Space biology initiative program definition review. Trade study 6: Space Station Freedom/spacelab modules compatibility

The differences in rack requirements for Spacelab, the Shuttle Orbiter, and the United States (U.S.) laboratory module, European Space Agency (ESA) Columbus module, and the Japanese Experiment Module (JEM) of Space Station Freedom are identified. The feasibility of designing standardized mechanical, structural, electrical, data, video, thermal, and fluid interfaces to allow space flight hardware designed for use in the U.S. laboratory module to be used in other locations is assessed

Space biology initiative program definition review. Trade study 3: Hardware miniaturization versus cost

The optimum hardware miniaturization level with the lowest cost impact for space biology hardware was determined. Space biology hardware and/or components/subassemblies/assemblies which are the most likely candidates for application of miniaturization are to be defined and relative cost impacts of such miniaturization are to be analyzed. A mathematical or statistical analysis method with the capability to support development of parametric cost analysis impacts for levels of production design miniaturization are provided

Space biology initiative program definition review. Trade study 4: Design modularity and commonality

The relative cost impacts (up or down) of developing Space Biology hardware using design modularity and commonality is studied. Recommendations for how the hardware development should be accomplished to meet optimum design modularity requirements for Life Science investigation hardware will be provided. In addition, the relative cost impacts of implementing commonality of hardware for all Space Biology hardware are defined. Cost analysis and supporting recommendations for levels of modularity and commonality are presented. A mathematical or statistical cost analysis method with the capability to support development of production design modularity and commonality impacts to parametric cost analysis is provided

Expression of innate immune complement regulators on brain epithelial cells during human bacterial meningitis

BACKGROUND: In meningitis, the cerebrospinal fluid contains high levels of innate immune molecules (e.g. complement) which are essential to ward off the infectious challenge and to promote the infiltration of phagocytes (neutrophils, monocytes). However, epithelial cells of either the ependymal layer, one of the established niche for adult neural stem cells, or of the choroid plexus may be extremely vulnerable to bystander attack by cytotoxic and cytolytic complement components. METHODS: In this study, we assessed the capacity of brain epithelial cells to express membrane-bound complement regulators (ie, CD35, CD46, CD55 and CD59) in vitro and in situ by immunostaining of control and meningitis human brain tissue sections. RESULTS: Double immunofluorescence experiments for ependymal cell markers (GFAP, S100, ZO-1, E-cadherin) and complement regulators indicated that the human ependymal cell line model was strongly positive for CD55, CD59 compared to weak stainings for CD46 and CD35. In tissues, we found that CD55 was weakly expressed in control choroid plexus and ependyma but was abundantly expressed in meningitis. Anti-CD59 stained both epithelia in apical location while increased CD59 staining was solely demonstrated in inflamed choroid plexus. CD46 and CD35 were not detected in control tissue sections. Conversely, in meningitis, the ependyma, subependyma and choroid plexus epithelia were strongly stained for CD46 and CD35. CONCLUSION: This study delineates for the first time the capacity of brain ependymal and epithelial cells to respond to and possibly sustain the innate complement-mediated inflammatory insult