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Santiago Soliveres David J. Eldridge Fernando T. Maestre Matthew A. Bowker Matthew Tighe Adrián Escudero 《Perspectives in Plant Ecology, Evolution and Systematics》2011,13(4):247
Studies of facilitative interactions as drivers of plant richness along environmental gradients often assume the existence of an overarching stress gradient that equally affects the performance of all the species in a given community. However, co-existing species differ in their ecophysiological adaptations, and do not experience the same stress level under particular environmental conditions. Moreover, these studies assume a unimodal relationship between richness and biomass, which is not as general as previously thought. We ignored these assumptions to assess changes in plant–plant interactions and their effect on local species richness across environmental gradients in semi-arid areas of Spain and Australia. We aimed to understand the relative importance of direct (microhabitat amelioration) and indirect (changes in the competitive relationships among the understorey species: niche segregation, competitive exclusion or intransitivity) mechanisms that might underlie the effects of nurse plants on local species richness. By jointly studying these direct and indirect mechanisms using a unifying framework, we found that nurse plants (trees, shrubs and tussock grasses) increased local richness not only by expanding the niche of neighbouring species but also by increasing niche segregation among them, though the latter was not important in all cases. The outcome of the competition-facilitation continuum varied depending on the study area, likely because the different types of stress gradient considered. When driven by both rainfall and temperature, or rainfall alone, the community-wide importance of nurse plants remained constant (Spanish sites), or showed a unimodal relationship along the gradient (Australian sites). This study expands our understanding of the relative roles of plant–plant interactions and environmental conditions as drivers of local species richness in semi-arid environments. The results can also be used to refine predictions about the response of plant communities to environmental change, and to clarify the relative importance of biotic interactions as drivers of such responses. 相似文献
153.
Cinzia Antognelli Rodolfo Cecchetti Francesca Riuzzi Matthew J. Peirce Vincenzo N. Talesa 《Journal of cellular and molecular medicine》2018,22(5):2865-2883
Metastasis is the primary cause of death in prostate cancer (PCa) patients. Effective therapeutic intervention in metastatic PCa is undermined by our poor understanding of its molecular aetiology. Defining the mechanisms underlying PCa metastasis may lead to insights into how to decrease morbidity and mortality in this disease. Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs). Hydroimidazolone (MG‐H1) and argpyrimidine (AP) are AGEs originating from MG‐mediated post‐translational modification of proteins at arginine residues. AP is involved in the control of epithelial to mesenchymal transition (EMT), a crucial determinant of cancer metastasis and invasion, whose regulation mechanisms in malignant cells are still emerging. Here, we uncover a novel mechanism linking Glo1 to the maintenance of the metastatic phenotype of PCa cells by controlling EMT by engaging the tumour suppressor miR‐101, MG‐H1‐AP and TGF‐β1/Smad signalling. Moreover, circulating levels of Glo1, miR‐101, MG‐H1‐AP and TGF‐β1 in patients with metastatic compared with non‐metastatic PCa support our in vitro results, demonstrating their clinical relevance. We suggest that Glo1, together with miR‐101, might be potential therapeutic targets for metastatic PCa, possibly by metformin administration. 相似文献
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Visually guided action and interaction depends on the brain’s ability to (a) extract and (b) discriminate meaningful targets from complex retinal inputs. Binocular disparity is known to facilitate this process, and it is an open question how activity in different parts of the visual cortex relates to these fundamental visual abilities. Here we examined fMRI responses related to performance on two different tasks (signal-in-noise “coarse” and feature difference “fine” tasks) that have been widely used in previous work, and are believed to differentially target the visual processes of signal extraction and feature discrimination. We used multi-voxel pattern analysis to decode depth positions (near vs. far) from the fMRI activity evoked while participants were engaged in these tasks. To look for similarities between perceptual judgments and brain activity, we constructed ‘fMR-metric’ functions that described decoding performance as a function of signal magnitude. Thereafter we compared fMR-metric and psychometric functions, and report an association between judged depth and fMRI responses in the posterior parietal cortex during performance on both tasks. This highlights common stages of processing during perceptual performance on these tasks. 相似文献
157.
Emma C. Wall Katharine Cartwright Matthew Scarborough Katherine M. Ajdukiewicz Patrick Goodson James Mwambene Eduard E. Zijlstra Stephen B. Gordon Neil French Brian Faragher Robert S. Heyderman David G. Lalloo 《PloS one》2013,8(7)
Mortality from bacterial meningitis in African adults is significantly higher than those in better resourced settings and adjunctive therapeutic interventions such as dexamethasone and glycerol have been shown to be ineffective. We conducted a study analysing data from clinical trials of bacterial meningitis in Blantyre, Malawi to investigate the clinical parameters associated with this high mortality.
Methods
We searched for all clinical trials undertaken in Blantyre investigating bacterial meningitis from 1990 to the current time and combined the data from all included trial datasets into one database. We used logistic regression to relate individual clinical parameters to mortality. Adults with community acquired bacterial meningitis were included if the CSF culture isolate was consistent with meningitis or if the CSF white cell count was >100 cells/mm3 (>50% neutrophils) in HIV negative participants and >5 cells/mm3 in HIV positive participants. Outcome was measured by mortality at discharge from hospital (after 10 days of antibiotic therapy) and community follow up (day 40).Results
Seven hundred and fifteen episodes of bacterial meningitis were evaluated. The mortality rate was 45% at day 10 and 54% at day 40. The most common pathogens were S.pneumoniae (84% of positive CSF isolates) and N.meningitidis (4%). 607/694 (87%) participants tested were HIV antibody positive. Treatment delays within the hospital system were marked. The median presenting GCS was 12/15, 17% had GCS<8 and 44.9% had a seizure during the illness. Coma, seizures, tachycardia and anaemia were all significantly associated with mortality on multivariate analysis. HIV status and pneumococcal culture positivity in the CSF were not associated with mortality. Adults with community acquired bacterial meningitis in Malawi present with a severe clinical phenotype. Predictors of high mortality are different to those seen in Western settings. Optimising in-hospital care and minimising treatment delays presents an opportunity to improve outcomes considerably. 相似文献158.
Toshchakov VY Fenton MJ Vogel SN 《Journal of immunology (Baltimore, Md. : 1950)》2007,178(5):2655-2660
We designed cell-penetrating peptides comprised of the translocating segment of Drosophila antennapedia homeodomain fused with BB loop sequences of TLR2, TLR4, and TLR1/6. TLR2- and TLR4-BB peptides (BBPs) inhibited NF-kappaB translocation and early IL-1beta mRNA expression induced by LPS, and the lipopeptides S-[2,3-bis(palmitoyloxy)-(2-RS)-propyl]-N-palmitoyl-(R)-Cys-Ser-Lys(4)-OH (P3C) and S-[2,3-bis(palmitoyloxy)-(2-RS)-propyl]-Cys-Ser-Lys(4)-OH (P2C). TLR4- and TLR2-BBPs also strongly inhibited LPS-induced activation of ERK. Only TLR2-BBP significantly inhibited ERK activation induced by P3C, which acts via TLR2/1 heterodimers. BBPs did not inhibit activation of ERK induced by P2C, a TLR2/6 agonist. The TLR2-BBP induced weak activation of p38, but not ERK or cytokine mRNA. The TLR1/6-BBP failed to inhibit NF-kappaB or MAPK activation induced by any agonist. Our results suggest that the receptor BBPs selectively affect different TLR signaling pathways, and that the BB loops of TLR1/6 and TLR2 play distinct roles in formation of receptor heterodimers and recruitment of adaptor proteins. 相似文献
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