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T Aoki

Publications and source records attributed to T Aoki.

At least 1,279 records · Page 71Linked to original sources
PubMed1972

[Stomal ulcer].

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Gastrectomy↗
PubMed1971

Activation of spontaneous murine leukemia virus-related antigen by lymphocytic choriomeningitis virus.

Persistent infection with lymphocytic choriomeningitis (LCM) virus activates a phenotypic expression of murine leukemia viruis-related antigen. NZB and (NZB x NZW)F(1) mice, which normally carry large amounts of Gross virus, and C57BL/6 and NZW mice, which normally carry little virus, were infected with LCM virus. All had Gross soluble antigen in their plasmas at 3 months of age, while noninfected matched controls of all strains did not. This effect was seen after infection with LCM virus that was tissue passed or plaque purified. Similarly, cultures of mouse-embryo fibroblasts produced Gross soluble antigen when infected with LCM virus, but noninfected cultures failed to do so.

Animals↗
PubMed1971

Cell surface antigens: serial sectioning of single cells as an approach to topographical analysis.

The topographical distribution of H-2 antigens on the surfaces of C57BL/6 mouse thymocytes and lymph-node lymphocytes was investigated by a new technique. Single cells were reacted with visually labeled antibody directed against H-2 antigen. Each cell was processed for electron microscopy individually and was serially sectioned. Models constructed from serial electron micrographs provided detailed views of the entire cell surface and showed that H-2 antigen occurs on thymocytes in small isolated regions and on lymphocytes in large interconnected regions.

Animals↗
PubMed1971

Human sarcomas in culture. Foci of altered cells and a common antigen; induction of foci and antigen in human fibroblast cultures by filtrates.

In a study of human sarcomas maintained in culture for periods up to two years, the following observations were made. The most prominent cell type in serially cultured osteosarcomas was fibroblastic in appearance. After 16-20 wk in culture some lines spontaneously developed foci of altered cells resembling the foci produced in monolayer cultures by oncogenic viruses. The presence of these foci in the sarcoma cultures was transient, and usually they did not reappear; but in one instance they recurred with a characteristic periodicity of several weeks. From one of the sarcoma lines, in which foci appeared after 5 months in culture, two subcultures were established from stored frozen cells and these both exhibited foci after approximately the same lapse of time. The same phenomenon has been seen with another line, suggesting that the time of appearance of foci is characteristic for particular sarcomas. Foci of similar type could sometimes be induced in monolayer cultures of human fibroblasts by filtered medium from cultured sarcomas; this bore no relation to the presence or absence of foci in the sarcoma cultures at the time the filtrate was prepared. Electron microscopy of the spontaneous and induced foci, and of the sarcoma cultures, revealed no demonstrable virus. 12 out of 15 sarcoma cultures contained an antigen (S) demonstrable by indirect immunofluorescence with human sera. It was not present in any of the original sarcoma specimens, nor in any culture lines other than sarcomas. At least 3-4 wk in culture appear to be required for its demonstration. The antigen was cytoplasmic, occurred in only a small proportion of the cells, and was unpredictably variable in its expression, even in the same culture line. It could be induced in monolayer cultures of human fibroblasts by filtrates of medium from sarcoma cultures. As with the foci, the induction of S antigen in indicator cultures was not dependent upon the expression of antigen in the sarcoma line from which the filtrates were obtained. There was no association between the presence of foci and of antigen, nor was there any apparent relation between the ability of filtrates to induce foci and their ability to induce antigen. 80% or more of the general population have S antibody, and the titer of antibody in patients with sarcoma is no higher than in normal subjects. Thus, as in the case of Burkitt's lymphoma antigen, it appears that most individuals have been exposed to S antigen. But unlike Burkitt's lymphoma, no relation has so far been established between any particular disease and a corresponding high titer or frequency of occurrence of S antibody. The occurrence of foci of altered cells and of a common antigen, and the transmission of these two characters to indicator cells by filtrates, are all suggestive of a virus specifically associated with human sarcomas, one to which the general population is widely exposed, as indicated by the prevalence of antibody.

Adenocarcinoma↗
PubMed1971

Wild-type Gross leukemia virus and the pathogenesis of the glomerulonephritis of New Zealand mice.

The pathogenesis of the spontaneous glomerulonephritis of NZB and (NZB x NZW) F(1) hybrid mice is related at least in part to the formation of natural antibody against antigens of the G (Gross) system, and apparently to the deposition in the glomeruli of immune complexes of G natural antibody with G soluble antigen (GSA), type-specific antigen specified by wild-type Gross leukemia virus. G natural antibody and GSA are detectable in the acid-buffer eluate of the kidneys of NZB mice during the course of the glomerulonephritis. (NZB x NZW) F(1) hybrid mice develop glomerulonephritis and produce GSA and free G natural antibody earlier in life than do NZB mice. The proteinuria manifestation of the gomerulonephritis of (NZB x NZW) F(1) hybrid mice becomes increasingly prevalent as GSA undergoes immune elimination from the circulation. Gross leukemia virus-specified antigens together with bound immunoglobulins are located in the glomerular lesions of (NZB x NZW) F(1) hybrid mice, both in the mesangium as observed in NZB mice and also in the wall of the peripheral capillary loops of the glomeruli.

AKR murine leukemia virus↗