Using Lyman-α\alpha transits to constrain models of atmospheric escape

Lyman-$\alpha$ transits provide an opportunity to test models of atmospheric escape directly. However, translating observations into constraints on the properties of the escaping atmosphere is challenging. The major reason for this is that the observable parts of the outflow often comes from material outside the planet's Hill sphere, where the interaction between the planetary outflow and circumstellar environment is important. As a result, 3D models are required to match observations. Whilst 3D hydrodynamic simulations are able to match observational features qualitatively, they are too computationally expensive to perform a statistical retrieval of properties of the outflow. Here, we develop a model that determines the trajectory, ionization state and 3D geometry of the outflow as a function of its properties and system parameters. We then couple this model to a ray tracing routine in order to produce synthetic transits. We demonstrate the validity of this approach, reproducing the trajectory of the outflows seen in 3D simulations. We illustrate the use of this model by performing a retrieval on the transit spectrum of GJ 436 b. Our model constrains the sound speed of the outflow $\gtrsim 10 \text{ km s}^{-1}$, indicating that we can rule out core-powered mass loss as the mechanism driving the outflow for this planet. The bound on planetary outflow velocity and mass loss rates are consistent with a photoevaporative wind

This New Ocean: A History of Project Mercury

When Congress created the National Aeronautics and Space Administration (NASA) in 1958, it charged NASA with the responsibility "to contribute materially to . . . the expansion of human knowledge of phenomena in the atmosphere and space" and "provide for the widest practicable and appropriate dissemination of information concerning its activities and the results thereof." NASA wisely interpreted this mandate to include responsibility for documenting the epochal progress of which it is the focus. The result has been the development of a historical program by NASA as unprecedented as the task of extending man's mobility beyond his planet. This volume is not only NASA's accounting of its obligation to disseminate information to our current generation of Americans. It also fulfills, as do all of NASA's future-oriented scientific-technological activities, the further obligation to document the present as the heritage of the future. The wide-ranging NASA history program includes chronicles of day-to-day space activities; specialized studies of particular fields within space science and technology; accounts of NASA's efforts in organization and management, where its innovations, while less known to the public than its more spectacular space shots, have also been of great significance; narratives of the growth and expansion of the space centers throughout the country, which represent in microcosm many aspects of NASA's total effort; program histories, tracing the successes- and failures- of the various projects that mark man's progress into the Space Age; and a history of NASA itself, incorporating in general terms the major problems and challenges, and the responses thereto, of our entire civilian space effort. The volume presented here is a program history, the first in a series telling of NASA's pioneering steps into the Space Age. It deals with the first American manned-spaceflight program: Project Mercury. Although some academicians might protest that this is "official" history, it is official only in the fact that it has been prepared and published with the support and cooperation of NASA. It is not "official" history in the sense of presenting a point of view supposedly that of NASA officialdom-if anyone could determine what the "point of view" of such a complex organism might be. Certainly, the authors were allowed to pursue their task with the fullest freedom and in accordance with the highest scholarly standards of the history profession

Extending Optical Flare Models to the UV: Results from Comparing of TESS and GALEX Flare Observations For M Dwarfs

The ultraviolet (UV) emission of stellar flares may have a pivotal role in the habitability of rocky exoplanets around low-mass stars. Previous studies have used white-light observations to calibrate empirical models which describe the optical and UV flare emission. However, the accuracy of the UV predictions of models have previously not been tested. We combined TESS optical and GALEX UV observations to test the UV predictions of empirical flare models calibrated using optical flare rates of M stars. We find that the canonical 9000 K blackbody model used by flare studies underestimates the GALEX NUV energies of field age M stars by up to a factor of 6.5$\pm$0.7 and the GALEX FUV energies of fully convective field age M stars by 30.6$\pm$10.0. We calculated energy correction factors that can be used to bring the UV predictions of flare models closer in line with observations. We calculated pseudo-continuum flare temperatures that describe both the white-light and GALEX NUV emission. We measured a temperature of 10,700 K for flares from fully convective M stars after accounting for the contribution from UV line emission. We also applied our correction factors to the results of previous studies of the role of flares in abiogenesis. Our results show that M stars do not need to be as active as previously thought in order to provide the NUV flux required for prebiotic chemistry, however we note that flares will also provide more FUV flux than previously modelled.Comment: 20 pages, 9 figures, 4 tables. Accepted for publication in the Monthly Notices of the Royal Astronomical Societ

Clinical and molecular genetic features of pulmonary hypertension in patients with hereditary hemorrhagic telangiectasia

BACKGROUND: Most patients with familial primary pulmonary hypertension have defects in the gene for bone morphogenetic protein receptor II (BMPR2), a member of the transforming growth factor beta (TGF-beta) superfamily of receptors. Because patients with hereditary hemorrhagic telangiectasia may have lung disease that is indistinguishable from primary pulmonary hypertension, we investigated the genetic basis of lung disease in these patients. METHODS: We evaluated members of five kindreds plus one individual patient with hereditary hemorrhagic telangiectasia and identified 10 cases of pulmonary hypertension. In the two largest families, we used microsatellite markers to test for linkage to genes encoding TGF-beta-receptor proteins, including endoglin and activin-receptor-like kinase 1 (ALK1), and BMPR2. In subjects with hereditary hemorrhagic telangiectasia and pulmonary hypertension, we also scanned ALK1 and BMPR2 for mutations. RESULTS: We identified suggestive linkage of pulmonary hypertension with hereditary hemorrhagic telangiectasia on chromosome 12q13, a region that includes ALK1. We identified amino acid changes in activin-receptor-like kinase 1 that were inherited in subjects who had a disorder with clinical and histologic features indistinguishable from those of primary pulmonary hypertension. Immunohistochemical analysis in four subjects and one control showed pulmonary vascular endothelial expression of activin-receptor-like kinase 1 in normal and diseased pulmonary arteries. CONCLUSIONS: Pulmonary hypertension in association with hereditary hemorrhagic telangiectasia can involve mutations in ALK1. These mutations are associated with diverse effects, including the vascular dilatation characteristic of hereditary hemorrhagic telangiectasia and the occlusion of small pulmonary arteries that is typical of primary pulmonary hypertension

Altered prostanoid production by fibroblasts cultured from the lungs of human subjects with idiopathic pulmonary fibrosis

BACKGROUND: Prostanoids are known to participate in the process of fibrogenesis. Because lung fibroblasts produce prostanoids and are believed to play a central role in the pathogenesis of idiopathic pulmonary fibrosis (IPF), we hypothesized that fibroblasts (HF) cultured from the lungs of patients with IPF (HF-IPF) have an altered balance between profibrotic (thromboxane [TX]A(2)) and antifibrotic (prostacyclin [PGI(2)]) prostaglandins (PGs) when compared with normal human lung fibroblasts (HF-NL). METHODS: We measured inducible cyclooxygenase (COX)-2 gene and protein expression, and a profile of prostanoids at baseline and after IL-1β stimulation. RESULTS: In both HF-IPF and HF-NL COX-2 expression was undetectable at baseline, but was significantly upregulated by IL-1β. PGE(2) was the predominant COX product in IL-1β-stimulated cells with no significant difference between HF-IPF and HF-NL (28.35 [9.09–89.09] vs. 17.12 [8.58–29.33] ng/10(6) cells/30 min, respectively; P = 0.25). TXB(2) (the stable metabolite of TXA(2)) production was significantly higher in IL-1β-stimulated HF-IPF compared to HF-NL (1.92 [1.27–2.57] vs. 0.61 [0.21–1.64] ng/10(6) cells/30 min, respectively; P = 0.007) and the ratio of PGI(2) (as measured by its stable metabolite 6-keto-PGF(1α)) to TXB(2) was significantly lower at baseline in HF-IPF (0.08 [0.04–0.52] vs. 0.12 [0.11–0.89] in HF-NL; P = 0.028) and with IL-1β stimulation (0.24 [0.05–1.53] vs. 1.08 [0.51–3.79] in HF-NL; P = 0.09). CONCLUSION: An alteration in the balance of profibrotic and antifibrotic PGs in HF-IPF may play a role in the pathogeneses of IPF

Decreased dyskerin levels as a mechanism of telomere shortening in X-linked dyskeratosis congenita

Dyskeratosis congenita (DC) is a premature ageing syndrome characterised by short telomeres. An X-linked form of DC is caused by mutations in DKC1 which encodes dyskerin, a telomerase component that is essential for telomerase RNA stability. However, mutations in DKC1 are identifiable in only half of X-linked DC families. A four generation family with pulmonary fibrosis and features of DC was identified. Affected males showed the classic mucocutaneous features of DC and died prematurely from pulmonary fibrosis. Although there were no coding sequence or splicing variants, genome wide linkage analysis of 16 individuals across four generations identified significant linkage at the DKC1 locus, and was accompanied by reduced dyskerin protein levels in affected males. Decreased dyskerin levels were associated with compromised telomerase RNA levels and very short telomeres. These data identify decreased dyskerin levels as a novel mechanism of DC, and indicate that intact dyskerin levels, in the absence of coding mutations, are critical for telomerase RNA stability and for in vivo telomere maintenance