Biomedical subjects

R Tanaka

Publications and source records attributed to R Tanaka.

At least 793 records · Page 44Linked to original sources

PubMed1982

The induction of glial proliferation by an astrocytoma-derived growth factor resembling glia maturation factor.

Glia maturation factor (GMF)-like activity which induces DNA synthesis and morphological differentiation of density-inhibited glioblasts was detected in various glial tumor cells. A polypeptide from C6 cells (rat astrocytoma) which has a molecular weight range of 40,000-50,000 showed the highest activity. This factor also induced DNA synthesis in glioma cells (354A and LRM55) and fibroblast (Swiss 3T3). The activity was susceptible to heat treatment at 70 degrees C for 5 min, or to proteases such as trypsin, chymotrypsin, papain, and subtilisin, but it was devoid of esteropeptidase activity. The isoelectric point was found to be 5.3. Subcellular fractionation localized the activity in cytosomal and microsomal fractions. These properties closely resemble those of GMF from pig and bovine brain.

Animals↗

PubMed1982

Interaction of glia maturation factor with the glial cell membrane.

Glia maturation factor (GMF) immobilized on agarose beads retained the same mitogenic and morphological transforming activities as free GMF when tested on glioblasts. The exposure of glioblasts to immobilized GMF for 5 min provoked the initiation of DNA synthesis and maximal stimulation was obtained within 30 min. Thiol-reducing agents, such as dithiothreitol and cysteine, increased the biological activity of GMF. These data suggest the presence of a surface receptor to GMF on the glioblasts, while the reduction of the thiol group(s) in GMF promotes the binding to its receptor. Repeated use of immobilized GMF decreased both the mitogenic and the morphological transforming activities. Immobilized GMF used for the third time lost its biological activity. This implies the existence of a certain kind of degradation system such as a proteolytic enzyme located close to the GMF receptor on the glial cell surface.

Animals↗

PubMed1982

Divalent cation, ATP-dependent [3H]leu-enkephalin uptake by synaptic vesicle fraction isolated from bovine caudate nucleus.

The mechanism of [3H]Leu-enkephalin uptake into synaptic vesicle fraction from bovine caudate nucleus was investigated. The simultaneous addition of 2 mM MgCl2, 2 mM CaCl2, and 2 mM ATP stimulated the uptake 22 times over the control, whereas the separate addition of these agents augmented the uptake 2.4 times at most. The addition of 2 mM MGCl2 plus 2 mM ATP and of 2 mM CaCl2 plus 2 mM ATP increased the uptake 6.6 times and 4.5 times, respectively. The cation, ATP-dependent uptake reached its half-maximal level within 10 min after the initiation of incubation at 25 degrees C, and little Leu-enkephalin was taken up at 0 degree C. The apparent Km for the uptake of [3H]Leu-enkephalin was 1.8 x 10(-7) M. Guanosine triphosphate stimulated the uptake as well as ATP, whereas CTP and ITP were only one-fourth effective of ATP. The cation, ATP-dependent uptake was inhibited by 25% and 20% in the presence of 0.1 mM colchicine and 1 microM reserpine, respectively.

Adenosine Triphosphate↗

PubMed1982

Inhibition of growth of mouse neuroblastoma cels by protein factor derived from rat glioblasts.

Growth inhibitory factor for mouse neuroblastoma cells was detected in the culture medium of fetal rat glioblasts, and was partially purified and characterized. The factor had an apparent molecular weight of 75,000 and an isoelectric point of 5.8, and showed no esterase activity. It possessed the activity to promote morphological differentiation including the formation of neural processes and the inhibition of cell division when tested on mouse neuroblastoma cell lines (Neuro 2a, NS-20Y, and NIE-115). The activity was susceptible to protease digestion and heat treatment. The serum over 25% cancelled the inhibitory activity of this factor. The factor failed to increase the intracellular contents of cAMP and cGMP. It showed no effect on either morphological differentiation or proliferation of glial cell lines, suggesting that under physiological conditions the factor acts specifically on neuronal cells.

Animals↗

PubMed1982

Inhibition by calmodulin antagonists of glioblast DNA synthesis and morphological changes induced by glia maturation factor.

Calmodulin antagonists, N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide hydrochlorides (W-7) and trifluoperazine (TFP), markedly inhibited both morphological transforming and mitogenic activities of glia maturation factor (GMF) on rat fetal glioblasts in culture. In the presence of W/-7 (16.5 microM) or TFP (9 microM) the formation of glial processes of glioblasts caused by GMF was decreased, and DNA synthesis (measured by the incorporation of [methyl-3H]thymidine into DNA was inhibited by 50% without changing cell viability. Kinetic analysis of dose-response experiments revealed a noncompetitive fashion of inhibition by W-7 and a mixed fashion by TFP. W-7 appeared to inhibit DNA synthesis at the G1 phase immediately before the beginning of the S phase. The results strongly suggest that calmodulin exerts a significant role on cell multiplication induced by the growth factor.

Animals↗

PubMed1982

Lymphocyte-conditioned medium protects human monocyte-macrophages from cholesteryl ester accumulation.

Exposure of human monocyte-macrophages to as little as 50 microliters of cultured medium from lymphocytes stimulated by concanavalin A (Con A) resulted in a dramatic decrease in the activities of the low density lipoprotein (LDL) receptor pathway, the LDL-dextran sulfate pathway, and the scavenger receptor pathway. This effect was not seen when the monocyte-macrophages were exposed to culture medium from lymphocytes cultured without Con A or with Con A together with alpha-methyl mannoside or control medium without lymphocytes. The activity of 3-hydroxy-3-methyglutaryl-coenzyme A reductase also decreased in monocyte-macrophages exposed to culture medium from stimulated lymphocytes. Acyl-CoA:cholesterol O-acyltransferase activity, protein synthesis, protein content, phagocytosis of heat-killed yeast, and non-receptor-mediated endocytosis were not inhibited. Monocyte-macrophages exposed to malondialdehyde altered-LDL in the presence of stimulated lymphocyte culture medium accumulated substantially less cholesteryl esters than did cells in control medium. We propose that substances produced by stimulated lymphocytes may be useful in protecting macrophages from cholesteryl ester accumulation.

Cells, Cultured↗

PubMed1982

Computed tomography in moyamoya disease.

Eighteen patients with moyamoya disease were examined by computed tomography (CT). At the first examination, CT findings were normal in one patient and abnormal in 17 patients. Significant abnormalities on precontrast CT were characterized by low density lesions in 14, ventricular dilatation in 9, and cerebral atrophy in 11 patients. Postcontrast CT showed the presence of contrast enhanced lesions in three patients. Follow-up examinations were performed in 13 patients, and the following changes on CT were found in 10 of them: increase or development of low density lesions in 10, ventricular dilatation in 4, cerebral atrophy in 5, appearance of a contrast enhanced lesion in 1, and disappearance of the enhanced lesion in 3. The patient with normal findings at the first examination showed a low density lesion on the second examination. The abnormal vascular networks in the region of the basal ganglia were visualized successfully in six examinations of five patients by higher concentration of contrast medium in blood than usual. Abnormal CT findings consisted of those seen in multiple cerebral infarctions and the visualization of the abnormal vascular networks. Computed tomographic findings on these patients showed evolution as seen in clinical and angiographic findings.

Adolescent↗

PubMed1982

Dynamics of contrast enhancement in delayed computed tomography of brain tumors: tissue-blood ratio and differential diagnosis.

Thirty-one patients with brain tumors were studied by delayed computed tomographic (CT) scanning performed one and two hours after intravenous administration of contrast medium. Dynamics of contrast enhancement in the lesion were analyzed quantitatively and qualitatively by calculating the tissue-blood ratio (TBR) at each scan, and are expressed as relative TBR (R-TBR). The R-TBRs obtained two hours after the first contrast-enhanced scan were found to be most useful in diagnosis, and were classified into three groups: less than 1.5 (Class I), 1.5 to 3.0 (Class II), and more than 3.0 (Class III). In the glioma group, seven of eight anaplastic gliomas were Class III and all of three anaplastic astrocytomas were Class II. All of seven meningiomas were Class I. Four of five pituitary adenomas were Class II. Three of four neurinomas were Class III. This method is potentially useful in differential diagnosis of some brain tumors.

Adenoma↗

PubMed1982