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Biomedical subjects

T Ebina

Publications and source records attributed to T Ebina.

At least 127 records · Page 7Linked to original sources
PubMed1982

Isolation of human rotavirus subgroups 1 and 2 in cell culture.

One strain of human rotavirus subgroup 1 (KUN) and one strain of subgroup 2 (MO) were isolated with the MA104 cell line, a fetal rhesus monkey kidney cell line. Their subgroup specificities and RNA patterns were identical to those of rotaviruses present in stools before cultivation. Distinct cytopathic effects consisting of obscure cell boundaries, cell fusion, cell rounding, cell detachment, and lytic foci were recognized at passage 3 of MO and passage 6 of KUN. No differences in cytopathic changes were found between the two isolates.

Animals↗
PubMed1982

Increased frequency of lymphocytotoxic antibodies in patients with multiple sclerosis correlated with disease activity.

Cold-reactive lymphocytotoxic antibodies (LCA) were investigated in sera from patients with multiple sclerosis (MS) in relation to disease activity. When a serum with more than 20% cytotoxicity is considered positive for the presence of LCA, the positive frequency at remission was 21% (6/28), but at exacerbation it was 83% (10/12). All the sera from normal controls were negative. The average of cytotoxicity expressed as a % killing of target cells by sera at remission was 13%; on the other hand, at exacerbation it was 39%. These results showed that in multiple sclerosis the level of LCA was not persistently high, but increased correlating with the disease activity. From these findings and previous experiments of rescue of measles virus antigens, it was suggested that multiple sclerosis is likely a virus-induced autoimmune disease.

Adult↗
PubMed1982

[Induction of interferon and activation of NK cells and macrophages in mice by oral administration of Ge-132, an organic germanium compound].

After oral administration of an organic germanium compound, Ge-132 (300 mg/kg), a significant level of interferon (IFN) activity was detected in the sera of mice at 20 hr and it reached a maximum of 320 U/ml at 24 hr. This IFN activity was lost after heat- or acid-treatment, suggesting that the induced IFN is of gamma nature. The molecular weight of this IFN was estimated to be 19,000 daltons by gel filtration. After the oral administration of Ge-132, NK activity of spleen cells had increased at 24 hr and cytotoxic macrophages were induced in the peritoneal cavity at 48 hr. In mice, receiving intraperitoneal (i.p.) injections of trypan blue or carrageenan 2 days before oral administration of Ge-132, neither induction of IFN nor augmentation of NK activity followed. X ray irradiation of mice also rendered the mice incapable of producing IFN, all suggesting that both macrophages and lymphocytes are required for this IFN induction. After i.p. administration of induced IFN, both NK and cytotoxic macrophage activities appeared at 48 hr with as little as 20 U/ml titered IFN. These facts may indicate that the augmentation of NK and activation of macrophages in mice after oral administration of Ge-132 is mediated by induced IFN.

Administration, Oral↗
PubMed1982

Antitumor and interferon-inducing activities of TH69, a whole bacterial preparation of Streptococcus faecalis, in mice.

The antitumor effect of TH69, a lyophilized whole cell preparation of Streptococcus faecalis, was examined in mice using four experimental tumors: Ehrlich carcinoma and sarcoma-180 in DDI mice, MCA tumor in syngeneic C3H mice and Meth-A tumor in syngeneic BALB/c mice. Consecutive intraperitoneal injections of TH69 started one day after the tumor implantation markedly inhibited the growth of the two allogeneic ascites tumors and two syngeneic solid tumors. However, even with the most sensitive Ehrlich ascites tumor, TH69 was ineffective when the tumor cell inoculum was more than 2 X 10(6) cells per mouse. Neither oral nor subcutaneous administrations of TH69 produced significant antitumor effects. After a single intraperitoneal administration of TH69 (300 mg/kg) to mice, interferon was induced in the serum with a titer of 220 U/ml at 14 hr after administration. As TH69 has no direct cytotoxic activity against Ehrlich tumor cells, the antitumor effect of TH69 in mice must be ascribed to some immunopotentiating activity including interferon induction.

Animals↗
PubMed1982

[Characterization and bioactivity of interferon induced by Streptococcus faecalis preparation, TH69].

It was demonstrated that TH69, an lyophylized preparation of streptococcus faecalis TH001 (ATCC No. 31663) induced interferon gamma (IFN gamma) in spleen cell cultures. The IFN activity was found in 8 hrs and reached to the peak of 120-240 U/ml 24-48 hrs after incubation in every concentration of 4, 20, and 100 micrograms/ml of TH69. TH69-induced IFN (TH69-IFN) was produced by T cells assisted by macrophages which were stimulated with TH69, and the activity was neutralized by 80-90% with anti-IFN gamma serum but hardly neutralized with anti-IFN alpha, beta serum. Therefore, TH69-IFN was found to be mostly gamma type. The elution profile of TH69-IFN activity on a column with Toyopearl HW-55S showed that molecular weight of IFN was estimated at 18,000-28,000. Sequential purification on this column of TH69-IFN increased the specific activity to approximately 2.5 X 10(4) U/mg protein (partially purified TH69-IFN: TH69-IFNp). A small amount of TH69-IFNp (5-50 U/ml) augmented NK activity and induced cytotoxic macrophages in vitro. Growth of Meth-A tumor cells exposed to TH69-IFNp of 100 U/ml in vitro declined to 50% and three times injection of TH69-IFN (200 U/50 microliters) into the tumor sites of mice given implants of Meth-A suppressed the tumor growth.

Animals↗
PubMed1981

Morphogenesis of human rotavirus type 2 Wa strain in MA 104 cells.

Morphogenesis of human rotavirus type 2 Wa strain in MA 104 cells was observed. The virus antigen in the cytoplasm was detected by indirect immunofluorescence twelve hours after infection. The cytopathic effect occurred 24 hours after infection when virus particles were detected by EM in the culture fluid as well as in thin sections of the infected cells. Virus particles were observed in the dilated RER, nuclear envelope (perinuclear space), viroplasm, and a lysosome-like body. Three types of virus particles were noted: double-shelled particles 75-85 nm in diameter, single-shelled particles 64-68 nm in diameter and electron-dense nucleoids or cores 32-40 nm in diameter. The outer shell of virus particles was acquired by budding through the membrane of the dilated RER. Tubular structures, similar in diameter to the single-shelled particles, were found in the cytoplasm and nucleus of infected MA 104 cells. Bundles of filaments or the leaflet-like inclusion bodies of membrane-bounded bundles of filaments were found in the cytoplasm and seemed to be associated with virus particles.

Animals↗
PubMed1981

Interferon-inducing activity of an immunotherapeutic anticancer agent, SSM, prepared from Mycobacterium tuberculosis strain Aoyama B.

The interferon-inducing capacity of arabinomannan-lipid preparation (SSM) extracted from Mycobacterium tuberculosis Aoyama B in both BCG-sensitized and unsensitized mice was studied in comparison with that of purified protein derivative (PPD) prepared from the same tubercle bacillus. Although it is known that PPD cannot stimulate interferon production in BCG-unsensitized mice, interferon activity was found in sera of both groups of mice after intravenous injection of SSM at a dose of 5 mg/kg. The maximum titer was detected 5 hr after injection. The interferon induced by SSM in both groups of mice shared certain physicochemical properties with the immune interferon induced by PPD in BCG-sensitized mice. In BCG-unsensitized mice, interferon induction by SSM was markedly inhibited by pretreatment with trypan blue and carrageenan, whereas it was not depressed in BCG-sensitized mice given the same treatment or when interferon was induced by PPD. In addition, induction of interferon in BCG-sensitized mice by SSM and PPD and in unsensitized mice by SSM was completely abrogated by pretreatment with hydrocortisone acetate and whole-body x-irradiation (700 R). These results suggest that in BCG-unsensitized mice macrophages, in addition to X-ray or hydrocortisone-sensitive cells, may be required for interferon induction by SSM.

Animals↗
PubMed1981

Lactate dehydrogenase-elevating agent is responsible for interferon induction and enhancement of natural killer cell activity by inoculation of Ehrlich ascites carcinoma cells into mice.

Inoculation of Ehrlich ascites carcinoma cells (EAC) into the peritoneal cavities of outbred ddY mice induced interferon (IFN) in the circulation. The maximum titer (1,280 U) was obtained at 24 hr after inoculation. This induced IFN had the characteristics of type I IFN, i.e., stability at pH2 and lability at 56 C. An increase in natural killer cell (NK) activity was also observed for the first 3 days after inoculation. In addition, plasma lactate dehydrogenase (LDH) activity was elevated in these mice. Inoculation of ascitic fluid or serum of EAC-bearing mice into normal mice increased plasma LDH activity six- to sevenfold over normal levels and elevated activities persisted throughout the life of the mice. These results suggest that the LDH-elevating agent was responsible for IFN induction and for enhancing NK activity. Because lactate dehydrogenase-elevating virus (LDV) can be eliminated from tumor cells by passage in vitro, we attempted to grow EAC in tissue culture for several months and re-examined whether the inoculation of such cells could elevate plasma LDH activity induce IFN and enhance NK activity. The results showed that inoculation of the passaged cells had no effect on these activities in normal mice. Therefore, we concluded that the IFN inducer was LDV which contaminated the EAC and then enhanced the NK activity. N-tropic murine leukemia virus also contaminated EAC, but this virus was not responsible because cultured cells of EAC still shed this virus.

Animals↗
PubMed1980

Caffeine-induced recovery from G2 block caused by neocarzinostatin.

Caffeine was found to act as a stimulator of the recovery of HeLa-S3 cells from the G2 phase arrest induced by a cancer chemotherapeutic agent, neocarzinostatin (NCS). When the cells were incubated in the presence of caffeine after removal of NCS, the time required for the recovery of mitosis was dependent on the concentration of NCS and was markedly shortened by caffeine treatment in a concentration-dependent manner. When puromycin, a specific protein synthesis inhibitor, was added together with caffeine, a temporary recovery of mitosis was observed, followed by an irreversible arrest of mitosis, suggesting that the terminal point of action of NCS resides closer to the M phase than that of puromycin. These results indicate that the mechanism of NCS-induced G2 block is closely related to that of X-ray-induced G2 block.

Antibiotics, Antineoplastic↗
PubMed1980

Effects of caffeine on neocarzinostatin-induced inhibition of cell cycle traverse in HeLa-S3 cells.

Caffeine was found to suppress the cell cycle effects of the cancer chemotherapeutic agent neocarzinostatin (NCS). When caffeine was added together with NCS to the culture of HeLa-S3 cells, NCS-induced inhibition of DNA synthesis and of mitosis was markedly reduced in the presence of caffeine. Theophylline was also effective, but N6, O2'-dibutyryl cyclic adenosine 3':5'-monophosphate was not. The caffeine-caused reduction of cell cycle effects was also observed in several other cancer chemotherapeutic agents, including bleomycin and Adriamycin. In contrast, the single-strand scission of cellular DNA and the final cell lethality induced by NCS were not affected by caffeine. These results suggest that the mechanism by which NCS inhibits the cell cycle traverse involves a kind of cell damage which is repairable in a manner promoted by caffeine and hence is different from single-strand scission of DNA. Such a mechanism might be common to the cell cycle effects of X-irradiation and several cancer chemotherapeutic agents including NCS.

Antibiotics, Antineoplastic↗