Gastrointestinal motility investigations involve the study of the motions of the bowel. Their goal is to understand the nature of the physical interactions that take place between the gut wall and its contents in both health and disease. The aim of this project was to develop a computerised system for the measurement, inspection, analysis and collation of prolonged, ambulatory manometric records from within the human small bowel. This was planned to evolve from existing analogue techniques using a specially commissioned digital data-logger. This thesis describes the testing of the data-logger by comparison with an accepted standard technique, investigating its long-term stability and the effect of different sampling rates. Then the development of a means of detecting intestinal contractions with minimal artefact is described. When validated against 6 experienced human observers the program had a sensitivity of between 84-95 % and a positive predictability of 98% in a noise free signal falling to 37% in a signal containing many movement artifacts and few contractions. The inter- and intra-observers response was found to be variable displaying a high degree of subjectivity in their assessment with respect to the computer. Further methods for the classification of intestinal activity in the temporal domain such as contraction frequency and the occurrence of clusters of contractions are described. A new parameter, Psw is proposed which provides an indication of the relative inter-contractile separations. The effect of meals and disease on Psw, contraction and cluster incidence is investigated and all three parameters are found to be markedly affected by feeding. A program for the identification of contractile propagation across adjacent sites is described, with reference to both a computer model and data from healthy subjects. A cross-correlation method is devised for the accurate assessment of propagation velocities. Finally, the form of database currently used for the clinical reporting of routine small bowel motility investigations is described with suggestions for improvements and additions to this database which are planned.

The Irritable Bowel Syndrome (IBS) is one of the most common conditions referred to a gastroenterologist, but there is no consensus of opinion regarding either its aetiology or its treatment. This is partly due to an absence of any physiological marker, and to the variability of presenting symptoms. It has been suggested that it is due to a fibre depleted diet, although this has never been shown. The diets of 187 patients with the IBS and 61 control subjects were investigated using a validated dietary diary method. The patients were subdivided according to presenting complaint. It was found that patients had a lower intake of dietary fibre than controls,and in particular those with diarrhoea had a low intake of fruit fibre. Patients with constipation had a lower food intake. To help in the dietary assessment of patients a computer programme based on a simple prospective dietary questionnaire was written. It proved to be an effective and rapid guide to fibre intakes. Gut transit times were measured using the breath hydrogen technique for mouth to caecum transit times and the continuous marker technique for whole gut transit times. The possible effect of abnormal transit through the gut on food handling was investigated. It was found that patients presenting with diarrhoea had significantly shorter mouth to caecum transit times (with implications for the absorption of food) and that patients with constipation had lengthened transit times, both mouth to caecum and whole gut. Malabsorption of simple sugar solutions leading to gut symptoms was demonstrated both in patients and controls. Finally, 11 patients with food intolerance were investigated, as it has been suggested that food intolerance is a major factor in the aetiology of the IBS. The results suggest that low fibre intakes are probably important in the aetiology of IBS and that, at least in some individuals, carbohydrate malabsorption may also be a significant factor.

M.Tech.

No description available.

No description available.

Vitreous hemorrhages are uncommon in the neonatal period. This article describes a neonatal who had bilateral vitreous hemorrhages after intrauterine bowel infarction.

Abdominal pain is a common symptom of inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). Although the extent differs, visceral inflammation is thought to play a significant role in nociception in these disorders. This thesis describes studies examining mechanisms of inflammation-induced changes in nociceptive signaling from the colon using human colonic biopsy and animal models of the conditions. Citrobacter rodentium infection in mice produced profound colitis at day 10 post-infection which resolved by day 30. Perforated current clamp recordings showed that inflammation induced hyperexcitability of colonic DRG neurons that persisted at day 30 post-infection. Similarly, multi-unit afferent nerve recordings revealed enhanced firing of colonic afferents following colon distension at this time. In voltage clamp studies, suppression of IA K+ currents in post-infected C. rodentium neurons was observed. Combining water-avoidance stress (WAS) and C. rodentium infection exaggerated these effects. Interactions between proteases and stress mediators underlie these actions. In vivo studies revealed WAS combined with C. rodentium post-infection induced visceral hyperalgesia and allodynia. A separate series of studies examined the possible role of cysteine proteases in post-infectious IBS. The cysteine protease cathepsin-s (Cat-S) induced neuronal excitability and, provoked visceral hypersensitivity in mice. Human IBS supernatants increased neuronal excitability, but this was reversed in neurons pre-treated with the cysteine protease inhibitor E-64. Together these data suggest that Cat-S is a secreted neuromodulator in human IBS supernatants and could be important in nociceptive signaling in IBS. In studies examining whether similar mechanisms operate in a traditional inflammatory condition, IBD, human ulcerative colitis (UC) supernatants showed elevated TNF-α levels. Exogenous TNF-α and UC-supernatants increased colonic nociceptor excitability, which was attenuated in neurons from TNFR knock-out animals. TNF-α and UC-supernatants both increased TTX-R Nav1.8 and suppressed IA and IK K+ currents. Together these results suggest that inflammation significantly increases and sustains peripheral nociceptive signaling in IBD and IBS. These effects involve changes in the properties of nociceptive DRG neurons through actions of specific secreted factors which modulate specific voltage-gated ion channels. Chronic stress exaggerates these changes through synergistic actions of stress hormones and local mediators, suggesting an interplay between central and peripheral mechanisms. / Thesis (Ph.D, Physiology) -- Queen's University, 2011-07-28 10:17:58.863

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2007. / Härtill 4 uppsatser.