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Biomedical subjects

C W Song

Publications and source records attributed to C W Song.

198 records · Page 11Linked to original sources
PubMedDate not supplied

Changes in blood flow in locally heated intestine of rats.

Male Fischer rats were surgically castrated through a lower midline incision and a 5-8 cm long segment of small intestine was fixed to the interior of the right scrotum. Two weeks after the surgery, the herniated intestine was heated by immersing the scrotum into a water bath at different temperatures and the blood flow in the intestine was measured with the radioactive microsphere method. The blood flow in the herniated intestine increased 1.5-2.0 times when the scrotum was heated with 42.5 and 43.5 degrees C water baths for 60-90 min, but began to decrease when heated longer, although the blood flow after heating for 120 min at these temperatures was still slightly larger than the blood flow before heating. Upon heating the scrotum with 44.5 degrees C water bath, the blood flow in the herniated intestine increased to 3-fold of control by 90 min and then rapidly recessed. Massive histological damage was observed 24 h after heating with 44.5 degrees C water bath for 60 min. The blood flow in the intestine measured 1 day after 60 min heating with 43.5 degrees C and 44.5 degrees C water bath was found to be only slightly decreased. Given the relatively small decrease in blood flow, the severe damage in the intestine 24 h after heating may be attributed to direct damage to parenchymal cells.

Animals↗
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Acute histological effects of interstitial hyperthermia on normal rat brain.

Histological changes in the brains of Fischer rats at different times after interstitial heating with various thermal doses were studied. The brains, subjected to sham-heating, and heating at 39 and 40 degrees C for 30 min showed mild capillary congestion and minimal vacuolation at 4, 24 and 72 h. In the brains heated to 41, 42 and 43 degrees C for 30 min, there was local vascular congestion, petechiae, vacuolation and cellular shrinkage with nuclear pyknosis at 4 h; enhanced congestion and petechiae, acute cellular necrosis, infiltration of polymorphonuclear leukocytes and marked vacuolation at the margin at 24h; total coagulative necrosis of all parenchymal and vascular elements, early liquefaction necrosis and vascular hyperplasia at the margin at 72 h; enhanced vascular hyperplasia at the margin at 120 h and 168 h. The threshold thermal dose for the histopathological damage in the rat brain was heating at 41 degrees C for 30 min.

Animals↗
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Effect of acidic environment and p53 on apoptosis induction by hyperthermia.

The effect of environmental acidity on the induction of apoptosis by heat was investigated. Human colorectal tumour RKO.C cells, carrying wild-type p53 and isogenic RC10.1 cells deficient in p53, were heated at 42.0 degrees C for 1 h in pH 7.5 or pH 6.6 medium and the apoptosis was assessed based on the flow cytometic determination of DNA content, DNA fragmentation, and PARP cleavage. The degree of apoptosis after heating in pH6.6 medium was greater than that in pH 7.5 medium in both RKO.C cells and RC10.1 cells. When heated in the same pH medium, more apoptosis occurred in the RC10.1 cells than in the RKO.C cells. Heating increased the expression of p53 protein and p21 protein markedly in RKO.C cells and slightly in RC10.1 cells. Expression of these proteins was slightly greater in pH 7.5 medium than in pH 6.6 medium. The expressions of Bax protein and Bcl-2 protein, which are known to control apoptosis, were not altered by heating. It was concluded that an acidic environment enhances heat-induced apoptosis. It was also concluded that heat-induced apoptosis is lessened by p53 and that Bcl-2 and Bax are not involved in the induction of apoptosis by hyperthermia.

Apoptosis↗
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Arsenic trioxide induces selective tumour vascular damage via oxidative stress and increases thermosensitivity of tumours.

It has previously been found that the anti-leukaemia agent Arsenic Trioxide (ATO) causes vascular shutdown in solid tumours and markedly sensitizes tumours to hyperthermia. The present study was designed to evaluate the mechanism of action and dose-dependence of ATO-induced thermosensitization in FSaII and SCK murine tumours. The role of oxidative stress was studied by observing ATO-induced vascular shutdown in vivo and ATO-induced endothelial cell adhesion molecule expression in vitro in the presence or absence of an anti-oxidant. It was found that a dose as low as 2 mg/kg ATO impaired vascular function, as estimated by 86Rb uptake, in the tumour. The degree of tumour growth delay induced by 1 h of hyperthermia at 42.5 degrees C, applied 2 h after ATO injection, was proportional to the dose of ATO administered. In addition, it was found that ATO can directly thermosensitize tumour cells in vitro. The development of massive tissue necrosis in the tumour was observed in the days after treatment, especially with the combination of ATO and heating. ATO-induced adhesion molecule expression in vitro was abolished when the anti-oxidant n-acetyl-cysteine (NAC) was introduced prior to exposure, while the addition of NAC in vivo partially blocked ATO-induced vascular shutdown. These results suggest that the expression of adhesion molecules by the vasculature due to oxidative stress contribute to the ATO-induced selective tumour vascular effects observed and that the clinical use of ATO to increase tumour thermosensitivity via direct cellular and vascular effects appears feasible.

Animals↗
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Reduction of tumour blood flow with KB-R8498 potentiates the response of tumours to hyperthermia.

The anti-tumour activity and the effect on tumour and normal tissue perfusion of a newly discovered anticancer agent, KB-R8498 (Kanebo Ltd., Osaka, Japan), were investigated in FSa II tumours of C3H mice. The tumour perfusion, as measured by the 86Rb-uptake method, markedly decreased with relatively little change in the normal tissue perfusion after an i.v. injection of KB-R8498. Furthermore, the drug potentiated the effect of hyperthermia at 42.5 degrees C for 60 min to suppress the tumour growth. The results suggest that the preferential reduction in tumour blood flow relative to normal tissue blood flow by KB-R8498 may be exploited to enhance the anti-tumour effect of hyperthermia.

Animals↗
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Effect of glycolic acid on UVB-induced skin damage and inflammation in guinea pigs.

OBJECTIVES: Recently the use of glycolic-acid-containing cosmetics has received increased public interest in their supposed ability to reduce wrinkles, roughness, age spots and other skin damage. However, the safety of such products when used excessively or chronically, especially by photosensitive people, is being questioned. The purpose of this study was to examine the effects of glycolic acid alone or in combination with UVB on skin damage and inflammatory response. METHOD: Guinea pigs were treated with glycolic acid (from 1 to 7 mg/cm(2)) alone or in combination with UVB (0.4 or 3 J/cm(2)) for 14 days. Skin damage was evaluated by scoring the skin irritation value by the method of Draize and by histopathological observations. Cyclooxygenase 2 (COX-2) expression and prostaglandin E(2) (PGE(2)) production were also assessed. RESULTS: Glycolic acid caused an increase in the level of skin damage in a dose- and time-dependent manner. Lower doses (1 and 3 mg/cm(2)) of glycolic acid mostly caused erythema and eschar, and these consequently formed scales, whereas higher doses (5 and 7 mg/cm(2)) of glycolic acid caused redness, edema and necrotic ulceration. Glycolic acid also increased the thickness of the epidermal layer, reduced the organization of the stratum corneum and eventually destroyed some parts of the epidermal layer at 7 mg/cm(2). UVB (0.4 and 3 J/cm(2)) caused redness and edema as well as reduced the integrity of the stratum corneum. Glycolic acid enhanced the UVB-induced skin damage. The magnitude of the damage caused by combined UVB and glycolic acid treatment was much greater than that caused by glycolic acid or UVB alone. Moreover, partial destruction of the epidermal layer was observed in skin treated with 3 J/cm(2) UVB and 3 mg/cm(2) glycolic acid. However, glycolic acid did not change the basal and UVB-induced PGE(2) production and COX-2 protein expression. CONCLUSION: These results show that glycolic acid causes skin damage in a dose- and time-dependent manner and that it enhances UVB-induced skin damage without accompanying PGE(2) production or COX-2 protein expression. Therefore, caution should be exercised by those using glycolic acid on a chronic basis or excessively. Moreover, those with photosensitive skins and those more exposed to the sun should be particularly careful.

Animals↗
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Effect of fractionated heating on the blood flow in normal tissues.

The changes in blood flow in the skin and muscle of rat by single, two or six heatings, were measured with the radioactive microsphere method. The blood flow rose continuously during the 2 h heatings at temperatures up to 43.0 degrees C and 44.0 degrees C in the skin and muscle, respectively. When heated at higher temperatures, the blood flow increased and then decreased. When heated twice at 43.5 degrees C for 1 h each, the magnitude of the increase in blood flow by the second heating varied depending on the time interval between the two heatings; e.g., the second heating on the 14th day after the first heating induced an increase in blood flow much greater than that by the first heating. When the heating at 43.5 degrees C for 1 h was repeated at intervals of five days, the second and third heatings were as effective as the first heating in increasing the skin blood flow. In the muscle, the second and third heatings were 2-3-fold more effective than the first heating in raising the blood flow. The heat-induced increase in blood flow in the skin and muscle gradually diminished from the fourth heating. The tissue temperature varied considerably during heating with a water bath at a constant temperature, due probably to the changes in blood flow.

Animals↗
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Effect of hyperthermia on the lactic acid and beta-hydroxybutyric acid content in tumour.

The effects of hyperthermia on the content of lactic acid and beta-hydroxybutyric acid in the SCK mammary carcinoma and the leg muscle of A/J mice were studied. The contents of lactic acid in the SCK tumour before heating was 9.32 mumol/g, and the content of beta-hydroxybutyric acid was only 0.013 mumol/g. The lactic acid content in the tumour increased to 17.5 mumol/g at 0 h after heating at 41.5 degrees C for 30 min and then decreased to the control level 3 h later. When heated at 43.5 degrees C for 30 min, the lactic acid content in the tumour increased to 24 mumol/g at the end of heating and remained elevated for 24 h. The content of beta-hydroxybutyric acid increased continuously reaching 0.45 mumol/g at 5 h after heating at 43.5 degrees C for 30 min, and then declined thereafter. The contents of lactic acid and beta-hydroxybutyric acid in the muscle also increased after heating, but these increases were far less than those observed in the tumours. The absolute amount of lactic acid in the heated tumours was far greater than that of beta-hydroxybutyric acid, and thus appeared to play the major role for the increased acidity in the heated tumours.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Continuous and non-invasive quantification of heat-induced changes in blood flow in the skin and RIF-1 tumour of mice by laser Doppler flowmetry.

The changes in blood flow in the skin and in the periphery of RIF-1 tumours of C3H mice could be monitored continuously during heating with the use of the laser doppler flowmetry. The laser probe was placed gently on the skin or tumour surface and the change in blood flow was quantified from the output signal from the monitor during the heating of the tissues with temperature-controlled water. The blood flow in the tumour increased significantly during the first 20-30 min of heating at 42.5-44.5 degrees C and then began to decline during the second half of one hour of heating. The skin blood flow either continuously increased or remained elevated during 1 h heating at 42.5-44.5 degrees C. These results were generally similar to the previous reports on the heat-induced changes in blood flow in the skin and tumours measured by other methods.

Animals↗
PubMedDate not supplied

Effect of multiple heatings on the blood flow in RIF-1 tumours, skin and muscle of C3H mice.

The effect of one to five multiple heatings on blood flow in the RIF-1 tumour, skin and muscle of C3H mice was studied. When heated for 1 h at 43.5 degrees C the tumour blood flow increased 1.8 times, and rapidly decreased after the heating to less than half the control value. The 2nd-5th heatings at 43.5 degrees C, applied at 1- or 3-day intervals, caused no further significant change in the tumour blood flow. In the skin and muscle the blood flow increased 5 times when heated for 1 h at 43.5 degrees C, and remained at 1.5-2.0 times of control for 1-3 days after the heating. The blood flow in the skin and muscle, particularly in the skin, was further increased by the 2nd-5th heatings applied at 3-day intervals, but not at 1-day intervals, albeit the additional increase was very small. Consequently, whereas the tumour blood flow was 5-6 times greater than that in the skin and muscle before heating, it was only about 1.5-2.0 times greater than that in the skin and muscle during the 1st heating. The tumour blood flow became more or less similar to the normal tissue blood flow during the 2nd-5th heatings given at 3-day intervals. The decline in the vascular response in normal and tumour tissues to the 2nd-5th heatings suggested development of vascular thermotolerance.

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Effect of regional heating of upper body on the liver blood flow in rats.

The changes in rat liver blood flow, caused by hyperthermia, were studied. The liver region of rats was heated with Thermotron IV, an experimental capacitive heating device utilizing 8 MHz RF, and the liver blood flow was measured with radioactive microspheres. Portal venous blood flow slightly decreased during 30 min heating of the liver at 41 degrees C and returned to control level after the heating. When the liver was heated at 43 degrees C, portal venous blood flow decreased initially by about 20%, but gradually returned to control level during the 30 min heating. Hepatic arterial blood flow increased slightly during 30 min heating at 41 degrees C and 43 degrees C. Because almost 85% of the liver blood flow is portal venous blood flow, the change in total liver blood flow paralleled the change in portal venous blood flow. During regional heating of the liver the cardiac output declined significantly, which may account in part for the decrease in splanchnic blood flow, and thus portal venous blood flow. Changes in vascular resistance in the viscera may be another reason for the decrease in portal venous blood flow during heating of the liver region.

Animals↗
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A differential low pH effect on tumour cells grown in vivo and in vitro when treated with hyperthermia.

The effectiveness of low extracellular pH in sensitizing cells to heat was studied using SCK mammary carcinoma cells of A/J mice. Solid tumours of 400-600 mg or cells grown in vitro for less than 13 weeks were dispersed to single cells and the in vivo- or in vitro-derived cells were suspended in a medium of pH 7.2 or 5.5-6.6 and then heated at 41-44 degrees C in vitro using a water bath. The dispersion procedure did not alter the heat sensitivity of these cells, but acidic medium of pH below 6.6 caused an increase in heat sensitivity. This effect of low pH decreased with increasing temperature of heating for both cell types. However, the effect was much smaller on in vivo-derived cells than that on in vitro-derived cells for any heating temperature tested. This reduction of the pH effect was also observed for cells derived from larger tumours as well as tumours at an early stage of growth in which the internal milieu was not acidic. This indicates that cellular adaptation to low intratumour pH was not the cause of the reduced pH effect; instead, factors other than low pH must cause the reduced pH effect seen in tumour-derived cells.

Animals↗
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Thermal sensitivity and kinetics of thermotolerance in bovine aortic endothelial cells in culture.

The effect of heat on the clonogenicity of bovine aortic endothelial (BAE) cells in vitro was measured. Continuous heating of cells at 43 degrees C or 43.5 degrees C produced survival curves exhibiting thermoresistant tails. When heated at 44 degrees C the survival curve of BAE cells was exponential except for a small shoulder. The BAE cells heated at 44 degrees C and 45 degrees C had D0 values of 33 min and 19 min, respectively. The development of thermotolerance in BAE cells was studied by measuring the sensitivity of cells to a 44 degrees C heating at various times following a priming heat treatment at 43 degrees C or 44 degrees C for 30 min. The thermotolerance ratio in BAE cells preheated at 43 degrees C for 30 min reached a peak of 3.8 at 3 h and declined to 1.9 at 24 h after the prime heating. After prime heating at 44 degrees C for 30 min the thermotolerance ratio increased rapidly to 5.4 in 5 h, remained elevated at 12 h and then declined to a value of 2.1 at 24 h. Thermotolerance in endothelial cells may be partially responsible for the thermotolerance in blood vessels of normal tissues and tumours.

Animals↗
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3D rendering of SAR distributions from Thermotron RF-8 using a ray casting technique.

A comprehensive 3D visualization package developed for CT-based 3D radiation treatment planning has been modified to volume-render SAR data. The program accepts data from sequential thermographic thermometry measurements as well as calculated data from thermal models. In this presentation sample data obtained from a capacitive heating system 'Thermotron-RF8' is presented. This capability allows the generation of accurate standardized volumetric images of SAR and provides a valuable tool to better preplan hyperthermia treatments.

Evaluation Studies as Topic↗
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Effects of a second heating on rat liver blood flow.

Effects of a second heating on blood flow in the liver and cardiac output were studied in Fischer rats. Heating was done by an experimental capacitive heating device using 8 MHz radiofrequency. Thermometry was performed at seven points around the liver with thermocouples. Blood flow and cardiac output were measured with the radioactive microsphere method. The liver was preheated for 30 min at 41 or 43 degrees C, and then reheated 1-7 days later at 41 degrees C for 15 min. Hepatic arterial blood flow, portal venous blood flow and the cardiac output were measured immediately before and at the end of the reheating. Heating the liver at 41 degrees C for 15 min without preheating slightly increased the hepatic arterial blood flow, and reheating 1-7 days after the first heating caused a greater increase in the hepatic arterial blood flow. Increase in hepatic arterial blood flow caused by reheatings pointed to the development of thermotolerance or thermal adaptation in the hepatic artery. When the liver was heated at 41 degrees C for 15 min without preheating, the portal venous blood flow remained almost unchanged 1-7 days after the heating. On the other hand, a reheating at 41 degrees C for 15 min applied 1-7 days after the preheating reduced the portal venous blood flow. Reduction in portal venous blood flow was approximately parallel to reduction in cardiac output by reheating, pointing to the existence of a causal relationship. Reduction in portal venous blood flow by reheating may also be, in part, due to the decrease in the splanchnic blood flow resulting from a systemic adaptation to the heat stress.

Animals↗
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Combined treatment of IL-1 alpha and TNF-alpha potentiates the antitumour effect of hyperthermia.

Vasoactive cytokines, such as IL-1 alpha and TNF-alpha, modulate the homeostatic state at the endothelial surface and cause various types of pathological damage in vascular systems. We investigated the potential therapeutic effects of IL-1 alpha and TNF-alpha in combination with hyperthermia on SCK tumours grown in the legs of A/J mice. We first determined the effect of cytokines on tumour blood perfusion with the (86)Rb uptake method. When the host mice were given an i.p. injection of 25 mu g/kg IL-1 alpha or 50 mu g/kg TNF-alpha, the tumour blood perfusion markedly declined to 46 and 82% of control, respectively. The combination of IL-1 alpha and TNF-alpha reduced the 86Rb uptake to 41% bf control. Hyperthermia at 42.5 degrees C for 1 h reduced the tumour blood flow to 71% of control. The tumour blood perfusion decreased further to 20% of control when the tumours were heated for 1 h at 42.5 degrees C starting 4h after the injection of both IL-1 alpha and TNF-alpha. The changes in clonogenic cell numbers in SCK tumours, as determined by the in vivo-in vitro assay, following various treatments was also investigated. At 4 h after an i.p. injection of 25 mu g/kg IL-1 alpha or 50 mu g/kg TNF-alpha, the clonogenicity of SCK tumours significantly decreased to 29 or 37% of control, respectively. Heating at 42.5 degrees C for 1 h caused a decline in the clonogenic cell number to 30% of control. When both IL-1 alpha and TNF-alpha were given and tumours were heated 4h later at 42.5 degrees C for 1 h, the clonogenic cell number markedly declined to 0.4% of control. The time needed for control tumours to reach 4 x their initial volume was about 3 days, and treatment with IL-1 alpha or hyperthermia alone induced a tumour delay growth by about 1 day. The combined injection of IL-1 alpha and TNF-alpha followed by a heating at 42.5 degrees C for 1 h delayed the tumour growth by 6 days. The results in this study suggest that prior impairment of blood circulation by the combined treatment of IL-1 alpha and TNF-alpha potentiates hyperthermic damage in tumours.

Animals↗
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Tumour oxygenation is increased by hyperthermia at mild temperatures.

The effects of hyperthermia on the oxygenation status in R3230 AC tumours of Fischer rats were measured using a polarographic oxygen electrode system. The median pO2 in about 10 mm diameter tumours grown s.c. in the leg of rats was 3.7 +/- 0.3 mm Hg and it significantly increased upon heating at modest temperatures. For example, the tumour pO(2) measured within 10-15 min after heating for 30 min at 42.5 degrees C was about three-fold greater than that in the control tumours. About 62% of PO(2) values measured in control tumours were < 5 mm Hg. After heating at 42.5 degrees C for 30 min, 37% of PO(2) values were < 5 mm Hg. Such an increase in tumour oxygenation or reoxygenation of hypoxic cells appeared to result from an increase in tumour blood flow caused by the mild temperature hyperthermia. The presence of hypoxic cells in tumours is believed to be a major factor in limiting the effectiveness of radiotherapy, certain chemotherapy drugs and phototherapy. Hyperthermia at mild temperatures easily achievable with the use of presently available clinical hyperthermia devices may be an effective means to overcome the hypoxic protection in the treatment of human tumours.

Adenocarcinoma↗