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S Yui

Publications and source records attributed to S Yui.

52 records · Page 3Linked to original sources

Induction of macrophage growth by lipoprotein.

Cell-free tumorous ascitic fluid stimulated growth of variously induced mouse peritoneal macrophages and resident macrophages in vitro. This induction of macrophage growth by the tumorous ascitic fluid was confirmed by autoradiography. The macrophage growth-stimulating activity was stable on heating at 100 degrees C, in contrast to that of macrophage growth factor (colony stimulating factor) previously reported. This heat-stable macrophage growth-stimulating activity was recovered in the lipoprotein fraction of tumorous ascitic fluid. The lipoprotein from heat-treated normal mouse serum also induced growth of macrophages. These results indicate that lipoprotein can induce macrophage proliferation, at least in vitro.

Animals↗

A new reaction useful for chemical cross-linking between nucleic acids and proteins.

Cytosine in nucleic acids can be converted into N4-aminocytosine by treatment with a mixture of hydrazine and bisulfite. The hydrazino group thus formed at position 4 of the pyrimidine ring can be linked to a sulhydryl group in proteins by the use of bromopyruvate as a linker. Successful use of this scheme of chemical cross-linking between nucleic acid and protein was demonstrated in the linking of poly(C) with glutathione, and of RNA with protein in the E. coli 30 S ribosomal subunit.

Cross-Linking Reagents↗

Induction of macrophage growth by heat-stable factor in tumorous ascitic fluid.

Peritoneal macrophages from mice synthesized DNA and proliferated in vitro in the presence of cell-free tumorous ascites. The growth stimulating activity of ascitic fluid was stable on heat treatment (100 degrees C, 30 min). In contrast, the macrophage growth stimulating activity of L cell-conditioned medium was inactivated by heat treatment. The growth factor(s) in heat-treated ascitic fluid was stable at pH 2 and 10, and on treatment with 2-mercaptoethanol or urea. Treatments, with enzymes such as trypsin, pronase, phospholipase and neuraminidase, and with sodium periodate oxidation partially inactivated the macrophage growth stimulating activity of the heat-stable factor(s). The adherent cultured cells that proliferated in heat-treated ascitic fluid were macrophages, as indicated by their nonspecific esterase staining, pinocytosis and phagocytosis. These macrophages showed cytolytic activity against a murine tumor in the presence of wheat germ agglutinin, but not antitumor antibody. These results indicate that tumorous ascitis fluid contains a heat-stable macrophage growth factor(s) distinct from the colony stimulating factor and that the proliferated macrophages killed tumor cells in cooperation with a lectin.

Animals↗

Antitumor activity of macrophages grown in tumorous ascitic fluid.

Peritoneal macrophages from mice injected with glycogen proliferated in vitro in the presence of cell-free tumorous ascites. DNA synthesis of macrophages was also induced by ascitic fluid, but did not occur in the absence of the fluid. However, macrophage growth was inhibited at a higher concentration of ascitic fluid (greater than 20%). The growth stimulating activity of this fluid was stable on heat treatment. The adherent cultured cells that proliferated were typical macrophages, as indicated by nonspecific esterase staining, pinocytosis and phagocytosis. These macrophages showed cytolytic activity against a murine tumor in the presence of wheat germ agglutinin. However, their cytotoxicity with antitumor antibody decreased during the culture period. These results indicate that tumorous ascitic fluid contains a macrophage growth factor(s) and that macrophages cultured with, and induced to proliferate by, ascitic fluid can kill tumor cells in cooperation with lectin but not antibody.

Animals↗

N-Sulfomethylation of guanine, adenine and cytosine with formaldehyde-bisulfite. A selective modification of guanine in DNA.

When guanine-, adenine- and cytosine-nucleosides and nucleotides were treated with formaldehyde and then with bisulfite, stable N-sulfomethyl compounds were formed. N2-Sulfomethylguanine, N6-sulfomethyladenine, N4-sulfomthylcytosine and N6-sulfomethyl-9-beta-D-arabinofuranosyladenine were isolated as crystals and characterized. A guanine-specific sulfomethylation was brought about by treatment and denatured single-stranded DNA with formaldehyde and then with bisulfite at pH 7 and 4 degrees C. Since native double-stranded DNA was not modified by this treatment, this new method of modification is expected to be useful as a conformational probe for polynucleotides.

Adenine↗

Idiopathic portal hypertension associated with progressive systemic sclerosis.

Herein we describe the clinical course of a case of idiopathic portal hypertension accompanied by splenomegaly, portal hypertension, and pancytopenia in addition to progressive systemic sclerosis. Immunological studies revealed positive antinuclear antibodies, hypergammaglobulinemia with increases in IgG and IgA, a decrease in peripheral T lymphocytes, and a decrease in the rate of lymphocyte blast transformation induced with phytohemagglutinin. The spleen weighed 1070 g, and the portal pressure was 270 nm H2O. Esophageal varices were also noted. These findings suggest the possibility of association of some immunological abnormalities with the etiology of idiopathic portal hypertension.

Adult↗