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Notes: A detailed experimental investigation of plasma fluctuation and its modification due to radial electric field effects, both its shear and curvature, has been carried out on the Current Sustained Torus IV at Nagoya University [Takamura et al., J. Plasma Fusion Res. 74, 38 (1998)] through measurement with an array of Langmuir probes. The observed statistical dispersion relation indicates a drift-wave-type turbulence. An examination of the radial electric field shear and curvature effects on the fluctuations as well as comparisons to theoretical predictions are presented. The decorrelation of turbulence is found to be influenced by the radial electric field shear in our experiment. A modification of the poloidal correlation length and the two-poloidal-point coherency due to the radial electric field has also been identified. Nonlinear analysis of quadratic mode coupling indicates that the radial electric field can affect the fluctuation amplitudes by modifying the coupling between different spectral components of the fluctuations. © 2000 American Institute of Physics.

Notes: The frequency dependence of the tokamak plasma response to the externally applied rotating helical field was investigated by measuring the radial profile of the perturbation field with small magnetic probes which were inserted in the plasma. The experimental results are discussed, directly comparing with the generally accepted linear theory, and taking into account the E×B drift and diamagnetic effect of the plasma. It was found that the experimental results are in good agreement with the simple linear analysis based on the single helicity approximation in a cylindrical geometry, except for the ergodic region, which comes from the overlapping of several sideband components of the perturbation. It is also found that the radial component of the perturbation field is still amplified inside the resonance surface (r〈rs), even when a partial shielding takes place at r(approximate)rs. © 2000 American Institute of Physics.

Notes: Co–P powders were produced by chemical reduction. The powders had a spherical shape with an average diameter of about 1 μm. X-ray diffraction and differential scanning calorimetry studies confirmed that the powders were amorphous. The amorphous powders showed higher saturation magnetization than the crystalline counterparts. Heat treatment of the powders above the crystallization temperature resulted in the formation of fcc Co, hcp Co, and Co2P phases. The saturation magnetization of the annealed powders monotonically decreased as the annealing temperature increased. On the other hand, the coercivity of the annealed powders rapidly increased with increasing annealing temperature. The powders annealed at 600 °C had a saturation magnetization of 100 emu/g with a coercivity of 500 Oe. © 2000 American Institute of Physics.

Notes: Objectives:  CD14, toll-like receptor 4 (TLR4) and MyD88 have been shown to mediate responsiveness in host cells to lipopolysaccharide. We investigated here the regulatory effects of inflammatory cytokines on the expression of membrane CD14 (mCD14), TLR4 and MyD88, and on subsequent responsiveness to lipopolysaccharide from Actinobacillus actinomycetemcomitans in human gingival fibroblasts.Materials and methods:  Following treatment with either interleukin-1β, tumor necrosis factor-α (TNF-α) or γ-interferon (IFN-γ), expression of mCD14/TLR4 and MyD88 was determined by flow cytometry and western blotting, respectively. After pretreatment with IFN-γ, cells were pre-incubated with either anti-CD14 antibody MY4 or anti-TLR4 antibody HTA125 and subsequently treated with A. actinomycetemcomitans lipopolysaccharide. Then, phosphorylation of mitogen-activated protein (MAP) kinases and IκBα was examined by western blotting, and production of interleukin-6 and interleukin-8 was measured by their respective enzyme-linked immunosorbent assay (ELISA) kits.Results:  IFN-γ stimulated expression of mCD14, whereas -1β and TNF-α did not. Expression of MyD88 but not TLR4 was also enhanced by IFN-γ. The lipopolysaccharide activated MAP kinases, such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38, and IκBα and stimulated production of interleukin-6 and interleukin-8. The lipopolysaccharide-stimulated interleukin-6 and interleukin-8 production was markedly inhibited by MY4 or HTA125. Pretreatment with IFN-γ augmented the following activation of MAP kinases and IκBα and production of interleukin-6 and interleukin-8 in response to the lipopolysaccharide.Conclusions:  These results suggest that the augmentation by IFN-γ of the responsiveness to A. actinomycetemcomitans lipopolysaccharide, such as activation of MAP kinases and IκBα and terminal cytokine production in human gingival fibroblasts, may be partially mediated by up-regulation of CD14 and MyD88 expression.

Notes: Objectives:  Previous studies have suggested an association between chronic infection and cardiovascular disease, and combined infection/inflammation is frequently related with hypertriglyceridemia, which may be a risk factor of cardiovascular disease. In fact, experimental transient or intermittent administration of lipopolysaccharide (LPS) is known to cause hypertriglyceridemia. We investigated the effects of subcutaneous and continuous administration of LPS in rats, which was considered to mimic chronic infection such as periodontal disease, on the serum levels of lipids [triglyceride (TG), total cholesterol (TC) and free fatty acid (FFA)] and cytokines [tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1)], all of which are thought to be etiological factors of atherosclerotic cardiovascular disease.Methods:  Ten fasted Wistar rats were subcutaneously injected with LPS (500 µg/100 g of body weight) (LPS-injected rats; n = 5) or saline (saline-injected rats; n = 5) as a model of transient infection. Further, mini-osmotic pumps containing the same concentration of LPS (LPS-implanted rats; n = 5) or saline (saline-implanted rats; n = 5) were subcutaneously implanted into an additional 10 rats as a model of chronic infection. After the injection or implantation, time-dependent changes in serum levels of TG, TC, FFA, TNF-α, MCP-1 and LPS were determined.Results:  LPS was detected in serum until 24 h in LPS-injected rats and until day 5 in LPS-implanted rats. Serum TG levels significantly increased from 6 to 24 h in LPS-injected rats and from day 5 to 14 in LPS-implanted rats. In both LPS-injected and LPS-implanted rats, serum FFA levels increased only slightly, whereas serum TC levels did not appreciably change. Both types of LPS administration increased serum TNF-α levels transiently and MCP-1 levels continuously.Conclusions:  These findings suggest that chronic infection such as periodontal disease induces hypertriglyceridemia and increases serum MCP-1 levels in a manner that increases the risk of atherosclerotic cardiovascular disease.

Notes: Previous studies have provided the biological basis for the therapeutic use of enamel matrix derivative (EMD) at sites of periodontal regeneration. A purpose of this study is to determine effects of EMD on cell growth, osteoblastic differentiation and insulin-like growth factor-I (IGF-I) and transforming growth factor-β1 (TGF-β1) production in human periodontal ligament cells (HPLC). We also examined participation of endogenous IGF-I and TGF-β1 with EMD-stimulated cell growth in these cells. HPLCs used in this study were treated with EMD alone or in combination with antihuman IGF-I antibody (anti-hIGF-I) or anti-hTGF-β1, recombinant human bone morphogenetic protein-2 (rhBMP-2), 1,25-dihydroxyvitamin D3[1,25(OH)2D3], rhTGF-β1 or rhIGF-I. After each treatment, cell growth, the production of IGF-I and TGF-β1 and the expression of osteoblastic phenotypes were evaluated. EMD stimulated cell growth in dose-dependent and time-dependent manners. EMD was also stimulated to express IGF-I and TGF-β1 at protein and mRNA levels. The EMD-stimulated cell growth was partially suppressed by cotreatment with anti-hIGF-I or anti-hTGF-β1, and cell growth was also stimulated by treatment with rhIGF-I or rhTGF-β1. rhBMP-2 stimulated alkaline phosphatase (ALPase) activity and ALPase mRNA expression, and 1,25(OH)2D3 stimulated ALPase and osteocalcin mRNA expression. However, EMD showed no effect on the osteoblastic phenotypes expression. These results demonstrated that EMD has no appreciable effect on osteoblastic differentiation, however it stimulates cell growth and IGF-I and TGF-β1 production in HPLC, and that these endogenous growth factors partially relate to the EMD-stimulated cell growth in HPLC.

Notes: Background: Although there is increasing evidence of the importance of cysteinyl leukotrienes (LT) as mediators of aspirin-induced bronchoconstriction in aspirin-sensitive asthma, the cellular origin of the LT is not yet clear. Methods: Urinary concentrations of leukotriene E4 (LTE4), 11-dehydrothromboxane B2, 9α,11β-prostaglandin F2, and Nτ-methylhistamine were measured during the 24 h following cumulative intravenous administration of increasing doses of lysine aspirin to asthmatic patients. In addition, the urinary concentrations of these metabolites were measured on 5 consecutive days in a patient who suffered an asthma attack after percutaneous administration of nonsteroidal anti-inflammatory drugs. Results: In aspirin-induced asthma patients (AIA, n=10), the basal concentration of urinary LTE4, but not the other metabolites, was significantly higher than that in aspirin-tolerant asthma patients (ATA, n=10). After intravenous aspirin provocation, the AIA group showed a 13.1-fold (geometric mean) increase in excretion of LTE4 during the first 3 h, and 9α,11β-prostaglandin F2 also increased in the AIA group during the first 0–3 h and the 3–6 h collection period. Nτ-methylhistamine excretion was also increased, but to a lesser degree. Adminis-tration of aspirin caused significant suppression of 11-dehydrothromboxane B2 excretion in both the AIA and ATA groups. When the percentage of maximum increase of each metabolite from the baseline concentrations was compared between the AIA group and the ATA group, a significantly higher increase in excretion of LTE4, 9α,11β-prostaglandin F2, and Nτ-methylhistamine was observed in the AIA group than the ATA group. An increased excretion of LTE4 and 9α,11β-prostaglandin F2 has been detected in a patient who suffered an asthma attack after percutaneous administration of nonsteroidal anti-inflammatory drugs. Conclusions: Considering that human lung mast cells are capable of producing LTC4, prostaglandin D2, and histamine, our present results support the concept that mast cells, at least, may participate in the development of aspirin-induced asthma.

Notes: Summary Background Pemphigus is an antidesmoglein (Dsg) autoimmune disease that is divided into two major subtypes: pemphigus foliaceus (PF) and pemphigus vulgaris (PV). We previously developed enzyme-linked immunosorbent assays (ELISAs) using recombinant Dsg1 and Dsg3 to detect IgG autoantibodies in patients with pemphigus. The protocol for the ELISAs was optimized for serological diagnosis, but under the conditions used, these assays were not particularly useful for monitoring disease activity in certain patients. That is, the sera from some patients with high-titre antibodies continued to show high index values in the ELISA after clinical improvement. Objectives In the study reported here, we modified the ELISA protocol to obtain ‘true’ index values that exhibit a better correlation with disease activity. Methods We tested two cases of pemphigus foliaceus (PF) and four cases of pemphigus vulgaris (PV), each with ELISA index values greater than 150 for Dsg1 or Dsg3. We ran an ELISA with sera from these patients serially diluted from 1 : 100 to 1 : 12,800. We then performed ELISA with a series of PV No. 1 sera diluted to 1 : 800 and PV No. 2–4 and PF No. 1–2 sera diluted to 1 : 1600, after which we plotted the ELISA index values against the time course of disease activity. Results In each of these cases, there was no apparent decline, over the course of the disease activity, in the ELISA index values at a serum dilution of 1 : 100, probably because the antigen–antibody reaction was saturated at that dilution. After running an ELISA with sera serially diluted from 1 : 100 to 1 : 12,800 we found that a linear dose-dependency between the dilution value and the index value was only observed when sera were diluted to 1 : 800 or more in one case (PV No.1) and to 1 : 1600 or more in the other five cases (PV No. 2–4, PF No. 1–2). After performing ELISA with these series as outlined above we plotted the ELISA index values against the time course of disease activity and found that the index values obtained from these appropriately diluted sera fluctuated in parallel with disease activity, and declined with clinical improvement. Conclusions These findings indicate that when appropriate dilutions are used in Dsg1 and Dsg3 ELISA, these assays can provide useful serological information for assessing disease activity in PF and PV.

Notes: Aims:  To investigate the expression of the cadherin complex in human crescentic glomerulonephritis to elucidate the role of intercellular adherens junction molecules in crescent formation.Methods and results:  Immunostaining revealed cadherin complexes localized in Bowman's epithelial cells, but not in podocytes, of normal human glomeruli. Eight adult cases with myeloperoxidase anti-neutrophil cytoplasmic autoantibodies (MPO-ANCA)-related (pauci-immune type) crescentic glomerulonephritis were examined on immunofluorescence microscopy with anti-pan cadherin, p120 catenin, and β-catenin antibodies. The specimens provided six cellular crescents, 12 fibrocellular crescents, and four fibrotic crescents. Immunofluorescence was semiquantitatively estimated by the rate of the field of localization within the whole area of the crescent, according to the four-grade system [(–) − (++)]. All the tested molecules consisting of the cadherin complex were abundantly observed in cytokeratin-positive epithelial components in crescents, each with an equivalent area of localization. The expression of the cadherin complex was closely associated with that of cytokeratin and both diminished as the crescents developed from cellular to fibrotic.Conclusions:  The cadherin–catenin complex is a specific marker of Bowman's epithelial cells in human glomeruli. The cellular crescents in pauci-immune-type crescentic glomerulonephritis possess adherens junction molecules, indicating a principle parietal epithelial cell phenotype.

Notes: The effect of Helicobacter pylori infection on non-steroidal anti-inflammatory drug-induced gastric mucosal injury is controversial.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To examine the effect of the interaction between H. pylori and non-steroidal anti-inflammatory drugs on gastric mucosal injury.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Mongolian gerbils infected with H. pylori were treated with indometacin at 8 mg/kg for 2 days or 7 days. Mucosal damage was assessed by macroscopic and histological examination, and myeloperoxidase activity was measured as an index of neutrophil infiltration. The expression levels of cyclo-oxygenase proteins were determined by Western blot analysis and cyclo-oxygenase activity.〈section xml:id="abs1-4"〉〈title type="main"〉Results:A 2-day course of indometacin did not cause an increase in gastric damage in H. pylori-infected Mongolian gerbils compared to uninfected gerbils, while a 7-day course of indometacin caused additive gastric damage in H. pylori-infected animals. H. pylori infection induced cyclo-oxygenase-2 expression in the stomach. Treatment with indometacin for 2 days did not significantly affect cyclo-oxygenase activity in H. pylori-infected animals, while treatment for 7 days inhibited both cyclo-oxygenase-1 and cyclo-oxygenase-2 activities. Pre-treatment with a selective cyclo-oxygenase-2 inhibitor aggravated mucosal injury in H. pylori-infected animals treated or not treated with indometacin for 2 days.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:Our results suggest that cyclo-oxygenase-2 protein induced by H. pylori infection may be involved in the defence of the gastric mucosa against damage caused by non-steroidal anti-inflammatory drugs. Therefore, inhibition of cyclo-oxygenase-2 activity may enhance non-steroidal anti-inflammatory drug-caused gastric damage in H. pylori-infected animals.