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Biomedical subjects

C Yamamoto

Publications and source records attributed to C Yamamoto.

At least 109 records · Page 6Linked to original sources
PubMed1996

[The clinical usefulness of the combined use of inhaled beta 2-agonist and inhaled steroid in asthma].

Treatment with inhaled steroid has become increasingly important in asthma. However there are also many patients with asthma whose symptoms are uncontrolled by beclomethasone dipropionate (BDP) alone. For these patients we have tried the regular use of inhaled procaterol or inhaled fenoterol with BDP, and some of these patients have got good control. Recent studies show that, in patients whose asthma is inadequately controlled with BDP, better control can be achieved by adding inhaled long-acting beta 2-agonist rather than by doubling the dose of BDP. In the near future inhaled long-acting beta 2-agonist will be possible for clinical use in our country, and the combined use of it and BDP as preventive therapy will be the mainstay of treatment for patients with moderate-to-severe asthma.

Adrenergic beta-Agonists↗
PubMed1996

Gene expressions of basic fibroblast growth factor and its receptor in healing of rat retina after laser photocoagulation.

Basic fibroblast growth factor (bFGF) stimulates the mitogenesis of various cells and plays a key role in wound repair. Using in situ hybridization, we studied mRNA expressions of bFGF and one of its receptors, FGF receptor 1 (FGFR1), during wound repair of the rat retina after laser photocoagulation. Gene expressions of bFGF and FGFR1 were detected in the ganglion cell and inner nuclear layers of the normal adult rat retina. On day 3 following laser photocoagulation, proliferating retinal pigment epithelial (RPE) cells of the lesion showed intense gene expressions of bFGF and FGFR1. Macrophage-like cells that migrated into the lesion also showed gene expression of bFGF. These gene expressions decreased over time. The finding of elevated gene expressions of bFGF and FGFR1 after laser photocoagulation suggests the bFGF may be a factor in retinal wound repair.

Animals↗
PubMed1996

[Clinical benefit of nutritional assessment and support in patients with chronic obstructive pulmonary disease].

Weight loss is common in patients with chronic obstructive pulmonary disease (COPD). Comprehensive nutritional assessment was conducted in two large groups of patients with COPD who were enrolled in the Respiratory Failure Research Program sponsored by the Japanese Ministry of Health and Welfare and the Kinki COPD Research Group. The incidences of mild malnutrition (%IBW < 90%) were 74% and 62%, respectively. The incidences of hypoalbuminemia were low: 10.0% and 6.5%, respectively. The incidence of imbalance in plasma amino acids, which was defined as an abnormally low BCAA/AAA ratio, was as high as 93% in patients with COPD and chronic respiratory failure. The %IBW was significantly related to the FEV1 and to the DLco/VA. The moderately-malnourished subpopulation was characterized by a greater degree of hyperinflation and hypercapnea: the measured resting energy expenditure (REE) was significantly higher than the values in age-matched healthy controls. REE/REEpred was significantly and inversely related to BCAA/AAA and to Pimax. REE was inversely related to FEV1%. REE in the subgroup with severe hyperinflation was significantly higher than REE in those with milder hyperinflation. Among patients with an FEV1% of less than 50%, mortality tended to be higher in those with lower body weight, and this relationship was stronger in patients with an FEV1% of more than 50%. When patients were given a BCAA-enriched enteral formula in addition to their usual diet for 3 months, there was a significant increase in body weight, transferrin level, and Pimax.

Amino Acids, Branched-Chain↗
PubMed1995

Effects of metabotropic glutamate receptor agonists on excitatory and inhibitory transmissions in cultured rat hippocampal neurons.

Effects of the metabotropic glutamate receptor agonist, trans-ACPD (tACPD), on the excitatory and the inhibitory transmissions were examined with cultured rat hippocampal neurons, by recording monosynaptic excitatory (EPSCs) and inhibitory postsynaptic currents (IPSCs) evoked by electrical stimulation of single presynaptic neurons. EPSCs were suppressed reversibly by application of 100 microM tACPD in almost all the tested neuron pairs with excitatory connections. Effects of tACPD on IPSCs were variable. Application of tACPD did not affect IPSCs in 15 pairs, suppressed them in eight pairs and enhanced them in the remaining eight pairs out of 31 neuron pairs with inhibitory connections. The study demonstrated that in the hippocampus the activation of metabotropic glutamate receptors modulated the inhibitory transmission differently at different synapses, whereas it always suppressed the excitatory transmission.

Animals↗
PubMed1995

Stimulatory effect of lead on the proliferation of cultured vascular smooth-muscle cells.

The effect of lead nitrate on the DNA synthesis of cultured bovine aortic smooth-muscle cells has been studied. Lead at 0.5-10 microM stimulated the incorporation of [3H]thymidine into the acid-insoluble fraction of the cells in a dose-dependent manner. However, other heavy metals including zinc, copper, manganese and nickel did not show such a stimulatory effect. Stimulation of [3H]thymidine incorporation by basic fibroblast growth factor was additive to that by lead. However, stimulation by either platelet-derived growth factor or acidic fibroblast growth factor was reduced by the metal. The leakage of lactate dehydrogenase into the medium from smooth-muscle cells, a marker of cell death, was not changed by the metal. Calcium ionophore A23187 inhibited [3H]thymidine incorporation in vascular endothelial cells but stimulated it in vascular smooth-muscle cells. These results suggest that lead may stimulate the proliferation of cultured vascular smooth-muscle cells probably via a calcium-dependent pathway; the metal may mimic calcium within the cells.

Animals↗
PubMed1995

Baclofen inhibits GABAergic transmission after treatment with type-specific calcium channel blockers in cultured rat hippocampal neurons.

Effects of the GABAB agonist baclofen on GABAergic transmission were examined before and after treatment with N-type (CgTX) and P-type (AGTX) Ca2+ channel blockers in cultured rat hippocampal neurons. Baclofen reduced GABAergic synaptic currents (IPSCs) without affecting the postsynaptic sensitivity to GABA. The presynaptic inhibition by baclofen was not blocked by Ba2+, a K+ channel blocker. IPSCs were reduced by treatment with either CgTX or AGTX, and completely abolished by treatment with both toxins. Both IPSCs after treatment with CgTX and those after AGTX treatment were similarly reduced by baclofen. The results indicate that both the transmission mediated by AGTX-sensitive Ca2+ channels and that by CgTX-sensitive Ca2+ channels are sensitive to baclofen, suggesting that activation of presynaptic GABAB receptors might inhibit both types of Ca2+ channels contributing to the GABAergic transmission in the hippocampus.

Animals↗
PubMed1995

Inhibitory effect of lead on the proliferation of cultured vascular endothelial cells.

We investigated the effect of lead nitrate (0.5, 1.0, 2.0 or 5.0 microM) on the proliferation of cultured bovine aortic endothelial cells. After exposure to lead, the number of cells and the incorporation of [3H]thymidine into the acid-insoluble fraction of the cells were reduced in parallel in a concentration-dependent manner. Histologically, lead treatment resulted in a decrease in the cell number accompanied by a change in the cell shape from polygonal to spindle; however, no degenerative change was observed except in 5.0 microM lead-treated cells. Furthermore, stimulation of [3H]thymidine incorporation by either basic or acidic fibroblast growth factor was significantly reduced by lead. However, the leakage of lactate dehydrogenase into the medium from the cells, a marker of nonspecific cell damage, was not changed by lead. From these results, it was revealed that lead inhibits the proliferation of cultured vascular endothelial cells without nonspecific cell damage. Although lead does not destroy the monolayer of endothelial cells, the metal may exhibit its noxious effect in the repair process of the vascular endothelium.

Animals↗
PubMed1995

Regulation by basic fibroblast growth factor of glycosaminoglycan biosynthesis in cultured vascular endothelial cells.

The alteration of glycosaminoglycans (GAGs) in cultured bovine aortic endothelial cells after exposure to basic fibroblast growth factor (bFGF) was investigated. It was found that the incorporation of [3H]glucosamine into GAGs was markedly increased by bFGF in both the cell layer and the conditioned medium; however, that of [35S]sulfate was not changed by the growth factor. These results indicated that bFGF enhanced the sugar-chain formation but did not affect their sulfation in endothelial GAG production. Similar changes were observed in either bovine aortic smooth-muscle cells and human fibroblastic IMR-90 cells to greater and lesser degrees, respectively. Characterization of GAGs in the endothelial cell layer and the conditioned medium revealed that bFGF enhanced both heparan sulfate and the other GAGs to a similar degree. The present data suggest that bFGF may be involved in the regulation of the blood coagulation system via altering GAGs of the vascular tissue when the endothelium was damaged.

Animals↗
PubMed1995

Severe damage of cultured vascular endothelial cell monolayer after simultaneous exposure to cadmium and lead.

This study evaluates the toxicity of lead in the presence or absence of cadmium on the maintenance of a monolayer of cultured bovine aortic endothelial cells. It was histologically shown that lead at 50 microM or less induced a slight formation of de-endothelialized areas on the monolayer after a 24-h incubation. Although lead accumulated in endothelial cells in a dose-dependent manner, the cytotoxicity (evaluated by the [3H]adenine release assay) was not detected. However, cadmium (1.0 or 2.0 microM)-induced de-endothelialized areas on the monolayer was considerably larger in the presence of lead at 10 microM; the cytotoxicity of cadmium was significantly enhanced by lead. It was concluded that vascular endothelial cell monolayer is severely destroyed by a greater cytotoxicity of combination of cadmium with lead.

Animals↗
PubMed1995

Zinc-induced tolerance to cadmium cytotoxicity without metallothionein induction in cultured bovine aortic endothelial cells.

We investigated the cytotoxicity of cadmium in cultured vascular endothelial cells from bovine aorta pretreated with zinc. The cytotoxicity was evaluated by the [3H]adenine release assay. It was shown that the increase in the [3H]adenine release after challenge with cadmium was significantly prevented by pretreatment with zinc. It was histologically observed that cadmium-induced occurrence of the de-endothelialized areas was reduced in zinc-pretreated cell layer. Intracellular accumulation of cadmium was significantly less but that of zinc was more in zinc-pretreated cells. The content of cadmium in both the particulate and the cytosol fraction was decreased by zinc pretreatment; however, metallothionein content after challenge with cadmium was not changed. It was therefore concluded that zinc is capable of inducing a tolerance to cadmium cytotoxicity in cultured vascular endothelial cells; this tolerance is postulated to be due to a decrease in the intracellular cadmium accumulation rather than a metallothionein induction.

Adenine↗
PubMed1995

Effect of galactosamine-induced hepatitis on the aerobic and anaerobic metabolism of the rat exposed to high-altitude hypoxia.

Galactosamine-induced hepatitis caused a marked increase in plasma lactate and pyruvate, but completely abolished the increase in ketone bodies in the rat exposed to an 8000 m simulated altitude. Plasma free fatty acid as the precursor of ketone bodies was higher in the galactosamine-treated rats during and after an exposure to 8000 m altitude. Treatment of the rat with galactosamine markedly reduced activities of citrate synthase, fumarase, glutamate dehydrogenase and fructose 1,6-bisphosphatase, but increased hexokinase and glucose 6-phosphate dehydrogenase in the liver. The effect of galactosamine-induced hepatitis on the energy metabolism can be explained by a reduction of mitochondrial oxidative enzymes and gluconeogenesis, and involves a shift of the aerobic metabolism to anaerobic glycolysis at high altitude.

Aerobiosis↗
PubMed1995

Temperature effects on Legionella pneumophila killing by and multiplication in phagocytes of guinea pigs.

We examined the effects of temperature on the interaction between Legionella pneumophila and phagocytes of guinea pigs. The body temperatures of guinea pigs infected with a sublethal dose (1.2 x 10(4) CFU) or a lethal dose (1.0 x 10(5) CFU) of L. pneumophila elevated from 38.4 +/- 0.15 C to 40.2 +/- 0.42 C or 40.3 +/- 0.62 C, respectively. The intracellular bacterial killing by and bacterial proliferation in the phagocytes were examined at 33, 37, 40, and 42 C, using in vitro culture systems of peritoneal macrophages or polymorphonuclear leukocytes (PMN) of guinea pigs. In all the macrophages incubated at different temperatures, significant intracellular bacterial killings were observed at 4 hr after in vitro phagocytosis. After 24 hr of incubation, there was about a 100-fold increase of CFU and the number reached a maximum after 48 hr of incubation in the macrophages incubated at 42 C as well as 37 and 40 C, suggesting that macrophages support the intracellular bacterial growth in hyperthermia. In the PMN, L. pneumophila CFU 4 hr or 12 hr after the infection were significantly lower at 42 C than those at 37 C (P < 0.05), indicating that the bactericidal capacity of PMN was enhanced at 42 C compared to 37 C. However, in all the PMN incubated at different temperatures, there were about 10-fold increases of CFU 24 hr after the infection, suggesting that PMN as well as macrophages support intracellular bacterial growth in hyperthermia. The extracellular bacterial growth was examined at 33, 37, 40, and 42 C in buffered yeast extract (BYE) broth or RPMI 1640 medium containing 50% guinea pig serum as a permissive or non-permissive liquid medium for the bacterial growth, respectively. Inhibition of bacterial growth in BYE broth at 42 C, and a decrease of CFU in RPMI 1640 medium containing 50% guinea pig serum at 42 C were observed. In conclusion, hyperthermia may be beneficial by restricting extracellular bacterial survival, but it exerts no beneficial effect on the restriction of intracellular bacterial growth in phagocytes, though PMN showed enhanced initial killing at 42 C. These results suggest that fever, or hyperthermia itself, may not largely contribute as a nonspecific host defense early in the course of legionellosis.

Animals↗
PubMed1995

Comparison of full-length sequences of interferon-sensitive and resistant hepatitis C virus 1b. Sensitivity to interferon is conferred by amino acid substitutions in the NS5A region.

We have previously demonstrated that sensitivity to interferon is different among hepatitis C virus (HCV) quasispecies simultaneously detected in same individuals and that interferon-resistant HCV quasispecies are selected during the treatment. To determine the genetic basis of their resistance to interferon, HCV genotype-1b was obtained from serum of three patients before and during interferon therapy, and their full-length nucleotide and deduced amino acid sequences were determined. Comparison of the pairs of interferon-resistant and interferon-sensitive HCV isolates in respective individuals demonstrated clusters of amino acid differences in the COOH-terminal half of the NS5A region (codon 2154-2383), which contained a common unique amino acid difference at codon 2218. Additional sequence data of the COOH-terminal half of the NS5A region obtained from six interferon-resistant and nine interferon-sensitive HCV confirmed the exclusive existence of missense mutations in a 40 amino acid stretch of the NS5A region around codon 2218 (from codon 2209 to 2248) in interferon-sensitive HCV. On the other hand, this region of interferon-resistant HCV was identical to that of prototype HCV genotype-1b (HCV-J, HCV-JTa, or HC-J4). We designated this region as the interferon sensitivity determining region. Thus, HCV genotype-1b with the prototype interferon sensitivity determining region appears to be interferon-resistant strains. The specific nature of these mutations might make it possible to predict prognostic effects of interferon treatment.

Adult↗
PubMed1995

Stimulation of cultured vascular smooth muscle cell proliferation by thrombospondin is potentiated by zinc.

The interaction of zinc sulfate with thrombospondin (TSP) derived from bovine platelets, on the proliferation of bovine aortic smooth muscle cells was investigated using cell culture. Zinc alone has no effect but potentiates the stimulatory effect of TSP on the incorporation of [3H]thymidine into the acid-insoluble cell fraction. Other heavy metals including copper, lead, manganese and nickel did not exhibit a similar effect. In bovine aortic endothelial cells, [3H]thymidine incorporation was stimulated by zinc alone and suppressed by TSP alone; the stimulation by zinc was significantly reduced by TSP. In human fibroblastic IMR-90 cells, [3H]thymidine incorporation was stimulated by either zinc or TSP; a simultaneous treatment with zinc and TSP showed an additive effect. The present data suggest that zinc may be a unique heavy metal that potentiates the proliferation of vascular smooth muscle cells stimulated by TSP; in addition, such an interaction was observed selectively in this cell type. Since a large amount of TSP is released from alpha-granules of aggregated platelets, zinc may augment TSP activity which is involved in the physiology of vascular tissues.

Animals↗
PubMed1995

Induction of metallothionein by thrombin in cultured vascular endothelial and smooth muscle cells.

Metallothionein induction by thrombin was investigated using a culture system of vascular endothelial and smooth muscle cells. It was found that the protease induced metallothionein in endothelial cells derived from human aorta and umbilical vein as well as bovine aorta in a concentration-dependent manner. Thrombin also induced metallothionein in vascular smooth muscle cells derived from bovine aorta but not in cells derived from human, rabbit and rat aortas. In bovine aortic endothelial and smooth muscle cells, induction of metallothionein by thrombin was unaffected by the protein kinase C inhibitor staurosporine; in addition, a protein kinase C activator, phorbol 12-myristate 13-acetate, failed to induce metallothionein, suggesting that the induction by thrombin occurred through pathway(s) other than protein kinase C activation. It is suggested that metallothionein may be induced during hemostasis in the vascular tissue through protein kinase C-independent pathway(s).

Animals↗
PubMed1995

Vascular smooth muscle cells in culture are highly sensitive to cadmium cytotoxicity without species-related differences: comparison with Chang liver cells.

Human, rabbit and rat aortic smooth muscle cells (hSMC, rSMC and A10 cells, respectively) were cultured with cadmium chloride and compared with human Chang liver cells to characterize the response of vascular smooth muscle cells to the metal. It was revealed that all tested vascular smooth muscle cells were markedly more sensitive to cadmium cytotoxicity than Chang liver cells. Cadmium accumulated more markedly in vascular smooth muscle cells than in Chang liver cells. After exposure to cadmium, metallothionein was induced in a concentration-dependent manner in Chang liver cells, it was constitutively high in hSMC, sensitively induced in rSMC and was constitutively low and induced within narrow limits in A10 cells. The intracellular content of reduced glutathione was greater and significantly enhanced by cadmium only in A10 cells. The present data suggest that vascular smooth muscle cells are, in general, sensitive to cadmium cytotoxicity without any species-related differences, mainly due to a higher accumulation of the metal within cells.

Animals↗