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Biomedical subjects

S Ida

Publications and source records attributed to S Ida.

At least 109 records · Page 6Linked to original sources
PubMed1981

Alteration of GABA system in frog retina following short light and dark adaptations - a quantitative comparison with retinal taurine.

Effect of short light and dark adaptations on retinal GABA and taurine was studied using bull frog (Rana catesbiana). The retinal GABA was increased significantly in light-adapted state, and this increase was accompanied by the increases of L-glutamate decarboxylase (GAD) activity and [3H]-GABA release. The activation of retinal GABA-transaminase succinic semialdehyde dehydrogenase (GABA-T:SSADH) was also observed after a lag period of several hours. Under the same experimental conditions, however, no significant changes were noted in retinal taurine content and cysteine sulfinate decarboxylase (CSD) activity. These findings suggest that a short light adaptation induces differential effects on retinal GABA and taurine, and the activation of GABAergic neurons in the retina may be involved in the process of short light adaptation.

Adaptation, Ocular↗
PubMed1981

Alteration of metabolism of retinal taurine following prolonged light and dark adaptation: a quantitative comparison with gamma-aminobutyric acid (GABA).

Alteration of metabolism of taurine in prolonged light- and dark-adapted frog retinae were studied in comparison with that of gamma-aminobutyric acid (GABA) and the following results were obtained. (1) Statistically significant alterations in retinal taurine, an increase in dark-adapted, and a decrease in light-adapted states, respectively, occurred when frogs were adapted continuously to light or dark for more than 3 weeks. Under the same experimental conditions, no alteration in retinal GABA was noted. (2) At 3 weeks and thereafter, a significant increase of retinal cysteine sulfinic acid decarboxylase (CSD; EC 4.1.1.12) activity, an enzyme involved in the biosynthetic pathway of taurine, also occurred in the dark, whereas the activity in the light-adapted retina was reduced. On the other hand, the retinal activity of L-glutamate decarboxylase (GAD; EC 1.1.1.15), the rate-limiting enzyme of GABA biosynthesis, was not altered in dark- as well as light-adapted state. Similarly, retinal GABA-transaminase (GABA-T; EC 2.6.1.19)-succinic semialdehyde dehydrogenase (SSADH; EC 1.2.1.16) was unaltered. (3) These alterations in retinal taurine were, however, unaccompanied by any changes in factors related to transmitter actions such as evoked release, high affinity uptake, and specific binding to synaptic membranes. The above results suggest that, different from GABA as a potent candidate for inhibitory neurotransmitter, retinal taurine may act as neuromodulator and/or may play an important role as a basic factor for maintaining cellular integrity under certain pathophysiological conditions.

4-Aminobutyrate Transaminase↗
PubMed1981

[Effect of Bromovincamine on noradrenaline and 5-hydroxytryptamine contents, and glucose metabolism in rat brain: analysis using spontaneously hypertensive rats (SHR) (author's transl)].

Effects of Bromovincamine (BV) on cerebral noradrenaline (NA) and 5-hydroxytryptamine (5-HT) contents, and glucose metabolism in the brain were studied using stroke-prone spontaneously hypertensive (SHR-SP), stroke-resistant spontaneously hypertensive (SHR), age-matched normotensive Wistar Kyoto (WKR) and Wistar rats. In the SHR-SP which have a low level of NA in the hypothalamus, a continuous administration of BV for 1 week induced a normalization of the hypothalamic NA content. Under the same experimental conditions, a tendency toward normalization of hypothalamic NA was also observed in SHR. 5-HT contents in the cerebellum, striatum, hypothalamus, midbrain and hippocampus of SHR showed a significant increase following a single injection of BV. Similarly, 5-HT contents in the cerebellum and cerebral cortex of Wistar, WKR and SHR showed a significant increase following a continuous administration of BV for 1 week. Both in vitro and in vivo administration of BV significantly inhibited the high concentration of K+ evoked glucose consumption in cerebral cortical slices from SHR, WKR and Wistar rats, whereas glucose consumption in cerebral cortical slices from SHR determined in the absence of high concentration of K+ increased significantly following continuous in vivo administration of BV. The present results suggest that BV may be an useful drug for improving abnormal cerebral metabolisms of NA, 5-HT and glucose.

Animals↗
PubMed1980

Enhancement of IgE-mediated histamine release from human basophils by immune-specific lymphokines.

Human leucocytes (basophils) release histamine when exposed to ragweed antigen E or anti-IgE. The present study shows that when leucocytes from BCG-positive donors are first incubated with PPD and then challenged with anti-IgE, histamine release is enhanced. In contrast, when leucocytes from BCG-negative donors are incubated with PPD and then challenged with anti-IgE there is no enhancement of histamine release. The enhancement of histamine release was detected within 24 hr after addition of PPD, but was maximal at 48 to 72 hr. Supernatant fluids collected from these leucocyte cultures revealed the presence of a soluble mediator(s) which, when incubated with leucocytes from BCG-negative donors, enhanced the release of histamine. Examination of the supernatant fluids from BCG-positive leucocyte cultures stimulated with PPD showed a correlation between histamine-release enhancing activity and interferon. Treatment of the culture fluids at pH 2.0 abolished the anti-viral activity, indicating that the interferon was of the type II or 'immune' class. The same treatment only partly abolished the histamine-release enhancing activity. It is concluded that immune-specific stimulation of leucocytes results in the release of soluble mediators that are capable of enhancing IgE-mediated histamine release.

Adult↗
PubMed1979

Interferon-induced enhancement of IgE-mediated histamine release from human basophils requires RNA synthesis.

Incubation of human leukocytes with certain viruses results in the enhancement of IgE-mediated release of histamine. This enhancement is produced by interferon. The present experiments show that an induction period of 6 to 9 hr and new RNA synthesis are required for interferon to enhance histamine release. This points to the possibility that interferon may exert its antiviral and histamine-release enhancing activities by acting through a common pathway.

Allergens↗
PubMed1978

Excretion of porphyrins in urine and bile after the administration of delta-aminolevulinic acid.

Excretion of porphyrins into bile and urine after intravenous injection of delta-ALA was studied in three patients with catheters inserted into the bile duct because of biliary obstruction and in two healthy volunteers. Excretion of porphyrins into bile increased in response to increasing doses of delta-ALA--up to 18 mumol/kg. On the other hand, excretion into urine reached a constant rate at 2 to 4 mumol/kg delta-ALA and did not increase further with larger doses. These findings suggest that transport of porphyrins across the liver cell membrane to the blood must be an important factor in determining the rate of excretion into the urine. After administration of delta-ALA,excretion of coproporphyrin III into urine increased more than that of coproporphyrin I. As a result, the former was the predominant form of urinary coproporphyrin. When radioactive delta-ALA was administered intravenously, far greater radioactivity was recovered in urine as coproporphyrin III than as coproporphyrin I. These results indicate that only a small portion of urinary coproporphyrin I is derived from the liver. A possible source of coproporphyrin I may be erythropoietic tissues, since the amount of urinary coproporphyrin I was considerably decreased in patients with severely suppressed erythropoiesis.

Aminolevulinic Acid↗
PubMed1977

Enhancement of IgE-mediated histamine release from human basophils by viruses: role of interferon.

Human leukocytes maintained in culture are induced to release histamine when exposed to ragweed antigen E or anti-IgE. Leukocyte cultures incubated with virus (i.e. HSV-1, Influenza A, and Adeno-1) but not exposed to ragweed antigen E or anti-IgE fail to release histamine. If, however, leukocyte cultures are first exposed to virus and then to ragweed antigen E or anti-IgE, significant enhancement of histamine release occurs. Both infectious and inactivated virus enhance histamine release and the degree of enhancement is related to the concentration of virus and the length of the incubation. Tissue culture fluid harvested 8 h after exposure of leukocytes to virus contains a soluble factor which is capable of enhancing histamine release when added to fresh leukocyte cultures. This factor has all the properties of interferon including species specificity and cannot be dissociated from the antiviral activity of interferon. Moreover, both known inducers of interferon (poly I:poly C) and standard preparations of interferon are capable of enhancing histamine release. The enhancement of histamine release by interferon represents a new biological role for interferon.

Adenoviridae↗
PubMed1977

Purification to homogeneity of spinach nitrite reductase by ferredoxin-sepharose affinity chromatography.

Assimilatory nitrite reductase was purified 1,700-fold with a yield of 22% from spinach leaves with a procedure involving ammonium sulfate fractionation, DEAE-cellulose and DEAE-Sephadex chromatography, gel filtration and ferredoxin-Sepharose affinity chromatography. The purified enzyme was apparently homogeneous as shown by disc and SDS-gel electrophoresis with a specific activity (mumol NO2-reduced/min/mg protein) of 140.

Chromatography, Affinity↗