Process control in agile supply chain network.

The work comprises a new theoretical development applied to aid decision making in an increasingly important commercial sector. Agile supply, where small volumes of high margin, short life cycle innovative products are offered, is increasingly carried out through a complex global supply chain network. We outline an equilibrium solution in such a supply chain network, which works through limited cooperation and coordination along edges (links) in the network. The links constitute the stochastic modelling entities rather than the nodes of the network. We utilise newly developed phase plane analysis to identify, model and predict characteristic behaviour in supply chain networks. The phase plane charts profile the flow of inventory and identify out of control conditions. They maintain quality within the network, as well as intelligently track the way the network evolves in conditions of changing variability. The methodology is essentially distribution free, relying as it does on the study of forecasting errors, and can be used to examine contractual details as well as strategic and game theoretical concepts between decision-making components (agents) of a network. We illustrate with typical data drawn from supply chain agile fashion products.

GABAA receptor chloride channels are involved in the neuroprotective role of GABA following oxygen and glucose deprivation in the rat cerebral cortex but not in the hippocampus.

Assays on "ex vivo" sections of rat hippocampus and rat cerebral cortex, subjected to oxygen and glucose deprivation (OGD) and a three-hour reperfusion-like (RL) recovery, were performed in the presence of either GABA or the GABA(A) receptor binding site antagonist, bicuculline. Lactate dehydrogenase (LDH) and propidium iodide were used to quantify cell mortality. We also measured, using real-time quantitative polymerase chain reaction (qPCR), the early transcriptional response of a number of genes of the glutamatergic and GABAergic systems. Specifically, glial pre- and post-synaptic glutamatergic transporters (namely GLAST1a, EAAC-1, GLT-1 and VGLUT1), three GABAA receptor subunits (α1, β2 and γ2), and the GABAergic presynaptic marker, glutamic acid decarboxylase (GAD65), were studied. Mortality assays revealed that GABAA receptor chloride channels play an important role in the neuroprotective effect of GABA in the cerebral cortex, but have a much smaller effect in the hippocampus. We also found that GABA reverses the OGD-dependent decrease in GABA(A) receptor transcript levels, as well as mRNA levels of the membrane and vesicular glutamate transporter genes. Based on the markers used, we conclude that OGD results in differential responses in the GABAergic presynaptic and postsynaptic systems.