Cost Analysis In A Multi-Mission Operations Environment

Spacecraft control centers have evolved from dedicated, single-mission or single missiontype support to multi-mission, service-oriented support for operating a variety of mission types. At the same time, available money for projects is shrinking and competition for new missions is increasing. These factors drive the need for an accurate and flexible model to support estimating service costs for new or extended missions; the cost model in turn drives the need for an accurate and efficient approach to service cost analysis. The National Aeronautics and Space Administration (NASA) Huntsville Operations Support Center (HOSC) at Marshall Space Flight Center (MSFC) provides operations services to a variety of customers around the world. HOSC customers range from launch vehicle test flights; to International Space Station (ISS) payloads; to small, short duration missions; and has included long duration flagship missions. The HOSC recently completed a detailed analysis of service costs as part of the development of a complete service cost model. The cost analysis process required the team to address a number of issues. One of the primary issues involves the difficulty of reverse engineering individual mission costs in a highly efficient multimission environment, along with a related issue of the value of detailed metrics or data to the cost model versus the cost of obtaining accurate data. Another concern is the difficulty of balancing costs between missions of different types and size and extrapolating costs to different mission types. The cost analysis also had to address issues relating to providing shared, cloud-like services in a government environment, and then assigning an uncertainty or risk factor to cost estimates that are based on current technology, but will be executed using future technology. Finally the cost analysis needed to consider how to validate the resulting cost models taking into account the non-homogeneous nature of the available cost data and the decreasing flight rate. This paper presents the issues encountered during the HOSC cost analysis process, and the associated lessons learned. These lessons can be used when planning for a new multi-mission operations center or in the transformation from a dedicated control center to multi-center operations, as an aid in defining processes that support future cost analysis and estimation. The lessons can also be used by mature serviceoriented, multi-mission control centers to streamline or refine their cost analysis process

Evidence That Separate Neural Circuits in the Nucleus Accumbens Encode Cocaine Versus “Natural” (Water and Food) Reward

Electrophysiological recording procedures were used to examine nucleus accumbens (Acb) cell firing in rats trained to press a lever on a multiple schedule [ fixed ratio (FR)1, FR1] for either two "natural" reinforcers (food and water), or a natural reinforcer and intravenous self-administration of cocaine. Of 180 cells recorded during water and food reinforcement (n = 13 rats), 77 neurons were classified as phasically active, exhibiting one of three well-defined types of patterned discharges relative to the reinforced-response (Carelli and Deadwyler, 1994). Of the 77 phasic cells, the majority (68%) showed similar types of patterned discharges across the two natural reinforcer conditions. In contrast, of 127 neurons recorded during water and cocaine reinforcement (n = 8 rats), only 5 of 60 phasically active cells (8%) exhibited similar types of patterned discharges relative to water- and cocaine-reinforced responding. The remaining 55 phasic cells (92%) displayed patterned discharges relative to the cocaine-reinforced response (n = 26 cells), or relative to the water-reinforced response (n = 29 cells), but not both. For some rats (n = 3), food was substituted for water in the task. Again, the majority of phasic neurons (13 of 14 cells, 93%) exhibited nonoverlapping firing patterns across the drug and natural reinforcer conditions. These findings indicate that in the well-trained animal, cocaine activates a neural circuit in the Acb that is largely separate from the circuit that processes information about food and water reward

Neuroimmune mechanisms of opioid-mediated conditioned immunomodulation

Morphine administration elicits pronounced effects on the immune system, including decreases in natural killer (NK) cell activity and lymphocyte mitogenic responsiveness. These immune alterations can become conditioned to environmental stimuli that predict morphine as a result of Pavlovian conditioning processes. Prior work in our laboratory has shown that acute morphine exposure produces dopamine-dependent reductions of NK cell activity that are mediated peripherally by neuropeptide Y Y1 receptors. The present study examined the involvement of dopamine D1 and neuropeptide Y Y1 receptors in the conditioned immunomodulatory effects of morphine. Rats received two conditioning sessions during which an injection of morphine was paired with a distinctive environment which served as the conditioned stimulus (CS). The results show that systemic administration of the D1 antagonist SCH-23390 prior to CS re-exposure prevented the conditioned suppression of splenic NK activity but did not alter conditioned decreases in mitogen-induced lymphocyte proliferation. Furthermore, bilateral microinjections of SCH-23390 directly into the nucleus accumbens shell fully blocked conditioned changes in NK activity. In a subsequent manipulation, subcutaneous injection of the Y1 receptor antagonist BIBP3226 prior to CS re-exposure was also shown to prevent conditioned effects on NK activity. Collectively, these findings provide evidence that the nucleus accumbens shell plays an important role in conditioned immunomodulation and further suggest that the conditioned and unconditioned immunomodulatory effects of opioids involve similar receptor mechanisms

Evidence for the Nucleus Accumbens as a Neural Substrate of Heroin-Induced Immune Alterations

Administration of opioid drugs such as heroin produces several immunosuppressive effects, including decreases in natural killer (NK) cell activity, lymphocyte proliferative responses, and nitric oxide production. Interestingly, opioids have been shown to alter many immune parameters indirectly by modulating the immunoregulatory actions of the central nervous system. Recently, it has been demonstrated that morphine inhibits NK cell activity through a neural pathway that requires the activation of dopamine D1 receptors in the nucleus accumbens shell. The present study examined whether the nucleus accumbens also mediates the effects of heroin, a more commonly abused opioid, on several parameters of immune status in Lewis rats. The results showed that bilateral administration of the dopamine D1 receptor antagonist R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (SCH-23390; 0.015 and 0.15 μg/side) into the nucleus accumbens shell blocked decreases in splenic NK activity produced by heroin (3 mg/kg s.c.) but did not attenuate the suppression of splenocyte proliferative responses to concanavalin-A or lipopolysaccharide (LPS). A subsequent experiment was performed to evaluate the effect of D1 receptor antagonism on LPS-induced expression of inducible nitric-oxide synthase (iNOS) in vivo. These results showed that intra-accumbens SCH-23390 administration prevented heroin-induced reductions of iNOS mRNA expression in spleen, liver, and lung tissues and attenuated the suppression of nitric oxide levels in plasma. Collectively, these findings indicate that nucleus accumbens dopamine D1 receptors are critically involved in heroin-induced immune alterations