111 research outputs found
Proton induced leakage current in CCDs
The effect of different proton fluences on the performance of two E2V Technologies CCD47-20 devices was investigated with particular emphasis given to the analysis of 'random telegraph signal' (RTS) generation, bright pixel generation and induced changes in base dark current level. The results show that bright pixel frequency increases as the mean energy of the proton beam is increased, and that the base dark current level after irradiation scales with the level of ionization damage. For the RTS study, 500 pixels on one device were monitored over a twelve hour period. This data set revealed a number of distinct types of pixel change level fluctuation and a system of classification has been devised. Previously published RTS data is discussed and reviewed in light of the new data
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The impact of low energy proton damage on the operational characteristics of EPIC-MOS CCDs
The University of Tübingen 3.5 MeV Van de Graaf accelerator facility was used to investigate the effect of low energy protons on the performance of the European Photon Imaging Camera (EPIC), metal–oxide semiconductor (MOS), charge coupled devices (CCDs). Two CCDs were irradiated in different parts of their detecting areas using different proton spectra and dose rates. Iron-55 was the calibration source in all cases and was used to measure any increases in charge transfer inefficiency (CTI) and spectral resolution of the CCDs. Additional changes in the CCD bright pixel table and changes in the low X-ray energy response of the device were examined.
The Monte Carlo code Stopping Range of Ions in Matter (SRIM) was used to model the effect of a 10 MeV equivalent fluence of protons interacting with the CCD. Since the non-ionising energy loss (NIEL) function could not be applied effectively at such low proton energies. From the 10 MeV values, the expected CTI degradation could be calculated and then compared to the measured CTI changes
MOS CCDs for the wide field imager on the XEUS spacecraft
In recent years the XEUS mission concept has evolved and has been the subject of several industrial studies. The mission concept has now matured to the point that it could be proposed for a Phase A study and subsequent flight programme. The key feature of XEUS will be its X-ray optic with collecting area ~30-100x that of XMM. The mission is envisaged at an orbit around the L2 point in space, and is formed from two spacecraft; one for the mirrors, and the other for the focal plane detectors. With a focal length of 50m, the plate scale of the optic is 6.5x that of XMM, which using existing focal plane technology will reduce the effective field of view to a few arc minutes. Cryogenic instrumentation, with detector sizes of a few mm can only be used for narrow field studies of target objects, and a wide field instrument is under consideration using a DEPFET pixel array to image out to a diameter of 5 arcminutes, requiring an array of dimension 70mm. It is envisaged to extend this field of view possibly out to 15 arcminutes through the use of an outer detection ring comprised of MOS CCD
Analytical and numerical analyses of the micromechanics of soft fibrous connective tissues
State of the art research and treatment of biological tissues require
accurate and efficient methods for describing their mechanical properties.
Indeed, micromechanics motivated approaches provide a systematic method for
elevating relevant data from the microscopic level to the macroscopic one. In
this work the mechanical responses of hyperelastic tissues with one and two
families of collagen fibers are analyzed by application of a new variational
estimate accounting for their histology and the behaviors of their
constituents. The resulting, close form expressions, are used to determine the
overall response of the wall of a healthy human coronary artery. To demonstrate
the accuracy of the proposed method these predictions are compared with
corresponding 3-D finite element simulations of a periodic unit cell of the
tissue with two families of fibers. Throughout, the analytical predictions for
the highly nonlinear and anisotropic tissue are in agreement with the numerical
simulations
The adipocyte: a model for integration of endocrine and metabolic signaling in energy metabolism regulation
The ability to ensure continuous availability of energy despite highly variable
supplies in the environment is a major determinant of the survival of all
species. In higher organisms, including mammals, the capacity to efficiently
store excess energy as triglycerides in adipocytes, from which stored energy
could be rapidly released for use at other sites, was developed. To orchestrate
the processes of energy storage and release, highly integrated systems operating
on several physiological levels have evolved. The adipocyte is no longer
considered a passive bystander, because fat cells actively secrete many members
of the cytokine family, such as leptin, tumor necrosis factor-alpha, and
interleukin-6, among other cytokine signals, which influence peripheral fuel
storage, mobilization, and combustion, as well as energy homeostasis. The
existence of a network of adipose tissue signaling pathways, arranged in a
hierarchical fashion, constitutes a metabolic repertoire that enables the
organism to adapt to a wide range of different metabolic challenges, such as
starvation, stress, infection, and short periods of gross energy excess
Constitutive modelling of skin ageing
The objective of this chapter is to review the main biomechanical and structural aspects associated with both intrinsic and extrinsic skin ageing, and to present potential research avenues to account for these effects in mathematical and computational models of the skin. This will be illustrated through recent work of the authors which provides a basis to those interested in developing mechanistic constitutive models capturing the mechanobiology of skin across the life course
Growth-induced buckling of an epithelial layer
We use a proof-of-concept experiment and two mathematical models to explore growth-induced tissue buckling, as may occur in colorectal crypt formation. Our experiment reveals how growth of a cultured epithelial monolayer on a thin flexible substrate can cause out-of-plane substrate deflections. We describe this system theoretically using a 'bilayer' model in which a growing cell layer adheres to a thin compressible elastic beam. We compare this with the 'supported-monolayer' model due to Edwards and Chapman (Bull Math Biol 69:1927-1942, 2007) for an incompressible expanding beam (representing crypt epithelium), which incorporates viscoelastic tethering to underlying stroma. We show that the bilayer model can exhibit buckling via parametric growth (in which the system passes through a sequence of equilibrium states, parameterised by the total beam length); in this case, non-uniformities in cell growth and variations in cell-substrate adhesion are predicted to have minimal effect on the shape of resulting buckled states. The supported-monolayer model reveals how competition between lateral supports and stromal adhesion influences the wavelength of buckled states (in parametric growth), and how non-equilibrium relaxation of tethering forces influences post-buckled shapes. This model also predicts that non-uniformities in growth patterns have a much weaker influence on buckled shapes than non-uniformities in material properties. Together, the experiment and models support the concept of patterning by growth-induced buckling and suggest that targeted softening of a growing cell layer provides greater control in shaping tissues than non-uniform growth
Electrophysiological and Structural Remodeling in Heart Failure Modulate Arrhythmogenesis. 1D Simulation Study
Background: Heart failure is a final common pathway or descriptor for various cardiac pathologies. It is associated with
sudden cardiac death, which is frequently caused by ventricular arrhythmias. Electrophysiological remodeling, intercellular
uncoupling, fibrosis and autonomic imbalance have been identified as major arrhythmogenic factors in heart failure
etiology and progression.
Objective: In this study we investigate in silico the role of electrophysiological and structural heart failure remodeling on the
modulation of key elements of the arrhythmogenic substrate, i.e., electrophysiological gradients and abnormal impulse
propagation.
Methods: Two different mathematical models of the human ventricular action potential were used to formulate models of
the failing ventricular myocyte. This provided the basis for simulations of the electrical activity within a transmural
ventricular strand. Our main goal was to elucidate the roles of electrophysiological and structural remodeling in setting the
stage for malignant life-threatening arrhythmias.
Results: Simulation results illustrate how the presence of M cells and heterogeneous electrophysiological remodeling in the
human failing ventricle modulate the dispersion of action potential duration and repolarization time. Specifically, selective
heterogeneous remodeling of expression levels for the Na+
/Ca2+ exchanger and SERCA pump decrease these
heterogeneities. In contrast, fibroblast proliferation and cellular uncoupling both strongly increase repolarization
heterogeneities. Conduction velocity and the safety factor for conduction are also reduced by the progressive structural
remodeling during heart failure.
Conclusion: An extensive literature now establishes that in human ventricle, as heart failure progresses, gradients for
repolarization are changed significantly by protein specific electrophysiological remodeling (either homogeneous or
heterogeneous). Our simulations illustrate and provide new insights into this. Furthermore, enhanced fibrosis in failing
hearts, as well as reduced intercellular coupling, combine to increase electrophysiological gradients and reduce electrical
propagation. In combination these changes set the stage for arrhythmias.This work was partially supported by (i) the "VI Plan Nacional de Investigacion Cientifica, Desarrollo e Innovacion Tecnologica" from the Ministerio de Economia y Competitividad of Spain (grant number TIN2012-37546-C03-01) and the European Commission (European Regional Development Funds - ERDF - FEDER), (ii) the Direccion General de Politica Cientifica de la Generalitat Valenciana (grant number GV/2013/119), and (iii) Programa Prometeo (PROMETEO/2012/030) de la Conselleria d'Educacio Formacio I Ocupacio, Generalitat Valenciana. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.GĂłmez GarcĂa, JF.; Cardona, K.; Romero PĂ©rez, L.; Ferrero De Loma-Osorio, JM.; TrĂ©nor Gomis, BA. (2014). Electrophysiological and Structural Remodeling in Heart Failure Modulate Arrhythmogenesis. 1D Simulation Study. PLoS ONE. 9(9). https://doi.org/10.1371/journal.pone.0106602S9
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