OPTIC: Orbiting Plutonian Topographic Image Craft Proposal for an Unmanned Mission to Pluto

The proposal for an unmanned probe to Pluto is presented and described. The Orbiting Plutonian Topographic Image Craft's (OPTIC's) trip will take twenty years and after its arrival, will begin its data collection which includes image and radar mapping, surface spectral analysis, and magnetospheric studies. This probe's design was developed based on the request for proposal of an unmanned probe to Pluto requirements. The distinct problems which an orbiter causes for each subsystem of the craft are discussed. The final design revolved around two important factors: (1) the ability to collect and return the maximum quantity of information on the Plutonian system; and (2) the weight limitations which the choice of an orbiting craft implied. The velocity requirements of this type of mission severely limited the weight available for mission execution-owing to the large portion of overall weight required as fuel to fly the craft with present technology. The topics covered include: (1) scientific instrumentation; (2) mission management; (3) power and propulsion; (4) attitude and articulation control; (5) structural subsystems; and (6) command, control, and communication

Bunyamwera Bunyavirus Nonstructural Protein NSs Counteracts the Induction of Alpha/Beta Interferon

Production of alpha/beta interferons (IFN-α/β) in response to viral infection is one of the main defense mechanisms of the innate immune system. Many viruses therefore encode factors that subvert the IFN system to enhance their virulence. Bunyamwera virus (BUN) is the prototype of the Bunyaviridae family. By using reverse genetics, we previously produced a recombinant virus lacking the nonstructural protein NSs (BUNdelNSs) and showed that NSs is a nonessential gene product that contributes to viral pathogenesis. Here we demonstrate that BUNdelNSs is a strong inducer of IFN-α/β, whereas in cells infected with the wild-type counterpart expressing NSs (wild-type BUN), neither IFN nor IFN mRNA could be detected. IFN induction by BUNdelNSs correlated with activation of NF-κB and was dependent on virally produced double-stranded RNA and on the IFN transcription factor IRF-3. Furthermore, both in cultured cells and in mice lacking a functional IFN-α/β system, BUNdelNSs replicated to wild-type BUN levels, whereas in IFN-competent systems, wild-type BUN grew more efficiently. These results suggest that BUN NSs is an IFN induction antagonist that blocks the transcriptional activation of IFN-α/β in order to increase the virulence of Bunyamwera virus

Functional characterization of coronary vascular adenosine receptors in the mouse

1. Coronary responses to adenosine agonists were assessed in perfused mouse and rat hearts. The roles of nitric oxide (NO) and ATP-dependent K(+) channels (K(ATP)) were studied in the mouse. 2. Resting coronary resistance was lower in mouse vs rat, as was minimal resistance (2.2±0.1 vs 3.8±0.2 mmHg ml(−1) min(−1) g(−1)). Peak hyperaemic flow after 20–60 s occlusion was greater in mouse. 3. Adenosine agonists induced coronary dilation in mouse, with pEC(50)s of 9.4±0.1 for 2-[p-(2-carboxyethyl)phenethylamino]-5′-N-ethyl carboxamidoadenosine (CGS21680, A(2A)-selective agonist), 9.3±0.1 for 5′-N-ethylcarboxamidoadenosine (NECA, A(1)/A(2) agonist), 8.4±0.1 for 2-chloroadenosine (A(1)/A(2) agonist), 7.7±0.1 for N(6)-(R)-(phenylisopropyl)adenosine (R-PIA, A(1)/A(2B) selective), and 6.8±0.2 for adenosine. The potency order (CGS21680=NECA>2-chloroadenosine>R-PIA>adenosine) supports A(2A) adenosine receptor-mediated dilation in mouse coronary vessels. 0.2–2 μM of the A(2B)-selective antagonist alloxazine failed to alter CGS21680 or 2-chloroadenosine responses. 4. pEC(50)s in rat were 6.7±0.2 for CGS21680, 7.3±0.1 for NECA, 7.6±0.1 for 2-chloroadenosine, 7.2±0.1 for R-PIA, and 6.2±0.1 for adenosine (2-chloroadenosine>NECA=R-PIA>CGS21680> adenosine), supporting an A(2B) adenosine receptor response. 5. NO-synthase antagonism with 50 μM N(G)-nitro L-arginine (L-NOARG) increased resistance by ∼25%, and inhibited responses to CGS21680 (pEC(50)=9.0±0.1), 2-chloroadenosine (pEC(50)=7.3±0.2) and endothelial-dependent ADP, but not sodium nitroprusside (SNP). K(ATP) channel blockade with 5 μM glibenclamide increased resistance by ∼80% and inhibited responses to CGS21680 in control (pEC(50)=8.3±0.1) and L-NOARG-treated hearts (pEC(50)=7.3±0.1), and to 2-chloroadenosine in control (pEC(50)=6.7±0.1) and L-NOARG-treated hearts (pEC(50)=5.9±0.2). 6. In summary, mouse coronary vessels are more sensitive to adenosine than rat vessels. A(2A) adenosine receptors mediate dilation in mouse coronary vessels vs A(2B) receptors in rat. Responses in the mouse involve a sensitive NO-dependent response and K(ATP)-dependent dilation