SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Bergstedt K) ;lar1:(gu)"

Sökning: WFRF:(Bergstedt K) > Göteborgs universitet

  • Resultat 1-2 av 2
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Deshpande, J, et al. (författare)
  • Ultrastructural changes in the hippocampal CA1 region following transient cerebral ischemia: evidence against programmed cell death.
  • 1992
  • Ingår i: Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. - 0014-4819. ; 88:1, s. 91-105
  • Tidskriftsartikel (refereegranskat)abstract
    • The ultrastructural changes in the pyramidal neurons of the CA1 region of the hippocampus were studied 6 h, 24 h, 48 h, and 72 h following a transient 10 min period of cerebral ischemia induced by common carotid occlusion combined with hypotension. The pyramidal neurons showed delayed neuronal death (DND), i.e. at 24 h and 48 h postischemia few structural alterations were noted in the light microscope, while at 72 h extensive neuronal degeneration was apparent. The most prominent early ultrastructural changes were polysome disaggregation, and the appearance of electron-dense fluffy dark material associated with tubular saccules. Mitochondria and nuclear elements appeared intact until frank neuronal degeneration. The dark material accumulated with extended periods of recirculation in soma and in the main trunks of proximal dendrites, often beneath the plasma membrane, less frequently in the distal dendrites and seldom in spines. Protein synthesis inhibitors (anisomycin, cycloheximide) and an RNA synthesis inhibitor (actinomycin D), administered by intrahippocampal injections or subcutaneously, did not mitigate neuronal damage. Therefore, DND is probably not apoptosis or a form of programmed cell death. We propose that the dark material accumulating in the postischemic period represents protein complexes, possibly aggregates of proteins or internalized plasma membrane fragments, which may disrupt vital cellular structure and functions, leading to cell death.
  •  
2.
  • Petersson, L. K., et al. (författare)
  • Changing land use and increasing abundance of deer cause natural regeneration failure of oaks: Six decades of landscape-scale evidence
  • 2019
  • Ingår i: Forest Ecology and Management. - : Elsevier BV. - 0378-1127 .- 1872-7042. ; 444, s. 299-307
  • Tidskriftsartikel (refereegranskat)abstract
    • Many tree species worldwide are suffering from slow or failed natural regeneration with dramatic consequences for biodiversity and ecosystem services. However, it is difficult to disentangle the complex effects of factors influencing regeneration processes on long-lived tree species at large scales. In this study, we use long-term data from the Swedish National Forest Inventory (1953-2015) combined with deer hunting data (1960-2015) to reveal experimentally-intractable processes impeding oak (Quercus spp.) regeneration in southern Sweden. Oak-dominated ecosystems are widespread in northern temperate regions, where oaks are foundation species with disproportionate importance for biodiversity and ecosystem functions. Our study reveals that during the last six decades, oak tree numbers and standing volume have continuously increased, while natural regeneration of oak declined steeply after the early 1980s. We connect this decline to denser and darker forests, combined with increased abundance of deer. Land use changes during the six decades, such as abandonment of traditional practices and large-scale introduction of forest management oriented towards high volume production, led to continuously denser forests and thereby reduced the oak regeneration niche. In addition, the impact of changed game management was evident. This was particularly clear from a natural experiment on Gotland, a large island free of deer until roe deer were introduced in the late 20th century, at which point oak regeneration began a steep decline. At the stand level, natural oak regeneration could be expected to mainly occur in pulses after disturbance events, followed by a period of low regeneration success as the cohort ages. However, at a landscape scale one would expect a mix of successional stages that would even out such demographic patterns. A prolonged period of low regeneration at a landscape scale will eventually lead to a large gap in the oak size distribution as was observed in this study. This could eventually hurt the many species dependent on old and large oak trees. Active management to restore the oak regeneration niche, i.e. forest habitats with more light and less browsing pressure, therefore seems essential. The latter includes developing strategies that manage both deer populations and their available food across landscapes. Our study is the first to link oak regeneration failure to long-term changes in land use and increased deer populations at a landscape scale in this region. Furthermore, our study show how historical data can clarify confounded processes impacting long-lived forest species.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-2 av 2

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