Fluid permeability of deformable fracture networks

The authors consider the problem of defining the fracture permeability tensor for each grid lock in a rock mass from maps of natural fractures. For this purpose they implement a statistical model of cracked rock due to M. Oda [1985], where the permeability tensor is related to the crack geometry via a volume average of the contribution from each crack in the population. In this model tectonic stress is implicitly coupled to fluid flow through an assumed relationship between crack aperture and normal stress across the crack. The authors have included the following enhancements to the basic model: (1) a realistic model of crack closure under stress has been added along with the provision to apply tectonic stresses to the fracture system in any orientation, the application of stress results in fracture closure and consequently a reduction in permeability; (2) the fracture permeability can be superimposed onto an arbitrary anisotropic matrix permeability; (3) the fracture surfaces are allowed to slide under the application of shear stress, causing fractures to dilate and result in a permeability increase. Through an example, the authors demonstrate that significant changes in permeability magnitudes and orientations are possible when tectonic stress is applied to a fracture system

Tectonic geomorphology and late Quaternary deformation on the Ragged Mountain fault, Yakutat microplate, south coastal Alaska

The 33 km-long Ragged Mountain fault (RMF) forms the northwestern corner of the Yakutat Terrane, which is colliding with the North American plate in south coastal Alaska at ~5.5 cm/yr. The fault zone contains three types of scarps in a zone up to 175 m wide: (1) antislope scarps on the lower range front, (2) a sinuous thrust scarp at the toe of the range front, and (3) a swarm of flexural-slip scarps on the footwall. Trenches across the first two scarp types reveal evidence for two Holocene surface ruptures, plus several late Pleistocene ruptures. In the antislope scarp trench, ruptures occurred at 0.5–3.9 ka; slightly younger than 8.3 ka; and at 18.1–21.8 ka (recurrence intervals 4.4–8 kyr and 9.8–13.3 kyr). Displacements per event ranged from 15 to 40 cm. In the thrust trench ruptures are dated at 2.8–5.9 ka; 5.9–17.2 ka, and 17.2–44.9 ka (mean recurrence intervals 7.2 kyr and 19.5 kyr). Displacements per event ranged from 26 to 77 cm. We interpret the thrust fault as the primary seismogenic structure, and its largest trench displacement (77 cm) equates to the average displacement expected for a 33 km-long reverse rupture. The flexural-slip scarp, in contrast, was rapidly formed ca. 4 ka but its sag pond sediments have continued to slowly fold up to present. The southern third of the fault is dominated by large gravitational failures of the range front (as large as 2.5 km wide, 0.6-0.7 km long, and 200–250 m thick), which head in a linear, 40 m-deep range-crest trough filled with lakes, a classic expression of deep-seated gravitational slope deformation

An assessment of Evans' unified field theory I

Evans developed a classical unified field theory of gravitation and electromagnetism on the background of a spacetime obeying a Riemann-Cartan geometry. This geometry can be characterized by an orthonormal coframe theta and a (metric compatible) Lorentz connection Gamma. These two potentials yield the field strengths torsion T and curvature R. Evans tried to infuse electromagnetic properties into this geometrical framework by putting the coframe theta to be proportional to four extended electromagnetic potentials A; these are assumed to encompass the conventional Maxwellian potential in a suitable limit. The viable Einstein-Cartan(-Sciama-Kibble) theory of gravity was adopted by Evans to describe the gravitational sector of his theory. Including also the results of an accompanying paper by Obukhov and the author, we show that Evans' ansatz for electromagnetism is untenable beyond repair both from a geometrical as well as from a physical point of view. As a consequence, his unified theory is obsolete.Comment: 39 pages of latex, modified because of referee report, mistakes and typos removed, partly reformulated, taken care of M.W.Evans' rebutta

Chondroprotection by urocortin involves blockade of a mechanosensitive piezo1 ion channel: novel, exploitable pathways for the treatment and prevention of osteoarthritis?

Purpose: Currently, the only treatments for Osteoarthritis (OA) are steroidal and non-steroidal anti-inflammatory drugs, and in severe cases total joint replacement surgery. However, these strategies only ameliorate symptoms but do not address the fundamental cause of the disease. Clearly therefore, there is a need for better therapies which address the underlying cause of OA. Importantly, this includes a reduction in the number of viable chondrocytes in articular cartilage, as the severity of cartilage damage has been shown to correlate negatively with the number of remaining chondrocytes. To develop a treatment strategy at a more fundamental level therefore, it is crucial to understand the nature of this chondrocyte cell death. We have previously found that the small endogenous peptide Urocortin (Ucn) and its two cognate G protein coupled receptors (CRF-R1 and CRF-R2) are expressed by human chondrocytes and crucially, its removal from the surrounding milieu using a Ucn depleting antibody or a pan receptor antagonist (as Ucn can bind to both receptor subtypes) causes profound chondrocyte cell death. Therefore, we believe that Ucn is an essential autocrine/paracrine pro-survival factor for human chondrocytes. Here we examine the pathways involved in this chondroprotective effect of Ucn. Methods: Selective pharmacological antagonists to CRF-R1 (CP-154526, 1–50μM; Tocris) and CRF-R2 (astressin2B 1–50μM; Tocris) were used to determine the receptor subtype responsible for the pro-survival effect of Ucn in human primary articular chondrocytes. Cell death was detected using the Annexin V-FITC Apoptosis Detection Kit I (BD Bioscience) and Western immunoblotting was used to determine the status of pro-apoptotic markers. Downstream signalling pathways involved in antagonist induced cell death were investigated using the adenylate cyclase activator forskolin (0.1μM; Tocris), the phospholipase C (PLC) activator m3M3FBS (0.1μM; Tocris), and the phospholipase A2 (PLA2) inhibitor OBAA (0.1μM; Tocris). Changes in intracellular Ca2+ were detected using Fluo-4 AM permeant dye (Thermo Fisher Scientific) and this effect was studied using the non-selective cation channel blocker Gadolinium (Gd3+ 100μM; Tocris). Human chondrocytes were transfected with siRNAs derived from a selected panel (Dharmacon), to knock down and identify specific ion channel species involved in chondrocyte survival/death. Results: We found that only inhibition of CRF-R1 using CP 154526 caused antagonist induced cell death, suggesting that the chondrocyte pro-survival effect is caused by Ucn binding to CRF-R1 alone (p < 0.05). This cell death was associated with an increased expression of p53 and cleavage of both caspases 9 and 3 but not caspase 8, implicating the intrinsic apoptotic pathway in this process. Furthermore, we were able to rescue chondrocyte cell death in the presence of antagonist, with the adenylate cyclase activator forskolin and the phospholipase A2 inhibitor OBAA but not with the phospholipase C activator m3M3FBS, suggesting a role for cAMP and PKA activation and a decrease in PLA2 activity in this process. Antagonist induced cell death initially involved a large inward flux of Ca2+ resulting in Ca2+ overload. This inward movement of Ca2+ and subsequent cell death could be prevented by Gd3+ p < 0.05, implying that this process involves a non-selective cation channel and that when Ucn is present, this channel is in a closed conformation. Using an siRNA array panel, we identified Piezo1 as the target ion channel responsible for chondrocyte cell death in the absence of Ucn. Conclusions: These findings are of great interest because Piezo1 is a novel type of mechanosensor and has recently been found to be highly expressed in chondrocytes and responsible for chondrocyte cell death in a porcine acute mechanical injury model of OA. This is the first study to bring together all of these critical mediators of chondrocyte survival/death and elucidating fully the relationship between Ucn receptor activation and gating of Piezo1, may highlight novel targets as potential therapy nodes for the treatment/prevention of OA. Additionally, because of the crucial role of Ucn in chondrocyte survival, a study of the molecular status of this peptide and/or its receptor could represent novel biomarkers of OA severity and progression