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Biomedical subjects

N Ueda

Publications and source records attributed to N Ueda.

At least 487 records · Page 27Linked to original sources
PubMed1981

Hormone dependency of chromosome aberrations induced by 7,12-dimethylbenz[a]anthracene in rat bone marrow cells: site-specific increase by erythropoietin.

The frequency of chromosome aberrations (CA) 6 hours after iv injection of 50 mg 7,12-dimethylbenz[a]anthracene (DMBA)/kg was studied in bone marrow cells of the noninbred Long-Evans rat under various hematopoietic conditions. The percentage of metaphase cells with CA was enhanced by anemia and suppressed by polycythemia. The low incidence of CA in polycythemic rats was reversed by 6 U of sheep erythropoietin (EP) injected at the time of DMBA treatment. The interchromosomal and intrachromosomal distribution of CA indicated that hematopoietic stimuli, more specifically EP, greatly enhanced DMBA-induced CA in specific chromosomal regions.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

Chemical carcinogenesis in the rat: common mode of action of carcinogens at the chromosome level.

The chromosomal distribution of chromosome aberrations (CA) and sister chromatid exchanges (SCE) induced by various chemical carcinogens such as 7,12-dimethylbenz[a]anthracene, 7,8,12-trimethylbenz[a]anthracene, 1-butyl-1-nitrosourea, urethan, 4-nitroquinoline 1-oxide, 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide, and the antineoplastic compound mitomycin C was studied with the use of noninbred Long-Evans male rat bone marrow cells in vivo and in vitro. The CA and SCE induced by these structurally different chemicals were distributed in a similar pattern among and along chromosomes when the chemicals were given a short time (6 hr) before the metaphase cells were harvested. The specific distribution pattern of chemically induced CA and SCE along chromosomes was attributed to the late DNA replication of the vulnerable chromosome regions. Conversely, X-ray-induced CA were distributed more randomly. Thus the different chemical carcinogens were shown to exert a similar genetic effect at the chromosome level.

Animals↗
PubMed1981

[Evaluation of pancreatic scintigram in the diagnosis of pancreatic diseases (author's transl)].

The classification of accumulative patterns with the pancreatic scintigram findings of chronic pancreatitis and carcinoma of the pancreas were compared with endoscopic retrograde pancreatography (ERP) findings and Pancreozymin-Secretin test (P-S test). I) The frequency of pancreatic cancer was 93%, whilst, the chronic pancreatitis was 88% in the abnormal pancreatic scintigram. II) In the scintigram the type II (localized defect shadows) of pancreatic cancer was comparatively high and it is proportional to evidence derived from ERP. Localized diagnostic certainty is helpful, although the two tests are related. The P-S test is only restricted to the carcinoma of head, whilst, scintigram is more useful to detect the carcinoma of the body and tail of the pancreas. II) As for the chronic pancreatitis, there are various accumulative patterns. This is resemblance to that of ERP findings, but in the P-S normal test, it showed discrepancy in part of the result. Particularly, in the type I (slightly generalized low uptake with density silhouette) and type II. Therefore in order to obtain an accurate diagnosis, it is essential to have both the P-S test and scintigram.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1980

Nevoid basal cell epithelioma syndrome in Japan.

A 49-year-old Japanese man with typical features of nevoid basal cell epithelioma syndrome is reported. The patient had cystic lesions of the jaw bone, multiple basal cell epitheliomas of the scalp and face, pits on the palms and soles, bifid ribs, scoliosis and calcification of the falx cerebri. In Japan five certain cases have been reported previously. We added one new case and reviewed the other five cases briefly.

Basal Cell Nevus Syndrome↗
PubMed1980

Establishment and chromosome studies of in vitro lines of chemically induced rat erythroblastic leukemia cells.

Eight cultured lines with a normal diploid karyotype, no. 2 trisomy, and markers involving chromosome No. 2 were established from three 7,12-dimethylbenz[a]anthracene (DMBA)- and two N-butyl-N-nitrosourea (BNU)-induced erythroblastic leukemias in noninbred Long-Evans rats. Serial in vivo and in vitro passage of these cells frequently evoked karyotype changes in stemline cells. In both lines from DMBA- and BNU-induced leukemias, ordinary and translocation no. 2 trisomy cells appeared and gradually replaced the normal diploid stemline cells. Obvious secondary karyotypic changes were also recognized in the "cloned" leukemia cells. Nucleolar chromosomes such as chromosomes no. 3 and no. 12 were frequently involved in aneuploidy and translocation. One cell line from a BNU-induced leukemia did not change its normal diploid karyotype during 12 months of in vitro passage. The above preferential growth of cells with no. 2 trisomy and the related changes during in vivo and in vitro passage as well as in-colony formation in soft agar suggest that these chromosome changes are somehow associated with the growth behavior of the leukemia cells. No positive correlation was demonstrated between karyotype and dimethyl sulfoxide-induced erythroid differentiation of the leukemia cells.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

Hypouricemia due to an isolated defect in renal tubular urate reabsorption.

During investigation of chronic glomerulonephritis, a 24-year-old man was found to have a low serum urate concentration (0.6-1.3 mg/100 ml). Daily urinary excretion of urate and oxypurines was normal. His urate clearance was markedly increased (43.3-98.0 ml/min), and was substantially unchanged after both the administration of pyrazinamide, an inhibitor of the renal tubular secretion of uric acid, and the administration of probenecid, an inhibitor of the renal tubular reabsorption of uric acid. No other renal tubular abnormalities were detected. It was concluded that the patient had an isolated defect in the renal tubular reabsorption of uric acid. The patient's brother was also found to have hypouricemia due to renal uricosuria, suggesting a genetic origin of the defect.

Adult↗
PubMed1979

Macroglobulinemia Waldenström complicated by autoimmune hemolytic anemia, meningeal sign and femoral lysis.

A necropsied case of macroglobulinemia Waldenström with unusual complications was presented; the patient was found to have autoimmune hemolytic anemia, first. During the course of its treatment, he developed monoclonal immunoglobulin M in serum together with lytic osseous lesion in both femurs, and died of meningeal involvement by tumor cells. Clinically, he had hepatosplenomegaly and generalized lymphadenopathy. The macroglobulin was kappa type of light chain, ultracentrifugation showed sharp spike of 21S in 18.6%, and myelogram revealed increased lymphocytoid series of 29.6%. It was proved that autoantibody causing autoimmune hemolytic anemia was composed of IgG and macroglobulin itself had no activity as an anti-red cell antibody. An emphasis was made that autoimmune hemolytic anemia followed by macroglobulinemia is based on the state of immunodeficiency of this patient.

Anemia, Hemolytic, Autoimmune↗