Modelling the interaction of tidal range power systems for renewable energy conversion

Tidal range power plants (TPPs) have the potential to provide a reliable and long-term source of renewable power. The inherent predictability and operation flexibility of TPPs presents opportunities regarding the phasing of energy supply. However, TPPs can notably impact the surrounding coastal system. These benefits and challenges could be magnified in scenarios where a national energy system incorporates multiple schemes. This thesis investigates interactions between TPPs that are sited within the same geographical region, with regards to their combined energy supply phasing and impacts. Depth-averaged coastal models are applied in characterising the ambient tidal resource. Techniques for numerically parameterising the presence, operation and power output of TPPs are established. Particular focus is granted to methods for optimising operation characteristics. A model of Ramsey Sound is employed in investigating common numerical model configuration choices. An extended model domain, to include the entire west coast of Great Britain, is then configured. Benefits and challenges associated with how multiple TPPs interact are explored: - A system of TPPs sited across the Bristol Channel and Irish Sea regions is implemented in the model, with their designs based on existing proposals. Operation control schedules targeting continuous power generation are optimised. The notable tidal phase difference between the two regions permits cumulative continuous supply for approximately half of the year during periods around spring tides. Financial incentives associated with reliable, baseload supply are proposed. - Combinations of seven consistently designed TPPs in the Bristol Channel and Irish Sea are investigated regarding their hydro-environmental and energy resource impacts. Scheme design consistency provides a basis to focus solely on impacts associated with development sites, by minimising differences in impacts that occur from TPP design variations. Results indicate that the more constrained geometry of the Bristol Channel contributes to higher individual and cumulative impacts than TPP developments in the Irish Sea.Open Acces

Deletion of Fibroblast Growth Factor Receptor 2 from the Peri-Wolffian Duct Stroma Leads to Ureteric Induction Abnormalities and Vesicoureteral Reflux

Purpose: Pax3cre-mediated deletion of fibroblast growth factor receptor 2 (Fgfr2) broadly in renal and urinary tract mesenchyme led to ureteric bud (UB) induction defects and vesicoureteral reflux (VUR), although the mechanisms were unclear. Here, we investigated whether Fgfr2 acts specifically in peri-Wolffian duct stroma (ST) to regulate UB induction and development of VUR and the mechanisms of Fgfr2 activity. Methods: We conditionally deleted Fgfr2 in ST (Fgfr2 ST-/- ) using Tbx18cre mice. To look for ureteric bud induction defects in young embryos, we assessed length and apoptosis of common nephric ducts (CNDs). We performed 3D reconstructions and histological analyses of urinary tracts of embryos and postnatal mice and cystograms in postnatal mice to test for VUR. We performed in situ hybridization and real-time PCR in young embryos to determine mechanisms underlying UB induction defects. Results: We confirmed that Fgfr2 is expressed in ST and that Fgfr2 was efficiently deleted in this tissue in Fgfr2 ST-/- mice at embryonic day (E) 10.5. E11.5 Fgfr2 ST-/- mice had randomized UB induction sites with approximately 1/3 arising too high and 1/3 too low from the Wolffian duct; however, apoptosis was unaltered in E12.5 mutant CNDs. While ureters were histologically normal, E15.5 Fgfr2 ST-/- mice exhibit improper ureteral insertion sites into the bladder, consistent with the ureteric induction defects. While ureter and bladder histology appeared normal, postnatal day (P) 1 mutants had high rates of VUR versus controls (75% versus 3%, p = 0.001) and occasionally other defects including renal hypoplasia and duplex systems. P1 mutant mice also had improper ureteral bladder insertion sites and shortened intravesicular tunnel lengths that correlated with VUR. E10.5 Fgfr2 ST-/- mice had decreases in Bmp4 mRNA in stromal tissues, suggesting a mechanism underlying the ureteric induction and VUR phenotypes. Conclusion: Mutations in FGFR2 could possibly cause VUR in humans. © 2013 Walker et al

Modelling an energetic tidal strait:investigating implications of common numerical configuration choices

Representation of the marine environment is key for reliable coastal hydrodynamic models. This study investigates the implications of common depth-averaged model configuration choices in sufficiently characterising seabed geometry and roughness. In particular, applications requiring a high level of accuracy and/or exhibiting complex flow conditions may call for greater detail in marine environment representation than typically adopted in coastal models. Ramsey Sound, a macrotidal strait in Pembrokeshire, Wales, UK is considered as a case study. The site contains various steeply inclined bathymetric features, including a submerged pinnacle named Horse Rock and a rocky reef called “The Bitches”. The available energy in Ramsey Sound’s tidal currents has attracted attention from tidal energy developers. There is interest in accurately modelling the energetic hydrodynamics surrounding its pronounced bathymetry. The coastal flow solver Thetis is applied to simulate the flow conditions in Ramsey Sound. It is shown that notable prominent bathymetric features in the strait influence localised and, most importantly, regional hydrodynamic characteristics. “The Bitches” consistently accelerate flow in the strait while Horse Rock induces a notable wake structure and flow reversals. The model is calibrated against bed- and vessel-mounted Acoustic Doppler Current Profiler (ADCP) observations, by altering seabed roughness parameterisations. A spatially variable and locally scaled Manning coefficient based on diverse seabed classification observations is found to improve model performance in comparison to uniformly applied constants, the latter a more common approach. The local impact of altering the Manning coefficient configuration is found to be greatest during spring flood periods of high velocity currents. Meanwhile, the effect of coarsening the computational mesh around bathymetric features towards values more typically applied in coastal models is investigated. Results indicate severe misrepresentation of seabed geometry and subsequent wake hydrodynamics unless refined to a mesh element size that adequately represents Horse Rock and “The Bitches”

CB1 cannabinoid receptors promote oxidative stress and cell death in murine models of doxorubicin-induced cardiomyopathy and in human cardiomyocytes

Aims Here we investigated the mechanisms by which cardiovascular CB1 cannabinoid receptors may modulate the cardiac dysfunction, oxidative stress, and interrelated cell death pathways associated with acute/chronic cardiomyopathy induced by the widely used anti-tumour compound doxorubicin (DOX). Methods and results Both load-dependent and -independent indices of left-ventricular function were measured by the Millar pressure-volume conductance system. Mitogen-activated protein kinase (MAPK) activation, cell-death markers, and oxidative/nitrosative stress were measured by molecular biology/biochemical methods and flow cytometry. DOX induced left-ventricular dysfunction, oxidative/nitrosative stress coupled with impaired antioxidant defense, activation of MAPK (p38 and JNK), and cell death and/or fibrosis in hearts of wide-type mice (CB1+/+), and these effects were markedly attenuated in CB1 knockouts (CB1−/−). In human primary cardiomyocytes expressing CB1 receptors (demonstrated by RT-PCR, western immunoblot, and flow cytometry) DOX, likewise the CB1 receptor agonist HU210 and the endocannabinoid anandamide (AEA), induced MAPK activation and cell death. The DOX-induced MAPK activation and cell death were significantly enhanced when DOX was co-administered with CB1 agonists AEA or HU210. Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX ± AEA/HU210 were largely attenuated by either CB1 antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs. Furthermore, AEA or HU210 in primary human cardiomyocytes triggered increased reactive oxygen species generation. Conclusion CB1 activation in cardiomyocytes may amplify the reactive oxygen/nitrogen species-MAPK activation-cell death pathway in pathological conditions when the endocannabinoid synthetic or metabolic pathways are dysregulated by excessive inflammation and/or oxidative/nitrosative stress, which may contribute to the pathophysiology of various cardiovascular disease

Resource-Bound Quantification for Graph Transformation

Graph transformation has been used to model concurrent systems in software engineering, as well as in biochemistry and life sciences. The application of a transformation rule can be characterised algebraically as construction of a double-pushout (DPO) diagram in the category of graphs. We show how intuitionistic linear logic can be extended with resource-bound quantification, allowing for an implicit handling of the DPO conditions, and how resource logic can be used to reason about graph transformation systems

Evolutionary biology and anthropology suggest biome reconstitution as a necessary approach toward dealing with immune disorders

Industrialized society currently faces a wide range of non-infectious, immune-related pandemics. These pandemics include a variety of autoimmune, inflammatory and allergic diseases that are often associated with common environmental triggers and with genetic predisposition, but that do not occur in developing societies. In this review, we briefly present the idea that these pandemics are due to a limited number of evolutionary mismatches, the most damaging being ‘biome depletion’. This particular mismatch involves the loss of species from the ecosystem of the human body, the human biome, many of which have traditionally been classified as parasites, although some may actually be commensal or even mutualistic. This view, evolved from the ‘hygiene hypothesis’, encompasses a broad ecological and evolutionary perspective that considers host-symbiont relations as plastic, changing through ecological space and evolutionary time. Fortunately, this perspective provides a blueprint, termed 'biome reconstitution', for disease treatment and especially for disease prevention. Biome reconstitution includes the controlled and population-wide reintroduction (i.e. domestication) of selected species that have been all but eradicated from the human biome in industrialized society and holds great promise for the elimination of pandemics of allergic, inflammatory and autoimmune diseases