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 s\sqrt{s} = 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 $\sqrt{s}$ = 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.