Hybrid global-local optimisation algorithms for the layout design of tidal turbine arrays

Tidal stream power generation represents a promising source of renewable energy. In order to extract an economically useful amount of power, tens to hundreds of tidal turbines need to be placed within an array. The layout of these turbines can have a significant impact on the power extracted and hence on the viability of the site. Funke et al. formulated the question of the best turbine layout as an optimisation problem constrained by the shallow water equations and solved it using a local, gradient-based optimisation algorithm. Given the local nature of this approach, the question arises of how optimal the layouts actually are. This becomes particularly important for scenarios with complex bathymetry and layout constraints, both of which typically introduce locally optimal layouts. Optimisation algorithms which find the global optima generally require orders of magnitude more iterations than local optimisation algorithms and are thus infeasible in combination with an expensive flow model. This paper presents an analytical wake model to act as an efficient proxy to the shallow water model. Based upon this, a hybrid global-local two-stage optimisation approach is presented in which turbine layouts are first optimised with the analytical wake model via a global optimisation algorithm, and further optimised with the shallow water model via a local gradient-based optimisation algorithm. This procedure is applied to a number of idealised cases and a more realistic case with complex bathymetry in the Pentland Firth, Scotland. It is shown that in cases where bathymetry is considered, the two-stage optimisation procedure is able to improve the power extracted from the array by as much as 25% compared to local optimisation for idealised scenarios and by as much as 12% for the more realistic Pentland Firth scenario whilst in many cases reducing the overall computation time by approximately 35%

Surrogate-based optimization of tidal turbine arrays: a case study for the Faro-Olhão inlet

This paper presents a study for estimating the size of a tidal turbine array for the Faro-Olhão Inlet (Potugal) using a surrogate optimization approach. The method compromises problem formulation, hydro-morphodynamic modelling, surrogate construction and validation, and constraint optimization. A total of 26 surrogates were built using linear RBFs as a function of two design variables: number of rows in the array and Tidal Energy Converters (TECs) per row. Surrogates describe array performance and environmental effects associated with hydrodynamic and morphological aspects of the multi inlet lagoon. After validation, surrogate models were used to formulate a constraint optimization model. Results evidence that the largest array size that satisfies performance and environmental constraints is made of 3 rows and 10 TECs per row.Eduardo González-Gorbeña has received funding for the OpTiCA project (http://msca-optica.eu/) from the Marie Skłodowska-Curie Actions of the European Union's H2020-MSCA-IF-EF-RI-2016 / GA#: 748747. The paper is a contribution to the SCORE pro-ject, funded by the Portuguese Foundation for Science and Technology (FCT–PTDC/AAG-TEC/1710/2014). André Pacheco was supported by the Portuguese Foun-dation for Science and Technology under the Portuguese Researchers’ Programme 2014 entitled “Exploring new concepts for extracting energy from tides” (IF/00286/2014/CP1234).info:eu-repo/semantics/publishedVersio

Automated adjoints of coupled PDE-ODE systems

Mathematical models that couple partial differential equations (PDEs) and spatially distributed ordinary differential equations (ODEs) arise in biology, medicine, chemistry, and many other fields. In this paper we discuss an extension to the FEniCS finite element software for expressing and efficiently solving such coupled systems. Given an ODE described using an augmentation of the Unified Form Language (UFL) and a discretization described by an arbitrary Butcher tableau, efficient code is automatically generated for the parallel solution of the ODE. The high-level description of the solution algorithm also facilitates the automatic derivation of the adjoint and tangent linearization of coupled PDE-ODE solvers. We demonstrate the capabilities of the approach on examples from cardiac electrophysiology and mitochondrial swelling

Reconstructing wave profiles from inundation data

This paper applies variational data assimilation to inundation problems governed by the shallow water equations with wetting and drying. The objective of the assimilation is to recover an unknown time-varying wave profile at an open ocean boundary from inundation observations. This problem is solved with derivative-based optimisation and an adjoint wetting and drying scheme to efficiently compute sensitivity information. The capabilities of this approach are demonstrated on an idealised sloping beach setup in which the profile of an incoming wave is reconstructed from wet/dry interface observations. The method is robust to noise in the observations if a regularisation term is added to the optimisation objective. Finally, the method is applied to a laboratory experiment of the Hokkaido-Nansei-Oki tsunami, where the wave profile is reconstructed with a relative L∞ error of less than 1%

High-level python abstractions for optimal checkpointing in inversion problems

Inversion and PDE-constrained optimization problems often rely on solving the adjoint problem to calculate the gradient of the objec- tive function. This requires storing large amounts of intermediate data, setting a limit to the largest problem that might be solved with a given amount of memory available. Checkpointing is an approach that can reduce the amount of memory required by redoing parts of the computation instead of storing intermediate results. The Revolve checkpointing algorithm o ers an optimal schedule that trades computational cost for smaller memory footprints. Integrat- ing Revolve into a modern python HPC code and combining it with code generation is not straightforward. We present an API that makes checkpointing accessible from a DSL-based code generation environment along with some initial performance gures with a focus on seismic applications

Monocytes of patients with familial hypercholesterolemia show alterations in cholesterol metabolism

<p>Abstract</p> <p>Background</p> <p>Elevated plasma cholesterol promotes the formation of atherosclerotic lesions in which monocyte-derived lipid-laden macrophages are frequently found. To analyze, if circulating monocytes already show increased lipid content and differences in lipoprotein metabolism, we compared monocytes from patients with Familial Hypercholesterolemia (FH) with those from healthy individuals.</p> <p>Methods</p> <p>Cholesterol and oxidized cholesterol metabolite serum levels of FH and of healthy, gender/age matched control subjects were measured by combined gas chromatography – mass spectroscopy. Monocytes from patients with FH and from healthy subjects were isolated by antibody-assisted density centrifugation. Gene expression profiles of isolated monocytes were measured using Affymetrix HG-U 133 Plus 2.0 microarrays. We compared monocyte gene expression profiles from FH patients with healthy controls using a Welch T-test with correction for multiple testing (p < 0.05; Benjamini Hochberg correction, False Discovery Rate = 0.05). The differential expression of FH associated genes was validated at the mRNA level by qRT-PCR and/or at the protein level by Western Blot or flow cytometry. Functional validation of monocyte scavenger receptor activities were done by binding assays and dose/time dependent uptake analysis using native and oxidized LDL.</p> <p>Results</p> <p>Using microarray analysis we found in FH patients a significant up-regulation of 1,617 genes and a down-regulation of 701 genes compared to monocytes from healthy individuals. These include genes of proteins that are involved in the uptake, biosynthesis, disposition, and cellular efflux of cholesterol. In addition, plasma from FH patients contains elevated amounts of sterols and oxysterols. An increased uptake of oxidized as well as of native LDL by FH monocytes combined with a down-regulation of NPC1 and ABCA1 explains the lipid accumulation observed in these cells.</p> <p>Conclusion</p> <p>Our data demonstrate that circulating FH monocytes show differences in cell physiology that may contribute to the early onset of atherosclerosis in this disease.</p

Identification of IGF1, SLC4A4, WWOX, and SFMBT1 as Hypertension Susceptibility Genes in Han Chinese with a Genome-Wide Gene-Based Association Study

Hypertension is a complex disorder with high prevalence rates all over the world. We conducted the first genome-wide gene-based association scan for hypertension in a Han Chinese population. By analyzing genome-wide single-nucleotide-polymorphism data of 400 matched pairs of young-onset hypertensive patients and normotensive controls genotyped with the Illumina HumanHap550-Duo BeadChip, 100 susceptibility genes for hypertension were identified and also validated with permutation tests. Seventeen of the 100 genes exhibited differential allelic and expression distributions between patient and control groups. These genes provided a good molecular signature for classifying hypertensive patients and normotensive controls. Among the 17 genes, IGF1, SLC4A4, WWOX, and SFMBT1 were not only identified by our gene-based association scan and gene expression analysis but were also replicated by a gene-based association analysis of the Hong Kong Hypertension Study. Moreover, cis-acting expression quantitative trait loci associated with the differentially expressed genes were found and linked to hypertension. IGF1, which encodes insulin-like growth factor 1, is associated with cardiovascular disorders, metabolic syndrome, decreased body weight/size, and changes of insulin levels in mice. SLC4A4, which encodes the electrogenic sodium bicarbonate cotransporter 1, is associated with decreased body weight/size and abnormal ion homeostasis in mice. WWOX, which encodes the WW domain-containing protein, is related to hypoglycemia and hyperphosphatemia. SFMBT1, which encodes the scm-like with four MBT domains protein 1, is a novel hypertension gene. GRB14, TMEM56 and KIAA1797 exhibited highly significant differential allelic and expressed distributions between hypertensive patients and normotensive controls. GRB14 was also found relevant to blood pressure in a previous genetic association study in East Asian populations. TMEM56 and KIAA1797 may be specific to Taiwanese populations, because they were not validated by the two replication studies. Identification of these genes enriches the collection of hypertension susceptibility genes, thereby shedding light on the etiology of hypertension in Han Chinese populations

Organization of multiprotein complexes at cell–cell junctions

The formation of stable cell–cell contacts is required for the generation of barrier-forming sheets of epithelial and endothelial cells. During various physiological processes like tissue development, wound healing or tumorigenesis, cellular junctions are reorganized to allow the release or the incorporation of individual cells. Cell–cell contact formation is regulated by multiprotein complexes which are localized at specific structures along the lateral cell junctions like the tight junctions and adherens junctions and which are targeted to these site through their association with cell adhesion molecules. Recent evidence indicates that several major protein complexes exist which have distinct functions during junction formation. However, this evidence also indicates that their composition is dynamic and subject to changes depending on the state of junction maturation. Thus, cell–cell contact formation and integrity is regulated by a complex network of protein complexes. Imbalancing this network by oncogenic proteins or pathogens results in barrier breakdown and eventually in cancer. Here, I will review the molecular organization of the major multiprotein complexes at junctions of epithelial cells and discuss their function in cell–cell contact formation and maintenance

Network Analyses Reveal Novel Aspects of ALS Pathogenesis

Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by selective loss of motor neurons, muscle atrophy and paralysis. Mutations in the human VAMP-associated protein B (hVAPB) cause a heterogeneous group of motor neuron diseases including ALS8. Despite extensive research, the molecular mechanisms underlying ALS pathogenesis remain largely unknown. Genetic screens for key interactors of hVAPB activity in the intact nervous system, however, represent a fundamental approach towards understanding the in vivo function of hVAPB and its role in ALS pathogenesis. Targeted expression of the disease-causing allele leads to neurodegeneration and progressive decline in motor performance when expressed in the adult Drosophila, eye or in its entire nervous system, respectively. By using these two phenotypic readouts, we carried out a systematic survey of the Drosophila genome to identify modifiers of hVAPB-induced neurotoxicity. Modifiers cluster in a diverse array of biological functions including processes and genes that have been previously linked to hVAPB function, such as proteolysis and vesicular trafficking. In addition to established mechanisms, the screen identified endocytic trafficking and genes controlling proliferation and apoptosis as potent modifiers of ALS8-mediated defects. Surprisingly, the list of modifiers was mostly enriched for proteins linked to lipid droplet biogenesis and dynamics. Computational analysis reveals that most modifiers can be linked into a complex network of interacting genes, and that the human genes homologous to the Drosophila modifiers can be assembled into an interacting network largely overlapping with that in flies. Identity markers of the endocytic process were also found to abnormally accumulate in ALS patients, further supporting the relevance of the fly data for human biology. Collectively, these results not only lead to a better understanding of hVAPB function but also point to potentially relevant targets for therapeutic intervention