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Robert M. Scheller Alec M. Kretchun E. Louise Loudermilk Matthew D. Hurteau Peter J. Weisberg Carl Skinner 《Ecosystems》2018,21(4):643-656
Climate-driven increases in wildfires, drought conditions, and insect outbreaks are critical threats to forest carbon stores. In particular, bark beetles are important disturbance agents although their long-term interactions with future climate change are poorly understood. Droughts and the associated moisture deficit contribute to the onset of bark beetle outbreaks although outbreak extent and severity is dependent upon the density of host trees, wildfire, and forest management. Our objective was to estimate the effects of climate change and bark beetle outbreaks on ecosystem carbon dynamics over the next century in a western US forest. Specifically, we hypothesized that (a) bark beetle outbreaks under climate change would reduce net ecosystem carbon balance (NECB) and increase uncertainty and (b) these effects could be ameliorated by fuels management. We also examined the specific tree species dynamics—competition and release—that determined NECB response to bark beetle outbreaks. Our study area was the Lake Tahoe Basin (LTB), CA and NV, USA, an area of diverse forest types encompassing steep elevation and climatic gradients and representative of mixed-conifer forests throughout the western United States. We simulated climate change, bark beetles, wildfire, and fuels management using a landscape-scale stochastic model of disturbance and succession. We simulated the period 2010–2100 using downscaled climate projections. Recurring droughts generated conditions conducive to large-scale outbreaks; the resulting large and sustained outbreaks significantly increased the probability of LTB forests becoming C sources over decadal time scales, with slower-than-anticipated landscape-scale recovery. Tree species composition was substantially altered with a reduction in functional redundancy and productivity. Results indicate heightened uncertainty due to the synergistic influences of climate change and interacting disturbances. Our results further indicate that current fuel management practices will not be effective at reducing landscape-scale outbreak mortality. Our results provide critical insights into the interaction of drivers (bark beetles, wildfire, fuel management) that increase the risk of C loss and shifting community composition if bark beetle outbreaks become more frequent. 相似文献
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Kinga Michno David Knight Jorge M. Campussano Diana van de Hoef Gabrielle L. Boulianne 《PloS one》2009,4(9)
Much of our current understanding about neurodegenerative diseases can be attributed to the study of inherited forms of these disorders. For example, mutations in the presenilin 1 and 2 genes have been linked to early onset familial forms of Alzheimer''s disease (FAD). Using the Drosophila central nervous system as a model we have investigated the role of presenilin in one of the earliest cellular defects associated with Alzheimer''s disease, intracellular calcium deregulation. We show that expression of either wild type or FAD-mutant presenilin in Drosophila CNS neurons has no impact on resting calcium levels but does give rise to deficits in intracellular calcium stores. Furthermore, we show that a loss-of-function mutation in calmodulin, a key regulator of intracellular calcium, can suppress presenilin-induced deficits in calcium stores. Our data support a model whereby presenilin plays a role in regulating intracellular calcium stores and demonstrate that Drosophila can be used to study the link between presenilin and calcium deregulation. 相似文献
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A gene encoding the endogenous superantigen Mlsc, which deletes Tcrb-V3+ T cells in the NOD inbred mouse strain, was found to co-segregate with Mtv-3 on chromosome 11. This identifies a fourth gene encoding a deletion ligand for Tcrb-V3+ T cells and extends recently published observations in support of the hypothesis that a number of endogenous superantigens are the products of Mtv proviruses.
Address correspondence and offprint requests to : K. Tomonari. 相似文献
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We have identified and partially purified a growth inhibitor protein secreted by human diploid fibroblast cells. This protein is not secreted constitutively but only after induction with the double stranded hetero duplex polyriboinosinic:polyribocytidylic acid. The growth inhibitory activity has been purified 3,800-fold and has an estimated molecular mass of 12,000 daltons. The protein will inhibit the growth in culture of human diploid fibroblast cells, human cells derived from tumors, and mouse L cells. Although interferon-beta is secreted with the growth inhibitory protein, the partially purified growth inhibitory protein has no antiviral activity, and its activity is not neutralized by antibodies to interferon-alpha, interferon-beta, and interferon-gamma. We believe this growth inhibitory activity to reside in a newly defined protein and have named it fibroblast-derived growth inhibitor. 相似文献