146 research outputs found

    Triggered massive-star formation on the borders of Galactic HII regions. IV- Star formation at the periphery of Sh2-212

    Full text link
    Aims: We wish to establish whether sequential star formation is taking place at the periphery of the Galactic HII region Sh2-212. Methods: We present CO millimetre observations of this region obtained at the IRAM 30-m telescope to investigate the distribution of associated molecular material. We also use deep JHK observations obtained at the CFHT to study the stellar content of the region, and radio observations obtained at the VLA to look for the presence of an ultra-compact (UC) HII region and for maser emission. Results: In the optical, Sh2-212 is spherically symmetric around its central exciting cluster. This HII region is located along a molecular filament. A thin, well-defined half ring of molecular material surrounds the brightest part of the HII region at the rear and is fragmented. The most massive fragment (~200 solar masses) contains a massive young stellar object displaying a near-IR excess; its spectral energy distribution indicates a high-mass (~14solar masses), high-temperature (~30000K), and high-luminosity (~17000 solar luminosities) source. This object ionizes a UC HII region. Conclusions: Sh2-212 is a good example of massive-star formation triggered via the collect and collapse process. The massive YSO observed at its periphery is a good candidate for a massive star formed in isolation.Comment: 12 pages, 14 figures. To be published in A&

    Leveraging Terrestrial Industry for Utilization of Space Resources

    Get PDF
    NASA's Journey to Mars: Pioneering Next Steps in Space Exploration released in October of 2015 states that NASA is working toward the capability to work, operate, and sustainably live safely beyond Earth. To progress from our current "Earth-Reliant" approach to exploration and eventually become "Earth Independent", we need to first identify resources in space and then learn to use and harvest them to minimize logistics from Earth, reduce costs, and enable sustainable and affordable space transportation and surface operations. Known as In Situ Resource Utilization (ISRU), the collection and conversion of space resources into products such as propellants, fuel cell reactants, and life support consumables can greatly reduce the mass, cost, and risk of space exploration. Also, the ability to perform civil engineering, construction, and manufacturing at sites of exploration can also allow for increased crew safety and sustainable growth in critical infrastructure. Much of what NASA wants to do on the Moon and Mars with respect to harnessing and utilizing space resources has been performed and perfected on Earth over the centuries. While minimizing mass and operating in the vacuum of space may be unique challenges to NASA, both terrestrial industry and NASA face many of the same challenges associated with operating in severe environments, minimizing maintenance and logistics, maximizing performance per unit mass and volume, performing remote and autonomous operations, and integrating hardware from many vendors and countries. In the end, both NASA and terrestrial industry need to obtain a return on the investment for the development and deployment of these capabilities. This paper will first examine what is ISRU and what are the space resources of interest. The paper will than discuss what are NASA's approach, life cycle, and economic considerations for implementing ISRU. The paper will outline the site and infrastructure needs associated with a phased implementation of ISRU into human missions to the Moon and Mars. The paper will than assess what technologies and operations from terrestrial industries are relevant and synergistic with ISRU (from prospecting to product storage), and what challenges and similarities between the two can be exploited. Lastly, the paper will end with a discussion on where do we go from here for industry and NASA to collaborate

    Results from the NASA Capability Roadmap Team for In-Situ Resource Utilization (ISRU)

    Get PDF
    On January 14, 2004, the President of the United States unveiled a new vision for robotic and human exploration of space entitled, "A Renewed Spirit of Discovery". As stated by the President in the Vision for Space Exploration (VSE), NASA must "... implement a sustained and affordable human and robotic program to explore the solar system and beyond " and ".. .develop new technologies and harness the moon's abundant resources to allow manned exploration of more challenging environments." A key to fulfilling the goal of sustained and affordable human and robotic exploration will be the ability to use resources that are available at the site of exploration to "live off the land" instead of bringing everything from Earth, known as In-Situ Resource Utilization (ISRU). ISRU can significantly reduce the mass, cost, and risk of exploration through capabilities such as: mission consumable production (propellants, fuel cell reagents, life support consumables, and feedstock for manufacturing & construction); surface construction (radiation shields, landing pads, walls, habitats, etc.); manufacturing and repair with in-situ resources (spare parts, wires, trusses, integrated systems etc.); and space utilities and power from space resources. On January 27th, 2004 the President's Commission on Implementation of U.S. Space Exploration Policy (Aldridge Committee) was created and its final report was released in June 2004. One of the report's recommendations was to establish special project teams to evaluate enabling technologies, of which "Planetary in situ resource utilization" was one of them. Based on the VSE and the commission's final report, NASA established fifteen Capability Roadmap teams, of which ISRU was one of the teams established. From Oct. 2004 to May 2005 the ISRU Capability Roadmap team examined the capabilities, benefits, architecture and mission implementation strategy, critical decisions, current state-of-the-art (SOA), challenges, technology gaps, and risks of ISRU for future human Moon and Mars exploration. This presentation will provide an overview of the ISRU capability, architecture, and implementation strategy examined by the ISRU Capability Roadmap team, along with a top-level review of ISRU benefits, resources and products of interest, and the current SOA in ISRU processes and systems. The presentation will also highlight the challenges of incorporating ISRU into future missions and the gaps in technologies and capabilities that need to be filled to enable ISRU

    The state of the Martian climate

    Get PDF
    60°N was +2.0°C, relative to the 1981–2010 average value (Fig. 5.1). This marks a new high for the record. The average annual surface air temperature (SAT) anomaly for 2016 for land stations north of starting in 1900, and is a significant increase over the previous highest value of +1.2°C, which was observed in 2007, 2011, and 2015. Average global annual temperatures also showed record values in 2015 and 2016. Currently, the Arctic is warming at more than twice the rate of lower latitudes

    Rho Signaling Regulates Pannexin 1-mediated ATP Release from Airway Epithelia

    Get PDF
    ATP released from airway epithelial cells promotes purinergic receptor-regulated mucociliary clearance activities necessary for innate lung defense. Cell swelling-induced membrane stretch/strain is a common stimulus that promotes airway epithelial ATP release, but the mechanisms transducing cell swelling into ATP release are incompletely understood. Using knockdown and knockout approaches, we tested the hypothesis that pannexin 1 mediates ATP release from hypotonically swollen airway epithelia and investigated mechanisms regulating this activity. Well differentiated primary cultures of human bronchial epithelial cells subjected to hypotonic challenge exhibited enhanced ATP release, which was paralleled by the uptake of the pannexin probe propidium iodide. Both responses were reduced by pannexin 1 inhibitors and by knocking down pannexin 1. Importantly, hypotonicity-evoked ATP release from freshly excised tracheas and dye uptake in primary tracheal epithelial cells were impaired in pannexin 1 knockout mice. Hypotonicity-promoted ATP release and dye uptake in primary well differentiated human bronchial epithelial cells was accompanied by RhoA activation and myosin light chain phosphorylation and was reduced by the RhoA dominant negative mutant RhoA(T19N) and Rho and myosin light chain kinase inhibitors. ATP release and Rho activation were reduced by highly selective inhibitors of transient receptor potential vanilloid 4 (TRPV4). Lastly, knocking down TRPV4 impaired hypotonicity-evoked airway epithelial ATP release. Our data suggest that TRPV4 and Rho transduce cell membrane stretch/strain into pannexin 1-mediated ATP release in airway epithelia

    Aboveground Biomass Accumulation in a Tropical Wet Forest in Nicaragua Following a Catastrophic Hurricane Disturbance 1

    Full text link
    Among their effects on forest structure and carbon dynamics, hurricanes frequently create large-scale canopy gaps that promote secondary growth. To measure the accumulation of aboveground biomass (AGBM) in a hurricane damaged forest, we established permanent plots 4 mo after the landfall of Hurricane Joan on the Atlantic coast of Nicaragua in October 1988. We quantified AGBM accumulation in these plots by correlating diameter measurements to AGBM values using a published allometric regression equation for tropical wet forests. In the first measurement year following the storm, AGBM in hurricane-affected plots was quite variable, ranging from 26 to 153 Mg/ha, with a mean of 78 (±15) Mg/ha. AGBM was substantially lower than in two control plots several kilometers outside the hurricane's path (331 ±15 Mg/ha). Biomass accumulation was slow (5.36 ± 0.74 Mg/ha/yr), relative to previous studies of forest regeneration following another hurricane (Hugo) and agricultural activity. We suggest that large-scale, homogenous canopy damage caused by Hurricane Joan impeded the dispersal and establishment of pioneer trees and led to a secondary forest dominated by late successional species that resprouted and survived the disturbance. With the relatively slow rate of biomass accumulation, any tightening in disturbance interval could reduce the maximum capacity of the living biomass to store carbon.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73646/1/j.1744-7429.2005.00077.x.pd

    Thrombin Induces Macrophage Migration Inhibitory Factor Release and Upregulation in Urothelium: A Possible Contribution to Bladder Inflammation

    Get PDF
    Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine expressed by urothelial cells that mediates bladder inflammation. We investigated the effect of stimulation with thrombin, a Protease Activated Receptor-1 (PAR1) agonist, on MIF release and MIF mRNA upregulation in urothelial cells.MIF and PAR1 expression was examined in normal human immortalized urothelial cells (UROtsa) using real-time RT-PCR, Western blotting and dual immunostaining. MIF and PAR1 immunostaining was also examined in rat urothelium. The effect of thrombin stimulation (100 nM) on urothelial MIF release was examined in UROtsa cells (in vitro) and in rats (in vivo). UROtsa cells were stimulated with thrombin, culture media were collected at different time points and MIF amounts were determined by ELISA. Pentobarbital anesthetized rats received intravesical saline (control), thrombin, or thrombin +2% lidocaine (to block nerve activity) for 1 hr, intraluminal fluid was collected and MIF amounts determined by ELISA. Bladder or UROtsa MIF mRNA was measured using real time RT-PCR.UROtsa cells constitutively express MIF and PAR1 and immunostaining for both was observed in these cells and in the basal and intermediate layers of rat urothelium. Thrombin stimulation of urothelial cells resulted in a concentration- and time-dependent increase in MIF release both in vitro (UROtsa; 2.8-fold increase at 1 hr) and in vivo (rat; 4.5-fold) while heat-inactivated thrombin had no effect. In rats, thrombin-induced MIF release was reduced but not abolished by intravesical lidocaine treatment. Thrombin also upregulated MIF mRNA in UROtsa cells (3.3-fold increase) and in the rat bladder (2-fold increase) where the effect was reduced (1.4-fold) by lidocaine treatment.Urothelial cells express both MIF and PAR1. Activation of urothelial PAR1 receptors, either by locally generated thrombin or proteases present in the urine, may mediate bladder inflammation by inducing urothelial MIF release and upregulating urothelial MIF expression
    corecore