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Register a new userIs the track-event theory of cell survival internally consistent?
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The track event theory (TET) has been developed in recent years as an alternative to the phenomenological linear-quadratic model for cell survival under exposure to ionizing radiation, particularly for heavy charged particles. The TET is based on a few simple model assumptions including the possibility to derive some of the model parameters from nanodosimetry. This work intends to carve out more clearly the basic assumptions behind the TET and to critically review the resulting mathematical model equations. It is demonstrated that the model assumptions of Poisson distribution and statistical independence of the frequency distributions of so-called one-track and two-track events follow from the Poisson distribution of the number of tracks affecting the considered target volume. It is also shown that the modified TET model equation used in the literature for consideration of repair is inconsistent with the model assumptions and requires an additional model parameter. Furthermore, the derivation of the model parameters from nanodosimetric properties of particle track structure is revealed to lead to a pure exponential dose dependence when the potentially large number of relevant nanometric target volumes inside a cell nucleus is accounted for.
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This work aims at carving out more clearly the basic assumptions behind the track-event theory (TET) and its derivate radiation action model based on nanodosimetry (RAMN) by clearly distinguishing between effects of tracks at the cellular level and the induction of lesions in subcellular targets. It is demonstrated that the model assumptions of Poisson distribution and statistical independence of the frequency of single and clustered DNA lesions are dispensable for multi-event distributions, because they follow from the Poisson distribution of the number of tracks affecting the considered target volume. It is also shown that making these assumptions for the single-event distributions of the number of lethal and sublethal lesions within a cell would lead to an essentially exponential dose dependence of survival for practically relevant values of the absorbed dose. Furthermore, it is elucidated that the model equation used in the literature for consideration of repair within the TET is based on the assumption that DNA lesions induced by different tracks are repaired independently and that the model equation is presumably inconsistent with the model assumptions and requires an additional model parameter. Furthermore, the methodology for deriving model parameters from nanodosimetric properties of particle track structure is critically assessed. Based on data from proton track simulations it is shown that the assumption of statistically independent targets leads to a prediction of negligible frequency of clustered DNA damage. An approach is outlined how track structure could be considered in determining the model parameters, and the implications for TET and RAMN are discussed.
Beams of $^{4}$He and $^{16}$O nuclei are considered for ion-beam cancer therapy as alternative options to protons and $^{12}$C nuclei. Spread-out Bragg peak (SOBP) distributions of physical dose and relative biological effectiveness for 10% survival are calculated by means of our Geant4-based Monte Carlo model for Heavy Ion Therapy (MCHIT) and the modified microdosimetric kinetic model. The depth distributions of cell survival fractions are calculated for $^{1}$H, $^{4}$He, $^{12}$C and $^{16}$O for tissues with normal (HSG cells), low and high radiosensitivity. In each case the cell survival fractions were compared separately for the target volume, behind and in front of it. In the case of normal radiosensitivity $^{4}$He and $^{12}$C better spare tissues in the entrance channel compared to protons and $^{16}$O. The cell survival fractions calculated, respectively, for the entrance channel and target volume are similar for $^{4}$He and $^{12}$C. When it is important to spare healthy tissues located after the distal edge of the SOBP plateau, $^{4}$He can be recommended due to reduced nuclear fragmentation of these projectiles. No definite advantages of $^{16}$O with respect to $^{12}$C were found, with the except of an enhanced impact of these heavier projectiles on radioresistant tumors.
The quantum adiabatic theorem states that if a quantum system starts in an eigenstate of the Hamiltonian, and this Hamiltonian varies sufficiently slowly, the system stays in this eigenstate. We investigate experimentally the conditions that must be fulfilled for this theorem to hold. We show that the traditional adiabatic condition as well as some conditions that were recently suggested are either not sufficient or not necessary. Experimental evidence is presented by a simple experiment using nuclear spins.
In this article, we study the kinetics of reversible ligand binding to receptors on a spherical cell surface using a self-consistent stochastic theory. Binding, dissociation, diffusion and rebinding of ligands are incorporated into the theory in a systematic manner. We derive explicitly the time evolution of the ligand-bound receptor fraction p(t) in various regimes . Contrary to the commonly accepted view, we find that the well-known Berg-Purcell scaling for the association rate is modified as a function of time. Specifically, the effective on-rate changes non-monotonically as a function of time and equals the intrinsic rate at very early as well as late times, while being approximately equal to the Berg-Purcell value at intermediate times. The effective dissociation rate, as it appears in the binding curve or measured in a dissociation experiment, is strongly modified by rebinding events and assumes the Berg-Purcell value except at very late times, where the decay is algebraic and not exponential. In equilibrium, the ligand concentration everywhere in the solution is the same and equals its spatial mean, thus ensuring that there is no depletion in the vicinity of the cell. Implications of our results for binding experiments and numerical simulations of ligand-receptor systems are also discussed.
We follow the evolution of the Ionization Potential (IP) for the paradigmatic quasi-one-dimensional trans-acetylene family of conjugated molecules, from short to long oligomers and to the infinite polymer trans-poly-acetylene (TPA). Our results for short oligomers are very close to experimental available data. We find that the IP varies with oligomer length and converges to the given value for TPA with a smooth, coupled inverse-length-exponential behavior. Our prediction is based on an internally-consistent scheme to adjust the exchange mixing parameter $alpha$ of the PBEh hybrid density functional, so as to obtain a description of the electronic structure consistent with the quasiparticle approximation for the IP. This is achieved by demanding that the corresponding quasiparticle correction, in the GW@PBEh approximation, vanishes for the IP when evaluated at PBEh($alpha^{ic}$). We find that $alpha^{ic}$ is also system-dependent and converges with increasing oligomer length, allowing to capture the dependence of IP and other electronic properties.
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