87 research outputs found

    Prospectus, February 27, 2002

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    https://spark.parkland.edu/prospectus_2002/1007/thumbnail.jp

    Prospectus, February 20, 2002

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    https://spark.parkland.edu/prospectus_2002/1006/thumbnail.jp

    Prospectus, April 10, 2002

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    https://spark.parkland.edu/prospectus_2002/1012/thumbnail.jp

    Prospectus, April 17, 2002

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    https://spark.parkland.edu/prospectus_2002/1013/thumbnail.jp

    On-Orbit Data and Validation of Astra\u27s ACE Electric Propulsion System

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    The first ACE propulsion system reached orbit on July 1st 2021 as part of Spaceflight’s demonstration of the Sherpa-LTE all-electric Orbital Transfer Vehicle (OTV). We are now able to share on-orbit data and have successfully verified the on-orbit performance of the ACE propulsion system, using xenon propellent. The mission objective was to lower altitude and use on-orbit data to derive performance, correlating the propulsion system’s performance to ground test data. The demonstration consisted of activating the propulsion system for 5- minute durations at a total input power of 340 W into the Power Processing Unit (PPU). Altitude change and propellant usage were used to derive thrust and total specific impulse. On-orbit performance is compared to ground test data in Table 1. Averaged performance is within one standard deviation of ground test data. Astra considers this a validation of system performance, as well as the ground test facilities used to test propulsion systems. On-orbit thrust has a large standard deviation as a result of the limited data sampling rate and measurement errors, rather than variability in thruster performance. Figure 1 shows the thruster operating on-orbit. The Astra team gratefully acknowledges the support of Spaceflight, Inc., the U.S. Air Force, and Defense Innovation Unit (DIU) without which this mission would not have been possible

    Formation of Chimeric Genes by Copy-Number Variation as a Mutational Mechanism in Schizophrenia

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    Chimeric genes can be caused by structural genomic rearrangements that fuse together portions of two different genes to create a novel gene. We hypothesize that brain-expressed chimeras may contribute to schizophrenia. Individuals with schizophrenia and control individuals were screened genome wide for copy-number variants (CNVs) that disrupted two genes on the same DNA strand. Candidate events were filtered for predicted brain expression and for frequency < 0.001 in an independent series of 20,000 controls. Four of 124 affected individuals and zero of 290 control individuals harbored such events (p = 0.002); a 47 kb duplication disrupted MATK and ZFR2, a 58 kb duplication disrupted PLEKHD1 and SLC39A9, a 121 kb duplication disrupted DNAJA2 and NETO2, and a 150 kb deletion disrupted MAP3K3 and DDX42. Each fusion produced a stable protein when exogenously expressed in cultured cells. We examined whether these chimeras differed from their parent genes in localization, regulation, or function. Subcellular localizations of DNAJA2-NETO2 and MAP3K3-DDX42 differed from their parent genes. On the basis of the expression profile of the MATK promoter, MATK-ZFR2 is likely to be far more highly expressed in the brain during development than the ZFR2 parent gene. MATK-ZFR2 includes a ZFR2-derived isoform that we demonstrate localizes preferentially to neuronal dendritic branch sites. These results suggest that the formation of chimeric genes is a mechanism by which CNVs contribute to schizophrenia and that, by interfering with parent gene function, chimeras may disrupt critical brain processes, including neurogenesis, neuronal differentiation, and dendritic arborization

    Adaptation and validation of a computerized neurocognitive battery in the Xhosa of South Africa

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    Objective: Large-scale studies have revolutionized biomedical research, and neurocognitive tests can help elucidate the biological basis of neuropsychiatric diseases. However, studies have predominantly been conducted in Western settings. We describe the development and validation of a computerized battery (PennCNB) with the Xhosa population of South Africa. Method: Individuals with schizophrenia (n = 525) and a normative comparison group (n = 744) were balanced on age, sex, education, and region. Participants provided blood samples, were assessed psychiatrically, and were administered a PennCNB translation to isiXhosa, including measures of executive functions, episodic memory, complex cognition, social cognition, and sensorimotor speed. Feasibility was examined with test completion rates and input from administrators, and psychometric structural validity and associations with clinical and demographic characteristics were examined. Results: Tests were well tolerated by participants, as >87% had one (or fewer) test missing. Results suggested a similar factor structure to prior PennCNB studies in Western contexts, and expected age and sex effects were apparent. Furthermore, a similar profile of schizophrenia was observed, with neurocognitive deficits most pronounced for executive functions, especially attention, as well as memory, social cognition, and motor speed relative to complex cognition and sensorimotor speed. Conclusions: Results support the feasibility of implementing a culturally adapted computerized neurocognitive battery in sub-Saharan African settings and provide evidence supporting the concurrent validity of the translated instrument. Thus, the PennCNB is implementable on a large scale in non-Western contexts, shows expected factor structure, and can detect cognitive deficits associated with neuropsychiatric disorders. Obtaining valid measures of cognition by nonspecialized proctors is especially suitable in resource-limited settings, where traditional testing is prohibitive. Future work should establish normative standards, test–retest reliability, and sensitivity to treatment
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