[A case of multiple bypass procedures for multiple arteriosclerotic cardiovascular lesions].
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Biomedical subjects
Publications and source records attributed to N Watanabe.
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In order to investigate the role of T cells in the production of tumor necrosis factor (TNF), a reconstitution experiment was performed with nude mice (Balb/c, nu/nu). The results obtained were as follows: The cytotoxic activity of tumor necrosis serum (TNS) from Balb/c, nu/nu mice treated with P. acnes-LPS was 1/22 against that from Balb/c, nu/+ mice. TNF activity increased 14 times in reconstituted nude mice against Balb/c, nu/nu mice. Investigation of the production of the cytotoxic activity per cell was carried out using T cell and macrophage fractions separated from the spleens of both Balb/c, nu/nu and Balb/c, nu/+ mice treated with P. acnes as a priming agent. Elicitation employing LPS was done in vitro. Cytotoxic activity released into culture medium was observed in the macrophage fraction, but not in the T cell fraction. However, no significant difference was shown in species. With P. acnes treatment, the population of macrophages in the spleens from Balb/c, nu/+ mice increased 25.5 times, whereas that from Balb/c, nu/nu mice only increased 6.8 times. The above results suggest that the mechanism of the incremental effect of T cells on TNF production was due to the promotion of macrophage proliferation during the priming period after injection of P. acnes.
There is significant evidence that the macrophage plays a critical role in the host's defense against neoplasia. Tumor-necrosis factor was recognized by Carswell et al. during a study of the antitumor activity of serum from mice infected with BCG and subsequently injected with endotoxin. The same procedure was applied to rabbits in order to obtain serum containing tumor-necrosis factor (TNF). Sera from these mice and rabbits contained a factor that induced hemorrhagic necrosis of certain mouse sarcomas in vivo and had cytotoxic effects on mouse and human tumor cells in vitro. Sera from mice and rabbits singly treated with BCG or endotoxin did not have these properties. Other agents such as C. parvum, OK-432, lentinan or zymosan, that cause hyperplasia of reticuloendothelial system and increase sensitivity to endotoxin lethality, could substitute for BCG in priming for TNF release. However, the use of P. acnes as a priming agent was the most effective and lipopolysaccharide from gram-negative bacteria appeared to be unique in its ability to elicit TNF release. TNF is a protein with a molecular weight, ranging from 40,000 to 60,000 that has both tumor necrotizing activity in vitro and tumor killing activity in vitro. It is relatively stable to heating at up 70 degrees C. This result indicated that both in vitro and in vitro activities of mouse and rabbit TNF are a property of one and the same molecule. TNF is thought to be produced by macrophage and is distinguished from the other know macrophage products in serum containing TNF. TNF is cytotoxic to several but not all tumor cell lines. Its most interesting feature is that it reportedly dose not affect any non-transformed cell types, implying that it somehow recognizes transformed cells.
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The induction of tumor necrosis factor (TNF) by OK-432 was investigated. The results were as follows: Serum from OK-432 injected into NZW rabbits treated with LPS was cytotoxic to tumor cells in vitro. With respect to the target cell spectrum this factor was cytotoxic to L929, Lewis, M7609 and K562, but not to Chang liver cells, HMV cells or HeLa cells. The cytotoxic activity of this factor was found to be M.W. 48,000 on H.P.L.C., and the pI was revealed to be 5.4 by isoelectric focusing. These results were consistent with previously reported findings on TNF.
Isoelectric focusing profiles of ferritins isolated from livers of anemic rats and 3'-methyl-4-dimethylaminoazobenzene-induced hepatomas were more acidic than their normal counterparts, and exhibited patterns similar to those of heart ferritin. Iron administration induced a shift to more basic components for the normal and tumor ferritins. The isoferritin patterns reflected the subunit populations of the protein, as the more acidic components had greater proportions of H-type subunits and iron induced an increase in L subunits with concomitant increases in more basic isoferritins. For both normal and malignant tissues there was a direct correlation between iron content of the tissue and subunit composition. The apparently unique isoferritin patterns in the tumor tissue may, therefore, be ascribed primarily to the lower iron contents.
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It is important to know the possibilities of allogenic transplantation of the joint in the present modes of the artificial joint replacement. In order to clarify the fate of osteochondral allograft, an experimental study of fresh "shell" transplantation was made on the femoral head of the dogs. Fifteen adult mongrels, around 15 kg in weight, were used as a recipient, and the same number as a donor. Special instruments of the same sized male and female reamer were made to cut an osteochondral shell with 2 to 4 mm thickness. Transplanted animals were killed at the interval from 2 weeks to 3 years. Femoral heads from the transplanted side and the opposite side for control were observed by histo-morphometric techniques. Usual decalcified sections were stained with H-E and safranin-O to observe the articular cartilage, and undecalcified ground specimens were made to understand the remodeling of the subchondral bone. The underlying subchondral bone was completely remodeled by 1 year, the grafted shells were well adapted and fixed to the host bone. Although a number of cartilage cells on the superficial layer were decreased from an early stage, the whole articular cartilage could possess its original thickness and well functioned for three years. However, in some animals, the pannus formation and chondrolytic reaction which is thought to be an immunological rejection were observed at the margin of the grafted articular cartilage. This experiment has demonstrated that allogenic osteochondral graft with 2 to 4 mm thickness was very successful even on the femoral head, and clinical trials might be expected if the histocompatibility of the tissue is settled.
Sixty-nine patients have shown recurrence after curative (standard, extended and modified) mastectomy from 1969 to 1978 in our department. Recurrence patterns and prognostic factors were analyzed using life-table and log-rank methods. Thirty-four patients (49%) developed their first recurrence within two years after surgery and died within two years after that. This period seemed to be high-risk after surgery and first recurrence. The disease-free interval and survival after first recurrence seemed to be shorter with the more advanced presenting Tnm stage. The disease-free and recurrence-to-death intervals of patients with first loco-regional recurrence seemed to be longer than those with first distant metastases.
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