2,791 research outputs found
Effects of normal stress variation on the strength and stability of creeping faults
Author Posting. © American Geophysical Union, 2004. 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 109 (2004): B03406, doi:10.1029/2003JB002824.A central problem in studies of fault interaction and earthquake triggering is that of quantifying changes in frictional strength and the constitutive response caused by dynamic stressing. We imposed normal stress vibrations on creeping laboratory shear zones to investigate the process of dynamic weakening and the conditions under which resonant frictional behavior occurs. Layers of quartz powder were sheared at room temperature in a double-direct shear geometry at normal stress sigma barn = 25–200 MPa, vibration amplitude A = 0.1–10 MPa, period T = 0.1–200 s, and loading rate V = 1–1000 μm/s. Frictional response varied systematically with A, T, and V. Small-amplitude, short-period vibrations had no effect on frictional strength, but large-amplitude, short-period vibrations reduced shear zone strength by about 1%. Intermediate periods caused phase lags between shear strength and imposed vibrations. During long-period vibrations, frictional strength varied sinusoidally, in phase with vibrations and with an amplitude consistent with a constant coefficient of friction. Our data show that friction exhibits a critical vibration period, as predicted by theory. At long periods, the Dieterich (aging) friction law, with the Linker and Dieterich modification to describe step changes in normal stress, provides a good fit to our experimental results for all A and V. At short periods, however, theory predicts more dynamic weakening than we observed experimentally, suggesting that existing rate and state friction laws do not account for the full physics of our laboratory experiments. Our data show that normal-force vibrations can weaken and potentially destabilize steadily creeping fault zones.This research was supported by NSF grant EAR 01-96570 and
USGS grant 02HQGR0156, and M.B. was supported by a NSF Graduate
Research Fellowship
Innate effector cells in angiogenesis and lymphangiogenesis
Angiogenesis and lymphangiogenesis are distinct and complex processes requiring a finely tuned balance between stimulatory and inhibitory signals. During adulthood, angiogenesis and lymphangiogenesis are activated at sites of tumor growth, tissue injury and remodeling, and chronic inflammation. Vascular endothelial growth factors (VEGFs), angiopoietin (ANGPTs) and a multitude of additional signaling molecules play distinct roles in the modulation of angiogenesis/lymphangiogenesis. VEGFs and ANGPTs activate specific tyrosine kinase receptor (e.g., VEGFR1, VEGFR-2, VEGFR-3 and TIE2 respectively), expressed on blood endothelial cells (angiogenesis) and lymphatic endothelial cells (lymphangiogenesis). Although tumor cells produce VEGFs and other proangiogenic mediators, tissue resident (e.g., macrophages, mast cells) and circulating immune cells (e.g., basophils, neutrophils, monocytes, eosinophils) are an important source of angiogenic/lymphangiogenic mediators in inflammation and in tumor microenvironment and at site of chronic inflammation. Certain immune cells can also release anti-angiogenic factors. Mast cells, basophils, neutrophils and presumably other immune cells are not only a source of angiogenic/lymphangiogenic molecules, but also their target. Cells of the immune system need consideration as major players and possible targets for therapeutic manipulation of angiogenesis/lymphangiogenesis in chronic inflammatory disorders and tumors
Diffraction dissociation in proton-proton collisions at = 0.9 TeV, 2.76 TeV and 7 TeV with ALICE at the LHC
The relative rates of single- and double- diffractive processes were measured
with the ALICE detector by studying properties of gaps in the pseudorapidity
distribution of particles produced in proton-proton collisions at =
0.9 TeV, 2.76 TeV and 7 TeV. ALICE triggering efficiencies are determined for
various classes of events, using a detector simulation validated with data on
inclusive particle production. Cross-sections are determined using van der Meer
scans to measure beam properties and obtain a measurement of the luminosity
Frictional state evolution during normal stress perturbations probed with ultrasonic waves
Fault normal stress changes dynamically during earthquake rupture; however, the impact of these changes on dynamic frictional strength is poorly understood. Here we report on a laboratory study to investigate the effect of normal stress perturbations on the friction of westerly granite surfaces sheared under normal stresses of 1-25 MPa. We measure changes in surface friction and elastic properties, using acoustic waves, for step changes in normal stress of 1–50% and shearing velocities of 1-100 μm/s. We demonstrate that transmitted elastic wave amplitude is a reliable proxy for the real contact area at the fault interface at steady state. For step increases in normal stress, wave amplitude increases immediately and then continues to increase during elastic shear loading to a peak value from which it decreases as fault slip rate increases. Friction changes in a similar fashion, showing an inelastic increase over a characteristic shear displacement that is independent of loading rate. Perturbations in normal stress during shear cause excursions in the frictional slip rate that must be accounted for in order to accurately predict the evolution of fault strength and elastic properties. Our work improves understanding of induced seismicity and triggered earthquakes with particular focus on simulating static triggering and stress transfer phenomena using rate-and-state frictional formulations in earthquake rupture models
Signaling events involved in cytokine and chemokine production induced by secretory phospholipase A2 in human lung macrophages.
7openopenGranata F; Frattini A; Loffredo S; Del Prete A; Sozzani S; Marone G; Triggiani M.Granata, F; Frattini, A; Loffredo, S; DEL PRETE, Annalisa; Sozzani, Silvano; Marone, G; Triggiani, M
Mechanisms for slow strengthening in granular materials
Several mechanisms cause a granular material to strengthen over time at low
applied stress. The strength is determined from the maximum frictional force
F_max experienced by a shearing plate in contact with wet or dry granular
material after the layer has been at rest for a waiting time \tau. The layer
strength increases roughly logarithmically with \tau -only- if a shear stress
is applied during the waiting time. The mechanisms of strengthening are
investigated by sensitive displacement measurements and by imaging of particle
motion in the shear zone. Granular matter can strengthen due to a slow shift in
the particle arrangement under shear stress. Humidity also leads to
strengthening, but is found not to be its sole cause. In addition to these time
dependent effects, the static friction coefficient can also be increased by
compaction of the granular material under some circumstances, and by cycling of
the applied shear stress.Comment: 21 pages, 11 figures, submitted to Phys. Rev.
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