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This document lists key Lessons Learned from the Startup Team for the 200 West Pump and Treat Facility Project. The Startup Team on this Project was an integrated, multi-discipline team whose scope was Construction Acceptance Testing (CAT), functional Acceptance Testing Procedures (ATP), and procedure development and implementation. Both maintenance and operations procedures were developed. Included in the operations procedures were the process unit operations. In addition, a training and qualification program was also part of the scope.

This is the post-print version of the Article. The official published version can be accessed from the link below - Copyright @ QASS 2011 This article describes a characterisation of competitive market behaviour using the concepts of cointegration analysis. It requires all (n) firms to set prices to follow a single stochastic trend (equivalently the vector of n prices should relate to cointegrating rank n- 1). This implies that, in the long run, prices are driven by the shocks that impact on all companies, ruling out the possibility that the price set by any one firm is weakly exogenous for the set of cointegrating vectors.

This report delineates the results obtained from laboratory testing of IONISIV{reg_sign} IE-95 to determine the efficacy of the zeolite for the removal of radioactive cesium from the KE Basin water prior to transport to the Effluent Treatment Facility, as described in RPP-PLAN-36158, IONSIV{reg_sign} IE-95 Studies for the removal of Radioactive Cesium from KE Basin Spent Nuclear Fuel Pool during Decommissioning Activities. The spent nuclear fuel was removed from KE Basin and the remaining sludge was layered with a grout mixture consisting of 26% Lehigh Type I/II portland cement and 74% Boral Mohave type F fly ash with a water-to-cement ratio of 0.43. The first grout pour was added to the basin floor to a depth of approximately 14 in. covering an area of 12,000 square feet. A grout layer was also added to the sludge containers located in the attached Weasel and Technical View pits.

Copyright @ 2005 Palgrave Macmillan Cointegration, equilibrium and equilibrium correction are key concepts in modern applications of econometrics to real world problems. This book provides direction and guidance to the now vast literature facing students and graduate economists. Econometric theory is linked to practical issues such as how to identify equilibrium relationships, how to deal with structural breaks associated with regime changes and what to do when variables are of different orders of integration.

The effects of glucose deficiency on (1) the K+-evoked release of glutamate and aspartate and (2) excitatory synaptic transmission were studied in the Schaffer collateral-commissural-ipsilateral associational (SCCIA) projection to area CA1 of the rat hippocampal formation in vitro. Compared with 1 or 10 mM glucose, superfusion of CA1 slices with 0.1 mM glucose enhanced the K+-evoked release of both glutamate and aspartate, increased the ratio of aspartate release to glutamate release and did not affect the release of GABA. With both high and low glucose concentrations, the K+-evoked release of glutamate and aspartate originated predominantly from a Ca2+-sensitive store associated with the SCCIA projection. Superfusion with glucose-deficient medium abolished the inhibitory effect of adenosine on glutamate and aspartate release, but augmented the enhancing effect of the adenosine antagonist 8-phenyltheophylline. These results suggest that enough endogenous adenosine was released from the slices under these conditions to saturate the presynaptic A1 receptors. Despite its facilitatory effect on excitatory transmitter release, glucose-deficient medium inhibited transmission at Schaffer collateral-commissural synapses. Even when the postsynaptic response to a single electrical pulse was abolished, however, a substantial response could still be evoked through paired-pulse or frequency potentiation and the inhibition promptly reversed upon superfusion with 10 mM glucose. The increased ratio of aspartate release to glutamate release appears to reflect changes in the tissue content of these amino acids. The enhanced release of both excitants is suggested to result partly from a rise in intraterminal Ca2+ concentration and partly from inhibition of glutamate/aspartate uptake. Enhanced aspartate release may be particularly relevant to hypoglycemic damage in the CA1 area, because aspartate is a more potent hippocampal excitotoxin than glutamate.

Glutamate and/or aspartate is the probable transmitter released from synaptic terminals of the CA3-derived Schaffer collateral, commissural, and ipsilateral associational fibers in area CA1 of the rat hippocampal formation. Slices of the CA1 area were employed to test the effects of adenosine- and gamma-aminobutyrate (GABA)-related compounds on the release of glutamate and aspartate from this projection. Under the conditions of these experiments, the release of glutamate and aspartate evoked by 50 mM K+ was more than 90% Ca2+-dependent and originated predominantly from the CA3-derived pathways. Adenosine reduced the K+-evoked release of glutamate and aspartate by a maximum of about 60%, but did not affect the release of GABA. This action was reversed by 1 microM 8-phenyltheophylline. The order of potency for adenosine analogues was as follows: L-N6-phenylisopropyladenosine greater than N6-cyclohexyladenosine greater than D-N6-phenylisopropyladenosine approximately equal to 2-chloroadenosine greater than adenosine much greater than 5'-N-ethylcarboxamidoadenosine. 8-Phenyltheophylline (10 microM) by itself enhanced glutamate/aspartate release, whereas dipyridamole alone depressed release. These results support the view that adenosine inhibits transmission at Schaffer collateral-commissural-ipsilateral associational synapses mainly by reducing transmitter release and that these effects involve the activation of an A1 receptor. Neither adenosine, L-N6-phenylisopropyladenosine, nor 8-phenyltheophylline affected the release of glutamate or aspartate evoked by 10 microM veratridine. The differing effects of adenosine compounds on release evoked by K+ and veratridine suggest that A1 receptor activation either inhibits Ca2+ influx through the voltage-sensitive channels or interferes with a step subsequent to Ca2+ entry that is coupled to the voltage-sensitive Ca2+ channels in an obligatory fashion. Neither baclofen nor any other agent active at GABAB or GABAA receptors affected glutamate or aspartate release evoked by elevated K+ or veratridine. Therefore, either baclofen does not inhibit transmission at these synapses by depressing transmitter release or else it does so in a way that cannot be detected when a chemical depolarizing agent is employed.