Global Carbon Budget: Ocean carbon sink.

CO2 emissions from human activities, the main contributor to global climate change, are set to rise again in 2014 reaching 40 billion tonnes CO2 The natural carbon ‘sinks’ on land and in the ocean absorb on average 55% of the total CO2 emissions, thus slowing the rate of global climate change Increasing CO2 in the oceans is causing ocean acidificatio

Integration von Wasserstoffenergiespeichern - Nutzen für Stromnetze?

Der Beitrag gibt einen Überblick über die Anforderungen an eine netzorientierte Integration von Wasserstoffenergiespeichern und -komponenten in das Stromnetz. Vor dem Hintergrund einer allgemeinen Definition von Wasserstoffenergiespeichern und möglichen Komponenten werden der zukünftige Wasserstoffbedarf, Elektrolyseleistung und Speicherkapazität vorgestellt, der in verschiedenen aktuellen Gesamtsystemstudien mit Ziel der Klimaneutralität im Jahr 2045 bestimmt wurde. Durch den angestrebten beschleunigten Ausbau erneuerbarer Erzeugungskapazität ergibt sich weiterer Netzausbaubedarf zusätzlich zu dem Ausbaubedarf durch bisherige Netzengpässen. Elektrolyseanlagen könnten also bereits im heutigen Stromnetz zur verbesserten Integration von EE-Anlagen eingesetzt werden. Derzeit bestehen allerdings kaum Anreize für netzdienliche Allokation und Betrieb von Elektrolyse bzw. Power-to-Gas Anlagen. Als Praxisbeispiele werden zwei mögliche Standorte für Wasserstoffanlagen aus zwei aktuellen Forschungsprojekten HyCavMobil und dem Innovationslabor Wasserstoffregion Nordwest (H2-ReNoWe) vorgestellt. Anhand von Stromnetzmodellen wird die Integration von Elektrolyseanlagen an diesen Standorten im derzeitigen Hoch- bzw. Höchstspannungsnetz untersucht

Review of Hydrogen Production Techniques from Water Using Renewable Energy Sources and Its Storage in Salt Caverns

Hydrogen is becoming an increasingly important energy carrier in sector integration for fuel cell transportation, heat and electricity. Underground salt caverns are one of the most promising ways to store the hydrogen obtained from water electrolysis using power generation from renewable energy sources (RES). At the same time, the production of hydrogen can be used to avoid energy curtailments during times of low electricity demand or low prices. The stored hydrogen can also be used during times of high energy demand for power generation, e.g., with fuel cells, to cover the fluctuations and shortages caused by low RES generation. This article presents an overview of the techniques that were used and proposed for using excess energy from RES for hydrogen production from water and its storage techniques, especially in underground salt caverns, for the aforementioned purpose, and its feasibility. This paper compares and summarizes the competing technologies based on the current state-of-the-art, identifies some of the difficulties in hydrogen production and storage, and discusses which technology is the most promising. The related analysis compares cost and techno-economic feasibility with regard to hydrogen production and storage systems. The paper also identifies the potential, technical challenges and the limitations associated with hydrogen integration into the power grid

Identification of a non-canonical chemokine-receptor pathway suppressing regulatory T cells to drive atherosclerosis

CCL17 is produced by conventional dendritic cells, signals through CCR4 on regulatory T (Treg) cells and drives atherosclerosis by suppressing Treg functions through yet undefined mechanisms. Here we show that conventional dendritic cells from CCL17-deficient mice display a pro-tolerogenic phenotype and transcriptome that is not phenocopied in mice lacking its cognate receptor CCR4. In the plasma of CCL17-deficient mice, CCL3 was the only decreased cytokine/chemokine. We found that CCL17 signaled through CCR8 as an alternate high-affinity receptor, which induced CCL3 expression and suppressed Treg functions in the absence of CCR4. Genetic ablation of CCL3 and CCR8 in CD4+ T cells reduced CCL3 secretion, boosted FoxP3+ Treg numbers and limited atherosclerosis. Conversely, CCL3 administration exacerbated atherosclerosis and restrained Treg differentiation. In symptomatic versus asymptomatic human carotid atheroma, CCL3 expression was increased, whereas FoxP3 expression was reduced. Together, we identified a non-canonical chemokine pathway whereby CCL17 interacts with CCR8 to yield a CCL3-dependent suppression of atheroprotective Treg cells. Doring, van der Vorst, Yan, Neideck et al. present a non-canonical chemokine pathway involving CCL17 signaling through CCR8, which induces CCL3 expression independent of CCR4 and suppresses the functions of atheroprotective Treg cells

Genome-wide meta-analysis of 241,258 adults accounting for smoking behaviour identifies novel loci for obesity traits

Few genome-wide association studies (GWAS) account for environmental exposures, like smoking, potentially impacting the overall trait variance when investigating the genetic contribution to obesity-related traits. Here, we use GWAS data from 51,080 current smokers and 190,178 nonsmokers (87% European descent) to identify loci influencing BMI and central adiposity, measured as waist circumference and waist-to-hip ratio both adjusted for BMI. We identify 23 novel genetic loci, and 9 loci with convincing evidence of gene-smoking interaction (GxSMK) on obesity-related traits. We show consistent direction of effect for all identified loci and significance for 18 novel and for 5 interaction loci in an independent study sample. These loci highlight novel biological functions, including response to oxidative stress, addictive behaviour, and regulatory functions emphasizing the importance of accounting for environment in genetic analyses. Our results suggest that tobacco smoking may alter the genetic susceptibility to overall adiposity and body fat distribution.Peer reviewe

Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci.

We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease