Stokesian Dynamics simulation of Brownian suspensions

The non-equilibrium behaviour of concentrated colloidal dispersions is studied by Stokesian Dynamics, a general molecular-dynamics-like technique for simulating particles suspended in a viscous fluid. The simulations are of a suspension of monodisperse Brownian hard spheres in simple shear flow as a function of the Péclet number, Pe, which measures the relative importance of shear and Brownian forces. Three clearly defined regions of behaviour are revealed. There is first a Brownian-motion-dominated regime (Pe ≤ 1) where departures from equilibrium in structure and diffusion are small, but the suspension viscosity shear thins dramatically. When the Brownian and hydrodynamic forces balance (Pe ≈ 10), the dispersion forms a new ‘phase’ with the particles aligned in ‘strings’ along the flow direction and the strings are arranged hexagonally. This flow-induced ordering persists over a range of Pe and, while the structure and diffusivity now vary considerably, the rheology remains unchanged. Finally, there is a hydrodynamically dominated regime (Pe > 200) with a dramatic change in the long-time self-diffusivity and the rheology. Here, as the Péclet number increases the suspension shear thickens owing to the formation of large clusters. The simulation results are shown to agree well with experiment

Cardiac-specific Conditional Knockout of the 18-kDa Mitochondrial Translocator Protein Protects from Pressure Overload Induced Heart Failure.

Heart failure (HF) is characterized by abnormal mitochondrial calcium (Ca2+) handling, energy failure and impaired mitophagy resulting in contractile dysfunction and myocyte death. We have previously shown that the 18-kDa mitochondrial translocator protein of the outer mitochondrial membrane (TSPO) can modulate mitochondrial Ca2+ uptake. Experiments were designed to test the role of the TSPO in a murine pressure-overload model of HF induced by transverse aortic constriction (TAC). Conditional, cardiac-specific TSPO knockout (KO) mice were generated using the Cre-loxP system. TSPO-KO and wild-type (WT) mice underwent TAC for 8 weeks. TAC-induced HF significantly increased TSPO expression in WT mice, associated with a marked reduction in systolic function, mitochondrial Ca2+ uptake, complex I activity and energetics. In contrast, TSPO-KO mice undergoing TAC had preserved ejection fraction, and exhibited fewer clinical signs of HF and fibrosis. Mitochondrial Ca2+ uptake and energetics were restored in TSPO KO mice, associated with decreased ROS, improved complex I activity and preserved mitophagy. Thus, HF increases TSPO expression, while preventing this increase limits the progression of HF, preserves ATP production and decreases oxidative stress, thereby preventing metabolic failure. These findings suggest that pharmacological interventions directed at TSPO may provide novel therapeutics to prevent or treat HF

IoT-enabled emergency information supply chain architecture for elderly people: The Australian context

© 2016 Elsevier Ltd. All rights reserved. The effective delivery of emergency information to elderly people is a challenging task. Failure to deliver appropriate information can have an adverse impact on the well-being of the elderly people. This paper addresses this challenge and proposes an IoT-enabled information architecture driven approach, which is called "Resalert". Resalert offers IoT-enabled emergency information supply chain architecture pattern, IoT device architecture and system architecture. The applicability of the Resalert is evaluated by the means of an example scenario, a portable Raspberry Pi based system prototype and user evaluation. The results of this research indicate that the proposed approach seems useful to the effective delivery of emergency information to elderly people

K Pair of disjoint paths Algorithm for Protection in WDM Optical Networks

Survivable routing in wavelength division multiplexing (WDM) optical networks has been proven to be NP-hard problem. There is a trade-off between the computational time and the optimality of solutions in existing approaches to the problem. Existing heuristic approaches purely based the graph algorithms are efficient in computational time but do not offer optimal solutions and may fail in some cases even when a solution exists. Meanwhile, the integer linear programming (ILP) models offer optimal solutions but are intractable even with moderate scale networks. In this paper, we introduce a new algorithm for finding K pairs of disjoint paths which are employed as K candidate pairs for each connection in the ILP models. We introduce an ILP model for dedicated path protection in which the number of decision variables is mainly dependant on traffic requests and the constant K, not on the network siz

A Bacterial Toxin Inhibits DNA Replication Elongation through a Direct Interaction with the β Sliding Clamp

Toxin-antitoxin (TA) systems are ubiquitous on bacterial chromosomes, yet the mechanisms regulating their activity and the molecular targets of toxins remain incompletely defined. Here, we identify SocAB, an atypical TA system in Caulobacter crescentus. Unlike canonical TA systems, the toxin SocB is unstable and constitutively degraded by the protease ClpXP; this degradation requires the antitoxin, SocA, as a proteolytic adaptor. We find that the toxin, SocB, blocks replication elongation through an interaction with the sliding clamp, driving replication fork collapse. Mutations that suppress SocB toxicity map to either the hydrophobic cleft on the clamp that binds DNA polymerase III or a clamp-binding motif in SocB. Our findings suggest that SocB disrupts replication by outcompeting other clamp-binding proteins. Collectively, our results expand the diversity of mechanisms employed by TA systems to regulate toxin activity and inhibit bacterial growth, and they suggest that inhibiting clamp function may be a generalizable antibacterial strategy.Howard Hughes Medical Institute (Summer Medical Fellowship)National Science Foundation (U.S.). Graduate Research Fellowship ProgramNational Institutes of Health (U.S.) (R01GM082899