30 research outputs found

    Conservative tracer study of horizontal sediment mixing rates in a bathyal basin, California borderland

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    In situ tracer (50–125 μm plastic particles) experiments conducted using the DSV Alvin over a two year period in the 1240 m deep Santa Catalina Basin (eastern Pacific) have yielded near-surface (0–1.5 cm) horizontal bioturbation rates of order 1–10 cm2yr–1. Vertical biodiffusivities obtained from the same and similar particulate tracers at the same site are approximately an order of magnitude less. Mixing of near-surface, coarse sediment in Santa Catalina Basin is anisotropic. Deeper within the sediment horizontal bioturbation is not diffusive on a two-year time scale, but would appear to be a form of mixing termed nonlocal symmetric by Boudreau and Imboden (1987), whereby particles are moved appreciable distances advectively. The finding that bioturbation in near-surface sediments is anisotropic in Santa Catalina Basin and the likelihood that this phenomenon is widespread in deep-ocean sediments calls into question the present parameterization of the effect sediment mixing has on various early diagenetic processes. Specifically, the contribution of bioturbation to organic carbon remineralization rates via microbial intermediaries may be underestimated. Bioturbation rates represent more than simply vertical mass transfer coefficients and should be incorporated into models of early diagenesis accordingly

    Spatial variation in short-term (234Th) sediment bioturbation intensity along an organic-carbon gradient

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    Natural and human-induced spatial gradients provide a useful vehicle with which to better understand diverse marine processes. On the Palos Verdes margin (S. California), historical and ongoing waste-water discharge has created an along-shelf gradient in organic C and total N, as well as various trace metals and other pollutants (e.g., DDT). To better understand the impact of such pollution on bioturbation and to develop a more general understanding of the controlling factors of sediment bioturbation intensity, a series of stations representing severely, moderately and negligibly impacted sediments was studied. Vertical profiles of the naturally occurring radionuclide, 234Th, as well as the abundance and species composition of macrofauna were measured from box cores collected at three sites during July 1992. During a March 1993 cruise, radionuclide profiles were collected at an additional eleven sites on the margin. Excess 234Th profiles are, in general, consistent with a steady-state model that balances vertical biodiffusive mixing with radioactive decay. Biodiffusivities determined from the 234Th profiles yield a spatial pattern in which sediments near the outfall are mixed at intensities of ≈10 cm2/yr, and bioturbation intensities are five times as rapid at sites 5–7 km from the outfall. Average mixing intensities are between these extremes (28 cm2/yr) at a nearby unimpacted site. Despite the overall consistency of this pattern the reasons behind it remain unclear. Structural aspects of the macrofauna either do not vary between the three intensively studied stations (e.g., depth distribution, size) or do so in a manner that would suggest an opposite effect on the biodiffusivity (e.g., abundance). There is also little variability in trophic groupings along the enrichment gradient. Behavioral modifications, such as: (1) sublethal pollution effects caused by elevated contaminant (e.g., organic carbon and DDT) concentrations, and (2) inhibition by a tube-building polychaete, Mediomastus sp., are postulated to suppress mixing intensities near the outfall. The results of this study suggest that, at least in shallow-water settings, the general controls of bioturbation intensity are still poorly understood

    Particle bioturbation in Massachusetts Bay: Preliminary results using a new deliberate tracer technique

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    To better understand temporal and particle size-dependent bioturbation processes, we conducted a study of sediment mixing in Massachusetts Bay using a newly developed deliberate tracer technique. Sediments from a 32-m, fine-grained site were collected and the 38–62 (“silt”) and 63–125 (“sand”) μm fractions isolated. These particle-size fractions were labeled with two different noble metals (Au: silt & Ag: sand) using a thermal diffusion technique. Mixtures of the tracers were spread onto the seafloor in April and July 1992 by divers and were tube-cored (3 replicates) ˜ 80 d later in each case. Vertical profiles of the tracers were measured at μg/g (Ag) and ng/g (Au) levels by instrumental neutron activation analysis. During the spring experiment, Au (silt) was mixed to depths \u3e 15 cm and displayed multiple subsurface maxima, whereas Ag (sand) was confined to the upper 5 cm of the bed and showed a near monotonic decrease in concentration with depth. In the fall experiment, the tracers displayed more congruent down-core profiles consisting of near-surface maxima and several subsurface peaks. Two nonlocal bioturbation modes are suggested by the tracer data: reverse conveyor-belt transport and head-down deposit feeding or excavation. A particle caching strategy by an unidentified macrofaunal species is postulated to explain the subsurface peaks, but remains conjectural without better species-level natural history information regarding solid-phase bioturbation

    Inhibition of plasmin-mediated TAFI activation may affect development but not progression of abdominal aortic aneurysms

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    Objective: Thrombin-activatable fibrinolysis inhibitor (TAFI) reduces the breakdown of fibrin clots through its action as an indirect inhibitor of plasmin. Studies in TAFI-deficient mice have implicated a potential role for TAFI in Abdominal Aortic Aneurysm (AAA) disease. The role of TAFI inhibition on AAA formation in adult ApoE-/- mice is unknown. The aim of this paper was to investigate the effects of TAFI inhibition on AAA development and progression. Methods: Using the Angiotensin II model of AAA, male ApoE-/- mice were infused with Angiotensin II 750ng/kg/min with or without a monoclonal antibody inhibitor of plasmin-mediated activation of TAFI, MA-TCK26D6, or a competitive small molecule inhibitor of TAFI, UK-396082. Results: Inhibition of TAFI in the Angiotensin II model resulted in a decrease in the mortality associated with AAA rupture (from 40.0% to 16.6% with MA-TCK26D6 (log-rank Mantel Cox test p = 0.16), and 8.3% with UK-396082 (log-rank Mantel Cox test p = 0.05)). Inhibition of plasmin-mediated TAFI activation reduced the incidence of AAA from 52.4% to 30.0%. However, late treatment with MA-TCK26D6 once AAA were already established had no effect on the progression of AAA in this model. Conclusions: The formation of intra-mural thrombus is responsible for the dissection and early rupture in the angiotensin II model of AAA, and this process can be prevented through inhibition of TAFI. Late treatment with a TAFI inhibitor does not prevent AAA progression. These data may indicate a role for inhibition of plasmin-mediated TAFI activation in the early stages of AAA development, but not in its progression
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