1,720,983 research outputs found
A Ottolenghi, F Ballarini, M Merzagora, Modelling radiation induced biological lesions: from initial energy depositions to chromosome aberrations.
No full textOpening lecture of the session DNA damage and radiation quality: experiments versus modelling.
No full textA Monte Carlo calculation of cell inactivation by light ions
No full textThis study simulates the exposure of V79 Chinese hamster fibroblasts to low-energy protons, deuterons and alpha-particles in the LET range 10-200 keV/mu-m. The starting assumption is that the induction of clustered lesions in DNA is a fundamental step for cell inactivation. A non-homogeneous cell population was simulated by a computer program, using as input measured morphological parameters reported in the literature. Variations in the number of traversals through each cell of the population and in the length of the traversal, depending on actual nuclear thickness and position of the traversal, the energy spread of the incident beam, and the change of LET along the tracks were included in the simulation. Microdosimetric spectra were computed and compared with spectra obtained neglecting Simulated cell survival was estimated under the assumption that particle slowing-down and stochastic aspects of cell morphology. surviving cells are those with no clustered DNA lesions or no passages. The main features of experimental RBE versus LET and particle type were reproduced by the simulations. The energy of the incident particles on survival were investigated under different assumptions about the correlation between morphological parameters. Results support the hypothesis of a relevant role of clustered DNA damage in cell killing and point out the importance of target-cell morphology and its variability in beam dosimetry and computer simulations of low-energy particle radiation effects
Modelling radiation induced biological lesions: from initial energy depositions to chromosome aberrations.
No full textThe development of biophysical models of
chromosome aberration induction has undergone considerable
improvements in the past few years. This is mainly
due to the development of new experimental techniques,
such as fluorescence in situ hybridization (FISH) and premature
chromosome condensation (PCC), and to a better
knowledge of track structure characteristics (both in the
physical and chemical stages). In particular, track structure
simulations, providing a detailed description of the
spatial distribution of energy depositions and relevant
DNA lesions, represent a useful starting point for the development
of ‘ab initio’ models. Various aspects of the processes
determining the induction and the formation kinetics
of chromosome aberrations are still under debate, concerning
in particular the target description (interphase
chromosome organization), the characterization of relevant
DNA lesions, the possibility of inducing exchanges
starting from single radiation-induced lesions, the rejoining
mechanisms (proximity effects and possible induction
of incomplete exchanges, i.e. one-way exchanges) and the
influence of specific scoring criteria adopted both in experiments
and models. Starting from Lea’s breakage-andreunion
theory and Revell’s exchange theory, an overview
is given of various models recently reported in the literature.
The assumptions adopted by the authors concerning
the various processes involved in aberration formation are
analysed in detail, in order to clarify the different approaches
adopted in treating the open questions outlined
above
Confronto fra RBE per inattivazione, single track lethal damage e qualità dei dsb al variare del LET di protoni e particelle alfa
No full textUso delle strutture di traccia per la comprensione dei meccanismi di induzione dei danni radiobiologici
No full textTheoretical and experimental bases for mechanistic models of radiation-induced DNA damage
No full textStudio del danno al DNA indotto da radiazioni ionizzanti mediante simulazioni Montecarlo
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A mechanistic approach to evaluate biological effectiveness of hadrons, based on DNA damage simulations
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