Thermally activated crack fronts propagating in pinning disorder: simultaneous brittle/creep behaviour depending on scale.

We study theoretically the propagation of a crack front in mode I along an interface in a disordered elastic medium, with a numerical model considering a thermally activated rheology, toughness disorder and long-range elastic interactions. This model reproduces not only the large-scale dynamics of the crack front position in fast or creep loading regimes, but also the small-scale self-affine behaviour of the front. Two different scaling laws are predicted for the front morphology, with a Hurst exponent of 0.5 at small scales and a logarithmic scaling law at large scales, consistently with experiments. The prefactor of these scaling laws is expressed as a function of the temperature, and of the quenched disorder characteristics. The cross-over between these regimes is expressed as a function of the quenched disorder amplitude, and is proportional to the average energy release rate, and to the inverse of temperature. This model captures as well the experimentally observed local velocity fluctuation probability distribution, with a high-velocity tail P(v)∼v -2.6 This feature is shown to arise when the quenched disorder is sufficiently large, whereas smaller toughness fluctuations lead to a lognormal-like velocity distribution. Overall, the system is shown to obey a scaling determined by two distinct mechanisms as a function of scale: namely, the large scales display fluctuations similar to an elastic line in an annealed noise excited as the average front travels through the pinning landscape, while small scales display a balance between thresholds in possible elastic forces and quenched disorder.This article is part of the theme issue 'Statistical physics of fracture and earthquakes'.

Dynamic friction and the origin of the complexity of earthquake sources.

We study a simple antiplane fault of finite length embedded in a homogeneous isotropic elastic solid to understand the origin of seismic source heterogeneity in the presence of nonlinear rate- and state-dependent friction. All the mechanical properties of the medium and friction are assumed homogeneous. Friction includes a characteristic length that is longer than the grid size so that our models have a well-defined continuum limit. Starting from a heterogeneous initial stress distribution, we apply a slowly increasing uniform stress load far from the fault and we simulate the seismicity for a few 1000 events. The style of seismicity produced by this model is determined by a control parameter associated with the degree of rate dependence of friction. For classical friction models with rate-independent friction, no complexity appears and seismicity is perfectly periodic. For weakly rate-dependent friction, large ruptures are still periodic, but small seismicity becomes increasingly nonstationary. When friction is highly rate-dependent, seismicity becomes nonperiodic and ruptures of all sizes occur inside the fault. Highly rate-dependent friction destabilizes the healing process producing premature healing of slip and partial stress drop. Partial stress drop produces large variations in the state of stress that in turn produce earthquakes of different sizes. Similar results have been found by other authors using the Burridge and Knopoff model. We conjecture that all models in which static stress drop is only a fraction of the dynamic stress drop produce stress heterogeneity.

Effects of arginine, growth hormone-releasing hormone (GHRH) and neostigmine administered singly or in paired combinations on growth hormone (GH) release in pigs.

In human, arginine (ARG) induces growth hormone (GH) release, probably via a decrease in somatostatinergic tone. To assess the mechanism by which ARG mediates GH release in pigs, the effects on plasma GH release of ARG (1 g/kg body weight, infused between times -15 and -5 min), growth hormone-releasing hormone (GHRH, 2 micrograms/kg, at time 0 min) and neostigmine, a cholinesterase inhibitor (NEO, 50 micrograms/kg, at time 4 min), administered intravenously singly or in paired combinations were investigated in piglets between times -30 and 100 min. ARG and GHRH had additive effects on GH release. No potentialization was observed between the two treatments. GH response was higher following the combination of NEO and GHRH treatments than after NEO or GHRH given alone. NEO had no further effect on ARG-induced GH secretion. Therefore, our results suggest that the mechanism by which ARG stimulates GH secretion in pig is the same as in human.

Plasma growth hormone (GH), insulin and amino acid responses to arginine with or without aspartic acid in pigs. Effect of the dose.

The aim of the present study was to examine, for the first time in pigs, the dose-dependent effect of arginine (ARG) on growth hormone (GH) and insulin release and the effect of the combined ARG and aspartic acid (ASP) treatment on GH and insulin release. ARG (0.5 or 1 g/kg body weight) with or without an equimolar supplement of ASP (0.38 or 0.76 g/kg, respectively) was administered in piglets via the duodenum. ARG increased plasma arginine, ornithine, urea, proline and branched chain amino acid concentrations. ASP increased specifically plasma aspartic acid, glutamic acid, alanine and citrulline concentrations. Plasma insulin increased with no apparent difference between treatments. Maximum GH level and the area under the GH curve (AUC) were increased in a dose-dependent manner in response to ARG treatment. GH response to the combined ARG and ASP treatment (ARGASP) was delayed compared to ARG alone and was not dose-dependent. AUC for GH after ARGASP treatments were intermediate between those observed after the two ARG doses. Our data suggest that high ASP doses transiently inhibit and delay ARG-induced GH release in pigs and that an equimolar supplement of ASP stimulates or inhibits ARG-induced GH release depending on the dose used.

Developmental changes in insulin-like growth factor-I (IGF-I) receptor levels and plasma IGF-I concentrations in large white and Meishan pigs.

The developmental pattern of insulin-like growth factor-I receptor (IGF-IR) and plasma IGF-I concentrations were examined in longissimus dorsi (LD), trapezius (TR), and liver from the last third of gestation up to 1 year of age in male Large White (LW) and Meishan (MS) pigs. Plasma IGF-I concentrations increased between 75 days of gestation and 180 days of age with a 100-fold increase and decreased thereafter. At 180 and 365 days of age, plasma IGF-I concentrations were higher in LW than in MS pigs. 125I-IGF-I specific binding was detected in liver and skeletal muscle (not determined in fetal TR) from 75 days of gestation until the adult stage in both breeds. Affinity cross-linking experiments followed by electrophoresis under reducing conditions revealed the presence of one band with an apparent molecular weight of 140 kDa in fetal liver and LD. In displacement experiments, data indicated that IGF-I bound specifically to IGF-IR in both prenatal and postnatal tissues. Specific binding increased between 75 and 90 days of gestation in both liver and LD. It remained elevated until 103-113 days of gestation and tended to be higher in MS than in LW fetal liver. After birth, it decreased to remain stable thereafter. The developmental pattern of IGF-IR is concluded to be similar in liver and skeletal muscle of LW and MS pigs. The few differences observed between LW and MS pigs cannot account for their different growth performances. The high binding in fetus suggests that IGF-IR may play an important role in fetal growth and development.