Pathogens are powerful evolutionary forces shaping the structure and dynamics of both individual species and of the communities of which they are part, at a broad range of genetic, ecological, spatial, and temporal scales. At all these levels their impact varies from the subtle and little recognized through to the most obvious destruction. Today the direct role of pathogens in natural plant communities is better recognized than at previous times, although the nuances of their interactions and the cascade of ramifications that can flow through changing biotic and abiotic effects are only now gaining recognition. However, as human influence on pathogens increases--either directly through enhanced if accidental dispersal, or through anthropogenic impacts on climate--we may expect to see increasing evidence of pathogens affecting plant species, community structure, and ecosystem function.
Altogether clinical, radiographic, and histologic findings indicated that two major etiologic factors might have been implicated in the failure process of the investigated implants: excessive occlusal load in relation to the bone-supporting capacity and, in two cases, infection.
Enhancement of tumor cell growth and invasiveness by transforming growth factor-β (TGF-β) requires constitutive activation of the ras/MAPK pathway. Here we have investigated how MEK activation by epidermal growth factor (EGF) influences the response of fully differentiated and growth-arrested pig thyroid epithelial cells in primary culture to TGF-β1. The epithelial tightness was maintained after single stimulation with EGF or TGF-β1 (both 10 ng/ml) for 48 hours. In contrast, co-stimulation abolished the transepithelial resistance and increased the paracellular flux of [3H]inulin within 24 hours. Reduced levels of the tight junction proteins claudin-1 and occludin accompanied the loss of barrier function. N-cadherin, expressed only in few cells of untreated or single-stimulated cultures, was at the same time increased 30-fold and co-localised with E-cadherin at adherens junctions in all cells. After 48 hours of co-stimulation, both E- and N-cadherin were downregulated and the cells attained a fibroblast-like morphology and formed multilayers. TGF-β1 only partially inhibited EGF-induced Erk phosphorylation. The MEK inhibitor U0126 prevented residual Erk phosphorylation and abrogated the synergistic responses to TGF-β1 and EGF. The observations indicate that concomitant growth factor-induced MEK activation is necessary for TGF-β1 to convert normal thyroid epithelial cells to a mesenchymal phenotype.
The objective was to examine injury rates and associated risk factors in a representative sample of climbers. A random sample (n=606) of the Swedish Climbing Association members was sent a postal survey, with an effective response rate of 63%. Self-reported data regarding climbing history, safety practices and retrospective accounts of injury events (recall period 1.5 years) were obtained. Descriptive statistical methods were used to calculate injury incidences, and a two-step method including zero-inflated Poisson's regression analysis of re-injuries was used to determine the combination of risk factors that best explained individual injury rates. Overall, 4.2 injuries per 1000 climbing hours were reported, overuse injuries accounting for 93% of all injuries. Inflammatory tissue damages to fingers and wrists were the most common injury types. The multivariate analysis showed that overweight and practicing bouldering generally implied an increased primary injury risk, while there was a higher re-injury risk among male climbers and a lower risk among the older climbers. The high percentage of overuse injuries implies that climbing hours and loads should be gradually and systematically increased, and climbers regularly controlled for signs and symptoms of overuse. Further study of the association between body mass index and climbing injury is warranted.
The aim of this study was to detect vegetation change and to examine trophic interactions in a Sphagnum-dominated mire in response to raised temperature and nitrogen (N) addition. A long-term global-change experiment was established in 1995, with monthly additions of N (30 kg x ha(-1) x yr(-1)) and sulfur (20 kg x ha(-1) x yr(-1)) during the vegetation period. Mean air temperature was raised by 3.6 degrees C with warming chambers. Vegetation responses were negligible for all treatments for the first four years, and no sulfur effect was seen during the course of the experiment. However, after eight years of continuous treatments, the closed Sphagnum carpet was drastically reduced from 100% in 1995 down to 41%, averaged over all N-treated plots. Over the same period, total vascular plant cover (of the graminoid Eriophorum vaginatum and the two dwarf-shrubs Andromeda polifolia and Vaccinium oxycoccos) increased from 24% to an average of 70% in the N plots. Nitrogen addition caused leaf N concentrations to rise in the two dwarf-shrubs, while for E. vaginatum, leaf N remained unchanged, indicating that the graminoid to a larger extent than the dwarf-shrubs allocated supplemented N to growth. Concurrent with foliar N accumulation of the two dwarf-shrubs, we observed increased disease incidences caused by parasitic fungi, with three species out of 16 showing a significant increase. Warming caused a significant decrease in occurrence of three parasitic fungal species. In general, decreased disease incidences were found in temperature treatments for A. polifolia and in plots without N addition for V. oxycoccos. The study demonstrates that both bryophytes and vascular plants at boreal mires, only receiving background levels of nitrogen of about 2 kg x ha(-1) x yr(-1), exhibit a time lag of more than five years in response to nitrogen and temperature rise, emphasizing the need for long-term experiments. Moreover, it shows that trophic interactions are likely to differ markedly in response to climate change and increased N deposition, and that these interactions might play an important role in controlling the change in mire vegetation composition, with implications for both carbon sequestration and methane emission.
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