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S Nishimura

Publications and source records attributed to S Nishimura.

At least 721 records · Page 40Linked to original sources
PubMed1986

Possible role of surface potential in the gating mechanism of Ca channels concerned with catecholamine secretion in the adrenal.

Cat adrenal gland was perfused retrogradely with modified Locke's medium and we investigated the effect of divalent cations on catecholamine release in response to KCl depolarization and to substitution of sucrose for NaCl in order to study the role of surface potential in the gating mechanism of Ca channels. The response to 20 mM KCl was largest at 10 mM Sr and it was less at 20 and 40 mM. Inhibition by the higher concentration of Sr was weakened by the addition of 10 mM Mg to the medium or by raising the concentration of KCl. The response to 30 mM KCl at 10 mM Sr was much larger than that at 10 mM Ca, and it was reduced by the addition of Ca. Stronger depolarization tended to reduce the difference between Ca and Sr in supporting secretion. The addition of 10 mM Sr increased the response to 30 mM KCl in the presence of 0.1 or 0.5 mM Ca, but tended to reduce the response in the presence of 2 or 10 mM Ca. Response to sucrose substitution was also reduced by increasing the concentration of Ca or Sr. Inhibition by Ca was counteracted by raising the concentration of K, Rb, or Cs so that the concentration of Ca producing the maximum response tended to be higher. Similarly, inhibition by Sr was partially reversed by raising the KCl concentration to 15 mM. These results are in accord with the idea that a high concentration of permeant divalent cations reduces the number of activated Ca channels by decreasing the surface potential, and also that Ca is more effective than Sr in decreasing the surface potential by binding to the surface negative charges. Increase of catecholamine secretion by a novel dihydropyridine BAY K 8644 was greater in the presence of Sr than with Ca.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Nucleotide sequence of cDNA and derived amino acid sequence of rabbit complement component C3 alpha-chain.

The nucleotide sequence coding for 726 amino acid residues of the alpha-chain of rabbit C3 was determined from a cDNA clone. Subfragments of the cDNA produced by restriction endonucleases were inserted into the bacteriophage M13 and sequenced using the dideoxynucleotide technique. The derived amino acid sequence was compared with those of human and mouse C3, which have been previously reported [by De Brujn, M.H.L. and Fey, G.H. (1985) Proc. Natl. Acad. sci. USA 82, 708, and Westel, R.A. et al. (1984) J. Biol. chem. 259, 13857, respectively]. There was 79% or 78% homology in amino acid sequence between rabbit and human or mouse C3, respectively. All of the cysteinyl residues were conserved among the three molecules, and the sequence around the thioester site was also highly conserved. Several regions having low homology were found: one of them was the small fragment released by factor I cleavage.

Amino Acid Sequence↗
PubMed1986

Mechanism of hematuria. I. Electron microscopic demonstration of the passage of a red blood cell through a glomerular capillary wall in rat masugi nephritis.

Masugi nephritis was induced in Sprague-Dawley rats by an intravenous injection of rabbit anti-rat kidney serum. In the autologous phase of the disease, three of 18 rats manifested continuous hematuria. Ultrastructural examination of renal glomeruli by transmission and scanning microscopy revealed gaps in the basement membranes, and the transcapillary passage of red blood cells through the discontinuous regions in the hematuric rats. Control animals revealed no gaps in the glomerular basement membranes regardless of the method used in their preparation for electron microscopy. These data support the hypothesis that hematuria is a result of the passage of red blood cells through gaps in the glomerular basement membrane in Masugi nephritis.

Animals↗
PubMed1986

Amplifications of both c-Ki-ras with a point mutation and c-myc in a primary pancreatic cancer and its metastatic tumors in lymph nodes.

Activated c-Ki-ras with a point mutation (GGT to CGT) at codon 12, resulting in the substitution of arginine for glycine, was found in DNA from metastatic pancreatic adenocarcinoma in a lymph node. By means of restriction endonuclease length polymorphism with SacI digestion, we were able to demonstrate that the same point mutation of c-Ki-ras was present in the primary tumor and in metastases in lymph nodes. DNA from the normal spleen of the patient did not have this type of point mutation. Moreover, amplifications of 3- to 6-fold of the activated c-Ki-ras and 50-fold of c-myc were found in the primary tumor and the metastases in the two lymph nodes, indicating that point mutation had occurred at a relatively early stage of the tumor development, before amplification of the gene. This is the first clear demonstration of amplification of activated c-Ki-ras accompanied by amplification of c-myc in both primary and metastatic human tumors in vivo.

Base Sequence↗
PubMed1986

[Study of chemotherapy in the field of internal medicine--clinical experience with SF-SP].

UNLABELLED: An SF-SP Tegafur spansule preparation was administered to 26 patients with advanced cancer (24 evaluable), and the clinical effectiveness and toxicity were studied. In most of cases, daily dosages of 800 mg were administered in two parts, in a few cases, daily dosages of 1,000 mg or 1,200 mg were given. Clinical effectiveness: The evaluation of effectiveness was based on the Koyama-Saito group criteria. Of the 24 evaluable cases, PR was observed in 3 cases of gastric cancer, one of colon cancer, and one of liver cancer, a total of 5 cases (20.8%). In these 5 cases the daily dosage was 800 mg, and the median duration of PR was 51 days. TOXICITY: TOXICITY was observed in 3 (11.5%) of the 26 cases.

Administration, Oral↗
PubMed1986

Teratocarcinoma derived from mouse zygotes after the introduction of activated human c-Ha-ras DNA.

We attempted to produce transgenic mice harboring the normal or activated human c-Ha-ras gene in order to examine the function of activated oncogenes in tumorigenesis. During the process of development, it happened that not only normal looking fetuses were obtained but also malformants, developmentally arrested conceptuses and tumors. Six such abnormally developed embryos were found to have been integrated with the activated human c-Ha-ras gene. One of the two tumors thus obtained was formed after the injection of 6.3 kb DNA fragment containing the gene for p21 with valine at the twelfth position. This tumor was integrated with two copies of the introduced DNA at a particular site in a chromosome and arranged in tandem in a head to tail direction. Histological analysis revealed that this tumor was constructed from at least three types of cells: two originating from different germ layers (one endoderm and the other mesoderm) and the third from an extra-embryonic ectoderm. The other tumor revealed similar features. Thus, it was strongly suggested that these tumors were derived from the very early developmental stage of the embryo, and had features very similar to those of teratocarcinoma.

Animals↗