Mainshocks are aftershocks of conditional foreshocks: How do foreshock statistical properties emerge from aftershock laws

The inverse Omori law for foreshocks discovered in the 1970s states that the rate of earthquakes prior to a mainshock increases on average as a power law ~ 1/(t_c-t)^p' of the time to the mainshock occurring at t_c. Here, we show that this law results from the direct Omori law for aftershocks describing the power law decay ~ 1/(t-t_c)^p of seismicity after an earthquake, provided that any earthquake can trigger its suit of aftershocks. In this picture, the seismic activity at any time is the sum of the spontaneous tectonic loading and of the activity triggered by all preceding events weighted by their corresponding Omori law. The inverse Omori law then emerges as the expected (in a statistical sense) trajectory of seismicity, conditioned on the fact that it leads to the burst of seismic activity accompanying the mainshock. The often documented apparent decrease of the b-value of the GR law at the approach to the main shock results straightforwardly from the conditioning of the path of seismic activity culminating at the mainshock. In the space domain, we predict that the phenomenon of aftershock diffusion must have its mirror process reflected into an inward migration of foreshocks towards the mainshock. In this model, foreshock sequences are special aftershock sequences which are modified by the condition to end up in a burst of seismicity associated with the mainshock.Comment: Latex document of 35 pages, 10 figure

Investigations of the radial propagation of blob-like structure in a non-confined electron cyclotron resonance heated plasma on Q-shu University Experiment with a Steady-State Spherical Tokamak

A study of radial propagation and electric fields induced by charge separation in blob-like structures has been performed in a non-confined cylindrical electron cyclotron resonance heating plasma on Q-shu University Experiment with a Steady-State Spherical Tokamak using a fast-speed camera and a Langmuir probe. The radial propagation of the blob-like structures is found to be driven by E × B drift. Moreover, these blob-like structures were found to have been accelerated, and the property of the measured radial velocities agrees with the previously proposed model [C. Theiler et al., Phys. Rev. Lett. 103, 065001 (2009)]. Although the dependence of the radial velocity on the connection length of the magnetic field appeared to be different, a plausible explanation based on enhanced short-circuiting of the current path can be proposed

Earthquake scaling relations for mid-ocean ridge transform 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): B12302, doi:10.1029/2004JB003110.A mid-ocean ridge transform fault (RTF) of length L, slip rate V, and moment release rate dot above M can be characterized by a seismic coupling coefficient χ = A E/A T, where A E ∼ dot above M/V is an effective seismic area and A T ∝ L 3/2 V −1/2 is the area above an isotherm T ref. A global set of 65 RTFs with a combined length of 16,410 km is well described by a linear scaling relation (1) A E ∝ A T, which yields χ = 0.15 ± 0.05 for T ref = 600°C. Therefore about 85% of the slip above the 600°C isotherm must be accommodated by subseismic mechanisms, and this slip partitioning does not depend systematically on either V or L. RTF seismicity can be fit by a truncated Gutenberg-Richter distribution with a slope β = 2/3 in which the cumulative number of events N 0 and the upper cutoff moment M C = μD C A C depend on A T. Data for the largest events are consistent with a self-similar slip scaling, D C ∝ A C 1/2, and a square root areal scaling (2) A C ∝ A T 1/2. If relations 1 and 2 apply, then moment balance requires that the dimensionless seismic productivity, ν0 ∝ inline equation 0/A T V, should scale as ν0 ∝ A T −1/4, which we confirm using small events. Hence the frequencies of both small and large earthquakes adjust with A T to maintain constant coupling. RTF scaling relations appear to violate the single-mode hypothesis, which states that a fault patch is either fully seismic or fully aseismic and thus implies A C ≤ A E. The heterogeneities in the stress distribution and fault structure responsible for relation 2 may arise from a thermally regulated, dynamic balance between the growth and coalescence of fault segments within a rapidly evolving fault zone.M.B. was supported by a NSF Graduate Research Fellowship, a MIT Presidential Fellowship, and the WHOI DOEI Fellowship. This research was supported by the Southern California Earthquake Center. SCEC is funded by NSF Cooperative Agreement EAR-0106924 and USGS Cooperative Agreement 02HQAG0008

Identification of the human eosinophil lineage-committed progenitor: revision of phenotypic definition of the human common myeloid progenitor

To establish effective therapeutic strategies for eosinophil-related disorders, it is critical to understand the developmental pathway of human eosinophils. In mouse hematopoiesis, eosinophils originate from the eosinophil lineage-committed progenitor (EoP) that has been purified downstream of the granulocyte/macrophage progenitor (GMP). We show that the EoP is also isolatable in human adult bone marrow. The previously defined human common myeloid progenitor (hCMP) population (Manz, M.G., T. Miyamoto, K. Akashi, and I.L. Weissman. 2002. Proc. Natl. Acad. Sci. USA. 99:11872–11877) was composed of the interleukin 5 receptor α chain+ (IL-5Rα+) and IL-5Rα− fractions, and the former was the hEoP. The IL-5Rα+CD34+CD38+IL-3Rα+CD45RA− hEoPs gave rise exclusively to pure eosinophil colonies but never differentiated into basophils or neutrophils. The IL-5Rα− hCMP generated the hEoP together with the hGMP or the human megakaryocyte/erythrocyte progenitor (hMEP), whereas hGMPs or hMEPs never differentiated into eosinophils. Importantly, the number of hEoPs increased up to 20% of the conventional hCMP population in the bone marrow of patients with eosinophilia, suggesting that the hEoP stage is involved in eosinophil differentiation and expansion in vivo. Accordingly, the phenotypic definition of hCMP should be revised to exclude the hEoP; an “IL-5Rα–negative” criterion should be added to define more homogenous hCMP. The newly identified hEoP is a powerful tool in studying pathogenesis of eosinophilia and could be a therapeutic target for a variety of eosinophil-related disorders

Seismicity rate immediately before and after mainshock rupture from high-frequency waveforms in Japan

International audienceWe analyze seismicity rate immediately before and after 82 mainshocks with the magnitudes ranging from 3 to 5 using waveforms recorded by the Hi-net borehole array in Japan. By scrutinizing high-frequency signals, we detect ~5 times as many aftershocks in the first 200 s as in the Japan Meteorological Agency catalogue. After correcting for the changing completeness level immediately after the mainshock, the aftershock rate shows a crossover from a slower decay with an Omori's law exponent p = 0.58±0.08 between 20 and 900 s after the mainshock, to a faster decay with p = 0.92±0.04 after 900 s. The foreshock seismicity rate follows an inverse Omori's law with p = 0.73±0.07 from several tens of days up to several hundred seconds before the mainshock. The seismicity rate in the 200 s immediately before the mainshock appears steady with p = 0.36±0.45. These observations can be explained by the epidemic-type aftershock sequence (ETAS) model, and the rate-and-state model for a heterogeneous stress field on the mainshock rupture plane. Alternatively, non-seismic stress changes near the source region, such as episodic aseismic slip, or pore fluid pressure fluctuations, may be invoked to explain the observation of small p values immediately before and after the mainshock

Upregulation of ANGPTL6 in mouse keratinocytes enhances susceptibility to psoriasis

Psoriasis is a chronic inflammatory skin disease marked by aberrant tissue repair. Mutant mice modeling psoriasis skin characteristics have provided useful information relevant to molecular mechanisms and could serve to evaluate therapeutic strategies. Here, we found that epidermal ANGPTL6 expression was markedly induced during tissue repair in mice. Analysis of mice overexpressing ANGPTL6 in keratinocytes (K14-Angptl6 Tg mice) revealed that epidermal ANGPTL6 activity promotes aberrant epidermal barrier function due to hyperproliferation of prematurely differentiated keratinocytes. Moreover, skin tissues of K14-Angptl6 Tg mice showed aberrantly activated skin tissue inflammation seen in psoriasis. Levels of the proteins S100A9, recently proposed as therapeutic targets for psoriasis, also increased in skin tissue of K14-Angptl6 Tg mice, but psoriasis-like inflammatory phenotypes in those mice were not rescued by S100A9 deletion. This finding suggests that decreasing S100A9 levels may not ameliorate all cases of psoriasis and that diverse mechanisms underlie the condition. Finally, we observed enhanced levels of epidermal ANGPTL6 in tissue specimens from some psoriasis patients. We conclude that the K14-Angptl6 Tg mouse is useful to investigate psoriasis pathogenesis and for preclinical testing of new therapeutics. Our study also suggests that ANGPTL6 activation in keratinocytes enhances psoriasis susceptibility