Search PubMed⌕ Search

Biomedical subjects

K Arima

Publications and source records attributed to K Arima.

At least 289 records · Page 16Linked to original sources
PubMed1969

Antiviral and antitumor antibiotics. XIV. Effects of ascochlorin and other respiration inhibitors on multiplication of Newcastle disease virus in cultured cells.

Antiviral activity on Newcastle disease virus was examined with some respiration inhibitors including ascochlorin, rotenone, antimycin A(3), piericidin A, dicoumarol, 2, 4-dinitrophenol, pentachlorophenol, and fatty acids. Of the chemicals tested, ascochlorin and rotenone showed significant inhibitory effect on the viral growth in cultured cells as determined by the plate and tube assay methods. Dose response of ascochlorin and rotenone was observed in rate and final yield of hemagglutinin synthesis. Ratio of infectivity for hemagglutinin was nearly equal at any test concentrations of ascochlorin. Thus, the possibility of inhibition of virus maturation by the antibiotic was excluded. Ascochlorin had no activity on virus particles and on viral adsorption onto host cells.

Adsorption↗
PubMed1969

Antiviral and antitumor antibiotics. XX. Effects of rotenone, deguelin, and related compounds on animal and plant viruses.

Rotenoids and related compounds were investigated for their effects on animal and plant viruses. Of 35 compounds examined, rotenone, rotenone norketone, acetylrotenone, acetylrotenone norketone, deguelin, deguelic acid, dehydrodeguelin, and isotubanol norketone, all used at low concentrations, suppressed the growth of Newcastle disease and herpes simplex viruses as determined by the agar diffusion, plaque inhibition method. Most of the compounds likewise decreased the number of necrotic spots on tobacco mosaic virus-infected leaf discs. Only derrisic acid completely inhibited the local lesion formation at subphytotoxic concentrations. Correlation of antiviral activity with respiratory inhibition of these compounds is discussed.

Animals↗
PubMed1969

Induction by mercuric ion of extensive degradation of cellular ribonucleic acid in Escherichia coli.

Low concentrations of HgCl(2) were found to induce extensive degradation of ribonucleic acid (RNA) in exponentially growing Escherichia coli cells but not in stationary-phase cells. Whereas 80% of cellular RNA was degraded during 90 min of incubation with 10(-5)m HgCl(2) at 37 C, HgCl(2) caused only slight degradation in stationary cells, even when present at concentrations higher than 5 x 10(-5)m. Inhibition of RNA synthesis occurred at almost the same concentration of HgCl(2) as degradation, and the ability of stationary-phase cells to synthesize RNA was also resistant to HgCl(2). The transition of cells from complete sensitivity to HgCl(2) to a fully insensitive state took place simultaneously with the cessation of growth. p-Chloromercuribenzoate was also found to induce remarkable degradation of RNA. In E. coli Q13, a mutant deficient for ribonuclease I, no degradation of RNA was evident, even in the exponential growth phase. 3'-Mononucleotides but not 5'-mononucleotides were found among the degradation products of cellular RNA. 2',3'-Cyclic mononucleotides were produced when RNA was degraded by the cell-free extracts of the Hg treated cells. Almost complete unmasking of the latent ribonuclease occurred in the particle fraction containing subribosomal particles of the Hg-treated cells. These data suggest that the incubation of exponentially growing E. coli cells with HgCl(2) led to the unmasking of ribonuclease I, which resulted in the extensive degradation of cellular RNA. The activation of ribonuclease by HgCl(2) in the isolated particulate fraction of E. coli K-12 which occurred in vitro suggested the presence of an Hg-sensitive inhibitor for ribonuclease I.

Bacterial Proteins↗