[The analysis of Tc-99m RBCs time activity curve on liver tumor--differentiation between hemangioma and hepatocellular carcinoma].
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Biomedical subjects
Publications and source records attributed to T Inomata.
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Tumor infiltrating lymphocytes induced by radiotherapy were analyzed by the biotin-avidin-horseradish peroxidase method. At the early dose of 4 Gy (400 rad) of irradiation (2 Gy X 2), remarkable infiltration of lymphocytes was observed surrounding cancer cells. This infiltration was mainly composed of Leu-3a+3b-positive lymphocytes, and human leukocyte antigen DR-positive tumor and interstitial cells were remarkably observed.
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We analysed various subsets of lymphocytes infiltrated into cancer tissues from 15 patients (10 cases of oropharyngeal cancer and 5 of hypopharyngeal cancer) at pretreatment and at about 10 Gy and 30 Gy of irradiation by the method of biotin-avidin-horseradish peroxidase using mouse monoclonal antibodies. In 3 cases, tumor infiltrating lymphocytes were remarkably increased at the delivery of small dose of irradiation: Two of them showed remarkable radiosensitivity, and the lymphocyte subpopulation of the cancer tissue was mainly composed of Leu3a + 3b positive, Leu-8 negative and Leu-HLA-DR positive lymphocytes (activated helper inducer T lymphocytes). On the other hand, the third one proved to be rather radioresistant and the lymphocyte subpopulation was mainly composed of Leu-14 positive lymphocytes (B lymphocytes). These findings indicate that the analysis of the lymphocyte subpopulation infiltrating into cancer tissues at the delivery of small dose of irradiation is applicable as a predictive assay in radiotherapy of squamous cell carcinoma of oropharynx and hypopharynx.
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The pathogenetic role of lipid peroxidation in ethanol-induced liver injury was previously supported by demonstration of increased formation of diene conjugates and decreased hepatic levels of reduced glutathione in ethanol-fed animals and alcoholic patients with liver injury. The present study was carried out to investigate whether these findings can be extended to a rat model that was shown to produce a spontaneous ethanol-induced liver injury progressing from steatosis to necrosis and fibrosis (Hepatology 6: 814, 1986). Despite the histological evidence of progression from hepatic steatosis to centrilobular necrosis in these animals, diene conjugate formation in mitochondrial and microsomal lipids was not enhanced when compared to pair-fed controls. In addition, hepatic levels of neither methionine nor glutathione were decreased in the ethanol-fed animals. The fatty acid composition of mitochondrial phospholipids from these animals was similar to that in the controls. However, in the microsomal phospholipids, the level of arachidonate (20:4) was depressed by about 50% as compared to the controls. These results demonstrate the lack of evidence for a pathogenetic relationship between lipid peroxidation and ethanol-induced liver injury progressing to centrilobular necrosis. They further suggest that the decreased levels of 20:4 commonly seen after chronic ethanol intake may not be due to a peroxidative loss.
Serial frozen sections were prepared from 22 squamous cell carcinomas of oral cavity and paranasal sinus. Mononuclear cell infiltrates were stained by the biotin-avidin-horseradish peroxidase method using a panel of 10 mouse monoclonal antibodies to human leukocyte antigens. The degree of infiltration was graded from + + + (marked) to - (absent). The infiltration of anti-Leu-4-reactive cells (Leu-4+ cells) was grade + + or + + + in 14 of 22 cases. In 13 of 22 cases, infiltration of Leu-3a + 3b+ cells (helper/inducer T lymphocytes) was grade + + (moderate). In 5 of 20 cases, infiltration of Leu-2a+ cells (cytotoxic/suppressor T lymphocytes) was grade + +. As for B lymphocytes, infiltration of Leu-12+ cells was grade + + in only 2 of 19 cases. In conclusion, T lymphocyte infiltrates were commonly seen in squamous cell carcinoma in oral cavity and paranasal sinus and the number of patients with grade + + infiltration of helper/inducer T lymphocytes significantly predominated over that of patients with infiltration of cytotoxic/suppressor T lymphocytes grade + +.
In order to better understand the immunologic effects of irradiation, blood levels of lymphocyte subsets were sequentially monitored in 37 patients before and during irradiation treatment for lung cancer. Tumor infiltrating lymphocytes induced by radiotherapy were analysed by the avidin-biotin-horseradish peroxidase method. 49 cases of head and neck cancer were examined. In some cases, remarkable infiltration of lymphocytes was observed surrounding cancer cells during radiotherapy. This infiltration was mainly composed of anti-Leu-3a + 3b positive lymphocytes, and HLA-DR positive cancer cells were remarkably observed.
Female C3H/HeN mice bearing solid FM3A tumors were treated with a combination of ACNU (or Nimustine hydrochloride) and radiation in order to investigate the antitumor effects and also to determine the optimal treatment schedule of ACNU in such combined therapy. ACNU was intravenously injected either twice with an interval of 2 weeks and a dose of 30 mg/kg (intermittent large-dose treatment), or as 4 weekly doses of 15 mg/kg (fractionated small-dose treatment). Local irradiation (5 Gy) at the tumor site was performed twice with an interval of 2 weeks between the doses. Synergistic effects were obtained by the combination of ACNU and radiotherapy in terms of tumor growth inhibition and prolongation of survival. Histology also revealed much greater reduction of viable tumor cells in the case of combination treatment. With either treatment with ACNU alone or in combination with irradiation, the intermittent large-dose injections resulted in better inhibition of tumor growth than did the fractionated small-dose injections, but the survival times with the intermittent treatments were not as prolonged as would be expected from the direct effects. Loss of body weight and depression of WBC number were also much more severe in the intermittent treatment group. Thus, it may be concluded that when ACNU is combined with radiotherapy, the intermittent large-dose regimen is not necessarily superior to the fractionated small-dose one.
Female C3H/HeN mice were irradiated in the thorax at a dose ranging from 10 to 25 Gy with or without ACNU (nimustine hydrochloride) treatment in order to determine whether the chemotherapeutic agent would lead to an enhancement of radiation-induced lung damage. ACNU given intravenously at 15 mg/kg immediately prior to irradiation reduced the mortality of mice irradiated with a low dose; mortality with either radiation alone or radiation plus ACNU was 4/10 (40%) or 0/10 (0%) at 13.1 Gy, and 9/10 (90%) or 6/10 (60%) at 15 Gy, respectively. The presence of ACNU during thoracic irradiation also prolonged the survival time of mice approximately 2-fold over that of animals given radiation alone. Histological examination of mice sacrificed 80 days after treatments revealed that the combination of drug and irradiation produced no radiation pneumonitis, which was predominant in mice given radiation alone. It is unexpectedly concluded that ACNU may have a protective effect against radiation-induced lung injury.
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