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31.
32.
Gavin M. Jones John J. Keane R. J. Gutiérrez M. Zachariah Peery 《Diversity & distributions》2018,24(3):341-351
Aim
Global declines in large old trees from selective logging have degraded old‐forest ecosystems, which could lead to delayed declines or losses of old‐forest‐associated wildlife populations (i.e., extinction debt). We applied the declining population paradigm and explored potential evidence for extinction debt in an old‐forest dependent species across landscapes with different histories of large tree logging.Location
Montane forests of the Sierra Nevada, California, USA.Methods
We tested hypotheses about the influence of forest structure on territory extinction dynamics of the spotted owl (Strix occidentalis) using detection/non‐detection data from 1993 to 2011 across two land tenures: national forests, which experienced extensive large tree logging over the past century, and national parks, which did not.Results
Large tree/high canopy cover forest was the best predictor of extinction rates and explained 26%–77% of model deviance. Owl territories with more large tree/high canopy cover forest had lower extinction rates, and this forest type was ~4 times more prevalent within owl territories in national parks ( = 19% of territory) than national forests ( = 4% of territory). As such, predicted extinction probability for an average owl territory was ~2.5 times greater in national forests than national parks, where occupancy was declining () and stable (), respectively. Large tree/high canopy cover forest remained consistently low, but did not decline, during the study period on national forests while owl declines were ongoing—an observation consistent with an extinction debt.Main conclusions
In identifying a linkage between large trees and spotted owl dynamics at a regional scale, we provide evidence suggesting past logging of large old trees may have contributed to contemporary declines in an old‐forest species. Strengthening protections for remaining large old trees and promoting their recruitment in the future will be critical for biodiversity conservation in the world's forests.33.
Role of lipid peroxidation in the inhibition of mononuclear cell proliferation by normal lipoproteins 总被引:1,自引:0,他引:1
Stimulated peripheral blood mononuclear cells (PBMC) can oxidize normal lipoproteins, and sufficiently oxidized lipoproteins are cytotoxic. However, the role of lipid peroxidation in the inhibition of mitogen-stimulated PBMC proliferation by physiologic concentrations of normal lipoproteins is unclear. In the present investigation, normal low density lipoprotein (LDL) and very low density lipoprotein (VLDL) suppressed [3H]thymidine incorporation and gamma interferon production in concanavalin A-stimulated PBMC without causing cell death. This suppression was accompanied by parallel increases in lipid peroxidation products measured as thiobarbituric acid reactive substances (TBARS). In contrast, high density lipoprotein (HDL) failed to inhibit PBMC and TBARS remains low. Differences between the PBMC suppression from LDL, VLDL, and HDL were best accounted for by normalizing the lipoprotein concentrations by their total lipid content. Moreover, the antioxidants superoxide dismutase and butylated hydroxytoluene each substantially ameliorated the inhibition of PBMC caused by LDL, and reduced the levels of lipid peroxidation products that were generated. Altogether, these results suggest that reactive oxygen species generated by stimulated PMBC may cause oxidative alterations of normal lipoproteins that may, in turn, account for much of the previously reported inhibition of PBMC by normal lipoproteins. 相似文献
34.
D Taruscio C Morciano P Laricchiuta P Mincarone F Palazzo CG Leo S Sabina R Guarino J Auld T Sejersen D Gavhed K Ritchie M Hilton-Boon J Manson PG Kanavos D Tordrup V Tzouma Y Le Cam J Senecat G Filippini S Minozzi C Del Giovane H Schünemann JJ Meerpohl B Prediger L Schell R Stefanov G Iskrov T Miteva-Katrandzhieva P Serrano-Aguilar L Perestelo-Perez MM Trujillo-Martín J Pérez-Ramos A Rivero-Santana A Brand H van Kranen K Bushby A Atalaia J Ramet L Siderius M Posada I Abaitua-Borda V Alonso Ferreira M Hens-Pérez FJ Manzanares 《Orphanet journal of rare diseases》2014,9(Z1):O14
35.
Evaluating future success of whitebark pine ecosystem restoration under climate change using simulation modeling 下载免费PDF全文
Robert E. Keane Lisa M. Holsinger Mary F. Mahalovich Diana F. Tomback 《Restoration Ecology》2017,25(2):220-233
Major declines of whitebark pine forests throughout western North America from the combined effects of mountain pine beetle (Dendroctonus ponderosae) outbreaks, fire exclusion policies, and the exotic disease white pine blister rust (WPBR) have spurred many restoration actions. However, projected future warming and drying may further exacerbate the species' decline and possibly compromise long‐term success of today's restoration activities. We evaluated successes of restoration treatments under future climate using a comprehensive landscape simulation experiment. The spatially explicit, ecological process model FireBGCv2 was used to simulate whitebark pine populations on two U.S. Northern Rocky Mountain landscapes over 95 years under two climate, three restoration, and two fire management scenarios. Major findings were that (1) whitebark pine can remain on some high mountain landscapes in a future climate albeit at lower basal areas (50% decrease), (2) restoration efforts, such as thinning and prescribed burning, are vital to ensure future whitebark pine forests, and (3) climate change impacts on whitebark pine vary by local setting. Whitebark pine restoration efforts will mostly be successful in the future but only if future populations are somewhat resistant to WPBR. Results were used to develop general guidelines that address climate change impacts for planning, designing, implementing, and evaluating fine‐scale restoration activities. 相似文献
36.
Andrew Lucas Michaela Lucas Anette Strhyn Niamh M. Keane Elizabeth McKinnon Rebecca Pavlos Ellen M. Moran Viola Meyer-Pannwitt Silvana Gaudieri Lloyd D’Orsogna Spyros Kalams David A. Ostrov S?ren Buus Bjoern Peters Simon Mallal Elizabeth Phillips 《PloS one》2015,10(2)
BackgroundFifty-five percent of individuals with HLA-B*57:01 exposed to the antiretroviral drug abacavir develop a hypersensitivity reaction (HSR) that has been attributed to naïve T-cell responses to neo-antigen generated by the drug. Immunologically confirmed abacavir HSR can manifest clinically in less than 48 hours following first exposure suggesting that, at least in some cases, abacavir HSR is due to re-stimulation of a pre-existing memory T-cell population rather than priming of a high frequency naïve T-cell population.MethodsTo determine whether a pre-existing abacavir reactive memory T-cell population contributes to early abacavir HSR symptoms, we studied the abacavir specific naïve or memory T-cell response using HLA-B*57:01 positive HSR patients or healthy controls using ELISpot assay, intra-cellular cytokine staining and tetramer labelling.ResultsAbacavir reactive CD8+ T-cell responses were detected in vitro in one hundred percent of abacavir unexposed HLA-B*57:01 positive healthy donors. Abacavir-specific CD8+ T cells from such donors can be expanded from sorted memory, and sorted naïve, CD8+ T cells without need for autologous CD4+ T cells.ConclusionsWe propose that these pre-existing abacavir-reactive memory CD8+ T-cell responses must have been primed by earlier exposure to another foreign antigen and that these T cells cross-react with an abacavir-HLA-B*57:01-endogenous peptide ligand complex, in keeping with the model of heterologous immunity proposed in transplant rejection. 相似文献
37.
38.
Common dandelions (Taraxacum officinale Weber, sensu lato; Asteraceae) introduced to North America form an assemblage of asexual (agamospermous), clonal lineages derived from Eurasian mixed sexual and asexual populations. We investigated whether selection for more pollution tolerant clonal lineages occurs at polluted sites and selection for more pollution intolerant lineages occurs at unpolluted sites. We tested the above hypothesis by performing reciprocal greenhouse productivity experiments in which unique dandelion clones (12 clones, identified by DNA fingerprinting, from each site type) sampled from two unpolluted and two polluted (moderately enhanced Cu, Pb and Zn soil concentrations) sites were grown pairwise in both unpolluted (nutrient solution only) and polluted (nutrient solution + Cu, Pb and Zn) media (n?=?48 paired tests for each media type). Dandelion clones from polluted sites produced fewer and smaller leaves, shorter roots and smaller root diameters, reduced shoot and root dry weights, and reduced total biomass compared to clones from unpolluted sites when clones were grown in unpolluted-media (P?≤?0.05). In contrast, clones taken from unpolluted sites were shown to produce significantly fewer and shorter leaves, shorter roots and smaller root diameters, reduced shoot and root dry weights, reduced total biomass, a reduced shoot : root biomass ratio, and have much lower survival compared to clones from polluted sites when both were grown in polluted-media (P?≤?0.05). These results reveal that there was increased selection against unpolluted-site clonal lineages in polluted-media and against polluted-site clonal lineages in unpolluted-media. Across all treatments, clones from unpolluted sites growing in unpolluted-media had the highest proximate measures of fitness. Overall, these findings provide insight into the relationships among anthropogenic environmental contamination and the consequent effects of selective forces acting on dandelion clones and their population genetic architecture. 相似文献
39.
Ilaria Guerini Nicola J Geisler Hengyao Niu Mareike Herzog Israel Salguero Bernardo Ochoa‐Montaño Emmanuelle Viré Patrick Sung David J Adams Thomas M Keane Stephen P Jackson 《The EMBO journal》2015,34(11):1509-1522
DNA double-strand break (DSB) repair by homologous recombination (HR) requires 3′ single-stranded DNA (ssDNA) generation by 5′ DNA-end resection. During meiosis, yeast Sae2 cooperates with the nuclease Mre11 to remove covalently bound Spo11 from DSB termini, allowing resection and HR to ensue. Mitotic roles of Sae2 and Mre11 nuclease have remained enigmatic, however, since cells lacking these display modest resection defects but marked DNA damage hypersensitivities. By combining classic genetic suppressor screening with high-throughput DNA sequencing, we identify Mre11 mutations that strongly suppress DNA damage sensitivities of sae2Δ cells. By assessing the impacts of these mutations at the cellular, biochemical and structural levels, we propose that, in addition to promoting resection, a crucial role for Sae2 and Mre11 nuclease activity in mitotic DSB repair is to facilitate the removal of Mre11 from ssDNA associated with DSB ends. Thus, without Sae2 or Mre11 nuclease activity, Mre11 bound to partly processed DSBs impairs strand invasion and HR. 相似文献
40.