Micro-mechanical Modeling for Rate-Dependent Behavior of Salt Rock under Cyclic Loading

Copyright © 2020 John Wiley & Sons, Inc.The dependence of rock behavior on the deformation rate is still not well understood. In salt rock, the fundamental mechanisms that drive the accumulation of irreversible deformation, the reduction of stiffness and the development of hysteresis during cyclic loading are usually attributed to intracrystalline plasticity and diffusion. We hypothesize that at low pressure and low temperature, the rate-dependent behavior of salt rock is governed by water-assisted diffusion along grain boundaries. Accordingly, a chemo-mechanical homogenization framework is proposed, in which the Representative Elementary Volume (REV) is viewed as a homogeneous polycrystalline matrix that contains sliding grain-boundary cracks. The slip is related to the mass of salt ions that diffuse along the crack surface. The relationship between fluid inclusion-scale and REV-scale stresses and strains is established by using the Mori-Tanaka homogenization scheme. It is noted from the model that a lower strain rate and a larger number of sliding cracks enhance stiffness reduction and hysteresis. Thinner sliding cracks (i.e. thinner brine films) promote stiffness reduction and accelerate stress redistributions. The larger the volume fraction of the crack inclusions, the larger the REV deformation and the larger the hysteresis. Results presented in this study shed light on the mechanical behavior of salt-rock that is pertinent to the design of geological storage facilities that undergo cyclic unloading, which could help optimize the energy production cycle with low carbon emissions

Micro-mechanical Modeling for Rate-Dependent Behavior of Salt Rock under Cyclic Loading

The dependence of rock behavior to the deformation rate is still not well understood. In salt rock, the fundamental mechanisms that drive the accumulation of irreversible deformation, the reduction of stiffness and the development of hysteresis during cyclic loading are usually attributed to intracrystalline plasticity and diffusion. We hypothesize that at low pressure and low temperature, the rate-dependent behavior of salt rock is governed by water-assisted diffusion along grain boundaries. Accordingly, a chemo-mechanical homogenization framework is proposed, in which the Representative Elementary Volume (REV) is viewed as a homogeneous polycrystalline matrix that contains sliding grain-boundary cracks. The slip is related to the mass of salt ions that diffuse along the crack surface. The rate of diffusion is calculated by a pressure solution model. The relationship between fluid inclusion-scale and REV-scale stresses and strains is established by using the Mori-Tanaka homogenization scheme. The proposed rate-dependent homogenization model is calibrated against cyclic compression tests. It is noted from the model that a lower strain rate and a larger number of sliding cracks enhances stiffness reduction and hysteresis. Thinner sliding cracks (i.e. thinner brine films) promote stiffness reduction and accelerate stress redistributions in the crack inclusions. Higher roughness angles lead to an increased difference of normal stress along the different segments of the crack plane and to a reduced diffusion path, which both amplify the reduction of stiffness and the development of hysteresis. The larger the volume fraction of the crack inclusions, the larger the REV deformation and the larger the hysteresis. Results presented in this study shed light on the mechanical behavior of salt-rock that is pertinent to the design of geological storage facilities that undergo cyclic unloading, which could help optimize the energy production cycle with low carbon emissions

Stat3 isoforms, α and β, demonstrate distinct intracellular dynamics with prolonged nuclear retention of Stat3β mapping to its unique C-terminal end

Two isoforms of Stat3 (signal transducer and activator of transcription 3) are expressed in cells, alpha (p92) and beta (p83), both derived from a single gene by alternative mRNA splicing. The 55-residue C-terminal transactivation domain of Stat3alpha is deleted in Stat3beta and replaced by seven unique C-terminal residues (CT7) whose function remains uncertain. We subcloned the open reading frames of Stat3alpha and Stat3beta into the C terminus of green fluorescent protein (GFP). Fluorescent microscopic analysis of HEK293T cells transiently transfected with GFP-Stat3alpha or GFP-Stat3beta revealed similar kinetics and cytokine concentration dependence of nuclear accumulation; these findings were confirmed by high throughput microscope analysis of murine embryonic fibroblasts that lacked endogenous Stat3 but stably expressed either GFP-Stat3alpha or GFP-Stat3beta. However, although time to half-maximal cytoplasmic reaccumulation after cytokine withdrawal was 15 min for GFP-Stat3alpha, it was >180 min for GFP-Stat3beta. Furthermore, although the intranuclear mobility of GFP-Stat3alpha was rapid and increased with cytokine stimulation, the intranuclear mobility of GFP-Stat3beta in unstimulated cells was slower than that of GFP-Stat3alpha in unstimulated cells and was slowed further following cytokine stimulation. Deletion of the unique CT7 domain from Stat3beta eliminated prolonged nuclear retention but did not alter its intranuclear mobility. Thus, Stat3alpha and Stat3beta have distinct intracellular dynamics, with Stat3beta exhibiting prolonged nuclear retention and reduced intranuclear mobility especially following ligand stimulation. Prolonged nuclear retention, but not reduced intranuclear mobility, mapped to the CT7 domain of Stat3beta

Experimental Implementation of the Quantum Random-Walk Algorithm

The quantum random walk is a possible approach to construct new quantum algorithms. Several groups have investigated the quantum random walk and experimental schemes were proposed. In this paper we present the experimental implementation of the quantum random walk algorithm on a nuclear magnetic resonance quantum computer. We observe that the quantum walk is in sharp contrast to its classical counterpart. In particular, the properties of the quantum walk strongly depends on the quantum entanglement.Comment: 5 pages, 4 figures, published versio

Implementing universal multi-qubit quantum logic gates in three and four-spin systems at room temperature

In this paper, we present the experimental realization of multi-qubit gates $$ in macroscopic ensemble of three-qubit and four-qubit molecules. Instead of depending heavily on the two-bit universal gate, which served as the basic quantum operation in quantum computing, we use pulses of well-defined frequency and length that simultaneously apply to all qubits in a quantum register. It appears that this method is experimentally convenient when this procedure is extended to more qubits on some quantum computation, and it can also be used in other physical systems.Comment: 5 Pages, 2 Figure

The discovery of potent, selective, and reversible inhibitors of the house dust mite peptidase allergen Der p 1: an innovative approach to the treatment of allergic asthma.

Blocking the bioactivity of allergens is conceptually attractive as a small-molecule therapy for allergic diseases but has not been attempted previously. Group 1 allergens of house dust mites (HDM) are meaningful targets in this quest because they are globally prevalent and clinically important triggers of allergic asthma. Group 1 HDM allergens are cysteine peptidases whose proteolytic activity triggers essential steps in the allergy cascade. Using the HDM allergen Der p 1 as an archetype for structure-based drug discovery, we have identified a series of novel, reversible inhibitors. Potency and selectivity were manipulated by optimizing drug interactions with enzyme binding pockets, while variation of terminal groups conferred the physicochemical and pharmacokinetic attributes required for inhaled delivery. Studies in animals challenged with the gamut of HDM allergens showed an attenuation of allergic responses by targeting just a single component, namely, Der p 1. Our findings suggest that these inhibitors may be used as novel therapies for allergic asthma

Microbiological, histological, immunological, and toxin response to antibiotic treatment in the mouse model of Mycobacterium ulcerans disease.

Mycobacterium ulcerans infection causes a neglected tropical disease known as Buruli ulcer that is now found in poor rural areas of West Africa in numbers that sometimes exceed those reported for another significant mycobacterial disease, leprosy, caused by M. leprae. Unique among mycobacterial diseases, M. ulcerans produces a plasmid-encoded toxin called mycolactone (ML), which is the principal virulence factor and destroys fat cells in subcutaneous tissue. Disease is typically first manifested by the appearance of a nodule that eventually ulcerates and the lesions may continue to spread over limbs or occasionally the trunk. The current standard treatment is 8 weeks of daily rifampin and injections of streptomycin (RS). The treatment kills bacilli and wounds gradually heal. Whether RS treatment actually stops mycolactone production before killing bacilli has been suggested by histopathological analyses of patient lesions. Using a mouse footpad model of M. ulcerans infection where the time of infection and development of lesions can be followed in a controlled manner before and after antibiotic treatment, we have evaluated the progress of infection by assessing bacterial numbers, mycolactone production, the immune response, and lesion histopathology at regular intervals after infection and after antibiotic therapy. We found that RS treatment rapidly reduced gross lesions, bacterial numbers, and ML production as assessed by cytotoxicity assays and mass spectrometric analysis. Histopathological analysis revealed that RS treatment maintained the association of the bacilli with (or within) host cells where they were destroyed whereas lack of treatment resulted in extracellular infection, destruction of host cells, and ultimately lesion ulceration. We propose that RS treatment promotes healing in the host by blocking mycolactone production, which favors the survival of host cells, and by killing M. ulcerans bacilli