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Elevated atmospheric CO2 concentrations increase plant productivity and affect soil microbial communities, with possible consequences for the turnover rate of soil carbon (C) pools and feedbacks to the atmosphere. In a previous analysis (Van Groenigen et al., 2014), we used experimental data to inform a one‐pool model and showed that elevated CO2 increases the decomposition rate of soil organic C, negating the storage potential of soil. However, a two‐pool soil model can potentially explain patterns of soil C dynamics without invoking effects of CO2 on decomposition rates. To address this issue, we refit our data to a two‐pool soil C model. We found that CO2 enrichment increases decomposition rates of both fast and slow C pools. In addition, elevated CO2 decreased the carbon use efficiency of soil microbes (CUE), thereby further reducing soil C storage. These findings are consistent with numerous empirical studies and corroborate the results from our previous analysis. To facilitate understanding of C dynamics, we suggest that empirical and theoretical studies incorporate multiple soil C pools with potentially variable decomposition rates.  相似文献   
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Temporal increases of tree mortality have been observed in regions where global warming has decreased long‐term water availability and/or induced droughts. However, temporal decreases in water availability are not a global phenomenon. Understanding how water deficit‐free forests respond to the recent effects of climate change is paramount towards a full appreciation of the impacts of climate change on global forests. Here, we reveal temporally increasing tree mortality across all study species over the last three decades in the central boreal forests of Canada, where long‐term water availability has increased without apparent climate change‐associated drought. In addition, we find that the effects of conspecific tree‐to‐tree competition have intensified temporally as a mechanism for the increased mortality of shade‐intolerant tree species. Our results suggest that the consequences of climate change on tree mortality are more profound than previously thought.  相似文献   
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Background

Respiratory syncytial virus (RSV) is one of the most frequently observed pathogens during infancy and childhood. However, the corresponding pathogenesis has not been determined to date. We previously demonstrated that IFN-γ plays an important role in RSV pathogenesis, and SARM-TRIF-signaling pathway could regulate the production of IFN-γ. This study is to investigate whether T cells or innate immune cells are the predominant producers of IFN-γ, and further to explore other culprits in addition to IFN-γ in the condition of RSV infection.

Methods

Normal BALB/c mice and nude mice deficient in T cells were infected intranasally with RSV. Leukocytes in bronchoalveolar lavage fluid were counted, lung histopathology was examined, and airway hyperresponsiveness (AHR) was measured by whole-body plethysmography. IFN-γ and MMP-12 were detected by ELISA. MMP408, a selective MMP-12 inhibitor, was given intragastrically. Resveratrol, IFN-γ neutralizing antibody and recombinant murine IFN-γ were administered intraperitoneally. SARM and TRIF protein were semi-quantified by Western blot. siRNA was used to knock-down SARM expression.

Results

RSV induced significant airway inflammation and AHR in both mice; IFN-γ was significantly increased in BALB/c mice but not in nude mice. MMP-12 was dramatically increased in both mice but earlier in nude mice. When MMP-12 was inhibited by MMP408, RSV-induced respiratory symptoms were alleviated. SARM was significantly suppressed while TRIF was significantly enhanced in both mice strains. Following resveratrol administration in nude mice, 1) SARM inhibition was prevented, 2) TRIF and MMP-12 were correspondingly down-regulated and 3) airway disorders were subsequently alleviated. Moreover, when SARM was efficiently knocked down using siRNA, TRIF and MMP-12 were markedly enhanced, and the anti-RSV effects of resveratrol were remarkably abrogated. MMP-12 was significantly increased in the IFN-γ neutralizing antibody-treated BALB/c mice but reduced in the recombinant murine IFN-γ-treated nude mice.

Conclusions

MMP-12 can result in at least part of the airway inflammation and AHR independent of IFN-γ. And SARM-TRIF- signaling pathway is involved in regulating the overproduction of MMP-12. To the best of our knowledge, this study is the first that has examined the effects of SARM on MMP-12 and further highlights the potential to target SARM-TRIF-MMP-12 cascades to treat RSV infection.

Electronic supplementary material

The online version of this article (doi:10.1186/s12931-015-0176-8) contains supplementary material, which is available to authorized users.  相似文献   
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