The container relocation problem, where containers that are stored in bays are retrieved in a fixed sequence, is a crucial port operation. Existing approaches using branch and bound algorithms are only able to optimally solve small cases in a practical time frame. In this paper, we investigate iterative deepening A* algorithms (rather than branch and bound) using new lower bound measures and heuristics, and show that this approach is able to solve much larger instances of the problem in a time frame that is suitable for practical application. We also examine a more difficult variant of the problem that has been largely ignored in existing literature.Note to Practitioners-Container retrieval is an important operation in a container port. When a ship arrives, containers stored in the port yard are first retrieved by yard crane, loaded onto autoguided vehicles, transported to quay cranes, and loaded onto the ship by quay crane. Due to various operational constraints, e.g., maintenance of vessel balance and safety issues, the containers in a storage bay are retrieved one by one in a fixed sequence. When the next container to be retrieved is not at the top of its stack, all other containers above it must then be first relocated onto other stacks within the bay. The relocation of a container is a time-consuming operation that essentially dominates all other aspects of the problem, and therefore it is important that the retrieval plan minimizes the number of such relocations. This study proposes a method to generate a near-optimal retrieval plan for yard cranes. This often arises as a subproblem when devising an overall plan for port operations that maximizes throughput, which involves the coordination of multiple pieces of machinery. Our approach produces significantly better results than all existing approaches.Index Terms-Container relocation problem, container yard operation, iterative deepening A*.

SEVO anaesthesia induced widespread apoptosis in infant rat brain. Co-administration of DEX (1 µg kg -1 ) provided significant protection, whereas DEX (5 µg kg -1 or higher) plus SEVO increased mortality. Our findings suggest that DEX could be an attractive therapeutic for future studies investigating its neuroprotective potential in a translational animal model.

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Acute cardiorenal syndrome is a common complication of acute cardiovascular disease. Studies of acute kidney injury (AKI) to chronic kidney disease (CKD) transition, including patients suffering acute cardiovascular disease, report high rates of CKD development. Therefore, acute cardiorenal syndrome associates with CKD, but no study has established causation. To define this we used a murine cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) model or sham procedure on male mice. CA was induced with potassium chloride while CPR consisted of chest compressions and epinephrine eight minutes later. Two weeks after AKI was induced by CA/CPR, the measured glomerular filtration rate (GFR) was not different from sham. However, after seven weeks the mice developed CKD, recapitulating clinical observations. One day, and one, two, and seven weeks after CA/CPR, the GFR was measured, and renal tissue sections were evaluated for various indices of injury and inflammation. One day after CA/CPR, acute cardiorenal syndrome was indicated by a significant reduction of the mean GFR (649 in sham, vs. 25 mL/min/ 100g in CA/CPR animals), KIM-1 positive tubules, and acute tubular necrosis. Renal inflammation developed, with F4/80 positive and CD3-positive cells infiltrating the kidney one day and one week after CA/CPR, respectively. Although there was functional recovery with normalization of GFR two weeks after CA/CPR, deposition of tubulointerstitial matrix proteins a-smooth muscle actin and fibrillin-1 progressed, along with a significantly reduced mean GFR (623 in sham vs. 409 mL/min/100g in CA/CPR animals), proteinuria, increased tissue transforming growth factor-b, and fibrosis establishing the development of CKD seven weeks after CA/CPR. Thus, murine CA/CPR, a model of acute cardiorenal syndrome, causes an AKI-CKD transition likely due to prolonged renal inflammation.

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GABAA receptors are ligand-gated CI- ion channels with multiple clinically relevant drug-recognition sites. We have previously shown that stimulation of N-methyl-D-aspartic acid (NMDA)-specific glutamate receptors quantitatively alters selected GABAA receptor subunit mRNAs and proteins in primary cultures of rat cerebellar granule neurons. We used whole-cell recordings of GABA-elicited CI- currents and flunitrazepam binding experiments in granule cell cultures maintained in low K+ (12.5 mM), cells maintained in low K+ and treated with a single dose of NMDA (10 microM), and cell cultures maintained in depolarizing concentrations of K+ (25 mM). The EC50 obtained from the dose-response curves for GABA in eliciting a maximal response was comparable in neurons maintained in high K+ or in low K+ and treated with a single dose of NMDA, but that it increased significantly in cells maintained in low K+. The potentiation of GABA-gated CI- currents by flunitrazepam increased significantly, while the negative allosteric modulator methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM) was significantly more effective in cultures either maintained in high K+ or treated with NMDA. This was coincident with a twofold increase in the Bmax associated with flunitrazepam binding. To further characterize the receptor assemblies present in the depolarization and NMDA induced paradigms, the Zn(2+)-induced inhibition of GABA-gated CI- currents was reduced as was the inhibition mediated by furosemide. Our data indicate that GABAA receptor assemblies alter their composition in response to excitatory afferent receptor stimulation.