bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of One‐to‐One Midwifery: Women's Responses to Care
Authors: McCourt Christine , Page Lesley , Hewison Jenny , Vail Andy 
Published: March 2003

Background:One‐to‐one midwifery was a demonstration project introduced into a London‐based maternity service in 1993 to put into practice the new government policy for maternity services in England. Evaluation was integral to the development of the project.Methods:The evaluation of women's responses was conducted between August 1994 and August 1995 based on a longitudinal, self‐completion questionnaire, interviews, and focus groups. Women in the study group (n= 728) received the new service and women in the control group (n= 675) received conventional care. The study design integrated quantitative and qualitative methods and went beyond a simple estimation of satisfaction with care.Results:Satisfaction with antenatal and birth care was generally high, but study group women showed more positive responses overall. Both groups showed a preference for continuity of caregiver, but expectations were higher in the study group (72% of the study group and 42% of the control group preferred to see one caregiver). Both groups had less satisfied responses to hospital postnatal care (50% study and 54% control group were very satisfied). Study group women showed greater preparedness for birth than control group women (18% vs 12%“very well prepared”) and for the time after the baby's birth (26% vs 15%“very prepared”).Conclusions:The study demonstrated that women were more satisfied with the one‐to‐one model of care. Taken together with the results of clinical and economic audit and professional responses, the evaluation suggests that this model should be developed and evaluated further to gain a greater understanding of women's needs of the maternity service. (BIRTH 25:2 June 1998)
The Role of Gastric Helicobacter and N‐methyl‐N′‐nitro‐ N‐nitrosoguanidine in Carcinogenesis of Mice
Authors: Danon Stephen J. , Eaton Kathryn A. 
Published: March 2003

Background.The aim of this study was to determine whether gastric epithelial proliferation due to gastric Helicobacter infection in mice represents a preneoplastic lesion.Materials and Methods. Helicobacter heilmannii infected and uninfected mice were treated with 150 μg/ml N‐methyl‐N′‐nitro‐N‐nitrosoguanidine in drinking water for either 20 or 38 weeks. Mice were killed 12 or 18 months after bacterial inoculation.Results.All infected mice developed lymphoplasmocytic gastritis and epithelial hyperplasia. Proliferative gastric lesions were characterised by nodular hypertrophy of the glandular mucosa, multifocal epithelial hyperplasia, and elevated BrdU labeling index. Intestinal metaplasia and true atrophy were not present but proliferative glands were poorly differentiated, lined by mucus‐type epithelial cells with no parietal, chief or other specialized cell types. Neoplasms developed only in MNNG‐treated mice. of the 180 treated mice the following neoplasms developed: 14 squamous cell carcinomas of mouth and forestomach; 37 hemangiosarcomas of the intestinal serosa; and 15 splenic lymphomas. No tumors were present in the glandular gastric mucosa, and infection did not affect tumor incidence. p53 overexpression occurred in 79% of hemangiosarcomas and 71% of squamous cell carcinomas but not in normal or proliferative gastric glandular mucosa.Conclusions.Gastric proliferative lesions in Helicobacter‐infected mice are not preneoplastic, and the combination of an alkylating agent and non‐neoplastic proliferation does not result in gastric carcinogenesis in mice.
Optimal PPI‐based Triple Therapy for the Cure of Helicobacter pylori Infection: A Single Center Comparison of Four 14‐day Schedules
Authors: Battaglia Guiseppe , Mario Francesco Di , Leandro Gioacchino , Benvenuti Maria Eugenia , Donisi Pietro Maria , Vianello Fabio , Bò Nadia Dal , Pasini Michele , Pasquino Marcello , Vigneri Sergio 
Published: March 2003

Background. Helicobacter pylori eradication is accomplished using a wide array of drugs combined in a multitude of dosage schedules. The aim of the present study was to define the best 14‐day eradication schedule using a PPI plus either two antibiotics or one antibiotic and bismuth.Material and Methods.For this study, 367 subjects (198 males, 169 females, age 22–87 years) with document H. pylori infection of the stomach were recruited from outpatients of the Gastroenterology Department of the Venezia Hospital. In all patients, H. pylori infection was identified by histology and the CLO‐test. Patients were treated as follows: 1) PPI (P) plus clarithromycin (C) 250 mg plus amoxicillin (A) 1000mg bid (P+C+A); 2) P plus C plus bismuth subcitrate (B) 120 mg qid (P+C+B); 3) P plus C plus tinidazole (T) 500 mg bid (P+C+T); and 4) P plus A plus T bid (P+A+T). After two months, an upper gastrointestinal endoscopy was repeated for end point histological evaluation and the CLO‐ test. Positivity of one of the two methods was considered sufficient to define H. pylori as “not eradicated”. Statistics: Chi‐squared test and Fisher exact test.Results.Thirty‐three subjects dropped out (six due to adverse events). P+C+B was proven significantly less effective than P+C+A, P+C+T and P+A+T, eradication rates being, respectively, 75.0%, 90.5%, 87.6%, 92.0%, (p = .005, per protocol analysis).Conclusions.All PPI‐based triple therapies tested in this study were effective in curing H. pylori infection; however, P+C+B resulted in rates too low (< 85%) to be recommended. P+C+A and P+A+T resulted in the high cure rates and thus may be considered the treatment of choice.
Follow‐Up of Helicobacter pylori Positive Gastritis and Argyrophil Cells Pattern During the Natural Course of Gastric Ulcer
Authors: Maaroos Heidi‐Ingrid , Havu Niilo , Sipponen Pentti 
Published: March 2003

Background.A follow‐up of argyrophil cell hyperplasia in Helicobacter pylori‐positive corpus gastritis in gastric ulcer patients during the natural course of ulcer disease.Methods.Endoscopic biopsies (4 specimens) were obtained step‐wise from the posterior wall of the corpus mucosa in 55 gastric ulcer (GU) patients. The natural course of GU was followed up in 38 patients during more than 10~years (maximum 19~years), and altogether 115 endoscopic examinations were made: 20 patients were re‐examined once, 14 twice, and 4 three times. A total of 364 biopsies from 307 biopsy sites were stained by Grimelius’ silver, hematoxylin‐eosin, and Giemsa method for the analysis of the argyrophil endocrine cells, chronic gastritis, and H. pylori colonization, respectively, according to the Sydney System.Results.Of 307 biopsy sites, 153 (50%) showed some grade of ACH. Focal (linear/micronodular) hyperplasia was found in 118 (77%) of biopsy sites; it was detected in 78 (66%) cases of atrophic corpus mucosa, but was present in only 14 (12%) cases of gastritis without atrophy or in the normal mucosa. In the follow‐up patients, ACH evolved in 17 and progressed in 6 cases, and a simultaneous development of atrophic corpus gastritis was found in 20 cases.Conclusion.This study demonstrates that ACH evolves during the natural course of GU, alongside the development of chronic atrophic gastritis.
The Ideal Therapy Must Be Def ined in Each Geographical Area: Experience with a Quadruple Therapy in Spain
Authors: Gomollón F. , Ducóns J.A. , Gimeno L. , Fuentes J. , García S. , Vera J. , Montoro M. 
Published: March 2003

Background. Multiple therapeutic combinations have been tested to determine the optimal regimen(s) for Helicobacter pylori eradication, leading to very different results depending on the geographical area. Our goal was to evaluate the efficacy of a “quadruple” therapy with omeprazole, tetracycline, bismuth and metronidazole in our area. Materials and Methods. We investigate 106 consecutive patients with active peptic ulcer disease (duodenal, gastric or both) and Helicobacter pylori infection. One‐week therapy with omeprazole 20 mg b.i.d., tetracycline hydrochloride 500 mg q.i.d., colloidal bismuth subcitrate 120 mg q.i.d., and metronidazole 250 mg t.i.d was prescribed. Between the days 30 and 40 after treatment ended follow‐up endoscopy was performed. Eradication was defined as both negative urease test and histology. Between days 90 and 360 a 13C urea breath test was performed in 100 patients. Results. Of the 106 patients in the study, 91 had duodenal ulcer, 12 had gastric ulcer, and 3 had both. Side effects were observed in 25% of the cases. Eradication was achieved in 87.7% (93/106; CI 79.9–93.3). Healing was obtained in 95.2% (100/105; CI 89.2–98.4); 97.8% (CI 92.4–99.7) in those eradicated and 75% (CI 42.8–94.5) in non‐eradicated (p < .01). Conclusions. Quadruple therapy with omeprazole, tetracycline, bismuth subcitrate and metronidazole achieves healing rates up to 95–100%. The 87.7% eradication rate obtained suggests that the regimen we used is a reasonable therapeutic alternative in our area.
Risk of Gastrointestinal Bleeding Associated with Helicobacter pylori Infection in Patients with Hemophilia or von Willebrand’s Syndrome
Authors: Braden Barbara , Wenke Andrea , Karich Hans‐Joachim , Dietrich Christoph F. , Scharrer Inge , Caspary Wolfgang F. , Lembcke Bernhard 
Published: March 2003

Background.Many episodes of bleeding in the upper gastrointestinal tract are caused by Helicobacter pylori infection. Because these episodes present a life‐threatening complication in patients with bleeding disorders, we prospectively investigated the prevalence of H. pylori infection in patients with hemophilia A or B and with the von Willebrand syndrome.Methods.Seventy patients (54 men, 16 women, ages 40 ± 11 years) and 100 age‐related volunteers (63 men, 37 women, ages 39 ± 9 years) were tested for H. pylori infection using the 13C urea breath test. Fifty‐four patients with hemophilia and 16 patients with von Willebrand syndrome participated.Results.Thirty‐three (33%) of the controls and 24 (34.3%) of the patients showed positive 13C urea breath tests (p = .97). Nineteen (35.2%) patients with hemophilia and 5 (31.3%) patients with von Willebrand syndrome were positive for H. pylori. History of dyspeptic symptoms (28% vs. 26%) were not different in patients and controls (p = .91). Gastric ulcers (20% vs. 5%) and duodenal ulcers (7% vs. 5%) were diagnosed more often in patients with bleeding disorders. Fourteen of the patients (20%), but none of the controls had a history of gastrointestinal bleeding (p < .001).Conclusions.The rate of H. pylori infection and dyspepsia in patients with bleeding disorders is similar to the prevalence in the normal population. Due to increased bleeding complications, H. pylori screening and therapy appears mandatory in patients with bleeding disorders.
Characterization of Helicobacter felis by Pulsed‐Field Gel Electrophoresis, Plasmid Profiling and Ribotyping
Authors: Jalava, Katri , De Ungria, Maria Corazon , O’Rourke, Jani , Lee, Adrian , Hirvi, Urszula , Hänninen Marja‐Liisa 
Published: March 2003

Background. Helicobacter felis, an organism naturally infecting both canine and feline gastric mucosa, has been largely used as in animal models to study the ecology and treatment of human Helicobacter pylori infections. H. felis has not yet been studied at the genetic level.Methods.The aims of this study were to modify an in situ DNA isolation method suitable for H. felis and, by the use of pulsed‐field gel electrophoresis (PFGE), plasmid profiling, and ribotyping, to determine the degree of genetic variation among H. felis strains isolated from cats and dogs from various geographic locations, and to determine the genome size of H. felis. Furthermore, the ability of these new H. felis strains to colonize mice was tested.Results.Most H. felis strains were distinguishable from each other, and 20 distinct PFGE types were detected. Four pairs of strains within a country and animal species produced identical patterns. All strains tested were found to carry several plasmids and plasmid profiling was equally discriminatory to PFGE. Ribotyping was not able to discriminate all the strains.Conclusions.The genome size of H. felis was found to be ≈ 1.6 Mb.
Role of Hpn and NixA of Helicobacter pylori in Susceptibility and Resistance to Bismuth and Other Metal Ions
Authors: Mobley Harry L.T. , Garner Rachel M. , Chippendale Gwynn R. , Gilbert Joanne V. , Kane Anne V. , Plaut Andrew G. 
Published: March 2003

Background. Helicobacter pylori produces Hpn, a 60‐amino acid, histidine‐rich protein that avidly binds nickel and zinc ions, and NixA, a high‐affinity nickel transporter in the cytoplasmic membrane. We tested the hypothesis that Hpn and NixA govern susceptibility to metal ions in H. pylori.Materials and Methods. Hpn‐negative mutants of four H. pylori strains were constructed by standard allelic exchange techniques to yield isogenic Hpn+/Hpn‐deficient pairs. A metal concentration that inhibited growth by 50% (IC50) was calculated for Ni2+, Zn2+, Cu2+, and Co2+ by comparing OD600 of cultures in metal‐supplemented and control media.Results. Among all four pairs of isogenic strains, the tolerance for Ni2+ was reduced significantly (p < .001) in the Hpn mutants; the mean IC50 value for wild‐type strains was 1.9 mM; for the mutant, it was 0.8 mM. In   contrast, growth inhibition by Zn2+ was identical within the fours pairs, as was Cu2+ and Co2+ tolerance in one pair tested. We also found that deletion of the hpn gene increases susceptibility to therapeutic forms of bismuth by testing a mutant and wild‐type pair with ranitidine bismuth citrate, bismuth citrate, and four antibiotics. Minimal inhibitory concentrations of ranitidine bismuth citrate dropped from 9.2 to 2.3 μg/ml, and those of bismuth citrate dropped from 7.4 to 3.2 μg/ml (p < .05 for both comparisons), while susceptibility to the antibiotics was unaffected. Disruption of the nixA gene encoding the specific Ni2+ transport protein of H. pylori did not change susceptibility to bismuth.Conclusion. We concluded that bacteria lacking Hpn, cultured in vitro, are more susceptible than is the wild type to bismuth and Ni2+.
Changing Patterns of Helicobacter pylori Gastritis in Long‐Standing Acid Suppression
Authors: Moayyedi Paul , Wason Catriona , Peacock Robert , Walan Anders , Bardhan Karna , Axon Anthony T. R. , Dixon Michael F. 
Published: March 2003

Background. Helicobacter pylori colonization and associated inflammation are influenced by local acid output. Infected subjects with acid‐related diseases, such as gastroesophageal reflux disease (GERD) are likely to have an antral‐predominant gastritis. We hypothesized that long‐term acid suppression would result in relatively greater bacterial colonization in the corpus leading to diffuse or corpus‐predominant gastritis and that this would be prevented by prior H. pylori eradication.Materials and Methods. To investigate this, we conducted a prospective, double‐blind trial of the effect on gastric histology of 12‐month maintenance treatment with omeprazole in H. pylori–positive GERD patients randomly assigned to either an eradication or omeprazole‐alone regime. A control group of 20 H. pylori–negative GERD patients also received omeprazole throughout the study period. Biopsies taken at baseline and at 12 months were graded “blind” by a single observer according to the updated Sydney System. The 41 H. pylori‐positive subjects with grade B or C esophagitis were randomly assigned (20 to omeprazole alone, 21 to eradication) and 33 subjects completed the 12‐month study.Results. There was a significant decline in antral chronic inflammation in initially positive patients between baseline and end in both the eradication group (p = .035) and the omeprazole‐alone group (p = .008). However, corpus chronic inflammation increased in the omeprazole‐alone group (p = .0156) but decreased in the eradication group. The change toward corpus predominance between baseline and end for the omeprazole‐alone group is highly significant (p = .0078). Furthermore, 5 of 11 in the omeprazole‐alone group developed mild corpus atrophy, compared to 0 of 8 who had undergone H. pylori eradication. The change in frequency of corpus atrophy between the two groups is significant (p = .02).Conclusion. In H. pylori–positive subjects with GERD, long‐term acid suppression leads to a shift from antral‐ to corpus‐predominant gastritis that can be prevented by prior eradication. The shift is accompanied by an increase in corpus atrophy. H. pylori infection should be eradicated prior to long‐term acid suppression with proton pump inhibitors.
A Possible Relation of the Helicobacter pylori pfr Gene to Iron Deficiency Anemia?
Authors: Choe Yon Ho , Hwang Tae Sook , Kim Hyun Joo , Shin Seok Hwan , Song Sun Uk , Choi Mi Sook 
Published: March 2003

AbstractBackground. H. pylori infection is thought to contribute to iron‐deficiency anemia, especially during puberty. The ferritin protein Pfr of H. pylori is homologous to eukaryotic and prokaryotic ferritins. The purpose of this study was to analyze the H. pylori pfr status in gastric biopsy specimens according to clinical data, including antral gastritis with or without iron‐deficiency anemia.Methods.A total of 26 H. pylori‐positive patients aged from 10–18 years were categorized into subgroups based on the presence or absence of iron‐deficiency anemia. All of them had antral gastritis. Sixteen patients were proved to have iron‐deficiency anemia by hematological study, two of which had a duodenal ulcer. The other 10 patients showed normal hematological findings. DNA isolation was performed from each of the gastric biopsy specimens. PCR amplification of the pfr gene coding was done using two sets of primers. The pfr region, 501 bp, was generated by linking the sequences of the two PCR products. The nucleotide and protein sequences were compared between the pfr regions from Korean H. pylori strains and the NCTC 11638 strain, which was obtained from the Genbank. Sequence comparisons were also performed for the pfr regions between the iron‐deficiency anemia (+) and (−) groups.Results.Analysis of the complete coding region of the pfr gene revealed three sites of mutation. The Ser39Ala mutation was found in 100% (26/26), Gly111Asn in 26.9% (7/26), and Gly82Ser in 11.5% (3/26). There were no significant differences in the mutations of the pfr regions between the iron deficiency anemia (+) and (−) groups.Conclusion.The mutation in the pfr gene did not relate with the clinical phenotype, iron deficiency anemia. Further studies are needed on the aspects of host side or other complex factors to elucidate the mechanisms by which the H. pylori infection might lead to iron deficiency anemia.
Cell Lysis is Responsible for the Appearance of Extracellular Urease in Helicobacter pylori
Authors: Marcus Elizabeth A. , Scott David R. 
Published: March 2003

AbstractBackground. Helicobacter pylori is a neutralophilic bacterium that colonizes the acidic human gastric surface using the neutralizing capacity of a constitutively produced urease. Urease is present both in the cytoplasm and bound to the outside surface of the bacteria. The origin of the surface urease continues to be controversial. This study provides additional evidence that the origin of surface urease is cell lysis, not secretion.Methods. H. Pylori was transformed with a plasmid encoding green fluorescent protein (GFP), a non‐native cytoplasmic protein. Cultures supplemented with β‐cyclodextrin or horse serum were collected over various time periods and spun through a ficoll cushion to gently separate whole bacteria from released protein. The pellet and supernatant fractions were analyzed by fluorimetry, SDS‐PAGE and Coomassie blue or Western analysis.Results.GFP fluorescence and antigenic reactivity in the supernatant increased at each time point. GFP, the non‐native cytoplasmic protein, and UreB, a native cytoplasmic protein, increased over time in the supernatant and both proteins were always present in the pellet fraction. UreI, an inner membrane protein, was only present in the pellet fraction. β‐galactosidase, a protein not found in H. pylori, was used as a negative control.Conclusions.Since it is unlikely that there is an intrinsic secretion system for GFP, a non‐native protein, its increasing presence over time in the supernate fraction along with UreB, and retention of UreI in the pellet fraction implies that cell lysis accounts for the presence of urease on the surface of H. pylori.
Inhibitory Action of a Novel Proton Pump Inhibitor, Rabeprazole, and its Thioether Derivative Against the Growth and Motility of Clarithromycin‐Resistant Helicobacter pylori
Authors: Ohara Tatsuki , Goshi Satoshi , Taneike Ikue , Tamura Yukiko , Zhang Hui‐Min , Yamamoto Tatsuo 
Published: March 2003

ABSTRACTBackground. Clarithromycin‐resistant Helicobacter pylori (CRHP) has increasingly been isolated from patients in Japan. The aim of our study was to test whether proton pump inhibitors (PPIs) and their thioether derivatives, which are secreted into the gastric mucosa, could inhibit the growth and motility (a factor in colonization) of CRHP.Materials and Methods. CRHP was isolated from patients who had experienced gastritis or peptic ulcers in Tokyo and Niigata. Drugs and related agents tested were omeprazole, lansoprazole, rabeprazole, the thioether derivative of rabeprazole (rabeprazole‐TH), clarithromycin, amoxicillin and metronidazole. The MICs of the drugs and agents for H. pylori strains were determined by the agar dilution method. Bacterial swimming in a liquid layer was examined under an inverted, phase‐contrast microscope.Results. The PPIs and rabeprazole‐TH, but not the anti‐H. pylori agents, inhibited the motility of CRHP at both pH 7.4 and 6.0. The concentrations (µg/ml) necessary to inhibit 50% of the motility at pH 7.4 were 0.25–0.5, 8–32, 8–16 and 128–256 for rabeprazole‐TH, rabeprazole, lansoprazole and omeprazole, respectively. Rabeprazole‐TH exibited the strongest inhibitory effect against the growth of CRPH (MIC, 0.5 µg/ml).Conclusion. Rabeprazole‐TH, which is secreted into the gastric mucosa, had the strongest inhibitory action against both the growth and motility of CRHP, suggesting that it is a potential novel agent for CRHP eradication.
Normalization of Phospholipids Concentration of the Gastric Mucosa was Observed in Patients with Peptic Ulcer after Eradication of Helicobacter pylori
Authors: Ishibashi Sadatoshi , Iwakiri Ryuichi , Shimoda Ryo , Ootani Hibiki , Kawasaki Seiji , Tadano Jutarou , Kikkawa Atsushi , Ootani Akifumi , Oda Kayoko , Fujise Takehiro , Yoshida Toshifumi , Tsunada Seiji , Sakata Hiroyuki , Fujimoto Kazuma 
Published: March 2003

AbstractBackground. Phospholipids concentration in the gastric mucosa decreased in patients with Helicobacter pylori infection. The aim of this study is to examine the effects of eradication of H. pylori on decreasing the phospholipids concentration in the gastric mucosa in patients with gastric or duodenal ulcer.Materials and Methods. Phospholipids (phosphatidylcholine, phosphatidylethanolamine, and sphingonomyeline) were measured in biopsy specimens from the antrum and corpus using thin‐layer chromatography. In H. pylori positive patients with gastric ulcer (n = 26) and duodenal ulcer (n = 13), and H. pylori negative controls (n = 20), the biopsy specimens were obtained before and 3 months after eradication. Eradication was performed using lansoprazole, amoxycillin, and clarithromycin.Results. Compared with the H. pylori negative control group, the concentrations of phosphatidylcholine and phosphatidylethanolamine decreased significantly in the gastric ulcer group in both antrum and corpus mucosa, and in the duodenal ulcer group in antrum mucosa. This decrease returned to the control level after eradication.Conclusions. This study demonstrates that the eradication of H. pylori in patients with peptic ulcer normalized the decrease of phosphatidylcholine and phosphatidylethanolamine in the gastric mucosa.