Paper Session III-A - Space Shuttle Avionics Upgrade: Issues and Opportunities

The Space Shuttle uses a complex set of software and hardware to guide, navigate and control it through all phases of flight. Five IBM AP-101B flight computers host a set of highly critical and complex programs. The current man-machine interface consists of a series of dedicated electromechanical instruments and switches combined with specialized displays with limited function. The exponential growth of microprocessor technology combined with the approaching obsolescence of the Space Shuttle cockpit avionics have driven NASA to explore a Product Improvement Plan for the Space Shuttle which includes the cockpit displays and controls. The IBM Systems Integration Division (SID) in Houston is currently studying alternatives for upgrading the Shuttle\u27s cockpit. Some goals of the upgrade include: Offloading of the main computers by distributing some of the avionics display functions, reducing crew workload, reducing maintenance cost, and providing display reconfigurability and context sensitivity. These goals are being met by using a combination of offthe- shelf and newly-developed software and hardware. The software will be developed using Ada, and must meet the timing constraints imposed by existing Shuttle Systems. Advanced active matrix liquid crystal displays are being used to meet the tight space, weight and power consumption requirements. These displays are tied to commercially available 80386 microprocessors. On top of the challenges presented by the software and hardware development are programmatic constraints. These include: Transparency to existing Shuttle avionics and data processing systems, Integration into training facilities: avionics labs, simulators, aircraft, etc., Development of ground support systems: Software Development facilities, verification capabilities, systems integration environments, etc. and Installation into the operational Shuttle fleet without impacting current flight rates. Of course, this all has to be done within cost and timing constraints in a dynamic environment. This upgrade holds promise for future improvements to the onboard avionics systems. An example is online storage and display of crew checklists and procedures. This and other potential growth paths must be accounted for in the design of this upgrade. The opportunities for laying the groundwork of a cohesive strategy for avionics in the nation\u27s space fleet are many and the issues are complex but the technology has advanced far enough that significant benefits can be achieved by upgrading the current system making this a worthwhile if not mandatory task

The intrafamilial transmission of rheumatoid arthritis: An unusual study

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/32903/1/0000283.pd

Local Ca2+ Entry Via Orai1 Regulates Plasma Membrane Recruitment of TRPC1 and Controls Cytosolic Ca2+ Signals Required for Specific Cell Functions

Store-operated Ca2+ entry (SOCE) has been associated with two types of channels: CRAC channels that require Orai1 and STIM1 and SOC channels that involve TRPC1, Orai1, and STIM1. While TRPC1 significantly contributes to SOCE and SOC channel activity, abrogation of Orai1 function eliminates SOCE and activation of TRPC1. The critical role of Orai1 in activation of TRPC1-SOC channels following Ca2+ store depletion has not yet been established. Herein we report that TRPC1 and Orai1 are components of distinct channels. We show that TRPC1/Orai1/STIM1-dependent ISOC, activated in response to Ca2+ store depletion, is composed of TRPC1/STIM1-mediated non-selective cation current and Orai1/STIM1-mediated ICRAC; the latter is detected when TRPC1 function is suppressed by expression of shTRPC1 or a STIM1 mutant that lacks TRPC1 gating, STIM1(684EE685). In addition to gating TRPC1 and Orai1, STIM1 mediates the recruitment and association of the channels within ER/PM junctional domains, a critical step in TRPC1 activation. Importantly, we show that Ca2+ entry via Orai1 triggers plasma membrane insertion of TRPC1, which is prevented by blocking SOCE with 1 µM Gd3+, removal of extracellular Ca2+, knockdown of Orai1, or expression of dominant negative mutant Orai1 lacking a functional pore, Orai1-E106Q. In cells expressing another pore mutant of Orai1, Orai1-E106D, TRPC1 trafficking is supported in Ca2+-containing, but not Ca2+-free, medium. Consistent with this, ICRAC is activated in cells pretreated with thapsigargin in Ca2+-free medium while ISOC is activated in cells pretreated in Ca2+-containing medium. Significantly, TRPC1 function is required for sustained KCa activity and contributes to NFκB activation while Orai1 is sufficient for NFAT activation. Together, these findings reveal an as-yet unidentified function for Orai1 that explains the critical requirement of the channel in the activation of TRPC1 following Ca2+ store depletion. We suggest that coordinated regulation of the surface expression of TRPC1 by Orai1 and gating by STIM1 provides a mechanism for rapidly modulating and maintaining SOCE-generated Ca2+ signals. By recruiting ion channels and other signaling pathways, Orai1 and STIM1 concertedly impact a variety of critical cell functions that are initiated by SOCE