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Biomedical subjects

J Wondergem

Publications and source records attributed to J Wondergem.

At least 55 records · Page 3Linked to original sources
PubMed1989

A comparison of thermal enhancement of cis-diamminedichloroplatinum (II) induced renal and intestinal toxicities by whole body hyperthermia in the rat.

Thermal enhancement of cis-diamminedichloroplatinum (II) (DDP) induced renal and intestinal toxicities by whole body hyperthermia (WBH) were compared using a F344 rat model. Thermal enhancement ratios (TER) for DDP-induced nephrotoxicity were calculated using renal functional assays and morphological techniques. TER values for gastrointestinal (G.I.) toxicity were calculated using "severity of diarrhea" and jejunal crypt cell survival as assays. TER's for renal damage varied between 3 and 3.4, whereas the TER measured for G.I.-toxicity was 1.8. Physiological changes caused by WBH or intrinsic differences in the sensitivities of normal tissues to DDP +/- WBH may be responsible for the differences in thermal enhancement of DDP-induced renal and intestinal toxicities.

Animals↗
PubMed1989

Gd-DTPA as a contrast agent in CT.

An evaluation was done of the effect of gadolinium diethylenetriaminepentaacetic acid (DTPA) on computed tomographic (CT) studies performed after magnetic resonance (MR) imaging. CT scans of two solutions of Gd-DTPA demonstrated substantial attenuation. In two patients who underwent CT after Gd-DTPA-enhanced MR imaging, the high attenuation of concentrated Gd-DTPA was seen in the urinary bladder and renal collecting system. However, in the concentration presently used in MR imaging, Gd-DTPA results in only minor enhancement of renal cortex.

Contrast Media↗
PubMed1989

Early detection of delayed myelination in preterm infants.

Myelination of the central nervous system can be demonstrated with magnetic resonance imaging. The influence of periventricular-intraventricular hemorrhage and periventricular leukomalacia on cerebral myelination was studied using magnetic resonance imaging. The subjects were 33 preterm infants of less than 30 weeks' gestation studied at 44 weeks' postmenstrual age: 11 infants with periventricular-intraventricular hemorrhage, 7 with periventricular leukomalacia, and 15 without periventricular-intraventricular hemorrhage or periventricular leukomalacia. There were no differences in mean gestational age and birth weight between the three groups. However, infants without periventricular-intraventricular hemorrhage or periventricular leukomalacia had significantly less respiratory distress syndrome. At 44 weeks postmenstrual age, infants with periventricular leukomalacia had a significantly delayed myelination pattern (stage M2) in comparison with infants without periventricular-intraventricular hemorrhage or periventricular leukomalacia and infants with periventricular-intraventricular hemorrhage (stages M3 and M4). The latter two groups had myelination stages that were similar to those of healthy term infants at 44 weeks' postmenstrual age. The results demonstrate that periventricular leukomalacia causes delayed myelination of the cerebrum, whereas periventricular-intraventricular hemorrhage does not.

Brain↗
PubMed1988

Effect of cis-diamminedichloroplatinum(II) combined with whole body hyperthermia on renal injury.

The effect of whole body hyperthermia (WBH) on cis-diamminedichloroplatinum (II) (DDP) induced renal toxicity and antitumor effect was studied using a F344 rat model. Renal injury at 5 and 14 days after treatment was evaluated using animal mortality, renal functional assays (blood urea nitrogen, creatinine), and histopathological methods. WBH (120 min at 41.5 degrees C) enhanced both antitumor effects and toxic side effects. The latter included increased mortality, increased blood urea nitrogen and creatinine levels, and increased renal damage. After simultaneous treatment with WBH and DDP, thermal enhancement ratios (TER) for renal damage between 2.5 and 3.0 were calculated. The histopathological changes observed in the kidney after DDP alone or combined with WBH were primarily found in the proximal pars recta tubules (S3 segment) in the outer stripe of the outer medulla. There was no qualitative difference in tubular damage between rats treated with DDP alone or those treated with DDP combined with WBH. However, at a fixed DDP dose, damage in the combined treatment modality group was significantly greater than in the DDP-only treated group.

Animals↗
PubMed1988

Cell proliferation in the murine epidermis and subcutaneous vascular endothelium after hyperthermia.

The skin of mouse legs was exposed to 44 degrees C hyperthermia using a thermostatically controlled waterbath. Treatment at 44 degrees C, for 15 or 30 min, led to oedema in the dermis immediately after treatment and to an infiltration by neutrophils within 7 h. The oedema disappeared in 2 days. Treatment for 60 min at 44 degrees C led to subepidermal blistering and as a result of this a considerable area of the tissue became necrotic 4 days after treatment. A repair reaction followed, and 3 weeks after heating for 60 min at 44 degrees C the epithelium was again completely or almost completely covering the underlying tissue. Shortly (7 h) after 15 or 30 min at 44 degrees C an increase was observed in the number of basal cells in the epithelium incorporating [3H]thymidine. This increase declined slowly with time: 3 weeks after treatment the number of labelled basal cells was not significantly different from that in untreated skin. Shortly after 60 min at 44 degrees C some basal cells of the epidermis still incorporated [3H]thymidine. The labelling index dropped to near-zero at day 2 after 60 min at 44 degrees C. Thereafter repopulation started and in the areas next to the granulation tissue the labelling index of basal cells reached values close to 100 per cent, 2 or 3 weeks after treatment. Treatment for 15 min at 44 degrees C did not lead to a stimulation of the proliferation of subcutaneous endothelial cells. Both 30 min and 60 min at 44 degrees C led to a greatly enhanced proportion of labelled subcutaneous endothelial cells after 2 days and 4 weeks, respectively (labelling index between 35 and 40 per cent). After this peak value the labelling index declined rapidly. However, in granulation tissue it remained high for about 10 days after the peak on day 4. The stimulated proliferation of subcutaneous endothelial cells after heating for 30 and 60 min at 44 degrees C correlated well with the finding that these heat treatments, given after or shortly before X-irradiation, led to a greatly reduced (X-ray-induced) tumour bed effect.

Animals↗
PubMed1988

Effects of local hyperthermia on the motor function of the rat sciatic nerve.

The effect of local heat treatment of the sciatic nerve was assessed using the toe-spreading test, which mainly assesses the motor function of the sciatic nerve. A 5 mm long segment of the nerve was heated at temperatures from 42.0 to 45.0 degrees C in vivo using a brass thermode. Hyperthermia led to a decrease in spreading of the toes. Recovery from functional loss took place in all cases, and this recovery was completed in 4 weeks. A 50 per cent functional loss in 50 per cent of the treated animals was observed after 58, 32 and 12 min of heating at 43.0, 44.0 and 45.0 degrees C respectively.

Animals↗
PubMed1987

The effect of previous treatment on the response of mouse feet to irradiation and hyperthermia.

The response of mouse feet to irradiation and heat was studied 90 days after a first treatment with X-rays, hyperthermia or both. Residual damage after a single dose of 20-30 Gy enhanced both the acute reaction and "late" deformity following a second treatment with radiation or hyperthermia. There was often a larger "memory" of the first radiation treatment for late deformity compared with the acute skin response, especially in the case of retreatment by hyperthermia. Prior treatment of the foot with a moderate heat dose (60 min at 44 degrees C), which by itself did not lead to deformity, had only a small effect on the response to retreatment with irradiation or heat, both with respect to the acute and "late" response. Residual damage after more severe hyperthermia (90 min at 44 degrees C) obscured the evaluation of deformity after a second treatment with radiation or hyperthermia. Feet treated with irradiation followed immediately or after 3 days by heat, show a larger "memory" when retreated with hyperthermia than with irradiation, both with regard to the acute and "late" response. Experiments using misonidazole indicated that the oxygenation status of previously treated skin (pretreatment not leading to deformity) had not changed significantly.

Animals↗
PubMed1987

Thermal radiosensitization and thermotolerance in cultured cells from a murine mammary carcinoma.

Cultured murine mammary carcinoma cells M8013 could be made thermotolerant by a priming heat treatment, 30 min at 43 degrees C, applied 5 h prior to subsequent heat treatment. The sensitivity of non-tolerant and thermotolerant cells to either radiation or heat combined with radiation was investigated. Analysis of survival curves with respect to D0 and N showed that thermotolerance had no influence on the radiation sensitivity of the cells. Thermal enhancement of radiation effects (in combined heat/irradiation treatments) was however reduced as a result of thermotolerance. When thermal enhancement ratios were (D0) plotted as a function of the cell killing effects of heat treatment alone, thermotolerance did not seem to have any influence. This latter observation suggests that thermotolerance modifies the effectiveness of the heat treatment for heat-induced cell lethality and radiosensitization equally. Comparison of our in vitro results with several in vivo data on normal tissues suggest that the reduction in 'effective' treatment temperature which has been observed in the in vivo studies as a result of thermotolerance may be explained by equal modification of the effects of heat by thermotolerance both for its direct effects and the radiosensitization.

Acclimatization↗
PubMed1987

Influence of prior heat treatment on the effects of heat alone or combined with X-rays on mouse stromal tissue.

The tumour bed effect assay was used to study the sensitivity of mouse stromal tissue to heat applied alone or combined with irradiation. Prior heat treatment, 30 min at 43 degrees C, of the tumour bed led to thermotolerance. After priming, thermotolerance developed fully within 24 h and it had disappeared completely after about 10 days. The kinetics of development and decay of thermotolerance in this slowly dividing tissue is similar to that which we had observed previously in skin. When decay rates of several normal tissues with different proliferation characteristics are compared, it is obvious that there is not a clear relationship between proliferation rate of the presumed target cells in the tissue and thermotolerance decay rate.

Acclimatization↗
PubMed1986

Effects of hyperthermia and X-irradiation on mouse stromal tissue.

The sensitivity of normal stroma to heat, irradiation and heat combined with irradiation has been studied using the tumour bed effect (TBE) assay. Irradiation before implantation led to a TBE. This TBE was dose dependent below 15 Gy, the TBE remaining relatively constant above 15 Gy. The interval (0-90 days) between irradiation and tumour implantation did not influence the magnitude of the TBE. Hyperthermia with large heat doses (45-60 min at 44 degrees C) before implantation may lead to a TBE. The interval between hyperthermia and tumour implantation proved to be very important. Our results show that the recovery from heat-induced stromal damage is very rapid. When the interval between hyperthermia and tumour implantation is 10 days or longer, no TBE could be observed. Irradiation combined with large heat doses (30-60 min at 44 degrees C) decreased the radiation-induced TBE. However, the combination of irradiation with mild heat treatments (15 min at 44 degrees C) could lead to a larger TBE than after irradiation alone. When hyperthermia was given prior to irradiation, the interval between heat and irradiation proved to be very important. With large intervals (21 days or longer) the TBE values were about the same as with irradiation alone. When heat was given after irradiation it always reduced the irradiation-induced TBE.

Animals↗
PubMed1985

Influence of thorax irradiation on the survival of mice with spontaneous or artificial lung metastases from a transplantable mammary adenocarcinoma.

The effect of thorax irradiation on lung metastases, either occurring spontaneously from a primary mammary adenocarcinoma (M8013X) transplanted on the leg or artificially induced by intravenous injection of tumor cells was studied. Increasing the interval between the moment at which lung metastases are supposed to originate and the thorax irradiation resulted in a rapid decrease of the effectiveness of this treatment in preventing the development of lung metastases. Early treatment of the mice not only resulted in a considerable number of animals that were cured, but also in a significant decrease in the number of tumor localizations in the lung of those animals still developing metastases. Thorax irradiation performed later was much less effective; at autopsy the lung showed a large number of small metastases. Increasing the radiation dose led to an increased number of cures; however, an increased number of mice dying of lethal lung damage was also observed. Irradiation of the lungs of mice with 5 or 10 Gy, 24 hours, 7 days or 14 days prior to i.v. injection with tumor cells, did not significantly increase the number of mice with lung metastases. Immunological resistance against the tumor played a role in our experiments with both spontaneous and artificial lung metastases.

Adenocarcinoma↗
PubMed1985

Thermal enhancement of the radiation damage in the mouse foot at different heat and radiation dose: influence of thermotolerance.

We studied the reaction of the mouse foot after combined X-irradiation and heat treatment. Acute reactions after heat differ from those after irradiation, however, after healing of the lesions, the same symptoms of deformity of the mouse foot remain. Prior heat treatment, 30 min at 43 degrees C, of the foot led to thermotolerance and this thermotolerance resulted in resistance to combined irradiation-heat treatments and hence to a decreased thermal enhancement of radiation effects. Resistance could be observed up to 168 h after prior heat treatment. The development of resistance to combined treatment at higher irradiation dose (15 or 20 Gy) and less severe heating was slower than at lower irradiation dose (10 Gy) and more severe heating. Thermal enhancement was confirmed to be dependent on the sequence of, and the interval between irradiation and heat treatment. When the mouse foot was made thermotolerant by prior heat treatment, thermal enhancement was always reduced, regardless of the sequence, when the combined heat and radiation treatments were given with an interval of less than 12 h. Thermotolerance led to an apparent decrease in the effective temperature employed in a combined treatment equivalent to approximately 1.0 degrees C, at temperatures above 43 degrees C in a 1 h heat treatment.

Animals↗
PubMed1984

A study of the effects of prior heat treatment on the skin reaction of mouse feet after heat alone or combined with X-rays: influence of misonidazole.

The skin of mouse feet was used to study the effects of hyperthermic treatment, either alone or combined with irradiation. The present experiments show that a priming heat treatment induces resistance both to a subsequent heat treatment and to a subsequent combined irradiation-heat treatment. The development of resistance to a combined irradiation-heat treatment after a priming heat treatment (30 min at 43 degrees C) was relatively slow (18-24 h) compared to development of resistance to a heat treatment without irradiation (6 h). Misonidazole, when administered prior to heat treatment only, did not influence the heat-induced skin reaction. However, when misonidazole was administered prior to combined irradiation-heat treatment, a slight but significant increase of the skin reaction was observed. Also, in combination with misonidazole resistance to combined treatment was observed by a priming heat treatment.

Animals↗
PubMed1983

The response of previously irradiated mouse skin to heat alone or combined with irradiation: influence of thermotolerance.

The skin of the mouse foot was used to study the effects of previous irradiation on the response to hyperthermia (44 degrees C), to irradiation, or to irradiation combined with hyperthermia (43 degrees C or 44 degrees C). Hyperthermia was applied by immersing the mouse foot into a hot waterbath and irradiation was performed using a 250 kV X-ray generator. Previous irradiation of the feet of mice 90 days before, with 20 Gy, increased the subsequent response to heat alone, or when combined with irradiation, as well as to irradiation alone. It had little effect on the thermal enhancement ratio's for both acute and late skin reactions. Memory of the previous irradiation treatment could be masked when the temperature of the subsequent heat treatment alone, or when combined with irradiation, was 44 degrees C. A priming heat treatment induced resistance both to a subsequent heat treatment and to a subsequent combined irradiation-heat treatment in normal skin as well in previously irradiated skin. This 'resistance' is probably mainly the result of thermotolerance induced in cells in the skin by the priming heat treatment. In thermotolerant skin a 'memory' of the previous irradiation was always evident when the reaction after heat alone or heat combined with irradiation was measured. When the late skin reaction was considered, a larger 'memory' of the previous irradiation treatment was always evident, compared to the acute skin reaction: the 'remembered' dose in the late skin reaction was about two times the 'remembered dose' in the acute skin reaction.

Acclimatization↗
PubMed1982

Effect of hyperthermia and misonidazole on the radiosensitivity of a transplantable murine tumor: influence of factors modifying the fraction of hypoxic cells.

Hypoxia has been demonstrated to play an important role in the effect of hyperthermia on tumors. We have studied the influence of different factors modifying the oxygenation status of a transplantable murine mammary adenocarcinoma (tumor volume and pentobarbital sodium anesthesia). The effect of hyperthermia alone on the tumor is not significantly influenced by the change in oxygenation status during the growth of the tumor. Also, the large increase of the acutely hypoxic cell fraction, as a result of anesthesia, does not change the effect of hyperthermia alone. In the combined irradiation-heat treatment there is a clear influence of the chronically hypoxic cell fraction on the response to hyperthermia: an increase in tumor size, resulting in a larger hypoxic cell fraction, leads to an increase in thermal enhancement ratio. However, the increased acutely hypoxic cell fraction, resulting from anesthesia, did not lead to an increase in thermal enhancement ratio; in fact the enhancement ratio apparently decreased. In spite of the fact that hyperthermia was applied immediately after irradiation no potentiation of radiation effects was found. The thermal enhancement of the radiation response was never larger than the enhancement as a result of misonidazole. All thermal enhancement could be explained by effects of heat on the chronically hypoxic cell fraction. Misonidazole had no effect on the response of tumors to heat alone, but greatly enhanced the effect of heat combined with irradiation. Anesthesia of the animals did not influence these effects of misonidazole.

Anesthesia↗