bluuebunny/crossref_metadata_2025_split huggingface dataset:
Direct detection of Helicobacter pylori resistance to macrolides by a polymerase chain reaction/DNA enzyme immunoassay in gastric biopsy specimens
Authors: Marais A , Monteiro L , Occhialini A , Pina M , Lamouliatte H , Mégraud F 
Published: January 2010

BACKGROUNDThe increasing use of macrolides especially in the treatment ofHelicobacter pylori infection has led to an increase in resistant strains. The resistance of H pylori to macrolides, especially clarithromycin, is one of the major causes of eradication failure. In H pylori, clarithromycin resistance is due to point mutations localised in domain V of 23S rRNA.AIMTo develop a molecular technique based on amplification of a relevant fragment of the 23S rRNA and colorimetric hybridisation in liquid phase to detect directly in biopsy specimens the type of mutation associated with resistance of H pylori to clarithromycin.METHODSGastric biopsy samples from 61 patients were submitted to this test. The results were compared with standard methods (determination of minimal inhibition concentration, polymerase chain reaction/restriction fragment length polymorphism, and/or DNA sequencing) in order to evaluate the test and to define the cut off values, specificity, and sensitivity.RESULTSThe 14 biopsy samples in which H pylori was not detected did not give a positive result in any assay, and the 14 samples harbouring strains susceptible to clarithromycin gave a positive result with the wild type probe as expected. The 33 biopsy specimens containing resistant strains always gave a positive signal with one of the probes detecting resistant organisms, but in eight cases they also reacted with the wild type probe, indicating that a mixture of resistant and susceptible organisms was present.CONCLUSIONThe importance of this new assay is that it allows the detection of multiple genotypes corresponding to either heterogeneous genotypes or mixed infections. Moreover, it allows in a single step not only the detection of H pylori but also the determination of its susceptibility to clarithromycin directly in biopsy specimens without the need for culture.
Helicobacter pylori infection potentiates the inhibition of gastric acid secretion by omeprazole
Authors: Gillen D , Wirz A A , Neithercut W D , Ardill J E S , McColl K E L 
Published: January 2010

BACKGROUNDOmeprazole has a greater intragastric pH elevating effect in Helicobacter pylori positive than negative subjects. Ammonia production byH pylori has been suggested as a probable mechanism.AIMSTo assess the effect ofH pylori status on gastric acid secretion during omeprazole treatment, and to examine the possible role of ammonia neutralisation of intragastric acid in increased omeprazole efficacy in infected subjects.METHODSTwentyH pylori positive and 12H pylori negative healthy volunteers were examined before and six to eight weeks after commencing omeprazole 40 mg/day. On both occasions plasma gastrin and acid output were measured basally and in response to increasing doses of gastrin 17 (G-17). Gastric juice ammonium concentrations were also measured.RESULTSPrior to omeprazole, measurements were similar in the H pyloripositive and negative subjects. During omeprazole, median basal intragastric pH was higher in the H pyloripositive (7.95) versus negative (3.75) subjects (p<0.002). During omeprazole basal, submaximal (180 pmol/kg/h G-17), and maximal acid outputs (800 pmol/kg/h G-17) were lower in H pylori positive subjects (0.0, 3.6, 6.0 mmol/h respectively) versus negative subjects (0.3, 14.2, 18.6 mmol/h) (p<0.03 for each). This effect was not explained by neutralisation by ammonia.CONCLUSIONThe presence ofH pylori infection leads to a more profound suppression of acid secretion during omeprazole treatment. The effect cannot be explained by neutralisation of intragastric acid by bacterial ammonia production and its precise mechanism has to be explained.
The effect of hiatus hernia on gastro-oesophageal junction pressure
Authors: Kahrilas P J , Lin S , Chen J , Manka M 
Published: January 2010

BACKGROUNDHiatus hernia and lower oesophageal sphincter hypotension are often viewed as opposing hypotheses for gastro-oesophageal junction incompetence.AIMSTo examine the interaction between hiatus hernia and lower oesophageal sphincter hypotension.METHODSIn seven normal subjects and seven patients with hiatus hernia, the squamocolumnar junction and intragastric margin of the gastro-oesophageal junction were marked with endoscopically placed clips. Axial and radial characteristics of the gastro-oesophageal junction high pressure zone were mapped relative to the hiatus and clips during concurrent fluoroscopy and manometry. Responses to inspiration and abdominal compression were also analysed.RESULTSIn normal individuals the squamocolumnar junction was 0.5 cm below the hiatus and the gastro-oesophageal junction high pressure zone extended 1.1 cm distal to that. In those with hiatus hernia, the gastro-oesophageal junction high pressure zone had two discrete segments, one proximal to the squamocolumnar junction and one distal, attributable to the extrinsic compression within the hiatal canal. Inspiration and abdominal compression mainly augmented the distal one. Simulation of hernia reduction by algebraically summing the proximal segment pressures with the hiatal canal pressures restored normal maximal pressure, radial asymmetry, and dynamic responses of the gastro-oesophageal junction.CONCLUSIONSHiatus hernia reduces lower oesophageal sphincter pressure and alters its dynamic responsiveness by spatially separating pressure components derived from the intrinsic lower oesophageal sphincter and the extrinsic compression of the oesophagus within the hiatal canal.
Geography of intestinal permeability and absorption
Authors: Menzies I S , Zuckerman M J , Nukajam W S , Somasundaram S G , Murphy B , Jenkins A P , Crane R S , Gregory G G 
Published: January 2010

BACKGROUNDIntestinal morphology and function vary geographically.AIMSThese functions were assessed in asymptomatic volunteers in European, North American, Middle Eastern, Asian, African, and Caribbean countries.METHODSFive hour urine collections were obtained from each subject following ingestion of a 100 ml iso-osmolar test solution containing 3–0-methyl-d-glucose,d-xylose, l-rhamnose, and lactulose after an overnight fast, to assess active (3–0-methyl-d-glucose) and passive (d-xylose) carrier mediated, and non-mediated (l-rhamnose) absorption capacity, as well as intestinal permeability (lactulose:rhamnose ratio).RESULTSA comparison of results for subjects from tropical countries (n=218) with those resident in the combined temperate and subtropical region (Europe, United States, Qatar) (n=224) showed significant differences. Residents in tropical areas had a higher mean lactulose:rhamnose ratio and lower mean five hour recoveries of 3–0-methyl-d-glucose,d-xylose, and l-rhamnose, indicating higher intestinal permeability and lower absorptive capacity. Investigation of visiting residents suggested that differences in intestinal permeability and absorptive capacity were related to the area of residence. Subjects from Texas and Qatar, although comprised of several ethnic groups and resident in a subtropical area, showed no significant difference from European subjects.CONCLUSIONSThere are clearly demarcated variations in intestinal permeability and absorptive capacity affecting asymptomatic residents of different geographical areas which correspond with the condition described as tropical enteropathy. Results suggest the importance of environmental factors. The parameters investigated may be relevant to the predisposition of the indigenous population and travellers to diarrhoeal illness and malnutrition. Intestinal function in patients from the tropics may be difficult to interpret, but should take into account the range of values found in the asymptomatic normal population.
Acute increase, stimulated by prostaglandin E2, in glucose absorption via the sodium dependent glucose transporter-1 in rat intestine
Authors: Scholtka B , Stümpel F , Jungermann K 
Published: January 2010

BACKGROUND/AIMSAcute stimulation by cAMP of the sodium dependent glucose cotransporter SGLT1 has previously been shown. As prostaglandin E2(PGE2) increases intracellular cAMP concentrations via its receptor subtypes EP2R and EP4R, it was investigated whether PGE2 could enhance intestinal glucose absorption.METHODSThe action of PGE2 on carbohydrate absorption in the ex situ perfused rat small intestine and on 3-O-[14C]methylglucose uptake in isolated villus tip enterocytes was determined. Expression of mRNA for the PGE2 receptor subtypes 1–4 was assayed in enterocytes by reverse transcriptase polymerase chain reaction (RT-PCR).RESULTSIn the perfused small intestine, PGE2 acutely increased absorption of glucose and galactose, but not fructose (which is not a substrate for SGLT1); in isolated enterocytes it stimulated 3-O-[14C]methylglucose uptake. The 3-O-[14C]methylglucose uptake could be inhibited by the cAMP antagonist RpcAMPS and the specific inhibitor of SGLT1, phlorizin. High levels of EP2R mRNA and EP4R mRNA were detected in villus tip enterocytes.CONCLUSIONPGE2acutely increased glucose and galactose absorption by the small intestine via the SGLT1, with cAMP serving as the second messenger. PGE2 acted directly on the enterocytes, as the stimulation was still observed in isolated enterocytes and RT-PCR detected mRNA for the cAMP-increasing PGE2 receptors EP2R and EP4R.
Involvement of tachykinin receptors in sensitisation to cow’s milk proteins in guinea pigs
Authors: Gay J , Fioramonti J , Garcia-Villar R , Emonds-Alt X , Bueno L 
Published: January 2010

BACKGROUNDThere is growing evidence for a pivotal role for tachykinins in gut neuroimmune interactions.AIMSTo determine whether NK1, NK2, and NK3 tachykinin receptors are involved in milk protein induced allergic sensitisation.METHODSEight groups of 12 Dunkin-Hartley guinea pigs (250–300 g) were used. Four groups were sensitised to milk proteins for three weeks. During this period, these animals were injected intraperitoneally each day with NK1 (SR 140333; 0.3 mg/kg), NK2 (SR 48968; 5 mg/kg), or NK3 (SR 142801; 5 mg/kg) receptor antagonist or vehicle. The fifth group had water available instead of milk and was used as a non-sensitised control. The three other groups received the NK receptor antagonists for three weeks but were not sensitised to milk proteins.RESULTSSensitised animals treated with NK1 and NK3 receptor antagonists had both lower IgE and IgG serum titres, evaluated by passive cutaneous anaphylaxis, and lower specific IgG serum titres, determined by enzyme linked immunosorbent assay (ELISA), than vehicle treated animals. Sensitisation induced an increase in intestinal mast cell number which was abolished by treatment with the NK1 receptor antagonist. Antigenic challenge-induced jejunal hypersecretion was also blocked by treatment with the NK1 receptor antagonist.CONCLUSIONIn guinea pigs, NK1 and NK3 but not NK2 receptors are involved in sensitisation to cow’s milk. However, NK1 but not NK3 receptor antagonists abolish both the hypermastocytosis induced by food allergy and the hypersecretion induced by antigenic challenge, suggesting different roles for NK1 and NK3 receptors in the mechanisms of sensitisation to β-lactoglobulin.
Bacteroides fragilis toxin 2 damages human colonic mucosa in vitro
Authors: Riegler M , Lotz M , Sears C , Pothoulakis C , Castagliuolo I , Wang C C , Sedivy R , Sogukoglu T , Cosentini E , Bischof G , Feil W , Teleky B , Hamilton G , LaMont J T , Wenzl E 
Published: January 2010

BACKGROUNDStrains ofBacteroides fragilis producing a 20 kDa protein toxin (B fragilis toxin (BFT) or fragilysin) are associated with diarrhoea in animals and humans. Although in vitro results indicate that BFT damages intestinal epithelial cells in culture, the effects of BFT on native human colon are not known.AIMSTo examine the electrophysiological and morphological effects of purified BFT-2 on human colonic mucosa in vitro.METHODSFor resistance (R) measurements, colonic mucosa mounted in Ussing chambers was exposed to luminal or serosal BFT-2 (1.25–10 nM) and after four hours morphological damage was measured on haematoxylin and eosin stained sections using morphometry. F actin distribution was assessed using confocal microscopy.RESULTSSerosal BFT-2 for four hours was four-, two-, seven-, and threefold more potent than luminal BFT-2 in decreasing resistance, increasing epithelial3H-mannitol permeability, and damaging crypt and surface colonocytes, respectively (p<0.05). Confocal microscopy showed reduced colonocyte F actin staining intensity after exposure to BFT-2.CONCLUSIONSBFT-2 increases human colonic permeability and damages human colonic epithelial cells in vitro. These effects may be important in the development of diarrhoea and intestinal inflammation caused by B fragilis in vivo.
Clinical spectral characterisation of colonic mucosal lesions using autofluorescence and δ aminolevulinic acid sensitisation
Authors: Eker C , Montán S , Jaramillo E , Koizumi K , Rubio C , Andersson-Engels S , Svanberg K , Svanberg S , Slezak P 
Published: January 2010

BACKGROUND AND AIMSLaser induced fluorescence (LIF) from colonic mucosa was measured in vivo with and without δ aminolevulinic acid (ALA) in an attempt to differentiate between neoplasia and non-neoplasia in real time during colonoscopy.METHODSSpectra from 32 adenomas, 68 normal sites, and 14 hyperplastic polyps in 41 patients were obtained with a point monitoring system. Twenty one of the patients had been given a low dose of ALA as a photosensitiser before the examination. Light of 337, 405, or 436 nm wavelength was used as excitation. Stepwise multivariate linear regression analysis was performed.RESULTSWith 337 nm excitation, 100% sensitivity and 96% specificity was obtained between normal mucosa and adenomas. Seventy seven per cent of the hyperplastic polyps were classified as non-neoplastic. When exciting with 405 and 436 nm, the possibility of distinguishing different types of tissue was considerably better in the ALA patients than in the non-ALA patients.CONCLUSIONSThe in vivo point measurements imply that a good discrimination between normal tissue and adenomatous polyps can be obtained using the LIF technique. Excitation at 337 nm and at 405 nm or 436 nm using ALA gives good results. LIF also shows potential for distinguishing adenomatous from hyperplastic polyps. The number of detection wavelengths could be reduced if chosen properly.
Linkage of Crohn’s disease to the major histocompatibility complex region is detected by multiple non-parametric analyses
Authors: Yang H , Plevy S E , Taylor K , Tyan D , Fischel-Ghodsian N , McElree C , Targan S R , Rotter J I 
Published: January 2010

BACKGROUNDThere is evidence for genetic susceptibility to Crohn’s disease, and a tentative association with tumour necrosis factor (TNF) and HLA class II alleles.AIMSTo examine the potential of genetic linkage between Crohn’s disease and the MHC region on chromosome 6p.METHODSTNF microsatellite markers and, for some families, additional HLA antigens were typed for 323 individuals from 49 Crohn’s disease multiplex families to generate informative haplotypes. Non-parametric linkage analysis methods, including sib pair and affected relative pair methods, were used.RESULTSIncreased sharing of haplotypes was observed in affected sib pairs: 92% (48/52) shared one or two haplotypes versus an expected 75% if linkage did not exist (p=0.004). After other affected relative pairs were included, the significance level reached 0.001. The mean proportion of haplotype sharing was increased for both concordant affected (π=0.60, p=0.002) and unaffected sib pairs (π=0.58, p=0.031) compared with the expected value (π=0.5). In contrast, sharing in discordant sib pairs was significantly decreased (π=0.42, p=0.007). Linear regression analysis using all three types of sib pairs yielded a slope of −0.38 at p=0.00003. It seemed that the HLA effect was stronger in non-Jewish families than in Jewish families.CONCLUSIONSAll available analytical methods support linkage of Crohn’s disease to the MHC region in these Crohn’s disease families. This region is estimated to contribute approximately 10–33% of the total genetic risk to Crohn’s disease.
Validation of a specific quality of life questionnaire for functional digestive disorders
Authors: Chassany O , Marquis P , Scherrer B , Read N W , Finger T , Bergmann J F , Fraitag B , Geneve J , Caulin C 
Published: January 2010

BACKGROUNDDyspepsia and irritable bowel syndrome are suitable conditions for assessment of quality of life. Their similarities justify the elaboration of a single specific questionnaire for the two conditions.AIMSTo examine the process leading to the validation of the psychometric properties of the functional digestive disorders quality of life questionnaire (FDDQL).METHODSInitially, the questionnaire was given to 154 patients, to assess its acceptability and reproducibility, analyse its content, and reduce the number of items. Its responsiveness was tested during two therapeutic trials which included 428 patients. The questionnaire has been translated into French, English, and German. The psychometric validation study was conducted in France, United Kingdom, and Germany by 187 practitioners. A total of 401 patients with dyspepsia or irritable bowel syndrome, defined by the Rome criteria, filled in the FDDQL and generic SF-36 questionnaires.RESULTSThe structure of the FDDQL scales was checked by factorial analysis. Its reliability was expressed by a Cronbach’s α coefficient of 0.94. Assessment of its discriminant validity showed that the more severe the functional digestive disorders, the more impaired the quality of life (p<0.05). Concurrent validity was supported by the correlation found between the FDDQL and SF-36 questionnaire scales. The final version of the questionnaire contains 43 items belonging to eight domains.CONCLUSIONSThe properties of the FDDQL questionnaire, available in French, English, and German, make it appropriate for use in clinical trials designed to evaluate its responsiveness to treatment among patients with dyspepsia and irritable bowel syndrome.
Pancreatic stellate cells are activated by proinflammatory cytokines: implications for pancreatic fibrogenesis
Authors: Apte M V , Haber P S , Darby S J , Rodgers S C , McCaughan G W , Korsten M A , Pirola R C , Wilson J S 
Published: January 2010

BACKGROUNDThe pathogenesis of pancreatic fibrosis is unknown. In the liver, stellate cells play a major role in fibrogenesis by synthesising increased amounts of collagen and other extracellular matrix (ECM) proteins when activated by profibrogenic mediators such as cytokines and oxidant stress.AIMSTo determine whether cultured rat pancreatic stellate cells produce collagen and other ECM proteins, and exhibit signs of activation when exposed to the cytokines platelet derived growth factor (PDGF) or transforming growth factor β (TGF-β).METHODSCultured pancreatic stellate cells were immunostained for the ECM proteins procollagen III, collagen I, laminin, and fibronectin using specific polyclonal antibodies. For cytokine studies, triplicate wells of cells were incubated with increasing concentrations of PDGF or TGF-β.RESULTSCultured pancreatic stellate cells stained strongly positive for all ECM proteins tested. Incubation of cells with 1, 5, and 10 ng/ml PDGF led to a significant dose related increase in cell counts as well as in the incorporation of3H-thymidine into DNA. Stellate cells exposed to 0.25, 0.5, and 1 ng/ml TGF-β showed a dose dependent increase in α smooth muscle actin expression and increased collagen synthesis. In addition, TGF-β increased the expression of PDGF receptors on stellate cells.CONCLUSIONSPancreatic stellate cells produce collagen and other extracellular matrix proteins, and respond to the cytokines PDGF and TGF-β by increased proliferation and increased collagen synthesis. These results suggest an important role for stellate cells in pancreatic fibrogenesis.
Underestimation of acute pancreatitis: patients with only a small increase in amylase/lipase levels can also have or develop severe acute pancreatitis
Authors: Lankisch P G , Burchard-Reckert S , Lehnick D 
Published: January 2010

BACKGROUNDIn most treatment studies on acute pancreatitis, pancreatologists base their diagnosis on amylase/lipase levels more than three times above the upper limit of normal (>3n) and thus exclude patients with smaller enzyme level increases. The recommendations derived from the results of treatment studies do not take into account such patients. Non-pancreatologists frequently believe that only patients with high enzyme levels have a serious prognosis.AIMSTo question the assumption that high enzyme levels indicate severe, and conversely low enzyme levels indicate mild, acute pancreatitis.PATIENTS/METHODSThis retrospective study includes 284 consecutive patients with a first attack of acute pancreatitis. The cause was biliary in 114 (40%) patients, alcoholism in 83 (29%), other in 21 (7%), and unknown in 66 (23%). Patients were divided into two groups according to their serum enzyme levels (amylase: ⩽3n, n = 88; >3n, n = 196; lipase: ⩽3n, n = 51; >3n, n = 233). Renal impairment, indication for dialysis and artificial ventilation, development of pseudocysts, necessity for surgery, and mortality were taken as parameters of severity.RESULTSThe incidence of severity was the same for both the ⩽3n and >3n groups.CONCLUSIONSThe severity of acute pancreatitis is independent of the elevation in serum amylase/lipase level (⩽3n or >3n) on admission. Patients with only a slight increase can also have or develop severe acute pancreatitis. Patients with ⩽3n elevated enzyme levels on admission represent a substantial group that treatment studies have frequently overlooked. This is especially true for patients with alcohol induced acute pancreatitis whose amylase levels are lower than in other aetiological groups.
Immunoreactive pancreatic Reg protein in sera from cystic fibrosis patients with and without pancreatic insufficiency
Authors: Carrère J , Guy-Crotte O , Gaia E , Figarella C 
Published: January 2010

BACKGROUNDThe biological function of the Reg protein, a non-enzymic protein produced in fairly large amounts by pancreatic acinar cells, remains elusive. Its susceptibility to proteolysis leading to precipitation of the proteolysis product at neutral pH suggests that it could contribute to the protein plugging observed in cystic fibrosis (CF).AIMSTo study its behaviour in the serum of CF patients with or without pancreatic insufficiency and to compare it with that of other pancreatic secretory proteins.PATIENTS170 patients (93 with CF, 55 controls, and 22 with chronic pancreatitis) were studied.METHODSReg protein was measured using a specific enzyme immunoassay and its molecular form in CF sera was characterised by gel filtration. Molecular gene expression was investigated by dot-blot hybridisation.RESULTSReg protein was present in all CF sera studied from patients with or without pancreatic insufficiency, and in all cases the level was significantly higher than in controls. Its chromatographic behaviour in CF sera was identical with that of the protein present in normal serum. No correlation was found between the levels of Reg protein and trypsin(ogen) (or lipase) in CF, nor in control sera or normal pancreatic juice. Molecular gene expression of the corresponding proteins investigated in pancreatic tissues showed an absence of correlation between the mRNA levels.CONCLUSIONSReg protein may not be a secretory exocrine protein like the digestive enzymes but rather a hormone-like secretory substance with an endocrine or paracrine function.