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  • 11
    Electronic Resource
    Electronic Resource
    Differential expression of CR3, FcɛRll and FcγRlll on Polymorphonuclear leukocytes in gingival crevicular fluid (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of periodontal research 28 (1993), S. 0 
    Details
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Polymorphonuclear leukocytes (PMNLs) are the most numerous cell population among the cellular infiltrates in gingival crevicular fluid (GCF) and play important roles in the host-defensive system in the gingival crevices. We determined the percentage of neutrophils, cosinophils and basophils in total PMNLs by light microscopic observation using Randolph-methylene blue staining, then assessed flow cytometric differences in the expression of CR3, FcγRIII, FcɛRII. LFA-1α, and LFA-Iβ on PMNL in GCF and peripheral blood (PB) from 21 patients with adult periodontius (AP) and 13 healthy donors. Percentages of basophils and eosinophils were higher in GCF than in PB. In both AP patients and healthy subjects, expression of CR3 and FcɛRll was higher while FeγRIII was lower in GCF than in PB. The statistical analysis showed that the expressions of FcγRIII and FcɛRII on GCF PMNLs were lower in AP patients than in healthy subjects. Expressions of LFA-1α and β on GCF were similar to those on PB PMNLs. PB PMNLs stimulated in vitro with Porphyromonas gingivalts culture supernatant and fMLP displayed an expression pattern of CR3, FcγRIII and FcɛRII on GCF PMNLs. However, C5a and IL-I failed to induce changes in FcγRIII and FcɛRII. The results indicate that GCF neutrophils are activated, present enhanced adhesion and a decreased IgG-binding ability which would reflect that they are at the terminal stage of activation, and that GCF contains a larger eosinophil fraction than in PB. Moreover, these GCF eosinophils appear to be activated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0765.1993.tb01080.x
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  • 12
    Electronic Resource
    Electronic Resource
    Effect of mechanical pressure on the blood flow in human palatal mucosa measured by temperature controlled thermoelectrical method (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral rehabilitation 19 (1992), S. 0 
    Details
    ISSN: 1365-2842
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Mucosal blood flow in the human palate was measured by a temperature controlled thermoelectrical method based on the thermal conductivity of mucosal tissue using a blood flow monitor and a non-invasive surface probe.The effect of mechanical pressure on the palatal mucosal tissue was studied. Mechanical pressure (2.5, 5.0, 7.5, 10.0 or 15.0g mm−2) to the mucosal surface was exerted circumferentially around the surface probe. In five out of seven subjects, the blood flow showed a tendency to be almost constant under the mechanical pressures which are 10.0g mm−2 or higher. The effect of the duration of the pressure (10.0g mm−2) exertion on the blood flow was also investigated and it was revealed that the blood flow tended to be constant after 60s in every subject. In the present study, it was also demonstrated that the temperature controlled thermoelectrical method is appropriate for studying the blood flow dynamics in oral mucosa.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2842.1992.tb01116.x
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  • 13
    Electronic Resource
    Electronic Resource
    Multi-unit fixed partial denture for a bilateral cleft palate patient: a clinical report (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of oral rehabilitation 32 (2005), S. 0 
    Details
    ISSN: 1365-2842
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: summary  Patients with cleft palates eventually require definitive fixed or removable dental prostheses after the maintenance of arch alignment and occlusal relationship during adolescence. This case report presents application of a resin composite veneered fixed partial denture utilized as a definitive prosthesis for a bilateral cleft palate patient after stable occlusion had been established orthodontically. The composite veneered long span fixed partial denture provides adequate aesthetics and function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2842.2005.01468.x
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  • 14
    Electronic Resource
    Electronic Resource
    Effect of CYP2C19 polymorphism on the safety and efficacy of omeprazole in Japanese patients with recurrent reflux oesophagitis (2005)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 21 (2005), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : The polymorphic enzyme cytochrome P450 2C19 affects omeprazole metabolism. This influence on metabolism might affect serum gastrin levels, and safety, during long-term treatment of reflux oesophagitis.Aim : To examine the relationship between cytochrome P450 2C19 genotype and the safety profile of long-term omeprazole treatment.Methods : A total of 119 Japanese patients with recurrent reflux oesophagitis underwent cytochrome P450 2C19 genotyping prior to receiving daily omeprazole 10 mg or 20 mg for 6–12 months, during which adverse event frequency, serum gastrin levels and endoscopic findings were monitored.Results : The incidences of adverse events, serious adverse events and adverse events leading to withdrawal did not differ between homozygous extensive metabolizer (n = 46), heterozygous extensive metabolizer (n = 53) or poor metabolizer (n = 20) groups. In all genotype groups, serum gastrin increased during the first 3 months of dosing but stabilized thereafter. No significant differences were seen either in the rate of reflux oesophagitis healing or symptom improvement among genotype groups.Conclusions : Long-term treatment with omeprazole was well-tolerated in Japanese patients, irrespective of their cytochrome P450 2C19 metabolic genotype, indicating that dose adjustment depending on metabolic genotype is not required during treatment with omeprazole.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2005.02486.x
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  • 15
    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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  • 16
    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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  • 17
    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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  • 18
    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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  • 19
    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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  • 20
    Electronic Resource
    Electronic Resource
    Role of elastase and active oxygen species in gastric mucosal injury induced by aspirin administration in Helicobacter pylori-infected Mongolian gerbils (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: H. pylori infection potentiates aspirin-induced gastric mucosal injury by mechanisms that include accumulation of activated neutrophils.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To determine the role of elastase and active oxygen species (AOS) produced by activated neutrophils in the gastric mucosal injury induced by administration of acidified aspirin to H. pylori-infected Mongolian gerbils.〈section xml:id="abs1-3"〉〈title type="main"〉Methods: H. pylori ATCC43504 culture broth was administered by oral gavage to male Mongolian gerbils at 7 weeks of age. After 4 weeks, acidified aspirin (400 mg/kg) was administered orally, and 3 h later, the total area of gastric erosions, myeloperoxidase (MPO) activity (an index of neutrophil accumulation), thiobarbituric acid-reactive substances (TBARS, an index of lipid peroxidation), and KC/GRO (a chemo-attractive cytokine in rodents) were measured in gastric mucosa. To determine the role of elastase or AOS derived from neutrophils in these circumstances, ONO-5046 (an elastase inhibitor), a combination of superoxide dismutase (SOD) and catalase (scavengers of AOS), and polaprezinc (an anti-ulcer agent with anti-inflammatory effects) were administered before aspirin.〈section xml:id="abs1-4"〉〈title type="main"〉Results:ONO-5046 inhibited the increase in gastric erosions and mucosal TBARS induced by administration of aspirin to H. pylori-infected gerbils, but not the increases in MPO activity or KC/GRO contents. A combination of SOD and catalase or polaprezinc significantly reduced gastric erosions, TBARS concentrations, MPO activity and KC/GRO concentration.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:These results suggest that neutrophil-derived-elastase and -oxidants play an important role in the gastric mucosal injury induced by administration of aspirin to H. pylori-infected gerbils.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.16.s2.32.x
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