Biomedical subjects
Publications and source records attributed to M Oishi.
UV irradiation of African green monkey cells greatly stimulated efficiency of simian virus 40 induction from simian virus 40-transformed Syrian hamster cells after cell fusion. The maximum inducing activity was observed at 15 to 20 h after irradiation but remained only transiently. The addition of cycloheximide after UV irradiation eliminated the stimulation of the activity.
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The mechanism of in vitro erythroid differentiation in mouse Friend cells was studied by employing cell fusion between two genetically marked Friend cells and other nonerythroid cells. Erythroid differentiation was induced indirectly by fusing Friend cells that had been exposed briefly to dimethyl sulfoxide prior to fusion with nonerythroid cells that had been treated with ultraviolet light(or other DNA-damaging agents). The results suggest that two distinct reactions are involved in erythroid differentiation in Friend cells in vitro. One reaction, originating from the damaged DNA (or inhibition of DNA replication as a consequence), exhibits an inducible nature, is nonspecific to Friend cells, and is trans-acting. The other reaction is specific to Friend cells. Evidence that a typical tumor promoter, 12-O-tetradecanoylphorbol 13-acetate, inhibits erythroid differentiation by affecting the latter reaction is also presented. Brief exposure of Friend cells to DMSO was found to induce an early cellular activity required fusion for erythroid differentiation which is detected only by with UV irradiated cells. The induction process of this activity consists of at least two distinct stages. In the first stage, the reaction proceeds without supply of metabolites from the medium and exhibits sensitivity to tumor promoters. The second stage is closed involved with cellular metabolic activity, notably protein synthesis. Under normal conditions, the induced activity is short-lived, suggesting that turnover of the molecules responsible for this activity. There appears to be a signal produced following DMSO pulse which acts as an inducer for this activity. The signal remains active as long as 40 hr when protein synthesis is blocked. When permeabilized Friend cells, which had been briefly treated by DMSO, were exposed to cell-free extracts from UV irradiated cells, a small but significant number of the cells became reactive to benzidine, a characteristic of erythroid differentiation. The activity in the extracts was apparently induced following UV irradiation, reaching a maximum 25 to 30 hr after irradiation. After partial purification, the active factor seems to be a protein with a molecular weight of 35,000 to 40,000.
Cell fusion with two genetically marked Friend (murine erythroleukemia) cells has made it possible to characterize the very early events leading to erythroid differentiation, particularly the nature of reactions initiated by inducers such as dimethyl sulfoxide. We have found that brief exposure of Friend cells to dimethyl sulfoxide (as well as butyric acid or hexamethylene-bisacetamide) induces an early cellular activity required for erythroid differentiation which is detected only by fusion with ultraviolet-irradiated cells. The induction process of this activity consists of at least two distinct stages. In the first stage, the reaction proceeds without supply of metabolites from the medium and exhibits sensitivity to tumor promoters. The second stage is tightly coupled to cellular metabolic activity, notably protein synthesis. Under normal conditions, the induced activity is short-lived, suggesting turnover of the molecules responsible for this activity. There appears to be a signal produced following dimethyl sulfoxide pulse which acts as an inducer for this activity. The signal remains active for as long as 40 hr when protein synthesis is blocked.
Plasma histamine levels of rats anesthetized with pentobarbital sodium were significantly increased by intravenous administration of neurotensin (NT, 1 nmole/kg) with the maximum effect at 3 min, and a return to the initial levels in 20 min. Treatment of animals with compound 48/80 or disodium cromoglycate completely inhibited the elevation of histamine level by NT, however, treatment with reserpine or diphenhydramine and adrenalectomy did not affect the elevation. Plasma adrenaline levels increased transiently 1 min after NT injection, and adrenalectomy and treatment with compound 48/80 or diphenhydramine markedly reduced the elevation of adrenaline levels after NT injection. Plasma levels of noradrenaline were unchanged upon NT injection. These results provide direct evidence of the release of endogenous histamine and adrenaline following NT administration, and suggest the contribution of these amines to the NT-induced triphasic blood pressure responses (the first depressor, second pressor and third depressor responses) reported previously.
The mechanism of in vitro erythroid differentiation in mouse Friend cells was studied by employing cell fusion between two genetically marked Friend cells and other nonerythroid cells, including BHK (baby hamster kidney) and FM3A (mouse mammary gland) cells. We were able to induce erythroid differentiation indirectly by fusing Friend cells that had been exposed briefly to dimethyl sulfoxide prior to fusion with nonerythroid cells that had been treated with ultraviolet light (or other DNA-damaging agents). The results suggest that two distinct reactions are involved in erythroid differentiation in Friend cells in vitro. One reaction, originating from the damaged DNA (or inhibition of DNA replication as a consequence), exhibits an inducible nature, is nonspecific to Friend cells, and is trans-acting. The other reaction is specific to Friend cells and most likely is cis-acting. We also present evidence from the cell fusion experiments that a typical tumor promoter, 12-O-tetradecanoylphorbol 13-acetate, inhibits erythroid differentiation by affecting the latter reaction. The biological significance of these findings is discussed.
Simian virus 40 (SV40)-transformed Syrian hamster kidney cells produce infectious SV40 virus particles after treatments which damage DNA, such as UV irradiation or mitomycin C treatment. We have found that the induction of SV40 by DNA-damaging agents is greatly stimulated when a typical tumor promoter, 12-O-tetradecanoylphorbol 13-acetate (TPA), is present in the medium. Phorbol, which has a molecular structure similar to TPA but does not have any tumor-promoting activity, showed no such stimulatory effect on SV40 induction. This apparent synergistic effect of DNA-damaging agents and tumor promoter (TPA) was more pronounced when a tumor initiator, benzo [a]pyrene or 2-acetamido-fluorene, was combined with TPA. The effect of TPA on UV-triggered SV40 induction was greatly influenced by the timing of TPA addition to the culture medium, which was most efficient when addition of TPA was 5 to 20 h before UV irradiation. The effect of TPA, however, was not observed in SV40 rescue from hamster cells by cell fusion with permissive monkey (C7) cells.
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A cell preparation that is permeable to proteins and oligonucleotides yet produces infectious phage particles after induction treatments was obtained by plasmolysis of Escherichia coli cells lysogenic for phi 80. When the permeabilized cells were exposed to specific oligo(deoxynucleotides), prophage (phi 80) was induced during further incubation. Of the dinucleotides tested, only d(A-G), d(G-G), and d(I-G) induced prophage. The essential base sequence of the deoxydinucleotides for the induction was determined to be deoxy(purine-G). Among oligo(deoxynucleotides) with unique base composition examined, only oligo(deoxyguanylates) exhibited the inducing activity. Although this specific oligo(deoxynucleotide)-triggered induction occurred in recB- cells, the induction was not detected in recA- cells or in the cells lysogenic for induction-negative phi 80(ind-). Possible biological significance of the oligo(deoxynucleotide)-triggered prophage induction is discussed.
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Neurotensin administered intravenously in a dose of 1 nmole/kg produced triphasic blood pressure responses in anesthetized rats: the first depressor, second pressor and third depressor responses. The first depressor response was significantly suppressed by treatment of animals with a mixture of diphenhydramine and metiamide or chronic administration of compound 48/80, but was not modified by treatment with atropine, phentolamine, yohimbine, propranolol, sulpiride and adrenalectomy. The second pressor response was abolished by phentolamine, yohimbine and adrenalectomy. The second phase response was also markedly reduced by diphenhydramine in reserpinized rats and chronic administration of compound 48/80. The third depressor response was blocked by treatment of animals with diphenhydramine or chronic administration of compound 48/80. These results suggest that neurotensin may produce an immediate depressor response (the first phase) partly through a histamine-mediated process, and the second pressor response is produced by catecholamines released from the adrenal medulla through a histamine-mediated process. The third depressor response appears to be mediated mainly by histamine. The participation of mast cells as an origin of histamine which mediates these processes is suggested.
Described here is a 27-year-old female, who had centripetal obesity, broad reddish-purple striae on the lower abdomen and hypertension. Serum cortisol levels, the results of a dexamethasone suppression test and an adrenal scintigram with 131I-19-iodocholesterol were all compatible with Cushing's syndrome due to an adrenal adenoma that secretes cortisol autonomously. This was confirmed by gross and microscopic examination of the removed adrenal tumor. In addition, the patient had markedly diminished T4 and T3 concentrations in serum. Basal TSH levels were not elevated and did not rise significantly after TRH injection. Serum T4 and T3 concentrations were elevated to the normal range when the hyperadrenocorticism was corrected. The results indicate that the patient had "'corticogenic hypothyroidism."
A variety of complications are encountered in primary aldosteronism. Among them, less well known is the association of functioning adrenocortical adenoma with neoplasia of other organs. Described here is a patient with primary aldosteronism who had undergone a surgical operation for thyroid cancer and died of meningoencephalitis due to Listeria monocytogenes. Moreover, the autopsy revealed that he had an adenocarcinoma of the rectum. To our knowledge, this is the first documented case of a patient who had both primary aldosteronism and a primary double cancer of the thyroid and rectum.
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