31 research outputs found

    Tundra photosynthesis captured by satellite-observed solar-induced chlorophyll fluorescence

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    Accurately quantifying the timing and magnitude of respiration and photosynthesis by high‐latitude ecosystems is important for understanding how a warming climate influences global carbon cycling. Data‐driven estimates of photosynthesis across Arctic regions often rely on satellite‐derived enhanced vegetation index (EVI); we find that satellite observations of solar‐induced chlorophyll fluorescence (SIF) provide a more direct proxy for photosynthesis. We model Alaskan tundra CO2 cycling (2012–2014) according to temperature and shortwave radiation and alternately input EVI or SIF to prescribe the annual seasonal cycle of photosynthesis. We find that EVI‐based seasonality indicates spring “green‐up” to occur 9 days prior to SIF‐based estimates, and that SIF‐based estimates agree with aircraft and tower measurements of CO2. Adopting SIF, instead of EVI, for modeling the seasonal cycle of tundra photosynthesis can result in more accurate estimates of growing season duration and net carbon uptake by arctic vegetation

    Hypersensitivity to very-low single radiation doses: its relationship to the adaptive response and induced radioresistance.

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    There is now little doubt of the existence of radioprotective mechanisms, or stress responses, that are upregulated in response to exposure to small doses of ionizing radiation and other DNA-damaging agents. Phenomenologically, there are two ways in which these induced mechanisms operate. First, a small conditioning dose (generally below 30 cGy) may protect against a subsequent, separate, exposure to radiation that may be substantially larger than the initial dose. This has been termed the adaptive response. Second, the response to single doses may itself be dose-dependent so that small acute radiation exposures, or exposures at very low dose rates, are more effective per unit dose than larger exposures above the threshold where the induced radioprotection is triggered. This combination has been termed low-dose hypersensitivity (HRS) and induced radioresistance (IRR) as the dose increases. Both the adaptive response and HRS/IRR have been well documented in studies with yeast, bacteria, protozoa, algae, higher plant cells, insect cells, mammalian and human cells in vitro, and in studies on animal models in vivo. There is indirect evidence that the HRS/IRR phenomenon in response to single doses is a manifestation of the same underlying mechanism that determines the adaptive response in the two-dose case and that it can be triggered by high and low LET radiations as well as a variety of other stress-inducing agents such as hydrogen peroxide and chemotherapeutic agents although exact homology remains to be tested. Little is currently known about the precise nature of this underlying mechanism, but there is evidence that it operates by increasing the amount and rate of DNA repair, rather than by indirect mechanisms such as modulation of cell-cycle progression or apoptosis. Changed expression of some genes, only in response to low and not high doses, may occur within a few hours of irradiation and this would be rapid enough to explain the phenomenon of induced radioresistance although its specific molecular components have yet to be identified

    What mediates the link between childhood maltreatment and depression? The role of emotion dysregulation, attachment, and attributional style

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    Background: Childhood maltreatment (CM) has been shown to be related to a severe and/or chronic course of depression. This study investigated which psychological processes mediate this relationship. Method: A large sample of acute or recovered depressed individuals (N=340) participated in an online survey assessing characteristics of depression, trauma exposure, and potential mediators (emotion regulation difficulties, attributional style, and attachment). Results: The experience of CM was related to more severe depression and more depressive episodes. In multiple mediation models, emotion dysregulation, a depressogenic attributional style, and avoidance in close relationships conjointly mediated the relationship between CM and depression severity as well as number of depressive episodes. However, a significant direct path between CM and depression characteristics remained. Exploratory analyses suggested that posttraumatic stress disorder symptom severity was an important additional mediator in our sample. Conclusions: Our findings provide preliminary evidence for psychological mediators between CM and depression that may be promising targets for interventions tailored for the treatment of depression in this subgroup
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