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Sökning: WFRF:(Neilson E) > Lunds universitet

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1.
  • Jackson, R B, et al. (författare)
  • Belowground consequences of vegetation change and their treatment in models
  • 2000
  • Ingår i: Ecological Applications. - 1051-0761. ; 10:2, s. 470-483
  • Tidskriftsartikel (refereegranskat)abstract
    • The extent and consequences of global land-cover and land-use change are increasingly apparent. One consequence not so apparent is the altered structure of plants belowground. This paper examines such belowground changes, emphasizing the interaction of altered root distributions with other factors and their treatment in models. Shifts of woody and herbaceous vegetation with deforestation, afforestation, and woody plant encroachment typically alter the depth and distribution of plant rests, influencing soil nutrients, the water balance, and net primary productivity (NPP). For example, our analysis of global soil data sets shows that the major plant nutrients C, N, P, and K are more shallowly distributed than are Ca, Mg, and Na, but patterns for each element vary with the dominant vegetation type. After controlling for climate, soil C and N are distributed more deeply in arid shrublands than in arid grasslands, and subhumid forests have shallower nutrient distributions than do subhumid grasslands. Consequently, changes in vegetation may influence the distribution of soil carbon and nutrients over time (perhaps decades to centuries). Shifts in the water balance are typically much more rapid. Catchment studies indicate that the water yield decreases 25-40 mm for each 10% increase in tree cover, and increases in transpiration of water taken up by deep roots may account for as much as 50% of observed responses. Because models are increasingly important for predicting the consequences of vegetation change, we discuss the treatment of belowground processes and how different treatments affect model outputs. Whether models are parameterized by biome or plant life form (or neither), use single or multiple soil layers, or include N and water limitation will all affect predicted outcomes. Acknowledging and understanding such differences should help constrain predictions of vegetation change.
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2.
  • Jiang, Mingkai, et al. (författare)
  • The fate of carbon in a mature forest under carbon dioxide enrichment
  • 2020
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 580:7802, s. 227-231
  • Tidskriftsartikel (refereegranskat)abstract
    • Atmospheric carbon dioxide enrichment (eCO2) can enhance plant carbon uptake and growth1–5, thereby providing an important negative feedback to climate change by slowing the rate of increase of the atmospheric CO2 concentration6. Although evidence gathered from young aggrading forests has generally indicated a strong CO2 fertilization effect on biomass growth3–5, it is unclear whether mature forests respond to eCO2 in a similar way. In mature trees and forest stands7–10, photosynthetic uptake has been found to increase under eCO2 without any apparent accompanying growth response, leaving the fate of additional carbon fixed under eCO2 unclear4,5,7–11. Here using data from the first ecosystem-scale Free-Air CO2 Enrichment (FACE) experiment in a mature forest, we constructed a comprehensive ecosystem carbon budget to track the fate of carbon as the forest responded to four years of eCO2 exposure. We show that, although the eCO2 treatment of +150 parts per million (+38 per cent) above ambient levels induced a 12 per cent (+247 grams of carbon per square metre per year) increase in carbon uptake through gross primary production, this additional carbon uptake did not lead to increased carbon sequestration at the ecosystem level. Instead, the majority of the extra carbon was emitted back into the atmosphere via several respiratory fluxes, with increased soil respiration alone accounting for half of the total uptake surplus. Our results call into question the predominant thinking that the capacity of forests to act as carbon sinks will be generally enhanced under eCO2, and challenge the efficacy of climate mitigation strategies that rely on ubiquitous CO2 fertilization as a driver of increased carbon sinks in global forests.
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3.
  • Perez-Soriano, Alexandra, et al. (författare)
  • PBB3 Imaging in Parkinsonian disorders: Evidence for binding to abnormally aggregated proteins in addition to tau proteins
  • 2017
  • Ingår i: Movement Disorders. - : Wiley. - 1531-8257 .- 0885-3185. ; 32:Suppl 2, s. 585-587
  • Konferensbidrag (refereegranskat)abstract
    • Objective: To study selective regional binding for tau pathology in vivo, using PET with [11C]PBB3 ([11C]methylamino pyridin-3-yl buta-1,3-dienyl benzo[d]thiazol-6-ol) in tauopathies, and in conditions not typically associated with tauopathy. Background: Tau imaging is a promising tool to study the link between tau and neurodegeneration. The specificity of tracers in vivo however remains uncertain, and off target binding is frequently present, limiting its use in parkinsonian disorders. Methods: Dynamic PET scans were obtained for 70 min after the bolus injection of [11C]PBB3 (mean dose 518.97MBq) in five PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype,3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 7 healthy controls of similar age. The occipital cortex was used as reference region for the PSP , the DCTN1 mutation and the MSA subjects. The cerebellar white matter was used as a reference region for the SNCA duplication carriers. Tissue reference Logan analysis was applied to each region of interest (ROI) using the appropriate reference region. Results: In PSP subjects, the highest retention of [11C]PBB3 was observed in putamen, midbrain, globus pallidus and substantia nigra. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. The DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and globus pallidus. In SNCA duplication carriers there was a significant increase of [11C] PBB3 binding compared to controls in globus pallidus, putamen, thalamus, ventral striatum, substantia nigra, and pedunculopontine nucleus. The MSA case showed increased binding in comparison to the control group in frontal lobe, globus pallidus, midbrain, parietal lobe, putamen, temporal lobe, substantia nigra, thalamus and ventral striatum. Conclusions: All PSP patients showed increased retention of the tracer in the basal ganglia, as clinically expected. However, binding was also present in asymptomatic SNCA duplication carriers as well as the subject with MSA, which are not typically associated with pathological tau deposition. This suggests the possibility that [11C]PBB3 binds to alpha-synuclein or other proteins involved in neurodegeneration.
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4.
  • Perez-Soriano, Alexandra, et al. (författare)
  • PBB3 imaging in Parkinsonian disorders : Evidence for binding to tau and other proteins
  • 2017
  • Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 32:7, s. 1016-1024
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND OBJECTIVES: To study selective regional binding for tau pathology in vivo, using PET with [(11) C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy.METHODS: Dynamic PET scans were obtained for 70 minutes after the bolus injection of [(11) C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region.RESULTS: In comparison to the control group, PSP subjects showed specific uptake of [(11) C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [(11) C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum.CONCLUSIONS: All PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [(11) C]PBB3 binds to alpha-synuclein. © 2017 International Parkinson and Movement Disorder Society.
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