Radio-Frequency Spectroscopy

Contains reports on three research projects

Radiocarbon age-offsets in an arctic lake reveal the long-term response of permafrost carbon to climate change

Author Posting. © American Geophysical Union, 2014. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research: Biogeosciences 119 (2014): 1630–1651, doi:10.1002/2014JG002688.Continued warming of the Arctic may cause permafrost to thaw and speed the decomposition of large stores of soil organic carbon (OC), thereby accentuating global warming. However, it is unclear if recent warming has raised the current rates of permafrost OC release to anomalous levels or to what extent soil carbon release is sensitive to climate forcing. Here we use a time series of radiocarbon age-offsets (14C) between the bulk lake sediment and plant macrofossils deposited in an arctic lake as an archive for soil and permafrost OC release over the last 14,500 years. The lake traps and archives OC imported from the watershed and allows us to test whether prior warming events stimulated old carbon release and heightened age-offsets. Today, the age-offset (2 ka; thousand of calibrated years before A.D. 1950) and the depositional rate of ancient OC from the watershed into the lake are relatively low and similar to those during the Younger Dryas cold interval (occurring 12.9–11.7 ka). In contrast, age-offsets were higher (3.0–5.0 ka) when summer air temperatures were warmer than present during the Holocene Thermal Maximum (11.7–9.0 ka) and Bølling-Allerød periods (14.5–12.9 ka). During these warm times, permafrost thaw contributed to ancient OC depositional rates that were ~10 times greater than today. Although permafrost OC was vulnerable to climate warming in the past, we suggest surface soil organic horizons and peat are presently limiting summer thaw and carbon release. As a result, the temperature threshold to trigger widespread permafrost OC release is higher than during previous warming events.National Science Foundation. Grant Number: ARC-09021692015-02-2

Modeling sulfate reduction in methane hydrate-bearing continental margin sediments : does a sulfate-methane transition require anaerobic oxidation of methane?

Author Posting. © American Geophysical Union, 2011. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geochemistry Geophysics Geosystems 12 (2011): Q07006, doi:10.1029/2011GC003501.The sulfate-methane transition (SMT), a biogeochemical zone where sulfate and methane are metabolized, is commonly observed at shallow depths (1–30 mbsf) in methane-bearing marine sediments. Two processes consume sulfate at and above the SMT, anaerobic oxidation of methane (AOM) and organoclastic sulfate reduction (OSR). Differentiating the relative contribution of each process is critical to estimate methane flux into the SMT, which, in turn, is necessary to predict deeper occurrences of gas hydrates in continental margin sediments. To evaluate the relative importance of these two sulfate reduction pathways, we developed a diagenetic model to compute the pore water concentrations of sulfate, methane, and dissolved inorganic carbon (DIC). By separately tracking DIC containing 12C and 13C, the model also computes δ13C-DIC values. The model reproduces common observations from methane-rich sediments: a well-defined SMT with no methane above and no sulfate below and a δ13C-DIC minimum at the SMT. The model also highlights the role of upward diffusing 13C-enriched DIC in contributing to the carbon isotope mass balance of DIC. A combination of OSR and AOM, each consuming similar amounts of sulfate, matches observations from Site U1325 (Integrated Ocean Drilling Program Expedition 311, northern Cascadia margin). Without AOM, methane diffuses above the SMT, which contradicts existing field data. The modeling results are generalized with a dimensional analysis to the range of SMT depths and sedimentation rates typical of continental margins. The modeling shows that AOM must be active to establish an SMT wherein methane is quantitatively consumed and the δ13C-DIC minimum occurs. The presence of an SMT generally requires active AOM

Evaluation Of Groundwater Pathways And Travel Times From The Nevada Test Site To The Potential Yucca Mountain Repository

Yucca Mountain (YM), Nevada, has been recommended as a deep geological repository for the disposal of spent fuel and high-level radioactive waste. If YM is licensed as a repository by the Nuclear Regulatory Commission, it will be important to identify the potential for radionuclides to migrate from underground nuclear testing areas located on the Nevada Test Site (NTS) to the hydraulically downgradient repository area to ensure that monitoring does not incorrectly attribute repository failure to radionuclides originating from other sources. In this study, we use the Death Valley Regional Flow System (DVRFS) model developed by the U.S. Geological Survey to investigate potential groundwater migration pathways and associated travel times from the NTS to the proposed YM repository area. Using results from the calibrated DVRFS model and the particle tracking post-processing package MODPATH, we modeled three-dimensional groundwater advective pathways in the NTS and YM region. Our study focuses on evaluating the potential for groundwater pathways between the NTS and YM withdrawal area and whether travel times for advective flow along these pathways coincide with the prospective monitoring timeframe at the proposed repository. We include uncertainty in effective porosity, as this is a critical variable in the determination of time for radionuclides to travel from the NTS region to the YM withdrawal area. Uncertainty in porosity is quantified through evaluation of existing site data and expert judgment and is incorporated in the model through Monte Carlo simulation. Since porosity information is limited for this region, the uncertainty is quite large and this is reflected in the results as a large range in simulated groundwater travel times

Specific inhibition of p38 mitogen-activated protein kinase with FR167653 attenuates vascular proliferation in monocrotaline-induced pulmonary hypertension in rats

AbstractObjectivesp38 mitogen-activated protein kinase is associated with many clinical entities characterized by inflammation. We postulated that inhibition of p38 mitogen-activated protein kinase with FR167653 attenuates inflammation and the development of pulmonary hypertension in monocrotaline-treated rats.MethodsRats were divided into 4 groups: (1) the control group (daily 0.9% saline), (2) the FR group (daily FR167653, 2 mg · kg−1 · d−1), (3) the MCT group (daily 0.9% saline the day after a single monocrotaline dose, 60 mg/kg), and (4) the MCT+FR group (daily FR167653, 2 mg · kg−1 · d−1, the day after a single MCT dose). Body weight, pulmonary artery pressure, and morphometric changes of the pulmonary artery with the histopathologic method were observed weekly for 4 weeks. Also, p38 mitogen-activated protein kinase activity and inflammatory cytokine expression in the lung were measured.ResultsFour weeks after monocrotaline administration, mean pulmonary artery pressure in the MCT+FR group was lower than in the MCT group (MCT+FR vs MCT: 24.7 ± 1.9 vs 36.5 ± 2.1 mm Hg; P < .05). In morphometric analysis the percentage of medial wall thickness and the percentage of muscularization in the MCT+FR group were reduced compared with those in the MCT group after 4 weeks (P < .05); however, the number of macrophages was not significantly different. p38 mitogen-activated protein kinase activity was significantly attenuated in the MCT+FR group compared with in the MCT group (7.2 ± 0.52 vs 2.1 ± 0.23 fold-increase, P < .05, at 1 week). Although mRNA levels of tumor necrosis factor α and interleukin 1β were reduced in the MCT+FR group compared with in the MCT group (tumor necrosis factor α: 1.18 ± 0.36 vs 3.05 ± 1.12 fold-increase, P < .05, at 2 weeks; interleukin 1β: 2.2 ± 0.34 vs 4.4 ± 1.09 fold-increase, P < .05, at 1 week), FR167653 did not suppress increased monocyte chemotactic protein 1 mRNA expression induced by monocrotaline (3.2 ± 0.62 vs 3.1 ± 0.42 fold-increase, at 1 week).ConclusionFR167653 significantly attenuates the expression of inflammatory cytokines, ultimately preventing the progression of pulmonary hypertension. These results suggest that p38 mitogen-activated protein kinase might play a central role in the molecular events that underlie the development and progression of pulmonary hypertension

FK 506 pre-treatment is associated with reduced levels of tumor necrosis factor and interleukin 6 following hepatic ischemia/reperfusion

Using a rat model, the effect of pre-treatment with FK 506 on hepatic ischemia/reperfusion injury was investigated. All control animals died within 72 h of the ischemia/reperfusion injury. Pre-treatment of the animals with FK 506 (0.3 mg/kg in 0.5 ml saline) administered intravenously improved survival. The most striking protection against fatal ischemia/reperfusion injury was achieved in rats that were given FK 506 6 and 24 h prior to the induction of the hepatic ischemic insult (70% and 80% 10-day survival rates, respectively). The hepatoprotective effect of FK 506 was assessed further in a second experiment in which the serum levels of tumor necrosis factor (TNF) and interleukin 6 (IL-6) were measured. These results suggest that a 60-min period of hepatic ischemia and subsequent reperfusion triggers the release of both TNF and IL-6, and that FK 506 pre-treatment (6 h before the ischemic episode) significantly inhibits the production and/or release of these two cytokines compared to untreated controls. These data provide additional information concerning the immunosuppressive and hepatoprotective activities of FK 506. Based upon these data, it is probable that FK 506 attenuates hepatic ischemia/reperfusion injury, at least in part, by reducing TNF and IL-6 levels. © 1993 Elsevier Scientific Publishers Ireland Ltd. All rights reserved