A small satellite design for deep space network testing and training

With the continuing exploration of the Solar System and the reemphasis on Earth focused missions, the need for faster data transmission rates has grown. Ka-band could allow a higher data delivery rate over the current X-band, however the adverse effects of the Earth's atmosphere on Ka are as yet unknown. The Deep Space Network and Jet Propulsion Lab have proposed to launch a small satellite that would simultaneously transmit X and Ka signals to test the viability of switching to Ka-band. The Mockingbird Design Team at the University of Texas at Austin applied small satellite design principles to achieve this objective. The Mockingbird design, named BATSAT, incorporates simple, low-cost systems designed for university production and testing. The BATSAT satellite is a 0.64 m diameter, spherical panel led satellite, mounted with solar cells and omni-directional antennae. The antennae configuration negates the need for active attitude control or spin stabilization. The space-frame truss structure was designed for 11 g launch loads while allowing for easy construction and solar-panel mounting. The communication system transmits at 1 mW by carrying the required Ka and X-band transmitters, as well as an S band transmitter used for DSN training. The power system provides the 8.6 W maximum power requirements via silicon solar arrays and nickel-cadmium batteries. The BATSAT satellite will be lofted into an 1163 km, 70 deg orbit by the Pegasus launch system. This orbit fulfills DSN dish slew rate requirements while keeping the satellite out of the heaviest regions of the Van Allen radiation belts. Each of the three DSN stations capable of receiving Ka-band (Goldstone, Canberra, and Madrid) will have an average of 85 minutes of view-time per day over the satellites ten year design life. Mockingbird Designs hopes that its small satellite design will not only be applicable to this specific mission scenario, but that it could easily be modified for instrument capability for university, government, and/or commercial research

Depression of cell metabolism and proliferation by membrane-permeable and -impermeable modulators : role for AMP-to-ATP ratio.

The metabolic and developmental depression commonly observed during natural states of dormancy, such as diapause and quiescence, is typically accompanied by an increase in the intracellular ratio of AMP to ATP. We investigated the impact of artificially increasing the AMP-to-ATP ratio in mouse macrophages. Evidence is presented here that the P2X7 receptor channel can be used as an effective means to load cells with membrane-impermeable compounds. Intracellular loading of adenosine-5’-O-thiomonophosphate (AMPS), a nonhydrolyzable analog of 5’-AMP and potent activator of AMP-activated protein kinase, significantly depresses metabolism and proliferation of macrophages. The intracellular effective AMP-to-ATP ratio obtained (the sum of AMPS plus endogenous 5’-AMP) was 0.073, well above that reported to activate AMP-activated protein kinase in vitro. Optimizing both the conditions under which the P2X7 receptor channel is opened and the duration of opening facilitates high analog uptake and ~98% survivorship. An advantage to AMPS is its minimal impact on other components of the nucleotide pool, most notably the unchanged concentration of ADP. An alternative way to shift the effective AMP-to-ATP ratio is by incubation with the membranepermeable compound 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), which is phosphorylated intracellularly to form the 5’-AMP analog ZMP. Despite a rapid intracellular accumulation of AICAR, conversion to ZMP was slow and inefficient. Furthermore, AICAR incubation increased cellular ADP, and, although cell proliferation was depressed, the overall cellular energy flow was unchanged. The rapid action of AMPS avoids upregulation of compensatory metabolic pathways and may provide a viable approach for promoting cell stasis

Metabolic preconditioning of cells with AICAR-riboside : improved cryopreservation and cell-type specific impacts on energetics and proliferation.

In species whose evolutionary history has provided natural tolerance to dehydration and freezing, metabolic depression is often a pre-requisite for survival. We tested the hypothesis that preconditioning of mammalian cells with 5-aminoimidazole-4-carboxamide-1-b-D-ribofuranoside (AICAR) to achieve metabolic depression will promote greater survivorship during cryopreservation. AICAR is used extensively to stimulate AMP-activated protein kinase (AMPK), which can result in downregulation of biosynthetic processes. We showed that the metabolic interconversion of AICAR was cell-type dependent. Accumulation of 5-aminoimidazole-4-carboxamide-1b-D-ribofuranosyl-5′-monophosphate (ZMP), as well as other metabolites that possess multiple phosphates (i.e., ZDP, ZTP), varied approximately 3.5-fold across the cell lines tested. AICAR treatment also significantly influenced the concentrations of cellular adenylates (ATP, ADP, AMP). Depression of cell metabolism and proliferation with AICAR treatment differed among cell lines. Proliferation for a given cell line was negatively correlated with the fold-increase achieved in the ‘effective adenylate ratio’ ([AMP]+[ZMP])/[ATP]) after AICAR treatment. Metabolic preconditioning with AICAR promoted a significant increase in viability post-freezing in J774.A1 macrophages, HepG2/C3A cells and primary hepatocytes but not in NIH/3T3 fibroblasts or OMK cells. The effect of AICAR on viability after freezing was positively correlated (r2 = 0.94) with the fold-increase in the ‘effective adenylate ratio’. Thus for each cell line, the greater the depression of metabolism and proliferation due to preconditioning with AICAR, the greater was the survivorship post-freezing