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Biomedical subjects

C Yamamoto

Publications and source records attributed to C Yamamoto.

At least 181 records · Page 10Linked to original sources
PubMed1992

Inhibitory effect of lead on the release of tissue plasminogen activator from human vascular endothelial cells in culture.

To evaluate the toxicity of lead on the blood fibrinolytic system, vascular endothelial cells from human umbilical vein were cultured in the presence of lead and the content of tissue plasminogen activator antigen (t-PA:Ag) released into the medium was determined by enzyme immunoassay. It was found that lead significantly decreased the t-PA:Ag release from the cells. Although heavy metals including cadmium, mercury, cobalt, manganese, nickel, zinc and copper as well as lead each had an inhibitory effect, lead was the potent inhibitor. Lead significantly disturbed thrombin up-regulation of t-PA:Ag release and significantly amplified endothelin-1 down-regulation of it. Incorporation of [3H]thymidine into the acid-insoluble fraction of the cell layer was significantly increased by lead; however, that of [14C]leucine was unchanged by the metal. In lead-treated cells, a significant accumulation of lead was observed but calcium content was increased slightly. From these results, it was suggested that lead decreased the release of t-PA:Ag from cultured endothelial cells without nonspecific inhibition of protein synthesis; lead may stimulate the calcium-dependent down-regulation of endothelial cell t-PA:Ag release by calcium or by mimicking calcium.

Calcium↗
PubMed1992

Stabilization of the adenylate energy charge in erythrocytes of rats and humans at high altitude hypoxia.

1. Stabilization of adenylate energy charge and control of adenylate pool were analysed in the erythrocytes of the rat and the human exposed to highly hypoxic conditions. 2. Red cell energy charge was decreased in the rats exposed to a simulated altitude of 5000-8000 m, and then recovered to the normal value with the depletion of adenylate pool. 3. The energy charge and the adenylate pool size of the human erythrocytes did not show any change under highly hypoxic conditions. 4. Anaerobic incubation of rat erythrocytes caused a marked decrease in the energy charge, and its recovery was accompanied by the depletion of total adenylates. 5. The energy charge and total adenylates of human red cells did not change under the anaerobic incubation of erythrocytes. 6. These results suggest that the energy charge of rat erythrocytes can be controlled by depletion of the adenylate pool, but the adenylate degradation is not responsible for the stabilization of the energy charge in human erythrocytes.

Adenosine Diphosphate↗
PubMed1992

Reversibility of the inhibitory effect of rhodamine B on the proliferation of cultured human lip fibroblasts.

To investigate the reversibility of rhodamine B inhibition of cell proliferation, human lip fibroblast KD cells were cultured for 3 days in the presence of 25 or 50 micrograms/ml of the dye and the effect of removal of the dye from the culture medium on cell histology and on incorporation of [3H]thymidine into the acid-insoluble fraction of the cell layer was investigated. Removal of rhodamine B on the last 1 or 2 days resulted in an increase in cell number, and incorporation of [3H]thymidine was also restored after removal of the dye; [3H]thymidine incorporation by the cells treated with the dye for only the 1st day was the same as that by the control cells cultured without the dye. In conclusion, it was shown that the decrease in KD cell proliferation caused by rhodamine B can be reversed by removal of the dye.

Cell Division↗
PubMed1992

Rhodamine B inhibits collagen synthesis by human lip fibroblasts in culture.

To investigate the effect of the cosmetic dye, rhodamine B, on the metabolism of collagen in fibroblasts, confluent KD cells, an established cell line of fibroblasts from human lip, were cultured for 6 h in a serum-free medium in the presence of the dye at 100 micrograms/ml and below. It was found that rhodamine B significantly decreased the content of procollagen type I C-terminal peptide antigen in both the cell layer and the medium with an only slight decrease in the cell number. Rhodamine B significantly decreased the incorporation of [3H]proline into either the collagen-digestible protein or the non-collagen protein in the cell layer. The incorporation of both [3H]thymidine and [14C]leucine into the acid-insoluble fraction of the cell layer was significantly decreased by rhodamine B; the activity of lactate dehydrogenase that leaked into the medium was not changed by the dye. From these results, it was suggested that rhodamine B has the capacity of decreasing the collagen content of the fibroblast cell layer of the human lip, which may result from a non-specific inhibition of protein synthesis without non-specific cell damage. Rhodamine B may impair the formation of extracellular matrix which is important for the maintenance of the lip tissue.

Cell Count↗
PubMed1992

Protective effect of copper against cadmium cytotoxicity on cultured vascular endothelial cells.

We investigated the effect of copper on cadmium-induced cytotoxicity on vascular endothelial cells from bovine aorta in a culture system. Cytotoxicity was evaluated by the [3H]adenine release assay and the histological observation. After a 24-h incubation, cadmium exhibited a significant cytotoxicity on confluent cultures of endothelial cells in a dose-dependent manner, while copper only slightly did after a 24-h incubation. It was found that copper (5 microM) significantly decreased cadmium (1 and 2 microM) cytotoxicity; histologically, formation of de-endothelialized areas in the cell layer caused by cadmium was reduced by copper. The accumulation of cadmium in the cell layer was significantly decreased by copper; however, that of copper was unaffected by cadmium. It was therefore suggested that copper significantly protects cadmium-induced cytotoxicity on cultured endothelial cells primarily through decreasing the cellular cadmium accumulation.

Animals↗
PubMed1992

Endothelin modulation of tissue plasminogen activator release from human vascular endothelial cells in culture.

To clarify a possible involvement of the vasoconstrictive peptide endothelin in the regulation of endothelial cell-mediated fibrinolytic system, confluent cultures of vascular endothelial cells from human umbilical vein were incubated in serum-free medium in the presence of endothelin-1 at 100 nM and below, and tissue plasminogen activator antigen (t-PA:Ag) in the medium was determined by enzyme immunoassay. Endothelin-1 at 1 nM and above significantly decreased the release of t-PA:Ag from the endothelial cells after a 24 h incubation. The t-PA:Ag release was also decreased by either endothelin-2 or endothelin-3 at 10 nM. The activity of lactate dehydrogenase in the medium was not changed by endothelin-1 at 100 nM and below, suggesting that the peptide did not cause nonspecific cell damage. The decrease in the t-PA:Ag release induced by endothelin-1 occurred in the presence or absence of 8-bromo cyclic AMP, which is an active congener of cyclic AMP; 3-isobutyl-1-methylxanthine, which is an inhibitor of phosphodiesterase; and forskolin, which is a stimulator of adenylate cyclase. These results strongly indicated that cyclic AMP which is known to down-regulate t-PA:Ag release was not involved in the endothelin-1 effect. However, endothelin-1 failed to decrease the t-PA:Ag release in the presence of either calcium ionophore A23187 or EGTA; the ionophore itself markedly decreased the release. The cytosolic calcium accumulation was significantly increased by endothelin-1. These results suggest that endothelin-1 decreases the release of t-PA:Ag from human endothelial cells through an excess accumulation of intracellular, especially cytosolic which would be mediated by an extracellular, calcium-dependent mechanism.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Disodium cromoglycate in the treatment of bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD) has become the most common form of chronic lung disease in the neonate. Recently, we have experienced a severe case of BPD and examined the effect of disodium cromoglycate (DSCG) on BPD. The gestational age and birthweight of the patient were 27 weeks and 1,000 g, respectively. Although RDS subsided after surfactant replacement therapy, the arterial-alveolar oxygen tension ratio (a/APO2) gradually decreased and FiO2 increased with age, respectively, and pure oxygen supplementation was eventually required after 67 days of life. The DSCG treatment was commenced at 80 days of life. After 6 days of the inhalation therapy, a/APO2 gradually increased. After 10 days of the treatment, the baby was extubated. While the baby was intubated, intratracheal lavage fluid samples were obtained. Eosinophilic cationic protein (ECP) and polymorphonuclear (PMN) elastase concentrations were determined. ECP and PMN elastase concentrations of intratracheal lavage fluids gradually decreased with the DSCG treatment. These results may indicate that DSCG has led to an improvement of pulmonary function and facilitated weaning from mechanical ventilation in an infant with BPD.

Bronchoalveolar Lavage Fluid↗
PubMed1992

Phagocytosis of polymorphonuclear leukocytes by guinea pig peritoneal macrophages: effects of serum and temperature in vitro.

The regulation of phagocytosis of neutrophils by peritoneal macrophages was studied in vitro. Peritoneal exudate cells (PECs) of guinea pigs were lavaged 15 h after the i.p. injection of thioglycollate medium and were cultured in chamber-slides. When PECs were cultured in RPMI 1640 medium in the absence of serum, approximately 20% of the macrophages phagocytized autologous neutrophils during 48-72 h of culture. Addition of guinea pig serum to the culture (2.5-20% v/v) suppressed the extent of the phagocytosis. The suppression was induced by globulin-rich ammonium sulfate fractions of the serum. Sera from rat, mouse, hamster, horse or calf also suppressed the phagocytosis, but fetal bovine serum (FBS) supported the phagocytosis, which was inhibited by globulin-rich Cohn fractions of bovine serum. The rate of neutrophil-phagocytosing macrophages was proportional to the rate of the pyknotic change of neutrophils. At a high temperature (42 degrees C), the autophagocytosis took place at 12 h of culture when fresh, but not heat-inactivated, autologous serum was added, implying that complement components may play a role in the hyperthermia-induced phagocytosis of neutrophils by macrophages. At 42 degrees C, ingested neutrophils did not show the pyknotic changes, indicating that intact neutrophils were ingested by macrophages.

Animals↗
PubMed1992

Modification of water and electrolyte metabolism during head-down tilting by hypoglycemia in men.

The effect of hypoglycemic stress on the changes in water and electrolyte metabolism induced by head-down tilting (HDT) was studied. Six healthy men were subjected to postural changes (30 min standing, 2 h HDT, 1 h standing), with or without the intravenous administration of insulin at the beginning of HDT. When insulin was not given, antidiuretic hormone (ADH), cortisol, plasma renin activity (PRA), aldosterone, and catecholamine levels were decreased and atrial natriuretic polypeptide (ANP) levels increased during HDT. These changes were associated with 2.5- and 1.5-fold increases in urine flow and sodium excretion, respectively, when compared with the amounts before HDT. On the other hand, insulin-induced hypoglycemia during HDT produced increases in ADH, cortisol, PRA, aldosterone, and catecholamine levels. At the same time, an exaggerated ANP response by HDT was observed. These hormonal changes were associated with an abolishment of the increases in urine flow and sodium excretion. It is suggested that acute stress modifies the changes in fluid and electrolyte metabolism induced by HDT.

Adult↗
PubMed1992

[Glutamic acid as an excitatory neurotransmitter].

The role of L-glutamic acid (Glu) as an excitatory neurotransmitter is reviewed. The idea that Glu is a main excitatory transmitter in the central nervous system (CNS) is now well supported by several lines of evidence, including its excitatory action, presence in the CNS, release, uptake mechanisms and suppression of synaptic transmission by its antagonists. Receptors for Glu are classified into ionotropic and metabotropic receptors. The former is further classified into non-NMDA and NMDA subgroups. The non-NMDA receptor mediates signal transduction between central neurons. Activation of the NMDA receptor causes an increase in intracellular calcium concentration in the postsynaptic neuron and thereby induces plastic changes such as, memory and learning. The function of the metabotropic receptor is yet to be elucidated.

Calcium↗
PubMed1991

Specific inhibition of cytoplasmic protein tyrosine kinases by herbimycin A in vitro.

Herbimycin A is an antibiotic which reverses transformation caused by various src related oncogenes. The reversion of transformation is restricted to cells transformed by tyrosine kinase coding oncogenes, and accompanies a decrease in kinase activity of the oncogene products. We have shown in vitro that herbimycin A directly inactivates p60v-src kinase by conjugating with SH group(s) of the kinase, raising the possibility that the molecular target of the antibiotic for reversion of v-src transformation is the p60v-src itself. To investigate the relevance of its in vitro tyrosine kinase inactivating activity to in vivo transformation reversing activity, we examined the specificity of herbimycin A for inhibition of cAMP-dependent kinase, protein kinase C and p210bcr-abl tyrosine kinase in vitro. Herbimycin A had no inhibitory effect on the activities of cAMP-dependent kinase or protein kinase C, whereas the SH-reagent N-(9-acridinyl)maleimide, which inactivates p60v-crc in vitro by a mechanism similar to that of herbimycin A, blocked the two serine/threonine kinases. On the other hand, the activity of p210bcr-abl tyrosine kinase was inhibited by herbimycin A treatment. The results indicate that herbimycin A specifically binds to reactive SH group(s) of cytoplasmic protein tyrosine kinases, and confer the biochemical basis for its selectivity in reversing cell transformation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Persistent enhancement of transmitter release accompanying long-term potentiation in the guinea pig hippocampus.

In order to examine temporal changes in enhancement of transmitter release during long-term potentiation (LTP), we examined amplitude fluctuation of excitatory postsynaptic potentials (EPSPs) for longer periods than 2 h after tetanic stimulation (up to 4 h in the longest observation). The relative magnitude of excitatory postsynaptic potentiation (EPSP) fluctuation (coefficient of variation, CV) reduced throughout the observation periods in association with an increase in EPSP amplitude after tetanic stimulation. The reciprocals of squared CVs (= mean2/variance) were almost in proportion to the magnitude of LTP, and the ratio of 1/CV2 and the LTP magnitude did not change significantly for up to 4 h. These findings suggest that a prolonged enhancement of transmitter release from presynaptic terminals underlies LTP, and the relative contribution of this presynaptic enhancement does not change significantly for 2 h (maybe up to 4 h, or longer) after tetanic stimulation.

Animals↗
PubMed1991

Enhancement of transmitter release accompanying with long-term potentiation in synapses between mossy fibers and CA3 neurons in hippocampus.

This study was performed to answer the question whether long-term potentiation (LTP) in mossy fiber-CA3 synapses is accompanied by an enhanced release of transmitter. For this purpose, the relative magnitude of amplitude fluctuation (coefficient of variation, CV) of excitatory postsynaptic potentials (EPSPs) and the probability of transmission failures were examined in thin hippocampal sections from the guinea pig before and after tetanic stimulation of mossy fibers or alteration of Ca2+ concentration. The values of CV were reduced in association with increases in EPSP amplitude after tetanic stimulation or at high Ca2+ concentration. The probability of failures decreased after tetanic stimulation. These findings indicate an enhancement of release of transmitter from mossy fiber terminals after induction of LTP.

Animals↗
PubMed1991

Quantal components of the synaptic potential induced in hippocampal neurons by activation of granule cells, and the effect of 2-amino-4-phosphonobutyric acid.

The probabilistic nature of excitatory postsynaptic potentials (EPSPs) induced monosynaptically in CA3 neurons by impulses of granule cells was studied in thin transverse sections of the guinea pig hippocampus. More than 600 EPSPs were recorded under several conditions, their amplitudes were measured, and histograms representing the EPSP amplitude distribution were constructed. Quantal parameters were estimated by the method of maximum likelihood. Of 9 neurons examined in the control solution, one neuron showed an exceptionally large number of transmission failures. The amplitude distribution of EPSPs recorded from this neuron could be described by Pascal statistics, but not by binomial or Poisson statistics. The EPSP amplitude distribution from the other neurons could be described by either binomial, Poisson, or Pascal predictions with a minor preference for the last statistic. When an apparently homogeneous group of data was divided into two subgroups and parameters were estimated separately, inconsistent values were obtained in some neurons with no failures. 2-Amino-4-phosphonobutyric acid (APB) suppressed the EPSPs reversibly at relatively low concentrations. Theoretical curves calculated according to the Pascal statistics fit quite well to the entire amplitude distribution of EPSPs recorded under the action of APB. The suppression of EPSPs by APB was accompanied by a marked decrease in mean quantal content (m) with no significant reduction in mean quantal amplitude (q). A quantum induced an increase in membrane conductance of about 150 pS. These results suggest that the release probability of the mossy fiber terminal fluctuates temporally according to a gamma distribution, and that APB reduces the liberation of the transmitter from mossy fiber terminals, thereby suppressing transmission between mossy fibers and CA3 neurons.

Aminobutyrates↗