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Y Ono

Publications and source records attributed to Y Ono.

At least 1,045 records · Page 58Linked to original sources

[Myelography].

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Contrast Media↗

[Clinical study on the angiotensin I-converting enzyme in human urine. (I) Partial purification, enzymic characteristics and excretion in normal subjects].

The angiotensin I-converting enzyme in normal human urine was partially purified with ammonium surfate (3.2M), DEAE-Cellulose ion exchange chromatography (0-0.5M NaCl gradient), and Sephadex G 200 gel filtration. The enzyme was separated into three forms which had different molecular weights of 700000, 290000 and 40000, respectively. The enzymic biochemical characteristics of these three enzymes, however, were identical with regard to their inhibitory effects (bradykinin potentiator c, arg-pro-pro, o-phenanthroline and EDTA), Cl- dependency, optimal pH (8.3) and temperature (37 degrees C), and Km value (2.3mM). The enzymic activity was determined in five normal subjects in three conditions of dietary sodium intake (51, 153 and 340mEq for 5 days, respectively). The enzymic activity correlated well with the concentration of the excreted sodium (r = 0.87, p less than 0.001). There was no significant relation between the enzymic excretion and the concentration of the excreted potassium, nor between the activity and the creatinine excretion. It is suggested that the origin of urinary angiotensin I-converting enzyme is the kidney, and that the enzyme might regulate sodium excretion in cooperation with renal kallikrein-kinin system.

Adult↗

Neurotoxicity of petroleum benzine compared with n-hexane.

Petroleum benzine is one of the mixtures of organic solvents containing n-hexane. The occurrence of polyneuropathy in the workers using petroleum benzines is attributed mainly to n-hexane, though other hydrocarbons present are also suspected of having some neurotoxicity or some potential which could modify the neurotoxicity of n-hexane. The present experiment was performed in order to clarify the toxicity of petroleum benzine to the peripheral nerve and compare it with that of n-hexane. Forty rats were randomly divided into five groups. The groups were exposed to 200 ppm n-hexane, 500 ppm n-hexane, and petroleum benzine vapor containing 200 ppm n-hexane or 500 ppm n-hexane, together with aliphatic and aromatic hydrocarbons for 12 h a day for 24 weeks. The body weight, motor nerve conduction velocity, motor distal latency, and mixed nerve conduction velocities were measured before exposure and every 4 weeks of exposure. A rat from each exposed group was histopathologically examined after 24 weeks' exposure. The function of the peripheral nerve was conspicuously impaired by 500 ppm n-hexane, slightly impaired by 200 ppm n-hexane and petroleum benzine containing 500 ppm n-hexane, and even less impaired by petroleum benzine containing 200 ppm n-hexane. Degenerations of the myelin sheaths and axons were demonstrated in all exposed groups upon examination of the revealed tail nerves. Thus, the experiment revealed that petroleum benzine could impair the peripheral nerves, while some components of petroleum benzine were considered to inhibit the neurotoxicity of n-hexane.

Alkanes↗

Frequencies of specific antibody-producing cells for sheep red blood cells and for phosphorylcholine in human tonsillar B lymphocytes transformed by Epstein-Barr virus.

The frequencies of transformed B cells and of transformed specific antibody-producing cells in human tonsillar lymphocytes infected with Epstein-Barr virus (EBV) were determined by limiting dilution analyses. The latter was corrected by the former and the frequencies of specific antibody-producing cells in EBV-transformed B cell populations were obtained. The frequencies of specific B cells for sheep red blood cells were calculated to be one in 500 to 2,000 EBV-transformed tonsillar B cells obtained from four donors, while those of specific B cells for a hapten, phosphorylcholine, were one in 700 to 5,000. The method may be useful to define the repertoire of specificities in the human B cell populations.

Antibody Formation↗

Antitumor and cytocidal activities of a newly isolated benzenoid ansamycin, macbecin I.

Macbecin I showed marked antitumor activity against intraperitoneally (ip) inoculated leukemia P388, melanoma B16, and Ehrlich carcinoma in mice on ip administration. The maximum effect measured in terms of ILS% (increase of life span) was 97 at a daily dose level of 10 mg/kg for leukemia P388, 103 at 5 mg/kg for melanoma B16, and 206 at 10 mg/kg for Ehrlich carcinoma. The effect of macbecin I on leukemia L1210 was slight (39 ILS%) and no activity was observed against leukemia L5178Y or P388/P-3 (a line of P388 resistant to ansamitocin P-3), or MOPC-104E myloma. Three to six hours after administration of 0.5 mg/kg or more of macbecin I to mice bearing ascites leukemia P388 cells, typical karyorrhexis followed by cytolysis in P388 cells was observed. Cytocidal changes induced by macbecin I were also observed in cells which were temporarily prevented from entering mitosis by treatment with known antitumor agents such as 5-fluorouracil, cyclophosphamide, and neocarzinostatin, whereas such cytolysis was not observed in cells which were arrested in metaphase by treatment with ansamitocin P-3. Cytotoxicity of macbecin I to cultured KB cells was observed at doses of 10(-1) micrograms/ml and more. Reverse transcriptase and terminal deoxynucleotidyl transferase activities were not inhibited by macbecin I.

Animals↗