Rheological factor in the thermal problem of SHF-hyperthermia treatment. I. Homogeneous tissue

In an excursus developing a modern view of the Carnot-Kelvin aspect of thermodynamics, appended recently to the letters from Clerk Maxwell to his friend W. Thomson reporting the early tentative evolution of the theory of the electro-dynamic field, the account presented by the writer stopped short at putting emphasis on the mystery of temperature, as a unique and supremely significant property of matter in bulk, with its trend to uniformity as presenting the basic thermal problem. The side of the subject involving dynamical analogy was there absent from the development, which was purely formal. It may be well, however, now to offer some general notions such as may be put on record, which arise naturally from that mode of approach to the subject.

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Mathematical model for the thermal enhancement of radiation response: thermodynamic approach

Scientific Reports ◽

10.1038/s41598-021-84620-z ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Adriana M. De Mendoza ◽

Soňa Michlíková ◽

Johann Berger ◽

Jens Karschau ◽

Leoni A. Kunz-Schughart ◽

...

Keyword(s):

Protein Denaturation ◽

Collateral Damage ◽

Hyperthermia Treatment ◽

Reversible Process ◽

Technological Advances ◽

Thermal Enhancement ◽

Main Driver ◽

Definition Of

AbstractRadiotherapy can effectively kill malignant cells, but the doses required to cure cancer patients may inflict severe collateral damage to adjacent healthy tissues. Recent technological advances in the clinical application has revitalized hyperthermia treatment (HT) as an option to improve radiotherapy (RT) outcomes. Understanding the synergistic effect of simultaneous thermoradiotherapy via mathematical modelling is essential for treatment planning. We here propose a theoretical model in which the thermal enhancement ratio (TER) relates to the cell fraction being radiosensitised by the infliction of sublethal damage through HT. Further damage finally kills the cell or abrogates its proliferative capacity in a non-reversible process. We suggest the TER to be proportional to the energy invested in the sensitisation, which is modelled as a simple rate process. Assuming protein denaturation as the main driver of HT-induced sublethal damage and considering the temperature dependence of the heat capacity of cellular proteins, the sensitisation rates were found to depend exponentially on temperature; in agreement with previous empirical observations. Our findings point towards an improved definition of thermal dose in concordance with the thermodynamics of protein denaturation. Our predictions well reproduce experimental in vitro and in vivo data, explaining the thermal modulation of cellular radioresponse for simultaneous thermoradiotherapy.

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