SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Dankel D. J.) "

Sökning: WFRF:(Dankel D. J.)

  • Resultat 1-4 av 4
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Clay, P. M., et al. (författare)
  • Implementation of integrated ecosystem assessments in the International Council for the Exploration of the Sea-conceptualizations, practice, and progress
  • 2023
  • Ingår i: Ices Journal of Marine Science. - 1054-3139. ; 80:5, s. 1516-1528
  • Tidskriftsartikel (refereegranskat)abstract
    • With increasing activities of multiple sectors in marine spaces, management of marine social-ecological systems requires more holistic approaches. Adopting such an approach, however, presents difficult institutional and disciplinary challenges. Here, we use the International Council for the Exploration of the Sea (ICES) as a case study on the implementation of ecosystem-based management (EBM) and integrated ecosystem assessments (IEAs). ICES includes EBM and IEAs in its Science Priorities and established IEA Working Groups (WGs) to carry out regional IEAs. But to what degree does this IEA WG work follow best practices? We examine policy documents, academic literature, and interview data from chairs of all IEA WGs. Results indicate mixed success. All groups acknowledge the holistic goals of IEA, and many use the IEA model as laid out by Levin et al. However, we found a significant variation in the degree to which the full model is applied. We identified two primary areas for improvement: (1) integration of social and economic issues and (2) involvement of stakeholders. We offer examples of how WGs have been making progress towards full IEAs, discuss how ICES can further support this transition, and suggest lessons with respect to the adoption of EBM and IEAs more broadly.
  •  
2.
  • Jersin, R. A., et al. (författare)
  • Role of the Neutral Amino Acid Transporter SLC7A10 in Adipocyte Lipid Storage, Obesity, and Insulin Resistance
  • 2021
  • Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 70:3, s. 680-695
  • Tidskriftsartikel (refereegranskat)abstract
    • Elucidation of mechanisms that govern lipid storage, oxidative stress, and insulin resistance may lead to improved therapeutic options for type 2 diabetes and other obesity-related diseases. Here, we find that adipose expression of the small neutral amino acid transporter SLC7A10, also known as alanine-serine-cysteine transporter-1 (ASC-1), shows strong inverse correlates with visceral adiposity, insulin resistance, and adipocyte hypertrophy across multiple cohorts. Concordantly, loss of Slc7a10 function in zebrafish in vivo accelerates diet-induced body weight gain and adipocyte enlargement. Mechanistically, SLC7A10 inhibition in human and murine adipocytes decreases adipocyte serine uptake and total glutathione levels and promotes reactive oxygen species (ROS) generation. Conversely, SLC7A10 overexpression decreases ROS generation and increases mitochondrial respiratory capacity. RNA sequencing revealed consistent changes in gene expression between human adipocytes and zebrafish visceral adipose tissue following loss of SLC7A10, e.g., upregulation of SCD (lipid storage) and downregulation of CPT1A (lipid oxidation). Interestingly, ROS scavenger reduced lipid accumulation and attenuated the lipid-storing effect of SLC7A10 inhibition. These data uncover adipocyte SLC7A10 as a novel important regulator of adipocyte resilience to nutrient and oxidative stress, in part by enhancing glutathione levels and mitochondrial respiration, conducive to decreased ROS generation, lipid accumulation, adipocyte hypertrophy, insulin resistance, and type 2 diabetes.
  •  
3.
  • Claussnitzer, M., et al. (författare)
  • FTO Obesity Variant Circuitry and Adipocyte Browning in Humans
  • 2015
  • Ingår i: New England Journal of Medicine. - 0028-4793. ; 373:10, s. 895-907
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND Genomewide association studies can be used to identify disease-relevant genomic regions, but interpretation of the data is challenging. The FTO region harbors the strongest genetic association with obesity, yet the mechanistic basis of this association remains elusive. We examined epigenomic data, allelic activity, motif conservation, regulator expression, and gene coexpression patterns, with the aim of dissecting the regulatory circuitry and mechanistic basis of the association between the FTO region and obesity. We validated our predictions with the use of directed perturbations in samples from patients and from mice and with endogenous CRISPR-Cas9 genome editing in samples from patients. Our data indicate that the FTO allele associated with obesity represses mitochondrial thermogenesis in adipocyte precursor cells in a tissue-autonomous manner. The rs1421085 T-to-C single-nucleotide variant disrupts a conserved motif for the ARID5B repressor, which leads to derepression of a potent preadipocyte enhancer and a doubling of IRX3 and IRX5 expression during early adipocyte differentiation. This results in a cell-autonomous developmental shift from energy-dissipating beige (brite) adipocytes to energy-storing white adipocytes, with a reduction in mitochondrial thermogenesis by a factor of 5, as well as an increase in lipid storage. Inhibition of Irx3 in adipose tissue in mice reduced body weight and increased energy dissipation without a change in physical activity or appetite. Knockdown of IRX3 or IRX5 in primary adipocytes from participants with the risk allele restored thermogenesis, increasing it by a factor of 7, and overexpression of these genes had the opposite effect in adipocytes from nonrisk-allele carriers. Repair of the ARID5B motif by CRISPR-Cas9 editing of rs1421085 in primary adipocytes from a patient with the risk allele restored IRX3 and IRX5 repression, activated browning expression programs, and restored thermogenesis, increasing it by a factor of 7. Our results point to a pathway for adipocyte thermogenesis regulation involving ARID5B, rs1421085, IRX3, and IRX5, which, when manipulated, had pronounced pro-obesity and anti-obesity effects. (Funded by the German Research Center for Environmental Health and others.)
  •  
4.
  • Stenseth, N. C., et al. (författare)
  • Attuning to a changing ocean
  • 2020
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 117:34, s. 20363-20371
  • Tidskriftsartikel (refereegranskat)abstract
    • The ocean is a lifeline for human existence, but current practices risk severely undermining ocean sustainability. Present and future social-ecological challenges necessitate the maintenance and development of knowledge and action by stimulating collaboration among scientists and between science, policy, and practice. Here we explore not only how such collaborations have developed in the Nordic countries and adjacent seas but also how knowledge from these regions contributes to an understanding of how to obtain a sustainable ocean. Our collective experience may be summarized in three points: 1) In the absence of long-term observations, decision-making is subject to high risk arising from natural variability; 2) in the absence of established scientific organizations, advice to stakeholders often relies on a few advisors, making them prone to biased perceptions; and 3) in the absence of trust between policy makers and the science community, attuning to a changing ocean will be subject to arbitrary decision-making with unforeseen and negative ramifications. Underpinning these observations, we show that collaboration across scientific disciplines and stakeholders and between nations is a necessary condition for appropriate actions.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-4 av 4

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy