Erosion, sediment production, and routing on a tectonically active continental margin reflect both tectonic and climatic processes; partitioning the relative importance of these processes remains controversial. Gulf of Alaska contains a preserved sedimentary record of the Yakutat Terrane collision with North America. Because tectonic convergence in the coastal St. Elias orogen has been roughly constant for 6 My, variations in its eroded sediments preserved in the offshore Surveyor Fan constrain a budget of tectonic material influx, erosion, and sediment output. Seismically imaged sediment volumes calibrated with chronologies derived from Integrated Ocean Drilling Program boreholes show that erosion accelerated in response to Northern Hemisphere glacial intensification (∼2.7 Ma) and that the 900-km-long Surveyor Channel inception appears to correlate with this event. However, tectonic influx exceeded integrated sediment efflux over the interval 2.8-1.2 Ma. Volumetric erosion accelerated following the onset of quasi-periodic (∼100-ky) glacial cycles in the mid-Pleistocene climate transition (1.2-0.7 Ma). Since then, erosion and transport of material out of the orogen has outpaced tectonic influx by 50-80%. Such a rapid net mass loss explains apparent increases in exhumation rates inferred onshore from exposure dates and mapped out-of-sequence fault patterns. The 1.2-My mass budget imbalance must relax back toward equilibrium in balance with tectonic influx over the timescale of orogenic wedge response (millions of years). The St. Elias Range provides a key example of how active orogenic systems respond to transient mass fluxes, and of the possible influence of climate-driven erosive processes that diverge from equilibrium on the million-year scale. O rogenesis reflects the balance of crustal material entering a mountain belt to undergo shortening and uplift versus material leaving the orogen through exhumation, erosion, and sediment transport (1-5). Perturbations in the influx/efflux from the orogen are expected to result in predictable changes in deformation within the orogen as it attempts to reestablish equilibrium (3). The long-term sink for sediment transported out of mountain belts is often in the deep sea, particularly in large submarine fans where sediments accumulate at anomalously high rates (>10 cm/ky) compared with deep-sea pelagic sedimentation (6-8). Even higher sedimentation rates (>100 cm/ky) proximal to glacially eroded regions (9-14) imply that wet-based glaciers are extremely efficient agents of erosion. Observations and modeling have argued that erosion rates can influence tectonic processes (15)(16)(17)(18)(19), but the timescales of adjustment, and the role of landscape disequilibrium, remain unclear. For example, exceptionally high local sedimentation rates (100-1000 cm/ky) recorded on the century timescale (13) SignificanceIn coastal Alaska and the St. Elias orogen, over the past 1.2 million years, mass flux leaving the mountains due to glacial erosion exceeds the plate tectonic input. This...

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The acute phase response is a systemic reaction to inflammatory processes characterized by multiple physiological adaptations, including the hepatic synthesis of acute-phase proteins. In humans, serum amyloid A (SAA) is one of the most prominent of these proteins. Despite the huge increase of serum levels of SAA in inflammation, its biological role remains to be elucidated, even though SAA is undoubtedly active in neutrophils. In a previous study, we reported that SAA induces the release of tumor necrosis factor-alpha, interleukin (IL)-1beta and IL-8 from human blood neutrophils. Here, we extend our earlier study, focusing on the effect of SAA on neutrophil IL-8 transcription and on the signaling pathways involved. We demonstrate herein that SAA, in relatively low concentrations (0.4-100 microg/ml) compared with those found in plasma in inflammatory conditions, induces a dose-dependent release of IL-8 from neutrophils. The p38 mitogen-activated protein kinase inhibitor SB 203580 inhibits the IL-8 mRNA expression and the release of protein from neutrophils. The release of IL-8 from SAA-stimulated neutrophils is strongly suppressed by the addition of N-acetyl-l-cysteine, alpha-mercaptoethanol, glutathione, and dexamethasone. SAA also induces IL-8 expression and release from monocytes. In conclusion, SAA appears to be an important mediator of the inflammatory process, possibly contributing to the pool of IL-8 produced in chronic diseases, which may play a role in degenerative diseases.

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This work reports the effect of the apolipoproteins A-I and A-II (apoA-I and apoA-II) on the release of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-8, and IL-1 receptor antagonist (IL-1Ra) and on the oxidative burst of human neutrophils. By themselves, apoA-I and apoA-II do not affect the basal liberation of these cytokines, whereas apoA-I affects the release of IL-1beta from lipopolysaccharide (LPS)-stimulated neutrophils and apoA-II affects IL-8 released from LPS-stimulated neutrophils. ApoA-II also decreases the production of IL-8 released by neutrophils stimulated with the acute phase apolipoprotein serum amyloid A. Both apoA-I and apoA-II exerted approximately 30% inhibition on the oxidative burst of neutrophils stimulated by opsonized zymosan, as revealed by the luminol-enhanced chemiluminescence assay. These findings give additional support to the idea that the role of human plasma lipoproteins and apolipoproteins goes beyond their function in lipid transport and metabolism. HDL apolipoproteins appear to be a class of mediators that can participate in the regulation of the activity of neutrophils.