bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation of serum pepsinogen with histological atrophy following successful Helicobacter pylori eradication
Authors: KAWAI T. , KAWAKAMI K. , KATAOKA M. , TAKEI K. , TAIRA S. , ITOI T. , MORIYASU F. , TAKAGI Y. , AOKI T. , SERIZAWA H. , RIMBARA E. , NOGUCHI N. , SASATSU M. 
Published: July 2010

SummaryBackgroundLevels of pepsinogen have been reported to correlate with the degree of gastric atrophy in Helicobacter pylori‐infected gastric mucosa.AimTo investigate the relationship between PG levels and histological atrophy before and after H. pylori eradication.MethodsEradication therapy was conducted on 180 H. pylori‐positive patients with upper gastrointestinal conditions. Endoscopy was performed prior to and at 2, 12 and 24 months after successful eradication therapy. Histological findings were scored using the updated Sydney System in the antrum and the corpus of the stomach. Pepsinogen was measured.ResultsPepsinogen I levels dropped significantly at 2 months after the eradication. By 12 months and 24 months post‐eradication they had risen again. Histological improvement was seen in atrophy at all sites at 24 months after the eradication. A significant correlation between atrophy and pepsinogen I was seen from prior to eradication. The correlation coefficient was greater at 2 months post‐eradication, decreased again at 12 months and was no longer significant at 24 months.ConclusionsOur results suggest that pepsinogen levels correlate with the degree of gastric mucosal atrophy prior to and soon after successful eradication therapy, but that the degree of correlation subsequently declines over time.
Review article: is there a common principle in the development of gastrointestinal cancers? Stem cells in the origin of cancer
Authors: WRIGHT N. A. 
Published: July 2010

SummaryBackgroundAccumulating evidence, outlined in this review, at last provides some elucidation of the orgin of gastrointestinal epithelial tumours.MethodsNew techniques, such as following the process of crypt or gastric gland purification following mutation in genes encoded by the mitochondrial genome, have shown that mutations spead within the proliferative unit, either gastric gland or intestinal crypt, by clonal purification or monoclonal conversion. Spreading otside the crypt or gland then takes place by fission.ResultsFuture research should focus on the mecanisim by which mutated stem cells colonize crypts, and on the mechanisms of crypt fission itself.
Interactions between the grading of gastric atrophy associated with Helicobacter pylori infection and the severity of clinical symptoms and delay in gastric emptying in patients with functional dyspepsia
Authors: KADOUCHI K. , TOMINAGA K. , OCHI M. , KAWAMURA E. , SASAKI E. , SHIBA M. , WATANABE T. , FUJIWARA Y. , OSHITANI N. , HIGUCHI K. , SHIOMI S. , ARAKAWA T. 
Published: July 2010

SummaryBackgroundAtrophic and inflammatory changes in the gastric mucosa are commonly observed in Japanese patients with functional dyspepsia. However, detailed data regarding the correlation between the severity of these changes and the symptoms of functional dyspepsia are not available.AimTo evaluate grading scales of gastric atrophy and inflammation, severity of clinical symptoms, and gastric emptying in patients with functional dyspepsia.MethodsNinety‐three patients with dyspepsia were enrolled. The severity of gastric atrophy was graded through serological and histological examination, and gastric inflammation was evaluated histologically. Clinical symptoms were evaluated on the Gastrointestinal Symptoms Rating Scale, including subscales for abdominal pain, acid reflux, diarrhoea, indigestion and constipation. Gastric emptying half‐time was measured using a radioisotope technique.Results Helicobacter pylori infection and gastric inflammation influenced neither clinical symptoms nor gastric emptying time. However, a correlation was observed between gastric atrophy as graded by serological examination and indigestion (R = 0.31, P = 0.01). Histological examination also showed a correlation between gastric atrophy and abdominal pain and indigestion (R = 0.31, P = 0.04 and R = 0.35, P = 0.02 respectively).ConclusionGastric atrophy associated with H. pylori infection may be partly responsible for the clinical symptoms experienced by patients with functional dyspepsia.
Colonic mucosal lesions associated with long‐term administration of non‐steroidal anti‐inflammatory drugs
Authors: OHKUSA T. , TERAI T. , ABE S. , KOBAYASHI O. , BEPPU K. , SAKAMOTO N. , KUROSAWA A. , OSADA T. , HOJO M. , NAGAHARA A. , OGIHARA T. , SATO N. 
Published: July 2010

SummaryBackgroundEffects of long‐term administration of non‐steroidal anti‐inflammatory drugs (NSAIDs) on the colon have not been well characterized.AimTo investigate colonoscopic findings and prevalence of adverse events following long‐term use of NSAIDs.MethodsThe study included 425 patients (mean 66.4 years) treated for over one year with NSAIDs, and 2125 age‐ and sex‐matched patients without NSAIDs as controls. Eligible candidates were selected by medical record review for underlying diseases, pre‐endoscopic symptoms, category of NSAIDs used, and duration of use. We used endoscopy to study lesion characteristics.ResultsThe occurrence rate of colonic lesions or bleeding in the NSAIDs user (13/425, 3.1%) was higher than that in controls (28/2125, 1.3%) (p = 0.017). Colitis was found in 10 of the 13 patients. The sigmoid colon, descending colon or both (70.0%) was commonly involved, and showed segmental ischemic colitis features in 8 of the 13 patients (61.5%). Among these, duration of use ranged from 1‐30 years (mean 7.8). Nine of 13 patients (69.2%) took low‐dose aspirin.ConclusionThe prevalence of colonic lesions in long‐term NSAIDs users is much lower than that of upper gastrointestinal side effects, but higher than that of colonic lesions in non‐NSAIDs users. The most common features of NSAIDs‐associated colitis were segmental ischeznia.
Gastric motility and autonomic activity during obstructive sleep apnea
Authors: URATA M. , FUKUNO H. , NOMURA M. , OGATA T. , ITO S. , NAKAYASU K. , NAKAYA Y. 
Published: July 2010

SummaryBackgroundPatients with Obstructive Sleep Apnea Syndrome (OSAS) often experience gastroesophageal reflux disease (GERD).AimTo investigate gastric motility and autonomic nervous activity during sleep apnea.MethodsThe subjects of this study were 20 individuals with OSAS who experienced 10 or more sleep apnoea events per hour, as measured with a portable sleep polygraph. A percutaneous electrogastrography (EGG) and fast Fourier transformation analysis was carried out on the results. The mean amplitude was compared for bradygastria, normogastria and tachygastria. Spectral analysis of heart rate variability was performed, and low‐frequency (LF) power, high‐frequency (HF) power and the LF/HF ratio were measured. Oesophagogastroduodenal endoscopy was performed on each subject, and the presence of reflux oesophagitis (RE) was diagnosed according to the Los Angeles (LA) grade classification. Moreover, questionnaire for the diagnosis of reflux disease (QUEST) was carried out.ResultsNormogastria was significantly decreased, and brady‐, tachygastria, or both were increased during sleep apnea (P < 0.01). There was no significant relation between LA grade classification of RE and severity of OSAS. The LF/HF ratio was significantly higher during sleep apnea for patients with RE and OSAS, but the opposite for those with RE without OSAS. Decreased percutaneous arterial oxygen saturation and normogastria were independent risk factors for the severity of RE.ConclusionsThe present study suggested that, in addition to decreased pressure on the pleural cavity, factors affecting the development of RE might include abnormal gastric motility, low oxygen, and increased sympathetic nervous activity during sleep apnea.
Evaluation of gastro‐oesophageal flap valve is useful for diagnosing gastro‐oesophageal reflux disease
Authors: IWAMOTO M. , KATO K. , MIZUNO S. , MIYAMOTO S. , TAKEUCHI R. , IWASAKI A. , ARAKAWA Y. 
Published: July 2010

SummaryBackgroundGastro‐oesophageal flap valve (GEFV) grade correlated with endoscopic reflux oesophagitis (RE) prevalence.AimTo investigate relationships among gastro‐oesophageal reflux disease (GERD) symptoms, RE and/or non‐erosive reflux disease (NERD) and GEFV grades in subjects undergoing endoscopy.MethodsWe enrolled 1305 subjects from whom endoscopic results and the results of a self‐administered questionnaire (QUEST) were available. Subjects were evaluated for GERD symptoms (QUEST score), GEFV grade, RE and gastric mucosal atrophy.ResultsTotal GERD prevalence, including symptomatic GERD (QUEST score ≥ 4) and/or RE, was 27%. RE grade and prevalence increased with GEFV grade. QUEST scores and GEFV grades showed a positive correlation. NERD prevalence was 14% and increased with GEFV grade, but the relationship was weaker than that between RE and GEFV. Comparing RE‐negative subjects by GEFV grade, GERD symptoms were noted in 10%, 19%, 36% and 52% with GEFV grades I, II, III and IV, respectively. Neither type of gastric mucosal atrophy correlated with GEFV grade.ConclusionsTotal GERD, NERD and RE prevalences increased with GEFV grade. Subjects with high GEFV grades often complain of GERD symptoms, even without RE. Our findings suggest that endoscopic GEFV evaluation provides a useful clinical index for diagnosing GERD.
Differential expression of cyclo‐oxygenase‐2 and nuclear β‐catenin in colorectal cancer tissue
Authors: TATSUGUCHI A. , KISHIDA T. , FUJIMORI S. , TANAKA S. , GUDIS K. , SHINJI S. , FURUKAWA K. , TAJIRI T. , SUGISAKI Y. , FUKUDA Y. , SAKAMOTO C. 
Published: July 2010

SummaryBackgroundBoth adenomatous polyposis coli (APC) gene mutation and cyclo‐oxygenase (COX)‐2 are thought to play key roles in colorectal carcinogenesis. Nuclear accumulation of β‐catenin results from APC gene mutation, which leads to enhanced transcription and activation of target genes, including cyclin D1. In vitro studies suggest that Cox‐2 transcription is directly regulated by β‐catenin/TCF complexes.AimTo investigate the relationship between cellular localization of β‐catenin and COX‐2 in colorectal cancer.MethodsWe performed immunohistochemical analysis of β‐catenin, cyclin D1 and COX‐2 expression in 50 resected colorectal cancer cases.ResultsThe proportion of cases positive for cyclin D1 was higher in nuclear β‐catenin‐positive cases than in negative cases (P < 0.001). Serial sections revealed that the co‐localization of cyclin D1 and nuclear β‐catenin was most frequently evident in the tumour cells at the advancing margin of invasive carcinoma. Conversely, there was no association between COX‐2 and nuclear β‐catenin expression, either topographically or statistically. The staining patterns for COX‐2 and nuclear β‐catenin differed; COX‐2 was diffuse and homogeneous, whereas nuclear β‐catenin was focal and preferentially distributed at the invasive margin of cancer cells.ConclusionsThese two important modulators of colorectal tumourigenesis are differentially expressed. Cox‐2 and β‐catenin transcription may be activated by different pathways.
Hypoxia‐inducible factor‐1 alpha and vascular endothelial growth factor expression in ischaemic colitis and ulcerative colitis
Authors: OKUDA T. , AZUMA T. , OHTANI M. , MATSUNAGA S. , MASAKI R. , SATOMI S. , INAGAKI T. , MURAMATSU A. , LEE S. , SUTO H. , ITO Y. , YAMAZAKI Y. , ITO S. , KURIYAMA M. 
Published: July 2010

SummaryBackgroundHypoxia‐inducible factor‐1 alpha (HIF‐1 alpha) is a transcriptional factor induced by ischaemic crisis in many tissues. Vascular endothelial growth factor (VEGF) is an important growth factor that plays a major role in angiogenesis.AimWe examined the aetiology and pathophysiology of human ischaemic colitis and ulcerative colitis from the viewpoint of the expression of these two ischaemic factors.MethodsThirty‐two patients with ischaemic colitis, 16 with ulcerative colitis and 25 normal controls underwent colonoscopy. Biopsy samples were taken from a colitis lesion and a normal region in the same patient. In the normal controls, four biopsy samples were obtained from each subject. Biopsy samples were subjected to real‐time polymerase chain reaction.ResultsHypoxia‐inducible factor and VEGF were overexpressed in ischaemic colitis lesions and quickly decreased to normal levels in the healing phase. In contrast, HIF but not VEGF was overexpressed in active ulcerative colitis lesions. In the remission phase of ulcerative colitis, VEGF decreased to low levels, although HIF was continuously overexpressed.ConclusionsOverexpression of HIF and VEGF contribute to the tolerance of ischaemia in patients with active ischaemic colitis. The inconsistency in their expression might be associated with the chronic intestinal damage characteristic of ulcerative colitis.
Effect of eradication of Helicobacter pylori on genetic instabilities in gastric intestinal metaplasia
Authors: TANAKA A. , WATARI J. , TANABE H. , MAEMOTO A. , FUJIYA M. , ASHIDA T. , DAS K. M. , KOHGO Y. 
Published: July 2010

SummaryBackgroundThere is little evidence of changes in genetic variations in gastric intestinal metaplasia (GIM) after the eradication of Helicobacter pylori (H. pylori).AimTo investigate the effects of H. pylori eradication on genetic GIM variability in patients with and without gastric cancer in a one‐year prospective study.MethodsWe analysed microsatellite instability (MSI) and loss of heterozygosity (LOH) in GIM. Subjects included Gr. A (n = 39): chronic gastritis, and Gr. B (n = 53): intestinal‐type early gastric cancer patients who underwent endoscopic mucosal resection (n = 25) and surgical resection (n = 28).ResultsThe frequency of incidence of MSI in GIM was 10.3% and 28.3% for Gr. A and Gr. B, respectively. Gr. B showed a significantly (p = 0.03) higher incidence rate than Gr. A for MSI, but not for LOH. The frequency of MSI declined in both groups post‐eradication, and patients that were positive for MSI before treatment were negative after H. pylori eradication. Unfortunately, however, GIM scores did not decline significantly post‐treatment for either group.ConclusionsMSI in GIM may be associated with gastric carcinogenesis. H. pylori eradication reduced MSI during the one‐year post‐treatment period, although no histological improvement in GIM was observed. These changes in MSI may explain the decrease in gastric cancer incidence after the eradication of H. pylori.
Molecular mechanisms involved in interleukin‐8 production by normal human oesophageal epithelial cells
Authors: YOSHIDA N. , IMAMOTO E. , UCHIYAMA K. , KURODA M. , NAITO Y. , MUKAIDA N. , KAWABE A. , SHIMADA Y. , YOSHIKAWA T. , OKANOUE T. 
Published: July 2010

SummaryBackgroundIncrease in interleukin‐8 in the oesophageal mucosa has been associated with the pathogenesis of reflux oesophagitis.AimTo assess the effect of bile acids on the interleukin‐8 expression in normal human oesophageal epithelial cells and to determine its molecular mechanisms.MethodsHuman oesophageal epithelial cells were stimulated with unconjugated bile acids, conjugated bile acids and inflammatory cytokines. Protein and mRNA of interleukin‐8 were measured by enzyme‐linked immunosorbent assay and quantitative real‐time polymerase chain reaction, respectively. In addition, we examined protein kinases and transcription factors involved in interleukin‐8 synthetic pathways using protein kinase inhibitors and luciferase expression vectors, respectively.ResultsUnconjugated bile acids induced interleukin‐8 production from human oesophageal epithelial cells stronger than conjugated bile acids. However, conjugated bile acids in acidic media resulted in remarkable increase of interleukin‐8 production compared with those in neutral‐pH media. Mutation of the binding site of NF‐kB, AP‐1 and NF‐IL6 abrogated the induction of luciferase activities by 100%, 70% and 30%, respectively. Inhibitor of protein kinase A, protein kinase C or p38 mitogen‐activated protein kinase attenuated the production of interleukin‐8 by cholic acid.ConclusionsThese results indicate that bile acids induce interleukin‐8 expression from oesophageal epithelial cells mainly via the activation of NF‐kB as well as AP‐1.
Gene expression clusters of a lipopolysaccharide‐stimulated pathway in peripheral blood monocytes of Japanese patients with Crohn's disease
Authors: NAITO Y. , TAKAGI T. , MIZUSHIMA K. , UETA M. , KINOSHITA S. , HANDA O. , KOKURA S. , ICHIKAWA H. , YOSHIDA N. , YOSHIKAWA T. 
Published: July 2010

SummaryBackgroundRecent reports support the notion that patients with Crohn's disease have a dysregulated innate immune response to endogenous flora.AimTo reveal the distinct gene expression clusters of a lipopolysaccharide‐stimulated pathway in the peripheral blood monocytes of Japanese patients with Crohn's disease.Materials and methodsTotal RNA was extracted from peripheral blood monocytes of four patients in the remission stage of Crohn's disease as well as four controls, and gene expression profiles before and after lipopolysaccharide stimulation were investigated using a high‐density oligonucleotide probe array. To focus on innate immunity, the expression of genes to be studied was narrowed down to 118 probe sets which were selected using the following keywords: lipopolysaccharide, toll, myd and tir along with a software of NetAffx Analysis Center.ResultsUsing hierarchical clustering analysis, we picked up to 44 and 36 probe sets for which expression had decreased before and after lipopolysaccharide stimulation, respectively, in patients with Crohn's disease compared with healthy volunteers. The expression of TLR5, 7, MyD88, SIGIRR, and Tollip was decreased both before and after lipopolysaccharide stimulation in patients with Crohn's disease.ConclusionWe found several interesting clusters in monocytes before and after stimulation with lipopolysaccharide. These genes may have been responsible for the immunological differences between the Crohn's disease and control patients.
Inadequate dietary intake but not renal tubular acidosis is associated with bone demineralization in primary biliary cirrhosis
Authors: ALLOCCA M. , CROSIGNANI A. , GRITTI A. , BENETTI A. , ZUIN M. , PODDA M. , BATTEZZATI P. M. 
Published: July 2010

SummaryBackgroundMetabolic bone disease associated with primary biliary cirrhosis (PBC) is inadequately characterized. Renal tubular acidosis (RTA) may lead to bone loss through chronic mobilization of skeletal calcium salts to buffer increased acid load.AimTo evaluate the prevalence of RTA in PBC and establish the relationships among bone mineral density (BMD), renal function and nutritional status.MethodsWe enrolled 69 female patients with compensated PBC and 35 control patients with chronic hepatitis C. RTA was searched in all patients, and 24‐h dietary recalls were collected at enrolment. BMD was measured by dual‐energy X‐ray absorptiometry at the femur neck, lumbar spine and radius ultradistalis sites.ResultsNo patients received a diagnosis of RTA. BMD values (Z‐scores) showed only little deviation from normal population with no difference between PBC and controls. Osteopoenic PBC patients (T‐score < 1) showed significantly lower daily phosphorus intake [median: 672 (288–1374) vs. 921 (253–1923) mg/day; P = 0.037], with a trend towards lower caloric intake than their nonosteopoenic counterparts.ConclusionsRenal tubular acidosis is uncommon in compensated PBC. Cholestasis is not associated with an increased risk of bone demineralization. Inadequate dietary intake may be a preventable factor contributing to bone loss in PBC.
Systematic review: Helicobacter pylori eradication for the prevention of gastric cancer
Authors: FUCCIO L. , ZAGARI R. M. , MINARDI M. E. , BAZZOLI F. 
Published: July 2010

SummaryBackground Helicobacter pylori is recognized as one of the most significant risk factors for gastric cancer, and H. pylori eradication has been proposed as a possible primary chemo‐preventive strategy to reduce gastric cancer incidence.AimTo evaluate the available evidence on the efficacy of H. pylori eradication in the prevention of gastric cancer.MethodsEpidemiological, observational and interventional studies, as well as decisional models, were taken into account in this review.ResultsLarge‐scale epidemiological studies clearly link H. pylori infection with non‐cardia gastric cancer. Current evidence suggests that, in a subpopulation of treated subjects, H. pylori eradication prevents the progression of preneoplastic lesions. Studies that have attempted to evaluate the effect of H. pylori eradication on the incidence of gastric cancer have not provided definitive answers. H. pylori eradication seems to reduce the incidence of gastric cancer in patients without baseline precancerous gastric lesions. Decisional models suggest that H. pylori screening could be cost‐effective, but there is not yet sufficient evidence to support the setting up of a general screening programme.Conclusion Helicobacter pylori eradication is a plausible intervention for gastric cancer prevention; however, it seems to be relevant in only a subset of subjects.
Review article: fructose malabsorption and the bigger picture
Authors: GIBSON P. R. , NEWNHAM E. , BARRETT J. S. , SHEPHERD S. J. , MUIR J. G. 
Published: July 2010

SummaryFructose is found widely in the diet as a free hexose, as the disaccharide, sucrose and in a polymerized form (fructans). Free fructose has limited absorption in the small intestine, with up to one half of the population unable to completely absorb a load of 25 g. Average daily intake of fructose varies from 11 to 54 g around the world. Fructans are not hydrolysed or absorbed in the small intestine.The physiological consequences of their malabsorption include increasing osmotic load, providing substrate for rapid bacterial fermentation, changing gastrointestinal motility, promoting mucosal biofilm and altering the profile of bacteria. These effects are additive with other short‐chain poorly absorbed carbohydrates such as sorbitol.The clinical significance of these events depends upon the response of the bowel to such changes; they have a higher chance of inducing symptoms in patients with functional gut disorders than asymptomatic subjects. Restricting dietary intake of free fructose and/or fructans may have durable symptomatic benefits in a high proportion of patients with functional gut disorders, but high quality evidence is lacking.It is proposed that confusion over the clinical relevance of fructose malabsorption may be reduced by regarding it not as an abnormality but as a physiological process offering an opportunity to improve functional gastrointestinal symptoms by dietary change.