There is a great incentive for developing systematic approaches that effectively identify strategies for planning oilfield complexes. This paper proposes an MILP that relies on a reformulation of the model developed by Tsarbopoulou (UCL M.S. Dissertation, London, 2000). Moreover, a bilevel decomposition technique is applied to the MILP. A master problem determines the assignment of platforms to wells and a planning subproblem calculates the timing for fixed assignments. Furthermore, a heuristic search procedure that relies on the distance between platforms and wells is applied in order to reduce the search region. Results show that the decomposition approach using heuristic generates optimal solutions for instances of up to 500 wells and 25 platforms in 10 discrete time periods that otherwise could not be solved with a full-scale approach. One important feature regarding these instances is that they correspond to problems of real-world dimension.

Fibronectin (FN), a large family of plasma and extracellular matrix (ECM) glycoproteins, plays an important role in leukocyte migration. In normal central nervous system (CNS), a fine and delicate mesh of FN is virtually restricted to the basal membrane of cerebral blood vessels and to the glial limitans externa. Experimental autoimmune encephalomyelitis (EAE), an inflammatory CNS demyelinating disease, was induced in Lewis rats with a spinal cord homogenate. During the preclinical phase and the onset of the disease, marked immunolabelling was observed on the endothelial luminal surface and basal lamina of spinal cord and brainstem microvasculature. In the paralytic phase, a discrete labelling was evident in blood vessels of spinal cord and brainstem associated or not with an inflammatory infiltrate. Conversely, intense immunolabelling was present in cerebral and cerebellar blood vessels, which were still free from inflammatory cuffs. Shortly after clinical recovery minimal labelling was observed in a few blood vessels. Brainstem and spinal cord returned to normal, but numerous inflammatory foci and demyelination were still evident near the ventricle walls, in the cerebral cortex and in the cerebellum. Intense expression of FN in brain vessels ascending from the spinal cord towards the encephalon preceded the appearance of inflammatory cells but faded away after the establishment of the inflammatory cuff. These results indicate an important role for FN in the pathogenesis of CNS inflammatory demyelinating events occurring during EAE.