Time-temperature analysis of cell killing of BHK cells heated at temperatures in the range of 43.5°C to 57.0°C

Borrelli, Michael J.; Thompson, L. L.; Cain, Charles A.; Dewey, William C.

doi:10.1016/0360-3016(90)90548-x

Cited by 115 publications

(79 citation statements)

References 21 publications

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“…For very short exposure times, the hyperthermia literature shows only limited (Borrelli et al, 1990) t 43 thermal dose data points for exposure durations of less than 1 min. Two aspects of single-burst in vivo threshold lesion studies in brain (Fry et al, 1970;Dunn and Fry, 1971;Lerner et al, 1973) and liver (Chan and Frizzell, 1977;Frizzell et al, 1977;Frizzell, 1988) are germane to the thermal dose issue for exposures less than a few seconds.…”

Section: Thermal Dose Conceptmentioning

confidence: 99%

Ultrasound–biophysics mechanisms

O’Brien

2007

Progress in Biophysics and Molecular Biology

586

416

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Ultrasonic biophysics is the study of mechanisms responsible for how ultrasound and biological materials interact. Ultrasound-induced bioeffect or risk studies focus on issues related to the effects of ultrasound on biological materials. On the other hand, when biological materials affect the ultrasonic wave, this can be viewed as the basis for diagnostic ultrasound. Thus, an understanding of the interaction of ultrasound with tissue provides the scientific basis for image production and risk assessment. Relative to the bioeffect or risk studies, that is, the biophysical mechanisms by which ultrasound affects biological materials, ultrasound-induced bioeffects are generally separated into thermal and nonthermal mechanisms. Ultrasonic dosimetry is concerned with the quantitative determination of ultrasonic energy interaction with biological materials. Whenever ultrasonic energy is propagated into an attenuating material such as tissue, the amplitude of the wave decreases with distance. This attenuation is due to either absorption or scattering. Absorption is a mechanism that represents that portion of ultrasonic wave that is converted into heat, and scattering can be thought of as that portion of the wave, which changes direction. Because the medium can absorb energy to produce heat, a temperature rise may occur as long as the rate of heat production is greater than the rate of heat removal. Current interest with thermally mediated ultrasound-induced bioeffects has focused on the thermal isoeffect concept. The non-thermal mechanism that has received the most attention is acoustically generated cavitation wherein ultrasonic energy by cavitation bubbles is concentrated. Acoustic cavitation, in a broad sense, refers to ultrasonically induced bubble activity occurring in a biological material that contains pre-existing gaseous inclusions. Cavitation-related mechanisms include radiation force, microstreaming, shock waves, free radicals, microjets and strain. It is more challenging to deduce the causes of mechanical effects in tissues that do not contain gas bodies. These ultrasonic biophysics mechanisms will be discussed in the context of diagnostic ultrasound exposure risk concerns.

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Section: Thermal Dose Conceptmentioning

confidence: 99%

Ultrasound–biophysics mechanisms

O’Brien

2007

Progress in Biophysics and Molecular Biology

586

416

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“…where (t) is the degree of tissue injury, c(t) is the concentration of living cells, c(0) is the initial concentration of living cells, R is the universal gas constant, A is a "frequency" factor for the kinetic expression (s -1 ), and E is the activation energy for the irreversible damage reaction (Jmol -1 ) [37]. The kinetic parameters account for morphologic changes in tissue relating to the thermal degradation of proteins [35].…”

Section: Arrhenius Based Recursive Thermal Injurymentioning

confidence: 99%

“…When the CEM 43 value exceeds a critical threshold, the tissue is considered to be thermally necrosed. Thresholds for CEM 43 have been tabulated in the literature for several types of tissue based upon experimental observation of tissue injury at 43°C [34][35][36][37].…”

Section: Introductionmentioning

confidence: 99%

Considerations for Thermal Injury Analysis for RF Ablation Devices

Chang¹

2010

TOBEJ

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Abstract:Background: The estimation of lesion size is an integral part of treatment planning for the clinical applications of radiofrequency ablation. However, to date, studies have not directly evaluated the impact of different computational estimation techniques for predicting lesion size. In this study, we focus on three common methods used for predicting tissue injury: (1) iso-temperature contours, (2) Cumulative equivalent minutes, (3) Arrhenius based thermal injury. Methods:We created a geometric model of a multi-tyne ablation electrode and simulated thermal and tissue injury profiles that result from three calculation methods after 15 minutes exposure to a constant RF voltage source. A hybrid finite element technique was used to calculate temperature and tissue injury. Time-temperature curves were used in the assessment of iso-temperature thresholds and the method of cumulative equivalent minutes. An Arrhenius-based formulation was used to calculate sequential and recursive thermal injury to tissues. Results: The data demonstrate that while iso-temperature and cumulative equivalent minute contours are similar in shape, these two methodologies grossly over-estimate the amount of tissue injury when compared to recursive thermal injury calculations, which have previously been shown to correlate closely with in vitro pathologic lesion volume measurement. In addition, Arrhenius calculations that do not use a recursive algorithm result in a significant underestimation of lesion volume. The data also demonstrate that lesion width and depth are inadequate means of characterizing treatment volume for multi-tine ablation devices. Conclusions: Recursive thermal injury remains the most physiologically relevant means of computationally estimating lesion size for hepatic tumor applications. Iso-thermal and cumulative equivalent minute approaches may produce significant errors in the estimation of lesion size.

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“…Arrhenius plots of k for killing in the hyperthermic region (figure 2) have a sharp bend at 42-438C 6 , due to the induction of chronic thermotolerance during the survival assay, but there is evidence they are linear for temperatures above this critical temperature to at least 578C 7 . The linear relationship between ln k and 1=T implies that the temperature dependence of the rate constant for killing can be approximated by…”

Section: Arrhenius Plots Of Growth and Killingmentioning

confidence: 99%

Cellular effects of hyperthermia: relevance to the minimum dose for thermal damage

Lepock

2003

International Journal of Hyperthermia

318

224

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The specific mechanism of cell killing by hyperthermia is unknown, but the high activation energy of cell killing and other responses to hyperthermia suggest that protein denaturation is the rate-limiting step. Protein denaturation can be directly monitored by differential scanning calorimetry and in general there is a good correlation between protein denaturation and cellular response. Approximately 5% denaturation is necessary for detectable killing. Protein denaturation leads to the aggregation of both denatured and native protein with multiple effects on cellular function.

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Time-temperature analysis of cell killing of BHK cells heated at temperatures in the range of 43.5°C to 57.0°C

Cited by 115 publications

References 21 publications

Ultrasound–biophysics mechanisms

Ultrasound–biophysics mechanisms

Considerations for Thermal Injury Analysis for RF Ablation Devices

Cellular effects of hyperthermia: relevance to the minimum dose for thermal damage

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