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1.
Biosci Biotechnol Biochem ; 60(2): 325-7, 1996 Jan.
Article in English | MEDLINE | ID: mdl-27299405

ABSTRACT

A bioflocculant from a fungus, Aspergillus sp. JS-42, was purified by precipitations with acetone and cetylpyridinium chloride. The flocculating activity was not significantly affected by pH from 3 to 8, but was stimulated by the addition of CaCl2, and was effective only when the reaction mixture contained an adequate amount of flocculant. The flocculant could efficiently flocculate all tested solids suspended in aqueous solution, including various microorganisms, organic acids, and inorganic materials.

2.
J Biol Chem ; 264(28): 16351-4, 1989 Oct 05.
Article in English | MEDLINE | ID: mdl-2550437

ABSTRACT

Medium of untreated human FS-4 foreskin fibroblasts contained a factor which, upon the addition of exogenous tumor necrosis factor (TNF), inhibited encephalomyocarditis virus replication when neither medium alone nor TNF alone were effective. This antiviral activity was abolished by a monoclonal antibody to human interferon (IFN)-beta, suggesting that the active component in the medium from untreated FS-4 cells was IFN-beta, present at subeffective concentrations. In addition, we show that untreated FS-4 cells contain IFN-beta mRNA, demonstrable by the highly sensitive polymerase chain reaction after reverse transcription. Treatment of FS-4 cells with TNF produced an approximately 16-fold increase in the steady-state level of IFN-beta mRNA. Our results support the conclusion that autocrine IFN-beta is secreted by untreated normal fibroblasts and that TNF can enhance the production of autocrine IFN-beta by increasing the level of IFN-beta mRNA. Our study also demonstrates that subeffective concentrations of autocrine IFN-beta, which escape detection in conventional assays, are sufficient to produce a strong synergistic action with TNF.


Subject(s)
Interferon Type I/genetics , Interferon Type I/pharmacology , RNA, Messenger/genetics , Tumor Necrosis Factor-alpha/pharmacology , Antibodies, Monoclonal , Cell Line , Encephalomyocarditis virus/drug effects , Encephalomyocarditis virus/physiology , Fibroblasts/drug effects , Fibroblasts/immunology , Gene Amplification , Genes/drug effects , Humans , Interferon Type I/immunology , Male , RNA, Messenger/drug effects , Recombinant Proteins/pharmacology , Skin/immunology , Transcription, Genetic/drug effects , Virus Replication/drug effects
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