Earthquake Source Properties from Pseudotachylite

Earthquake‐radiated motions contain information that can be interpreted as source displacement and therefore related to stress drop. Except in a few notable cases, these displacements cannot be easily related to the absolute stress level or the fault strength, or attributed to a particular physical mechanism. In contrast, paleoearthquakes recorded by exhumed pseudotachylite have a known dynamic mechanism whose properties constrain the coseismic fault strength. Pseudotachylite can be used to directly address a discrepancy between seismologically measured stress drops, which are typically a few MPa, and much larger dynamic stress drops expected from thermal weakening during slip at seismic speeds in crystalline rock (Mckenzie and Brune, 1972; Sibson, 1973; Lachenbruch, 1980; Mase and Smith, 1987; Rice, 2006), and as have been observed in laboratory experiments at high slip rates (Di Toro, Hirose, Nielsen, Pennacchioni, et al., 2006). This places pseudotachylite‐derived estimates of fault strength and inferred crustal stress within the context and bounds of naturally observed earthquake source parameters: apparent stress, stress drop, and overshoot, including consideration of fault‐surface roughness, off‐fault damage, fracture energy, and the strength excess. The analysis, which assumes stress drop is related to corner frequency as in the Madariaga (1976) source model, is restricted to earthquakes of the Gole Larghe fault zone in the Italian Alps, where the dynamic shear strength is well constrained by field and laboratory measurements. We find that radiated energy is similar to or exceeds the shear‐generated heat and that the maximum strength excess is ∼16  MPa. These events have inferred earthquake source parameters that are rare, for instance, a low percentage of the global earthquake population has stress drops as large, unless fracture energy is routinely greater than in existing models, pseudotachylite is not representative of the shear strength during the earthquake that generated it, or the strength excess is larger than we have allowed

Stability of pulse-like earthquake ruptures

Pulse-like ruptures arise spontaneously in many elastodynamic rupture simulations and seem to be the dominant rupture mode along crustal faults. Pulse-like ruptures propagating under steady-state conditions can be efficiently analysed theoretically, but it remains unclear how they can arise and how they evolve if perturbed. Using thermal pressurisation as a representative constitutive law, we conduct elastodynamic simulations of pulse-like ruptures and determine the spatio-temporal evolution of slip, slip rate and pulse width perturbations induced by infinitesimal perturbations in background stress. These simulations indicate that steady-state pulses driven by thermal pressurisation are unstable. If the initial stress perturbation is negative, ruptures stop; conversely, if the perturbation is positive, ruptures grow and transition to either self-similar pulses (at low background stress) or expanding cracks (at elevated background stress). Based on a dynamic dislocation model, we develop an elastodynamic equation of motion for slip pulses, and demonstrate that steady-state slip pulses are unstable if their accrued slip $b$ is a decreasing function of the uniform background stress $\tau_\mathrm{b}$. This condition is satisfied by slip pulses driven by thermal pressurisation. The equation of motion also predicts quantitatively the growth rate of perturbations, and provides a generic tool to analyse the propagation of slip pulses. The unstable character of steady-state slip pulses implies that this rupture mode is a key one determining the minimum stress conditions for sustainable ruptures along faults, i.e., their ``strength''. Furthermore, slip pulse instabilities can produce a remarkable complexity of rupture dynamics, even under uniform background stress conditions and material properties

Direct vs. indirect optical recombination in Ge films grown on Si substrates

The optical emission spectra from Ge films on Si are markedly different from their bulk Ge counterparts. Whereas bulk Ge emission is dominated by the material's indirect gap, the photoluminescence signal from Ge films is mainly associated with its direct band gap. Using a new class of Ge-on-Si films grown by a recently introduced CVD approach, we study the direct and indirect photoluminescence from intrinsic and doped samples and we conclude that the origin of the discrepancy is the lack of self-absorption in thin Ge films combined with a deviation from quasi-equilibrium conditions in the conduction band. The latter is confirmed by a simple model suggesting that the deviation from quasi-equilibrium is caused by the much shorter recombination lifetime in the films relative to bulk Ge

Number of Common Sites Visited by N Random Walkers

We compute analytically the mean number of common sites, W_N(t), visited by N independent random walkers each of length t and all starting at the origin at t=0 in d dimensions. We show that in the (N-d) plane, there are three distinct regimes for the asymptotic large t growth of W_N(t). These three regimes are separated by two critical lines d=2 and d=d_c(N)=2N/(N-1) in the (N-d) plane. For d<2, W_N(t)\sim t^{d/2} for large t (the N dependence is only in the prefactor). For 2<d<d_c(N), W_N(t)\sim t^{\nu} where the exponent \nu= N-d(N-1)/2 varies with N and d. For d>d_c(N), W_N(t) approaches a constant as t\to \infty. Exactly at the critical dimensions there are logaritmic corrections: for d=2, we get W_N(t)\sim t/[\ln t]^N, while for d=d_c(N), W_N(t)\sim \ln t for large t. Our analytical predictions are verified in numerical simulations.Comment: 5 pages, 3 .eps figures include

Posterior stability of the shoulder depends on acromial anatomy: a biomechanical study of 3D surface models

PURPOSE Primary glenohumeral osteoarthritis is commonly associated with static posterior subluxation of the humeral head. Scapulae with static/dynamic posterior instability feature a superiorly and horizontally oriented acromion. We investigated whether the acromion acts as a restraint to posterior humeral translation. METHODS Five three-dimensional (3D) printed scapula models were biomechanically tested. A statistical shape mean model (SSMM) of the normal scapula of 40 asymptomatic shoulders was fabricated. Next, a SSMM of scapular anatomy associated with posterior subluxation was generated using data of 20 scapulae ("B1"). This model was then used to generate three models of surgical correction: glenoid version, acromial orientation, and acromial and glenoid orientation. With the joint axially loaded (100N) and the humerus stabilized, an anterior translation force was applied to the scapula in 35°, 60° and 75° of glenohumeral flexion. Translation (mm) was measured. RESULTS In the normal scapula, the humerus translates significantly less to contact with the acromion compared to all other configurations (p < .000 for all comparisons; i.e. 35°: "normal" 8,1 mm (± 0,0) versus "B1" 11,9 mm (± 0,0) versus "B1 Acromion Correction" 12,2 mm (± 0,2) versus "B1 Glenoid Correction" 13,3 mm (± 0,1)). Restoration of normal translation was only achieved with correction of glenoid and acromial anatomy (i.e. 75°: "normal" 11 mm (± 0,8) versus "B1 Acromion Correction" 17,5 mm (± 0,1) versus "B1 Glenoid Correction" 19,7 mm (± 1,3) versus "B1 Glenoid + Acromion Correction" 11,5 mm (± 1,1)). CONCLUSIONS Persistence or recurrence of static/dynamic posterior instability after correction of glenoid version alone may be related to incomplete restoration of the intrinsic stability that is conferred by a normal acromial anatomy. LEVEL OF EVIDENCE V biomechanical study

Indeterminacy of Spatiotemporal Cardiac Alternans

Cardiac alternans, a beat-to-beat alternation in action potential duration (at the cellular level) or in ECG morphology (at the whole heart level), is a marker of ventricular fibrillation, a fatal heart rhythm that kills hundreds of thousands of people in the US each year. Investigating cardiac alternans may lead to a better understanding of the mechanisms of cardiac arrhythmias and eventually better algorithms for the prediction and prevention of such dreadful diseases. In paced cardiac tissue, alternans develops under increasingly shorter pacing period. Existing experimental and theoretical studies adopt the assumption that alternans in homogeneous cardiac tissue is exclusively determined by the pacing period. In contrast, we find that, when calcium-driven alternans develops in cardiac fibers, it may take different spatiotemporal patterns depending on the pacing history. Because there coexist multiple alternans solutions for a given pacing period, the alternans pattern on a fiber becomes unpredictable. Using numerical simulation and theoretical analysis, we show that the coexistence of multiple alternans patterns is induced by the interaction between electrotonic coupling and an instability in calcium cycling.Comment: 20 pages, 10 figures, to be published in Phys. Rev.

Role for inducible cAMP early repressor in promoting pancreatic beta cell dysfunction evoked by oxidative stress in human and rat islets

Aims/hypothesis: Pro-atherogenic and pro-oxidant, oxidised LDL trigger adverse effects on pancreatic beta cells, possibly contributing to diabetes progression. Because oxidised LDL diminish the expression of genes regulated by the inducible cAMP early repressor (ICER), we investigated the involvement of this transcription factor and of oxidative stress in beta cell failure elicited by oxidised LDL. Methods: Isolated human and rat islets, and insulin-secreting cells were cultured with human native or oxidised LDL or with hydrogen peroxide. The expression of genes was determined by quantitative real-time PCR and western blotting. Insulin secretion was monitored by EIA kit. Cell apoptosis was determined by scoring cells displaying pycnotic nuclei. Results: Exposure of beta cell lines and islets to oxidised LDL, but not to native LDL raised the abundance of ICER. Induction of this repressor by the modified LDL compromised the expression of important beta cell genes, including insulin and anti-apoptotic islet brain 1, as well as of genes coding for key components of the secretory machinery. This led to hampering of insulin production and secretion, and of cell survival. Silencing of this transcription factor by RNA interference restored the expression of its target genes and alleviated beta cell dysfunction and death triggered by oxidised LDL. Induction of ICER was stimulated by oxidative stress, whereas antioxidant treatment with N-acetylcysteine or HDL prevented the rise of ICER elicited by oxidised LDL and restored beta cell functions. Conclusions/interpretation: Induction of ICER links oxidative stress to beta cell failure caused by oxidised LDL and can be effectively abrogated by antioxidant treatmen

Evidence for tuning adipocytes ICER levels for obesity care.

Abnormal adipokine production, along with defective uptake and metabolism of glucose within adipocytes, contributes to insulin resistance and altered glucose homeostasis. Recent research has highlighted one of the mechanisms that accounts for impaired production of adiponectin (ADIPOQ) and adipocyte glucose uptake in obesity. In adipocytes of human obese subjects and mice fed with a high fat diet, the level of the inducible cAMP early repressor (ICER) is diminished. Reduction of ICER elevates the cAMP response element binding protein (CREB) activity, which in turn increases the repressor activating transcription factor 3. In fine, the cascade triggers reduction in the ADIPOQ and GLUT4 levels, which ultimately hampers insulin-mediated glucose uptake. The c-Jun N-terminal kinase (JNK) interacting-protein 1, also called islet brain 1 (IB1), is a target of CREB/ICER that promotes JNK-mediated insulin resistance in adipocytes. A rise in IB1 and c-Jun levels accompanies the drop of ICER in white adipose tissues of obese mice when compared with mice fed with a chow diet. Other than the expression of ADIPOQ and glucose transport, decline in ICER expression might impact insulin signaling. Impairment of ICER is a critical issue that will need major consideration in future therapeutic purposes

Role for inducible cAMP early repressor in promoting pancreatic beta cell dysfunction evoked by oxidative stress in human and rat islets

AIMS/HYPOTHESIS: Pro-atherogenic and pro-oxidant, oxidised LDL trigger adverse effects on pancreatic beta cells, possibly contributing to diabetes progression. Because oxidised LDL diminish the expression of genes regulated by the inducible cAMP early repressor (ICER), we investigated the involvement of this transcription factor and of oxidative stress in beta cell failure elicited by oxidised LDL. METHODS: Isolated human and rat islets, and insulin-secreting cells were cultured with human native or oxidised LDL or with hydrogen peroxide. The expression of genes was determined by quantitative real-time PCR and western blotting. Insulin secretion was monitored by EIA kit. Cell apoptosis was determined by scoring cells displaying pycnotic nuclei. RESULTS: Exposure of beta cell lines and islets to oxidised LDL, but not to native LDL raised the abundance of ICER. Induction of this repressor by the modified LDL compromised the expression of important beta cell genes, including insulin and anti-apoptotic islet brain 1, as well as of genes coding for key components of the secretory machinery. This led to hampering of insulin production and secretion, and of cell survival. Silencing of this transcription factor by RNA interference restored the expression of its target genes and alleviated beta cell dysfunction and death triggered by oxidised LDL. Induction of ICER was stimulated by oxidative stress, whereas antioxidant treatment with N-acetylcysteine or HDL prevented the rise of ICER elicited by oxidised LDL and restored beta cell functions. CONCLUSIONS/INTERPRETATION: Induction of ICER links oxidative stress to beta cell failure caused by oxidised LDL and can be effectively abrogated by antioxidant treatment