Injection into the subsurface is carried out by industry for a variety of reasons: storage of waste-water; enhanced oil recovery; and for hydraulic fracture stimulation. By increasing subsurface pressures, injection can trigger felt seismicity (i.e. of sufficient magnitude to be felt at the surface) on pre-existing faults. As the number of cases of felt seismicity associated with hydraulic fracturing has increased, strategies for mitigating induced seismicity are required. However, most hydraulic stimulation activities do not induce felt seismicity. Therefore a mitigation strategy is required that is capable of differentiating the "normal" case from "abnormal" cases that trigger larger events. In this paper we test the ability of statistical methods to estimate the largest event size during stimulation, applying these approaches to two datasets collected during hydraulic stimulation in the Horn River Shale, British Columbia, where hydraulic fracturing was observed to reactivate faults. We apply these methods in a prospective manner: using the microseismicity recorded during the early phases of a stimulation stage to make forecasts about what will happen as the stage continues. We do so to put ourselves in the shoes of an operator or regulator, where decisions must be taken based on data as it is acquired, rather than a post hoc analysis once a stimulation stage has been completed. We find that the proposed methods can provide a reasonable forecast of the largest event to occur during each stage. This means that these methods can be used as the basis of a mitigation strategy for induced seismicity.

We investigate the physical processes that generate seismicity during hydraulic fracturing. Fluid processes (increases in pore pressure and poroelastic stress) are often considered to be the primary drivers. However, some recent studies have suggested that elastic stress interactions may significantly contribute to further seismicity. In this work we use a microseismic data set acquired during hydraulic fracturing to calculate elastic stress transfer during a period of fault activation and induced seismicity. We find that elastic stress changes may have weakly promoted initial failure, but at later times stress changes generally acted to inhibit further slip. Sources from within tight clusters are found to be the most significant contributor to the cumulative elastic stress changes. Given the estimated in situ stress field, relatively large increases in pore pressure are required to reach the failure envelope for these faults-on the order of 10 MPa. This threshold is far greater than the reliable cumulative elastic stress changes found in this study, with the vast majority of events receiving no more than 0.1 MPa of positive CFS, further indicating that elastic stress changes were not a significant driver, and that interaction with the pressurized fluid was required to initiate failure. Thus, cumulative stress transfer from small events near the injection well does not appear to play a significant role in the reactivation of nearby faults.

Organic shales generally have low permeability unless fractures are present. However, how gas, oil, and water flows into these fractures remains enigmatic. The alignment of clay minerals and the alignment of fractures and cracks are effective means to produce seismic anisotropy. Thus, the detection and characterization of this anisotropy can be used to infer details about lithology, rock fabric, and fracture and crack properties within the subsurface. We present a study characterizing anisotropy using S wave splitting from microseismic sources in a highly anisotropic shale. We observe very strong anisotropy (up to 30%) with predominantly VTI (vertical transverse isotropy) symmetry, but with evidence of an HTI (horizontal transverse isotropy) overprint due to a NE striking vertical fracture set parallel to the maximum horizontal compressive stress. We observe clear evidence of a shear wave triplication due to anisotropy, which to our knowledge is one of only a very few observations of such triplications in field‐scale data. We use modal proportions of minerals derived from X‐ray fluorescence data combined with realistic textures to estimate the contribution of intrinsic anisotropy as well as possible contributions of horizontally aligned cracks. We find that aligned clays can explain much of the observed anisotropy and that any cracks contributing to the vertical transverse isotropy (VTI) must have a low ratio of normal to tangential compliance (ZN/ZT), typical of isolated cracks with low hydraulic connectivity. Subhorizontal cracks have also been observed in the reservoir, and we propose that their reactivation during hydraulic fracturing may be an important mechanism to facilitate gas flow.

Cancer and dendritic cells recognize and migrate toward chemokines secreted from lymphatics and use this mechanism to invade the lymphatic system, and cancer cells metastasize through it. The lymphatic-secreted chemokine ligand CCL21 has been identified as a key regulatory molecule in the switch to a metastatic phenotype in melanoma and breast cancer cells. However, it is not known whether CCL21 inhibition is a potential therapeutic strategy for inhibition of metastasis. Here, we describe an engineered CCL21-soluble inhibitor, Chemotrap-1, which inhibits migration of metastatic melanoma cells in vivo. Two-hybrid, pull-down, and coimmunoprecipitation assays allowed us to identify a naturally occurring human zinc finger protein with CCL21 chemokine-binding properties. Further analyses revealed a short peptide (∼70 amino acids), with a predicted coiled-coil structure, which is sufficient for association with CCL21. This CCL21 chemokine-binding peptide was then fused to the Fc region of human IgG1 to generate Chemotrap-1, a human chemokine-binding Fc fusion protein. Surface plasmon resonance and chemotaxis assays showed that Chemotrap-1 binds CCL21 and inhibits CCL21-induced migration of melanoma cells in vitro with subnanomolar affinity. In addition, Chemotrap-1 blocked migration of melanoma cells toward lymphatic endothelial cells in vitro and in vivo. Finally, Chemotrap-1 strongly reduced lymphatic invasion, tracking, and metastasis of CCR7-expressing melanoma cells in vivo. Together, these results show that CCL21 chemokine inhibition by Chemotrap-1 is a potential therapeutic strategy for metastasis and provide further support for the hypothesis that lymphaticmediated metastasis is a chemokine-dependent process. Cancer Res; 70(20); 8138-48. ©2010 AACR.