often neglected by other works. From measurements of its radius and density, we also provide the mass of 55 Cnc independently of models. From the stellar masses, we provide new estimates of semi-major axes and minimum masses of exoplanets with reliable uncertainties. We also derive the radius, density, and mass of 55 Cnc e, a super-Earth that transits its stellar host. Our exoplanetary parameters reflect the known population of exoplanets.Comment: 23 pages, 9 figures, published in A&A. (This version includes proof corrections.

Congenital and Disseminated Pyogenic Granuloma-like Vascular Lesions

International audienceWe report an exceptional case of multiple cutaneous and visceral neonatal pyogenic granuloma (PG) initially suggestive of a diffuse neonatal haemangiomatosis. CASE REPORT A full-term female newborn, with no significant past medical history, was referred to our department for treatment of an acute respiratory distress syndrome of neurological origin at day 8 of life. At birth, she presented with 3 small angiomatous papules and 4 subcutaneous nodules suggestive of neonatal hae-mangiomatosis (NH) (Fig. 1). A brain MRI revealed a highly vascularised brain stem tumour suggestive of glioma (Fig. 2), associated with 2 abnormal hepatic lesions consistent with infantile haemangiomas (IH) on ultrasound and CT scan. Methylprednisolone was started for the suspected glioma-associated oedema, and vincristine and propranolol were introduced for NH. After initial improvement, an acute intracranial hypertension related to cystic evolution of the disease necessitated surgical resection at the age of 2 months. Pathological examinations of the brain, cutaneous and subcutaneous lesions were similar, showing a vascular lobular proliferation of capillaries highly suggestive of PG. The misdiagnosis of glioma was eliminated. The GLUT-1 antigen marker was negative, ruling out the diagnosis of NH-like infantile haemangioma (Fig. 3). Lymphatic marker (D2-40) was also negative and eliminated a multifocal lymphangioendotheliomato-sis with thrombocytopaenia (MLT). Cutaneous and hepatic lesions gradually regressed. She is currently in complete remission after completing a treatment over 18 months with propranolol but a spontaneous improvement can not be excluded. DISCUSSIO

The Intensity of IUGR-Induced Transcriptome Deregulations Is Inversely Correlated with the Onset of Organ Function in a Rat Model

A low-protein diet applied during pregnancy in the rat results in intrauterine growth restricted (IUGR) fetuses. In humans, IUGR is associated with increased perinatal morbidity, higher incidence of neuro-developmental defects and increased risk of adult metabolic anomalies, such as diabetes and cardiovascular disease. Development and function of many organs are affected by environmental conditions such as those inducing fetal and early postnatal growth restriction. This phenomenon, termed “fetal programming” has been studied unconnectedly in some organs, but very few studies (if any) have investigated at the same time several organs, on a more comparative basis. However, it is quite probable that IUGR affects differentially most organ systems, with possible persistent changes in gene expression. In this study we address transcriptional alterations induced by IUGR in a multi-organ perspective, by systematic analysis of 20-days rat fetuses. We show that (1) expressional alterations are apparently stronger in organs functioning late in foetal or postnatal life than in organs that are functioning early (2) hierarchical classification of the deregulations put together kidney and placenta in one cluster, liver, lungs and heart in another; (3) the epigenetic machinery is set up especially in the placenta, while its alterations are rather mild in other organs; (4) the genes appear deregulated in chromosome clusters; (5) the altered expression cascades varies from organ to organ, with noticeably a very significant modification of the complement and coagulation cascades in the kidney; (6) we found a significant increase in TF binding site for HNF4 proteins specifically for liver genes that are down-regulated in IUGR, suggesting that this decrease is achieved through the action of HNF transcription factors, that are themselves transcriptionnally induced in the liver by IUGR (x 1.84 fold). Altogether, our study suggests that a combination of tissue-specific mechanisms contributes to bring about tissue-driven modifications of gene cascades. The question of these cascades being activated to adapt the organ to harsh environmental condition, or as an endpoint consequence is still raised

Clinical research in newborn infants: difficulties and specificity

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Caractérisation des composants de la fonction endothéliale au cours du développement normal et pathologique.Implications sur la programmation précoce du risque cardio-vasculaire.

Le faible poids de naissance (FPN) est un facteur de risque indépendant reconnu de maladies cardiovasculaires et d'hypertension à l'âge adulte, mais les mécanismes physiopathologiques sous-tendant cette programmation précoce ne sont que partiellement connus. Chez l'adulte, la dysfonction endothéliale et l'altération tant quantitative que qualitative de la cellule progénitrice endothéliale (PEC) sont un marqueur précoce et sensible de risque cardiovasculaire. Des altérations vasculaires (raréfaction microvasculaire, anomalies de la structure vasculaire) et une dysfonction endothéliale (altération de la vasodilatation endothélium-dépendante) sont retrouvées chez le nouveau-né de FPN. Cependant, l'hypothèse d'une altération de la cellule progénitrice endothéliale chez le nouveau-né de FPN reste à être démontrée. Au cours de notre travail, nous avons montré une altération des capacités clonogéniques et angiogéniques des PECs des nouveau-nés de FPN, tant in vitro qu'in vivo. Cette dysfonction pourrait être liée à un déséquilibre antiangiogénique d'origine environnementale conduisant à un profil antiangiogénique d'expression génique de la PEC. Ainsi, nous avons pu montrer qu'une surexpression du gène de la thrombospondine-1 pouvait en partie expliquer la réduction du potentiel angiogénique des PECs du nouveau-né de FPN via une inhibition de la transduction du signal de la voie Akt/PI3K. D'autre part, une diminution des concentrations circulantes de VEGF, dont le rôle critique dans la néovascularisation est bien connu, peut-être liée à une augmentation de son inhibiteur circulant, sFlt1 (récepteur soluble au VEGF), a été retrouvée chez le nouveau-né de FPN.Low birth weight (LBW) is a risk factor for cardiovascular disease in adulthood. However, the mechanisms explaining cardiovascular programming are incompletely understood. In adults, a reduced level of circulating endothelial progenitor cells (EPCs) is correlated with cardiovascular disease and independently predicts atherosclerosis disease progression. Recent studies demonstrated an impairment of vascular structure (microvascular rarefaction) and function (impaired vasodilation) in LBW neonates. Thus, we hypothesized that LBW infants display an EPCs impairment.We demonstrated an alteration of clonogenic and angiogenic capacities of EPCs fropm LBW infants, both in vitro and in vivo. This could be due to a fetal antiangiogenic imbalance and a subsequent antiangiogenic gene expression profile in EPCs of LBW infants. Through an inhibition of Akt/PI3K signaling, an upregulation of thrombospondin-1 expression could partially explain such observations. Moreover, VEGF pathway, the main angiogenesis regulator, could be involved as we found reduced circulating levels of VEGF, probably due to an increase of its main inhibitor, sFlt1 (soluble receptor of VEGF 1) in LBW infants. The addition of VEGF reversed the in vitro negative effect of LBW infants' sera on EPCs angiogenic function.This investigation opens the way for more studies of EPCs function in LBW subjects. Indeed, many questions emerged about the impact of such dysfunction on the future health of LBW infants

Altered angiogenesis in low birth weight individuals: a role for anti-angiogenic circulating factors

International audienceObjective: Low birth weight (LBW) is a risk factor for hypertension at adulthood. Endothelial progenitor cells (EPCs) dysfunction has been characterized in LBW neonates. We hypothesized that changes in soluble, plasma pro-or anti-angiogenic factors are associated with EPCs dysfunction and impaired angiogenesis in LBW neonates. Method: Venous umbilical cord blood was collected from 42 normal, term neonates and 75 LBW neonates. Cord blood endothelial colony forming cells (ECFC) from control patients were cultured in the presence of 10% of serum obtained from both groups. Results: The proliferation and the migration of ECFC were significantly reduced when cultured with 10% of serum of LBW neonates compared to serum of control neonates. Matrigel invasion assay was not significantly altered. Umbilical vein plasma VEGF concentration was significantly reduced in LBW neonates while that of sVEGFR and PF4 were significantly higher. Addition of VEGF corrected the inhibitory effect of LBW serum on normal ECFC proliferation. Conclusions: Serum obtained from LBW babies contains factors that exhibit an antiangiogenic effect on ECFC proliferation and migration. VEGF/sVEGF/PF4 pathway seems to be involved in the EPCs dysfunction in LBW neonates

Outcomes at 7 Years of Age of Former Very Preterm Neonates with Repeated Surfactant Treatment for Prolonged Respiratory Distress in the Neonatal Period

International audienceThis study aimed at evaluating the 7-year outcomes of 118 very preterm newborns (VPNs, gestational age = 26 ± 1.4 w) involved in a randomized controlled trial. They presented neonatal respiratory distress (RDS), requiring ventilation for 14 ± 2 days post-natal age (PNA). A repeated instillation of 200 mg/kg poractant alfa (SURF) did not improve early bronchopulmonary dysplasia, but the SURF infants needed less re-hospitalization than the controls for respiratory problems at 1- and 2-year PNA. There was no growth difference at 7.1 ± 0.3 years between 41 SURF infants and 36 controls (80% of the eligible children), and 7.9% SURF infants vs. 28.6% controls presented asthma (p = 0.021). The children underwent cognitive assessment (WISC IV) and pulmonary function testing (PFT), measuring their spirometry, lung volume, and airway resistance. The spirometry measures showed differences (p 85 in both groups. Repeated surfactant treatment in VPNs presenting severe RDS led to the attenuation of early lung injuries, with an impact on long-term pulmonary sequelae, without differences in neurodevelopmental outcomes

Patent ductus arteriosus, tracheal ventilation, and the risk of bronchopulmonary dysplasia

International audienceAbstract Background An increased risk for bronchopulmonary dysplasia (BPD) exists when moderate-to-large patent ductus arteriosus shunts (hsPDA) persist beyond 14 days. Goal To examine the interaction between prolonged exposures to tracheal ventilation (≥10 days) and hsPDA on the incidence of BPD in infants 14 days, 41 died before 36 weeks. Among survivors, 93/266 had BPD. The association between BPD and hsPDA depended on the length of intubation. In multivariable analyses, prolonged hsPDA shunts were associated with increased BPD (odds ratio (OR) (95% confidence interval (CI)) = 3.00 (1.58–5.71)) when infants required intubation for ≥10 days. In contrast, there was no significant association between hsPDA exposure and BPD when infants were intubated <10 days (OR (95% CI) = 1.49 (0.98–2.26)). A similar relationship between prolonged hsPDA and length of intubation was found for BPD/death ( n = 307): infants intubated ≥10 days: OR (95% CI) = 2.41 (1.47–3.95)); infants intubated <10 days: OR (95% CI) = 1.37 (0.86–2.19)). Conclusions Moderate-to-large PDAs were associated with increased risks of BPD and BPD/death—but only when infants required intubation ≥10 days. Impact Infants with a moderate-to-large hsPDA that persist beyond 14 days are only at risk for developing BPD if they also receive prolonged tracheal ventilation for ≥10 days. Infants who receive less ventilatory support (intubation for <10 days) have the same incidence of BPD whether the ductus closes shortly after birth or whether it persists as a moderate-to-large shunt for several weeks. Early PDA closure may be unnecessary in infants who require short durations of intubation since the PDA does not seem to alter the incidence of BPD in infants who require intubation for <10 days

Effect of Early Targeted Treatment of Ductus Arteriosus with Ibuprofen on Survival Without Cerebral Palsy at 2 Years in Infants with Extreme Prematurity : A Randomized Clinical Trial

International audienceObjective: To examine the effects of early echocardiography-targeted ibuprofen treatment of large patent ductus arteriosus (PDA) on survival without cerebral palsy at 24 months of corrected age.Study design: We enrolled infants born at <28 weeks of gestation with a large PDA on echocardiography at 6-12 hours after birth to ibuprofen or placebo by 12 hours of age in a multicenter, double blind, randomized-controlled trial. Open-label ibuprofen was allowed for prespecified criteria of a hemodynamically significant PDA. The primary outcome was survival without cerebral palsy at 24 months of corrected age.Results: Among 337 enrolled infants, 109 had a small or closed ductus and constituted a reference group; 228 had a large PDA and were randomized. The primary outcome was assessed at 2 years in 108 of 114 (94.7%) and 102 of 114 (89.5%) patients allocated to ibuprofen or placebo, respectively. Survival without cerebral palsy occurred in 77 of 108 (71.3%) after ibuprofen, 73 of 102 (71.6%) after placebo (adjusted relative risk 0.98, 95% CI 0.83-1.16, P = .83), and 77 of 101 (76.2%) in reference group. Infants treated with ibuprofen had a lower incidence of PDA at day 3. Severe pulmonary hemorrhage during the first 3 days occurred in 2 of 114 (1.8%) infants treated with ibuprofen and 9 of 114 (7.9%) infants treated with placebo (adjusted relative risk 0.22, 95% CI 0.05-1.00, P = .05). Open-label rescue treatment with ibuprofen occurred in 62.3% of infants treated with placebo and 17.5% of infants treated with ibuprofen (P < .001), at a median (IQR) age of 4 (3, 5) and 4 (4, 12) days, respectively.Conclusions: Early echocardiography-targeted ibuprofen treatment of a large PDA did not change the rate of survival without cerebral palsy.Trial registration: Eudract 2011-003063-30 and ClinicalTrials.gov: NCT01630278

Effect of Early Targeted Treatment of Ductus Arteriosus with Ibuprofen on Survival Without Cerebral Palsy at 2&nbsp;Years in Infants with Extreme Prematurity: A Randomized Clinical Trial.

ObjectiveTo examine the effects of early echocardiography-targeted ibuprofen treatment of large patent ductus arteriosus (PDA) on survival without cerebral palsy at 24&nbsp;months of corrected age.Study designWe enrolled infants born at &lt;28&nbsp;weeks of gestation with a large PDA on echocardiography at 6-12&nbsp;hours after birth to ibuprofen or placebo by 12&nbsp;hours of age in a multicenter, double blind, randomized-controlled trial. Open-label ibuprofen was allowed for prespecified criteria of a hemodynamically significant PDA. The primary outcome was survival without cerebral palsy at 24&nbsp;months of corrected age.ResultsAmong 337 enrolled infants, 109 had a small or closed ductus and constituted a reference group; 228 had a large PDA and were randomized. The primary outcome was assessed at 2&nbsp;years in 108 of 114 (94.7%) and 102 of 114 (89.5%) patients allocated to ibuprofen or placebo, respectively. Survival without cerebral palsy occurred in 77 of 108 (71.3%) after ibuprofen, 73 of 102 (71.6%) after placebo (adjusted relative risk 0.98, 95% CI 0.83-1.16, P&nbsp;=&nbsp;.83), and 77 of 101 (76.2%) in reference group. Infants treated with ibuprofen had a lower incidence of PDA at day 3. Severe pulmonary hemorrhage during the first 3&nbsp;days occurred in 2 of 114 (1.8%) infants treated with ibuprofen and 9 of 114 (7.9%) infants treated with placebo (adjusted relative risk 0.22, 95% CI 0.05-1.00, P&nbsp;=&nbsp;.05). Open-label rescue treatment with ibuprofen occurred in 62.3% of infants treated with placebo and 17.5% of infants treated with ibuprofen (P&nbsp;&lt;&nbsp;.001), at a median (IQR) age of 4 (3, 5) and 4 (4, 12) days, respectively.ConclusionsEarly echocardiography-targeted ibuprofen treatment of a large PDA did not change the rate of survival without cerebral palsy.Trial registrationEudract 2011-003063-30 and ClinicalTrials.gov: NCT01630278