bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of gases responsible for the odour of human flatus and evaluation of a device purported to reduce this odour
Authors: Suarez F L , Springfield J , Levitt M D 
Published: June 2010

Background/Aims—While the social significance of flatus derives mainly from its odour, previous studies have focused on the non-odoriferous components of rectal gas. The aims of the present study were to determine the role of sulphur-containing gases in flatus odour and test the efficacy of a device purported to reduce this odour.Methods—Flatus was quantitatively collected via rectal tube from 16 healthy subjects who ingested pinto beans and lactulose to enhance flatus output. The concentrations of sulphur-containing gases in each passage were correlated with odour intensity assessed by two judges. Odour intensity was also determined after treatment of flatus samples with zinc acetate, which binds sulphydryl compounds (hydrogen sulphide and methanethiol), or activated charcoal. Utilising gas-tight Mylar pantaloons, the ability of a charcoal lined cushion to adsorb sulphur-containing gases instilled at the anus of eight subjects was assessed.Results—The main sulphur-containing flatus component was hydrogen sulphide (1.06 (0.2) μmol/l), followed by methanethiol (0.21 (0.04) μmol/l) and dimethyl sulphide (0.08 (0.01) μmol/l) (means (SEM)). Malodour significantly correlated with hydrogen sulphide concentration (p⩽0.001). Zinc acetate reduced sulphur gas content but did not totally eliminate odour, while activated charcoal removed virtually all odour. The cushion adsorbed more than 90% of the sulphur gases.Conclusion—Sulphur-containing gases are the major, but not the only, malodorous components of human flatus. The charcoal lined cushion effectively limits the escape of these sulphur-containing gases into the environment.
Patterns of alcohol consumption after liver transplantation
Authors: Tang H , Boulton R , Gunson B , Hubscher S , Neuberger J 
Published: June 2010

Background—Uncertainty exists about the extent and consequences of a return to alcohol consumption after liver transplantation for alcoholic liver disease (ALD).Aims—To determine the prevalence and consequences of alcohol consumption in patients transplanted for ALD.Methods—A retrospective case controlled study of all patients transplanted for ALD at the Queen Elizabeth Hospital, Birmingham, between 1987 and 1996.Results—Seventy patients with ALD were transplanted, of which 59 survived more than three months; 56 were interviewed. Twenty eight had consumed some alcohol after transplantation; for the nine “heavy drinkers” (HD), the median time to resumption of alcohol intake was six months and for the 19 “moderate drinkers” (MD) it was eight months. There was no significant difference in episodes of acute rejection or compliance with medication between those who were abstinent, MD, or HD. Histological evidence of liver injury was common in ALD patients who had returned to drink. Mild fatty change was found in 1/11 biopsy specimens from abstinent patients but moderate to severe fatty change and ballooned hepatocytes were seen in 3/5 MD and 2/5 HD specimens. Two HD patients had early fibrosis. One HD patient has died of alcohol related complications.Conclusions—Moderate to heavy alcohol consumption occurs in patients transplanted for ALD. Patient recall of abstinence advice is unreliable, and patients return to alcohol mainly within the first year after liver transplantation. Return to alcohol consumption after liver transplantation is associated with rapid development of histological liver injury including fibrosis.
A simple clinical colitis activity index
Authors: Walmsley R S , Ayres R C S , Pounder R E , Allan R N 
Published: June 2010

Background—The appropriate medical treatment of patients with ulcerative colitis is determined largely by the severity of symptoms. Hospital assessment of the severity of disease activity includes investigation of laboratory indices and sigmoidoscopic assessment of mucosal inflammation.Aims—To develop a simplified clinical colitis activity index to aid in the initial evaluation of exacerbations of colitis.Methods—The information for development of the simple index was initially evaluated in 63 assessments of disease activity in patients with ulcerative colitis where disease activity was evaluated using the Powell-Tuck Index (which includes symptoms, physical signs, and sigmoidoscopic appearance). The new index was then further evaluated in 113 assessments in a different group of patients, by comparison with a complex index utilising clinical and laboratory data, as well as five haematological and biochemical markers of disease severity.Results—The newly devised Simple Clinical Colitis Activity Index, consisting of scores for five clinical criteria, showed a highly significant correlation with the Powell-Tuck Index (r=0.959, p<0.0001) as well as the complex index (r=0.924, p<0.0001) and all laboratory markers (p=0.0003 to p<0.0001).Conclusions—This new Simple Colitis Activity Index shows good correlation with existing more complex scoring systems and therefore could be useful in the initial assessment of patients with ulcerative colitis.
High Fas ligand expression on lymphocytes in lesions of ulcerative colitis
Authors: Ueyama H , Kiyohara T , Sawada N , Isozaki K , Kitamura S , Kondo S , Miyagawa J , Kanayama S , Shinomura Y , Ishikawa H , Ohtani T , Nezu R , Nagata S , Matsuzawa Y 
Published: June 2010

Background—The pathogenesis of ulcerative colitis is unclear, but cytotoxic T lymphocytes infiltrating the mucosa have been implicated in mucosal damage. The Fas ligand (FasL), expressed on cytotoxic T lymphocytes, induces apoptosis in cells expressing Fas.Aim—To analyse FasL expression in affected colonic mucosa to ascertain Fas-FasL interaction in ulcerative colitis.Methods—FasL mRNA was quantified in colonic mucosal specimens from healthy subjects and patients with ulcerative colitis or Crohn’s disease, using the competitive reverse transcription polymerase chain reaction. FasL mRNA localisation was determined by in situ hybridisation. Expression of Fas in colonic mucosa was analysed immunohistochemically. Phenotypes of lamina propria lymphocytes that expressed FasL were analysed by flow cytometry.Results—FasL mRNA was strongly expressed in active ulcerative colitis lesions, but not in those associated with active Crohn’s disease or active proctitis-type ulcerative colitis. In situ hybridisation showed that FasL mRNA expression occurred in mononuclear cells infiltrating lesions. Fas was expressed in epithelial cells in ulcerative colitis and Crohn’s disease, and in normal subjects. Cytometry showed that FasL was expressed in CD3 lymphocytes infiltrating the lamina propria in active lesions.Conclusions—FasL is expressed in CD3 lymphocytes infiltrating into ulcerative colitis but not Crohn’s disease lesions, suggesting that Fas-FasL induced apoptosis participates in the mucosal damage of ulcerative colitis.
Colonic epithelial cell proliferation in hereditary non-polyposis colorectal cancer
Authors: Green S E , Chapman P , Burn J , Burt A D , Bennett M , Appleton D R , Varma J S , Mathers J C 
Published: June 2010

Background—Despite the recent discovery of four genes responsible for up to 90% of all cases of hereditary non-polyposis colorectal cancer (HNPCC), there will still be families in whom predictive testing is not possible. A phenotypic biomarker would therefore be useful. An upwards shift of the proliferative compartment in colonic crypts is reported to be one of the earliest changes in premalignant mucosa.Aims—To assess the role of crypt cell proliferation as a phenotypic biomarker in HNPCC.Patients—Thirty five patients at 50% risk of carrying the HNPCC gene (21 of whom subsequently underwent predictive testing and hence gene carrier status was known) and 18 controls.Methods—Crypt cell proliferation was measured at five sites in the colon using two different techniques. Labelling index was determined using the monoclonal antibody MIB1 and whole crypt mitotic index was measured using the microdissection and crypt squash technique. The distribution of proliferating cells within the crypts was also assessed.Results—There were no significant differences in the total labelling index or mean number of mitoses per crypt, nor in the distribution of proliferating cells within the crypt, between the study and control groups at any site. When the 21 patients in whom gene carrier status was known were analysed separately there were no significant differences in the measured indices of proliferation between the HNPCC gene carriers and non-gene carriers.Conclusion—Crypt cell proliferation is not a discriminative marker of gene carriage in HNPCC.
CTLA-4 gene polymorphism is associated with predisposition to coeliac disease
Authors: Djilali-Saiah I , Schmitz J , Harfouch-Hammoud E , Mougenot J-F , Bach J-F , Caillat-Zucman S 
Published: June 2010

Background—Susceptibility to coeliac disease is strongly associated with particular HLA class II alleles. However, non-HLA genetic factors are likely to be required for the development of the disease. Among candidate genes is the CTLA-4 (cytotoxic T lymphocyte associated) gene located on chromosome 2q33 in humans, which encodes a cell surface molecule providing a negative signal for T cell activation.Aims—To investigate CTLA-4 exon 1 polymorphism (position 49 A/G) in patients with coeliac disease.Patients—101 patients with coeliac disease and 130 healthy controls.Methods—Allele specific hybridisation and restriction enzyme digestion of polymerase chain reaction amplified genomic DNA.Results—The A allele of the CTLA-4 position 49 polymorphism was found on 82.2% of chromosomes in patients with coeliac disease compared with 65.8% in controls (p<0.0001), mostly in the homozygous form (68.3% in patients versus 47.7% in controls; odds ratio (OR) 2.36, 95% confidence interval (CI) 1.37 to 4.06, p=0.002). Four patients only had the G/G genotype compared with 21 controls (OR 0.21, CI 10.07 to 0.64, p=0.002). These differences were maintained when subjects were stratified according to the HLA class II phenotype, in particular when patients and controls were matched for the presence of the predisposing HLA DQB1*02 (DQ2) allele or HLA-DQA1*0501/DQB1*02 heterodimer.Conclusion—The CTLA-4 gene polymorphism is a non-HLA determinant that predisposes to coeliac disease. Whether it directly contributes to disease susceptibility or represents a marker for a locus in linkage disequilibrium with CTLA-4 needs further investigation.
Analysis of MHC class II DP, DQ and DR alleles in Crohn’s disease
Authors: Cariappa A , Sands B , Forcione D , Finkelstein D , Podolsky D K , Pillai S 
Published: June 2010

Background—Although inflammation in Crohn’s disease is believed to be mediated by activated T cells, genotyping of all MHC class II alleles in white people with this disease has not been reported.Aims—To perform a detailed molecular analysis of HLA DPB, DQB, and DRB genes in white patients with Crohn’s disease and controls in order to determine if the inheritance of any class II genes confers susceptibility or resistance to this disease.Methods—Complete molecular typing of HLA class II DPB, DQB, and DRB alleles was performed in 58 white patients with Crohn’s disease and 93 healthy controls using a polymerase chain reaction-sequence specific oligonucleotide based approach.Results—No significant association with any DPB or DQB alleles was noted in patients with Crohn’s disease. Since our previous studies had shown a strong association of an HLA DRB3*0301/DRB1*1302 haplotype with Crohn’s disease, we re-examined this association using more stringent genotyping criteria. This haplotype was present in 20.7% of patients and 5.4% of controls (p = 0.0066; relative risk = 4.59).Conclusions—The DRB3*0301/DRB1* 1302 haplotype is the only significant MHC class II association noted in white people with Crohn’s disease and represents the strongest association of any MHC or non-MHC locus with this disease.
Gastroenterology research in the United Kingdom: funding sources and impact
Authors: Lewison G 
Published: June 2010

Aims—To determine the sources of funding for UK gastroenterology research papers and the relative impact of papers funded by different groups and of unfunded ones.Methods—UK gastroenterology papers from 1988–94 were selectively retrieved from theScience Citation Index by means of a specially constructed filter based on their title keywords and journal names. They were looked up in libraries to determine their funding sources and these, together with their numbers of authors, numbers of addresses, and research category (clinical/basic) were considered as input parameters to the research. Output parameters analysed were mean journal impact category, citation counts by papers, and the frequency of citation by a US patent.Results—Gastroenterology papers comprise about 7% of all UK biomedical research and 46% of them have no acknowledged funding source. One quarter of the papers acknowledged government support, and a similar fraction a private, non-profit source; 11% were funded by the pharmaceutical industry. The papers acknowledging funding had significantly more impact than the others on all three measures. The citing patents had six times more UK inventors than the average for all US Patent and Trademark Office patents in the relevant classes and were mostly generic in application.Conclusion—The variation in impact of papers funded by different sources can mostly be explained by a simple model based on the input factors (numbers of funding bodies, numbers of authors, numbers of addresses, and research type). The national science base in gastroenterology is important for the underpinning of UK invented patents citing to it.
Poor diagnostic value of colonic CD44v6 expression and serum concentrations of its soluble form in the differentiation of ulcerative colitis from Crohn’s disease
Authors: Reinisch W , Heider K-H , Oberhuber G , Dejaco C , Müllner M , Adolf G R , Gasché C 
Published: June 2010

Background—Increased expression of CD44v6 on colonic crypt epithelial cells in ulcerative colitis has been suggested as a diagnostic tool to distinguish ulcerative colitis from colonic Crohn’s disease.Aims—To investigate colonic CD44v6 expression and serum concentrations of soluble CD44v6 (sCD44v6) in patients with ulcerative colitis and Crohn’s disease.Methods—Colonic biopsy samples were obtained from 16 patients with ulcerative colitis, 13 with ileocolonic Crohn’s disease, and 10 undergoing polypectomy. Serum samples were obtained from 15 patients with active ulcerative colitis, 20 with active Crohn’s disease, and 20 healthy donors. Colonic CD44v6 expression was evaluated immunohistochemically by monoclonal antibody 2F10 and the higher affinity monoclonal antibody VFF18. Serum sCD44v6 concentrations were measured by ELISA.Results—2F10 stained colonic epithelium of inflamed ulcerative colitis and Crohn’s disease samples in 80% and 40% of cases, respectively, and VFF18 in 95% and 87%, respectively. Both monoclonal antibodies displayed a sensitivity and specificity of 60% and 87% to differentiate ulcerative colitis from colonic Crohn’s disease. Serum concentrations of sCD44v6 were lower in patients with ulcerative colitis (median 153 ng/ml; interquartile range (IQR) 122–211) compared with Crohn’s disease (219; IQR 180–243) and healthy donors (221; IQR 197–241 (p=0.002)). Its sensitivity and specificity to discriminate ulcerative colitis from Crohn’s disease was 75% and 71%, respectively.Conclusion—Colonic CD44v6 and serum sCD44v6 concentrations do not facilitate reliable differential diagnosis between ulcerative colitis and Crohn’s disease.
bax, but notbcl-2, influences the prognosis of human pancreatic cancer
Authors: Friess H , Lu Z , Graber H U , Zimmermann A , Adler G , Korc M , Schmid R M , Büchler M W 
Published: June 2010

Background—bcl-2and bax belong to thebcl-2-related gene family, which marks a new class of genes that influence apoptosis. Thebcl-2 oncogene acts as a broad antiapoptotic factor and extends both normal and tumour cell survival. In contrast, the bax gene is a promoter of apoptosis.Aims—To analyse the expression of bcl-2 andbax in pancreatic cancer and correlate the results with clinical parameters.Patients—Pancreatic cancer tissue samples were obtained from 28 female and 32 male patients (median age 63, range 43–79 years) having surgery for pancreatic cancer. Normal pancreatic tissues obtained from 18 previously healthy organ donors served as controls.Methods—The levels ofbcl-2 and baxmRNA expression were analysed by northern blot and the exact site of mRNA transcription was determined by in situ hybridisation. The presence of the corresponding proteins was determined by immunohistochemistry.Results—Northern blot analysis indicated that, in comparison with the normal pancreas,bcl-2 mRNA was overexpressed in 30% andbax mRNA in 61% of the pancreatic cancer samples. Concomitant overexpression ofbcl-2 and bax was present in 26% of the cancer samples. Pancreatic adenocarcinomas exhibited 3.7-fold and 5.4-fold increases (p<0.001) inbcl-2 and baxmRNA levels respectively. In situ hybridisation showed that bothbcl-2 and baxmRNA were expressed in the cancer cells. Immunohistochemical analysis showed positive Bcl-2 and Bax immunostaining in 28 and 83% of the cancer samples respectively. In multivariate analysis (Cox regression model), bax expression was found to be a strong indicator of survival (p<0.001). Patients whose tumours exhibited Bax immunostaining lived significantly longer (12 months) than those whose tumours were Bax negative (five months) (p<0.039). In contrast, no relation was found between Bcl-2 and survival time.Conclusions—The data indicate that genes that are involved in the regulation of apoptosis are upregulated in human pancreatic cancer cells. Prolonged survival times in patients in whom apoptosis promoting factors are upregulated indicate that apoptotic pathways are of biological significance in pancreatic cancer.
Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently
Authors: Hackelsberger A , Platzer U , Nilius M , Schultze V , Günther T , Dominguez-Muñoz J E , Malfertheiner P 
Published: June 2010

Background—Gastric mucosal surface hydrophobicity (GMSH) is an essential component of the mucosal defence system that is decreased by Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in elderly subjects, and may thus reflect diminished mucosal resistance.Aims—To investigate whether aging decreases GMSH.Patients—One hundred and twenty patients without peptic ulcer disease were divided into three age groups: I (41 years or below); II (41–64 years); and III (65 years or above).Methods—Biopsy specimens were taken from the antrum, corpus, and cardia for histology (Sydney system), urease testing for H pylori, and for contact angle measurement of GMSH with a goniometer. The presence of specific H pyloriantibodies was checked by immunoblotting.Results—Fifty two patients (43%) were infected, and 68 were uninfected with H pylori. GMSH at all biopsy sites was lower in H pylori infected subjects (p=0.0001), but also decreased with age independently of infection status (p=0.0001). The most notable decrease in GMSH occurred between age groups I and II in those with, and between age groups II and III in those without, H pylori infection. GMSH was greater in antral than in corpus mucosa in both infected (p=0.0001) and uninfected patients (p=0.0003).Conclusions—A physiological decrease in GMSH with aging may contribute to the risk of ulcer development in the elderly, and may act synergistically with H pylori and/or NSAIDs on gastric mucosal defence.
Helicobacter pylori in vivo causes structural changes in the adherent gastric mucus layer but barrier thickness is not compromised
Authors: Newton J L , Jordan N , Oliver L , Strugala V , Pearson J , James O F W , Allen A 
Published: June 2010

Background—It has been proposed that a pathogenic effect of Helicobacter pylori is a weakening of the protective mucus barrier; however, this remains controversial.Aims—To clarify the effects of H pylori infection on the mucus gel barrier in vivo.Methods—Mucus gel polymeric structure and the thickness of the adherent mucus barrier were measured in endoscopic biopsy samples in subjects with and without H pyloriinfection.Results—There was a significant 18% reduction in the proportion of polymeric gel forming mucin in the adherent mucus layer in H pylori positive compared with negative subjects. There was no change in the adherent mucus thickness betweenH pylori positive and negative subjects without gastric atrophy (mean (SD): 104 (26) μm, 106 (30) μm respectively). There was however a significant reduction in mucus thickness in those H pylori positive subjects with underlying gastric atrophy (84 (13) μm, p=0.03) compared with those without atrophy.Conclusions—A partial breakdown in gel forming structure of the gastric mucus barrier does occur in H pylori infection per se but this is insufficient to cause a collapse of the mucus barrier.
Mucin gene expression in human embryonic and fetal intestine
Authors: Buisine M P , Devisme L , Savidge T C , Gespach C , Gosselin B , Porchet N , Aubert J P 
Published: June 2010

Background—The intestinal epithelium is covered by a continuous layer of mucus which is secreted by well differentiated epithelial cells. Disregulation of the expression of mucins has been reported to have possible implications in the neoplastic process which affects intestinal mucosae. It is well known that preneoplastic and neoplastic tissues can express fetal phenotypic characteristics.Aims—To assess whether the expression of mucin genes in the intestinal tract is linked to the stage of cellular differentiation and tissue development, by studying the expression of six mucin genes in human fetal small intestine and colon, and also adult tissues.Methods—In situ hybridisation was used to study mRNA expression of MUC2, MUC3, MUC4, MUC5B, MUC5AC, and MUC6 in 32 human embryos and fetuses (6.5–27 weeks gestation). Normal adult mucosae were used as controls.Results—Three mucin genes, MUC2, MUC4, and MUC5AC, were differently expressed in fetal intestine compared with expression in normal adults.Conclusion—These differences in mucin gene expression suggest a possible regulatory role for these products in intestinal epithelial cell differentiation.
Expression of basic fibroblast growth factor in intact and ulcerated human gastric mucosa
Authors: Hull M A , Brough J L , Powe D G , Carter G I , Jenkins D , Hawkey C J 
Published: June 2010

Background—Basic fibroblast growth factor (bFGF) promotes angiogenesis and healing of gastric ulcers in rats, and bFGF expression is up regulated in such ulcers. However, little is known about expression of bFGF in human gastric mucosa.Aims—To investigate bFGF expression in intact human gastric mucosa and gastric ulcers and to determine whether low bFGF content or altered binding by mucosa is associated with ulceration.Subjects—Endoscopy outpatients, gastrectomy patients, and organ donors.Methods—bFGF was isolated by heparin affinity chromatography and characterised by western blotting and endothelial cell bioassay. bFGF was measured by immunoassay and its distribution defined by immunohistochemistry and in situ hybridisation. Binding of bFGF by heparan sulphate proteoglycans was investigated by sodium chloride and heparin extraction.Results—Bioactive bFGF (19 kDa) was detected in normal mucosa but bFGF mRNA was not found. bFGF expression was up regulated in granulation tissue endothelial cells, mononuclear cells, and epithelial cells at the ulcer rim. Gastric ulcer patients had constitutively low bFGF concentrations in intact antral mucosa which were not explained by changes in binding to heparan sulphate proteoglycans.Conclusions—bFGF expression is up regulated in human gastric ulcers. Low intact mucosal bFGF content is associated with gastric ulceration.