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Tesis sobre el tema "Duodecim"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 14 de febrero de 2022

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1

Hedkvist, Daniel. "Medicin på finska : Det medicinska ordförrådets utveckling i finskan i slutet av 1800-talet". Thesis, Umeå universitet, Institutionen för språkstudier, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-91516.

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In the beginning of the 19th century, Swedish was the only official language of Finland, and thus the dominating language in administration and higher education. However, during the latter part of the century, efforts were made to develop Finnish into a language which could be used in every part of society. In 1881, the medical society Suomalainen Lääkäriseura Duodecim was founded with the development of a medical terminology in Finnish as one of its main purposes. In 1885, a medical paper, Duodecim, and a medical dictionary were published. The aim of this study is to illuminate the vocabulary of the dictionary. The articles published in Duodecim about the dictionary during the same time are used to get to know the context into which the dictionary was published. In this study, the medical dictionary published in 1885, Duodecim’in Sanaluettelo Suomen lääkäreille, and relevant articles in Duodecim are examined. Relevant articles are read and summarized. From the dictionary, relevant words are selected. The method is qualitative and grounded theory is used. The discussion in Duodecim is mainly, except for some discussion about minor linguistic errors, about what vocabulary is to be used for such a basic phenomenon as respiration. In the dictionary, the most striking trait is the presence of Finnish translations of almost every anatomic term in Latin mentioned. A fear of loan-words is observed. This has also been seen by other authors. Other words are translated directly from Swedish. Some translations are more like explanations than translations.

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2

Chiffre, Pierre-Alain. "Le style historique dans les biographies de Suétone". Paris 4, 2000. http://www.theses.fr/2000PA040119.

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Trop souvent considéré comme un écrivain mineur et sans grand intérêt, Suétone est resté longtemps porteur d'une image très négative. Son style notamment, décrié chez de nombreux commentateurs pour sa fadeur et son manque de relief, semblait ne pas présenter d'originalité véritable. Il recèle pourtant des qualités réelles qui le rapprochent tout particulièrement du style historique, le modeste biographe qu'est apparemment Suétone révélant en fait une vraie capacité à mettre en oeuvre toute une série de techniques d'écriture fréquemment employées chez les historiens latins. C'est donc un style beaucoup plus élaboré qu'on ne pourrait le croire au premier abord qui ressort des vies des douze césars, le lexique et la phrase apparaissant notamment comme deux domaines ou Suétone a su exercer son talent, manifester son originalité et témoigner d'une réelle maitrise dans les procédés employés. C'est pourquoi en se rapprochant dans bien des cas du style historique, Suétone, dans son désir de donner a son écriture une qualité littéraire a part entière, contraint le lecteur à considérer les vies des douze Césars sous un jour nouveau.

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3

Rogier, Michel. "Les cancers du duodenum". Montpellier 1, 1990. http://www.theses.fr/1990MON11161.

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4

Mulholland, Gary. "Pig Duodenum Derivative : biological properties". Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335588.

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5

Cheng, Wei. "Development of duodenum and duodenal atresia". Click to view the E-thesis via HKUTO, 2000. http://sunzi.lib.hku.hk/hkuto/record/B31979646.

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6

Cheng, Wei y 鄭偉. "Development of duodenum and duodenal atresia". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31979646.

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7

Smith, Julie A. "Adenylate cyclase in the human duodenum". Thesis, Nottingham Trent University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304059.

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8

Eriksen, Craig Alexander. "Duodenal pH : new aspects of physiology and pathophysiology". Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27222.

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The pathogenesis of duodenal ulcer is believed to centre around the presence of gastric acid, yet the exact role that acid plays is poorly understood. Previous investigations of the duodenal pH have been restricted by methodological and technical difficulties, and have, for the most part, only monitored the pH in the short-term. A new reliable system for long-term (twenty-four hour), ambulatory, simultaneous measurement of intra-luminal antral and duodenal bulb pH has been developed. The system comprises two glass pH electrodes, a small portable recording unit and a computer-based system for data storage and analyses. Validation of this pH monitoring system was first performed, and the 24-hour ambulatory profiles of antral and duodenal pH of normal healthy subjects were subsequently recorded. Periods of cephalic stimulation and ingestion of a solid meal were included during the study period. Having established the normal profiles, the investigation was repeated in patients with active duodenal ulcer, off-treatment. The gastric pH profile was similar of both study groups. There were no significant differences between the fasting duodenal bulb pH and the total 24-hour duodenal acid exposure of the ulcer patients and healthy subjects. Acid peak analysis demonstrated that the duodenal ulcer patients exhibited a defect in the propulsive duodenal bulb motility. Gastric stimulation caused a similar pattern of duodenal acidification in the two groups. These results suggest that gastric acid is not of primary pathophysiological importance in duodenal ulcer disease. The effects of cephalic stimulation and a meal on plasma gastrin, secretin and somatostatin and duodenal pH were examined in healthy subjects and duodenal ulcer patients. The results showed: vagally-released gastrin is not a significant contributor to stimulation of gastric acid secretion in either health or duodenal ulcer disease; duodenal ulcer patients have excessive basal and post-stimulation plasma gastrin levels but a subset of ulcer patients exists, the "Hypergastrinaemic" patients, who exhibit exaggerated gastrin responses, vagal hyperactivity, a defective somatostatin-induced inhibition of gastrin release and a defect in the "switch-off" mechanism of gastric acid secretion. In addition, the physiological role of secretin in inhibiting gastrin release in Man is questionable. This study reveals new aspects in the physiology and pathophysiology of the duodenal bulb pH.

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9

COURT, JEAN-YVES. "Hematome intra-mural du duodenum d'origine pancreatique". Amiens, 1992. http://www.theses.fr/1992AMIEM047.

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10

DARRIEUTORT, NICOLE. "A propos d'un melanome malin primitif du duodenum". Toulouse 3, 1989. http://www.theses.fr/1989TOU31032.

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11

Lam, Chi-ming. "The standard of pancreatoduodenectomy in Hong Kong". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B4189716X.

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12

CONSOLINI, TURQUIN-TRAORE NICOLE. "Une cause rare de stenose duodenale chez l'adulte : les diaphragmes duodenaux congenitaux : a propos de deux cas et revue de la litterature". Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20220.

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13

Huck, Patricia Marie Liliane. "Place des anastomoses cholédoco-duodénales dans le traitement des affections bilio-pancréatiques non cancéreuses : à propos de 182 cas". Université Louis Pasteur (Strasbourg) (1971-2008), 1990. http://www.theses.fr/1990STR1M087.

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14

KONDO, TATSUHEI, HIROSHI TAKAGI y TAKESHI MORIMOTO. "Canine Pancreatic Allotransplantation with Duodenum (Pancreaticoduodenal Transplantation) Using Cyclosporin A". Nagoya University School of Medicine, 1985. http://hdl.handle.net/2237/17478.

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15

Demenis, Claire. "Cellular expression and function of CCK in the mouse duodenum". Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/cellular-expression-and-function-of-cck-in-the-mouse-duodenum(171573ca-8a23-459f-8233-b48da346016b).html.

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Enteroendocrine cells (EECs) express key gastrointestinal (GI) hormones including cholecystokinin (CCK), gastric inhibitory peptide (GIP), peptide tyrosine tyrosine(PYY), glucagon‐like peptide‐1 (GLP‐1) and ghrelin. EECs are characterised to contain the hormones derived from one precursor protein. Of these, CCK‐cells are typically concentrated in the proximal small intestine and release CCK upon stimulation by nutrient ligands and in so doing signal to multiple tissues to co‐ordinate and optimise digestive, absorptive functions, and instil hunger or satiety. The aims of this study were to establish whether EECs co‐expressed CCK alongside other key GI peptides and to determine a paracrine role for CCK to increase FA uptake in intestinal cells. These studies utilised an eGFP‐CCK transgenic mouse model. Tissue sections frome GFP‐CCK mice were paraffin embedded and immunostained against an array of targets. Firstly, an anti‐GFP antiserum was employed to visualise eGFP‐cells along the GI tract, and duodenal sections were dual stained for anti‐GFP and an anti‐proCCK antiserum to confirm eGFP‐cells represented CCK‐cells. A series of dual immunostaining experiments ensued to probe duodenal eGFP‐cells for a range of different hormonal targets and demonstrated that a significant number of eGFP‐CCK cells contained GIP (37%), PYY (45%), proglucagon (14%) and ghrelin (50%). Further dual‐staining experiments were carried out to stain for CCK alongside PYY, GIP or ghrelin and enabled analysis of the intracellular localisation of co‐expressing peptides, which indicated that these peptides were packaged in the same and also with indistinctly separate vesicles. These data demonstrate CCK‐cells can co‐express more than one peptide and analysis of intracellular labelling indicates they may have the ability to co‐release CCK alongside other peptides. To investigate a potential paracrine‐signalling pathway for CCK a FA uptake assay was performed using a fluorescent C12‐fatty acid (FA) analogue (Bodipy‐FA) that was analysed using fluorescent activated cell sorting (FACS). Single small intestinal cells of eGFP‐CCK mice were prepared using an EDTA chemical/mechanical dissociation method. Cell samples were either non‐treated (control) or pre‐treated with a targeted compound prior to incubation with Bodipy‐FA. Treatment of cells witholeoylethanolamide, glucagon‐like peptide‐2 (GLP‐2) or CCK increased FA uptake 2 to3‐fold and this increase was demonstrated to be carrier‐mediated. Experiments ensued employing CCK‐cell ligands to implicate activity of CCK‐cells in this process. Bombesin and L‐amino acids induced a dynamic increase in FA uptake comparable to that achieved by pre‐treatment with CCK. However, implementation of the protocol using cells from a CCK KO model achieved replicate data and therefore demonstrated these effects were not exclusive to CCK‐cells. In conclusion, data presented in this thesis establish that a spectrum of key gut hormones is expressed in individual EECs. Furthermore, a paracrine action of CCK signalling is implicated to increase the absorptive ability of neighbouring enterocytes. These data suggest that CCK‐cells have the ability to integrate nutrient signals and secrete a cocktail of hormones in response. These findings imply an increased complexity to the enteroendocrine system whereby GI peptides may work together to potentiate a desired response without requirement of signals from higher centres.

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16

An, Rong. "Pancreatic duodenum homeobox 1 (PDX-1) phosphorylation in pancreatic β-cells". Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5270.

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Pancreatic Duodenum Homeobox (PDX-1) is a homeodomain transcription factor and a key regulator of β-cell development and differentiation. In mice and humans, mutations of the Pdx1 gene in β-cells have been linked to MODY and type 2 diabetes. Therefore, the regulation of PDX-1 transcriptional activity is very important. Phosphorylation is known to be a pivotal regulatory mechanism for several transcription factors. Therefore in this study, I focused on the regulation of phosphorylation on PDX-1 in intact β-cells and investigated the potential signalling pathways involved in its regulation. Firstly I showed that PDX-1 is phosphorylated under physiological conditions in pancreatic β-cell line. Additionally, recombinant PDX-1 is efficiently phosphorylated in vitro at Thr- 152 in the homeodomain by the nutrient-regulated protein kinase, PASK. To explore the physiological relevance of this site I made dephospho- (T152A) and phosphomimetic (T152E) mutants of PDX-1. In INSrαβ cells, a less differentiated cell line derived from INS-1 cells, wild-type PDX-1 and PDX-1T152A were partially redistributed from the cytosol to the nucleus in response to elevated glucose concentrations (20 vs 3 mM). By contrast, PDX-1T152D and PDX-1T152E displayed enhanced nuclear immunoreactivity at low glucose concentrations, and underwent nuclear export as glucose concentrations were raised. PDX- 1 binding to an oligonucleotide based on the consensus A3 binding site of the preproinsulin gene promoter was completely abolished by mutation of Thr-152 to an acidic amino acid. Furthermore, the PDX-1 phosphomimetic mutants failed to suppress preproglucagon gene expression in INSrαβ cells, an action fully preserved in the T152A mutant. However, metabolic labelling of INS-1(832/13) cells with 32Pi, as well as mass spectroscopic analysis, and the use of a phospho Thr-152-specific antibody, failed to reveal any clear evidence for phosphorylation at this site under a variety of in vivo conditions, including in cells overexpressing PASK. Thus, Thr-152 is not a major site of phosphorylation of PDX-1 in intact β-cells. However, a novel phosphorylation site, Ser-269, at the C-terminus of PDX-1 was identified by mass spectrometry. To explore the potential upstream regulatory kinase and the signalling pathway involved, I generated dephospho-(S269A) and phosphomimetic (S269E) mutant PDX-1 and a phospho-Ser-269-specific antibody. Candidate kinases were also identified using recombinant wild-type and mutant PDX-1 in in vitro phosphorylation experiments. In this thesis I demonstrate that PDX-1 is phosphorylated under physiological conditions in β-cell lines. I have shown that Thr152 is not a major phosphorylation site of PDX-1 in intact cells and we also defined the novel in vivo phosphorylation site of PDX-1. Moreover, we reported that PDX-1 is phosphorylated in vitro by a number of kinases including Aurora, Rsk1, PKCa, JNK. The work presented in the thesis provides evidence that PDX-1 phosphorylation is important in its role as a transcription regulator in mature β-cells; moreover, it suggests several physiological signalling networks to investigate.

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17

Chu, Kent-man. "Helicobacter pylori infection and gastroduodenal ulcer disease". Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23636555.

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18

PEROT, EMMANUEL. "Les tumeurs malignes de l'angle duodeno-jejunal : a propos de 4 cas". Lyon 1, 1992. http://www.theses.fr/1992LYO1M056.

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19

Simon, Jean-Claude. "Tumeurs endocrines duodeno-pancreatiques non fonctionnelles : a propos de 20 cas cliniques de 1980 a 1990". Lyon 1, 1992. http://www.theses.fr/1992LYO1M007.

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20

MARTINOD, JOCELYNE. "Les atresies et stenoses congenitales intrinseques du duodenum : a propos de 36 observations". Lyon 1, 1990. http://www.theses.fr/1990LYO1M107.

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21

BACHELIER, PIERRICK. "A propos d'un cas de syndrome de willebrand acquis associe a des angiodysplasies duodenales". Angers, 1988. http://www.theses.fr/1988ANGE1111.

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22

Lemaitre, Jean-François. "Adenocarcinome de l'angle duodeno-jejunal : a propos de 3 cas". Lille 2, 1988. http://www.theses.fr/1988LIL2M060.

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23

GARNIER, LUC. "Fistules pyelo-duodenales : observation personnelle ; revue de la litterature". Amiens, 1988. http://www.theses.fr/1988AMIEM037.

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24

PLANCQ, DEBURGHGRAEVE MARIE-CHRISTINE. "Les traumatismes duodeno-pancreatiques fermes chez l'enfant". Amiens, 1991. http://www.theses.fr/1991AMIEM111.

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25

Wong, Chun-yu Benjamin. "Helicobacter pylori : related diseases in the Chinese /". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22226977.

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26

Joo, Nam Soo. "Regulation of duodenal ion transport by uroguanylin and cloning of murine intestinal CIC-2 chloride channel". free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9924893.

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27

VINOGRAD, ALAIN. "Hemorragie digestive revelatrice d'une tumeur carcinoide du duodenum : a propos d'un cas". Reims, 1990. http://www.theses.fr/1990REIMM118.

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28

Sjöblom, Markus. "The duodenal mucosal bicarbonate secretion : role of melatonin in neurohumoral control and cellular signaling /". Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. {[distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3521.

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29

朱建民 y Kent-man Chu. "Helicobacter pylori infection and gastroduodenal ulcer disease". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B23685426.

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30

Bailbe, François. "Tumeurs villeuses du deuxième duodénum". Montpellier 1, 1990. http://www.theses.fr/1990MON11253.

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31

JAIS, FRANCK. "Dystrophie kystique sur pancreas aberrant de la paroi duodenale : a propos d'un cas". Nantes, 1992. http://www.theses.fr/1992NANT062M.

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32

Malfatti, Bruno. "Adénome villeux isolé du duodénum : à propos d'un cas". Bordeaux 2, 1999. http://www.theses.fr/1999BOR2M050.

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33

Claassen, Claudia. "Untersuchung über die Expression von Kalzium-Transportproteinen in kaninem Duodenum, Niere und Pankreas". Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-134785.

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34

Spiegel, Stefanie. "Untersuchungen zum Mechanismus und zur Regulation der intestinalen Anionensekretion im Duodenum des Kaninchens". [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968548776.

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35

Numrich, Joanne L. "Predicting CLA production in the rumen/duodenum by the use of mathematical models /". Available to subscribers only, 2005. http://proquest.umi.com/pqdweb?did=1075690481&sid=7&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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36

Dusfour, Bernard. "Les contusions du duodénum : un retard diagnostique, ses conséquences". Montpellier 1, 1990. http://www.theses.fr/1990MON11145.

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37

Laurent, Sophie. "Metastases gastroduodenales multiples d'un melanome malin cutane : a propos d'une observation". Besançon, 1993. http://www.theses.fr/1993BESA3054.

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38

Roman, Olivier. "A propos d'un cas de fistule paraprothetique aortique a expression uniquement septicemique". Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20372.

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39

TREDANIEL, CLAUDE. "Le choledochocele : a propos d'un cas et revue de la litterature". Nantes, 1988. http://www.theses.fr/1988NANT070M.

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40

Guérin, Cécile. "Enteropathie hypogammaglubinemique et pseudo-tumeur inflammatoire duodenale dans le cadre d'une sarcoidose". Lille 2, 1992. http://www.theses.fr/1992LIL2M135.

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41

Simpson, Janet Elizabeth. "The cystic fibrosis transmembrane conductance regulator and acid-base transporters of the murine duodenum". Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4391.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2006.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "August 2006" Includes bibliographical references.

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42

Gama, Carolina. "Investigation of splanchnic perfusion utilising an intraluminal opto-electronic sensor placed in the duodenum". Thesis, City University London, 2015. http://openaccess.city.ac.uk/14801/.

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The splanchnic region (abdominal gastrointestinal organs) is sometimes known as the “canary of the body” for its susceptibility to develop hypoxia at an earlier stage, analogue to the old times practice in coal mining. When the neuroendocrine response is activated, it exhibits regulation of blood flow and extraction of oxygen, facilitating redistribution of blood to vital organs. This can ultimately lead to systemic inflammatory response and multiple organ failure. The vital need to monitor the perfusion of the splanchnic region in critically ill patients has not yet been met by existing techniques. The goal of this research was to evaluate the feasibility of using the technique of photoplethysmography intraluminally in the duodenum in order to measure the haemodynamic changes occurring in the splanchnic circulation in a minimally invasive fashion. A bespoke processing system and data acquisition virtual instrument were designed and developed to allow continuous and simultaneous monitoring of two probes: an existing miniaturised PPG probe intended for intraluminal use and optically- identical finger PPG probe. Nine anaesthetised patients undergoing elective open laparotomy surgery were recruited and consented for the clinical trial at The Royal London Hospital. Due to the great proximity to the surgical site, monitoring of duodenal pulse oximetry signals could not be done in a continuous way. Also, the presence of moderate respiratory modulation in otherwise good quality, high amplitude signals seemed to result in an underestimation of arterial blood saturation of 2%. A frequency domain algorithm was thus applied to the data with results in agreement with both the finger PPG probe and commercial pulse oximeter. Blood oxygen saturation estimation at respiratory frequency yielded values within the physiological range expected for venous blood. For three of the patients, PPG signals were also acquired from the stomach, with results showing a similar pattern to the ones obtained from the duodenum. During the clinical trials, two patients experienced hypotension. PPG signals obtained before, during and after showed a great decrease in estimated blood oxygen saturations, which remained low even when monitored haemodynamical variables were back to normal values. Finger PPG probe estimations and commercial pulse oximetry values did not demonstrate this change. This suggests the possibility of photoplethysmography identifying changes in tissue oxygenation and blood volume in the splanchnic circulation resulting from external and/or internal regulatory mechanisms. This clinical trial thus show the great promise of pulse oximetry as complementary monitoring for patients at risk of developing splanchnic ischaemia.

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43

Gountounas, Nektaria. "Localisation of candidate sweet taste receptor molecules involved in glucose sensing in the rat duodenum /". Title page and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09SB/09sbg711.pdf.

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44

Brownhill, Varuni R. "Characterization and ontogeny of purinoceptors in the vas deferens and the duodenum of the rat". Thesis, University of Surrey, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320912.

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45

Rafiq, Imran. "Role of pancreatic duodenum homeobox 1 (PDX-1) in transcriptional regulation of the prepoinsulin gene". Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322013.

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46

Itier, Lambert Mireille. "Etude de la regulation transcriptionnelle de la calbindine-d9k dans le duodenum chez le rat". Paris 11, 1996. http://www.theses.fr/1996PA11T001.

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47

Dhir, Nirmal. "Structures of human gastric mucus glycoproteins : changes in Helicobacter pylori - associated gastroduodenal disease". Thesis, University of Westminster, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323003.

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48

Nicaud, Philippe. "Atrésies et sténoses duodénales intrinsèques congénitales : expérience du Service de chirurgie infantile de Montpellier sur la période 1980-1990". Montpellier 1, 1991. http://www.theses.fr/1991MON11118.

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49

PHAN, VAN JEAN-PIERRE. "Bulbite erosive et cytoprotection duodenale : etablissement de profils metaboliques quantitatifs de prostanoides dans la muqueuse bulbaire avant et apres repas-test". Besançon, 1990. http://www.theses.fr/1990BESA3099.

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50

Odes, Harold Selwyn. "Regulation of duodenal mucosal bicarbonate secretion". Thesis, University of Cape Town, 1993. http://hdl.handle.net/11427/25542.

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The present research studied the regulation of duodenal bicarbonate secretion in the anaesthetized guinea-pig, using a model that permitted the study of active transport of bicarbonate. It was determined that dibutyryl 3' ,5'-cyclic adenosine monophosphate, vasoactive intestinal polypeptide, prostaglandin E2, carbachol and theophylline are the chief agonists of duodenal bicarbonate secretion. Vasoactive intestinal polypeptide and prostaglandin E2 act directly via distinct receptors on the duodenal enterocytes, activating adenylate cyclase and protein kinase A in sequence to initiate bicarbonate secretion. In addition, there is good evidence that the inositol phospholipid and protein kinase C cascade is also involved, possibly to a lesser extent, since tetradecanoyl-phorbolacetate and prostaglandin F2a were agonists of bicarbonate secretion. Carbachol, using a m-cholinoceptor pathway, stimulates duodenal bicarbonate secretion by releasing vasoactive intestinal polypeptide. Consistent with this finding is the observation that carbachol has no receptors on duodenal enterocytes. The role of the nicotinic pathway in bicarbonate secretion, however, remains uncertain. Duodenal bicarbonate secretion can be inhibited by somatostatin and acetazolamide. Somatostatin selectively suppresses carbachol-stimulated and VIP-stimulated duodenal bicarbonate secretion, but not PGE2-stimulated bicarbonate secretion. Receptors for somatostatin coupled to adenylate cyclase could not be detected on isolated duodenal enterocytes, which strengthens the hypothesis that carbachol does not act directly on these epithelial cells, but via a second transmitter, vasoactive intestinal polypeptide. Carbonic anhydrase activity is necessary for secretion of bicarbonate, since acetazolamide-inhibition of this enzyme decreased bicarbonate secretion, both basal and stimulated by many different agonists. Carbonic anhydrase serves as a common final step in the generation of bicarbonate in duodenal enterocytes. This enzyme was located in the cytoplasm of cells in the villus as well as the crypt cells, implying that bicarbonate secretion occurs along the length of the villus and crypt. In summary, the present research has shown direct stimulation of duodenal bicarbonate secretion by vasoactive intestinal polypeptide, which participates also in themcholinergic pathway, and by prostaglandin E2. Adenylate cyclase and protein kinase A appear to be the intracellular messengers with the primary function of initiating duodenal bicarbonate secretion. However, there is convincing evidence that the inositol phospholipid and protein kinase C cascade also activates this secretion. Somatostatin selectively stops duodenal bicarbonate secretion. Carbonic anhydrase activity in the crypt and villus is required as the final common step in bicarbonate production.

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