Search PubMed⌕ Search

Biomedical subjects

S B Field

Publications and source records attributed to S B Field.

At least 55 records · Page 3Linked to original sources
PubMed1979

A microwave heating system for improving temperature uniformity in heated tissue.

A microwave heating system, designed to improve temperature uniformity in heated tissue, is described. The system employs parallel-opposed waveguide applicators, operating in the TE10 mode at 2450 MHz with the tissue to be heated (i.e. mouse intestine) immersed in a liquid which is both biologically compatible with and dielectrically similar to the tissue. The liquid improves the microwave coupling and avoids shape and size dependent absorption characteristics of the irregularly shaped tissue. Also, by maintaining this liquid at a suitable temperature with respect to that required in the tissue, the thermal losses and hence temperature gradients in the tissue are reduced compared with heating in hot liquid alone.

Animals↗
PubMed1979

Induced thermal resistance in the mouse ear.

The mouse ear (pinna) was used to investigate the effect of two hyperthermic treatments. Heating was by immersion in hot water at 43.5 degrees C. A single treatment of about 50 minutes was required to cause necrosis in 50% of the ears heated. When heat treatment was given in two equal fractions the total heating time had to be increased if the interval between fractions was greater than four hours. By 24 hours a total treatment of about 100 minutes was required, indicating almost complete recovery from the first heating. Priming treatments at 43.5 degrees C induced thermal resistance to a second heat treatment at 43.5 degrees C. Maximum resistance was observed one day after a 20 minute priming and two days after a 40 minute priming, when the heating time had to be increased to 120 minutes, an increase by a factor of 2.4. Shorter priming treatments induced less resistance, the minimum heating time to produce an effect being two minutes. In all cases the effect decreased during the next four to five days. These results indicate that the reduced response of tissues to fractionated hyperthermia is due both to the repair of sublethal heat damage and induction of thermal resistance.

Animals↗
PubMed1979

The effect of prior heat treatment on the thermal enhancement of radiation damage in the mouse ear.

The effects of prior heat treatment on the skin reaction produced by a subsequent treatment with combined heat and X-rays were investigated in the mouse ear. Ears were heated by immersion in hot water. The priming heat treatment was always 43.5 degrees C for 40 minutes. Its effect was transient, beginning between 24 and 48 hours after the priming treatment and reaching a maximum at 48 to 96 hours when there was a reduction in the skin response to combined heat and X rays, i.e. it caused a reduction in the thermal enhancement ratio (TER). The effect was lost by 192 hours. At 96 hours after the priming treatment the TER for 30 minutes at 42.5 degrees C or at 43.5 degrees C was reduced by a value equivalent to decreasing the temperature by about 0.4 degrees C. This was equivalent to increasing the heating at 43.5 degrees C required to produce a given enhancement of radiation damage by a factor of 1.4 relative to that required without prior heating. The effect was smaller than induced resistance to damage caused by severe heat treatment alone (i.e. necrosis) and it occurred later. These differences support the concept that two separate mechanisms underlie direct heat necrosis and thermal enhancement of radiation damage.

Animals↗
PubMed1979

The effect of local hyperthermia on the small intestine of the mouse.

Small loops of mouse jejunum were exteriorized and heated by immersion in a bath of Krebs-Ringer salt solution. Crypts were lost in the heated regions with a half-time of approximately six hours and reached a steady level of damage by 10--16 hours. There was no recovery in crypt number for one week after hyperthermia. Using a 24 hour assay, crypt survival curves were obtained using various heating times in the temperature range 37.5 degrees C--44.5 degrees C. These curves were qualitatively similar to those resulting from radiation damage, showing a shoulder followed by exponential killing. As the temperature was increased, progressive changes in shape of the curves indicated a proportional inhibition of accumulation of sublethal heat damage combined with increased rate of expression of lethal damage. Over the temperature range 42.3 degrees C--44.5 degrees C, a linear relationship was found between the rate of crypt loss and the reciprocal of the absolute temperature. An activation energy of 600 +/- 70 kJ mole-1 was calculated using the Arrhenius equation. In this temperature range, doubling the heating time had the same effect as increasing the temperature by 1 degree C. At temperatures below about 42.3 degrees C, the tissue became relatively less sensitive to increasing the treatment time.

Animals↗
PubMed1978

Two qualitatively different effects of hyperthermia on acid phosphatase staining in mouse spleen, dependent on the severity of the treatment.

Heating the lower body of the mouse for up to 1.5 hours at temperatures above 41.0 degrees C causes an increase in splenic lysosomal acid phosphatase activity. For mouse temperatures up to 42.3 degrees C the change is probably due to enzyme activation, which reaches a maximum 1.5 hours after heating and then decays in a way which may be related to the transient ability of moderate hyperthermia to potentiate X-ray damage. At temperatures above about 42.5 degrees C hyperthermia results in a qualitatively different lysomal response, probably due to an increased lysosomal membrane permeability. The change is observed immediately after heating and remains high for at least 4 hours. The resultant release of hydrolases into the cytoplasm may be involved in the irreversible cell damage caused by severe hyperthermia.

Animals↗
PubMed1978

Heat-induced thermal resistance and its relationship to lysosomal response.

Two separate effects of hyperthermia on mouse splenic lysosomes have been reported, dependent on the severity of the treatment. Heating to temperatures below 42.5 degrees C causes a transient increase in lysosomal acid phosphatase activity which can be correlated with the ability of moderate hyperthermia to potentiate X-ray damage. Heating to temperatures above 42.5 degrees C results in an immediate increase in lysosomal membrane permeability which may be involved in tissue necrosis. By giving a priming heat treatment at 41.8 degrees C, induced thermal resistance was demonstrated for the lysosomal membrane effect, but not for the enzyme activation. The degree of induced thermal resistance observed is similar to that reported for the cell-killing effect of heat on tissues in vivo and cells in vitro and occurs over a similar time course. The relevance of these results to the understanding of fractionated hyperthermia in cancer therapy is discussed.

Acid Phosphatase↗
PubMed1978

Hyperthermic sensitization of mouse intestine to damage by X rays: the effect of sequence and temporal separation of the two treatments.

Adult mice were irradiated with between 7 and 15 Gy of X rays to the abdomen either before or after immersion of the lower half of the body in water at various temperatures. The thermal enhancement of X-irradiation damage to the intestine was estimated using survival at five days as the endpoint. Thermal enhancement ratios (defined as the ratio between the dose of X rays and the dose of X rays plus heat to produce the same level of damage) were calculated at the 50% survival level. If only a few minutes separated the application of heat and irradiation, the values obtained were similar to those reported for other normal tissues. There was only a slight dependence on the sequence of the two treatments. As the time interval between the two treatments was increased the effect of heat was reduced and a normal irradiation response was obtained when the separation was greater than about four hours. The results are compared with those for other normal tissues and tumours and the relevance of these findings in the design of optimal therapeutic schedules of combined heat and X rays is discussed.

Animals↗
PubMed1977

The response of mouse skin to combined hyperthermia and X-rays.

The effects of combined hyperthermia and X-irradiation were studied in the skin of the mouse ear. Ears were heated for 1 hour by immersion in a waterbath at temperatures ranging from 37 degrees C--43 degrees C. These heat treatments had little visible effect alone, but when combined with X-rays, enhanced the radiation response. Enhancement depended on the degree of heating. When heat was given immediately after X-rays, the radiation dose to cause a given skin reaction had to be reduced by about 10 per cent for 37 degrees C and about 40 per cent of 43 degrees C. The timing and sequence of the two treatments were important. Heat after X-rays was less effective than heat before X-rays. When heat followed X-rays, the enhancing effect was lost completely if the interval exceeded 4 hours. When heat preceded X-rays, the effect was lost more slowly, depending on temperature. The implications of this for the treatment of cancer by combined therapy are discussed.

Animals↗
PubMed1977

The effects of fast neutrons and X rays on the subependymal layer of the rat brain.

Some effects of irradiation of rat brain with single doses of X rays or fast neutrons have been measured. This was done by estimating the total number of cells in the subependymal layer at various times after irradiation. The gross response to X rays and neutrons was somewhat different, and the results suggest that the two histologically distinguishable cell types in the subependymal layer have different values of RBE.

Animals↗
PubMed1977

The response of tissues to combined hyperthermia and X rays.

Three normal tissues in mice and rats (skin, intestine and cartilage) have been used to investigate the effects of combined hyperthermia and radiation. The heating time was kept constant at one hour and X rays were given either immediately before or after heating. Thermal enhancement ratios were measured as a function of temperature up to 43 degress C and were compared with data for other normal tissues and tumours taken from the literature. The variation from tissue to tissue was found to be fairly small within this temperature range, but there is some indication of a greater response of tumours.

Animals↗
PubMed1977

The response of the rat tail to hyperthermia.

When the cartilage of the tail of a baby rat is exposed to temperatures between 41 degrees C and 46 degrees C either necrosis or a small degree of stunting in growth may occur. Isoeffect curves relating time and temperature for both these endpoints for normal and clamped tissue were found to be parallel, a doubling of heating time or an increase in temperature of 1 degree C having the same effect in all cases. Clamping sensitizes the tails by a factor of about three in heating time, equivalent to a temperature difference of 1.5 degrees C. Arrhenius plots show an inactivation energy of 140 kcal/mole. This is similar to that found by other workers using different endpoints, and supports the suggestion that protein denaturation is a critical target for direct heat damage.

Animals↗
PubMed1977

The response of the rat tail to combined heat and x rays.

Moderate heat doses which, alone, cause no measurable response in the cartilage of the tail of the baby rat, may potentiate the effects of X-irradiation. The magnitude of the enhancement (the Thermal Enhancement Ratio, or TER) depends upon the heat dose in a similar way to that observed in other normal tissues. The thermal enhancement in the rat tail was also dependent on the dose of X rays, increasing with increasing dose. Potentiation was always greater when heat was applied before irradiation although the difference in TER between heating immediately before or after irradiation was less than 10%. Potentiation of X ray damage decreased steadily to zero as the heat and X-ray treatments were separated by increasing intervals of time. The loss of potentiation was more complete and more rapid when X rays were given before heating, but was also dependent on both the degree of heating and the dose of X rays.

Animals↗