bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stimulus and site specific induction of hiccups in the oesophagus of normal subjects
Authors: Fass R , Higa L , Kodner A , Mayer E A 
Published: June 2010

Background—Hiccups that are induced by a large meal have been suggested to result from gastric overdistension. The role of the oesophagus in precipitating hiccups has never been defined.Aims—To determine the involvement of oesophageal mechanoreceptors in the hiccup reflex.Methods—Ten normal healthy subjects were prospectively evaluated at a university affiliated hospital. Controlled inflation of a polyethylene bag in the proximal and distal oesophagus was carried out using slow ramp and rapid phasic distensions, by an electronic distension device.Results—Hiccups were induced in four subjects only during rapid phasic distensions and only in the proximal oesophagus. The mean (SEM) minimal volume threshold for the hiccup reflex was 32.5 (4.8) ml, which was above the perception threshold. Hiccups appeared during inflation and resolved after deflation.Conclusions—Sudden rapid stretch of the mechanoreceptors in the proximal oesophagus can trigger the hiccup reflex in normal subjects. Only rapid distensions above a determined volume threshold will predictably induce hiccups in a given subject. This mechanism may play a role in the physiological induction of hiccups.
Abnormal postprandial duodenal chyme transport in patients with long standing insulin dependent diabetes mellitus
Authors: Nguyen H N , Silny J , Wüller S , Marschall H-U , Rau G , Matern S 
Published: June 2010

AbstractBackground—Patients with long standing diabetes mellitus frequently have upper gut dysmotility. Gastroparesis has been well studied, whereas detailed data on duodenal motor function are limited.Aims—To characterise postprandial duodenal chyme transport in such patients.Methods—Intraluminal multiple impedance measurement, recently introduced as a novel technique for investigation of chyme transport, was used to study postprandial duodenal chyme flow in 10 patients with long standing insulin dependent diabetes mellitus with gastroparesis, and 10 healthy volunteers.Results—Four distinct transport patterns of chyme, termed bolus transport events (BTEs), were found in both groups and could be characterised as: short distance propulsive; simple long distance propulsive; retrograde; and complex long distance propulsive. Diabetic patients had significantly lower numbers of propulsive BTEs (p<0.01), and higher proportions of retrograde BTEs and complex long distance BTEs (p<0.05) than control subjects, whereas the proportion of simple long distance BTEs was significantly lower (p<0.05). The mean propagation velocities of the BTEs were similar in both groups.Conclusion—Abnormal postprandial duodenal chyme transport was found in patients with long standing insulin dependent diabetes mellitus. This is characterised by transport disorganisation and may result in disturbed chyme clearance.
Studies on the gastric mucosal microcirculation. 2.Helicobacter pylori water soluble extracts induce platelet aggregation in the gastric mucosal microcirculation in vivo
Authors: Kalia N , Jacob S , Brown N J , Reed M W R , Morton D , Bardhan K D 
Published: June 2010

Background—The exact mechanisms by whichHelicobacter pylori infection results in gastric mucosal injury are unclear.Aims—To assess in vivo whether H pylori extracts could initiate an inflammatory response in the rat gastric mucosal microcirculation.Methods—Extracts of H pylori, Escherichia coli, or distilled water were administered topically to the gastric mucosa of anaesthetised animals. Fluorescence in vivo microscopy assessed macromolecular leakage of labelled albumin from mucosal vessels, leucocyte adherence/rolling, and platelet activity for 90 minutes.Results—H pylori induced increases (p<0.001) in adherent platelet thrombi and circulating platelet emboli after five and 15 minutes respectively. Adherent platelet thrombi (mean of four per field of view) remained significantly increased throughout the experiment, but circulating emboli (maximum of five at 30 minutes) decreased with time. Leucocyte adherence did not occur although early transient rolling was observed. An 11% increase (p<0.02) in albumin leakage occurred after five minutes only. The induction of platelet aggregation was only observed following H pyloriadministration.Conclusion—This in vivo study demonstrated the ability of Hpylori extracts to promote platelet aggregation within gastric mucosal microvessels. Recruitment of leucocytes was not observed. The results suggest that the early events associated with H pylori infection are platelet aggregation with perhaps subsequent leucocyte recruitment by activated platelets.
Vascular anatomy defines sites of indomethacin induced jejunal ulceration along the mesenteric margin
Authors: Anthony A , Pounder R E , Dhillon A P , Wakefield A J 
Published: June 2010

Background—Indomethacin induces ulceration in the rat jejunum with sparing of the ileum. The ulcers localise between vasa recta along the mesenteric margin of the bowel, observations that have not been fully explained.Aim—To examine the relationship between the localisation of experimental ulcers and the vascular anatomy of the rat small intestine.Methods—The normal vascular anatomy of the rat jejunum and ileum was studied and compared using arterial carbon ink perfusion. The anatomical localisation of early and advanced lesions induced by indomethacin was examined with particular reference to the vasculature. Mucosal injury induced by feeding vessel ligation for 24 hours or brief ischaemia-reperfusion injury was examined. The existence of anatomically sensitive sites to indomethacin was tested in a two dose study.Results—In the rat jejunum, poorly vascularised sites along the mesenteric margin were highly susceptible to indomethacin induced injury, such sites being absent from the ileum. Villous contraction was a feature of both early indomethacin injury and ischaemia-reperfusion injury in the rat jejunum. Twenty four hour ligation of jejunal vasa brevia selectively induced ischaemic injury along the mesenteric margin. Two doses of indomethacin to rats did not induce greater injury than a single dose.Conclusions—Results support the hypothesis that the rat jejunum possesses vascularly compromised sites along the mesenteric margin that are susceptible to indomethacin induced injury. Indomethacin may cause ischaemia-reperfusion injury selectively at these sites.
Macronutrient intake and malabsorption in HIV infection: a comparison with other malabsorptive states
Authors: Carbonnel F , Beaugerie L , Rached A Abou , D’Almagne H , Rozenbaum W , Le Quintrec Y , Gendre J P , Cosnes J 
Published: June 2010

Background—Wasting is a major complication of HIV infection. The role of malabsorption in wasting is controversial.Aims—To assess oral intake and malabsorption in a cohort of weight losing HIV infected patients, with or without chronic diarrhoea.Methods—A prospective study using a predefined protocol for HIV infected patients was performed in a gastroenterology and nutrition unit in a university hospital. A retrospective comparison was made with HIV negative patients with malabsorption due either to small bowel disease or resection. Body weight and height, serum albumin, oral intake of macronutrients, faecal weight, and faecal fat were measured.Results—Seventy nine weight losing HIV infected patients were studied. Among the 66 patients with more than 5% lipid malabsorption, wasting was significantly greater in patients with cryptosporidiosis (n=22) than in patients with microsporidiosis (n=18) who exhibited significantly more wasting than patients with no identified enteropathogen (n=26) (body mass index 16.8 (14.0–20.7), 18.9 (16.5–21.3), 19.7 (15.9–23), respectively). When controlling for the level of lipid malabsorption, HIV infected patients had a significantly lower energy intake than HIV negative patients with chronic malabsorption. In HIV infected patients, but not in other categories of malabsorbers, body mass index correlated significantly with energy intake (r=0.33, 95% confidence intervals 0.12 to 0.51).Conclusion—In weight losing HIV infected patients, reduced energy intake is superimposed on malabsorption and significantly contributes to wasting.
A simple genetic test identifies 90% of UK patients with haemochromatosis
Authors:   The UK Haemochromatosis Consortium
Published: June 2010

Background—The diagnosis of genetic haemochromatosis (GH) before iron overload has developed is difficult. However a convincing candidate gene for GH, HFE (previously HLA-H), has been described recently.Aims—To determine the prevalence of the haemochromatosis associated HFE mutations C282Y and H63D in United Kingdom affected and control populations.Methods—The prevalence of the HFE C282Y and H63D mutations was determined by polymerase chain reaction amplification and restriction enzyme digestion in a cohort of 115 well characterised patients with GH and 101 controls from the United Kingdom.Results—One hundred and five of 115 (91%) patients with GH were homozygous for the C282Y mutation. Only one of 101 (1%) controls was homozygous for the C282Y mutation and this individual currently shows evidence of iron overload. Two of five patients who did not have either of the two described mutations of HFE had early onset iron overload (ages 16 and 24). One had a family history of cardiac failure and the second was subsequently hospitalised due to cardiac failure. These are the first phenotypic observations for patients without either C282Y or H63D mutation of HFE.Conclusion—This simple genetic test promises to be a highly effective tool in the diagnosis of GH.
Drinking habits as cofactors of risk for alcohol induced liver damage
Authors: Bellentani S , Saccoccio G , Costa G , Tiribelli C , Manenti F , Sodde M , Croce’ L Saveria , Sasso F , Pozzato G , Cristianini G , Brandi and the Dionysos Study Group G 
Published: June 2010

Background—The Dionysos Study is a cohort study of the prevalence of chronic liver disease in the general population of two northern Italian communities. It included 6917 subjects, aged 12–65 (69% of the total population).Aims—The aim of this part of the study was to examine the relationship of daily alcohol intake, type of alcoholic beverage consumed, and drinking patterns to the presence of alcohol induced liver damage in an open population.Patients and methods—6534 subjects, free of virus related chronic liver disease and participating in the first cross-sectional part of the study, were fully examined. Each subject underwent: (a) medical history and physical examination, (b) evaluation of alcohol intake using an illustrated dietary questionnaire, and (c) routine blood tests. More invasive diagnostic procedures were performed when indicated.Results—Multivariate analysis showed that the risk threshold for developing either cirrhosis or non-cirrhotic liver damage (NCLD) was ingestion of more than 30 g alcohol per day in both sexes. Using this definition, 1349 individuals (21% of the population studied) were at risk. Of these, only 74 (5.5% of the individuals at risk) showed signs of liver damage. The prevalence of “pure” alcoholic cirrhosis was 0.43% (30 of 6917), representing 2.2% of the individuals at risk, with a ratio of men to women of 9:1, while 44 (3.3% of the individuals at risk) showed persistent signs of NCLD. After 50 years of age, the cumulative risk of developing both NCLD and cirrhosis was significantly higher (p<0.0001) for those individuals who regularly drank alcohol both with and without food than for those who drank only at mealtimes.Conclusions—Our data show that in an open population the risk threshold for developing cirrhosis and NCLD is 30 g ethanol/day, and this risk increases with increasing daily intake. Drinking alcohol outside mealtimes and drinking multiple different alcoholic beverages both increase the risk of developing alcohol induced liver damage.
Hepatic histology in hepatitis C virus carriers coinfected with hepatitis G virus
Authors: Petrik J , Guella L , Wight D G D , Pearson G M , Hinton J , Parker H , Allain J-P , Alexander G J M 
Published: June 2010

Background—A novel flavivirus has been described recently and designated hepatitis G virus (HGV). The virus is transmitted by the parenteral route but it is uncertain whether it is associated with chronic liver disease because liver biopsy is difficult to justify in this group.Aims—To examine histological features of liver biopsy in patients infected with hepatitis C virus (HCV) according to the presence or absence of HCV and HGV RNA.Methods—One hundred and thirty one consecutive HCV carriers undergoing staging liver biopsy were studied retrospectively. In each, HCV RNA and HGV RNA were detected by reverse transcription polymerase chain reaction on serum samples collected at the time of biopsy. The presence of each RNA was correlated with histological features blind to the RNA results; individual histological features of inflammation or fibrosis were scored separately.Results—Nineteen patients were positive for both HGV and HCV RNA in serum, 91 were positive for HCV RNA alone, two were positive for HGV RNA alone, and 19 were negative for both RNA species. Neither age nor sex differed between the groups; a greater proportion of intravenous drug users were HGV RNA positive, but this was not statistically significant. There was no effect of HGV coinfection on the stage of fibrosis or any other histological parameter except steatosis; patients with HCV and HGV RNA had a higher mean score for fat than those patients with HCV RNA alone (p<0.05).Conclusions—HGV coinfection has no important effects on histological features in chronic HCV carriers. It is unlikely that HGV infection causes chronic liver disease.
The association between primary biliary cirrhosis and coeliac disease: a study of relative prevalences
Authors: Kingham J G C , Parker D R 
Published: June 2010

Background—Coexistent primary biliary cirrhosis (PBC) and coeliac disease has been recorded but the association has not been systematically studied.Aims—To determine relative prevalences of PBC and coeliac disease in a defined population over a 12 year period.Patients and methods—All patients with PBC or coeliac disease in a stable population of 250 000 in South Wales were identified from a clinical register and laboratory records.Results—Sixty seven patients with PBC and 143 patients with coeliac disease have been diagnosed and followed over a median of 86 (4–135) months; point prevalences in 1996 were 20 per 100 000 for PBC and 54 per 100 000 for coeliac disease. PBC in patients with coeliac disease was sought by investigating abnormal liver function tests. Ten (7%) had persistent abnormalities and three had PBC. Coeliac disease in patients with PBC was sought by investigating malabsorption, haematinic deficiency, positive antigliadin antibody, or coeliac disease family history. Eleven patients underwent duodenal biopsy revealing one further coeliac disease case. Four patients (three women) have both conditions giving a point prevalence for patients with both conditions of 1.6 per 100 000 (95% confidence limits 0.44 to 4.1 per 100 000). Prevalence of PBC in patients with coeliac disease was 3% and of coeliac disease in patients with PBC was 6%.Conclusion—A 12 year study of a stable 250 000 population revealed a relative prevalence of PBC in 3% of 143 patients with coeliac disease and of coeliac disease in 6% of 67 patients with PBC. PBC and coeliac disease are therefore associated. Screening for PBC in patients with coeliac disease using antimitochondrial antibody testing and screening for coeliac disease in patients with PBC with antigliadin antibody testing or duodenal biopsy are recommended.
Is the association between irritable bowel syndrome and abuse explained by neuroticism? A population based study
Authors: Talley N J , Boyce P M , Jones M 
Published: June 2010

Background—In outpatients and the community, an association between abuse (particularly sexual abuse) and irritable bowel syndrome (IBS) has been observed, but whether there is a causal link continues to be disputed.Aims—To test the hypothesis that psychological factors explain the apparent association between abuse and IBS.Methods—A sample of residents of Penrith (a Sydney suburb sociodemographically similar to the Australian population) selected randomly from the electoral rolls (that by law include the entire population of age 18 years and above) was mailed a validated self report questionnaire. Measured were gastrointestinal (GI) symptoms including the Rome criteria for IBS, abuse (including the standardised Drossman questions), neuroticism (Eysenck Personality Questionnaire), and psychological morbidity (General Health Questionnaire).Results—The response rate was 64% (n=730); 12% fulfilled the Rome criteria for IBS. Overall abuse in childhood (odds ratio (OR)=2.02, 95% confidence interval (CI) 1.29 to 3.15) but not adulthood (OR=1.39, 95% CI 0.88 to 2.19) was associazted with IBS univariately. Neuroticism and psychological morbidity were also univariately associated with abuse in childhood, abuse in adulthood, and IBS, respectively. However, by logistic regression, abuse in childhood was not associated with IBS after controlling for age, gender, and psychological factors (OR=1.34, 95% CI 0.83 to 2.17). The results were not altered by restricting the analyses to more severe forms of abuse, and were not explained by interactions between abuse and psychological variables.Conclusion—There is an association between abuse and IBS in the community, but this may be explained in part by other psychological factors. Based on a path analysis, we postulate that abuse may induce the expression of neuroticism that in turn leads to IBS.
Developmental expression of mucin genes in the human gastrointestinal system
Authors: Reid C J , Harris A 
Published: June 2010

Background and aims—Mucin glycoproteins play a key role in the normal function of the epithelium lining the gastrointestinal tract. The expression of mucin genes, MUC 3, 4, 5AC, 5B, 6, 7, and 8 in human fetal tissues was examined to establish the localisation and age of onset of expression of each mucin gene during human development.Methods—Mucin gene expression was assayed by mRNA in situ hybridisation.Results—Expression of MUC3 was detected in the small intestine and colon from 13 weeks gestation onwards and at low levels in the main pancreatic duct at 13 weeks only. MUC4 expression was seen at a low level in the colonic epithelium from 13 weeks of gestation but not elsewhere in the gastrointestinal tract. MUC5AC mRNA was detected in the colon at 17 weeks and at high levels in the stomach at 23 weeks. MUC6transcripts were evident in the pancreatic ducts from 13 weeks of gestation and at high levels in the stomach at 23 weeks.MUC5B, MUC7, and MUC8transcripts were not detected.Conclusions—Mucin genes are expressed from the early mid-trimester of gestation in the developing human fetal gastrointestinal tract.
Inhibition of phenolsulphotransferase by salicylic acid: a possible mechanism by which aspirin may reduce carcinogenesis
Authors: Harris R M , Hawker R J , Langman M J S , Singh S , Waring R H 
Published: June 2010

Background—Recent epidemiological evidence has shown that chronic use of aspirin decreases susceptibility to bowel cancer. Animal studies have shown that sulphotransferase inhibitors coadministered with sulphation activated carcinogens dramatically reduce the incidence of cancer.Aims—To investigate the effect of the main aspirin breakdown product, salicylic acid, on the P and M isoforms of phenolsulphotransferase from human platelets and colonic mucosa.Methods—Platelets were obtained from healthy blood donors and isolated within 24 hours after donation. Samples of colonic mucosa were obtained at resection for non-malignant disease. Phenolsulphotransferase activity was measured in cellular homogenates using a standard radiolabelling assay.Results—Salicylic acid consistently and selectively inhibited the P form of phenolsulphotransferase at subtherapeutic concentrations in both tissue samples. A 50% inhibition of sulphation by the P phenolsulphotransferase occurred at salicylic acid concentrations of about 40 and 130 μM in platelets and bowel mucosa respectively. M phenolsulphotransferase was virtually unaffected by salicylic acid up to a concentration of 1.5 mM (the therapeutic plasma concentration for salicylates when treating rheumatoid arthritis is about 1–2 mM).Conclusion—The action of salicylic acid on P phenolsulphotransferase, by preventing the excessive activation of carcinogens, is a possible additional pathway by which aspirin can reduce cancer risk.
Focal reduction of villous blood flow in early indomethacin enteropathy: a dynamic vascular study in the rat
Authors: Kelly D A , Piasecki C , Anthony A , Dhillon A P , Pounder R E , Wakefield A J 
Published: June 2010

Background—Oral indomethacin causes villous shortening, microvascular damage, and distortion, which might induce mucosal ischaemia and necrosis.Aims—In order to determine the early events in indomethacin induced jejunal injury we examined the temporal relations between morphological damage and changes in villous blood flow following indomethacin.Methods—In anaesthetised rats, mid jejunal villi were exteriorised in a chamber and observed by fluorescence microscopy. Blood flow in surface capillaries was calculated from velocities and diameters. Indomethacin was applied by both luminal and intravenous routes for 90 minutes, after which the animal was perfusion fixed and the villi were processed for histological examination. Control animals received intravenous or luminal bicarbonate (1.25%).Results—Blood flow slowed in individual villi at 20 minutes, and progressed to complete stasis (in another group) by 45 minutes. Histological examination at 20 minutes revealed microvascular distortion, but no villous shortening: crypt depth:villous height ratios were 0.356 (0.02) in test and 0.386 (0.01) in surrounding villi (p>0.5). At stasis, the villi under study showed epithelial clumping and were shortened: crypt depth:villous height ratios were 0.92 (0.2) in test and 0.42 (0.06) in surrounding villi (p<0.02). Vehicle alone had no effect on either blood flow or histology.Conclusions—Focal slowing of villous blood flow and microvascular distortion precede villus shortening and epithelial disruption, and indicate that damage to surface microvasculature is an early event in indomethacin induced mucosal injury in this model.