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Titlebook: Malabsorption in Coeliac Sprue; O. J. J. Cluysenaer,J. H. M. Tongeren Book 1977 Martinus Nijhoff, P.O. Box 442, The Hague, The Netherlands

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發(fā)表于 2025-3-21 19:34:13 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書(shū)目名稱(chēng)Malabsorption in Coeliac Sprue
編輯O. J. J. Cluysenaer,J. H. M. Tongeren
視頻videohttp://file.papertrans.cn/622/621868/621868.mp4
圖書(shū)封面Titlebook: Malabsorption in Coeliac Sprue;  O. J. J. Cluysenaer,J. H. M. Tongeren Book 1977 Martinus Nijhoff, P.O. Box 442, The Hague, The Netherlands
描述For at least three centuries, Holland has been at the centre of research on intestinal malabsorption. In the 17th and 18th centuries, early descriptions of coeliac disease and tropical sprue were published by physicians trained in Holland, and it was in 1950 that Dicke published his painstaking and vital observations that coeliac disease in children was caused by the inges- tion of wheat flour. Subsequent careful work with van de Kamer and Weijers showed that the harmful agent was gluten. Since these discoveries were made, research in intestinal malabsorption, particularly in the adult, has continued in several centres in Holland. At Nijmegen, for example, dr. Cluysenaer, dr. van Tongeren and their as- sociates have been involved in long-term studies of patients with intestinal disease for the past fifteen years. In this book they describe their experience of the investigation and treatment of fifty patients with the adult form of coeliac disease. Their monograph gives an account of the history, definition and incidence of the disorder, and then goes on to undertake a critical review of the pathogenesis of the coeliac lesion. Before embarking on the different patterns of malabsorpt
出版日期Book 1977
關(guān)鍵詞anatomy; bacteria; biopsy; blood; bone; fat; gastrointestinal tract; hormone; hormones; nervous system; pathog
版次1
doihttps://doi.org/10.1007/978-94-010-1093-1
isbn_softcover978-90-247-2000-2
isbn_ebook978-94-010-1093-1
copyrightMartinus Nijhoff, P.O. Box 442, The Hague, The Netherlands 1977
The information of publication is updating

書(shū)目名稱(chēng)Malabsorption in Coeliac Sprue影響因子(影響力)




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發(fā)表于 2025-3-21 22:19:12 | 只看該作者
Pathogenesis of Coeliac Sprue,enesis at the present time. On the other hand it cannot be denied that particularly in the past 25 years — unmistakable advances have been made in this respect. An important event in this context was the discovery that the presence in the diet of a protein fraction from certain cereals caused the sy
板凳
發(fā)表于 2025-3-22 02:10:09 | 只看該作者
Morphology of the Small Intestine Under Normal Conditions and in Coeliac Sprue,hand, the function of the small intestine is determined by its structure, and on the other hand the structure of the small intestine seems to be subservient to the function which this organ is expected to fulfil. This interdependence prevails in normal circumstances as well as in diseases. For a bet
地板
發(fā)表于 2025-3-22 06:05:18 | 只看該作者
Physiology of the Small Intestine,s the starch in the food. After passing through the oesophagus the food bolus enters the stomach, where it is further kneaded by vigorous contractions of the gastric wall and mixed with gastric juice, which contains pepsinogens and hydrochloric acid. The secretion of gastric juice is regulated by ne
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Pathophysiology of Coeliac Sprue,tention has so far been paid to possible changes of the physiological processes in the small intestine in patients with coeliac sprue. There are indeed some indications that these processes take an abnormal course. This is quite conceivable, because the inflammatory lesions in the intestinal wall do
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發(fā)表于 2025-3-22 17:24:16 | 只看該作者
Malabsorption in Coeliac Sprue,reference to distinct clinical symptoms of malabsorption (305, 385). The fact that this malabsorption can induce deficiencies of various nutrients, has been demonstrated by clinical surveys in the last 10–20 years. In most of these studies malabsorption was only broadly investigated, and but a few p
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發(fā)表于 2025-3-23 00:46:41 | 只看該作者
Clinical Features,861). The nature and severity of this malabsorption are largely determined by the extent of the intestinal lesions or, rather, by the capacity of the remaining unaffected intestine (647, 732, 817). Nevertheless, differences exist among individuals so that, given an apparently identical pathological
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