Component-Level Electronic-Assembly Repair (CLEAR) Analysis of the Problem Reporting and Corrective Action (PRACA) Database of the International Space Station On-Orbit Electrical Systems

The NASA Constellation Program is investigating and developing technologies to support human exploration of the Moon and Mars. The Component-Level Electronic-Assembly Repair (CLEAR) task is part of the Supportability Project managed by the Exploration Technology Development Program. CLEAR is aimed at enabling a flight crew to diagnose and repair electronic circuits in space yet minimize logistics spares, equipment, and crew time and training. For insight into actual space repair needs, in early 2008 the project examined the operational experience of the International Space Station (ISS) program. CLEAR examined the ISS on-orbit Problem Reporting and Corrective Action database for electrical and electronic system problems. The ISS has higher than predicted reliability yet, as expected, it has persistent problems. A goal was to identify which on-orbit electrical problems could be resolved by a component-level replacement. A further goal was to identify problems that could benefit from the additional diagnostic and test capability that a component-level repair capability could provide. The study indicated that many problems stem from a small set of root causes that also represent distinct component problems. The study also determined that there are certain recurring problems where the current telemetry instrumentation and built-in tests are unable to completely resolve the problem. As a result, the root cause is listed as unknown. Overall, roughly 42 percent of on-orbit electrical problems on ISS could be addressed with a component-level repair. Furthermore, 63 percent of on-orbit electrical problems on ISS could benefit from additional external diagnostic and test capability. These results indicate that in situ component-level repair in combination with diagnostic and test capability can be expected to increase system availability and reduce logistics. The CLEAR approach can increase the flight crew s ability to act decisively to resolve problems while reducing dependency on Earth-supplied logistics for future Constellation Program missions

Component-Level Electronic-Assembly Repair (CLEAR) Operational Concept

This Component-Level Electronic-Assembly Repair (CLEAR) Operational Concept document was developed as a first step in developing the Component-Level Electronic-Assembly Repair (CLEAR) System Architecture (NASA/TM-2011-216956). The CLEAR operational concept defines how the system will be used by the Constellation Program and what needs it meets. The document creates scenarios for major elements of the CLEAR architecture. These scenarios are generic enough to apply to near-Earth, Moon, and Mars missions. The CLEAR operational concept involves basic assumptions about the overall program architecture and interactions with the CLEAR system architecture. The assumptions include spacecraft and operational constraints for near-Earth orbit, Moon, and Mars missions. This document addresses an incremental development strategy where capabilities evolve over time, but it is structured to prevent obsolescence. The approach minimizes flight hardware by exploiting Internet-like telecommunications that enables CLEAR capabilities to remain on Earth and to be uplinked as needed. To minimize crew time and operational cost, CLEAR exploits offline development and validation to support online teleoperations. Operational concept scenarios are developed for diagnostics, repair, and functional test operations. Many of the supporting functions defined in these operational scenarios are further defined as technologies in NASA/TM-2011-216956

Component-Level Electronic-Assembly Repair (CLEAR) System Architecture

This document captures the system architecture for a Component-Level Electronic-Assembly Repair (CLEAR) capability needed for electronics maintenance and repair of the Constellation Program (CxP). CLEAR is intended to improve flight system supportability and reduce the mass of spares required to maintain the electronics of human rated spacecraft on long duration missions. By necessity it allows the crew to make repairs that would otherwise be performed by Earth based repair depots. Because of practical knowledge and skill limitations of small spaceflight crews they must be augmented by Earth based support crews and automated repair equipment. This system architecture covers the complete system from ground-user to flight hardware and flight crew and defines an Earth segment and a Space segment. The Earth Segment involves database management, operational planning, and remote equipment programming and validation processes. The Space Segment involves the automated diagnostic, test and repair equipment required for a complete repair process. This document defines three major subsystems including, tele-operations that links the flight hardware to ground support, highly reconfigurable diagnostics and test instruments, and a CLEAR Repair Apparatus that automates the physical repair process

Phenotyping acute and chronic atopic dermatitis-like lesions in Stat6VT mice identifies a role for IL-33 in disease pathogenesis

The Stat6VT mouse model of atopic dermatitis (AD) is induced by T-cell-specific expression of a constitutively active form of the protein signal transducer and activator of transcription 6 (STAT6). Although AD-like lesions are known to develop in Stat6VT mice, this study was designed to determine if these mice develop acute and chronic phases of disease similar to humans. To address this, AD-like lesions from Stat6VT mice were harvested at two different timepoints relative to their onset. Lesions harvested within 1 week after development were defined as acute lesions, and those present for 1 month or more were defined as chronic lesions. Acute and chronic AD-like lesions from Stat6VT mice exhibited histologic findings and cytokine expression patterns similar to acute and chronic AD lesions in humans. Further analysis revealed increased levels of interleukin (IL)-33 transcripts in AD-like lesions compared to Stat6VT nonlesional and wild-type skin controls. Immunofluorescence also revealed increased numbers of IL-33+ keratinocytes in Stat6VT lesional skin and localized IL-33+ keratinocytes to a keratin 5+ subset. Furthermore, AD-like disease was more severe in IL-33-deficient Stat6VT mice compared to IL-33-sufficient Stat6VT mice. These studies suggest that Stat6VT mice can serve as a model of acute and chronic AD and that IL-33 may attenuate inflammation in this system

Intravenously Administered Alphavirus Vector VA7 Eradicates Orthotopic Human Glioma Xenografts in Nude Mice

VA7 is a neurotropic alphavirus vector based on an attenuated strain of Semliki Forest virus. We have previously shown that VA7 exhibits oncolytic activity against human melanoma xenografts in immunodeficient mice. The purpose of this study was to determine if intravenously administered VA7 would be effective against human glioma.In vitro, U87, U251, and A172 human glioma cells were infected and killed by VA7-EGFP. In vivo, antiglioma activity of VA7 was tested in Balb/c nude mice using U87 cells stably expressing firefly luciferase in subcutaneous and orthotopic tumor models. Intravenously administered VA7-EGFP completely eradicated 100% of small and 50% of large subcutaneous U87Fluc tumors. A single intravenous injection of either VA7-EGFP or VA7 expressing Renilla luciferase (VA7-Rluc) into mice bearing orthotopic U87Fluc tumors caused a complete quenching of intracranial firefly bioluminescence and long-term survival in total 16 of 17 animals. In tumor-bearing mice injected with VA7-Rluc, transient intracranial and peripheral Renilla bioluminescence was observed. Virus was well tolerated and no damage to heart, liver, spleen, or brain was observed upon pathological assessment at three and ninety days post injection, despite detectable virus titers in these organs during the earlier time point.VA7 vector is apathogenic and can enter and destroy brain tumors in nude mice when administered systemically. This study warrants further elucidation of the mechanism of tumor destruction and attenuation of the VA7 virus