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1.
  • Cameron, Lachlan, et al. (författare)
  • NAMAs and INDCs : Interactions and opportunities
  • 2015
  • Rapport (övrigt vetenskapligt/konstnärligt)abstract
    • Countries representing more than 90 percent of global greenhouse gas emissions and population have submitted intendednationally determined contributions (INDCs) in anticipation of the 21st COP in Paris. In parallel, developing countries are designing at least 152 nationally appropriate mitigation actions (NAMAs) and 13 have secured implementation funding. Connecting these two concepts, more than a third of developing countries communicate a role for NAMAs in their INDCs. It is therefore vital to understand the potential role of NAMAs (here understood as specific actions) with respect to INDCs (which are often broader targets) and vice versa. This paper explores the links between NAMAs and INDCs with regard to various elements central to their implementation, including: access to finance; stakeholder engagement; sustainable development impacts; measurement, reporting and verification (MRV); and institutional frameworks.To avoid delaying mitigation action any further, it is important to keep momentum behind NAMAs. They represent one of the few tools at our disposal for countries to undertake mitigation actions, be recognised for these efforts, and mobilise climate finance and investment. The skills and learning on NAMA development can be seen more fundamentally as capacity for the design of bottom-up actions. Attention should be paid now to ensure that this capacity is maintained in the future. To do this, continued attention must be paid to NAMAs in Paris, as a key implementation tool for INDCs and, therefore, a key element of the success of a new global climate agreement.
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2.
  • Nicolas, Aude, et al. (författare)
  • Genome-wide Analyses Identify KIF5A as a Novel ALS Gene
  • 2018
  • Ingår i: Neuron. - : Cell Press. - 0896-6273 .- 1097-4199. ; 97:6, s. 1268-1283.e6
  • Tidskriftsartikel (refereegranskat)abstract
    • To identify novel genes associated with ALS, we undertook two lines of investigation. We carried out a genome-wide association study comparing 20,806 ALS cases and 59,804 controls. Independently, we performed a rare variant burden analysis comparing 1,138 index familial ALS cases and 19,494 controls. Through both approaches, we identified kinesin family member 5A (KIF5A) as a novel gene associated with ALS. Interestingly, mutations predominantly in the N-terminal motor domain of KIF5A are causative for two neurodegenerative diseases: hereditary spastic paraplegia (SPG10) and Charcot-Marie-Tooth type 2 (CMT2). In contrast, ALS-associated mutations are primarily located at the C-terminal cargo-binding tail domain and patients harboring loss-of-function mutations displayed an extended survival relative to typical ALS cases. Taken together, these results broaden the phenotype spectrum resulting from mutations in KIF5A and strengthen the role of cytoskeletal defects in the pathogenesis of ALS.
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