Orbit Determination During Spacecraft Emergencies with Sparse Tracking Data - THEMIS and TDRS-3 Lessons Learned

This paper provides an overview of the lessons learned from the National Aeronautics and Space Administration (NASA) Goddard Space Flight Center s (GSFC) Flight Dynamics Facility s (FDF) support of the Time History of Events and Macroscale Interactions during Substorms (THEMIS) spacecraft emergency in February 2007, and the Tracking and Data Relay Satellite-3 (TDRS-3) spacecraft emergency in March 2006. A successful and timely recovery from both of these spacecraft emergencies depended on accurate knowledge of the orbit. Unfortunately, the combination of each spacecraft emergency with very little tracking data contributed to difficulties in estimating and predicting the orbit and delayed recovery efforts in both cases. In both the THEMIS and TDRS-3 spacecraft emergencies, numerous factors contributed to problems with obtaining nominal tracking data measurements. This paper details the various causative factors and challenges. This paper further enumerates lessons learned from FDF s recovery efforts involving the THEMIS and TDRS-3 spacecraft emergencies and scant tracking data, as well as recommendations for improvements and corrective actions. In addition, this paper describes the broad range of resources and complex navigation methods employed within the FDF for supporting critical navigation activities during all mission phases, including launch, early orbit, and on-orbit operations

Trajectory Design for the Transiting Exoplanet Survey Satellite

The Transiting Exoplanet Survey Satellite (TESS) is a National Aeronautics and Space Administration (NASA) mission, scheduled to be launched in 2017. TESS will travel in a highly eccentric orbit around Earth, with initial perigee radius near 17 Earth radii (Re) and apogee radius near 59 Re. The orbit period is near 2:1 resonance with the Moon, with apogee nearly 90 degrees out-of-phase with the Moon, in a configuration that has been shown to be operationally stable. TESS will execute phasing loops followed by a lunar flyby, with a final maneuver to achieve 2:1 resonance with the Moon. The goals of a resonant orbit with long-term stability, short eclipses and limited oscillations of perigee present significant challenges to the trajectory design. To rapidly assess launch opportunities, we adapted the Schematics Window Methodology (SWM76) launch window analysis tool to assess the TESS mission constraints. To understand the long-term dynamics of such a resonant orbit in the Earth-Moon system we employed Dynamical Systems Theory in the Circular Restricted 3-Body Problem (CR3BP). For precise trajectory analysis we use a high-fidelity model and multiple shooting in the General Mission Analysis Tool (GMAT) to optimize the maneuver delta-V and meet mission constraints. Finally we describe how the techniques we have developed can be applied to missions with similar requirements. Keywords: resonant orbit, stability, lunar flyby, phasing loops, trajectory optimizatio

An illustrated anatomical ontology of the developing mouse lower urogenital tract

Malformation of the urogenital tract represents a considerable paediatric burden, with many defects affecting the lower urinary tract (LUT), genital tubercle and associated structures. Understanding the molecular basis of such defects frequently draws on murine models. However, human anatomical terms do not always superimpose on the mouse, and the lack of accurate and standardised nomenclature is hampering the utility of such animal models. We previously developed an anatomical ontology for the murine urogenital system. Here, we present a comprehensive update of this ontology pertaining to mouse LUT, genital tubercle and associated reproductive structures (E10.5 to adult). Ontology changes were based on recently published insights into the cellular and gross anatomy of these structures, and on new analyses of epithelial cell types present in the pelvic urethra and regions of the bladder. Ontology changes include new structures, tissue layers and cell types within the LUT, external genitalia and lower reproductive structures. Representative illustrations, detailed text descriptions and molecular markers that selectively label muscle, nerves/ganglia and epithelia of the lower urogenital system are also presented. The revised ontology will be an important tool for researchers studying urogenital development/malformation in mouse models and will improve our capacity to appropriately interpret these with respect to the human situation

DLG4-related synaptopathy: a new rare brain disorder

Purpose: Postsynaptic density protein-95 (PSD-95), encoded by DLG4, regulates excitatory synaptic function in the brain. Here we present the clinical and genetic features of 53 patients (42 previously unpublished) with DLG4 variants. Methods: The clinical and genetic information were collected through GeneMatcher collaboration. All the individuals were investigated by local clinicians and the gene variants were identified by clinical exome/genome sequencing. Results: The clinical picture was predominated by early onset global developmental delay, intellectual disability, autism spectrum disorder, and attention deficit–hyperactivity disorder, all of which point to a brain disorder. Marfanoid habitus, which was previously suggested to be a characteristic feature of DLG4-related phenotypes, was found in only nine individuals and despite some overlapping features, a distinct facial dysmorphism could not be established. Of the 45 different DLG4 variants, 39 were predicted to lead to loss of protein function and the majority occurred de novo (four with unknown origin). The six missense variants identified were suggested to lead to structural or functional changes by protein modeling studies. Conclusion: The present study shows that clinical manifestations associated with DLG4 overlap with those found in other neurodevelopmental disorders of synaptic dysfunction; thus, we designate this group of disorders as DLG4-related synaptopathy. [Figure not available: see fulltext.

DLG4-related synaptopathy: a new rare brain disorder.

PURPOSE: Postsynaptic density protein-95 (PSD-95), encoded by DLG4, regulates excitatory synaptic function in the brain. Here we present the clinical and genetic features of 53 patients (42 previously unpublished) with DLG4 variants. METHODS: The clinical and genetic information were collected through GeneMatcher collaboration. All the individuals were investigated by local clinicians and the gene variants were identified by clinical exome/genome sequencing. RESULTS: The clinical picture was predominated by early onset global developmental delay, intellectual disability, autism spectrum disorder, and attention deficit-hyperactivity disorder, all of which point to a brain disorder. Marfanoid habitus, which was previously suggested to be a characteristic feature of DLG4-related phenotypes, was found in only nine individuals and despite some overlapping features, a distinct facial dysmorphism could not be established. Of the 45 different DLG4 variants, 39 were predicted to lead to loss of protein function and the majority occurred de novo (four with unknown origin). The six missense variants identified were suggested to lead to structural or functional changes by protein modeling studies. CONCLUSION: The present study shows that clinical manifestations associated with DLG4 overlap with those found in other neurodevelopmental disorders of synaptic dysfunction; thus, we designate this group of disorders as DLG4-related synaptopathy.RD&E staff can access the full-text of this article by clicking on the 'Additional Link' above and logging in with NHS OpenAthens if prompted.Accepted version (6 month embargo), submitted versio

DLG4-related synaptopathy: a new rare brain disorder.

PURPOSE: Postsynaptic density protein-95 (PSD-95), encoded by DLG4, regulates excitatory synaptic function in the brain. Here we present the clinical and genetic features of 53 patients (42 previously unpublished) with DLG4 variants. METHODS: The clinical and genetic information were collected through GeneMatcher collaboration. All the individuals were investigated by local clinicians and the gene variants were identified by clinical exome/genome sequencing. RESULTS: The clinical picture was predominated by early onset global developmental delay, intellectual disability, autism spectrum disorder, and attention deficit-hyperactivity disorder, all of which point to a brain disorder. Marfanoid habitus, which was previously suggested to be a characteristic feature of DLG4-related phenotypes, was found in only nine individuals and despite some overlapping features, a distinct facial dysmorphism could not be established. Of the 45 different DLG4 variants, 39 were predicted to lead to loss of protein function and the majority occurred de novo (four with unknown origin). The six missense variants identified were suggested to lead to structural or functional changes by protein modeling studies. CONCLUSION: The present study shows that clinical manifestations associated with DLG4 overlap with those found in other neurodevelopmental disorders of synaptic dysfunction; thus, we designate this group of disorders as DLG4-related synaptopathy.Accepted version (6 month embargo), submitted versionRD&E staff can access the full-text of this article by clicking on the 'Additional Link' above and logging in with NHS OpenAthens if prompted

DLG4-related synaptopathy: a new rare brain disorder.

PURPOSE: Postsynaptic density protein-95 (PSD-95), encoded by DLG4, regulates excitatory synaptic function in the brain. Here we present the clinical and genetic features of 53 patients (42 previously unpublished) with DLG4 variants. METHODS: The clinical and genetic information were collected through GeneMatcher collaboration. All the individuals were investigated by local clinicians and the gene variants were identified by clinical exome/genome sequencing. RESULTS: The clinical picture was predominated by early onset global developmental delay, intellectual disability, autism spectrum disorder, and attention deficit-hyperactivity disorder, all of which point to a brain disorder. Marfanoid habitus, which was previously suggested to be a characteristic feature of DLG4-related phenotypes, was found in only nine individuals and despite some overlapping features, a distinct facial dysmorphism could not be established. Of the 45 different DLG4 variants, 39 were predicted to lead to loss of protein function and the majority occurred de novo (four with unknown origin). The six missense variants identified were suggested to lead to structural or functional changes by protein modeling studies. CONCLUSION: The present study shows that clinical manifestations associated with DLG4 overlap with those found in other neurodevelopmental disorders of synaptic dysfunction; thus, we designate this group of disorders as DLG4-related synaptopathy.RD&E staff can access the full-text of this article by clicking on the 'Additional Link' above and logging in with NHS OpenAthens if prompted.Accepted version (6 month embargo), submitted versio