Paper Session II-C - Commercial Partnering at CCAS: A Proactive Approach to the Commercial Launch Market

The reality of increased access to space for the commercial launch industry is that existing sites must foster an environment which is capable of compromise, responsive to the customers needs, and allows the customer to maximize their launch capabilities. In recent years the space industry has seen a dramatic shift in the launch customer. Prior to 1995 the majority of space launches were funded through the government with some commercial customers, since then this trend has reversed and the primary launch customer has become the commercial launch programs. All indications and future projections demonstrate that this trend will continue and will most likely accelerate. This activity has made the commercial space launch industry a highly competitive multi-billion dollar industry. Much has been done, and written concerning launch vehicle design, production, and processing and the steps that have been taken to reduce the launch customers costs and increase their commercial market share. However, very little has been documented as to the process renovations which the launch sites are going to have to undergo due to competition between the various foreign and domestic launch sites which are just beginning to develop. With new spaceports springing up all across North America(e.g. California, Florida, Virginia and Alaska) and overseas( e.g. Russia, Canada, China, Ukraine) all of which are looking to capitalize on this new and growing market, the efficient processing of requirements, the use of new and evolving technologies, responsive customer interface and reduction of launch support costs have become pressing issues

Impaired nigrostriatal function precedes behavioral deficits in a genetic mitochondrial model of Parkinson's disease

Parkinson's disease (PD) involves progressive loss of nigrostriatal dopamine (DA) neurons over an extended period of time. Mitochondrial damage may lead to PD, and neurotoxins affecting mitochondria are widely used to produce degeneration of the nigrostriatal circuitry. Deletion of the mitochondrial transcription factor A gene (Tfam) in C57BL6 mouse DA neurons leads to a slowly progressing parkinsonian phenotype in which motor impairment is first observed at ∼12 wk of age. l-DOPA treatment improves motor dysfunction in these “MitoPark” mice, but this declines when DA neuron loss is more complete. To investigate early neurobiological events potentially contributing to PD, we compared the neurochemical and electrophysiological properties of the nigrostriatal circuit in behaviorally asymptomatic 6- to 8-wk-old MitoPark mice and age-matched control littermates. Release, but not uptake of DA, was impaired in MitoPark mouse striatal brain slices, and nigral DA neurons lacked characteristic pacemaker activity compared with control mice. Also, hyperpolarization-activated cyclic nucleotide-gated (HCN) ion channel function was reduced in MitoPark DA neurons, although HCN messenger RNA was unchanged. This study demonstrates altered nigrostriatal function that precedes behavioral parkinsonian symptoms in this genetic PD model. A full understanding of these presymptomatic cellular properties may lead to more effective early treatments of PD.—Good, C. H., Hoffman, A. F., Hoffer, B. J., Chefer, V. I., Shippenberg, T. S., Bäckman, C. M., Larsson, N.-G., Olson, L., Gellhaar, S., Galter, D., Lupica, C. R. Impaired nigrostriatal function precedes behavioral deficits in a genetic mitochondrial model of Parkinson's disease