Letteratura scientifica selezionata sul tema "Troubles fonctionnels intestinaux – Chimiothérapie"
Cita una fonte nei formati APA, MLA, Chicago, Harvard e in molti altri stili
Consulta la lista di attuali articoli, libri, tesi, atti di convegni e altre fonti scientifiche attinenti al tema "Troubles fonctionnels intestinaux – Chimiothérapie".
Accanto a ogni fonte nell'elenco di riferimenti c'è un pulsante "Aggiungi alla bibliografia". Premilo e genereremo automaticamente la citazione bibliografica dell'opera scelta nello stile citazionale di cui hai bisogno: APA, MLA, Harvard, Chicago, Vancouver ecc.
Puoi anche scaricare il testo completo della pubblicazione scientifica nel formato .pdf e leggere online l'abstract (il sommario) dell'opera se è presente nei metadati.
Articoli di riviste sul tema "Troubles fonctionnels intestinaux – Chimiothérapie":
Jacquet, Alain, e Cécile Rémy. "Réflexothérapie et Troubles fonctionnels intestinaux". Hegel N° 4, n. 4 (2017): 368a. http://dx.doi.org/10.3917/heg.074.0368a.
Jouët, Pauline, e Jean-Marc Sabaté. "Troubles fonctionnels intestinaux et rhumatismes". Revue du Rhumatisme Monographies 83, n. 4 (settembre 2016): 213–17. http://dx.doi.org/10.1016/j.monrhu.2016.04.004.
Bueno, Lionel. "Immunité digestive et troubles fonctionnels intestinaux". Gastroentérologie Clinique et Biologique 29, n. 8-9 (agosto 2005): 828–31. http://dx.doi.org/10.1016/s0399-8320(05)86354-7.
Mennecier, D., H. Rimlinger, O. Mouline, C. Nizou, C. Thiolet, O. Farret e B. Vergeau. "Troubles fonctionnels intestinaux et maladie caeliaque". La Revue de Médecine Interne 23 (dicembre 2002): 693s. http://dx.doi.org/10.1016/s0248-8663(02)80679-8.
Mennecier, D., H. Rimlinger, O. Moulin, J. Dufeau, C. Nizou, C. Thiolet, O. Farret e B. Vergeau. "Troubles fonctionnels intestinaux et maladie cœliaque". La Revue de Médecine Interne 24, n. 3 (marzo 2003): 204–5. http://dx.doi.org/10.1016/s0248-8663(02)00803-2.
Wiesel, Paul, Gerold Schacher, Jean-François Schnegg, Alexandre Bertholz e Philippe De Saussure. "Troubles fonctionnels gastro-intestinaux en 2001". Revue Médicale Suisse -2, n. 2377 (2002): 218–26. http://dx.doi.org/10.53738/revmed.2002.-2.2377.0218.
Breton, Elisabeth. "Stimulation réflexe plantaire et Troubles fonctionnels intestinaux". Hegel N° 1, n. 1 (2018): 90. http://dx.doi.org/10.3917/heg.081.0090.
Ducrotté, P. "Physiopathologie et traitement des troubles fonctionnels intestinaux". EMC - Gastro-entérologie 1, n. 1 (gennaio 2006): 1–9. http://dx.doi.org/10.1016/s1155-1968(05)39221-2.
Ducrotté, P. "Physiopathologie et traitement des troubles fonctionnels intestinaux". EMC - Hépato-Gastroenterologie 2, n. 4 (ottobre 2005): 400–412. http://dx.doi.org/10.1016/j.emchg.2005.07.002.
Dapoigny, M. "Troubles fonctionnels intestinaux et impact en santé publique". Côlon & Rectum 1, n. 4 (novembre 2007): 255–58. http://dx.doi.org/10.1007/s11725-007-0063-7.
Tesi sul tema "Troubles fonctionnels intestinaux – Chimiothérapie":
Beutheu, Youmba Stéphanie. "Étude des protéines de jonctions serrées au cours de l'inflammation intestinale : impact des acides aminés". Rouen, 2011. http://www.theses.fr/2011ROUENR04.
La fonction de barrière peut être régulée en partie par les jonctions serrées (JS). Les JS sont des structures mufti-protéiques qui jouent un rôle important dans la polarité, la prolifération et la différenciation cellulaire. Plusieurs études ont suggéré que l'augmentation de la perméabilité intestinale pourrait être impliquée dans la survenue de phénomènes inflammatoires tels qu'observés au cours du syndrome de l'intestin irritable (Sul), ou de la mucite induite par le méthotrexate (MTX). Cependant, les régulations et les mécanismes mis en jeu ne sont pas clairement définis. Les objectifs de notre travail étaient d'une part d'étudier la régulation des protéines de JS, claudine-1, occludine et zonula occludens-1 (Z0-1) dans deux modèles i. E. Sur des biopsies coliques de patients atteints du SII et dans des modèles expérimentaux de mucite induite par le MTX in vivo chez le rat et in vitro sur des cellules Caco-2, et d'autre part d'évaluer les effets d'acides aminés dans les modèles expérimentaux de mucite. Nous avons observé des différences dans les altérations des protéines de JS en fonction du phénotype et des symptômes chez les patients SII. Les patients SII diarrhéiques présentaient d'importantes altérations d'expression de l'occludine et de la claudine-1. Cette perte d'expression protéique était corrélée à la durée des symptômes et à l'intensité de la douleur, suggérant donc que ces modifications seraient impliquées dans l'initiation du SIL Dans les modèles expérimentaux de mucite, nous avons observé une augmentation de la perméabilité intestinale induite par le MTX qui serait associée à des altérations de l'expression et de la localisation des protéines claudine-1, occludine et ZO-1. De plus, nous avons pu déterminer que les voies NF-kB, MEK1&2 et JNK seraient impliquées au cours de la perte de la fonction de barrière. Dans le cadre de stratégies nutritionnelles pour moduler ces altérations, nous avons montré que la glutamine prévenait l'augmentation de la perméabilité et restaurait l'expression des protéines de JS via les voies erk. Et NF-kB. La combinaison glutamine plus arginine n'aurait pas d'effet protecteur au cours de la rupture de la barrière intestinale dans ce modèle et semblerait être associée à une mortalité importante. Ces données incitent à poursuivre cette étude pour confirmer les effets préventifs et/ou thérapeutiques de la glutamine au cours de la mucite induite par le MTX mais également au cours du SII
STENGEL, CONRAD. "Mmpi et troubles fonctionnels intestinaux". Toulouse 3, 1988. http://www.theses.fr/1988TOU31151.
Bourdu, Sophie. "Mise au point d'un modèle d'hypersensibilité colique induite par le butyrate chez le rat : approches physiologiques et pharmacologiques". Clermont-Ferrand 1, 2005. http://www.theses.fr/2005CLF1MM05.
Duboc, Henri-Gérard. "Dysbiose et métabolisme des acides biliaires : implications au cours du syndrome de l’intestin irritable". Paris 6, 2013. http://www.theses.fr/2013PA066218.
The irritable bowel syndrome associates chronic abdominal pain and altered bowel transit. This is a common digestive disorder, which in its pathophysiology include the concept of dysbiosis, i. E disruption of the intestinal microbiota (overall micro organisms in a gut). Dysbiosis implies alterations of the host-microbiota dialogue leading to disease, a mainly descriptive concept to date. Bile acids are synthesized by the liver and metabolized by bacteria then reabsorbed from the intestine - so potentially involved in this dialogue. Other pathophysiological axes include motor, permeability, and intestinal secretion, and theses are functions also regulated by bile acids, through the membrane receptor TGR5. This work presents and discusses, through two scientific publications, the links between irritable bowel syndrome, dysbiosis, and TGR5 receptor
Langlois, Ludovic. "Caractérisation d'un effet sensitif de la neuromodulation des racines sacrées". Rouen, 2015. http://www.theses.fr/2015ROUENR05.
Fecal incontinence remains a therapeutic problem in patients when conservative measures fail and sphincter repair is unsuccessful or inappropriate. Sacral nerve stimulation (SNS) is an alternative surgical approach proposed initially to treat urinary incontinence, and has been used for the past decade as a successful treatment of fecal incontinence. Despite its overall efficacy, the mechanisms involved in this symptomatic effect remain unclear. The aim of this study was to evaluate the effect of SNS on rat visceral sensitivity. In an anesthetized rat model, mean arterial pressure variation was recorded in response to colorectal distension (CRD) in sham and effective SNS groups. Healthy and cross-organ sensitization models were studied. Characterization of the pathways involved in the effect of SNS was made by injecting pharmacological agents. Central neuronal activation and p-opioid receptor internalization were assessed by immunohistochemistry. In both models, SNS reduced mean arterial pressure variation. This effect was prevented by opioid receptor antagonist. CRD induced a rise in sacral dorsal horn of the spinal cord, parabrachial nucleus and solitary tract nucleus that was prevented by SNS. Finally, SNS induced an increase of p-opioid receptor internalization in a context of CRD. Concomitantly, we developed an implantable stimulating device in order to study chronic SNS on awaken rats. Implantation technique was validated by obtaining tail tremor response and by performing computed tomography imaging. Micturition frequency was assessed in rats undergoing 3 days of bipolar or unipolar SNS. In both groups, SNS reduced micturition frequency
Jie, Bai. "Effets d'un analogue de la somatostatine, l'octréotide sur la pathogénicité à court et long termes de l'infection par Cryptosporidium parvum dans un modèle de raton nouveau-né immunocompétent". Rouen, 2011. http://www.theses.fr/2011ROUENR03.
Tarrerias, Anne-Laure. "Relation nutrition et sensibilité colique : effet des fibres et des acides gras volatils chez le rat et chez l'homme". Clermont-Ferrand 1, 2003. http://www.theses.fr/2003CLF1MM18.
Thibault, Ronan. "Utilisation des substrats énergétiques par l'intestin en situation d'agression : utilisation du butyrate par le côlon au cours de l'inflammation intestinale : utilisation de la glutamine par l'intestin grêle dans un modèle de stress chez le volontaire sain". Nantes, 2009. http://www.theses.fr/2009NANT2016.
During intestinal inflammation or critical illness, the availability of the two preferred energy substrates of the intestine, butyrate and glutamine, is dramatically altered. The aim of this work was to obtain further insight into the mechanisms leading to alterations in butyrate and glutamine availability for the colon and the small intestine, respectively, during metabolic stress in vivo in humans. First, using various models of intestinal inflammation, we demonstrate that the defect in butyrate oxidation reported in inflammatory bowel diseases is the consequence of a decrease in butyrate transport into the colonocyte, itself related to a reduced expression of the butyrate intestinal transporter MCT1. We also clearly show that pro-inflammatory cytokines inhibit MCT1 transcription, and that this regulation involves the transcriptional factor USF2. The putative binding sequences involved in the cytokine-mediated inhibition of MCT1 transcription are located in the region -111/+213 of the promoter region. Last, our data indicate that the decrease in MCT1 expression alters cell metabolism, since it favours glucose utilization by the colonic mucosa, by increasing the expression of the glucose transporter GLUT1. This metabolic switch may be involved in the colonic carcinogenesis associated with chronic inflammation. Second, we have studied the effects of the metabolic stress on the glutamine utilization by the small intestine. In critically ill patients, glutamine is considered a conditionally essential amino acid, as muscle free glutamine pool is depleted in spite of high rates of de novo glutamine synthesis. To mimick the catabolic effects of severe illness, we studied the effect of oral corticosteroids on the splanchnic utilization of glutamine in healthy subjects. We show that a 6-day oral treatment with prednisone increases glutamine splanchnic extraction, but not its oxidation. These findings strongly suggest that the metabolic stress increases glutamine requirements by the small intestine, and may contribute to the depletion of muscle free glutamine concentration observed in critically ill patients
Khaldi, Samira. "Apport d'un modèle de rat d'hypersensibilité intestinale induite par Cryptosporidium parvum à la physiopathologie du syndrome de l'intestin irritable post-infectieux ; et transfert des oocystes de Cryptosporidium spp. Dans l'aquifère de la craie". Rouen, 2010. http://www.theses.fr/2010ROUES047.
Cryptosporidiosis, caused by Cryptosporidium spp. , is a self-limiting infection in immunocompetent individuals but may be life-threatening in immunocompromised individuals, in the absence of effective treatment. The pathophysiological mechanisms of cryptosporidiosis are not yet fully understood, but it has been shown that cryptosporidiosis can cause long-term sequelae. The first part of this work was aimed to highligt in a suckling rat model that infection with C. Parvum (isolate Nouzilly) leads to a more severe infection compared to rats that were infected with C. Parvum (isolate Iowa). Moreover, after clearance of infection, sub-mucosal infiltration of activated mast cells was observed in the jejunum. This infiltration is concomitant with the occurrence of a jejunal hypersensitivity to distention at day 50 post-infection. The anomalies observed are similar to those found in patients suffering from a post-infectious irritable bowel syndrome. The second part of the thesis was dedicated to the study of the transfer modalities of Cryptosporidium oocysts in a well-defined karst system, from the entry (swallow hole) to the exit of the system (spring and well-bore). It has been shown that the oocysts are transported in karst conduits, undergoing transfer, depostion and resuspention processes, under the influence of hydrodynamic gradient. Moreover, it was observed that the exploitation of the resource for the drinking water supply by sequences of continuous pumping promoted resuspension of sedimented oocysts and contributes to contamination of water resources
Coppet, Pierre de. "Expression du transporteur des monocarboxylates MCT1 dans le côlon sain et pathologique". Nantes, 2009. http://www.theses.fr/2009NANT2062.
Dietary fibers are digestible food ingredients that reach the colon and are then fermented by colonic bacteria, resulting mainly in the formation of short-chain fatty acids (SCFAs) such as acetate, propionate and butyrate. Especially butyrate plays an important part in maintaining the health and integrity of the colonic mucosa. It is the primary energy source for the colonic epithelium and has most important physiological effect, including regulation of cell proliferation, differentiation and apoptosis. Butyrate oxidation was decrease in pathological situations like chronic inflammatory bowel diseases or colorectoral cancer. The monocarboxylate transporter 1 (MCT1 = SLC16A1) transports butyrate across the apical membrane of human colonocytes. Thus, a decrease in MCT1 expression, which reduces the intra-cellular availability of butyrate could affect not only its oxidation, but also its cell regulatory effects. In this study, we investigated that MCT1 can be identified as a good marker of butyrate exposition in colon epithelial cells and we demonstrate that the defect in butyrate oxidation reported in inflammatory bowel diseases is the consequence of a decrease in butyrate transport into the colonocyte, itself related to a reduced expression of the butyrate intestinal transporter MCT1
Capitoli di libri sul tema "Troubles fonctionnels intestinaux – Chimiothérapie":
Chevallier, Laurent. "Troubles fonctionnels intestinaux". In Nutrition : principes et conseils, 223–35. Elsevier, 2009. http://dx.doi.org/10.1016/b978-2-294-70817-6.00028-x.
Chevallier, Laurent. "Troubles fonctionnels intestinaux". In 65 Ordonnances Alimentaires, 388–97. Elsevier, 2021. http://dx.doi.org/10.1016/b978-2-294-76804-0.00064-7.
Sarembaud, Alain, e Bernard Poitevin. "Les troubles fonctionnels intestinaux". In HoméOopathie, 189–94. Elsevier, 2011. http://dx.doi.org/10.1016/b978-2-294-70862-6.00018-5.