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  • 1
    Electronic Resource
    Electronic Resource
    Renal cell carcinoma with rhabdoid features: an aggressive neoplasm (2002)
    Oxford, UK : Blackwell Science Ltd
    Histopathology 41 (2002), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aims:  Only a few reports on renal cell carcinoma with rhabdoid features have been published. This study was performed to investigate the clinicopathological characteristics of renal cell carcinomas with rhabdoid features.Methods and results:  Among 253 cases of renal cell carcinoma in adults, eight cases with rhabdoid features were detected. Rhabdoid areas ranged from 10% to 90% of each of the cases. Seven of the eight cases were TNM stage III or IV, and four of the eight cases died within 8 months of surgery. Immunohistochemically, the rhabdoid areas were positive for CAM 5.2 (4/8), AE1/AE3 (6/8), epithelial membrane antigen (6/8) and vimentin (8/8), and negative for myogenetic markers (0/8). The mean MIB-1 labelling index in the rhabdoid areas was higher than that in the definite carcinomatous areas. Ultrastructurally, perinuclear whorls of intermediate filaments were demonstrated in three of the eight cases using paraffin-embedded blocks.Conclusions:  The rhabdoid areas in renal cell carcinoma have histological, immunohistochemical and ultrastructural similarities to malignant rhabdoid tumours. Renal cell carcinoma with rhabdoid features is a highly aggressive neoplasm and its malignant behaviour may be due to the high cell-proliferative activity of the rhabdoid areas. Rhabdoid features in renal cell carcinoma may represent the endpoint of clonal evolution of renal cell carcinoma (especially in clear cell type cases).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2559.2002.01427.x
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  • 2
    Electronic Resource
    Electronic Resource
    Safety and efficacy of glucagon as a premedication for upper gastrointestinal endoscopy—a comparative study with butyl scopolamine bromide (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: Glucagon inhibits digestive motility and is used for endoscopic premedication; however, its effect on cardiopulmonary function during endoscopy has not yet been fully investigated.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To clarify the efficacy and safety of glucagon compared with butyl scopolamine bromide as upper gastrointestinal endoscopy premedication.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Two hundred and forty consecutive patients over 40 years of age, referred for upper gastrointestinal endoscopy, without any complications, were studied. These patients were randomly premedicated with butyl scopolamine bromide (SC group) or glucagon (G group). Time course changes in blood pressure, arterial oxygen saturation, heart rate and the number of retching episodes during endoscopy were examined. The efficacy of glucose tablets after upper gastrointestinal endoscopy to prevent hypoglycaemia caused by glucagon was evaluated. Cardiopulmonary parameters were also examined in 77 complicated patients with glucagon premedication (GC group).〈section xml:id="abs1-4"〉〈title type="main"〉Results:A continuous increase in heart rate during upper gastrointestinal endoscopy was observed in the SC group, but not in the G and GC groups. Blood pressure, arterial oxygen saturation and number of retching episodes were not different between the groups. Hypoglycaemia-related symptoms were frequent in the G group without glucose tablets, but were prevented by the administration of glucose.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:Glucagon has a weaker effect on cardiopulmonary function during upper gastrointestinal endoscopy than butyl scopolamine bromide. Glucose administration prevents hypoglycaemia-related symptoms caused by glucagon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2002.01148.x
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  • 3
    Electronic Resource
    Electronic Resource
    Helicobacter pylori infection influences nocturnal gastric acid breakthrough (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: Nocturnal gastric acid breakthrough is defined as night-time periods when gastrin pH falls below 4.0 for greater than 1h during administration of a proton pump inhibitor. This phenomenon is a serious problem for patients who require strict control of their gastric acid secretions.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To investigate the prevalence of nocturnal gastric acid breakthrough in Japanese subjects during administration of rabeprazole, and to clarify the relationship between Helicobacter pylori infection and nocturnal gastric acid breakthrough.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Thirty-one normal male volunteers were examined by ambulatory 24 h gastric pH monitoring four times: without medication, after a morning or an evening dose of 20 mg rabeprazole, and after administration of an H2-receptor antagonist at bedtime, in addition to the morning dose of rabeprazole. H. pylori infection was determined by the 13C-urea breath test and an assay for serum anti-H. pylori antibody.〈section xml:id="abs1-4"〉〈title type="main"〉Result:Nocturnal gastric acid breakthrough was observed in 12 patients (39%) after the morning dose of 20 mg rabeprazole. In all cases, nocturnal gastric acid breakthrough was inhibited completely by administration of the H2-receptor antagonist at bedtime. Only one patient with nocturnal gastric acid breakthrough had H. pylori infection.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:The absence of H. pylori infection appears to be closely related to the occurrence of nocturnal gastric acid breakthrough during dosing with a proton pump inhibitor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2000.00799.x
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  • 4
    Electronic Resource
    Electronic Resource
    CYP2C19 genotype status and intragastric pH during dosing with lansoprazole or rabeprazole (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: CYP2C19 has an important role in the catabolism of several proton pump inhibitors. However, the relative contribution of CYP2C19-mediated metabolism varies among the different proton pump inhibitors.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To determine the effect of CYP2C19 genotype status on intragastric pH during dosing with lansoprazole or rabeprazole.〈section xml:id="abs1-3"〉〈title type="main"〉Subjects and methods:The subjects were 20 male volunteers without Helicobacter pylori infection. Their CYP2C19 genotype status was determined by a polymerase chain reaction-restriction fragment length polymorphism method. Twenty-four-hour monitoring of intragastric acidity was performed three times: once without medication, once on the last day of a 7-day course of rabeprazole, and once on the last day of a 7-day course of lansoprazole.〈section xml:id="abs1-4"〉〈title type="main"〉Results:Subjects were divided into three groups on the basis of their CYP2C19 genotype status: homozygous extensive metabolizers (homo-EMs, n=7), heterozygous extensive metabolizers (hetero-EMs, n=9), and poor metabolizers (PMs, n=4). The median pH during rabeprazole administration was not influenced by CYP2C19 genotype. On the other hand, the median pH in PMs during lansoprazole dosing was higher than in homo-EMs and hetero-EMs. The percentage of time with pH 〈 4.0 had a similar tendency to that of median pH.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:CYP2C19 genotype status influences gastric acid suppression by lansoprazole, but not by rabeprazole.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2000.00840.x
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  • 5
    Electronic Resource
    Electronic Resource
    Time-course changes of ECL cell markers in acetic acid-induced gastric ulcers in rats (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: Enterochromaffin-like (ECL) cells are the major source of histamine for the regulation of gastric acid secretion, and also contain histidine decarboxylase (HDC), vesicular monoamine transporter 2 (VMAT2), and chromogranin A (CgA). Although gastric acid secretion is suppressed during ulcer healing, the role of ECL cells in that process is not yet fully understood. In the present study, we investigated the changes in ECL cell number during healing of experimental ulcers in rats.〈section xml:id="abs1-2"〉〈title type="main"〉Materials and methods:Seven-week-old male Wistar rats were used. Acetic acid-induced ulcers were caused by an application of 100% acetic acid to the serosal surface of the rat stomachs. At different time points following the induction (12 h-15 days), time-course changes of HDC, VMAT2, and CgA mRNA expression were investigated by Northern blot analysis. The expressions of HDC, VMAT2, and CgA were immunostained on gastric mucosal sections with ulcers.〈section xml:id="abs1-3"〉〈title type="main"〉Results:HDC, VMAT2, and CgA mRNA in gastric mucosa each showed an initial marked transient decrease, followed by an increase on day 10 back to the initial value. HDC, VMAT2, and CgA-immunoreactive cells at the ulcer margin were reduced in number on day 3, compared with those in distant areas. On day 10, however, they returned to levels similar to those in distant areas.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusion:The present study revealed a local down-regulation of HDC, VMAT2, and CgA in ECL cells at the ulcer margin. As a result, we concluded that a suppression of ECL cell activity during ulcer healing may be involved in suppressed gastric acid secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.16.s2.10.x
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  • 6
    Electronic Resource
    Electronic Resource
    Nizatidine and cisapride enhance salivary secretion in humans (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: Salivation plays an important role in the defence of the oesophageal mucosa against gastric acidic reflux and can be evoked by cholinergic stimulation. Both nizatidine and cisapride have been reported to increase acetylcholine concentrations in the cholinergic system.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To investigate the effect of nizatidine and cisapride on salivary secretion, salivary epidermal growth factor and bicarbonate output.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:The salivary volume and concentration of salivary epidermal growth factor and bicarbonate were measured after the administration of nizatidine (150 mg), famotidine (20 mg) and cisapride (5 mg) in 30 male healthy volunteers.〈section xml:id="abs1-4"〉〈title type="main"〉Results:Basal and stimulated salivary secretions were found to be increased after the administration of nizatidine and cisapride. In contrast, salivary secretion was not increased by famotidine. Although epidermal growth factor content was not augmented, nizatidine and cisapride administration also increased the bicarbonate output in mastication-stimulated saliva.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:Increased salivary secretion and bicarbonate output induced by nizatidine may be useful for the treatment of patients with gastro-oesophageal reflux disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2002.01159.x
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  • 7
    Electronic Resource
    Electronic Resource
    Intragastric distribution of Helicobacter pylori during short-term omeprazole therapy: study using Carnoy’s fixation and immunohistochemistry for detection of bacteria (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: There is controversy about the effect of acid-suppressive therapy on Helicobacter pylori density and the severity of histological gastritis in the corpus.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To evaluate the precise distribution of H. pylori, both on the surface mucus cells and in the surface mucus gel layer, by using Carnoy’s fixation and immunostaining for the detection of bacteria.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:A total of 19 peptic ulcer patients with H. pylori infection were studied. All patients received a 6-week course of treatment with omeprazole (20 mg/day). Before and after the therapy, H. pylori density in Carnoy-fixed tissue sections was examined immunohistochemically. The effect of omeprazole therapy on the severity of gastritis was also evaluated.〈section xml:id="abs1-4"〉〈title type="main"〉Results: H. pylori density and the grade of gastritis significantly decreased in the antrum after omeprazole therapy. In the corpus, however, there were no significant changes in H. pylori density or the severity of gastritis after omeprazole therapy.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:Carnoy’s fixation and immunostaining was found to be useful for the detection of H. pylori in the surface mucus gel layer as well as on the surface mucus cells in biopsy tissue sections. By using this method, H. pylori density decreased in the antrum, but remained unchanged in the corpus after a 6-week course of omeprazole therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2001.01067.x
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  • 8
    Electronic Resource
    Electronic Resource
    Efficacy of ecabet sodium for Helicobacter pylori eradication triple therapy in comparison with a lansoprazole-based regimen (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: : The cytoprotective agent, ecabet sodium, inhibits urease activity and growth of Helicobacter pylori.〈section xml:id="abs1-2"〉〈title type="main"〉Aim: To evaluate the efficacy and safety of ecabet sodium-based eradication of H. pylori infection, compared with a lansoprazole-based regimen, in a randomized multicentre study.〈section xml:id="abs1-3"〉〈title type="main"〉Subjects and methods: A total of 120 H. pylori-positive patients were assigned to one of two treatment regimens for 2 weeks: ecabet sodium 1 g b.d., amoxicillin 500 mg t.d.s. and clarithromycin 400 mg b.d. (EAC: 60 patients); or lansoprazole 30 mg (o.m.) with the same antimicrobial agents (LAC: 60 patients). Cure of infection was assessed by a 13C-urea breath test 1 month after completion of treatment.〈section xml:id="abs1-4"〉〈title type="main"〉Results: One patient in the EAC group and two in the LAC group did not complete therapy because of an adverse event, and three did not undergo the 13C-urea breath test. Cure rates for the intention-to-treat, all-patients-treated and per protocol analysis in the EAC group were 85%, 86% and 88%, respectively, whereas those in the LAC group were 85%, 88% and 91%. There were no significant differences in cure rate or adverse events between the two regimens.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions: Ecabet sodium in combination with amoxicillin and clarithromycin is as effective as lansoprazole-based eradication therapy for H. pylori.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2001.01022.x
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  • 9
    Electronic Resource
    Electronic Resource
    Introduction (2004)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 20 (2004), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2004.02255.x
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  • 10
    Electronic Resource
    Electronic Resource
    Expression of midkine and receptor-like protein tyrosine phosphatase (RPTP)-β genes in the rat stomach and the influence of rebamipide (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 : Midkine has been reported to bind to receptor-like protein tyrosine phosphatase (RPTP)-β and to play important roles in growth and differentiation of various cells. Midkine is expressed in rat stomach during experimental ulcer healing, suggesting that the midkine-RPTP-β system has some physiological functions in the stomach. Rebamipide is a mucoprotective drug used for the treatment of gastric ulcers. We have tested the hypothesis that the ulcer healing mechanism stimulated by rebamipide is linked physiologically to the gastric midkine-RPTP-β system.Materials and methods : Seven-week-old-male Wistar rats were used. Midkine and RPTP-β gene expression in rat stomach was investigated by laser capture microdissection coupled with the reverse transcription-polymerase chain reaction (RT-PCR). The effects of rebamipide on midkine and RPTP-β expression in rat stomach and the gastric epithelial cell line RGM1 were evaluated by RT-PCR and Northern blot analyses.Results : Midkine and RPTP-β expression was detected in the gastric mucosal, submucosal and muscle layers. Rebamipide stimulated both midkine and RPTP-β expression in rat stomach and RGM1 cells.Conclusion : Rebamipide may protect the gastric mucosa by regulating midkine and RPTP-β expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.18.s1.12.x
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