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Right on track?
(2019)
Satellite telemetry is an increasingly utilized technology in wildlife research, and current devices can track individual animal movements at unprecedented spatial and temporal resolutions. However, as we enter the golden age of satellite telemetry, we need an in-depth understanding of the main technological, species-specific and environmental factors that determine the success and failure of satellite tracking devices across species and habitats. Here, we assess the relative influence of such factors on the ability of satellite telemetry units to provide the expected amount and quality of data by analyzing data from over 3,000 devices deployed on 62 terrestrial species in 167 projects worldwide. We evaluate the success rate in obtaining GPS fixes as well as in transferring these fixes to the user and we evaluate failure rates. Average fix success and data transfer rates were high and were generally better predicted by species and unit characteristics, while environmental characteristics influenced the variability of performance. However, 48% of the unit deployments ended prematurely, half of them due to technical failure. Nonetheless, this study shows that the performance of satellite telemetry applications has shown improvements over time, and based on our findings, we provide further recommendations for both users and manufacturers.
Moving in the Anthropocene
(2018)
Animal movement is fundamental for ecosystem functioning and species survival, yet the effects of the anthropogenic footprint on animal movements have not been estimated across species. Using a unique GPS-tracking database of 803 individuals across 57 species, we found that movements of mammals in areas with a comparatively high human footprint were on average one-half to one-third the extent of their movements in areas with a low human footprint. We attribute this reduction to behavioral changes of individual animals and to the exclusion of species with long-range movements from areas with higher human impact. Global loss of vagility alters a key ecological trait of animals that affects not only population persistence but also ecosystem processes such as predator-prey interactions, nutrient cycling, and disease transmission.
The majority of research on biodiversity ecosystem functioning in laboratories has concentrated on a few traits, but there is increasing evidence from the field that functional diversity controls ecosystem functioning more often than does species number. Given the importance of traits as predictors of niche complementarity and community structures, we (1) examine how the diversity sensu lato of forest trees, freshwater fishes and soil invertebrates might support ecosystem functioning and (2) discuss the relevance of productive biota for monophyletic assemblages (taxocenes).
In terrestrial ecosystems, correlating traits to abiotic factors is complicated by the appropriate choice of body-size distributions. Angiosperm and gymnosperm trees, for example, show metabolic incongruences in their respiration rates despite their pronounced macroecological scaling. Scaling heterotrophic organisms within their monophyletic assemblages seems more difficult than scaling autotrophs: in contrast to the generally observed decline of mass-specific metabolic rates with body mass within metazoans, soil organisms such as protozoans show opposite mass-specific trends.
At the community level, the resource demand of metazoans shapes multitrophic interactions. Hence, population densities and their food web relationships reflect functional diversity, but the influence of biodiversity on stability and ecosystem functioning remains less clear. We focused on fishes in 18 riverine food webs, where the ratio of primary versus secondary extinctions (hereafter, 'extinction partitioning') summarizes the responses of fish communities to primary species loss (deletions) and its consequences. Based on extinction partitioning, our high-diversity food webs were just as (or even more) vulnerable to extinctions as low-diversity food webs.
Our analysis allows us to assess consequences of the relocation or removal of fish species and to help with decision-making in sustainable river management. The study highlights that the topology of food webs (and not simply taxonomic diversity) plays a greater role in stabilizing the food web and enhancing ecological services than is currently acknowledged.
More than 80 years ago Otto Warburg suggested that cancer might be caused by a decrease in mitochondrial energy metabolism paralleled by an increase in glycolytic flux. In later years, it was shown that cancer cells exhibit multiple alterations in mitochondrial content, structure, function, and activity. We have stably overexpressed the Friedreich ataxia-associated protein frataxin in several colon cancer cell lines. These cells have increased oxidative metabolism, as shown by concurrent increases in aconitase activity, mitochondrial membrane potential, cellular respiration, and ATP content. Consistent with Warburg's hypothesis, we found that frataxin-overexpressing cells also have decreased growth rates and increased population doubling times, show inhibited colony formation capacity in soft agar assays, and exhibit a reduced capacity for tumor formation when injected into nude mice. Furthermore, overexpression of frataxin leads to an increased phosphorylation of the tumor suppressor p38 mitogen-activated protein kinase, as well as decreased phosphorylation of extracellular signal-regulated kinase. Taken together, these results support the view that an increase in oxidative metabolism induced by mitochondrial frataxin may inhibit cancer growth in mammals
We have disrupted expression of the mitochondrial Friedreich ataxia protein frataxin specifically in murine hepatocytes to generate mice with impaired mitochondrial function and decreased oxidative phosphorylation. These animals have a reduced life span and develop multiple hepatic tumors. Livers also show increased oxidative stress, impaired respiration and reduced ATP levels paralleled by reduced activity of iron-sulfur cluster (Fe/S) containing proteins (ISP), which all leads to increased hepatocyte turnover by promoting both apoptosis and proliferation. Accordingly, phosphorylation of the stress-inducible p38 MAP kinase was found to be specifically impaired following disruption of frataxin. Taken together, these findings indicate that frataxin may act as a mitochondrial tumor suppressor protein in mammals