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Biomedical subjects

T Kishida

Publications and source records attributed to T Kishida.

At least 253 records · Page 14Linked to original sources
PubMed1983

[Effect of interferon on mouse glioma].

Mouse interferon (IFN) induced in L 929 cells by Newcastle disease virus was examined for its effect on the growth of mouse brain tumor cell line. In this study, we used subcutaneously transplanted 203 Glioma model, which had been originally induced by methylcholanthrene in C 57 BL mice. After subcutaneous transplantation, intraperitoneal administration of IFN was started by following schedule; 5 X 10(3) IU twice a week, 5 X 10(4) IU twice a week, 2.5 X 10(5) IU twice a week, 5 X 10(3) IU every day and 2.5 X 10(4) IU every day. In all groups treated by IFN intraperitoneally, no inhibition of the tumor growth was seen. On the other hand, natural killer (NK) activity was augmented by IFN treatment. Therefore, we considered that augmentation of NK activity was not directly correlated with the antitumor effect of IFN. Then, local administration was examined. After subcutaneous tumor was recognized, 2.5 X 10(4) IU of IFN was injected intratumorally every day. About 20 days later, the tumor decreased its size less than that treated by local injection of saline. It was suggested that the local administration of IFN might be better than the systemic administration.

Animals↗
PubMed1983

[Production and characterization of human tumor degenerating factor (TDF)].

The culture supernatant of human fibroblasts caused degenerative changes in the target cells. This tumor degenerating factor in the supernatant (TDF) appeared already on the 1st day of culture and increased gradually to the 8th day. TDF was effective on human KB, HeLa, FL and of hepatoma cells, but neither on murine L929, 3T3, SV-3T3 cells nor MDBK cells. Furthermore, TDF was not effective on human non-transformed cells, namely various human fibroblasts. Human leukocyte interferon (HuIFN-alpha) enhanced TDF production. The coculture of human fibroblasts with KB cells augmented TDF production.

Animals↗
PubMed1983

Morphological study of neurotransmitter receptors in the rat brain.

1. We performed light and electron microscopic autoradiography of GABA and opiate receptors using 3H-muscimol and 3H-DAMA. 2. Selection of development method is important for electron microscopic autoradiography. The authors obtained silver grains in a pattern precisely localized to the cytoplasmic membrane, i.e., the receptor site by means of EAA development. 3. We observed 3H-muscimol binding site in the neuropiles of the cerebellar molecular layer and the substantia nigra ultrastructurally. Receptor sites labeled with silver grains are located not only on the synaptic regions but also on the plasma membranes of the dendrites and axons not corresponding to synaptic sites. 3H-DAMA binding sites in the caudate nucleus and the amygdaloid nucleus are noticed on the plasma membranes of the axons, dendrites, and nerve cell somas, some corresponding to synapses, others not. There are still problems to be solved in the autoradiographical observation of neurotransmitter receptors. Nevertheless, this technique is very important in observing the morphological relationship between transmitters and their receptor sites.

Animals↗
PubMed1983

Tumor degeneration by human embryonic fibroblasts and its enhancement by interferon.

KB cells from a human nasopharyngeal tumor were cocultivated with human embryonic fibroblasts (HF 8101 cells); 7 to 14 days after incubation, "spongy degeneration"-like changes developed in the target cell-growing area. These changes developed in other target cells [HeLa cells from human cervical cancer, human hepatoma cells (PLC/PRF/5), and human amnion FL cells] cocultured with several kinds of human embryonic fibroblasts [HF 8101 cells, HF 8103 cells, and HEL cells]; however, HF 8101 cells did not cause degenerative changes in murine L929 cells. The degenerative changes were enhanced by treatment with human leukocyte interferon or human fibroblast interferon at a dose of 1,000 or 10,000 IU/ml, but there was no significant difference in the enhancing effect between human leukocyte and human fibroblast interferons. Mouse L929 interferon did not enhance the degenerative changes in KB cells caused by HF 8101 cells. It was concluded that human fibroblasts caused the degenerative changes in the human tumor cells and the continuous cell line and that the changes were enhanced by treatment with either human leukocyte interferon or human fibroblast interferon.

Animals↗
PubMed1983

Augmentation of natural killer activity of human peripheral blood lymphocytes by human leukocyte interferon: characterization of the augmented activity.

The characteristics of natural killer (NK) activity of human peripheral blood lymphocytes treated with human leukocyte interferon (HuIFN-alpha) were compared with those of the untreated original NK activity. HuIFN-alpha, at a concentration of 50 IU/ml or more, augmented the NK activity against BALL-1, Daudi, and Namalwa target cells. On the other hand, the augmentation was less evident for the activity against Raji and Molt-4 cells. Original NK activity was detected mainly in the fraction that passed through a nylon wool column. Nylon-retained cells, however, could be activated by the addition of HuIFN-alpha to express activity against BALL-1. The activity of the nylon-passed fraction was augmented by HuIFN-alpha as well as that of unfractionated cells. NK cells could be activated by HuIFN-alpha under calcium-free conditions that allow NK cells to bind but not to lyse the target cells; augmented cytotoxicity was observed when calcium was added 2 hr later. This suggests that the augmentation of NK activity by HuIFN-alpha may have resulted from an increase in the number of NK cells.

Animals↗
PubMed1983

Local administration of interferon for malignant brain tumors.

We investigated the effects of local administration of interferon (IFN) on 13 patients with recurrent brain tumors. Histologic diagnoses were glioblastoma (eight patients), medulloblastoma (one), ependymoma (one), ependymoblastoma (one), pontine glioma (one), and astrocytoma (one). When tumor recurrence was evident local administration of IFN was started through an Ommaya reservoir, which was placed during repeat craniotomy. No tumor regressions were seen in the patients given weekly injections of IFN; however, in two of six patients given daily injections, a decrease of tumor volume and augmentation of natural killer activity were seen.

Adult↗
PubMed1982

[Interferon therapy for brain tumor patients (author's transl)].

Nine cases of recurrent and metastatic brain tumors were treated by Hu-IFN-alpha. It was given intramuscularly and singly to those who finished the usual treatments of surgical removal and 60Co irradiation more than 6 months before, to exclude their effects on tumors. They were divided into 2 groups of small dosage (fifty thousands units weekly) and large dosage (3 million units every other day). The total dosage of IFN varied from about 2 million units for the small dosage group to 264 million units for the large dosage group. No side effects were noted. In two cases of six which were followed up over 4 months, the tumors regressed about 50% on serial CT. However, IFN was not effective on the tumors which had already showed a rapid growth before IFN administration. Almost all the patients showed improvements in their general condition, PPD and PHA skin test, peripheral lymphocyte counts and natural killer cell activities.

Adolescent↗
PubMed1982

Elimination of polynucleotide-induced hyporeactivity in mice treated with interferon and antitumor therapy.

Polyriboinosinic-polyribocytidylic acid (poly I:C) (100 microgram) induced hyporeactivity to interferon production 24, 48 and 72 hr after the injection. This hyporeactivity was eliminated by the injection of mouse brain interferon (more than 10,000 IU) 3 hr prior to the second injection of poly I:C. Even the hyporeactivity caused by the repeated administration of poly I:C was eliminated when interferon was injected 3 hr before each administration of poly I:C. It was surmised that one of the causes for the elimination of hyporeactivity may be the priming effect effect of interferon in mice. By utilizing the eliminating effect which interferon has on the hyporeactivity caused by poly I:C, the synergistically suppressive effect of interferon and poly I:C on the mortality and tumor growth in the neuroblastoma-bearing mice was found. These results suggest that the combined use of interferon and interferon-inducer may be applicable to cancers or viral diseases in humans.

Animals↗
PubMed1982

Binding experiments of muscarinic acetylcholine and dopamine receptors in human brains with emphasis on a case of striatonigral degeneration.

In the regional distribution of I-3H-quinuclindinyl benzilate (3H-QNB) binding in human brains of neurologically unaffected cases, it was highest in the caudate nucleus which was followed by the putamen, amygdala, cerebral corteces and olfactory bulb and lowest in the substantia nigra. As to the regional distribution of 3H-spiroperidol binding in human control brains, it was highest in the caudate nucleus and was followed by the cerebral corteces, amygdala and lowest in the cerebellar cortex. In a case of striatonigral degeneration (SND), 3H-QNB binding in the putamen and thalamus was lowered and 3H-spiroperidol binding was decreased in the putamen, frontal and parietal corteces, Ammon's horn, amygdala and substantia nigra as compared to human brains of control cases. These results were noteworthy since no pathological changes were observed in the thalamus, cerebral corteces, amygdala and Ammon's horn in this case. The 3H-spiroperidol binding was increased by injection of 6-hydroxydopamine (6-OHDA) into the substantia nigra of rat brains by 17% as compared to the contralateral intact side. Conversely, 3H-spiroperidol binding was decreased by injection of kainic acid (KA) into the striatum of rat brains by 43% as compared to the contralateral intact side. This meant that dopamine receptors labelled by 3H-spiroperidol were at least partially localized at the postsynaptic site of the nigrostriatal dopamine neuron.

Animals↗
PubMed1982

[Interferon production in human T lymphoblastoid cells].

Human T lymphoblastoid cell (RPMI 8402 cell) produced interferon (IFN) through the induction by Sendai virus. The priming effect on the interferon production in the RPMI 8402 cell could be found by the pretreatment of human leukocyte IFN (Hu IFN-alpha), but not by that of the IFN produced in the RPMI 8402 cell (T-IFN). The superinduction by the irradiation of ultraviolet rays or the treatment of antimetabolites (actinomycin D and cycloheximide) or 5-bromodeoxyuridine was not found. The T-IFN was completely neutralized by the anti-Hu IFN-beta serum, but not by the anti-Hu IFN-alpha serum at all. In conclusion, it was confirmed that the IFN produced in the RPMI 8402 cell through the induction by Sendai virus was antigenically identical to Hu IFN-beta.

Antigen-Antibody Complex↗
PubMed1982

Effects of interferon on C1300 mouse neuroblastoma.

The effects of murine interferon (MuIFN) with and without cyclophosphamide (CY) were evaluated in C1300 neuroblastoma-bearing mice. Mean survival times were prolonged by administration of 25,000 IU of MuIFN three times per week by ip injection. The combination of MuIFN and CY was more effective in the treatment of mouse neuroblastoma than either agent alone. Our results suggested that MuIFN is synergistic in combination with moderate amounts of CY in mouse neuroblastoma cells and may be given for the treatment of neuroblastoma.

Animals↗
PubMed1982

Different susceptibilities of cultured mouse cell lines to mouse interferon.

Cultured mouse cells were treated with 3.3 approximately 10,000 units of mouse interferononon for 3 days and further cultivated in fresh medium for 2 days (recovery incubation). The IC50 (concentration of drug required for 50% inhibition) of interferon was not changed much after the recovery incubation. The most susceptible cell line to interferon was B16 melanoma; the IC50 was 10.5 units per ml of medium on day 3 after the start of treatment. P388 leukemic cells, Lewis lung carcinoma cells, and colon adenocarcinoma 38 cells were moderately susceptible to interferon and the IC50s of these cell lines were 200, 80, and 180 units per ml medium, respectively, on day 3. The cells least susceptible to interferon were those of colon adenocarcinoma 26; IC50 was greater than 10,000 units per ml. In the recovery incubation, the growth of B16 melanoma cells, P388 leukemic cells, Lewis lung carcinoma cells and colon adenocarcinoma 38 cells was considerably inhibited when these cells were treated with more than 100 approximately, 1,000 units of interferon per ml medium. The rate of multiplication was usually more than 1 for these cell lines, except for Lewis lung carcinoma cells where the rate of multiplication was less than 1. This indicates that interferon is not cytocidal towards B16 melanoma cells, P388 leukemic cells, or colon adenocarcinoma 38 cells, but mouse interfer is cytocidal towards Lewis lung carcinoma cells when the cells are treated with a relatively high concentration of interferon and then cultured in the medium without interferon.

Adenocarcinoma↗
PubMed1982

Enhancement of bactericidal activity of mouse peritoneal macrophages against Staphylococcus aureus by mouse interferon preparations.

The effect of mouse interferon on the bactericidal activity of macrophages against pyogenic cocci was examined. Mouse peritoneal macrophages were cultivated with Staphylococcus aureus in vitro and viable Staphylococcus was recovered by treatment of the mixed macrophage-bacteria culture with sodium dodecyl sulphate (SDS) solution. Results showed that S. aureus was phagocytized and killed by the macrophages. Mouse L cell interferon enhanced the bactericidal activity of macrophages. A mouse brain interferon preparation also enhanced this activity. However, heat-inactivated L cell interferon and heterologous rabbit RK-13 cell interferon and human leukocyte interferon did not enhance it. This suggests that interferon enhances the bactericidal activity of macrophages against S. aureus.

Animals↗