DNA diagnosis of Plasmodium falciparum malaria by single-tube PCR.
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DNA, Protozoan↗
Biomedical subjects
S Kano
Publications and source records attributed to S Kano.
Regulation of MHC class I expression by inflammatory cytokines in rat mesangial cells.
We investigated the regulation of major histocompatibility complex (MHC) class I expression by inflammatory cytokines and nitric oxide (NO) in rat mesangial cells by enzyme-linked immunosorbent assay and flow cytometry. MHC class I molecule expression on mesangial cells was significantly stimulated by interferon gamma, tumor necrosis factor alpha and interleukin 1beta, but not by interleukin 6, in a dose-dependent manner. Addition of SIN-1, an NO donor, did not affect the expression of cytokine-induced MHC class I expression. These results suggest that under inflammatory conditions mesangial cells may act as antigen-presenting cells in response to stimulation by cytokines and may be involved in the pathogenesis of immune-mediated glomerular disease.
Animals↗
Inhibitory effects of glibenclamide and pertussis toxin on the attenuation of ischemia-induced myocardial acidosis following ischemic preconditioning in dogs.
Ischemic preconditioning is known to be mediated by several humoral factors, such as adenosine, norepinephrine, and bradykinin. We examined intracellular signal transduction of ischemic preconditioning following receptor stimulation. Alterations in the pH of the ischemic bed were monitored to assess the response of control and ischemic-preconditioned myocardium to glibenclamide and pertussis toxin. Pentobarbital-anesthetized open-chest dogs were subjected to 40 min of ligation of the left anterior descending coronary artery. Ischemic preconditioning was elicited by 25-min periods of coronary ligation followed by 5 min of reperfusion before a 40-min period of ligation. Glibenclamide (0.3 mg/kg)was given i.v. 20 min before the onset of ischemic preconditioning. Pertussis toxin (6-10 micrograms/kg) was given i.v. 3 days before the experiment. Tissue myocardial pH was measured by a glass micro-pH electrode. Ischemia for 5 min decreased myocardial pH and reperfusion returned it to the preischemic levels. Ischemia for 40 min decreased the myocardial pH from 7.43 +/- 0.06 to 6.43 +/- 0.08. Ischemic preconditioning significantly attenuated the decrease in myocardial pH (6.57 +/- 0.06) induced by 40 min of ischemia. Pretreatment with either glibenclamide or pertussis toxin completely abolished the effect of ischemic preconditioning on ischemic myocardial acidosis. Ischemic preconditioning can attenuate ischemia-induced myocardial acidosis in dogs, and this effect is mediated by activation of adenosine triphosphate-sensitive potassium channels and pertussis toxin-sensitive guanosine triphosphate-binding protein.
Acetylcholine↗
Association of interleukin 6 release from endothelial cells and pulmonary hypertension in SLE.
OBJECTIVE: To investigate how sera from 37 patients with systemic lupus erythematosus (SLE) stimulate interleukin (IL) 6 release from IL-1beta pretreated endothelial cells and compare these effects to those of sera from 16 normal controls. METHODS: Endothelial cells pretreated 18 h with IL-1beta (5 U/ml) were incubated 2 h with sera diluted 10-fold with phosphate buffered saline (PBS). IL-6 concentrations in endothelial culture supernatants collected after incubation were measured by ELISA. RESULTS: Compared with PBS, sera from controls and 24 patients with SLE suppressed IL-6 release from IL-1beta pretreated cells. However, sera from 13 patients with SLE augmented IL-6 release. Of note, sera from 5 patients with pulmonary hypertension induced the highest level of IL-6 release. IgG from control sera suppressed IL-6 release, whereas F(ab')2 did not. Both IgG and F(ab')2 from the sera of patients with SLE with pulmonary hypertension augmented IL-6 release from IL-1beta pretreated cells. CONCLUSION: IgG antiendothelial cell antibodies from patients with SLE may be associated with the pathogenesis of SLE and pulmonary hypertension.
Adolescent↗
Detection of large macrophage colony forming cells in the peripheral blood of patients with rheumatoid arthritis.
OBJECTIVE: To test for the presence of colony forming cells, that form large macrophage colonies (> 2.5 mm in diameter, > 10,000 cells), in the peripheral blood of patients with rheumatoid arthritis (RA) and to determine its association with the clinical and laboratory features of RA. METHODS: Peripheral blood mononuclear cells (PBMC) from 96 patients with RA and 20 healthy controls were assayed for in vitro colony formation. In addition, PBMC from 38 patients with other rheumatic diseases including systemic lupus erythematosus (SLE), progressive systemic sclerosis (SSc), and polymyositis/dermatomyositis (PM/DM); 23 patients with infectious inflammatory diseases were also assayed. RESULTS: Large macrophage colony forming cells were detected in the peripheral blood of 19% of patients with RA (18/96), but not in that of healthy controls. In addition, these cells were detected in the peripheral blood of 11 of the 38 patients with other rheumatic disease (7/13 SSc and 4/11 PM/DM), but not in the 23 patients with infectious diseases. In the patients with RA, interstitial lung disease was significantly more frequently observed among patients in whom colony forming cells were found than among those in whom they were not found (p < 0.001). CONCLUSION: Based on the size of the colonies they formed, the macrophage colony forming cells detected in patients with RA probably corresponded to primitive hematopoietic progenitor cells, defined as high proliferative potential colony forming cells (HPP-CFC). Our observations provide preliminary evidence of the appearance of HPP-CFC in the circulation during inflammation of RA, and during that in other rheumatic diseases such as SSc and PM/DM, and of the association of HPP-CFC with interstitial lung disease in patients with RA.
Adult↗
[Pathogenetic mechanisms of autoimmunity in collagen diseases].
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Antibody Formation↗
[Characterization of antibodies against core, NS3, NS4, NS5 region of hepatitis C virus in patients with hepatitis C].
Third-generation screening assays for HCV antibodies were recently developed, in which a mixture of recombinant antigens from four different regions of the viral protein (core, NS3, NS4, NS5) was used. We reported the analytical performance and clinical usefulness of a third-generation counting immunoassay (RANREAM HCV) with PAMIA 30 (Toa Medical Electronics Inc., Kobe). In the present study, we investigated a modified assay of RANREAM HCV to detect region-specific antibody by using single antigen from four different regions, and studied response pattern of HCV antibodies and region-specific antibody in the patients with HCV infection. HCV antibodies of the seroconversion panel serum samples (BBI, USA) measured by RANREAM HCV were greatly coincident with those obtained by Ortho RIBA 3.0. The region-specific assay of serial sera from the patient with acute hepatitis revealed that anti-core antibody was produced at the initial stage of infection. In 165 patients with chronic hepatitis, pattern of region-specific antibody was different from case to case, although anti-NS3 and anti-core antibodies seemed to be predominant. The change of pattern was not observed for at least one year. All 2 cases who achieved complete remission with interferon showed low serum titer of anti-core antibody, in contrast to partial or non remission patients in which the level of anti-core antibodies was low in 6 of 16 cases.
Hepatitis C↗
[Relationship between PEF and SpO2 on acute asthma attack in children].
We evaluated the relationship between PEF and SpO2 on 126 acute asthma attacks of 52 asthmatic children (25 males, 27 females, age 6-17 yrs-old) whose PEF and SpO2 being measured either before or after inhalation of beta-agonist at out-patient clinic. In the whole age group over 6 yrs-old, values of %PEF were proportional to individual SpO2 (n = 76, R = 0.472, p < 0.001). However, the relationship between %PEF and SpO2 in the present study was different from that of the guideline proposed by WHO (Global Initiative for asthma, GINA), showing that the value of SpO2 corresponding to %PEF was higher in the present study than in GINA. Regarding the difference in age group, significant relationship between %PEF and SpO2 was observed in both lower (6-9 yrs-old) and middle age group (10-12 yrs-old) but not in older age group (over 12 yrs-old). Also, there was a significant relationship between %PEF and SpO2 in cases whose pulmonary function during stable condition showed no-obstructive change (FEV1.0% > 80%), but not in cases with obstructive change. On the other hand, averaged values of %PEF, SpO2, heart rate (HR), respiratory rate (RR) before inhalation of beta-agonist at out-patient clinic in cases with or without admission were 32.3% vs 50.0%, 93.0%, vs 95.0%, 115 bpm vs 100 bpm, and 27/min vs 25/min respectively, those difference being statistically significant. Although measurement of SpO2 is thought to be a useful index for assessing severity of childhood asthma exacerbation, clinician should recognize that value of SpO2 could be greater than 91% even though % predicted PEF is less than 60%. Especially in older age group, obstructive change during stable condition may disturb the relation of SpO2 to %PEF. In such cases, not only SpO2 but also PEF, which is objective index of airway obstruction, should be taken into account for assessing severity of exacerbation.
Acute Disease↗
[Case of bilateral temporal skin ulcer with temporal arteritis].
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Aged↗
Effect of cilostazol, a cAMP phosphodiesterase inhibitor, on nitric oxide production by vascular smooth muscle cells.
We investigated the effects of cilostazol, a cAMP phosphodiesterase inhibitor, on nitric oxide (NO) synthesis in cultured rat vascular smooth muscle cells. Incubation of the cultures with interleukin-1 beta (10 ng/ml) for 24 h caused a significant increase in the accumulation of nitrite, a stable metabolite of NO. Although cilostazol itself showed no effect on nitrite accumulation, it stimulated interleukin-1 beta-induced nitrite accumulation in a concentration-dependent manner (10(-8)-10(-5) M). This effect of cilostazol was completely abolished in the presence of NG-monomethyl-L-arginine, actinomycin D or dexamethasone. The cilostazol-induced nitrite production was accompanied by increased inducible NO synthase protein expression. In the presence of dibutyryl-cAMP, interleukin-1 beta-induced nitrite accumulation was further increased, but the stimulatory effect of cilostazol on nitrite accumulation was blunted. The effect of cilostazol was also abolished in the presence of Rp-8-bromoadenosine-3',5-cyclic monophosphorothioate, a competitive inhibitor of protein kinase A. Addition of cilostazol to the cultures significantly increased intracellular cAMP levels of vascular smooth muscle cells. These results indicate that cilostazol increases NO synthesis in interleukin-1 beta-stimulated smooth muscle cells, at least partially through a cAMP-dependent pathway.
Animals↗
Local changes in oxygen tension and blood flow in the brain under hyperthermia induced by intracerebroventricular NMDA in rats.
Intracerebroventricular administration of N-methyl-D-aspartate (NMDA; 100 nmol) to rats increased oxygen tension and blood flow of the caudate putamen and the ventral hippocampus. The regional differences in the increase in oxygen tension could not be explained in terms of those in the blood flow. NMDA also increased the temperature of the two brain regions to a similar extent, and these increases preceded that in the rectum. These findings suggest that NMDA receptor stimulation leads to exposure of the brain to a higher oxygen level and higher temperature, which might be involved in NMDA neurotoxicity.
Animals↗
Human monocyte-endothelial cell interaction induces synthesis of granulocyte-macrophage colony-stimulating factor.
BACKGROUND: Adhesion of monocytes to the endothelium is an initial step in the early stages of atherosclerosis and inflammation. Granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulates a range of functional activities of monocytes, including regulation of monocyte adhesion and induction of cytokine production. We investigated in this study whether CM-CSF synthesis was induced by the direct cell-to-cell interaction between human monocytes and human umbilical vein endothelial cells (ECs). METHODS AND RESULTS: The expressions of GM-CSF mRNA and protein were analyzed by Northern blotting and ELISA, respectively. Coculture of monocytes and ECs induced the high levels of GM-CSF mRNA expression, whereas culture of ECs or monocytes alone or coculture of neutrophils with ECs induced no GM-CSF mRNA expression. A large amount of GM-CSF was secreted into the supernatant upon coculture of monocytes with ECs. The supernatant from the coculture markedly stimulated 02- release in neutrophils, and this effect was significantly inhibited by anti-GM-CSF antibody (Ab). Immunohistochemistry and in situ hybridization revealed that GM-CSF protein and mRNA were clearly detectable in both ECs and monocytes adhered to ECs but not in nonadherent monocytes. The GM-CSF production by the coculture was markedly inhibited by genistein and partially inhibited by Abs against interleukin-1 and tumor necrosis factor-alpha. CONCLUSIONS: The present results indicate that GM-CSF is produced by direct interaction between monocytes and ECs and suggest that GM-CSF produced locally by monocyte-EC adhesive interaction plays an important role in the pathogenesis of atherosclerosis and inflammation by modulating monocyte/macrophage functions in vivo.
Adult↗
[Recent topics on collagen diseases].
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Anti-Inflammatory Agents↗
Selective accumulation of anti-histone antibodies in glomeruli of lupus-prone lpr mice.
Immunoglobulins were eluted from glomeruli of 50 lupus-prone, lpr mice and their physicochemical properties and specificity were compared with those in sera pooled from the same mice. Although immunoglobulins in glomeruli had higher isoelectric points than those in sera, there were no appreciable differences in the relative contents of neutral and acidic immunoglobulins between them. The proportion of IgG3 subclass was slightly higher in glomerular than serum immunoglobulins. Both anti-single-stranded and anti double-stranded DNA antibodies were twofold higher in glomerular than serum immunoglobulins, while anti-Sm antibodies were not recovered in glomerular eluate despite their high activity in serum. Antibodies in glomerular eluate reacted most strongly with histones, especially with core histones, while those in sera bound preferentially with histone H1, Sm-B, -B', and -D antigens. Since histones are very basic, they would have a higher affinity for negatively charged glomerular constituents, leading to an in situ formation of immune complexes involving fixed histones and their binding with antibodies for the induction of nephritides. Otherwise, such immune complexes themselves might retain positive charges sufficient for an affinity with the glomerular basement membrane. These results indicate that histone-anti-histone antibody system may play a role in the perpetuation of murine lupus nephritis.
Animals↗
Regulation of ICAM-1 expression by inflammatory cytokines in rat mesangial cells.
We investigated the regulation of intercellular adhesion molecule 1 (ICAM-1) expression by the inflammatory cytokines interleukin 1 beta (IL-1), IL-6 and IL-8 in rat mesangial cells by enzyme-linked immunosorbent assay, flow cytometry and Northern blot analyses. ICAM-1 expression on mesangial cells was stimulated significantly by IL-1 beta, but not by IL-6 nor IL-8, in a dose-dependent manner. Levels of ICAM-1 mRNA were very low in unstimulated mesangial cells, while its expression was markedly induced by exposure to IL-1 beta for 3 h. IL-6 and IL-8 showed no effect on ICAM-1 mRNA accumulation. These results demonstrate that IL-1 beta, but not IL-6 nor IL-8, induces ICAM-1 mRNA and protein accumulation in rat mesangial cells.
Animals↗
Nitric oxide attenuates adhesion molecule expression in human endothelial cells.
Leukocyte adhesion to vascular endothelium is a crucial step in the early stages of atherosclerosis, which may be mediated by the interaction of adhesion molecules expressed on the surfaces of both cell types. In this study, we investigated the effects of nitric oxide (NO) on the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs). ICAM-1 and VCAM-1 protein and mRNA expression were determined by cellular ELISA and Northern blot analysis, respectively. Both ICAM-1 and VCAM-1 expression were increased markedly by interleukin-1 beta (IL-1 beta). This IL-1 beta-mediated induction of ICAM-1 and VCAM-1 expression was significantly inhibited in the presence of a NO donor 3-morpholino-sydnonimine (SIN-1) in a dose-dependent manner. The inhibitory effect of SIN-1 was abolished in the presence of a NO scavenger haemoglobin, while addition of 8-bromo-cGMP showed no significant effect on IL-1 beta-induced ICAM-1 or VCAM-1 expression. Northern blot analysis showed that IL-1 beta markedly increased ICAM-1 and VCAM-1 mRNA expression, while SIN-1 decreased the accumulation of these transcripts induced by IL-1 beta. These results suggest that NO could prevent the focal adhesion and accumulation of leukocytes through the inhibition of ICAM-1 and VCAM-1 expression in endothelial cells.
Cell Adhesion↗
Monocyte-endothelial cell interaction induces expression of adhesion molecules on human umbilical cord endothelial cells.
OBJECTIVE: The adhesive interaction of monocytes and endothelial cells has been implicated as a regulatory signal in the cell activation that is involved in the pathogenesis of atherosclerosis. We investigated the effect of monocyte-endothelial cell interaction on the expression of adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), in human umbilical cord vein endothelial cells (HUVECs). METHODS: ICAM-1 and VCAM-1 protein and mRNA expression were determined by cellular ELISA and Northern blot analysis, respectively. RESULTS: The addition of unstimulated human monocytes, as well as interleukin-1 beta (IL-1 beta: 25 U/ml) and tumor necrosis factor-alpha (TNF: 100 U/ml), to HUVECs rapidly induced the expression of ICAM-1 and VCAM-1 protein and mRNA in HUVECs, whereas the addition of polymorphonuclear leukocytes (PMNs) had no significant effect on their expression. The induction of ICAM-1 and VCAM-1 by the co-culture of HUVECs and monocytes was significantly, but partially, inhibited by the combination of anti-IL-1 alpha, anti-IL-1 beta and anti-TNF Abs. Actinomycin D and genistein, but not calphostin C, also significantly inhibited the co-culture-induced adhesion molecule expression. CONCLUSIONS: These results suggest that the monocyte-endothelial cell interaction induces the expression of ICAM-1 and VCAM-1 in endothelial cells partially through the production of IL-1 and TNF. These findings also suggest that the monocyte-endothelial interaction further augments their interaction through the up-regulation of endothelial adhesion molecules, as a positive feedback mechanism.
Arteriosclerosis↗
Distinct effects of N omega-nitro-L-arginine on seizures induced by several drugs in mice.
A potent nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine (L-NA), suppressed tonic seizure elicited by pentylenetetrazol (PTZ; 100 mg/kg, SC) in a dose-related manner (25 to 100 mg/kg, IP), but had no effect on clonic seizure. The effect was most potent at 1 h after the administration of L-NA. L-NA (100 mg/kg, IP) suppressed clonic seizure as well as tonic seizure in bicuculline-treated (3.0 or 4.5 mg/kg, SC) mice. However, it did not affect seizures elicited by picrotoxin (2.0 to 6.0 mg/kg, SC). On the other hand, N-methyl-DL-aspartate (NMDLA; 300 mg/kg or 350 mg/kg, IP) induced clonic seizure, but tonic seizure was not always noted. All mice with clonic and tonic seizures died, and some mice with clonic seizure died without accompanying tonic seizure. L-NA did not influence NMDLA-induced seizures, but it appeared to enhance NMDLA lethality, though without statistical significance. These findings suggest distinct roles of NO in seizures induced by different drugs in mice.
Animals↗