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Ulcer, experimental peptic

Prophylactic and therapeutic administration of Enterosgel to rats with experimental peptic ulcer and ulcerative colitis, significantly decreased the number and surface area of lesions on gastro-intestinal tract (GIT) mucosa and reduced the severity of the syndrome of endogenous intoxication that accompanied these injuries [21, 22]. The first evidence of clinical use of Enterosgel in combined therapy of peptic gastric ulcer and duodenum was reported by S.M. Tkach, who had noted that enterosorp-tion significantly reduced the number of side effects of treatment, and the rate of Helicobacter eradication increased from 83.3 to 93.3% [23]. [Pg.207]

Tani, S., A. Ishikawa, H. Yamazaki, and Y. Kudo. 1987. Serum pepsinogen levels in normal and experimental peptic ulcer rats measured by radioimmunoassay. Chemical and Pharmaceutical Bulletin (Tokyo) 35 1515-1522. [Pg.113]

Frank Mann and Experimental Peptic Ulceration, 153 Preventing Mann-Williamson Ulcers Urogastrone, 155 Charlie Code s Apprenticeship with Histamine, 157 Charlie Code s Apprenticeship as a Gastroenterologist, 159... [Pg.426]

Although these findings may apply to an experimental cortisone ulcer in animals, Hitzelberg in our laboratory obtained less definite results in man (H22, H23). Fifteen arthritic patients received 1 g prednisolone in 6 weeks. In the course of treatment, there was never an indication of peptic ulcer formation, although the output and concentration of pepsin in the basal secretion increased on the average about 2-fold. Paper electrophoresis of the dialyzed and lyophilized gastric juice, following steroid administration, frequently showed decrease of total carbohydrate... [Pg.268]

Secondly, a possible beneficial role of COX-2 on the stomach should also be taken into account. In mice, COX-2 is expressed at the borders of gastric ulcers and has been implicated as a critical factor in promoting repair (11). Whether these experimental data have any clinical relevance is unknown, but this issue raises the possibility that individuals with pre-existing peptic ulcers who take COX-2 selective drugs may be at risk of delayed ulcer healing and potential complications. This issue may be of particular concern in patients with ulcers due to Helicobacter pylori infection. [Pg.1007]

In summary, NSAIDs and H. pylori can cause adverse effects on gastroduodenal mucosal protective mechanisms in different ways, and so the interaction between these two susceptibility factors might allow damage to occur more readily when NSAIDs are taken in the presence of H. pylori infection. However, despite this experimental evidence, the interaction between H. pylori infection and use of NSAIDs in the pathogenesis of peptic ulcers and their complications is still unclear from clinical studies. [Pg.2562]

In 2005, J. Robin Warren and Barry J. Marshall shared the Nobel Prize in Medicine for discovery of the bacterium Helicobacter pylori, and for establishing experimental proof that it plays a major role in gastritis and peptic ulcer disease. The story began when Warren, a pathologist, noticed that bacilli were associated with the tissues taken from patients suffering from ulcers. Look up the history of this case and describe Warren s first hypothesis. What sorts of evidence did it take to create a credible theory based on it ... [Pg.39]

Code concluded that the experiments incriminated gastric juice as the factor in the production of peptic ulcer, but only later did he realize that he had produced the experimental equivalent of the Zollinger-Ellison syndrome. Frank Mann was pleased by the results, for up to that time he had not been able to produce experimental ulcers in the duodenum as the result of action of the animal s own gastric juice. [Pg.160]

Mann FC, Williamson CS. The experimental production of peptic ulcer. Ann Siirg 77 409-422, 1923. [Pg.371]

Mann FC, Bollman JL. Experimentally produced peptic ulcer. JAMA 99 1576-1582, 1932 idem. [Introduction to] A Symposium concerning duodenal factors in the neutralization of acid. Am J Dig Dis 2 284-285, 1935. [Pg.371]

Sandweiss (n. 494). The occurrence of fibroblastic proliferation was stated in all early papers but in particular in Beaver DC, Sandweiss DJ, Saltzmann HC, et al. The effect of urine extracts on the prevention and healing of experimental ulcers in dogs. Am J Clin Pathol 12 617-629, 1940. See also Sandweiss DJ, Sugarman MH, Friedman MHF, et al. The effect of urine extracts on peptic ulcer. Am J Dig Dis 8 371-382, 1941. [Pg.371]

Code CF. The role of gastric juice in experimental production of peptic ulcer. Surg Clin North Arniy.mx-xm, 1943. [Pg.373]

Subsequently, Frank Mann of the AAayo Clinic noted that the neostomal ulcers resulting from gastrojejunostomy reflected a critical relevance of the anatomic and physiologic location of the lesion. He devised the Mann-Williamson experimental operation, which was used for the next 30 years as the basic test for a new procedure to prevent or cure a peptic ulcer. [Pg.55]

The initial report of Williamson and Mann detailing the technique of the experimental preparation they had devised to generate peptic ulcer disease (top). The subsequent widespread usage of the Mann-Williamson nxidel provided the experimental surgical basis for the evaluation of the role of acid in the genesis of ulcer disease (bottom). [Pg.55]

Coffee causes peptic ulcers —The possible relationship between caffeine and peptic ulcers has long been debated. Stimulation of gastric secretion by caffeine has been shown in several experimental animals and with human subjects in single dose experiments. [Pg.219]


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See also in sourсe #XX -- [ Pg.241 ]




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Peptic ulceration experimental production

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