310 research outputs found

    Volume 29, issue 6

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    The mission of CJS is to contribute to the effective continuing medical education of Canadian surgical specialists, using innovative techniques when feasible, and to provide surgeons with an effective vehicle for the dissemination of observations in the areas of clinical and basic science research. Visit the journal website at http://canjsurg.ca/ for more.https://ir.lib.uwo.ca/cjs/1213/thumbnail.jp

    Observations on the metabolism of cholecystokinin

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    Highly selective vagotomy without a drainage procedure

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    From dyspepsia to Helicobacter: a history of peptic ulcer disease

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    Abstract This thesis is a historical study of peptic ulcer disease from the sixth decade of the eighteenth century until the end of the twentieth. Symptoms of dyspepsia or indigestion have affected more than twenty percent of the British population for most of that period and attracted the involvement of many medical practitioners and others with the provision of health care. Within this group of symptomatic dyspeptic patients were to be found gastric and duodenal ulcers which were capable of causing serious health problems. However the prevalence of stomach and duodenal peptic ulcers has declined markedly during the time course of this thesis and now they are relatively uncommon. Although peptic ulcers may still have a fatal outcome, they now are considered to be curable conditions for the majority of patients who suffer from them in the developed world. This thematic history of gastric and duodenal ulcer examines how medical practitioners worked in a changing climate of novel ideas about disease, often aided or driven by technological developments, from the nineteenth century onwards. It begins with a humoural approach to the understanding of disease, which concentrated upon a patient’s personality, lifestyle choices and circumstances but this was gradually displaced from the end of the eighteenth century by the clinico-anatomical approach, which sought to identify a specific lesion as the ‘seat’ of the disease. In the nineteenth century, the discoveries of pathology, physiology, chemistry and bacteriology became incorporated in clinical medical practice, involving the laboratory in the investigation and treatment of many diseases. In the twentieth century, medical research became rooted in experimentation using scientific technology and engineering to equip investigators with new methods which changed the ways in which diseases were understood and treated. Although there were many innovations in theoretical concepts of disease aetiology and empirical treatments, many were subsequently rejected for reasons of ineffectiveness or possible harm to the patient, sometimes after long periods of use. In its first part, the thesis draws upon publications from 1769 until 1950, mostly in the form of scientific articles and books. In the second part, the oral testimonies of health care professionals involved with the management and treatment of gastric and duodenal ulcers are added. The recorded testimonies of 28 witnesses have been preserved in written form as a supplement to this dissertation. Peptic ulcer disease was initially perceived as a whole-body ailment which was centred on the stomach as its symptomatic location and its treatment was intended to alter humoural imbalance or relieve symptoms. However after post-mortem examinations were increasingly performed from the seventeen-nineties, medical practitioners could see its complications in death and combine their findings with the clinical presentations of what was becoming recognised as a relatively common disorder. In the nineteenth century, physiologists investigated the workings of the stomach using vivisection and chemistry to analyse the stomach contents. The acid produced by the stomach was seen to play a part in ulcer genesis but there was no agreement as to what its precise contribution was for many years thereafter. Bacteriologists who found micro-organisms in the stomach assumed that they were pathogenically involved and subsequent experiments confirmed this. As a result of effective anaesthesia and antisepsis in the last decades of the nineteenth century, surgeons intervened increasingly in life-threatening complications of gastric and duodenal ulcers and their observations changed their perceptions of the diseases. In the twentieth century, opaque meal X-ray techniques began to allow doctors to see lesions inside the living stomach, as did improved endoscopes. In 1952, research suggested that stomach bacteria played no part in causing ulcers and further bacteriological research in the stomach was abandoned. By this time, surgeons had designed operations to reduce stomach acid production which healed most gastric and duodenal ulcers. Good therapeutic results were also achieved using medication and dietetic regimens, but it was recognised that only the surgeon could help patients who had failed to respond to medical treatments. In 1962 it was noted that deaths rates for gastric and duodenal ulcer were falling and fewer people were suffering from them, but they remained a serious cause of morbidity and mortality. A new acid-reducing operation was devised in 1969 that offered the hope that surgery could adequately treat ulcers without causing iatrogenic damage, and in 1976, a new drug was marketed which healed them if continuously taken. Then in 1983 it was asserted that peptic ulcers were caused by a bacterium which was later called Helicobacter pylori. In time and in the face of much opposition, it was shown that if this organism was eradicated in the stomach by medication then gastric ulcers and duodenal ulcers could be cured for the first time. This account of the history of peptic ulcer disease shows how medical practitioners adapted the theoretical basis of their medical practice as its evolved under the influence of scientific or societal changes and later abandoned concepts and therapeutic regimens which no longer were in accord with current thinking. Important issues which have arisen out of the testimonies include: medical involvement with the pharmaceutical industry, how doctors co-operate in the care of patients and how they respond to new theories and equipment and techniques as they became available. The history of peptic ulcer disease over the past two hundred years as described in this thesis follows a broadly similar course to that of other diseases such as tuberculosis, syphilis and chronic renal disease which once dominated the lives of those who suffered from them and have largely become curable in recent years. This thesis is offered as an account of an equally fascinating and complex disease

    Volume 18, issue 4

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    The mission of CJS is to contribute to the effective continuing medical education of Canadian surgical specialists, using innovative techniques when feasible, and to provide surgeons with an effective vehicle for the dissemination of observations in the areas of clinical and basic science research. Visit the journal website at http://canjsurg.ca/ for more.https://ir.lib.uwo.ca/cjs/1134/thumbnail.jp

    Volume 18, issue 5

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    The mission of CJS is to contribute to the effective continuing medical education of Canadian surgical specialists, using innovative techniques when feasible, and to provide surgeons with an effective vehicle for the dissemination of observations in the areas of clinical and basic science research. Visit the journal website at http://canjsurg.ca/ for more.https://ir.lib.uwo.ca/cjs/1135/thumbnail.jp

    Volume 29, issue 4

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    The mission of CJS is to contribute to the effective continuing medical education of Canadian surgical specialists, using innovative techniques when feasible, and to provide surgeons with an effective vehicle for the dissemination of observations in the areas of clinical and basic science research. Visit the journal website at http://canjsurg.ca/ for more.https://ir.lib.uwo.ca/cjs/1211/thumbnail.jp

    Method of biological assay of Gastrin and its application to the study of human tissue

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    The relatively small number of cases in this series, aggravated by the need for further division into subgroups, makes interpretation difficult. The situation is made worse by a number of factors as yet unknown, e.g., the effect of anaesthesia and duration of operation on the gastrin content, the rate of turnover of gastrin and the significance of a single estimate of extractable gastrin -like activity. Any comment on the above results must therefore be speculative.There is now good experimental evidence indicating that vagal excitation stimulates acid gastric secretion by (a), causing release of gastrin, (b), sensitizing the parietal cells to various stimuli including gastrin, and (c), direct stimulation of the parietal cell. If one assumes that, under strong and possibly maximal vagal stimulation by insulin- induced hypoglycaemia direct stimulation of the parietal cells is responsible for a constant proportion of the acid output, then the remainder of the acid secretory response to insulin would be accounted for by the amount of gastrin liberated. Since, however, there is a positive correlation between the insulin- stimulated acid secretion and the total gastrin-like activity in the uncomplicated D.U.'s in this study, it would seem reasonable to assume that, in these cases, the amount of gastrin liberated into circulation is proportional to the total gastrin -like activity extractable from the stomach. This is assumed to be true also for D.U.'s with stenosis.Hunt & Kay (1954) have suggested that the increase in parietal cell mass in D.U.'s with stenosis was a result of repeated distension of the stomach with consequent stimulation of the parietal cells. The data presented in Fig. 15 and 16 is compatible with this view. The cases with stenosis had more gastrin in the antral mucosa (and hence probably in the circulation) than the uncomplicated cases. The observation that cases with mild as well as severe stenosis had similar total gastrin -like activity could be explained by the possibility of operative intervention at different phases of progression of the disease, it being assumed that a considerable time lag exists between the increase in gastrin content (and production) and the associated growth in the parietal cell mass.The results in Fig. 16 indicate that the insulin -stimulated secretion per secretory unit, represented by the ratio 'insulin- secretion test/ maximal histamine output', remained about the same despite increase in the total gastrin -like activity beyond a point at about the equivalent of 100 pg of the Standard. This might represent a plateau response to maximal or supramaximal levels of circulating gastrin.The possible role of gastrin in the aetiology of duodenal ulceration has been suggested by Gillespie & Kay (1961) who showed that antrectomy alone led to healing of the duodenal ulcer in four patients. The Zollinger -Ellison syndrome provides an extreme example of possible effects of excessive gastrin (or gastrin -like substance) in circulation. The idea of gastrin possibly playing a role as a trophic hormone to the parietal cells has been summarized by Card (1962), who cited in support a case of Zollinger -Ellison syndrome of Dr. Bryan Alton when the 'maximal histamine output' of the patient progressively fell after partial resection of the pancreas and left adrenalectomy without any surgery on the stomach. The failure to demonstrate a correlation between the 'maximal histamine output' and gastrin -like activity in this present study does not support this idea but certainly does not exclude it, since apart from all the unknown factors mentioned above, this series could well have included cases with a large parietal cell mass to start with, irrespective of the gastrin content in the antrum.The whole problem of the clinical significance of gastrin is obviously a dynamic one, a better approach to which would probably be the assay of gastrin in blood or urine, methods for which remain to be devised
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