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Biomedical subjects

M Sekiguchi

Publications and source records attributed to M Sekiguchi.

At least 559 records · Page 31Linked to original sources
PubMed1984

[Combined therapy with microwave hyperthermia and adriamycin in MM2-bearing mice].

C3H/He mice were inoculated i.p. with synergic MM2 tumor cells(2 X 10(6) cells/mouse), and subsequently treated either by systemic hyperthermia induced by microwave irradiation (2450 MHz)alone, administration of ADM alone, or a combination of both. The mice were exposed to hyperthermia for 5 minutes everyday at an output of 10, 20 or 30 watts. ADM was administered i.p. for 3 days at dose levels of 0.025 mg/kg, 0.05 mg/kg or 0.075 mg/kg body weight. The mean survival time and the mean relative body weight were recorded. From these data, tumor-suppressing effects of the treatments were analysed by one-way or two-way variance analysis. Mice treated with 30-watt microwave irradiation survived significantly longer than control mice without treatment (P less than 0.05), as did mice treated with ADM alone (P less than 0.01). The mean relative body weight was similar among the microwave, ADM and control groups. When the mice were given microwave treatment combined with ADM, significant difference was observed in the mean survival time by one-way variance analysis (P less than 0.01), but no significant difference was observed by two-way variance analysis. The best condition of mice and the optimal dose of ADM still remain to be determined to facilitate more efficient tumor-suppression using this combination therapy.

Animals↗
PubMed1983

A dominant (mutD5) and a recessive (dnaQ49) mutator of Escherichia coli.

The two known strong mutators of Escherichia coli K12, mutD5 (Degnen & Cox, 1974) and dnaQ49 (Horiuchi et al., 1978), are located at almost the same position, at five minutes on the linkage map. To clarify the genetical and functional relationships between these two mutators, we have constructed hybrid plasmids and phages carrying dnaQ+ or mutD5 by using in vivo and in vitro recombination techniques and examined their effect on the phenotype of wild-type or mutant bacteria. The results indicated that the mutD5 mutator is dominant over the wild-type allele whereas dnaQ49 is recessive. Thus, mutD5 plasmid or mutD5 transducing lambda phage can be used to convert a wild-type strain to a highly mutable strain. Both dnaQ+ and mutD5 plasmids carried a 1.5 X 10(3) base DNA fragment derived from the E. coli chromosome and they were indistinguishable from each other by restriction enzyme analysis. Moreover, specific labeling of the plasmid-encoded proteins by the maxicell method revealed that the mutD5 plasmid codes for two proteins, one whose molecular weight is 25,000 and the other whose molecular weight is 21,000, which correspond to the dnaQ protein and RNase H, respectively. Insertion of the gamma delta sequence into the mutD gene of the plasmid resulted in disappearance of the 25,000 Mr protein. These results suggested that the dnaQ49 and mutD5 mutator are mutations that have arisen in a single gene, though they differ in many respects.

Bacteriophage lambda↗
PubMed1983

Transformation of temperature-sensitive growth mutant of BHK21 cell line to wild-type phenotype with hamster and mouse DNA.

A temperature-sensitive (ts) mutant, tsBN2, which was derived from BHK21 and is defective in the regulatory mechanism for chromosome condensation, was transformed to the temperature-resistant (ts+) phenotype by means of DNA-mediated gene transfer with hamster and mouse DNA. Treatment of mouse DNA with the restriction enzymes EcoRI, HindIII, PstI and SalI, but not with XhoI, almost completely abolished the transforming activity. A fluctuation test, originally devised by Luria and Delbrück, was used to estimate the reversion and transformation frequencies of tsBN2 cultures.

Animals↗
PubMed1983

Faulty development of cortical neurons in the Snell dwarf cerebrum.

In the Snell dwarf motor cortex, area 6 of Caviness, the cell number, the stratification of neurons and the portion of layer-widths were absolutely identical to those of the controls. By means of the Golgi-Cox method modified by Ramon-Moliner, however, the pyramidal neuron was found to have small perikarya, short primary dendrites with sparse branchings, and a low spine density on the dendrites. The corpus callosum of the dwarf contained a reduced number of fibers compared to that of the controls, and the staining for myelin basic protein revealed a considerable reduction of positive-fibers of radiation in this area. The content of Thy-1 antigen in the cerebrum, cerebellum and brainstem, was significantly lower than that of controls, but the monoamine content was normal in the cerebrum and brainstem. From these results, it appears that the Snell dwarf cerebrum shows retarded neuronal growth; a reduction in size of neurons, an underdevelopment of axons and dendrites, and a retarded maturation of spine, in addition to arrested glial proliferation. At present, it is unclear which hormone deficient in these mutants, growth hormone or thyroxine, is the essential potentiator for neuronal growth.

Animals↗
PubMed1983

Recovery of a hybrid vector, derived from bovine papilloma virus DNA, pBR322 and the HSV tk gene, by bacterial transformation with extrachromosomal DNA from transfected rodent cells.

A bovine papilloma virus (BPV)-pBR322-derived recombinant plasmid carrying a 2-kb fragment of Herpes simplex virus DNA containing the thymidine kinase (tk) gene is capable of transforming tk- cells of mouse L and Syrian hamster BHK21 lines to tk+. In transformed cells a small proportion of the plasmid DNA is present as extrachromosomal elements while the remainder appears to be integrated into the genome. It was possible to recover plasmids indistinguishable from the input DNA by transformation of Escherichia coli bacteria with low-molecular-weight DNA isolated from the transformed mouse and hamster cells and consisting of BPV-pBR322-HSV tk+ plasmids.

Animals↗
PubMed1983

Structure and expression of the dnaQ mutator and the RNase H genes of Escherichia coli: overlap of the promoter regions.

A 1.6-kilobase-pair DNA fragment derived from the Escherichia coli chromosome was analyzed by Tn3 transposon insertion and deletion mapping to locate a mutator gene, dnaQ (mutD), and the rnh gene that codes for RNase H. When a strong promoter, PL of lambda phage, was placed at the right- and left-side of the cloned DNA fragment, the dnaQ protein and RNase H, respectively were overproduced. These results suggested that the two genes are transcribed in opposite directions and that their promoters are located in a narrow region between the genes. Nucleotide sequence analysis confirmed this and further revealed that transcriptional and translational initiation signals for the two genes overlap. From the sequence data it was deduced that the dnaQ protein and RNase H consist of 243 and 155 triplets and have molecular weights of 27,500 and 17,500, respectively. dnaQ81 amber mutant showed two codon alterations, CAG(glutamine-195) leads to TAG(amber) and ACA(threonine-193) leads to ATA(isoleucine). The dnaQ-lacZ and the rnh-lacZ fused genes were constructed and hybrid proteins with beta-galactosidase activity were produced. From beta-galactosidase levels it was estimated that the promoter for dnaQ is 5 times more active than that for rnh.

Amino Acid Sequence↗
PubMed1983

Identification and cloning of the gene coding for lysophospholipase L2 of E. coli K-12.

E. coli bearing hybrid plasmid pKOl (Oeda et al. (1981) Mol. Gen. Genet. 184, 191-199) expressed a large amount of lysophospholipase L2 activity. When a mutant which was defective in lysophospholipase L2 activity was transformed with plasmid pKOl, it overproduced lysophospholipase L2 activity. The gene responsible for the lysophospholipase L2 activity was designated as pld B. On the same hybrid plasmid another gene (pld A) coding for detergent-resistant phospholipase A (DR-phospholipase A) was also identified. These facts together with the results of a Pl transduction experiment revealed that the pld B gene must be between the pld A and met E genes on the E. coli chromosome.

Cloning, Molecular↗