Food and nutrition guidelines.
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Biomedical subjects
Publications and source records attributed to C Tasman-Jones.
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Hepatic steatosis is a common liver biopsy finding. As a preamble to a study of nonA, nonB hepatitis we aimed to determine the clinical associations in patients who had hepatic steatosis on biopsy. All liver biopsies performed in the gastroenterology department at Auckland Hospital between 1986 and 1989 were reviewed for evidence of steatosis and the clinical associations analysed. Steatosis was present in 69 (43.7%) of 158 liver biopsy specimens with 35 being mild (47%), 29 moderate (45%) and five severe (7%). Excess alcohol intake was the probable aetiological association in 28 (45%), obesity in 17 (27%) and diabetes mellitus in seven (11%). No causal association could be identified in 17 (24%) and included three of the five cases with severe steatosis. There were no significant differences in clinical presentation, biochemistry or hepatic histopathology between alcoholic and nonalcoholic steatosis. Nonalcoholic steatosis appeared to be more benign with only one case of cirrhosis but further follow up is required to determine true prognosis.
Necropsy gastric mucus infected with Helicobacter pylori has a reduced capacity to concentrate colloidal bismuth subcitrate when compared with non-infected mucus. Mucus mounted in a modified in vitro diffusion chamber was bathed with colloidal bismuth subcitrate solutions at different concentrations and pH levels. Bismuth was measured by atomic absorption spectrophotometry to assess intramucus colloidal bismuth subcitrate concentrations. Bismuth concentrations in non-infected mucus were higher than in Helicobacter pylori infected mucus at all experimental colloidal bismuth subcitrate concentrations and pH levels. Regardless of the infection status, the intramucus concentration of colloidal bismuth subcitrate was dependent upon the concentration of the bathing solution and independent of the pH and the mucus thickness. Colloidal bismuth subcitrate solubility in saline solution varied with pH, and was least soluble in the pH range 1.1 to 3.25 and more soluble above and below this pH range. This study suggests that Helicobacter pylori infection is associated with physicochemical changes in the gastric mucus with a reduction in its capacity to concentrate colloidal bismuth subcitrate. Such a reduction may compromise the attainment of optimum colloidal bismuth subcitrate concentrations necessary for its bactericidal activity.
To establish a human model system for investigating control of mucus secretion by the small intestine, we have studied the output of mucus glycoprotein in the urine of patients with ileal conduits. A highly specific enzyme-linked immunosorbent assay (ELISA) was used to measure mucus glycoprotein with a sensitivity down to 0.3 ng protein of mucus glycoprotein. The assay detects human ileal mucus glycoprotein in the urine of ileal conduit patients; for an individual subject, the amount hardly varied from day to day, although there were substantial differences between individuals in the amounts secreted. Control urine from persons with normal bladders did not contain any mucus glycoprotein that reacted in the ELISA. The model has many advantages over other experimental systems for studying the rate of mucus glycoprotein secretion from the human ileum and can also be used as a reproducible resource of undegraded mucus glycoprotein.
Free vulpecholic acid (1 alpha,3 alpha,7 alpha-trihydroxy-5 beta-cholan-24-oic) is the major biliary component of the Australian opossum (Trichosurus vulpecula), accompanied only by a few percent of its taurine conjugate. In order to exclude a microbial involvement in its formation (i.e., secondary origin) four sets of experiments were performed. It was found that a) the level of vulpecholic acid remained unchanged in the bile of opossums fed with neomycin and kanamycin for 7 days prior to bile collection; b) it also remained unchanged after long bile drainage; c) in opossums prepared with biliary cannula, intraportally injected [24-14C]chenodeoxycholic acid was transformed to [24-14C]vulpecholic acid; and d) in a similar experiment, the detectable transformation of [1 alpha,2 alpha-3H2]cholesterol to vulpecholic acid was observed. In experiment c) 28-66% of the administered radioactivity was secreted in 2 h in the form of free biliary vulpecholic and chenodeoxycholic acids. Only a trace amount of the corresponding taurine conjugates (approximately 0.4%) was formed. Moreover, rapidly declining specific radioactivity of the unconjugated chenodeoxycholic acid indicated its probable participation in the native formation of vulpecholic acid.
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The stomach and small intestine are areas of major electrolyte and solute transport. Mechanisms of transport in these areas have been widely studied and basic understanding is available. However, the mucus that lines the stomach and intestine is an important layer whose properties and functions in electrolyte and solute transport are not well understood. In this study we examined the Na+/H+ exchange of mucus from the stomach body and antrum, the jejunum, and the ileum. Mucus from the stomach body and antrum is a cation exchanger, a property that aids the net unidirectional flux of H+ ions from parietal cells to lumen. In the jejunum and ileum, mucus is an anion exchanger, which may be important in solute transport and absorption in the small bowel. In both the stomach and small bowel, proton movement is slow, which helps maintain the uphill pH gradient across gastric mucus and the downhill pH gradient across small intestinal mucus.
The spatial relations between bacteria and the affected tissues can indicate pathogenic mechanisms. This study was undertaken to define the spatial relation of Helicobacter pylori to the human gastric mucosa. Antibodies against gastric mucus and ruthenium red were used to stabilise the glycoprotein structure of the mucus and glycocalyces in antral biopsy specimens from eight patients infected with H pylori. The location of organisms and ultrastructural features were assessed using systematic scanning and transmission electron microscopy: 92 (2)% (mean (SE] of H pylori were in the pit mucus, and 7 (3)% were in the surface mucus; 60 (12)% of H pylori were close to epithelial cells, with only 5 (2)% located near the epithelial intercellular junctions. Fine filamentous strands extended between organisms and nearby epithelial cells, with few organisms in membrane to membrane contact. H pylori were not observed between, beneath, or within cells of the gastric mucosa. The preferred location of H pylori in the gastric antrum is within the pit mucus close to the epithelial cell surface, with no evidence that they have a direct toxic effect on the mucosa.
Sucralfate protects the stomach against a number of experimental damaging agents and is efficacious in the treatment of peptic ulcer disease. It binds with acidity to the base of an ulcer to form a protective barrier. Sucralfate also enhances prostaglandin synthesis and release in the mucosa. In this study, the rat stomach was examined to determine sucralfate's interaction with gastric mucus. Mucus in the rat stomach forms a distinct and continuous blanket. In snap-frozen samples, pretreatment with phosphate-buffered saline as a control shows a layer of mucus of homogeneous structure thinner than the homogeneous layer after pretreatment with antibodies developed against rat gastric mucus. Pretreatment with the surface protective agent sucralfate shows some increase in the thickness of mucus with a thin dense sublayer adjacent to the epithelium and a less dense-appearing outer zone of variable thickness. Analysis of x-rays generated by the electron beam on windows of mucus and epithelium showed the expected gradients of sodium, potassium, chloride, and sulfur. The percentage of aluminum and sulfur in the mucus was higher in sucralfate-treated samples than in controls. Interaction between sucralfate and gastric mucus needs further investigation.
Lithium is widely used in the management of patients with manic depressive illnesses. It is a valuable drug with a good safety record but occasionally causes severe disorders. A 71-year-old woman is described who previously had a good response to lithium carbonate treatment of a manic depressive illness. Because the patient appeared depressed and withdrawn, lithium carbonate dosage was increased. The development of confusion and choreiform movements precipitated hospital admission. The symptoms were relieved when lithium was stopped but recurred with the reinstitution of lithium. Spontaneous choreiform movements were again relieved on lithium withdrawal. Associated with the abnormal movements were alterations in the serum calcium concentrations, a rise in the parathyroid hormone concentration and a rise in the serum amylase concentration without features of acute pancreatitis.
The effect of Campylobacter pylori infection and sucralfate treatment on the ion-exchange property of human gastric mucus from 17 human postmortem stomachs was investigated in an in vitro chamber. Of the 10 stomachs not infected with C. pylori mucus from 4 stomachs had a 'normal' Na+/H+ exchange capacity, whereas 6 were without a Na+/H+ exchange capacity. The Na+/H+ exchange capacity of the seven stomachs infected with C. pylori was half that of the four 'normal' uninfected stomachs. Sucralfate significantly improved the Na+/H+ exchange capacity of mucus from C. pylori-infected stomachs and from the uninfected stomachs without Na+/H+ exchange. This study shows that impairment of the Na+/H+ exchange capacity of gastric mucus is associated with C. pylori infection and that sucralfate improves the Na+/H+ exchange capacity of gastric mucus.
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We aimed to show that Campylobacter pylori infection increases the concentration of ammonia in the gastric mucus and alters the movement of H+ through the mucus. Mucus from uninfected and C. pylori-infected stomachs was collected at postmortem. Ammonia was measured enzymatically. The ammonia concentration in C. pylori-infected mucus was fourfold greater than in uninfected mucus. H+ movement experiments were carried out using an in vitro chamber, in which a layer of mucus separated a 0.1 M HCl solution from distilled H2O. The change in pH of the distilled H2O was measured over 30 min. A drop in pH was measured for uninfected mucus. A slight rise in pH was measured for C. pylori-infected mucus. We conclude that C. pylori infection is associated with reduced H+ movement through mucus and that this may be due to increased ammonia concentration within mucus.
The distribution of microorganisms in the mid-colon of the rat was studied by light and scanning electron microscopy. An antiserum against rat colon mucus was used to stabilize the mucus in situ. In samples not incubated with antiserum, the mucus disintegrated and contracted into patchy strands only partly covering the luminal surface of the colon. Bacteria were seen within fecal pellets, tangled among the strands of mucus, and scattered on the epithelial surface. However, when incubated with antiserum, mucus almost completely filled the lumen and coated the fecal pellets. Bacteria in these stabilized preparations were limited mainly to the fecal pellets, and there were small numbers scattered in the luminal mucus, but none were observed on the epithelial surface or within the crypts. Latex particles introduced into the lumen with the antiserum or with phosphate-buffered saline showed the same distribution as the bacteria. These findings are at variance with previous reports that organisms occur in abundance in the mucous layer, adjacent to cell surfaces, and inside crypts. Our results suggest that conventional preparation for microscopy without prior stabilization of the mucus in situ may lead to artifactual redistribution of microorganisms and emphasize the importance of mucus in maintaining mucosal-floral homeostasis in the colon.
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The digestion of cellulose, hemicellulose, and lignin has been investigated in humans. Two groups of subjects were studied--healthy subjects with an ileostomy and normal subjects. Both were put on a fixed diet of known cellulose, hemicellulose, and lignin content. From the feces excreted the fiber components were measured by the acid and neutral detergent method. From the small bowel 84.5% of the ingested cellulose was excreted from the ileostomy subjects. From the normal subjects 22.4% of the ingested cellulose was excreted, indicating approximately 80% of the cellulose was digested in the normal subjects. From the water insoluble ingested hemicelluloses 27.5% were excreted from the small bowel, 4.0% from normal subjects. That is approximately 96% digestion of the hemicelluloses in normal subjects. Lignin was found to be undigested in both the small and large bowel. This has important implications in future fiber research.