| 1. |
- Wang, F. M., et al.
(författare)
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Global blue carbon accumulation in tidal wetlands increases with climate change
- 2021
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Ingår i: National Science Review. - : Oxford University Press (OUP). - 2095-5138 .- 2053-714X. ; 8:9
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Tidskriftsartikel (refereegranskat)abstract
- Coastal tidal wetlands produce and accumulate significant amounts of organic carbon (C) that help to mitigate climate change. However, previous data limitations have prevented a robust evaluation of the global rates and mechanisms driving C accumulation. Here, we go beyond recent soil C stock estimates to reveal global tidal wetland C accumulation and predict changes under relative sea level rise, temperature and precipitation. We use data from literature study sites and our new observations spanning wide latitudinal gradients and 20 countries. Globally, tidal wetlands accumulate 53.65 (95%CI: 48.52-59.01) Tg C yr(-1), which is similar to 30% of the organic C buried on the ocean floor. Modeling based on current climatic drivers and under projected emissions scenarios revealed a net increase in the global C accumulation by 2100. This rapid increase is driven by sea level rise in tidal marshes, and higher temperature and precipitation in mangroves. Countries with large areas of coastal wetlands, like Indonesia and Mexico, are more susceptible to tidal wetland C losses under climate change, while regions such as Australia, Brazil, the USA and China will experience a significant C accumulation increase under all projected scenarios.
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| 2. |
- Dwibedi, Chinmay Kumar, et al.
(författare)
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Long-range dispersal moved Francisella tularensis into Western Europe from the East
- 2016
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Ingår i: Microbial Genomics. - : Microbiology Society. - 2057-5858. ; 2:12
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Tidskriftsartikel (refereegranskat)abstract
- For many infections transmitting to humans from reservoirs in nature, disease dispersal patterns over space and time are largely unknown. Here, a reversed genomics approach helped us understand disease dispersal and yielded insight into evolution and biological properties of Francisella tularensis, the bacterium causing tularemia. We whole-genome sequenced 67 strains and characterized by single-nucleotide polymorphism assays 138 strains, collected from individuals infected 1947-2012 across Western Europe. We used the data for phylogenetic, population genetic and geographical network analyses. All strains (n= 205) belonged to a monophyletic population of recent ancestry not found outside Western Europe. Most strains (n= 195) throughout the study area were assigned to a star-like phylogenetic pattern indicating that colonization of Western Europe occurred via clonal expansion. In the East of the study area, strains were more diverse, consistent with a founder population spreading from east to west. The relationship of genetic and geographic distance within the F. tularensis population was complex and indicated multiple long-distance dispersal events. Mutation rate estimates based on year of isolation indicated null rates; in outbreak hotspots only, there was a rate of 0.4 mutations/genome/year. Patterns of nucleotide substitution showed marked AT mutational bias suggestive of genetic drift. These results demonstrate that tularemia has moved from east to west in Europe and that F. tularensis has a biology characterized by long-range geographical dispersal events and mostly slow, but variable, replication rates. The results indicate that mutation-driven evolution, a resting survival phase, genetic drift and long-distance geographical dispersal events have interacted to generate genetic diversity within this species.
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| 3. |
- Losa, Marco, et al.
(författare)
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The ASC inflammasome adapter governs SAA-derived protein aggregation in inflammatory amyloidosis
- 2024
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Ingår i: EMBO Molecular Medicine. - : SPRINGERNATURE. - 1757-4676 .- 1757-4684.
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Tidskriftsartikel (refereegranskat)abstract
- Extracellularly released molecular inflammasome assemblies -ASC specks- cross-seed A beta amyloid in Alzheimer's disease. Here we show that ASC governs the extent of inflammation-induced amyloid A (AA) amyloidosis, a systemic disease caused by the aggregation and peripheral deposition of the acute-phase reactant serum amyloid A (SAA) in chronic inflammatory conditions. Using super-resolution microscopy, we found that ASC colocalized tightly with SAA in human AA amyloidosis. Recombinant ASC specks accelerated SAA fibril formation and mass spectrometry after limited proteolysis showed that ASC interacts with SAA via its pyrin domain (PYD). In a murine model of inflammatory AA amyloidosis, splenic amyloid load was conspicuously decreased in Pycard-/- mice which lack ASC. Treatment with anti-ASC(PYD) antibodies decreased amyloid loads in wild-type mice suffering from AA amyloidosis. The prevalence of natural anti-ASC IgG (-logEC(50 )>= 2) in 19,334 hospital patients was <0.01%, suggesting that anti-ASC antibody treatment modalities would not be confounded by natural autoimmunity. These findings expand the role played by ASC and IL-1 independent inflammasome employments to extraneural proteinopathies and suggest that anti-ASC immunotherapy may contribute to resolving such diseases.
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