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Uwe Schneider - One of the best experts on this subject based on the ideXlab platform.

  • Track-event theory of Cell Survival with second-order repair
    Radiation and Environmental Biophysics, 2015
    Co-Authors: Jürgen Besserer, Uwe Schneider
    Abstract:

    When fractionation schemes for hypofractionation and stereotactic body radiotherapy are considered, a reliable Cell Survival model at high dose is needed for calculating doses of similar biological effectiveness. In this work, a simple model for Cell Survival which is valid also at high dose is developed from Poisson statistics. It is assumed that a Cell is killed by an event that is defined by two double-strand breaks on the same or different chromosomes. Two different mechanisms can produce events. A one-track event is always represented by two simultaneous double-strand breaks. A two-track event results in one double-strand break. Therefore, at least two two-track events on the same or different chromosomes are necessary to produce an event. It is assumed that two double-strand breaks can be repaired with a certain repair probability. Both the one-track events and the two-track events are statistically independent. From the stochastic nature of Cell killing which is described by the Poisson distribution, the Cell Survival probability was derived. The model was fitted to experimental data. It was shown that a solution based on Poisson statistics exists for Cell Survival. It exhibits exponential Cell Survival at high dose and a finite gradient of Cell Survival at vanishing dose, which is in agreement with experimental Cell studies. The model fits the experimental data as well as the LQ model and is based on two free parameters. It was shown that Cell Survival can be described with a simple analytical formula on the basis of Poisson statistics. This solution represents in the limit of large dose the typical exponential behavior and predicts Cell Survival as well as the LQ model.

  • A track-event theory of Cell Survival
    Zeitschrift Fur Medizinische Physik, 2014
    Co-Authors: Jürgen Besserer, Uwe Schneider
    Abstract:

    Abstract Purpose When fractionation schemes for hypofractionation and stereotactic body radiotherapy are considered, a reliable Cell Survival model at high dose is needed for calculating doses of similar biological effectiveness. In this work a simple model for Cell Survival which is valid also at high dose is developed from Poisson statistics. Materials and Methods An event is defined by two double strand breaks (DSB) on the same or different chromosomes. An event is always lethal due to direct lethal damage or lethal binary misrepair by the formation of chromosome aberrations. Two different mechanisms can produce events: one-track events (OTE) or two-track-events (TTE). The target for an OTE is always a lethal event, the target for an TTE is one DSB. At least two TTEs on the same or different chromosomes are necessary to produce an event. Both, the OTE and the TTE are statistically independent. From the stochastic nature of Cell kill which is described by the Poisson distribution the Cell Survival probability was derived. Results It was shown that a solution based on Poisson statistics exists for Cell Survival. It exhibits exponential Cell Survival at high dose and a finite gradient of Cell Survival at vanishing dose, which is in agreement with experimental Cell studies. The model fits the experimental data nearly as well as the three-parameter formula of Hug-Kellerer and is only based on two free parameters. It is shown that the LQ formalism is an approximation of the model derived in this work. It could be also shown that the derived model predicts a fractionated Cell Survival experiment better than the LQ-model. Conclusions It was shown that Cell Survival can be described with a simple analytical formula on the basis of Poisson statistics. This solution represents in the limit of large dose the typical exponential behavior and predicts Cell Survival after fractionated dose application better than the LQ-model.

Jürgen Besserer - One of the best experts on this subject based on the ideXlab platform.

  • Track-event theory of Cell Survival with second-order repair
    Radiation and Environmental Biophysics, 2015
    Co-Authors: Jürgen Besserer, Uwe Schneider
    Abstract:

    When fractionation schemes for hypofractionation and stereotactic body radiotherapy are considered, a reliable Cell Survival model at high dose is needed for calculating doses of similar biological effectiveness. In this work, a simple model for Cell Survival which is valid also at high dose is developed from Poisson statistics. It is assumed that a Cell is killed by an event that is defined by two double-strand breaks on the same or different chromosomes. Two different mechanisms can produce events. A one-track event is always represented by two simultaneous double-strand breaks. A two-track event results in one double-strand break. Therefore, at least two two-track events on the same or different chromosomes are necessary to produce an event. It is assumed that two double-strand breaks can be repaired with a certain repair probability. Both the one-track events and the two-track events are statistically independent. From the stochastic nature of Cell killing which is described by the Poisson distribution, the Cell Survival probability was derived. The model was fitted to experimental data. It was shown that a solution based on Poisson statistics exists for Cell Survival. It exhibits exponential Cell Survival at high dose and a finite gradient of Cell Survival at vanishing dose, which is in agreement with experimental Cell studies. The model fits the experimental data as well as the LQ model and is based on two free parameters. It was shown that Cell Survival can be described with a simple analytical formula on the basis of Poisson statistics. This solution represents in the limit of large dose the typical exponential behavior and predicts Cell Survival as well as the LQ model.

  • A track-event theory of Cell Survival
    Zeitschrift Fur Medizinische Physik, 2014
    Co-Authors: Jürgen Besserer, Uwe Schneider
    Abstract:

    Abstract Purpose When fractionation schemes for hypofractionation and stereotactic body radiotherapy are considered, a reliable Cell Survival model at high dose is needed for calculating doses of similar biological effectiveness. In this work a simple model for Cell Survival which is valid also at high dose is developed from Poisson statistics. Materials and Methods An event is defined by two double strand breaks (DSB) on the same or different chromosomes. An event is always lethal due to direct lethal damage or lethal binary misrepair by the formation of chromosome aberrations. Two different mechanisms can produce events: one-track events (OTE) or two-track-events (TTE). The target for an OTE is always a lethal event, the target for an TTE is one DSB. At least two TTEs on the same or different chromosomes are necessary to produce an event. Both, the OTE and the TTE are statistically independent. From the stochastic nature of Cell kill which is described by the Poisson distribution the Cell Survival probability was derived. Results It was shown that a solution based on Poisson statistics exists for Cell Survival. It exhibits exponential Cell Survival at high dose and a finite gradient of Cell Survival at vanishing dose, which is in agreement with experimental Cell studies. The model fits the experimental data nearly as well as the three-parameter formula of Hug-Kellerer and is only based on two free parameters. It is shown that the LQ formalism is an approximation of the model derived in this work. It could be also shown that the derived model predicts a fractionated Cell Survival experiment better than the LQ-model. Conclusions It was shown that Cell Survival can be described with a simple analytical formula on the basis of Poisson statistics. This solution represents in the limit of large dose the typical exponential behavior and predicts Cell Survival after fractionated dose application better than the LQ-model.

Eric A. Toth - One of the best experts on this subject based on the ideXlab platform.

Paul D. Mintz - One of the best experts on this subject based on the ideXlab platform.

  • Red Cell Survival Studies in a Patient with Anti-Tca
    American Journal of Clinical Pathology, 1991
    Co-Authors: Garth Anderson, Lloyd S. Gray, Paul D. Mintz
    Abstract:

    A radiolabeled, allogenic red Cell Survival study was performed on a patient who lacked the Cromer-related antigen Tca and who had developed the corresponding antibody. Red Cell Survival was 92% at 1 hour and 88% at 24 hours. Monocyte monolayer assays (MMA) and IgG subclass determinations were performed on samples from: (1) 1965, the period of initial antibody formation; (2) approximately two years before the red Cell Survival study; and (3) four months after the study. All samples reacted w+ to 1 + by the antiglobulin test. The earliest sample contained IgGl, IgG2, and IgG4 anti-Tca. Because there were 20.5% reactive monocytes in the MMA (normal range 0—3%), this antibody may have produced extravascular red Cell destruction. In contrast to the initial example, the samples before and after the red Cell Survival study both contained IgG2 and IgG4 subclasses with 1.3% and 2.2% MMA reactivity, respectively. The current pattern of antibody subclass, the lack of reactivity in the MMA, and a red Cell Survival of 88% at 24 hours indicate that shortterm transfusion support would have been well tolerated. This contrasts to the in vitro results obtained with the earliest sample, which suggest a clinically significant antibody. This appears to be the first report of a red Cell alloantibody that remained serologically reactive but underwent a loss of its IgGl fraction, which appeared capable of red Cell destruction based on the MMA results.

Sung-joon Ye - One of the best experts on this subject based on the ideXlab platform.

  • Theoretical Cell Survival Probability for Preclinical Evaluation of BNCT Treatment Conditions
    Frontiers in Neutron Capture Therapy, 2020
    Co-Authors: Sung-joon Ye
    Abstract:

    Conventionally, Cell Survival parameters can be experimentally measured in Cell culture system. Using these parameters, Cell Survival curves vs. absorbed dose are plotted. However, this classical approach cannot explicitly describe Cell Survival variation with individual treatment conditions, such as beam spectra and field sizes. The emphasis in this paper is on the development of a computational protocol to directly calculate the theoretical Cell Survival probability regarding BNCT treatment conditions. Macroscopic dosimetry is in principle not sufficient to accurately evaluate BNCT therapeutic efficacy, which depends on 10B-distributions at the Cellular and subCellular levels.1 Therefore, in this paper a treatment condition is characterized by the choice of boron carrier drugs (boronophenylalanine, BPA, or boron sulfhydryl hydride, BSH), two different neutron beam spectra, and single or bilateral exposures. The radiation transport from the neutron source to a patient’s tumor is calculated using Monte Carlo methods. With an assumed tolerance dose (l0.5Gy-Eq), a Cell Survival probability is determined for a given treatment condition. The Cell Survival probability applies to a simple model of tumor control probability (TCP) by radiotherapy,2 based on the principle that every tumor clonogen must be killed to achieve tumor control.3

  • Monte Carlo based protocol for Cell Survival and tumour control probability in BNCT
    Physics in Medicine and Biology, 1999
    Co-Authors: Sung-joon Ye
    Abstract:

    A mathematical model to calculate the theoretical Cell Survival probability (nominally, the Cell Survival fraction) is developed to evaluate preclinical treatment conditions for boron neutron capture therapy (BNCT). A treatment condition is characterized by the neutron beam spectra, single or bilateral exposure, and the choice of boron carrier drug (boronophenylalanine (BPA) or boron sulfhydryl hydride (BSH)). The Cell Survival probability defined from Poisson statistics is expressed with the Cell-killing yield, the (n, ) reaction density, and the tolerable neutron fluence. The radiation transport calculation from the neutron source to tumours is carried out using Monte Carlo methods: (i) reactor-based BNCT facility modelling to yield the neutron beam library at an irradiation port; (ii) dosimetry to limit the neutron fluence below a tolerance dose (10.5 Gy-Eq); (iii) calculation of the (n, ) reaction density in tumours. A shallow surface tumour could be effectively treated by single exposure producing an average Cell Survival probability of - for probable ranges of the Cell-killing yield for the two drugs, while a deep tumour will require bilateral exposure to achieve comparable Cell kills at depth. With very pure epithermal beams eliminating thermal, low epithermal and fast neutrons, the Cell Survival can be decreased by factors of 2-10 compared with the unmodified neutron spectrum. A dominant effect of Cell-killing yield on tumour Cell Survival demonstrates the importance of choice of boron carrier drug. However, these calculations do not indicate an unambiguous preference for one drug, due to the large overlap of tumour Cell Survival in the probable ranges of the Cell-killing yield for the two drugs. The Cell Survival value averaged over a bulky tumour volume is used to predict the overall BNCT therapeutic efficacy, using a simple model of tumour control probability (TCP).