Preliminary Pages |
| Acknowledgements |
| Abbreviations |
| Preface, philosophical observations on research and introductory comments |
| |
I. P. Semmelweiss |
| |
G. J. Mendel |
| |
W.S.Gosset |
| Figure 1 – 5. |
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Chapter 1. Helicobacter pylori and antigen presentation |
| 1.1 |
Can intestinal epithelial cells act as antigen presenting cells? |
| 1.2 |
Do gastric epithelial cells present antigen? |
| 1.3 |
Why do CD4 lymphocytes enter the gastric epithelium at sites of Helicobacter pylori infection? |
| 1.4 |
Can antigenic peptides influence the gastric epithelial cells in any other way? |
| 1.5 |
What causes changes to the tight junctions resulting in them becoming "leaky"? |
| 1.6 |
Lymphocyte nomenclature |
| 1.7 |
What happens to the gastric mucosal lymphocyte population in Helicobacter pylori infection? |
| 1.8 |
Are there any factors which would assist CD4 lymphocyte migration? |
| 1.9 |
Intracellular pathways in the mucus secreting epithelial cells of the pit region of the gastric glands in the body of the stomach. |
| Figure 6 – 39. |
| |
Chapter 2. Polymorphonuclear leucocytes and the stomach |
| 2.1 |
The migration of polymorphonuclear leucocytes in the stomach |
| 2.2 |
What causes polymorphonuclear leucocytes to migrate? |
| 2.3 |
What is the source of IL-8? |
| 2.4 |
What is the effect of Helicobacter pylori on IL-8 expression? |
| 2.5 |
What cell signalling proteins are implicated in the upregulation of IL-8? |
| 2.6 |
Chief cells and IL-8. |
| 2.7 |
Is the extent of the acute inflammatory response related to the magnitude of the Helicobacter pylori infection? |
| 2.8 |
What are the consequences of this polymorphonuclear leucocyte infiltration for the Helicobacter pylori? |
| 2.9 |
Does healing of benign peptic ulceration have an effect on the Helicobacter pylori colonisation of the stomach and the polymorphonuclear leucocyte epithelial infiltration? |
| Figure 40 – 64. |
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Chapter 3. Eosinophils and the stomach |
| 3.1 |
What causes the activation of eosinophils? |
| 3.2 |
What factors are responsible for the increase in gastric eosinophils associated with Helicobacter pylori infection? |
| |
3.2.2 |
Eotaxin. |
| 3.3 |
What are the sources of eotaxin? |
| |
3.3.1 |
Epithelial cells. |
| |
3.3.2 |
Endothelial cells. |
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3.3.3 |
Connective tissue cells. |
| 3.4 |
Are cytokines involved in eotaxin activation? |
| |
3.4.1 |
Interleukin 4. |
| |
3.4.2 |
Interleukin 5. |
| |
3.4.3 |
Tumour necrosis factor a. |
| 3.5 |
Conclusion. |
| Figure 65 – 91. |
| |
Chapter 4. Mast cells and the stomach |
| 4.1 |
What mast cell changes are associated with Helicobacter pylori infection? |
| 4.2 |
What roles do mast cells perform? |
| 4.3 |
Are any of the gastric enterochromaffin-like(ECL) cells a subpopulation of mast cells? |
| Figure 92 – 105. |
| |
Chapter 5. Secretory function and the stomach |
| 5.1 |
How are the stimuli received at the mucosal surface? |
| 5.2 |
Afferent input. |
| 5.3 |
Efferent response. |
| 5.4 |
Acid secretion. |
| 5.5 |
How is acid secretion regulated? |
| 5.6 |
What is the effect of substance P on gastric acid secretion? |
| 5.7 |
What effect does chronic Helicobacter pylori infection have on gastric acid secretion? |
| 5.8 |
What is the effect of a vagotomy on Helicobacter pylori infection of the stomach? |
| 5.9 |
Pepsinogen secretion. |
| 5.10 |
What is the gastric distribution of pepsinogen 11 and its relationship to parietal cells? |
| 5.11 |
Do chief cells contain any cytokines? |
| 5.12 |
What are the effects of neuropeptides on chief cells and other epithelial cells? |
| 5.13 |
How can the observations on the effects of toxin A be explained? |
| 5.14 |
Can substance P and NK1 receptors effect the functioning of epithelial cells? |
| 5.15 |
What is the source of the substance P that could interact with the connective tissue NK1 receptors causing cell signalling? |
| 5.16 |
What happens to continually produced chief cells? |
| 5.17 |
What is the mechanism responsible for inducing the shedding of these cells undergoing necrosis? |
| 5.18 |
Does apoptosis have a role in the shedding of chief cells and parietal cells? |
| 5.19 |
Are any of these types of lymphocytes responsible for the epithelial cell changes associated with the shedding of chief cells and parietal cells? |
| 5.20 |
Are any of these processes occurring in vivo in the gastric mucosa? |
| 5.21 |
Why are necrotic chief cells and necrotic parietal cells shed in this manner? |
| 5.22 |
How are the shed cells expelled from the gastric gland lumen? |
| 5.23 |
Interleukin 4 (IL-4) as a cell signalling mechanism. |
| |
5.23.1 |
Interleukin 4. |
| |
5.23.2 |
Signal transducer and activator of transcription 6. |
| |
5.23.3 |
Functions of interleukin 4. |
| Figure 106 – 139. |
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Chapter 6. Some cell signalling molecules affecting apoptosis |
| 6.1 |
Fas. |
| |
6.1.1 |
Why are there Fas receptors on Helicobacter pylori? |
| |
6.1.2 |
Could the presence of bacterial TNFα receptors be protective? |
| 6.2 |
Bcl-2. |
| 6.3 |
Bax. |
| Figure 140 – 152. |
| |
Chapter 7. Acid / base changes in the stomach |
| 7.1 |
What is the source of the hydrogen ions in the gastric juice? |
| 7.2 |
Water. |
| 7.3 |
Carbonic anhydrase. |
| 7.4 |
Carbon dioxide. What is the source of the carbon dioxide in the reaction catalysed by carbonic anhydrase? |
| 7.5 |
Arginine. |
| 7.6 |
Agmatine. |
| |
7.6.1 |
Is the cellular metabolism of arginine the only source of tissue agmatine? |
| 7.7 |
What happens to the agmatine produced in the parietal cell canaliculi? |
| 7.8 |
Some of the arginine containing molecules in the stomach apart from those proteins directly associated with nucleic acids? |
| 7.9 |
What about the bicarbonate ion and secretion? |
| Figure 153 – 169. |
| |
| References |
| Index |
| Appendix A |
| Appendix B |
| Appendix C |
| Appendix D |
| Notes |
| |
