[Fertility in Japan: 1993].
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Age Factors↗
Biomedical subjects
C Yamamoto
Publications and source records attributed to C Yamamoto.
[Nuptiality and divorce in Japan: 1993].
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Age Factors↗
[Studies on production of interleukin-1 beta (IL-1 beta) and granulocyte. Macrophage-colony stimulating factor (GM-CSF) by peripheral blood monocytes from patients with Mycobacterium avium-intracellulare complex (MAC) infection].
Production of Interleukin-1 beta (IL-1 beta) and granulocyte macrophage-colony stimulating factor (GM-CSF) by peripheral blood monocytes (PBMs) from patients with Mycobacterium avium-intracellulare complex (MAC) infection was assessed and the relationship with their clinical course was analyzed. PBMs were obtained from MAC-infected patients in their active stage as well as in the inactive stage and the healthy controls. Spontaneous release of IL-1 beta by PBMs from patients in the active stage was higher than those by the cells in the inactive stage or the healthy controls. On the other hand, spontaneous GM-CSF release by PBMs from patients in the active stage was higher than the healthy controls. When PBMs were stimulated with MAC-derived purified protein derivatives (PPD-B), increased production of both IL-1 beta and GM-CSF were obtained for PBMs in their active stage. While these enhanced production upon stimulation with PPD-B related to the persistent infection with MAC, the increased IL-1 beta production correlated with the exhausted nutritional state. Both IL-1 beta and GM-CSF produced by PBMs seemed to be closely related with the clinical course of human MAC infection.
Aged↗
[The evaluation of interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) level in peripheral blood of patients with active pulmonary tuberculosis].
We investigated the serum level of IL-8 and TNF-alpha using ELISA in 16 patients with active pulmonary tuberculosis before administration of antituberculous drugs and in age-, smoking habit-matched 20 healthy controls. The mean level of serum IL-8 in patients with active pulmonary tuberculosis was significantly higher than that in healthy controls (P < 0.001). The mean level of serum TNF-alpha in tuberculosis patients was also high, while TNF-alpha was not detectable in the sera of healthy controls. We also examined the relationship between clinical pictures mainly defined by radiographic findings and the serum levels of IL-8 and TNF-alpha. The serum IL-8 level of 9 patients with tuberculous cavity is significantly higher than that of 7 patients without cavity. (P < 0.05) We classified the patients with cavities into two subgroups according to the radiographic classification of the Japanese Society of Tuberculosis. Four patients with advanced lesions on chest X-ray showed higher serum IL-8 level than 5 patients with moderate lesions (P < 0.05). On the other hand, there was no correlation between serum TNF-alpha level and radiographic findings. These results suggest that IL-8 appears to be involved in the formation of tuberculous cavitary lesion.
Adult↗
[Studies on mucociliary transport in patients with pulmonary atypical mycobacteriosis--by aerosol inhalation cine-scintigraphy].
Mucociliary transport (MCT) was studied in 22 patients with atypical mycobacteriosis (Group I : 16 with M. avium-intracellulare complex (MAC), Group II : 6 with M. kansasii) by aerosol inhalation cine-scintigraphy. In most of the patients, the MCT was abnormally slow both in the main bronchus and in the trachea, while in healthy controls the transport of the inhaled aerosol in the bronchus and the trachea were rapid and smooth. In both groups, the tracheal MCT was impaired in two thirds of the patients, while the MCT in the main bronchus was impaired in all except one in Group I and in two-thirds in Group II. The results indicate that the grade of bronchial impairment was higher in MAC than in M. kansasii infections. In atypical mycobacteriosis, especially in MAC infections, such impairment of MCT could be closely related to the disruption of local defence mechanisms in the airways.
Adult↗
[Pulmonary infection due to Mycobacterium szulgai associated with multiple bullous disease of the lung].
A 46-years-old male was admitted to our hospital because of productive cough and infiltrates on the chest roentogenogram. The patient had a history of left upper bullectomy ten years prior to the admission. The CT scan of the chest on admission showed infiltrats with cavitation in the left apex and multiple bullae in almost whole lung. Microscopical examination of smears of sputum and bronchoalveolar lavage fluid revealed acid-fast bacilli. They were identified as Mycobacterium szulgai by DNA-DNA hybridization method. The patient was treated with isoniazid, streptomycin and rifampicin. After treatment for about a month, the culture of sputum converted to negative for M. szulgai. After about three months hospitalization, the infiltrates decreased and the cavity wall became thin, and no recurrence sign has been observed after the discharge. There are a few case reports of pulmonary infection due to M. szulgai associated with bullous disease of the lung in Japan.
Anti-Bacterial Agents↗
Contributions of multiple calcium channel types to GABAergic transmission in rat cultured hippocampal neurons.
Effects of Ca2+ channel blockers on GABAergic transmission were examined with rat cultured hippocampal neurons. The GABAergic synaptic currents (IPSCs) evoked by electrical stimulation of single presynaptic neurons were recorded from voltage-clamped postsynaptic neurons. The amplitude of IPSCs was not changed by 10 microM nifedipine (L-type Ca2+ channel blocker), but was decreased irreversibly to 37% of control by 1 microM omega-conotoxin GVIA (N-type blocker, CgTX), to 67% by 0.1 microM omega-agatoxin IVA (P-type blocker, AGTX), and to 1% by both toxins. From these data and the Ca(2+)-dependence of IPSCs, the contributions of CgTX-sensitive and AGTX-sensitive Ca2+ channels to the transmission were estimated at 59% and 36%, respectively.
Animals↗
Plasmin-induced reduction of heparan sulfate in cultured vascular endothelial cell layer.
Plasmin-induced alteration of glycosaminoglycans (GAGs) was investigated using a cell culture system of vascular endothelial cells derived from bovine aorta. In the cell layer, the incorporation of [3H]glucosamine into GAGs, a marker of the sugar chain formation, was slightly decreased by plasmin. On the other hand, the incorporation of [35S]sulfate, a marker of the sulfation, was markedly decreased by the protease. Plasminogen also induced a weak but similar change. Characterization of the cellular GAGs showed that plasmin inhibited the incorporation of both [3H]glucosamine and [35S]sulfate into the major component heparan sulfate at a similar degree. In the other GAGs, the [35S]sulfate incorporation was significantly decreased by plasmin without a change of the [3H]glucosamine incorporation. The leakage of lactate dehydrogenase from the endothelial cells was significantly increased by plasmin, suggesting that the protease exhibited cytotoxicity. The present data suggest that the anticoagulant activity on the surface of vascular endothelium mediated by the anticoagulant heparan sulfate may be reduced by plasmin which will be generated from plasminogen by plasminogen activators derived from endothelial cells.
Animals↗
Calcium regulation of tissue plasminogen activator and plasminogen activator inhibitor-1 release from cultured human vascular endothelial cells.
Tissue plasminogen activator (t-PA) produced by vascular endothelial cells converts plasminogen to plasmin which degrades fibrin. Since t-PA activity is greatly potentiated in the presence of fibrin (1,2), the activator is implicated in intravascular fibrinolysis. On the other hand, endothelial cells also produce plasminogen activator inhibitor-1 (PAI-1) (3). The inhibitor associated with vascular endothelium rapidly inhibits t-PA, while that released into the liquid phase has a little anti-activator activity (4). However, clinical studies have shown that elevation of plasma PAI-1 level is a risk factor of thrombosis (5,6). It is thus suggested that the balance between t-PA and PAI-1 is important for the regulation of fibrinolysis. The release of t-PA and PAI-1 from vascular endothelial cells is regulated by physiological factors including thrombin (3,7), histamine (8), vasoconstrictor peptide endothelins (9,10) and cytokines (11). In addition, the regulation of the t-PA release and that of the PAI-1 release are not necessarily coupled. It has been shown that activated protein kinase C and cyclic AMP are involved in the stimulation and suppression, respectively, of the endothelial t-PA and PAI-1 production (12,13). However, the role of intracellular calcium in the regulation of endothelial t-PA and PAI-1 release has remained to be elucidated. In the present study, we investigated the effect of calcium ionophore A23187 on the release of t-PA antigen (t-PA:Ag) and PAI-1 antigen (PAI-1:Ag) from cultured vascular endothelial cells derived from human umbilical vein.
Antigens↗
Transforming growth factor beta-induced tolerance to cadmium cytotoxicity in cultured vascular endothelial cells.
We investigated whether or not transforming growth factor beta (TGF beta 1) affects the sensitivity to cadmium of bovine aortic endothelial cell in a culture system. Cadmium cytotoxicity was evaluated by [3H]adenine release assay. It was found that pretreatment with recombinant human TGF beta 1 (rhTGF beta 1) of the confluent cultures resulted in a reduction of cadmium cytotoxicity, suggesting that the cytokine induced a tolerance to cadmium in the cells. Such a tolerance was induced slightly by either recombinant human tumor necrosis factor alpha or recombinant human basic fibroblast growth factor but not by recombinant human interleukin-1 beta and -6; rhTGF beta 1 was the most potent inducer. rhTGF beta 1 failed to induce the tolerance in the presence of anti-rhTGF beta 1 antibody. Pretreatment with the antibody alone caused a significantly sensitive response to cadmium, suggesting that endogenous TGF beta 1 can physiologically contribute to protection against cadmium cytotoxicity in endothelial cells. The accumulation of cadmium was increased in the extracellular fraction but significantly decreased in the intracellular fraction of the cells by pretreatment with rhTGF beta 1. The cadmium content was significantly decreased in the particulate fraction but not in the cytosol fraction. Gel filtration chromatography of the cytosol fraction revealed that cadmium was bound to high-molecular-weight protein and metallothionein; both peaks were slightly increased by pretreatment with rhTGF beta 1. It was concluded that rhTGF beta 1 induces a tolerance to cadmium in cultured endothelial cells, caused by a decrease in the cadmium accumulation in the particulate fraction of the cells. TGF beta 1 may serve as a protective factor against cadmium cytotoxicity in vascular endothelial cells.
Animals↗
Basic fibroblast growth factor suppresses tissue plasminogen activator release from cultured human umbilical vein endothelial cells but enhances that from cultured human aortic endothelial cells.
Since basic fibroblast growth factor (bFGF) modulates the functions of vascular endothelial cells, we hypothesized that this factor may be involved in the regulation of the blood coagulation-fibrinolytic system mediated by the cells. Confluent cultures of vascular endothelial cells from human umbilical vein were treated with recombinant human bFGF (bFGF) in a serum-free medium and the content of tissue plasminogen activator antigen (t-PA:Ag) in the medium was determined by EIA. Treatment with bFGF resulted in a significant decrease in the release of t-PA:Ag from the cells accompanied with a less t-PA activity in the medium. In contrast, the t-PA:Ag release from human aortic endothelial cells was significantly increased by bFGF. The bFGF-induced decrease in the t-PA:Ag release from the venous endothelial cells was completely blocked by anti-bFGF antibody. The incorporation of [3H]leucine into the acid-insoluble fraction of the cells was significantly increased by bFGF; however, the activity of lactate dehydrogenase leaked into the medium was significantly decreased, suggesting that the suppression of the t-PA:Ag release caused by bFGF in the venous endothelial cells was not due to either a nonspecific inhibition of protein synthesis or a nonspecific cell damage. Since bFGF is postulated to be released from damaged endothelial cells, the present data suggest the regulation by bFGF of hemostasis mediated by endothelial cells when the vascular endothelium was damaged.
Aorta↗
Suppression of hippocampal synaptic transmission by the spider toxin omega-agatoxin-IV-A.
Effects of omega-agatoxin-IV-A (AGTX) on synaptic transmissions were examined in thin transverse sections of the guinea pig hippocampus. AGTX suppressed, in a dose-dependent manner, field potentials elicited by mossy fiber stimulation in CA3 pyramidal cell layer. AGTX also suppressed field potentials elicited by perforant fiber stimulation in granular layer without marked changes in antidromic responses. These results suggest that Ca2+ entry into presynaptic terminals via P-like calcium channels is at least partly responsible for release of glutamate.
Animals↗
Alteration of glycosaminoglycans induced by cadmium in cultured vascular smooth muscle cells.
Alteration of glycosaminoglycans (GAGs) in cultured bovine aortic smooth muscle cells after exposure to cadmium was investigated. It was revealed that cadmium increased the accumulation of GAGs metabolically labeled with [3H]glucosamine but decreased that with [35S]sulfate in the cell fraction, the cell surface fraction and the medium fraction. This suggested that cadmium stimulated the biosynthesis of GAGs but inhibited their sulfation in the cells. A similar alteration was observed in cadmium-treated human aortic smooth muscle cell layer. Of tested cations including cadmium, bismuth, cobalt, copper, lead, manganese, nickel and zinc, only cadmium stimulated [3H]glucosamine incorporation, with a strong inhibition of the [35S]sulfate incorporation in the bovine cells. Characterization of bovine smooth muscle GAGs showed that the cadmium-induced increase in the [3H]glucosamine incorporation was mainly observed in heparan sulfate; the inhibition of the [35S]sulfate incorporation occurred non-selectively. Cadmium accumulated in bovine vascular smooth muscle cells in a dose-dependent manner with an increase in the leakage of lactate dehydrogenase into the medium. The present data suggest that vascular smooth muscle cells respond to the cytotoxicity of cadmium and promote the GAG synthesis with a reduction of their sulfation. It is postulated that this response may be a defensive one to the damage of the vascular tissue caused by cadmium but would be a component of the metal-induced atherosclerosis.
Animals↗
Suppression of plasminogen activator inhibitor type 1 release from cultured human umbilical vein endothelial cells by basic fibroblast growth factor.
We investigated the release of plasminogen activator inhibitor type 1 (PAI-1) from cultured vascular endothelial cells after exposure to basic fibroblast growth factor (bFGF). Treatment with human recombinant bFGF of confluent cultures of endothelial cells derived from human umbilical vein resulted in a reduction of the accumulation of PAI-1 antigen (PAI-1:Ag) in the conditioned medium. The suppressive effect of bFGF completely disappeared in the presence of anti-bFGF antibody. The reduction of endothelial PAI-1:Ag release induced by bFGF was suggested to be independent of intracellular accumulation of cyclic AMP. On the other hand, nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase pathway of arachidonic acid metabolism, suppressed the spontaneous release of PAI-1:Ag by itself; in the presence of NDGA, bFGF failed to further suppress the PAI-1:Ag release. The effect of bFGF and indomethacin, an inhibitor of the cyclooxygenase pathway, was additive on the PAI-1:Ag release. The present data suggest that bFGF reduces the endothelial PAI-1:Ag release via suppression of the putative lipoxygenase pathway which up-regulates a part of the spontaneous PAI-1:Ag release.
8-Bromo Cyclic Adenosine Monophosphate↗
Stimulation by zinc of cultured vascular endothelial cell proliferation: possible involvement of endogenous basic fibroblast growth factor.
Vascular endothelial cells from bovine aorta were cultured with zinc sulfate (20 microM or less) for 24 h and labeled with [3H]thymidine or [14C]leucine during the last 3 h of the culture. It was found that the cell number was significantly increased by zinc alone; the incorporation of both [3H]thymidine and [14C]leucine was also stimulated by the metal. The stimulation by zinc occurred in the presence or absence of exogenous basic fibroblast growth factor (bFGF). However, other heavy metals including copper, manganese and nickel did not exhibit such a stimulatory effect, suggesting that zinc plays a particular role in endothelial cell proliferation. Stimulation of the [3H]thymidine incorporation by zinc disappeared in the presence of either cycloheximide or anti-bFGF IgG; in addition, a lipoxygenase inhibitor nordihydroguaiaretic acid diminished the zinc stimulation but a cyclooxygenase inhibitor indomethacin did not exhibit such an inhibitory effect. These results indicated that zinc stimulated the proliferation of endothelial cells through the lipoxygenase pathway which mediates the stimulation by endogenous bFGF. In other words, the metal may amplify the endogenous bFGF-dependent proliferation of the cells.
Animals↗
Augmenting action of nicotine on population spikes in the dentate gyrus of the guinea pig.
Effects of nicotinic cholinergic agents on field potentials recorded from the dentate gyrus were studied in thin transverse sections of the hippocampus of the guinea pig. Nicotine augmented the population spike elicited by the second stimulus of a paired stimulation to the molecular layer. The threshold concentration of nicotine to cause this effect was 5-10 microM. The augmentation of the spike was not accompanied by an increase in the rising slope of population excitatory postsynaptic potentials, and was not observed in the presence of bicuculline. Carbamylcholine had a weak and inconsistent effect. D-tubocurarine and mecamylamine also augmented the population spike. The action of nicotine was blocked by hexamethonium. These results suggest that nicotine facilitates the generation of action potentials in granule cells by depressing inhibitory processes, and that properties of nicotinic cholinergic receptors are different in different subfields of the hippocampal formation, presumably reflecting the diversity of the receptors.
Action Potentials↗
Long-term potentiation and depression in the dentate gyrus, and effects of nicotine.
Effects of a brief high-frequency stimulation or a prolonged low-frequency stimulation in the presence and absence of nicotine were studied in thin transverse slices of the dentate gyrus prepared from the guinea pig. Test and conditioning stimulations were delivered to the middle one-third of the molecular layer, and the slope of the population excitatory postsynaptic potentials (EPSPs) elicited by the test stimulation was taken as an indicator of potentiation or depression. Nicotine was without effects on the N-methyl-D-aspartate (NMDA) component of EPSPs at 50 or 100 microM. A brief high-frequency stimulation induced long-term potentiation (LTP) in the presence of bicuculline. Nicotine (50 microM) almost doubled the magnitude of LTP. In the absence of bicuculline, an identical high-frequency stimulation induced a brief depression, the duration and magnitude of which were increased by nicotine. The increase was not statistically significant, however. In contrast to observations in the region CA1, 720 pulses at 1 Hz delivered after induction of LTP failed to induce long-term depression. Nicotine did not modify the after-effect of the low-frequency stimulation. It was discussed that the facilitation of LTP by nicotine probably resulted from suppression of inhibitory processes.
Animals↗
A comparison between potencies of external calcium, strontium and barium to support GABAergic synaptic transmission in rat cultured hippocampal neurons.
Relative potencies of external Ca2+, Sr2+ and Ba2+ to trigger GABAergic synaptic transmission were evaluated by applying the patch-clamp technique to both presynaptic and postsynaptic hippocampal neurons prepared from neonatal rats. Action potentials were evoked by application of voltage pulses to presynaptic neurons, and GABAergic synaptic currents were recorded in voltage-clamped postsynaptic neurons. No stimuli were delivered during replacement with test solutions and only five pulses were applied to the presynaptic neuron in each test solution. During the five-pulse application, the amplitude of synaptic currents was constant in Ca(2+)-containing solutions, but decreased successively in Ba(2+)- and Sr(2+)-containing solutions without Ca2+. Thus, the amplitude of synaptic currents induced by the first pulse in each ionic condition was used to evaluate the potency of divalent cations. The lowest external concentration required to trigger the transmission was 0.3 mM for Ca2+, 1 mM for Sr2+ and 2 mM for Ba2+, and the concentration required to achieve the same effect as with 2 mM Ca2+ was 6 mM for Sr2+ and 10 mM for Ba2+. These results strongly suggest that Ba2+ as well as Sr2+ can be substituted for Ca2+ in GABAergic synaptic transmission and the order of potency is Ca2+ > Sr2+ > Ba2+.
Animals↗