In this report, the details of an investigation into the e ect of the low induction wind turbines on the Levelised Cost of Electricity (LCoE) in a 1GW o shore wind farm is outlined. The 10 MW INNWIND.EU conventional wind turbine and its low induction variant, the 10 MW AVATAR wind turbine, are considered in a variety of 10x10 layout configurations. The Annual Energy Production (AEP) and cost of electrical infrastructure were determined using two in-house ECN software tools, namely FarmFlow and EEFarm II. Combining this information with a generalised cost model, the LCoE from these layouts were determined. The optimum LCoE for the AVATAR wind farm was determined to be 92.15 e/MWh while for the INNWIND.EU wind farm it was 93.85 e/MWh. Although the low induction wind farm o ered a marginally lower LCoE, it should not be considered as definitive due to simple nature of the cost model used. The results do indicate that the AVATAR wind farms require less space to achieve this similar cost performace, with a higher optimal wind farm power density (WFPD) of 3.7 MW/km2 compared to 3 MW/km2 for the INNWIND.EU based wind farm.
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From PLoS website: In general, dietary antigens are tolerated by the gut associated immune system. Impairment of this so-called oral tolerance is a serious health risk. We have previously shown that activation of the ligand-dependent transcription factor aryl hydrocarbon receptor (AhR) by the environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects both oral tolerance and food allergy. In this study, we determine whether a common plant-derived, dietary AhR-ligand modulates oral tolerance as well. We therefore fed mice with indole-3-carbinole (I3C), an AhR ligand that is abundant in cruciferous plants. We show that several I3C metabolites were detectable in the serum after feeding, including the high-affinity ligand 3,3´-diindolylmethane (DIM). I3C feeding robustly induced the AhR-target gene CYP4501A1 in the intestine; I3C feeding also induced the aldh1 gene, whose product catalyzes the formation of retinoic acid (RA), an inducer of regulatory T cells. We then measured parameters indicating oral tolerance and severity of peanut-induced food allergy. In contrast to the tolerance-breaking effect of TCDD, feeding mice with chow containing 2 g/kg I3C lowered the serum anti-ovalbumin IgG1 response in an experimental oral tolerance protocol. Moreover, I3C feeding attenuated symptoms of peanut allergy. In conclusion, the dietary compound I3C can positively influence a vital immune function of the gut.
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