History of POIC Capabilities and Limitations to Conduct International Space Station Payload Operations

Payload science operations on the International Space Station (ISS) have been conducted continuously twenty-four hours per day, 365 days a year beginning February, 2001 and continuing through present day. The Payload Operations Integration Center (POIC), located at the Marshall Space Flight Center in Huntsville, Alabama, has been a leader in integrating and managing NASA distributed payload operations. The ability to conduct science operations is a delicate balance of crew time, onboard vehicle resources, hardware up-mass to the vehicle, and ground based flight control team manpower. Over the span of the last ten years, the POIC flight control team size, function, and structure has been modified several times commensurate with the capabilities and limitations of the ISS program. As the ISS vehicle has been expanded and its systems changed throughout the assembly process, the resources available to conduct science and research have also changed. Likewise, as ISS program financial resources have demanded more efficiency from organizations across the program, utilization organizations have also had to adjust their functionality and structure to adapt accordingly. The POIC has responded to these often difficult challenges by adapting our team concept to maximize science research return within the utilization allocations and vehicle limitations that existed at the time. In some cases, the ISS and systems limitations became the limiting factor in conducting science. In other cases, the POIC structure and flight control team size were the limiting factors, so other constraints had to be put into place to assure successful science operations within the capabilities of the POIC. This paper will present the POIC flight control team organizational changes responding to significant events of the ISS and Shuttle programs

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

Leading-Edge Votex-System Details Obtained on F-106B Aircraft Using a Rotating Vapor Screen and Surface Techniques

A flight research program to study the flow structure and separated-flow origins over an F-106B aircraft wing is described. The flight parameters presented include Mach numbers from 0.26 to 0.81, angles of attack from 8.5 deg to 22.5 deg, Reynolds numbers from 22.6 x 10(exp 6) to 57.3 x 10(exp 6) and load factors from 0.9 to 3.9 times the acceleration due to gravity. Techniques for vapor screens, image enhancement, photogrammetry, and computer graphics are integrated to analyze vortex-flow systems. Emphasis is placed on the development and application of the techniques. The spatial location of vortex cores and their tracks over the wing are derived from the analysis. Multiple vortices are observed and are likely attributed to small surface distortions in the wing leading-edge region. A major thrust is to correlate locations of reattachment lines obtained from the off-surface (vapor-screen) observations with those obtained from on-surface oil-flow patterns and pressure-port data. Applying vapor-screen image data to approximate reattachment lines is experimental, but depending on the angle of attack, the agreement with oil-flow results is generally good. Although surface pressure-port data are limited, the vapor-screen data indicate reattachment point occurrences consistent with the available data

Blood-based protein mediators of senility with replications across biofluids and cohorts

Dementia severity can be quantitatively described by the latent dementia phenotype 'δ' and its various composite 'homologues'. We have explored δ's blood-based protein biomarkers in the Texas Alzheimer's Research and Care Consortium. However, it would be convenient to replicate them in the Alzheimer's Disease Neuroimaging Initiative. To that end, we have engineered a δ homologue from the observed cognitive performance measures common to both projects [i.e. 'd:Texas Alzheimer's Research and Care Consortium to Alzheimer's Disease Neuroimaging Initiative' (dT2A)]. In this analysis, we confirm 13/22 serum proteins as partial mediators of age's effect on dementia severity as measured by dT2A in the Texas Alzheimer's Research and Care Consortium and then replicate 4/13 in the Alzheimer's Disease Neuroimaging Initiative's plasma data. The replicated mediators of age-specific effects on dementia severity are adiponectin, follicle-stimulating hormone, pancreatic polypeptide and resistin. In their aggregate, the 13 confirmed age-specific mediators suggest that 'cognitive frailty' pays a role in dementia severity as measured by δ. We provide both discriminant and concordant support for that hypothesis. Weight, calculated low-density lipoprotein and body mass index are partial mediators of age's effect in the Texas Alzheimer's Research and Care Consortium. Biomarkers related to other disease processes (e.g. cerebrospinal fluid Alzheimer's disease-specific biomarkers in the Alzheimer's Disease Neuroimaging Initiative) are not. It now appears that dementia severity is the sum of multiple independent processes impacting δ. Each may have a unique set of mediating biomarkers. Age's unique effect appears to be at least partially mediated through proteins related to frailty. Age-specific mediation effects can be replicated across cohorts and biofluids. These proteins may offer targets for the remediation of age-specific cognitive decline (aka 'senility'), help distinguish it from other determinants of dementia severity and/or provide clues to the biology of Aging Proper