In vitro effects of chlorpromazine and meprobamate on blast transformation and chromosomes.
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Biomedical subjects
Publications and source records attributed to N Kamada.
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Tritiated water (HTO) is a major toxic effluent from the nuclear power industry, that is released into the environment in large quantities. The low dose radiation effect and dose rate effect of HTO on human lymphocytes and bone marrow cells have not been well studied. The present study was therefore undertaken to investigate the HTO dose-response relationship for chromosomal aberrations in human lymphocytes and bone marrow cells at low in vitro radiation doses ranging from 0.1 to 1 Gy. Lymphocytes (G0 stage) and bone marrow cells were incubated for 10-150 min with HTO at a dose rate of 2 cGy/min (555 MBq/ml). The relative biological effectiveness (RBE) of HTO was calculated with respect to 60Co gamma-rays for the induction of dicentric and centric ring chromosomes at low radiation doses. The RBE value for HTO beta-rays relative to 60Co gamma-rays was 2.7 for lymphocytes and 3.1 for chromatid aberrations in bone marrow cells. Lymphocytes were also chronically exposed to HTO for 6.7-80 h at dose rates of 0.5 cGy/min (138.5 MBq/ml) and 0.02 cGy/min (5.6 MBq/ml). There was a 71.5% decrease in the yield of dicentrics and centric rings at the dose rate of 0.02 cGy/min, indicating a clear dose rate effect of HTO. The RBE value for HTO relative to 137Cs gamma-rays was 2.0 at a dose rate of 0.02 cGy/min, suggesting that low HTO dose rates produce no increase of the RBE values and that the values may be constant between 2 and 3 within these dose rates. These results should prove useful in assessment of the health risk for humans exposed to low levels of HTO.
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BACKGROUND: Nijmegen breakage syndrome (NBS), also known as ataxia-telangiectasia (AT) variant, is an autosomal recessive disorder characterized by microcephaly, growth retardation, severe combined immunodeficiency and a high incidence of lymphoid carcinoma, the majority of which are B-cell lymphomas. To determine whether the NBS1 gene is a tumor suppressor gene in B-cell lymphoma, we screened B-cell malignant lymphoma (ML) for any evidence of NBS1 mutation. MATERIALS AND METHODS: Sequence analysis of the NBS1 gene was performed from PCR products amplified from the DNA of 12 extracranial ML or RT-PCR products amplified from cDNA of 8 primary central nervous system lymphoma. RESULTS: Direct sequence analysis revealed that no NBS1 mutations were present in any of these patients. CONCLUSION: The present results suggested that the contribution of NBS1 mutations to B-cell ML was minimal, despite the fact that the NBS1 gene was causative factor in these cases.
Seventeen patients with chronic liver disease underwent prolonged warm ischemia of hemi-lobe during liver resection. Those included 15 cirrhotic patients and two with chronic hepatitis. The hemi-hepatic ischemia was carried out with a liver clamp. The normothermic liver ischemia time of 40 to 70 minutes (53.8 +/- 10.4 minutes, mean +/- SD) were tolerated well with an acceptable postoperative course and no mortality. The liver with cirrhosis or chronic hepatitis can tolerate a hemi-hepatic ischemia of up to 70 minutes for patients with no high-risk factors.
This report describes a precise molecular analysis of a rare case of Philadelphia chromosome (Ph) positive acute myeloid leukemia (AML) (FAB classification M2). Phenotypic markers were positive for cells of the myeloid lineage, but negative for B cell and T cell lineage. The leukemic cells carried a Philadelphia chromosome. Major breakpoint cluster region (M-BCR) rearrangement was detected by the Southern blot analysis. Reverse transcriptase polymerase chain reaction analysis revealed the presence of b3a2 BCR/ABL mRNA transcripts. The patient achieved complete remission by conventional remission induction therapy for acute myeloid leukemia. M-BCR rearrangement could not be detected during complete remission. After hematological remission of an 8-month duration, the patient relapsed and died of respiratory distress due to pneumonia. Our case indicate Ph-positive AML with M-BCR rearrangement actually exists. Ph-positive AML carries either M-BCR rearrangement expressing the P210 BCR-ABL or minor breakpoint cluster region (m-BCR) rearrangement producing the P190 BCR-ABL. Therefore, additional other factor (s) apart from the Ph chromosome must be responsible for the acute malignant transformation.