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N Kanda

Publications and source records attributed to N Kanda.

At least 109 records · Page 6Linked to original sources
PubMed1985

Molecular and cytologic analysis of DNA amplification in retinoblastoma.

Amplification of two distinct genomic DNA segments is observed in homogeneously staining regions in two sets of retinoblastoma cell lines derived from two different patients. One DNA segment was known to have sequence homology to the c-myc oncogene, and both DNA segments had previously been shown to be amplified in neuroblastoma cells. The absolute degree of amplification differed in all cytogenetically distinct retinoblastoma cell lines tested. Also, the relative amplification of these two DNA segments was unequal within a given cell line. Minimal amplification of both DNA segments was also detected in DNA directly isolated from one primary retinoblastoma. Based on these and previous results, it is concluded that assembly of amplifiable, relocatable units in many human retinoblastoma and neuroblastoma cells may involve a complex process of differential recruitment of separate DNA segments that are located on human chromosome #2.

Cell Line↗
PubMed1984

A simple and convenient synthesis of 3'-5'- or 2'-5'-linked oligoribonucleotide by polymerization of unprotected ribonucleoside using phosphorus tris-azole.

Oligoribonucleotides have been synthesized directly from unprotected ribonucleosides by a chemical polymerization approach using phosphorus tris-azoles. The procedure involves two steps: (i) the reaction of unprotected ribonucleoside with phosphorus tris-azole and (ii) the in situ oxidation of the resulting phosphite with iodine and water. Several phosphorus tris-azoles were investigated for generating oligoribonucleotide chains. Phosphorus tris-azoles of which azoles are imidazole, 2-methylimidazole, and 2-ethyl-4-methylimidazole were found to be most effective. Uridine, adenosine, and cytidine oligonucleotides were obtained rapidly in high yields without any protection. The inter-ribonucleotidic linkage of the oligomers consists of 3'-5'- and 2'-5'-linkages. The linkage isomers were easily separated by a reverse phase column chromatography. The present approach provides a convenient and potentially useful method for preparing 3'-5'- or 2'-5'-linked oligoribonucleotides.

Animals↗
PubMed1984

Progressive foot swelling in BUF rats. A new animal model for screening of anti-inflammatory and anti-rheumatic drugs.

Buffalo rats of a low adjuvant-arthritis responder strain demonstrate a continually increasing swelling in the hind foot inoculated with mycobacterial adjuvant, characterized by extensive panostitis, new bone formation and long-delayed bony calcification. A rapid regression of foot swelling was produced by a three-day course of therapy with indomethacin (1 mg/kg) or with dexamethasone (0.1 mg/kg), but a definite rebound was followed soon after termination of the therapy. This recurrent episode occurred repeatedly in the second and third therapeutic trials with the anti-inflammatory drugs in the same animals. The 5 days treatment with either levamisole (5 mg/kg) or cyclophosphamide (5 mg/kg) prevented further increase in the swelling for a long time period after withdrawal of the drug, and enhanced bone mineralization.

Animals↗
PubMed1983

In vivo sister chromatid exchange analysis of a mouse plasmacytoma cell line NP-38.

In vivo sister chromatid exchange (SCE) frequencies have been compared between the mouse plasmacytoma NP-38 and normal bone marrow cells of the host BALB/c mouse. NP-38 cells, transplanted subcutaneously showed a two-fold increase in SCEs (4.35-5.76/cell) compared with the bone marrow cells of the host (1.65-2.14/cell). Such an increase in SCE rates was also observed in NP-38 cells metastasized in spleen, bone marrow, liver, or mesentery, upon inoculation of NP-38 cells by intravenous injection. Even in such tumor-bearing mice, the SCE rates of the bone marrow cells were equivalent to the SCE level found in uninfected mice. These results indicate that the high SCE incidence in NP-38 cells is an inherent characteristic of this tumor cell line.

Animals↗
PubMed1983

Transposition and amplification of oncogene-related sequences in human neuroblastomas.

We have cloned a 2.0-kb EcoRI fragment of human genomic DNA (NB-19-21) which has homology to the v-myc oncogene but is distinct from the classical c-myc gene. This sequence is amplified from 25- to 700-fold in eight of nine tested human neuroblastoma cell lines which contain either homogeneously staining regions or double minutes (HSRs or DMs), the caryological manifestations of amplified genes. In the remaining line, the c-myc proto-oncogene is amplified approximately 30-fold. NB-19-21 hybridizes to a 3.2-kb cytoplasmic, poly(A)+ RNA species that is abundant only in lines in which the sequence is amplified. We propose that the gene encoding the NB-19-21-related RNA species may represent a new oncogene, which we call N-myc. NB-19-21 derives from chromosome 2; but in the five HSR-containing lines that have amplified this sequence, none has HSRs on chromosome 2. NB-19-21 is associated with DMs in a DM-containing line. A second, randomly cloned, amplified DNA segment from the HSR of one of the neuroblastoma lines is amplified in a subset of the lines in which NB-19-21 is amplified. In addition, this probe identifies a novel joint in the amplification unit of one line relative to that of the others. We suggest that, in the eight lines which have amplified NB-19-21, the amplification units are overlapping, but not identical, and that transposition of the common sequences may occur prior to amplification.

Base Sequence↗
PubMed1983

Isolation of amplified DNA sequences from IMR-32 human neuroblastoma cells: facilitation by fluorescence-activated flow sorting of metaphase chromosomes.

Human neuroblastoma IMR-32 cells have large homogeneously staining regions (HSRs), primarily in the short arms of chromosome 1. We have constructed a recombinant phage library that is enriched for DNA present in the HSR of this chromosome by using fluorescence-activated flow sorting for initial chromosome purification. Eleven distinct cloned DNA segments were identified that showed significantly greater hybridization to IMR-32 genomic DNA, detected by Southern blotting, than to normal human genomic DNA. These sequences have also been localized to the HSR of chromosome 1 by in situ hybridization. Based on an approximate 50-fold sequence amplification for each cloned segment and a total HSR size of 150,000 kilobases, the amplified unit in the HSR is estimated to be 3,000 kilobases. Sequences homologous to all cloned HSR DNA segments were mapped to human chromosome 2 by using human-mouse hybrid cells. Further work using in situ hybridization demonstrated that cloned HSR segments were localized in the short arm of chromosome 2 in both normal and IMR-32 cells. Thus, the amplification of these sequences in IMR-32 cells may have involved transposition from chromosome 2 to chromosome I.

Base Composition↗
PubMed1981

Selective differential staining of sister chromatids of the facultative heterochromatic X chromosome in the female mouse.

Selective differential staining of sister chromatids for the facultative heterochromatic X chromosome in the female mouse has been achieved by the combination of two differential staining techniques; one for the heterochromatic X chromosome and the other for sister chromatids. Thermal hypotonic treatment moderately destroyed the chromosome structure except for the heterochromatic X in BrdU labelled metaphase cells, resulting in the selective sister chromatid differentiation of this X with Giemsa stain. This technique enables us to know the exact frequency of th spontaneous sister chromatid exchanges in the heterochromatic X without using 3H-TdR labelling for detecting the late DNA replication. The results indicate that the sister chromatid exchange frequency of the heterochromatic X chromosome is not affected by its late DNA replication during S phase, or by the genetic inactivation and the resulting heterochromatinization.

Animals↗
PubMed1981

Lipid peroxide formation and membrane damage in endotoxin-poisoned mice.

Lipid peroxide formation and plasma membrane damage in mouse liver following the administration of Salmonella endotoxin were examined. The liver lipoperoxide level was markedly elevated in animals given endotoxin compared with that in the controls, and returned to its normal range after 2 days. On the other hand, superoxide dismutase activity was decreased by 18--48 hr after endotoxin injection, thereafter tending to increase. Glutathione reductase and glutathione peroxidase activities declined in the liver 18 hr after the injection. The endotoxin resulted in much lower lipoperoxide formation in the livers of tolerant mice than in those of the poisoned mice. The lipoperoxide level in endotoxin-poisoned mice after the administration of alpha-tocopherol was lower than that in the controls, and alpha-tocopherol administration prevented completely the membrane protein damage that arose from endotoxin challenge. After glutathione administration the membranes of the poisoned mice also returned to almost the normal disk electrophoretic profile. These results suggest that lipid peroxide formation in the liver plasma membrane caused by free radicals might occur in a tissue ischemic state in endotoxicosis.

Adenosine Triphosphate↗
PubMed1981

Effect of alpha-Tocopherol on endotoxicosis.

The effect of alpha-tocopherol in endotoxicosis was studied. The alpha-tocopherol level significantly decreased in mouse liver 18 hr after endotoxin administration, thereafter tending to increase to approach the normal range. In endotoxin-tolerant mouse liver, the lipid peroxide level was reduced to less than half of that in nontolerant animals following endotoxin challenge. The liver lipid peroxide level and serum lactate dehydrogenase or acid phosphatase leakage were studied in mice fed a vitamin E-deficient (ED) diet and a vitamin E-supplemented (ES) diet for 40 days. ED mouse liver exhibited a higher formation of lipid peroxide after endotoxin was given while there was a markedly lower level in ES mouse liver. There was significantly more serum lactate dehydrogenase or acid phosphatase leakage in ED mice than in ES mice after endotoxin administration. There was about a 25% decrease in liver superoxide dismutase (SOD) activity in endotoxin-poisoned mice fed both the normal and the ED diets, while the activity was at a higher level in ES-fed mice. These results suggest that alpha-tocopherol may be helpful in preventing membrane instability in endotoxin poisoning.

Acid Phosphatase↗
PubMed1980

Analysis of crossing over in mouse meiotic cells by BrdU labelling technique.

Differential staining of sister chromatids in male mouse meiotic cells was achieved by continuous infusion with BrdU from the tail vein followed by Giemsa staining (the FPG technique of Perry and Wolff, 1974). Analysis of 341 bivalents including XY, and 21 univalents reveals that: (1) visible crossing over coincided exactly with the site of chiasmata; (2) no evidence was obtained in support of chiasma terminalisation; (3) an anomalous type of crossing over was found in the monochiasmatic bivalents, which could not be explained by the conventional hypothesis for crossing over; (4) some of the terminally associated bivalents might be achiasmatic, and univalents might have originated from such bivalents; (5) in XY bivalents, sister chromatid association was between lightly and darkly stained chromatids, suggesting a lack of crossing over and the existence of other genetic controls for this association; (6) during meiosis sister chromatid exchanges (SCEs) might be less frequent than crossovers.

Animals↗
PubMed1979

In vivo sister chromatid exchange in cells of various organs of the mouse.

In vivo sister chromatid exchange (SCE) in mouse cells derived from various organs was studied by infusing BrdU from the tail vein. It was found that at BrdU concentrations ranging from 2.2-13.5 micrograms/g/h, the SCE frequency in bone marrow cells seemed to stay at a constant level (1.5-2/cell/two cell cycles) whereas it started to rise as the BrdU dose exceeded this dose range. When BrdU within this dose range was infused continuously from the tail vein for appropriate hours to label chromosomes in various organs, the average SCE frequencies per cell were found to be 1.64 in bone marrow cells, 1.82 in spermatogonia, 1.99 in splenic cells, 2.89 in intestinal cells and 3.69 in cells from adjuvant stimulated lymph nodes. It is suggested that the spontaneous level of the in vivo SCE frequency might be about 1.5-2/cell/two cell cycles in the mouse. In cells derived from intestine and adjuvant stimulated lymph node, some unknown factors might work as a inducer of SCEs resulting in a significant increase in the SCE frequency in these organs.

Animals↗
PubMed1979

Identification of the facultative heterochromatic X chromosome in females of 25 rodent species.

Treatment of the chromosomes of 25 rodent species with a 50 degrees C hypotonic solution and Giemsa staining permitted identification of the heterochromatic X chromosome in 24 species. With this technique, the facultative of the heterochromatic X chromosome or the facultative portion of large, composite-type X chromosoms is stained darker than the other chromosomes, allowing it to be distinguished from the homologous euchromatic X chromosome in female metaphase cells. Intense staining of the single X chromosome was not observed in male metaphase cells. It is suggested that this differential staining of one of the two X chromosomes might be due to qualitative differences in chromosomal proteins rather than to differences in the degree of chromosomal condensation or in DNA base sequence.

Animals↗