704 research outputs found

    Time evolution of the QED vacuum in a uniform electric Field: Complete analytic solution by spinorial decomposition

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    Exact analytical solutions are presented for the time evolution of the density of pairs produced in the QED vacuum by a time-independent, uniform electric field. The mathematical tool used here to describe the pair production is the Dirac-Heisenberg-Wigner function introduced before [Phys. Rev. D 44, 1825 (1991)]. The initial value problem for this function is solved by decomposing the solution into a product of spinors. The equations for spinors are much simpler and are solved analytically. These calculations are nonperturbative since pair production is due to quantum-mechanical tunneling and the explicit solutions clearly exhibit their nonanalytic behavior.Comment: 6 pages, 1 figur

    Sample handling for kinetics and molecular assembly in flow cytometry

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    Matter of Salmon, 24 A.D.2d 962, 265 N.Y.S.2d 373 (1st Dep\u27t 1965)

    The Transition from Proliferation to Differentiation Is Delayed in Satellite Cells from Mice Lacking MyoD

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    AbstractSatellite cells from adult rat muscle coexpress proliferating cell nuclear antigen and MyoD upon entry into the cell cycle, suggesting that MyoD plays a role during the recruitment of satellite cells. Moreover, the finding that muscle regeneration is compromised in MyoD−/− mice, has provided evidence for the role of MyoD during myogenesis in adult muscle. In order to gain further insight into the role of MyoD during myogenesis in the adult, we compared satellite cells from MyoD−/− and wildtype mice as they progress through myogenesis in single-myofiber cultures and in tissue-dissociated cell cultures (primary cultures). Satellite cells undergoing proliferation and differentiation were traced immunohistochemically using antibodies against various regulatory proteins. In addition, an antibody against the mitogen-activated protein kinases ERK1 and ERK2 was used to localize the cytoplasm of the fiber-associated satellite cells regardless of their ability to express specific myogenic regulatory factor proteins. We show that during the initial days in culture the myofibers isolated from both the MyoD−/− and the wildtype mice contain the same number of proliferating, ERK+ satellite cells. However, the MyoD−/− satellite cells continue to proliferate and only a very small number of cells transit into the myogenin+ state, whereas the wildtype cells exit the proliferative compartment and enter the myogenin+ stage. Analyzing tissue-dissociated cultures of MyoD−/− satellite cells, we identified numerous cells whose nuclei were positive for the Myf5 protein. In contrast, quantification of Myf5+ cells in the wildtype cultures was difficult due to the low level of Myf5 protein present. The Myf5+ cells in the MyoD−/− cultures were often positive for desmin, similar to the MyoD+ cells in the wildtype cultures. Myogenin+ cells were identified in the MyoD−/− primary cultures, but their appearance was delayed compared to the wildtype cells. These “delayed” myogenin+ cells can express other differentiation markers such as MEF2A and cyclin D3 and fuse into myotubes. Taken together, our studies suggest that the presence of MyoD is critical for the normal progression of satellite cells into the myogenin+, differentiative state. It is further proposed that the Myf5+/MyoD− phenotype may represent the myogenic stem cell compartment which is capable of maintaining the myogenic precursor pool in the adult muscle

    Megf10 regulates the progression of the satellite cell myogenic program

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    We identify here the multiple epidermal growth factor repeat transmembrane protein Megf10 as a quiescent satellite cell marker that is also expressed in skeletal myoblasts but not in differentiated myofibers. Retroviral expression of Megf10 in myoblasts results in enhanced proliferation and inhibited differentiation. Infected myoblasts that fail to differentiate undergo cell cycle arrest and can reenter the cell cycle upon serum restimulation. Moreover, experimental modulations of Megf10 alter the expression levels of Pax7 and the myogenic regulatory factors. In contrast, Megf10 silencing in activated satellite cells on individual fibers or in cultured myoblasts results in a dramatic reduction in the cell number, caused by myogenin activation and precocious differentiation as well as a depletion of the self-renewing Pax7+/MyoD− population. Additionally, Megf10 silencing in MyoD−/− myoblasts results in down-regulation of Notch signaling components. We conclude that Megf10 represents a novel transmembrane protein that impinges on Notch signaling to regulate the satellite cell population balance between proliferation and differentiation

    Multiscale framework for predicting the coupling between deformation and fluid diffusion in porous rocks

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    In this project, a predictive multiscale framework will be developed to simulate the strong coupling between solid deformations and fluid diffusion in porous rocks. We intend to improve macroscale modeling by incorporating fundamental physical modeling at the microscale in a computationally efficient way. This is an essential step toward further developments in multiphysics modeling, linking hydraulic, thermal, chemical, and geomechanical processes. This research will focus on areas where severe deformations are observed, such as deformation bands, where classical phenomenology breaks down. Multiscale geometric complexities and key geomechanical and hydraulic attributes of deformation bands (e.g., grain sliding and crushing, and pore collapse, causing interstitial fluid expulsion under saturated conditions), can significantly affect the constitutive response of the skeleton and the intrinsic permeability. Discrete mechanics (DEM) and the lattice Boltzmann method (LBM) will be used to probe the microstructure---under the current state---to extract the evolution of macroscopic constitutive parameters and the permeability tensor. These evolving macroscopic constitutive parameters are then directly used in continuum scale predictions using the finite element method (FEM) accounting for the coupled solid deformation and fluid diffusion. A particularly valuable aspect of this research is the thorough quantitative verification and validation program at different scales. The multiscale homogenization framework will be validated using X-ray computed tomography and 3D digital image correlation in situ at the Advanced Photon Source in Argonne National Laboratories. Also, the hierarchical computations at the specimen level will be validated using the aforementioned techniques in samples of sandstone undergoing deformation bands

    Microstructural Shear Localization in Plastic Deformation of Amorphous Solids

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    The shear-transformation-zone (STZ) theory of plastic deformation predicts that sufficiently soft, non-crystalline solids are linearly unstable against forming periodic arrays of microstructural shear bands. A limited nonlinear analysis indicates that this instability may be the mechanism responsible for strain softening in both constant-stress and constant-strain-rate experiments. The analysis presented here pertains only to one-dimensional banding patterns in two-dimensional systems, and only to very low temperatures. It uses the rudimentary form of the STZ theory in which there is only a single kind of zone rather than a distribution of them with a range of transformation rates. Nevertheless, the results are in qualitative agreement with essential features of the available experimental data. The nonlinear theory also implies that harder materials, which do not undergo a microstructural instability, may form isolated shear bands in weak regions or, perhaps, at points of concentrated stress.Comment: 32 pages, 6 figure
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