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Biomedical subjects

T Kihara

Publications and source records attributed to T Kihara.

At least 127 records · Page 7Linked to original sources
PubMed1991

Lysis of fresh human tumor cells by autologous peripheral blood lymphocytes and tumor-infiltrating lymphocytes activated by PSK.

The protein-bound polysaccharide PSK was tested for the ability to induce in vitro autologous tumor killing (ATK) activity in human cancer patients. Peripheral blood lymphocytes (PBL) and tumor-infiltrating lymphocytes (TIL) demonstrated various levels of cytotoxicity against autologous, freshly isolated tumor cells. When PBL and TIL were cultured overnight with PSK, ATK activity was induced in previously non-reactive cases and augmented in previously reactive samples. The PSK effect was observed with PSK concentrations of 10-100 micrograms/ml that could be obtained in the blood of cancer patients who received standard oral administration of PSK. The manifestation of PSK-induced ATK required active cell metabolism and RNA and protein syntheses, but not DNA synthesis of lymphocytes. PSK-induced enhancement of ATK was not abrogated by monoclonal antibodies (mAb) directed against interferon (IFN) alpha or IFN gamma. In addition, mAb that neutralized interleukin-2 (IL-2) or mAb reactive with alpha-chain or beta-chain of IL-2 receptors (IL-2R) had no effect on PSK-induced ATK activity. Supernatants from PSK-stimulated lymphocyte cultures did not induce ATK. Cell fractionation experiments revealed that CD3-CD16+ large granular lymphocytes (LGL) and/or CD3+CD16- T lymphocytes were responsible for both spontaneous and PSK-induced ATK. PSK-activated LGL, but not T lymphocytes expressed lysis of fresh allogeneic tumor cells. These results indicate that PSK activates PBL and TIL to exhibit ATK independently of IL-2/IL-2R systems.

Adult↗
PubMed1990

Ceruletide, a cholecystokinin-related peptide, attenuates haloperidol-induced increase in dopamine release from the rat striatum: an in vivo microdialysis study.

The effects of ceruletide diethylamine (CLT), a cholecystokinin (CCK)-related peptide, on the spontaneous and haloperidol (HPD)-induced release of striatal dopamine (DA) were investigated with the in vivo microdialysis method. The striatum was perfused with Ringer solution containing different concentrations of K+. (1) When the dialysis tube was perfused with 4 mM K(+)-containing Ringer solution, CLT exerted no influence on the spontaneous and HPD-induced release of DA. (2) Increasing the K+ concentration in the perfusate from 4 to 15 mM failed to change the spontaneous and HPD-induced DA release. In this perfusion condition, the HPD-induced increase in DA release was significantly attenuated by CLT. (3) Perfusion of the striatum with the 20 mM K+ significantly reduced both the spontaneous and HPD-induced output of DA. (4) Even under the condition of perfusing the dialysis tube with the 4 mM K+, CLT significantly decreased the HPD-stimulated DA release in rats given HPD alone for the first 7 days and with CLT for the last 3 days. (5) Sixty consecutive daily administrations of HPD alone markedly reduced HPD-induced DA release from the striatum perfused with the Ringer solution containing 4 mM K+. From these results, we suggest that CLT, under the appropriate depolarization, can facilitate or induce depolarization inactivation of the A9 DA cells and/or nigrostriatal DA terminals, and consequently, produce significant inhibition of HPD-induced DA release from the rat striatum.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Discontinuity of primary and secondary neural tube in spina bifida induced by retinoic acid in mice.

This report shows by light microscopy the appearance of secondary neurulation separated from primary neurulation and its developmental fate in the spinal cord of mice exposed to retinoic acid in utero. The embryos and fetuses were derived from pregnant mice (ICR strain) given 60, 40, or 0 mg/kg of retinoic acid in olive oil on day 8 of gestation orally and killed 1, 2, or 10 days later. Separation of the primary neural fold from the secondary neural tube was seen in 9- and 10-day-old embryos: the caudal part of the neuroepithelium of the primary neural fold was disarranged with non-closed posterior neuropore, and underneath it the secondary neural tissue extended caudally with abnormal notochord. At term, fetuses showed spina bifida, including myeloschisis, myelocele, and diplomyelia (diastematomyelia) with abnormal distribution of ganglionic cells. These cord lesions were located between the third lumbar and second coccygeal levels. The former two cord anomalies were associated with diplomyelia and split the dorsal and ventral portions of the spinal cord with an overlapping zone between the third lumbar and third sacral levels. These findings suggest that the separation from primary neurulation is due to the lesions in both primary neural folds and notochord induced by retinoic acid and that the spinal cord caudal to the third lumbar level originates from both neuroectoderm and mesenchyme-like cells while that caudal to the third sacral level originates from mesenchyme-like cells only.

Abnormalities, Drug-Induced↗
PubMed1990

Interleukin-2 production of T cells in atopic dermatitis.

Patients with atopic dermatitis (AD) were treated with Tranilast, Interleukin-2 (IL-2) (production of T cells in vitro) and blood histamine values, before and after Tranilast therapy, were measured, and the following results were obtained: 1) Compared with healthy controls, the IL-2 producing ability of T cells in patients with AD was increased. 2) After Tranilast therapy, IL-2 production of T cells in AD decreased in quantity to the control level. 3) Skin lesion severities of AD were correlated with the quantity of IL-2 production of T cells. 4) Serum histamine levels were not significantly different between AD patients and healthy controls, before or after Tranilast therapy.

Adult↗
PubMed1990

Effect of diphenylthiocarbazone (dithizone) on glutamate level in hippocampus preparation in vitro and in vivo.

To assess the functional interaction between Zn2+ and glutamate in hippocampus, diphenylthiocarbazone (dithizone), a Zn2+ chelator, was used to alter the glutamate level in hippocampus in vitro and in vivo. Dithizone at the concentration of 1 microM stimulated high K(+)- and veratrine-induced release of [3H]glutamate both in the presence and absence of Ca2+ from rat hippocampal slices preloaded with [3H]glutamate without affecting the release of [3H]gamma-aminobutyric acid and [3H]acetylcholine. Metal chelators other than dithizone did not evoke the [3H]glutamate release at the concentration of 10 microM. Two weeks after the intrahippocampal injection of 20 micrograms of dithizone, both Zn2+ and glutamate levels of the hippocampus significantly decreased with no change in the levels of other metals, amino acids, monoamines and acetylcholine.

Acetylcholine↗
PubMed1990

Inhibition of [3H]glutamate release by Zn2+ in rat hippocampal slices.

Zn2+ at the concentration of 10 microM inhibited the depolarization-induced [3H]glutamate release from the preloaded rat hippocampal slices both in the presence and absence of Ca2+ without affecting [3H]GABA and [3H]ACh release. Of divalent cations tested, Zn2+ and Fe2+ had an inhibitory effect on the release of glutamate.

Acetylcholine↗
PubMed1989

Excitatory amino acids enhance dissociation of zinc from soluble protein in cytosol of rat hippocampus.

An ultra-filtration method for separating free Zn from its bound form with macromolecules was used to study the effect of excitatory amino acids on dissociation of Zn in the soluble fraction of rat hippocampus. L-Glutamate, L-aspartate and L-cysteic acid but not D-glutamate significantly increased the dissociated Zn at the concentration of 100 microM. 2-Amino-5-phosphonovalerate did not inhibit the effect of L-glutamate. Likewise, the stimulatory effect of N-methyl-DL-aspartate and quisqualate was observed at the concentration range between 1 and 100 microM. The effect of kainate was much less potent. Taurine and GABA had no stimulatory effect on the dissociation of Zn.

Amino Acids↗
PubMed1989

Aberrant differentiation of neuroepithelial cells in developing mouse brains subsequent to retinoic acid exposure in utero.

All-trans-retinoic acid induced 2 types of disorganized neuroepithelium, localized and continuous, in the exencephaly of 9-day-old mouse embryos exposed to 60 or 40 mg/kg for 27 to 30 hr in utero. The localized effect appeared as a protuberance in the wall of the telencephalon and thick neural folds in the mesencephalon with the discontinuity of the apical terminal sheet. The continuous disorganization was seen from the olfactory placode to the myelencephalon with rosettes of cells and many dense bodies in the neuroepithelium. Ultrastructurally, cells in the localized disorganizations showed swelling of Golgi complexes, coated vesicles, and rough endoplasmic reticulum resulting in degeneration. The continuous disorganizations consisted of undifferentiated homogeneous cells in which the nuclei exhibited expansion of nucleolar granular portions and coagulated heterochromatin, and cytoplasm showed monosomal dispersion. In both types of disorganized neuroepithelium, junctional complexes were seen focally at the apical side or apical processes of the rosette, with few or no microfilament bundles. A layer of microfilaments at the base of the neuroepithelial cells in controls, just above the basal lamina, was not present in the monosome dispersed cytoplasm. In the neuroepithelium of controls, one phagosome was seen in the perinuclear region in 0.8% of the cells examined, whereas in the experimental neuroepithelium 2 or more phagosomes were seen in a cell, and phagocytosis occurred by pseudopods. These findings suggest that all-trans-retinoic acid induces not only cytotoxicity but also dedifferentiation in the neuroepithelial cells leading to more cell death, which activates the phagocytosis. These lesions in the neuroepithelium may be a cause of exencephaly.

Abnormalities, Drug-Induced↗
PubMed1989

Morphogenesis of the secondary palate in mouse embryos with special reference to the development of rugae.

Morphological studies of secondary palate formation, with special reference to the development of rugae, were carried out on Jcl:ICR mouse embryos. Three rugae were observed on the anterior part of the future oral surface of the vertically developing palatal shelves in 13-day embryos. Rugae increased in number as the development of the palatal shelves proceeded, and five to six prominent rugae were observed in 14-day embryos just prior to shelf elevation. The folding of these five to six rugae progressed in conjunction with the formation of a sharp, valley-like groove at the base of the anterior two-fifths of the vertical palatal shelves. As palatal shelves elevated, the groove disappeared gradually, and, accordingly, the folding of rugae loosened. In the groove region, the superficial epithelial cells were roundish, while the basal ones were elongated. Such characteristic features were no longer observed when the disappearance of the groove was completed. Eight rugae were observed on the future hard palate of 14-day embryos with already completed palatal fusion. An additional ruga was frequently found in 15-day embryos, and the pattern then was almost the same as that of an adult. Epithelial thickening and condensation at the rugae region, as well as mesenchymal condensation under the epithelium of the rugae, were confirmed in embryos both before and after elevation of the palatal shelves. There is a possibility that these structural characteristics observed in the epithelial and mesenchymal cells of the rugae and groove regions may be related to palatal shelf elevation.

Animals↗
PubMed1989

Dental radiography exposure of the Hiroshima and Nagasaki populations.

Dental radiography doses in Hiroshima and Nagasaki were estimated on the basis of survey data from dental hospitals and clinics in Hiroshima and Nagasaki, and doses were measured by thermoluminescent dosimeters and a phantom. Doses to organs, including the lens, pituitary fossa, thyroid gland, and skin were calculated from data obtained during a 2-week survey in both cities. The mean caput doses were calculated from the data indicating frequency per year and were tabulated by organs, age, teeth examined, type of examination, population, sex, and city. No significant difference was observed by age, population, sex, or city. Currently the doses incurred during dental radiography may not be sufficiently high to cause bias in the assessments for late radiation effects among atomic-bomb survivors. However, the mean caput thyroid doses of 62 mrad and 67 mrad in Hiroshima and Nagasaki, respectively, cannot be ignored from the standpoint of their potential in contributing to radiation-induced carcinogenesis.

Adolescent↗
PubMed1989

Flow cytometric analysis of murine splenic cells after DNFB painting on Langerhans cell deficient skin.

One week after a single painting of 50 microliters of 0.5% DNFB in acetone-olive oil on the tail skin of C3H mice, the spleens were removed from the animals. A single cell suspension was prepared from the spleens, and flow cytometric analysis was performed for L3T4 and Lyt2 positive cells, as well as for the IJk expression of the Lyt2+ cells. Results showed that the percentages and absolute numbers of Lyt2+ L3T4- cells, Lyt2- L3T4+ cells, Lyt2+ IJk+ cells, and Lyt2+ IJk- cells in the spleens of the DNFB-treated mice were not significantly different from those in the non-treated mice. However, in the treated mice, the IJk expression of Lyt2+ cells intensified. These results indicate that, following a single painting of DNFB onto Langerhans cell-deficient skin, the numbers of Lyt2+ cells do not change significantly, but do change functionally.

Animals↗
PubMed1989

Effect of yohimbine on urethane-induced hyperglycemia in rats.

Urethane is a widely used anesthetic and yohimbine is a well-known alpha 2-adrenergic antagonist. In fasted Wistar rats urethane at an anesthetic dose (1.25 g/kg, i.p.) caused an increase in plasma glucose, while pentobarbital at an anesthetic dose (40 mg/kg, i.p.) did not. Urethane caused no change in plasma glucose in adrenalectomized rats. The hyperglycemic effect of urethane was not inhibited by pretreatment with propranolol (1 mg/kg, p.o.) or prazosin (10 mg/kg, p.o.), but was reduced by pretreatment with phentolamine (10 mg/kg, p.o.) or yohimbine (10 mg/kg, p.o.). Urethane caused an elevation of plasma adrenaline, and yohimbine reduced the elevation. In addition, the pretreatment of yohimbine potentiated the urethane-induced increase in plasma insulin. These results indicate that yohimbine may inhibit the urethane-induced hyperglycemia that is mediated by the central and peripheral alpha 2-adrenergic systems.

Animals↗
PubMed1989

Adrenergic function and the development of analgesic tolerance to morphine.

Whether or not the suppressive effect of alpha- and beta-adrenergic blockers, phentolamine and propranolol, on the development of tolerance to morphine could be substituted for each other was investigated in mice. Daily co-administration of either one of the blockers with morphine suppressed the development of analgesic tolerance to morphine as far as the treatment was continued without affecting the analgesic effect per se; however, the suppressive effect was lost from the day of the substitution for the other blocker and tolerance developed as rapidly as in the control group treated with morphine alone. Co-administration of both blockers with morphine also maintained the analgesic effect on the 1st day for 10 days, but when the administration of either one or both blockers was eliminated from the 6th day, the development of tolerance was initiated. These results suggest that the mechanisms of alpha- and beta-blockers for the suppression of the development of analgesic tolerance to morphine are different from each other and that adrenergic blockers may produce a specific alteration in the mechanism for the development of tolerance to morphine.

Analgesics↗
PubMed1989

Biosynthesis and 13C NMR assignment of cytovaricin, a neutral macrolide antibiotic.

13C NMR analysis of 13C-labeled cytovaricin which was obtained by feeding sodium [1-13C]-, [2-13C]-, and [1,2-13C]acetates, [1-13C]- and [3-13C]propionates, [1-13C]isobutyrate and [methyl-13C]methionine to cultures of Streptomyces diastatochromogenes showed that the aglycone of cytovaricin is derived from nine acetate units, six propionate units and one isobutyrate unit and the methoxy group at C-3' of cymarose moiety is derived from the methionine-S-methyl group. The 13C NMR spectra of 13C-labeled cytovaricins which were obtained from feeding experiments allowed the complete assignment of the 13C NMR spectrum of cytovaricin.

Anti-Bacterial Agents↗