Concepts for Life Cycle Cost Control Required to Achieve Space Transportation Affordability and Sustainability

Cost control must be implemented through the establishment of requirements and controlled continually by managing to these requirements. Cost control of the non-recurring side of life cycle cost has traditionally been implemented in both commercial and government programs. The government uses the budget process to implement this control. The commercial approach is to use a similar process of allocating the non-recurring cost to major elements of the program. This type of control generally manages through a work breakdown structure (WBS) by defining the major elements of the program. If the cost control is to be applied across the entire program life cycle cost (LCC), the approach must be addressed very differently. A functional breakdown structure (FBS) is defined and recommended. Use of a FBS provides the visibifity to allow the choice of an integrated solution reducing the cost of providing many different elements of like function. The different functional solutions that drive the hardware logistics, quantity of documentation, operational labor, reliability and maintainability balance, and total integration of the entire system from DDT&E through the life of the program must be fully defined, compared, and final decisions made among these competing solutions. The major drivers of recurring cost have been identified and are presented and discussed. The LCC requirements must be established and flowed down to provide control of LCC. This LCC control will require a structured rigid process similar to the one traditionally used to control weight/performance for space transportation systems throughout the entire program. It has been demonstrated over the last 30 years that without a firm requirement and methodically structured cost control, it is unlikely that affordable and sustainable space transportation system LCC will be achieved

Chandra Observations of the Interacting NGC 4410 Galaxy Group

We present high resolution X-ray imaging data from the ACIS-S instrument on the Chandra telescope of the nearby interacting galaxy group NGC 4410. Four galaxies in the inner portion of this group are clearly detected by Chandra, including the peculiar low luminosity radio galaxy NGC 4410A. In addition to a nuclear point source, NGC 4410A contains diffuse X-ray emission, including an X-ray ridge extending out to about 12" (6 kpc) to the northwest of the nucleus. This ridge is coincident with an arc of optical emission-line gas, which has previously been shown to have optical line ratios consistent with shock ionization. This structure may be due to an expanding superbubble of hot gas caused by supernovae and stellar winds or by the active nucleus. The Chandra observations also show four or five possible compact ultra-luminous X-ray (ULX) sources (L(x) >= 10^39 erg/s) associated with NGC 4410A. At least one of these candidate ULXs appears to have a radio counterpart, suggesting that it may be due to an X-ray binary with a stellar-mass black hole, rather than an intermediate mass black hole. In addition, a faint diffuse intragroup X-ray component has been detected between the galaxies (L(x) ~ 10^41 erg/s). This supports the hypothesis that the NGC 4410 group is in the process of evolving via mergers from a spiral-dominated group (which typically have no X-ray-emitting intragroup gas) to an elliptical-dominated group (which often have a substantial intragroup medium).Comment: 27 pages, 14 figures; Accepted by Astronomical Journal; color images at http://www.etsu.edu/physics/bsmith/research/n4410.htm

Differences in Falls and Recovery From a Slip Based On an Individual\u27s Lower Extremity Corrective Response

Background: Slips and falls account for high rates of injury and mortality in multiple populations. The corrective responses during the slip perturbation have been well documented. However, when a fall results from a slip, it is unclear which of these responses were inadequate. Objective: The purpose of this study was to examine differences in lower extremity corrective responses of the slip recovery response between individuals who fall and those who recover. Methodology: Sixty-four participants completed this study (32 males & 32 females). Participant’s gait kinematics and kinetics were collected during normal gait (NG) and an unexpected slip (US). A prediction equation for slip outcome and slip severity were created using a binary logistic regression model. Results: Our findings show an increased time to peak hip extension (OR = 1.006, CI: 1.000-1.011) and ankle dorsiflexion (OR = 1.005, CI: 1.001-1.009) moments increased the odds of falling, while the average ankle moment was negatively associated with falling (OR = 0.001, CI: 0.001-0.005). Conclusions: Rapid lower extremity corrective responses appear critical in arresting the slip and preventing a fall. While there are various strategies for slip recovery, our findings suggest that the primary recovery mechanism at the slipping hip may play a vital role in preventing the fall

Differences in falls and recovery from a slip based on an individual’s lower extremity corrective response

Copyright (c) the author(s). This is an open access article under CC BY license (https://creativecommons.org/licenses/by/4.0/) Background: Slips and falls account for high rates of injury and mortality in multiple populations. The corrective responses during the slip perturbation have been well documented. However, when a fall results from a slip, it is unclear which of these responses were inadequate. Objective: The purpose of this study was to examine differences in lower extremity corrective responses of the slip recovery response between individuals who fall and those who recover. Methodology: Sixty-four participants completed this study (32 males & 32 females). Participant’s gait kinematics and kinetics were collected during normal gait (NG) and an unexpected slip (US). A prediction equation for slip outcome and slip severity were created using a binary logistic regression model. Results: Our findings show an increased time to peak hip extension (OR = 1.006, CI: 1.000-1.011) and ankle dorsiflexion (OR = 1.005, CI: 1.001-1.009) moments increased the odds of falling, while the average ankle moment was negatively associated with falling (OR = 0.001, CI: 0.001-0.005). Conclusions: Rapid lower extremity corrective responses appear critical in arresting the slip and preventing a fall. While there are various strategies for slip recovery, our findings suggest that the primary recovery mechanism at the slipping hip may play a vital role in preventing the fall

Ecrg4 expression and its product augurin in the choroid plexus: impact on fetal brain development, cerebrospinal fluid homeostasis and neuroprogenitor cell response to CNS injury

<p>Abstract</p> <p>Background</p> <p>The content and composition of cerebrospinal fluid (CSF) is determined in large part by the choroid plexus (CP) and specifically, a specialized epithelial cell (CPe) layer that responds to, synthesizes, and transports peptide hormones into and out of CSF. Together with ventricular ependymal cells, these CPe relay homeostatic signals throughout the central nervous system (CNS) and regulate CSF hydrodynamics. One new candidate signal is augurin, a newly recognized 14 kDa protein that is encoded by <it>esophageal cancer related gene-4 </it>(<it>Ecrg4</it>), a putative tumor suppressor gene whose presence and function in normal tissues remains unexplored and enigmatic. The aim of this study was to explore whether <it>Ecrg4 </it>and its product augurin, can be implicated in CNS development and the response to CNS injury.</p> <p>Methods</p> <p><it>Ecrg4 </it>gene expression in CNS and peripheral tissues was studied by <it>in situ </it>hybridization and quantitative RT-PCR. Augurin, the protein encoded by <it>Ecrg4</it>, was detected by immunoblotting, immunohistochemistry and ELISA. The biological consequence of augurin over-expression was studied in a cortical stab model of rat CNS injury by intra-cerebro-ventricular injection of an adenovirus vector containing the <it>Ecrg4 </it>cDNA. The biological consequences of reduced augurin expression were evaluated by characterizing the CNS phenotype caused by <it>Ecrg4 </it>gene knockdown in developing zebrafish embryos.</p> <p>Results</p> <p>Gene expression and immunohistochemical analyses revealed that, the CP is a major source of <it>Ecrg4 </it>in the CNS and that <it>Ecrg4 </it>mRNA is predominantly localized to choroid plexus epithelial (CPe), ventricular and central canal cells of the spinal cord. After a stab injury into the brain however, both augurin staining and <it>Ecrg4 </it>gene expression decreased precipitously. If the loss of augurin was circumvented by over-expressing <it>Ecrg4 in vivo</it>, BrdU incorporation by cells in the subependymal zone decreased. Inversely, gene knockdown of <it>Ecrg4 </it>in developing zebrafish embryos caused increased proliferation of GFAP-positive cells and induced a dose-dependent hydrocephalus-like phenotype that could be rescued by co-injection of antisense morpholinos with <it>Ecrg4 </it>mRNA.</p> <p>Conclusion</p> <p>An unusually elevated expression of the <it>Ecrg4 </it>gene in the CP implies that its product, augurin, plays a role in CP-CSF-CNS function. The results are all consistent with a model whereby an injury-induced decrease in augurin dysinhibits target cells at the ependymal-subependymal interface. We speculate that the ability of CP and ependymal epithelium to alter the progenitor cell response to CNS injury may be mediated, in part by <it>Ecrg4</it>. If so, the canonic control of its promoter by DNA methylation may implicate epigenetic mechanisms in neuroprogenitor fate and function in the CNS.</p

Deficiency of annexins A5 and A6 induces complex changes in the transcriptome of growth plate cartilage but does not inhibit the induction of mineralization

Initiation of mineralization during endochondral ossification is a multistep process and has been assumed to correlate with specific interactions of annexins A5 and A6 and collagens. However, skeletal development appears to be normal in mice deficient for either A5 or A6, and the highly conserved structures led to the assumption that A5 and A6 may fulfill redundant functions. We have now generated mice deficient of both proteins. These mice were viable and fertile and showed no obvious abnormalities. Assessment of skeletal elements using histologic, ultrastructural, and peripheral quantitative computed tomographic methods revealed that mineralization and development of the skeleton were not significantly affected in mutant mice. Otherwise, global gene expression analysis showed subtle changes at the transcriptome level of genes involved in cell growth and intermediate metabolism. These results indicate that annexins A5 and A6 may not represent the essential annexins that promote mineralization in vivo