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Phase field approach to heterogeneous crystal nucleation in alloys
We extend the phase field model of heterogeneous crystal nucleation developed recently [L. Gránásy, T. Pusztai, D. Saylor, and J. A. Warren, Phys. Rev. Lett. 98, 035703 (2007)] to binary alloys. Three approaches are considered to incorporate foreign walls of tunable wetting properties into phase field simulations: a continuum realization of the classical spherical cap model (called Model A herein), a non-classical approach (Model B) that leads to ordering of the liquid at the wall, and to the appearance of a surface spinodal, and a non-classical model (Model C) that allows for the appearance of local states at the wall that are accessible in the bulk phases only via thermal fluctuations. We illustrate the potential of the presented phase field methods for describing complex polycrystalline solidification morphologies including the shish-kebab structure, columnar to equiaxed transition, and front-particle interaction in binary alloys
Nonequilibrium critical dynamics of the two-dimensional Ising model quenched from a correlated initial state
The universality class, even the order of the transition, of the
two-dimensional Ising model depends on the range and the symmetry of the
interactions (Onsager model, Baxter-Wu model, Turban model, etc.), but the
critical temperature is generally the same due to self-duality. Here we
consider a sudden change in the form of the interaction and study the
nonequilibrium critical dynamical properties of the nearest-neighbor model. The
relaxation of the magnetization and the decay of the autocorrelation function
are found to display a power law behavior with characteristic exponents that
depend on the universality class of the initial state.Comment: 6 pages, 5 figures, submitted to Phys. Rev.
Atomic Force Microscopy of height fluctuations of fibroblast cells
We investigated the nanometer scale height fluctuations of 3T3 fibroblast
cells with the atomic force microscope (AFM) under physiological conditions.
Correlation between these fluctuations and lateral cellular motility can be
observed. Fluctuations measured on leading edges appear to be predominantly
related to actin polymerization-depolymerization processes. We found fast (5
Hz) pulsatory behavior with 1--2 nm amplitude on a cell with low motility
showing emphasized structure of stress fibres. Myosin driven contractions of
stress fibres are thought to induce this pulsation.Comment: 6 pages, 5 figures, 1 tabl
Phase-field approach to polycrystalline solidification including heterogeneous and homogeneous nucleation
Advanced phase-field techniques have been applied to address various aspects of polycrystalline solidification including different modes of crystal nucleation. The height of the nucleation barrier has been determined by solving the appropriate Euler-Lagrange equations. The examples shown include the comparison of various models of homogeneous crystal nucleation with atomistic simulations for the single component hard-sphere fluid. Extending previous work for pure systems (Gránásy L, Pusztai T, Saylor D and Warren J A 2007 Phys. Rev. Lett. 98 art no 035703), heterogeneous nucleation in unary and binary systems is described via introducing boundary conditions that realize the desired contact angle. A quaternion representation of crystallographic orientation of the individual particles (outlined in Pusztai T, Bortel G and Gránásy L 2005 Europhys. Lett. 71 131) has been applied for modeling a broad variety of polycrystalline structures including crystal sheaves, spherulites and those built of crystals with dendritic, cubic, rhombododecahedral, truncated octahedral growth morphologies. Finally, we present illustrative results for dendritic polycrystalline solidification obtained using an atomistic phase-field model
Microglia protect against brain injury and their selective elimination dysregulates neuronal network activity after stroke
Microglia are the main immune cells of the brain and contribute to common brain diseases. However, it is unclear how microglia influence neuronal activity and survival in the injured brain in vivo. Here we develop a precisely controlled model of brain injury induced by cerebral ischaemia combined with fast in vivo two-photon calcium imaging and selective microglial manipulation. We show that selective elimination of microglia leads to a striking, 60% increase in infarct size, which is reversed by microglial repopulation. Microglia-mediated protection includes reduction of excitotoxic injury, since an absence of microglia leads to dysregulated neuronal calcium responses, calcium overload and increased neuronal death. Furthermore, the incidence of spreading depolarization (SD) is markedly reduced in the absence of microglia. Thus, microglia are involved in changes in neuronal network activity and SD after brain injury in vivo that could have important implications for common brain diseases
Low-energy excitations in the three-dimensional random-field Ising model
The random-field Ising model (RFIM), one of the basic models for quenched
disorder, can be studied numerically with the help of efficient ground-state
algorithms. In this study, we extend these algorithm by various methods in
order to analyze low-energy excitations for the three-dimensional RFIM with
Gaussian distributed disorder that appear in the form of clusters of connected
spins. We analyze several properties of these clusters. Our results support the
validity of the droplet-model description for the RFIM.Comment: 10 pages, 9 figure
Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms
Neurotropic herpesviruses can establish lifelong infection in humans and contribute to severe diseases including encephalitis and neurodegeneration. However, the mechanisms through which the brain's immune system recognizes and controls viral infections propagating across synaptically linked neuronal circuits have remained unclear. Using a well-established model of alphaherpesvirus infection that reaches the brain exclusively via retrograde transsynaptic spread from the periphery, and in vivo two-photon imaging combined with high resolution microscopy, we show that microglia are recruited to and isolate infected neurons within hours. Selective elimination of microglia results in a marked increase in the spread of infection and egress of viral particles into the brain parenchyma, which are associated with diverse neurological symptoms. Microglia recruitment and clearance of infected cells require cell-autonomous P2Y12 signalling in microglia, triggered by nucleotides released from affected neurons. In turn, we identify microglia as key contributors to monocyte recruitment into the inflamed brain, which process is largely independent of P2Y12. P2Y12-positive microglia are also recruited to infected neurons in the human brain during viral encephalitis and both microglial responses and leukocyte numbers correlate with the severity of infection. Thus, our data identify a key role for microglial P2Y12 in defence against neurotropic viruses, whilst P2Y12-independent actions of microglia may contribute to neuroinflammation by facilitating monocyte recruitment to the sites of infection
Viral epidemics in a cell culture: novel high resolution data and their interpretation by a percolation theory based model
Because of its relevance to everyday life, the spreading of viral infections
has been of central interest in a variety of scientific communities involved in
fighting, preventing and theoretically interpreting epidemic processes. Recent
large scale observations have resulted in major discoveries concerning the
overall features of the spreading process in systems with highly mobile
susceptible units, but virtually no data are available about observations of
infection spreading for a very large number of immobile units. Here we present
the first detailed quantitative documentation of percolation-type viral
epidemics in a highly reproducible in vitro system consisting of tens of
thousands of virtually motionless cells. We use a confluent astroglial
monolayer in a Petri dish and induce productive infection in a limited number
of cells with a genetically modified herpesvirus strain. This approach allows
extreme high resolution tracking of the spatio-temporal development of the
epidemic. We show that a simple model is capable of reproducing the basic
features of our observations, i.e., the observed behaviour is likely to be
applicable to many different kinds of systems. Statistical physics inspired
approaches to our data, such as fractal dimension of the infected clusters as
well as their size distribution, seem to fit into a percolation theory based
interpretation. We suggest that our observations may be used to model epidemics
in more complex systems, which are difficult to study in isolation.Comment: To appear in PLoS ONE. Supporting material can be downloaded from
http://amur.elte.hu/BDGVirus
Microglia modulate blood flow, neurovascular coupling, and hypoperfusion via purinergic actions
Microglia, the main immunocompetent cells of the brain, regulate neuronal function, but their contribution to cerebral blood flow (CBF) regulation has remained elusive. Here, we identify microglia as important modulators of CBF both under physiological conditions and during hypoperfusion. Microglia establish direct, dynamic purinergic contacts with cells in the neurovascular unit that shape CBF in both mice and humans. Surprisingly, the absence of microglia or blockade of microglial P2Y12 receptor (P2Y12R) substantially impairs neurovascular coupling in mice, which is reiterated by chemogenetically induced microglial dysfunction associated with impaired ATP sensitivity. Hypercapnia induces rapid microglial calcium changes, P2Y12R-mediated formation of perivascular phylopodia, and microglial adenosine production, while depletion of microglia reduces brain pH and impairs hypercapnia-induced vasodilation. Microglial actions modulate vascular cyclic GMP levels but are partially independent of nitric oxide. Finally, microglial dysfunction markedly impairs P2Y12R-mediated cerebrovascular adaptation to common carotid artery occlusion resulting in hypoperfusion. Thus, our data reveal a previously unrecognized role for microglia in CBF regulation, with broad implications for common neurological diseases
Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms
Neurotropic herpesviruses can establish lifelong infection in humans and contribute to severe diseases including encephalitis and neurodegeneration. However, the mechanisms through which the brain's immune system recognizes and controls viral infections propagating across synaptically linked neuronal circuits have remained unclear. Using a well-established model of alphaherpesvirus infection that reaches the brain exclusively via retrograde transsynaptic spread from the periphery, and in vivo two-photon imaging combined with high resolution microscopy, we show that microglia are recruited to and isolate infected neurons within hours. Selective elimination of microglia results in a marked increase in the spread of infection and egress of viral particles into the brain parenchyma, which are associated with diverse neurological symptoms. Microglia recruitment and clearance of infected cells require cell-autonomous P2Y12 signalling in microglia, triggered by nucleotides released from affected neurons. In turn, we identify microglia as key contributors to monocyte recruitment into the inflamed brain, which process is largely independent of P2Y12. P2Y12-positive microglia are also recruited to infected neurons in the human brain during viral encephalitis and both microglial responses and leukocyte numbers correlate with the severity of infection. Thus, our data identify a key role for microglial P2Y12 in defence against neurotropic viruses, whilst P2Y12-independent actions of microglia may contribute to neuroinflammation by facilitating monocyte recruitment to the sites of infection