SatNOGS: Satellite Networked Open Ground Station

Abstract—The SatNOGS, or Satellite Network Open Ground Stations, project promotes and supports free and open space applications. It seeks to solve the problem of connecting many satellite users/observers to many ground station operators. Modern open software, web, and hardware techniques are used in implementing the Network, Database, Client, and Ground Station sub- projects. Modularity in all the systems promotes the dual-use of ground stations by not interfering with local operation while utilizing the great amount of time a civilian, non-commercial ground station would otherwise sit idle

Overview of the Satellite Networked Open Ground Stations (SatNOGS) Project

The SatNOGS, or Satellite Network Open Ground Stations, project promotes and supports free and open space applications. It seeks to address the problem of connecting many satellite users/observers to many ground station operators. Modern Open Source software, web, and hardware techniques are used in implementing the Network, Database, Client, and Ground Station sub-projects. Modularity in all the systems promotes the dual-use of ground stations by not interfering with local operation while utilizing the great amount of time a civilian, non-commercial ground station would otherwise sit idle

Relationship of ERK1/2 phosphorylation to D1 dopamine receptor activation, behavioral sensitization, and structural plasticity in the neonate 6-hydroxydopamine-lesioned rat

Repeated administration of the D1-dopamine receptor agonist SKF-38393 to adult rats lesioned with 6-hydroxydopamine (6-OHDA) as neonates results in increasingly greater behavioral responsiveness with each dose, a phenomenon known as "priming of D1 receptor sensitivity." This dissertation examines the role of the extracellular signal-regulated kinase 1/2 (ERK), an intracellular mediator of signal transduction, in D1-dopamine receptor activation, priming of behavioral sensitivity, and structural plasticity in the neonate-lesioned rat. Using immunohistochemistry, I found that repeated administration of SKF-38393 produced a prolonged increase in phosphorylated (phospho-) ERK in the medial prefrontal cortex (mPFC) of neonate-lesioned rats. A corresponding increase in the phosphorylation of CREB (cyclic AMP-response element binding protein), a downstream target of ERK signaling, implied a functional consequence for the prolonged ERK activation in mPFC. Pretreatment with the D1 antagonist SCH-23390, but not the 5-HT2 antagonist ketanserin, prior to each dose of SKF-38393 blocked the persistently increased phospho-ERK. The competitive and non-competitive NMDA receptor antagonists MK-801 and CGS-19755, which inhibit the induction of behavioral sensitization in neonate-lesioned rats, also blocked the increased phospho-ERK. In addition, intracerebroventricular (ICV) and systemic administration of SL327 or PD98059, inhibitors of the upstream ERK activator MEK (mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2), prior to each SKF-38393 treatment eliminated mPFC phospho-ERK. Computer-monitored activity chambers and visual observation both revealed that the global MEK inhibition increased horizontal behavior and decreased certain stereotyped behaviors after an additional sensitizing dose of SKF-38393. In addition, intra-mPFC infusions with PD98059 only decreased stereotyped behaviors in primed animals. Finally, using immunohistochemistry for MAP2 combined with recombinant adenovirus (AAV) transduction of green fluorescent protein (GFP) in mPFC neurons, I found that repeated administration of SKF-38393 produces robust, long-lasting changes in the morphology of dendrites in mPFC of neonate-lesioned rats. Pretreatment with SL327 and PD98059 prevented these changes, suggesting that the alterations in dendritic morphology require ERK pathway activation. Collectively, these results demonstrate that D1 and NMDA receptors cooperatively produce prolonged ERK pathway activation in mPFC of primed neonate-lesioned rats, and suggest that persistent ERK phosphorylation in mPFC plays a pivotal role in long-lasting behavioral and structural adaptations in these animals

Frio pilot in CO2 sequestration in brine-bearing sandstones: The University of Texas at Austin, Bureau of Economic Geology, report to the Texas Commission on Environmental Quality to accompany a class V application for an experimental technology pilot injection well.

GEOSEQ project (LBNL, LLNL, ORNL), NETL, Schlumberger–Doll Research Center, Transpetco, Sandia TechnologiesJackson School of Geoscience

Sustained Extracellular Signal-Regulated Kinase 1/2 Phosphorylation in Neonate 6-Hydroxydopamine-Lesioned Rats after Repeated D1-Dopamine Receptor Agonist Administration: Implications for NMDA Receptor Involvement

Extracellular signal-regulated kinase (ERK) 1/2, a well known regulator of gene expression, is likely to contribute to signaling events underlying enduring neural adaptations. Phosphorylated (phospho)-ERK was examined immunohistochemically after both single and repeated (i.e., sensitizing) doses of the partial D1-dopamine (DA) receptor agonist SKF-38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benazepine HCl) to adult rats lesioned as neonates (neonate lesioned) with 6-hydroxydopamine. Remarkably, prolonged phospho-ERK accumulated primarily in layers II–III of medial prefrontal cortex (MPC), where it declined gradually yet remained significantly elevated for at least 36 d after repeated doses of SKF-38393. Sustained (≥7 d) phospho-ERK was observed for shorter periods in various other cortical regions but was not detectable in striatum or nucleus accumbens. At 36 d, an additional injection of SKF-38393 to sensitized rats restored phospho-ERK to maximal levels only in MPC when examined 7 d later. Phosphorylated cAMP response element-binding protein (CREB), examined 7 d after the sensitizing regimen, was observed exclusively in MPC, where it was abundant throughout all layers. Systemic injections of SL327 (α-[amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl)benzeneacetonitrile), an inhibitor of the upstream ERK activator mitogen ERK kinase, attenuated both ERK and CREB phosphorylation in layers II–III of MPC. Pretreatment with the D1 antagonist SCH-23390 ((R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-OL maleate) inhibited the prolonged increase in MPC phospho-ERK, whereas the 5-HT2 receptor antagonist ketanserin (3-[2-[4-(4-fluorobenzoyl)-1-piperidinyl]ethyl]-2,4(1H,3H)-quinazolinedione tartrate) was ineffective. Competitive and noncompetitive NMDA receptor antagonists also blocked sustained ERK phosphorylation. Collectively, the present results demonstrate coupling of D1 and NMDA receptor function reflected in sustained activation of the ERK signaling pathway in MPC of SKF-38393-sensitized neonate-lesioned rats. Ultimately, long-lasting phosphorylation of ERK and CREB in MPC may play a pivotal role in any permanent adaptive change(s) in these animals

Describing SmallSat Missions with MetaSat

Space mission metadata is not standardized and various mission outputs are typically disconnected. This situation makes it hard for different teams to share information, collaborate, or advise each other on best practices and lessons learned. The MetaSat team, made up of staff from both the Wolbach Library at the Center for Astrophysics (CfA) and the Libre Space Foundation (LSF), is addressing these issues by creating a metadata vocabulary and example JSON-LD schemas that can be used to describe small satellite missions. This work will help facilitate the ease of sharing information between missions and lower the barrier of entry into the field

Sustaining Agility: Organizational Change, Factors and Theoretical Lenses

Agile organizations have to deal regularly with change and at the same time adapt to sustain agility. In this paper, we present an initial study to identify factors considered when changes need to be made to sustain agility. We used a novel data collection approach, critical decision method (CDM), and investigated three theoretical lenses, paradox theory, situation awareness and shared mental models, to explore the kind of practical consequences they help to uncover. This paper presents the findings of this initial study together with reflections on the data collection method and the three theoretical lenses. Three key dimensions relevant to sustaining agility emerge from the use of these theoretical lenses: teams vs organization; understanding the environment vs the impact of change internally; and understanding “now” vs looking into the future

SatNOGS-COMMS: Turnkey Nanosatellite Communications

The SatNOGS-COMMS is a dual-band software configurable radio transceiver specifically designed for Telemetry and Telecommand (TMTC) in the UHF and S-band. It is designed to match best with nanosatellites and CubeSats missions operating in Low Earth Orbit (LEO) up to 800 km. The radio module supports full in-flight reconfiguration of the carrier and intermediate frequencies, bitrate, modulation options, and channel-filter bandwidth. SatNOGS-COMMS is fully compatible with SatNOGS Network for all TMTC functionality. The software and hardware are released as open source projects, which can be tailored to user needs

Changes in apical dendritic structure correlate with sustained ERK1/2 phosphorylation in medial prefrontal cortex of a rat model of dopamine D 1 receptor agonist sensitization

Rats lesioned with 6-hydroxydopamine (6-OHDA) as neonates exhibit behavioral and neurochemical abnormalities in adulthood that mimic Lesch-Nyhan disease, schizophrenia and other developmental disorders of frontostriatal circuit dysfunction. In these animals, a latent sensitivity to D1 agonists is maximally exposed by repeated administration of dopamine agonists in the post-pubertal period (D1 priming). In neonate-lesioned, adult rats primed with SKF-38393, we found selective, persistent alterations in the morphology of pyramidal neuron apical dendrites in the prelimbic area of the medial prefrontal cortex (mPFC). In these animals, dendrite bundling patterns and the typically straight trajectories of primary dendritic shafts were disrupted, whereas the diameter of higher-order oblique branches was increased. Although not present in neonate-lesioned rats treated with saline, these morphological changes persisted at least 21 days after repeated dosing with SKF-38393, and were not accompanied by markers of neurodegenerative change. A sustained increase in phospho-ERK immunoreactivity in wavy dendritic shafts over the same period suggested a relationship between prolonged ERK phosphorylation and dendritic remodeling in D1-primed rats. In support of this hypothesis, pretreatment with the MEK1/2-ERK1/2 pathway inhibitors PD98059 or SL327, prior to each priming dose of SKF-38393, prevented the morphological changes associated with D1 priming. Together, these findings demonstrate that repeated stimulation of D1 receptors in adulthood interacts with the developmental loss of dopamine to profoundly and persistently modify neuronal signaling and dendrite morphology in the mature prefrontal cortex. Furthermore, sustained elevation of ERK activity in mPFC pyramidal neurons may play a role in guiding these morphological changes in vivo