Drilling reveals fluid control on architecture and rupture of the Alpine Fault, New Zealand

Rock damage during earthquake slip affects fluid migration within the fault core and the surrounding damage zone, and consequently coseismic and postseismic strength evolution. Results from the first two boreholes (Deep Fault Drilling Project DFDP-1) drilled through the Alpine fault, New Zealand, which is late in its 200–400 yr earthquake cycle, reveal a >50-m-thick “alteration zone” formed by fluid-rock interaction and mineralization above background regional levels. The alteration zone comprises cemented low-permeability cataclasite and ultramylonite dissected by clay-filled fractures, and obscures the boundary between the damage zone and fault core. The fault core contains a <0.5-m-thick principal slip zone (PSZ) of low electrical resistivity and high spontaneous potential within a 2-m-thick layer of gouge and ultracataclasite. A 0.53 MPa step in fluid pressure measured across this zone confirms a hydraulic seal, and is consistent with laboratory permeability measurements on the order of 10?20 m2. Slug tests in the upper part of the boreholes yield a permeability within the distal damage zone of ?10?14 m2, implying a six-orders-of-magnitude reduction in permeability within the alteration zone. Low permeability within 20 m of the PSZ is confirmed by a subhydrostatic pressure gradient, pressure relaxation times, and laboratory measurements. The low-permeability rocks suggest that dynamic pressurization likely promotes earthquake slip, and motivates the hypothesis that fault zones may be regional barriers to fluid flow and sites of high fluid pressure gradient. We suggest that hydrogeological processes within the alteration zone modify the permeability, strength, and seismic properties of major faults throughout their earthquake cycles

Mechanism Underlying the Weight Loss and Complications of Roux-en-Y Gastric Bypass. Review

Various bariatric surgical procedures are effective at improving health in patients with obesity associated co-morbidities, but the aim of this review is to specifically describe the mechanisms through which Roux-en-Y gastric bypass (RYGB) surgery enables weight loss for obese patients using observations from both human and animal studies. Perhaps most but not all clinicians would agree that the beneficial effects outweigh the harm of RYGB; however, the mechanisms for both the beneficial and deleterious (for example postprandial hypoglycaemia, vitamin deficiency and bone loss) effects are ill understood. The exaggerated release of the satiety gut hormones, such as GLP-1 and PYY, with their central and peripheral effects on food intake has given new insight into the physiological changes that happen after surgery. The initial enthusiasm after the discovery of the role of the gut hormones following RYGB may need to be tempered as the magnitude of the effects of these hormonal responses on weight loss may have been overestimated. The physiological changes after RYGB are unlikely to be due to a single hormone, or single mechanism, but most likely involve complex gut-brain signalling. Understanding the mechanisms involved with the beneficial and deleterious effects of RYGB will speed up the development of effective, cheaper and safer surgical and non-surgical treatments for obesity