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  • 1
    Electronic Resource
    Electronic Resource
    Development of a multichord beam-attenuation probe of hydrogen and helium for plasma diagnostics : Proceedings of the 12th topical conference on high temperature plasma diagnostics (1999)
    [S.l.] : American Institute of Physics (AIP)
    Review of Scientific Instruments 70 (1999), S. 865-868 
    Details
    ISSN: 1089-7623
    Source: AIP Digital Archive
    Topics: Physics , Electrical Engineering, Measurement and Control Technology
    Notes: In order to estimate the density and the electron temperature profiles of a medium temperature plasma, a multichord beam probing system has been developed. The ion density can be estimated by hydrogen neutrals attenuation via charge exchange. The electron temperature could be inferred from the electron impact ionization attenuation of a helium atom beam under some assumption. Our beam system includes a large bucket ion source which can simultaneously emit both hydrogen and helium ions, a neutralization drift tube, a beam energy and momentum analyzer corresponding to six chords and a data acquisition system. The completed device is applied for the measurement of a field-reversed configuration plasma which has a typical electron temperature of 50 eV and a line density of 2.0×1015 cm−2. © 1999 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1149280
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  • 2
    Electronic Resource
    Electronic Resource
    Complete polarization control of 8×8 vertical-cavity surface-emitting laser matrix arrays (1995)
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 66 (1995), S. 908-910 
    Details
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Polarization of 8×8 vertical cavity surface emitting laser (VCSEL) arrays is completely controlled. These index-guided VCSELs have a 6×5 μm rectangular poststructure consisting of DBR mirrors. All 64 VCSELs emit fundamental single-mode and linearly polarized light with a polarization angle deviation of only 2.9°. Their light output characteristics are almost the same as those of conventional 6×6 μm polarization-uncontrolled VCSELs. © 1995 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.113593
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  • 3
    Electronic Resource
    Electronic Resource
    Rosmarinic acid in perilla extract inhibits allergic inflammation induced by mite allergen, in a mouse model (2004)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 34 (2004), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Perilla and its constituent rosmarinic acid have been suggested to have anti-allergic activity. However, few studies have examined the effects on allergic asthma.Objective The purpose of this study was to evaluate the effect of oral administration of perilla leaf extract, which contains high amount of rosmarinic acid, on a murine model of allergic asthma induced by house dust mite allergen.Methods C3H/He mice were sensitized by intratracheal administration of Dermatophagoides farinae (Der f). Mice were orally treated with rosmarinic acid in perilla extract (PE) (1.5 mg/mouse/day).Results Der f challenge of sensitized mice elicited pulmonary eosinophilic inflammation, accompanied by an increase in lung expression of IL-4 and IL-5, and eotaxin. Daily treatment with rosmarinic acid in PE significantly prevented the increases in the numbers of eosinophils in bronchoalveolar lavage fluids and also in those around murine airways. Rosmarinic acid in PE treatment also inhibited the enhanced protein expression of IL-4 and IL-5, and eotaxin in the lungs of sensitized mice. Der f challenge also enhanced allergen-specific IgG1, which were also inhibited by rosmarinic acid in PE.Conclusion These results suggest that oral administration of perilla-derived rosmarinic acid is an effective intervention for allergic asthma, possibly through the amelioration of increases in cytokines, chemokines, and allergen-specific antibody.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2004.01979.x
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  • 4
    Electronic Resource
    Electronic Resource
    Gonadal development and non-functional protogyny in a coral-reef damselfish, Dascyllus albisella Gill (2001)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of fish biology 58 (2001), S. 0 
    Details
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: All gonads of the Hawaiian dascyllus Dascyllus albisella, irrespective of the final sex of individuals, developed an ovarian lumen and primary-growth-stage oocytes after an initially undifferentiated state. From this ovarian state or from more differentiated ovaries, some gonads redifferentiated into testes. None of 117 individuals examined had a gonad containing degenerating vitellogenic oocytes and proliferating spermatogenic tissue. Eleven individuals had gonads containing degenerating cortical-alveolus-stage oocytes and developing spermatogenic tissue. The size of these individuals overlapped with the female size range in which the majority of the females were still in the middle of the maturation process. They were absent from the larger size range where the majority of females had vitellogenic oocytes. This indicated that the transition toward maleness is likely to have occurred after the onset of cortical-alveolus stage, but before final oocyte maturation and spawning as females. Therefore the protogynous pattern of gonadal development was non-functional. There was no dimorphism in the sperm duct configuration, and all the testes were secondary testes reported for diandric, protogynous species with undelimited gonads. Very early development of an ovarian lumen appeared to have resulted in a secondary-male configuration in all testes, although redifferentiation into males appeared to have occurred before sexual maturity and spawning as females.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1095-8649.2001.tb02315.x
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  • 5
    Electronic Resource
    Electronic Resource
    The effect of rebamipide on Helicobacter pylori extract-mediated changes of gene expression in gastric epithelial cells (2003)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 18 (2003), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Recent studies have shown that Helicobacter pylori affects intracellular signal transduction in host cells, leading to the activation of transcriptional factors and the induction of pro-inflammatory cytokines. On the other hand, rebamipide, an anti-gastritis and anti-ulcer agent, could scavenge reactive oxygen species and reduce interleukin-8 (IL-8) expression in gastric epithelial cells induced by H. pylori-stimulation through the attenuated activation of nuclear factor-κB (NF-κB).Aims : In this study, we investigated the effects of rebamipide on gene expression in H. pylori-stimulated epithelial cells using DNA chip.Methods : H. pylori water extract (HPE) was prepared from NCTC11637, the type strain of H. pylori. Total RNA was extracted from MKN45 cells, a human gastric cancer cell line, following HPE-stimulation with and without rebamipide for 3 h, and differences in gene expression profiles were observed using GeneChip and Human 6800 probe array.Results : The GeneChip analysis demonstrated that 132 up-regulated genes and 873 down-regulated genes, such as growth factors, chemokines and transcription factors, were detected in MKN45 cells 3 h after stimulation of H. pylori. Among them, several genes, including bFGF, RANTES and MIP-2β, were previously unknown to be expressed in H. pylori-stimulated human gastric cells. Rebamipide reduced expression of 119 genes encoding cytokines, growth factors and their receptors and transcription factors.Conclusions : These findings suggest that rebamipide could inhibit inflammatory reactions and tumour progression by modifying H. pylori infection-induced gene expression in gastric epithelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.18.s1.7.x
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  • 6
    Electronic Resource
    Electronic Resource
    Pioglitazone, a specific PPAR-γ ligand, inhibits aspirin-induced gastric mucosal injury in rats (2001)
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 15 (2001), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Neutrophils activation and tumour necrosis factor-α (TNF-α) induction play a critical role in aspirin-induced gastric mucosal injury. Peroxisome proliferator-activated receptor-γ (PPAR-γ), a member of the nuclear hormone receptor superfamily, has recently been implicated as a regulator of inflammatory responses. The aim of the present study was to determine whether pioglitazone, a specific PPAR-γ ligand, can ameliorate aspirin-induced gastric mucosal injury in rats, and whether the agent can inhibit the increase in neutrophil accumulation associated with TNF-α expression.〈section xml:id="abs1-2"〉〈title type="main"〉Methods:Aspirin-induced injury was produced by the intragastric administration of aspirin (200 mg/kg) and HCl (0.15 N, 8.0 mL/kg). Pioglitazone was given to the rats by gastric intubation 1 h before the aspirin administration. Thiobarbituric acid-reactive substances and tissue-associated myeloperoxidase activity were measured in gastric mucosa as indices of lipid peroxidation and neutrophil infiltration. The gastric concentration of TNF-α and the expression of TNF-α mRNA was determined by ELISA and reverse transcriptase-polymerase chain reaction.〈section xml:id="abs1-3"〉〈title type="main"〉Results:The intragastric administration of acidified aspirin induced hyperemia and haemorrhagic erosions in rat stomachs. The increase in the total gastric erosive area after aspirin administration was significantly inhibited by treatment with pioglitazone in a dose-dependent manner. The increases in thiobarbituric acid-reactive substances and myeloperoxidase activity after aspirin administration were both significantly inhibited by pre-treatment with pioglitazone (10 mg/kg). The gastric content of TNF-α increased and the expression of TNF-α mRNA was up-regulated after aspirin treatment. However, the peak TNF-α mRNA expression 1 h after aspirin administration was inhibited by pioglitazone.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusion:Based on these data, the beneficial effects of pioglitazone on aspirin-induced gastric mucosal injury may be attributed to its anti-inflammatory properties.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2001.00983.x
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  • 7
    Electronic Resource
    Electronic Resource
    Protective role of intracellular glutathione against nitric oxide-induced necrosis in rat gastric mucosal cells (2000)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 14 (2000), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Nitric oxide synthase activity is increased in the stomach in association with Helicobacter pylori infection and portal hypertension, but the mechanism by which nitric oxide contributes to mucosal damage remains unclear. Aim: To examine whether nitric oxide injures gastric mucosal cells and whether cellular glutathione affects nitric oxide-induced cytotoxicity. Methods: A confluent monolayer of RGM-1 gastric mucosal cells was exposed to nitric oxide donors (NOC5 or NOC12). Cell viability was determined by trypan blue dye exclusion, lactate dehydrogenase release and supravital staining with Hoechst 33342 and propidium iodide. The kinetics of the reduced/oxidized forms of glutathione were also measured, as well as the effect of glutathione-depletion or glutathione-precursor treatment on nitric oxide-induced cytotoxicity. Results: Excess exogenous nitric oxide produced by NOC5 or NOC12 induced necrosis in RGM-1 cells in a time- and concentration-dependent manner. The level of reduced glutathione drastically decreased prior to the loss of cell viability and remained low, but oxidized glutathione was not affected. Glutathione depletion increased necrosis of both NOCs in an NOC-concentration-related fashion, while pre-treatment with γ-glutamylcysteine ethyl ester reduced their necrotic susceptibility. Conclusion: Exogenous nitric oxide induced necrosis in gastric mucosal cells, and intracellular reduced glutathione protects gastric mucosal cells from damage by nitric oxide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2000.014s1145.x
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  • 8
    Electronic Resource
    Electronic Resource
    A new mechanism for anti-inflammatory actions of proton pump inhibitors – inhibitory effects on neutrophil–endothelial cell interactions (2000)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 14 (2000), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Neutrophil–endothelial cell interactions mediated by adhesion molecules may be involved in gastric mucosal inflammation associated with Helicobacter pylori or nonsteroidal anti-inflammatory drugs. Aim: To investigate the effects of proton pump inhibitors and histamine-2 receptor antagonists (HRA) on neutrophil-endothelial cell adhesive interactions induced by H. pylori water extract (HPE) or interleukin-1β (IL-1β). Methods: Human peripheral neutrophils and umbilical vein endothelial cells were incubated with either proton pump inhibitors (lansoprazole and omeprazole) or HRA (famotidine and ranitidine). Neutrophil surface expression of CD11b and CD18 and endothelial cell intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) were assessed by flow cytometry and an enzyme immunoassay, respectively. Neutrophil adherence was defined as the ratio of exogenous neutrophils that adhered to the endothelial monolayers. Results: The expression of CD11b and CD18 on neutrophils and neutrophil-dependent adhesion to endothelial cells elicited by HPE were inhibited by lansoprazole and omeprazole at clinical relevant doses, and the expression of ICAM-1 and VCAM-1 on endothelial cells and endothelial-dependent neutrophil adherence induced by IL-1β were also inhibited by lansoprazole and omeprazole at similar doses. Famotidine and ranitidine had no effect on neutrophil–endothelial cell interactions. Conclusions: These results indicate that proton pump inhibitors can attenuate neutrophil adherence to endothelial cells via inhibiting the expression of adhesion molecules, suggesting that proton pump inhibitors may have anti-inflammatory activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2000.014s1074.x
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  • 9
    Electronic Resource
    Electronic Resource
    Effects of rebamipide, a gastro-protective drug on the Helicobacter pylori status and inflammation in the gastric mucosa of patients with gastric ulcer: a randomized double-blind placebo-controlled multicentre trial (2003)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 18 (2003), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aims : To investigate the effects of rebamipide on the Helicobacter pylori eradication rate with amoxicillin and omeprazole. The trial also examined its histological effects on gastro-mucosal inflammation after eradication.Methods : Two hundred and six H. pylori-positive patients with active gastric ulcer underwent 8-week based therapy (OA) consisting of 2-week amoxicillin with omeprazole and subsequent 6-week omeprazole. They randomly received either rebamipide (OA-R) or placebo (OA-P) for 16 weeks: combined with the OA based therapy, and subsequently for another 8 weeks. Besides eradication rate, inflammatory findings of gastric mucosa after eradication were evaluated histologically.Results : Per Protocol Set analysis showed no significant difference in eradication rate between OA-R (64.6%; 95% confidence interval, 54.3–75.0%) and OA-P (67.9%; 95% CI, 57.6–78.3%). Histological findings in the gastric mucosa of the ulcer region, however, indicated a significant improvement (P = 0.017) in inflammation scores in OA-R (1.84 ± 0.41) compared with that in OA-P (2.02 ± 0.39) after 16-weeks of treatment. This suppressive effect on inflammation was observed even in the OA-R patients unsuccessfully eradicated.Conclusion : Rebamipide demonstrated a suppressive effect on the persistent and possibly chronic inflammation in the gastric mucosa of the ulcer region after eradication, but the drug did not improve the eradication rate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.18.s1.20.x
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  • 10
    Electronic Resource
    Electronic Resource
    Ubiquitin-proteasome inhibitor enhances tumour necrosis factor-α-induced apoptosis in rat gastric epithelial cells (2002)
    Oxford UK : Blackwell Science Ltd.
    Alimentary pharmacology & therapeutics 16 (2002), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Tumour necrosis factor (TNF-α) is a candidate factor for involvement in inflammation-mediated gastric mucosal injury. However, the effect of this cytokine on gastric epithelial cells has been poorly investigated. In the present study, we examined whether gastric epithelial cells are resistant to TNF- α-induced apoptosis, and whether this resistance is related to ubiquitin-proteasome-associated nuclear factor-κB (NF-κB) activation.〈section xml:id="abs1-2"〉〈title type="main"〉Methods:The rat gastric mucosal cell line RGM-1 was grown in DMEM/F12 medium supplemented with 10% FCS. Confluent monolayers of cells were pretreated or not for 60 min with PSI, a peptide aldehyde known to specifically inhibit the chymotrypsin-like activity of 26S proteasome. Cells were subsequently stimulated with recombinant rat TNF-α and their viability was determined by WST-1 assay. Apoptosis was confirmed by fluorescence microscopy after staining with Hoechst 33342 and propidium iodide, and DNA fragmentation was determined by flow cytometry using an APO-BRDU kit. IκB-α and the p65 binding subunit of NF-κB were detected by Western blots.〈section xml:id="abs1-3"〉〈title type="main"〉Results:Twenty-four-hour incubation with TNF-α alone or PSI alone did not affect the cell viability of RGM-1 cells. Pretreatment with PSI significantly enhanced the level of apoptosis induced by TNF-α. In RGM-1 cells treated with TNF-α, cytoplasmic IκB-α decreased and p65 in nuclear extracts increased markedly 30 min after cytokine stimulation. Pretreatment with PSI at 12.5 μmol/L blocked these TNF-α-induced changes.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusion:PSI enhances TNF-α-induced apoptosis through inhibition of NF-κB activation in RGM-1 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.16.s2.30.x
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