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S Masunaga

Publications and source records attributed to S Masunaga.

At least 73 records · Page 4Linked to original sources
PubMed1995

Clinical evaluation of 430 MHz microwave hyperthermia system with lens applicator for cancer therapy.

The clinical efficacy of a microwave (MW) hyperthermia system using an electric-field converging (lens) applicator is evaluated for 42 malignant tumours with a maximum tumour depth of less than 7 cm. The mean of the maximum, average and minimum tumour temperature of the 42 tumours are 44.5, 42.5 and 40.7 C, respectively. The thermal parameters are higher for tumours in the chest, abdominal walls and hip than for those in the neck, groin and extremities. No apparent difference in thermal parameters according to the depth of tumour is shown. Of 40 tumours treated by hyperthermia in combination with radiotherapy, 20 (50%) showed complete regression, 14 (35%) showed partial regression, and six (15%) showed no change. This phase I and II study indicates clinical feasibility of the newly developed MW heating apparatus, and strongly suggests the usefulness of thermoradiotherapy in the treatment of localised superficial and subsurface malignancies.

Adolescent↗
PubMed1995

[A case of successful acute revascularization using a long vein graft].

We experienced a case of successful acute revascularization using a long vein graft. A 68-year-old man was admitted to our department due to transient ischemic attack of the left hemiparesis. CT scan showed no infarction, but PAO-SPECT revealed moderate hypoperfusion in the right ACA and MCA area. Cerebral angiography demonstrated right IC occlusion at its origin and moderate collateral circulation via leptomeningeal anastomosis from the PCA area, and via the external carotid system, especially directly from STA. But the STA was very narrow. Three days after admission, left hemiparesis appeared again and deteriorated severely. This time the hemiparesis persisted. Although MRI demonstrated little infarction in the right frontal lobe, we decided to carry out revascularization on the same day. Right saphenous vein was harvested for a graft because of the narrow STA. The facial artery and angular artery was selected as a donor and a recipient respectively, to avoid a clamp of the EC and a craniotomy of the STA running area. Finally we performed a facial artery-vein graft-angular artery (M4) bypass. The patient showed no complication and the left hemiparesis improved enough to allow the patient to walk by himself. Revascularization using vein graft is dangerous for acute ischemia due to the possibility of a complication such as brain edema and hemorrhagic infarction. The usual style of vein graft bypass is an EC-vein graft-M2 or M3 bypass. Using this style, high pressure inside the EC is carried intracranially.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1995

[MRI of the pituitary adenomas with reference to the hormonal activity].

Many studies in Magnetic Resonance Imaging (MRI) of pituitary adenomas are already performed. However, few reports exist about MRI findings of pituitary adenomas with reference to the hormonal activity, therefore, we evaluated this problem on the viewpoint of the signal intensity in MRI and pathological features. Fifteen patients with growth hormone producing adenoma (GH-group), 6 patients with prolactin producing adenoma (PRL-group), 15 patients with endocrinologically non-functioning adenoma (Null-group) and 9 cases with normal pituitary gland (normal control group) were examined. Signal intensity values in adenoma (or anterior lobe in normal control group) and in pons as standard value were measured in each cases, then their rates were calculated as signal intensity ratio (SIR). In 24 cases (14 in GH-group, 3 in PRL-group, 7 in Null-group), cellular density were examined with surgically resected specimens. In the T1-weighted images (T1 WIs), PRL-group and Null-group presented more hypointense tendency than normal control group. In the T2-weighted images (T2 WIs), only Null-group presented more hyperintense tendency than other groups. But significant correlation was not observed between SIR and cellular density.

Adenoma↗
PubMed1994

The radiosensitivity of quiescent cell populations in murine solid tumors in irradiation with fast neutrons.

PURPOSE: We analyzed the characteristics of radiosensitivity and potentially lethal damage repair in the quiescent cell populations of murine SCC VII solid tumors irradiated with fast neutrons, in comparison with those irradiated with 10 MV X rays. METHODS AND MATERIALS: SCC VII tumor-bearing C3H/He mice were irradiated with 30 MeV fast neutrons or 10 MV X rays after receiving 10 injections of 5-bromo-2'-deoxyuridine (BUdR) to label all proliferating tumor cells. Immediately or 24 h after irradiation, the tumors were excised and trypsinized. The tumor cell suspensions thus obtained were incubated with cytochalasin-B (a cytokinesis blocker), and the micronucleus frequency in cells without BUdR labeling was determined using immunofluorescence staining to BUdR. This micronucleus frequency was then used to calculate the surviving fraction of unlabeled cells from the regression line for the relation between micronucleus frequency and the surviving fraction of all tumor cells. Thus, a cell survival curve could be determined for the cells not labeled by BUdR, which can be regarded as the quiescent cells for all practical purposes. RESULTS: The difference in intrinsic radiosensitivity between all tumor and quiescent cells became smaller by using fast neutrons, compared with X rays, especially when large radiation doses were given. Potentially lethal damage repair by quiescent cells was less evident following irradiation with fast neutrons than with X rays, especially when large doses were delivered. CONCLUSION: By using fast neutrons in clinical radiotherapy, the radiosensitivity of solid tumors is thought to depend on their heterogeneity less critically than for X rays.

Animals↗
PubMed1994

Middle dose rate irradiation in combination with carbogen inhalation selectively and more markedly increases the responses of SCCVII tumors.

PURPOSE: Carbogen increases the radiation response of tumors and reduced dose rate irradiation spares the damage of normal tissues. The purpose in this paper is to investigate the possibility of selective radiosensitization of tumors by reduced dose rate irradiation in combination with carbogen inhalation. METHODS AND MATERIALS: SCCVII tumors in C3H/He mice were irradiated at middle dose rate (0.1 Gy/min) or high dose rate irradiation (3.0 Gy/min) in combination with carbogen inhalation. The mice were enclosed in a box with carbogen flushing at 1.01/min. The tumor response was measured by a cytokinesis block micronucleus assay. The effects on intestinal crypt cells and bone marrow cells were investigated by microcolony assay or Hendry's method, respectively. RESULTS: The anti-tumor effect of middle dose rate irradiation was equal to that of a high dose rate irradiation. Carbogen inhalation, more efficiently, increased the antitumor effect when combined with middle and high dose rate irradiation, and yielded enhancement ratios of 1.6 at around 2 Gy. Middle dose rate irradiation produced less damage on intestinal crypt cells and bone marrow cells in comparison with high dose rate irradiation, and carbogen inhalation never enhanced the responses of these normal tissues in combination with middle dose rate irradiation. Dose modifying factors were 1.3-2.0. CONCLUSION: Since middle dose rate irradiation in combination with carbogen inhalation gave the therapeutic gain factors of 2.0-3.2, which were much larger than those obtained with any other radiosensitizers, this combination has a potential as a new modality for improving the results of cancer radiotherapy.

Animals↗
PubMed1994

Degradation of tri-n-butyltin in Ise Bay sediment.

The vertical distribution patterns of the transformation products of tri-n-butyltin (TBT) in sediment cores collected from 6 sites in Ise Bay, Japan indicated that TBT was transformed by two pathways: methylation and debutylation. Anaerobic incubation of sediment spiked with TBT showed that the methylation was mainly supported by sulfate reducing activity and debutylation was mainly supported by nitrate reducing activity. These results showed that contribution of the two transformation reactions of TBT varied according to the dominant microbial activities in the sediment. The two types of vertical distribution of butyltins observed in the sediment cores appear to be the result of different dominant microbial activity in the sediment.

Alkylation↗
PubMed1994

Determination of the target volume of HeLa cells treated with platinum-195 m radiolabeled cis-diammine(1, 1-cyclobutane-dicarboxylato)-platinum(II); comparison with cis- and trans-diamminedichloroplatinums(II).

HeLa S-3 cells were treated with 195mPt-radiolabeled cis-diammine(1, 1-cyclobutane-dicarboxylato)platinum(II) (carboplatin) under various conditions, and the relationship between lethal effect and the number of Pt atoms binding to DNA, RNA and proteins was examined. The mean lethal concentrations for the cells treated with carboplatin at 37 degrees C for 1, 2 and 3 h were 553.4, 194.3 and 68.7 microM, respectively. By using identically treated cells, the numbers of Pt-atoms combined with DNA, RNA and protein molecules were determined after fractionation of the cells. In this way the D0 values (D0, dose that would give an average of one lethal event per member of the population), expressed as the drug concentration, were substituted for the number of Pt atoms combined with each fraction. The target volumes, the efficiency of Pt atom to kill cells expressed as the reciprocals of the D0 values, were then calculated with each fraction. The results suggested that DNA was the primary target for cell killing by carboplatin. The target volumes for DNA were 0.891 x 10(4), 2.01 x 10(4) and 3.96 x 10(4) nucleotides for 1, 2 and 3 h treated cells, respectively. The cell killing effects of carboplatin were lower than those of cis-diamminedichloroplatinum(II) (CDDP) by factors of 6.0, 2.8 and 2.6 for 1, 2 and 3 h treatments at 37 degrees C, respectively, in terms of the target volume, while those in terms of the mean lethal dose (D0) were 59.5, 29.0 and 21.5, respectively.

Antineoplastic Agents↗
PubMed1994

Effect of hyperthermia on the number of platinum atoms binding to DNA of HeLa cells treated with 195mPt-radiolabelled cis-diaminedichloroplatinum(II).

HeLa S-3 cells were treated with 195mPt-radiolabelled cis-diaminedichloroplatinum II) (CDDP) for 60 min at various temperatures to examine the relationship between the lethal effect and the number of Pt atoms binding to DNA, RNA and protein molecules. The mean lethal concentration (Do) of CDDP for 60-min treatment at 0, 25, 37, 40, 42 and 44 degrees C was 233, 69.9, 15.9, 11.7, 8.3 and 4.7 microM respectively. By using identically treated cells, the number of Pt atoms combined with DNA, RNA and protein molecules was determined in the subcellular fractions prepared by the method of Schneider (1961). Thus, the Do's given as the drug concentrations were substituted for the number of Pt atoms combined with each fraction. Then the efficiency of the Pt atom to kill the cells was expressed as the reciprocal of the number of Pt atoms combined and was calculated for each molecule. The efficiency for DNA was 2.47, 2.75, 9.49, 9.66, 10.53 and 15.00 x 10(4) nucleotides respectively for the conditions described above. A detailed comparison of the Do's and efficiencies suggested that the supra-additive effect of the combination treatment could be explained by two mechanisms, i.e. the increased drug level in DNA (from 37 to 42 degrees C) and the increased efficiency of the Pt atoms to kill the cells (> 42 degrees C).

Cell Death↗
PubMed1994

Enhancement of chemosensitivity of quiescent cell populations in murine solid tumors using nicotinamide.

Cis-diamminedichloroplatinum(II) (CDDP) was intraperitoneally injected into mice bearing SCC VII or EMT6/KU tumors after 10 administrations of 5-bromo-2'-deoxyuridine (BUdR) to label all the proliferating tumor cells. One hour later, the tumors were excised, minced and trypsinized. The tumor cell suspensions were incubated with cytochalasin B (a cytokinesis blocker). The micronucleus (MN) frequency was determined using immunofluorescence staining to BUdR. The cells that were not labeled with BUdR could be regarded as the quiescent cells. The MN frequency in total tumor cells was determined from the tumors that were not pretreated with BUdR. To modify the sensitivity to CDDP, nicotinamide was intraperitoneally injected before CDDP administration. In both tumor system, the MN frequency in quiescent cells was lower than in total cells. Nicotinamide pretreatment increased the MN frequency in total and quiescent cells in both tumor systems, especially in total cells of the SCC VII tumor. The nicotinamide injection increased the uptake of 195mPt-CDDP into the total cells, especially in the SCC VII tumor. Nicotinamide administration before chemotherapy using CDDP was considered to be effective for tumor control, especially in tumors including large acutely hypoxic fractions such as the SCC VII murine tumor.

Animals↗
PubMed1994

The response of quiescent cell populations in murine solid tumors to irradiation with fast neutrons.

5-bromo-2'-deoxyuridine (BUdR) was injected into SCC VII tumor-bearing mice intraperitoneally to label all proliferating tumor cells. The mice were irradiated with fast neutrons or x-rays. Immediately, or 24 h after irradiation, the tumors were excised, minced and trypsinized. The tumor cell suspensions were incubated with cytochalasin-B (a cytokinesis blocker). The micronucleus frequency was determined using immunofluorescence staining to BUdR. The cells that were not labeled with BUdR could be regarded as the quiescent cells. The micronucleus frequency in total tumor cells was determined from the irradiated tumors that were not pretreated with BUdR. The difference in radiosensitivity between total and quiescent cells was markedly reduced with fast neutrons, especially at higher doses of radiation. Potentially lethal damage repair by total and quiescent cells was inhibited more strongly with neutrons than with x-rays. When using fast neutrons, the radiosensitivity of solid tumors depends on their heterogeneity less critically than for x-rays.

Animals↗
PubMed1994

Estimation of the initial slope of the cell survival curve after irradiation from micronucleus frequency in cytokinesis-blocked cells.

We have already reported that the alpha/beta ratio of the cell survival curve could be estimated from the micronucleus frequency in cytokinesis-blocked cells treated with cytochalasin-B after irradiation. In this paper, we investigate the direct relationship between the alpha value and the appearance of micronuclei. Cells of the SCCVII, RIF-1, EMT6, V-79, CHO, HeLa and human esophageal cancer cell lines were used for the study. Low-dose-rate irradiation was used to determine the alpha component of the relationship between dose and micronucleus frequency according to the linear-quadratic (LQ) model. A reduction of the dose rate from 3.09 to 0.0142 Gy/min correspondingly decreased the micronucleus frequency; however, the fraction of binucleate cells without micronuclei was not affected in SCCVII and RIF-1 cells. When this fraction was defined as the normal nuclear division fraction, it decreased exponentially as a function of radiation dose. Then dose vs normal nuclear division fraction (NNDF) was fitted as follows: -ln NNDF = aD + C, where D is radiation dose in grays and C is constant. The slope of the dose vs normal nuclear division fraction was not affected by dose rate. The correlation was also explored between the slope (a) and the alpha value of the cell survival curve determined by the colony formation assay in cells of eight cell lines. These two values showed extremely high agreement: alpha = 1.01 a + 0.00795 (r = 0.99, P < 0.01). This assay was applied to estimate the alpha value of the cell survival curve of human esophageal cancer cell lines established from surgical specimens.

Animals↗
PubMed1993

Radiosensitization of SCCVII tumours and normal tissues by nicotinamide and carbogen: analysis by micronucleus assay.

The radiosensitizing effect on SCCVII tumours of carbogen (95% O2 + 5% CO2) combined with nicotinamide was investigated using the micronucleus assay and an in vivo/in vitro colony formation assay following single irradiation. The effects on intestinal crypt cells and bone marrow cells were also examined in mice. The frequency of micronuclei in tumours increased with an increase in the nicotinamide dose (administered 1 h before the irradiation of 5 Gy) from 0.1 to 1.0 mg/g, and showed a 1.3-fold increase at 1.0 mg/g when compared with radiation alone. The micronucleus frequency showed a more marked increase following irradiation combined with nicotinamide and carbogen inhalation starting 15 min before irradiation. The radiosensitizing effect reached a plateau at a nicotinamide dose of 0.1 mg/g in combination with carbogen, giving an enhancement ratio (ER) of 1.8 relative to radiation alone at 2 Gy. In the radiation dose range of 5-20 Gy, ERs of 1.8-1.9 and 1.5 (at a 10% cell-survival level) were obtained for the combination of 0.1 or 1.0 mg/g nicotinamide and carbogen and for carbogen alone, respectively. A slight increase in the regeneration response of the jejunum and the bone marrow was observed following irradiation combined with 0.1 mg/g nicotinamide and carbogen, yielding ERs of 1.07 for the jejunum and 1.15 for the bone marrow. Thus, the nicotinamide/carbogen combination, with its large therapeutic gain factor at low doses and proven low toxicity in humans, seems to improve the response of cancer to radiotherapy.

Animals↗
PubMed1993

Alteration of radiosensitivity of quiescent cell populations in solid tumors irradiated with X-rays twice at various intervals.

5-Bromo-2'-deoxyuridine (BUdR) was injected into SCC VII or EMT6/KU tumor-bearing mice intraperitoneally to label all the proliferating tumor cells. First, the mice were irradiated with X-rays at a dose of 10 Gy, followed by a dose of 0-20 Gy at 0, 12, 24 or 48 h later. During the interval, no BUdR was injected. Immediately after the second irradiation, the tumors were excised and trypsinized. The micronucleus (MN) frequency in cells without BUdR labeling was determined by means of incubation with cytochalasin-B (a cytokinesis-blocker) and immunofluorescence staining for BUdR. When the tumors were not pretreated with BUdR before the first irradiation, the MN frequency in all tumor cells was determined. To determine the labeling indices of SCC VII and EMT6/KU tumors at the time of the second irradiation, each group also included mice that were continuously administered BUdR until just before the second irradiation using mini-osmotic pumps which had been implanted subcutaneously 5 days before the first irradiation. The MN frequency of all tumor cell populations obtained immediately after the second irradiation decreased in proportion to the increase in interval time. However, in both tumor systems, the MN frequency of unlabeled cell populations, which could be regarded as quiescent cells in the tumors at the time of the first irradiation, was raised with increase in the interval time. In addition, the labeling index at the second irradiation was higher than that at the first irradiation. These findings support the occurrence of recruitment from quiescent to proliferating state during fractionated irradiation.

Animals↗
PubMed1993

The detection and modification of the hypoxic fraction in quiescent cell populations in murine solid tumours.

Mice bearing SCC VII or EMT6/KU tumours were irradiated after receiving 10 injections of 5-bromo-2'-deoxyuridine (BUdR) to label all proliferating tumour cells, and the tumours were then excised and trypsinized. The tumour cell suspensions thus obtained were incubated with cytochalasin-B (a cytokinesis blocker), and the micronucleus (MN) frequency in cells without BUdR labelling was determined using immunofluorescence staining to BUdR. This MN frequency was then used to calculate the surviving fraction of unlabelled cells from the regression line for the relation between MN frequency and the surviving fraction of all tumour cells. Thus a cell survival curve could be determined for cells not labelled by BUdR, which can be regarded as quiescent tumour cells for all practical purposes. Assays performed immediately after irradiation of both normally aerated and hypoxic tumours showed that quiescent cells contained higher hypoxic fractions than the tumour cells as a whole. Furthermore, administration of nicotinamide before irradiation or the placement of mice in a circulating carbogen (95% O2, 5% CO2) chamber for 30 min before and during irradiation altered the acutely and chronically hypoxic fractions of the proliferating and quiescent tumour cell populations in a way which depended on the tumour system. Combined nicotinamide and carbogen therapy was shown to have a large potential to sensitize cells to low-dose radiation in vivo. In addition, this assay method appears to be useful for determining the size of the hypoxic fraction of quiescent tumour cells in murine solid tumours.

Animals↗
PubMed1993

[Current status of thermoradiotherapy in cancer therapy].

The current status of thermoradiotherapy for cancer is reviewed. The usefulness of this combined treatment for superficial tumors, in which heating and thermometry are relatively easy to apply, has been clearly demonstrated by many clinical results. With recent technological advancements, the application of thermoradiotherapy to deep-seated tumors is increasing, and encouraging results have been reported for various tumors including brain tumors, carcinomas of the breast, lung, esophagus, liver, rectum, urinary bladder, and soft tissue tumors. Thermoradiotherapy seems a very promising treatment modality for various refractory malignancies.

Brain Neoplasms↗
PubMed1992

Hyperthermia combined with radiation therapy for primarily unresectable and recurrent colorectal cancer.

The value of adjuvant hyperthermia to radiotherapy in the treatment of locally advanced colorectal cancers was investigated. Between 1981 and 1989, 71 primarily unresectable or recurrent colorectal tumors were treated with radiotherapy at the Department of Radiology, Kyoto University Hospital. Of the 71 tumors, 35 were treated with radiotherapy plus hyperthermia (group I), while 36 tumors (group II) were unsuitable for hyperthermia mainly because of difficulties with the insertion of temperature probes or the thickness of the patient's subcutaneous fat (greater than 2 cm). The mean total radiation dose was 58 Gy and 57 Gy for groups I and II, respectively. Thirty deep-seated pelvic tumors were treated with an 8 MHz radiofrequency capacitive heating device, and five subsurface tumors were treated with a 430 MHz microwave hyperthermia system. Hyperthermia was given following radiotherapy for 30-60 min for a total of 2-14 sessions (mean 5.7). In 32 of the 35 tumors heated, direct measurement of tumor temperature was performed. For the five tumors treated with the microwave heating device, the means of the mean maximum, average, and minimum measured intratumoral temperatures were 45.4 degrees C, 43.3 degrees C, and 40.6 degrees C, respectively. The corresponding values were 42.2 degrees C, 41.3 degrees C, and 40.3 degrees C for the 27 tumors treated with the capacitive heating device. Effective heating of deep-seated pelvic tumors was more difficult than heating of abdominal wall or perineal tumors. The local control rate at 6 months after the treatment, which was defined as absence of local progression of the tumors, was 59% (17/29) and 37% (11/30) for groups I and II, respectively. The objective tumor response rate (complete regression plus partial response) evaluated by computed tomography was 54% (19/35) in group I, whereas it was 36% (10/28) in group II. A better response rate of 67% was obtained in the 15 tumors with a mean average tumor temperature of greater than 42 degrees C. Although limitation of our current heating devices exist, the combination of hyperthermia with radiotherapy is a promising treatment modality in the treatment of locally advanced colorectal cancer.

Adenocarcinoma↗
PubMed1992

Potentially lethal damage repair by quiescent cells in murine solid tumors.

We investigated potentially lethal damage repair by quiescent tumor cells in vivo. SCC VII tumor-bearing C3H/He mice were irradiated after being given 10 injections of 5-bromo-2'-deoxyuridine (BUdR) to label all the proliferating cells in their tumors, and the tumors were then excised and trypsinized. The tumor cell suspensions thus obtained were incubated with cytochalasin-B (Cyt-B, a cytokinesis blocker), and the micronucleus frequency in cells without BUdR labelling was determined using immunofluorescence staining to BUdR. The micronucleus frequency was then used to determine the surviving fraction of unlabelled cells on the basis of the regression line obtained for the micronucleus frequency and the surviving fraction of all tumor cells not labeled by BUdR, which can be regarded as the quiescent cells in a tumor for all practical purposes. Assessment performed 0, 3, 6, 9, and 24 hr after irradiation showed that quiescent cells had more potentially lethal damage repair capacity than the tumor cell population as a whole. Assays were also performed immediately after irradiation alone, 24 hr after the injection of cis-diamminedichloroplatinum(II) (CDDP), mitomycin C (MMC), or misonidazole [1-(2-nitro-1-imidazolyl)-3-methoxy-2-propanol] (MISO) following irradiation, and 24 hr after irradiation alone. It was found that CDDP and MISO (especially the latter) inhibited potentially lethal damage repair more strongly in quiescent cells than in the tumor cell population as a whole. This assay method thus appears to be quite useful for detecting the responses of quiescent tumor cells to various chemical agents.

Animals↗