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T Uede

Publications and source records attributed to T Uede.

211 records · Page 12Linked to original sources
PubMed1981

[Mechanism of suppression on cellular immunity in experimental brain tumor rats (author's transl)].

The mechanism of the suppression on the cellular immunity was analysed in experimental brain tumor rats. The tumor used in this experiment was a 3-methylcholanthrene induced fibrosarcoma. The tumor cell was inoculated into the caudate nucleus of the rats with a Hamilton microsyringe. When spleen cells from brain tumor rats were added to the PHA blastogenesis system, impairment of the normal lymphoproliferative response to the PHA was detected as early as on the third day and continued until the ninth day after inoculation. After the depletion of glass adherent cells, the residual cells from the spleen could not suppress the normal lymphoblastogenesis by the PHA. After the depletion of T cells by anti-T cell sera and complement, however, the residual cells from the spleen still suppressed the normal lymphoblastogenesis. Glass adherent cells were able to phagocyte the latex particles. From these findings, the suppressor cell responsible for the suppression of the normal lymphoblastogenesis by the PHA was considered to be macrophage and suppressor T cell did not play a role in the suppression of the PHA responses in this experimental model. The sera from brain tumor rats could not inhibit the proliferative responses of lymphocytes to PHA. Thus the possibility of the existence of suppressive factors in the sera was also negligible.

Animals↗
PubMedDate not supplied

Prevention of cardiac reperfusion injury following global ischemia by a monoclonal antibody, R2-1A6.

The effect of R2-1A6 monoclonal antibody on the reperfusion injury of heterotopically transplanted rat cardiac tissues after global ischemia was studied. Histological, functional as well as myocardial energy status were evaluated in control and R2-1A6-treated rats. The strong binding of neutrophils to cardiac endothelial cell surface and strong tissue edema were present at 10 min after the initiation of reperfusion and subsequently interstitial hemorrhage and myocardial degeneration were present in the control group. The mean survival date of grafted hearts was about 7.7 days in the control group. In contrast, the significantly less severe binding of neutrophils to endothelial cells, tissue edema, interstitial hemorrhage, and myocardial degeneration were present in R2-1A6-treated rats. All grafted hearts survived up to 14 days in R2-1A6-treated group. Myocardial ATP content decreased from preischemic value of about 4 mumol/g to post-ischemic value of 0.57 mumol/g. After reperfusion of ischemic hearts, myocardial ATP values remained to be a range of 1.27-1.03 mumol/g in control group. However, myocardial ATP values recovered up to 2.28 mumol/g in R2-1A6-treated group. Thus, these experiments indicated that neutrophil adherence to endothelial cells is a critical early event in the process leading to post-ischemic reperfusion injury in global ischemia and the R2-1A6 treatment resulted in significant protection against cardiac reperfusion injury following global ischemia.

Adenosine Triphosphate↗
PubMedDate not supplied

Cardiac allografts in rat recipients with simultaneous use of anti-ICAM-1 and anti-LFA-1 monoclonal antibodies leads to accelerated graft loss.

Cardiac allografts from Fisher rats underwent acute rejection in Wistar King Aptekman/Hokkaido (WKAH) recipient rats. ICAM-1 molecule was induced in grafted myocytes and interstitial cells during the rejection. LFA-1 (+) inflammatory cells heavily infiltrated into rejected allografts. Monoclonal antibodies to rat ICAM-1 or LFA-1 were administered intravenously to WKAH rats receiving Fisher cardiac allografts for 3-7 consecutive days after transplantation. Anti-LFA-1 treatment for 7 consecutive days prolonged allograft survival, and two of these obtained a long-term survival. While 2 out of 13 allografts survived more than 100 days in the anti-ICAM-1-treated groups, anti-ICAM-1 treatment did not affect allograft survival in the other recipients. Surprisingly, simultaneous use of both anti-ICAM-1 and anti-LFA-1 antibodies resulted in accelerated graft loss with interstitial edema, diffuse myocardial degeneration, vascular injury and scattered hemorrhage. Thus, beneficial effects on allograft survival were partially seen when recipients were given anti-ICAM-1 or anti-LFA-1 antibody alone. However, serious disadvantage in preventing rejection was clearly seen when both anti-ICAM-1 and anti-LFA-1 antibodies were used together.

Animals↗
PubMedDate not supplied

A case of abducens neurinoma mimicking acoustic neurinoma.

Neurinoma arising from the abducens nerve independent of neurofibromatosis has been rarely reported in the existing literature. We present a case of abducens neurinoma which was confirmed during a surgical excision. A 31-year-old female had experienced a hearing disturbance for the past 8 months. Abduction of the right eye ball was almost full. Magnetic resonance images showed a tumor having a size of 44 x 33 X 33 mm at the right cerebellopontine angle. Neuro-otological examination revealed the findings specific to acoustic neurinoma. Surgical excision confirmed that the tumor originated from the abducens nerve. The tumor located at the cavernous sinus or cerebellopontine angle might originate from the abducens nerve, though the abduction of eye ball is not in any way impaired.

Abducens Nerve↗
PubMedDate not supplied

Effects of stress on growth of transplanted hepatic tumours and immune responses.

Growth of transplanted hepatic tumours (T-9) was enhanced in immune rats under stress, compared with immune rats in an unstressed condition. Compared with unstressed immune rats, killer activity of mononuclear cells infiltrating the tumours against T-9 cells was significantly reduced in stressed immune rats. In contrast, killer activity of splenocytes obtained from stressed immune rats against T-9 cells was elevated compared with that from unstressed immune rats. In addition, natural killer cell activity of mononuclear cells infiltrating the tumours obtained from stressed immune rats was significantly reduced compared with that from unstressed immune rats. Cell populations infiltrating tumour tissues were identified by flow cytometric analysis. The percentage of CD8+ cells in mononuclear cells isolated from tumour tissues of stressed immune rats was reduced compared with that of unstressed immune rats. Furthermore, interleukin-2 responsiveness of splenocytes was suppressed in stressed immune rats, whereas T cell function as reflected by phytohaemagglutinin- or Concanavalin A-reactivity was unaffected by stress. Collectively, it is likely that stress suppressed the generation of cytotoxic cells from the spleen cells of immune rats.

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