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Littérature scientifique sur le sujet « Gastrointestinal system Motility »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 30 juillet 2024

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Articles de revues sur le sujet "Gastrointestinal system Motility"

Wood, Jackie D. "Enteric Nervous System: Neuropathic Gastrointestinal Motility." Digestive Diseases and Sciences 61, no. 7 (May 3, 2016): 1803–16. http://dx.doi.org/10.1007/s10620-016-4183-5.

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BURKS, THOMAS F. "Central Nervous System Regulation of Gastrointestinal Motility." Annals of the New York Academy of Sciences 597, no. 1 Neurobiology (July 1990): 36–42. http://dx.doi.org/10.1111/j.1749-6632.1990.tb16156.x.

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Wang, Po-Min, Genia Dubrovsky, James C. Y. Dunn, Yi-Kai Lo, and Wentai Liu. "A Wireless Implantable System for Facilitating Gastrointestinal Motility." Micromachines 10, no. 8 (August 9, 2019): 525. http://dx.doi.org/10.3390/mi10080525.

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Gastrointestinal (GI) electrical stimulation has been shown in several studies to be a potential treatment option for GI motility disorders. Despite the promising preliminary research progress, however, its clinical applicability and usability are still unknown and limited due to the lack of a miniaturized versatile implantable stimulator supporting the investigation of effective stimulation patterns for facilitating GI dysmotility. In this paper, we present a wireless implantable GI modulation system to fill this technology gap. The system consists of a wireless extraluminal gastrointestinal modulation device (EGMD) performing GI electrical stimulation, and a rendezvous device (RD) and a custom-made graphical user interface (GUI) outside the body to wirelessly power and configure the EGMD to provide the desired stimuli for modulating GI smooth muscle activities. The system prototype was validated in bench-top and in vivo tests. The GI modulation system demonstrated its potential for facilitating intestinal transit in the preliminary in vivo chronic study using porcine models.

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Alqudah, M., O. Al-Shboul, A. Al-Dwairi, D. G. Al-U´Dat, and A. Alqudah. "Progesterone Inhibitory Role on Gastrointestinal Motility." Physiological Research, no. 2 (April 30, 2022): 193–98. http://dx.doi.org/10.33549/physiolres.934824.

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Progesterone is a steroidal hormone that is produced from the corpus luteum of the ovaries and from the placenta. The main function of progesterone is to promote the secretory differentiation in the endometrium of the uterus and to maintain pregnancy by inhibiting uterine contractions throughout pregnancy. Progesterone performs its actions by activating the classical progesterone nuclear receptors that affect gene transcription and by the non-classical activation of cell surface membrane receptors that accounts for the rapid actions of progesterone. Besides the reproductive roles of progesterone, it exerts functions in many tissues and systems such as the nervous system, the bone, the vascular system, and the gastrointestinal (GI) tract. This review will summarize the recent literature that investigated the role of progesterone in GI tract motility. Most literature indicates that progesterone exerts an inhibitory role on gut smooth muscle cells in part by elevating nitric oxide synthesis, which induces relaxation in smooth muscle. Moreover, progesterone inhibits the signaling pathways that lead to contraction such as Rho kinase inhibition. These data serve as a quick resource for the future directions of progesterone research that could lead to better understanding and more effective treatment of gender-related GI tract motility disorders.

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Stern, H. Patrick, Suzanne E. Stroh, Stephen C. Fiedorek, Kelly Kelleher, Michael W. Mellon, Sandra K. Pope, and Phillip L. Rayford. "Increased Plasma Levels of Pancreatic Polypeptide and Decreased Plasma Levels of Motilin in Encopretic Children." Pediatrics 96, no. 1 (July 1, 1995): 111–17. http://dx.doi.org/10.1542/peds.96.1.111.

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Objective. Abnormalities of hormones affecting gastrointestinal motility have been found in "functional" disorders of the gastrointestinal system in adults. One such disorder of childhood, encopresis, is frequently associated with constipation, the treatment of which often eliminates the soiling. We hypothesized that hormones affecting gastrointestinal motility were different between encopretic patients and matched controls. Methods. Ten encopretic patients were matched by age, race, and sex with controls who had no history of encopresis or constipation. After an overnight fast, each child consumed a meal of Ensure, the amount of which was based on body weight. Plasma levels of gastrin, pancreatic polypeptide, cholecystokinin, motilin, thyroxine, estrogen, and insulin were measured 20 and 5 minutes before the meal, and 5, 10, 15, 30, 45, 60, 90, 120, 150, and 180 minutes after the meal. Results. Postprandial levels of pancreatic polypeptide remained consistently higher and peaked earlier (P &lt; .05) for encopretic patients. The motilin response was lower (P &lt; .03) for encopretic children than for controls. Conclusions. We conclude that pancreatic polypeptide and motilin responses to a meal are different in encopretic children than in children in the control group. These gastrointestinal hormone findings may in part explain and/or be the result of the severe constipation that frequently underlies the fecal soiling found in these patients. These findings also suggest the motility of the stomach and small intestine may be abnormal in encopresis.

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Lee, Yunna, Jeongbin Jo, Hae Young Chung, Charalabos Pothoulakis, and Eunok Im. "Endocannabinoids in the gastrointestinal tract." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 4 (October 1, 2016): G655—G666. http://dx.doi.org/10.1152/ajpgi.00294.2015.

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The endocannabinoid system mainly consists of endogenously produced cannabinoids (endocannabinoids) and two G protein-coupled receptors (GPCRs), cannabinoid receptors 1 and 2 (CB1 and CB2). This system also includes enzymes responsible for the synthesis and degradation of endocannabinoids and molecules required for the uptake and transport of endocannabinoids. In addition, endocannabinoid-related lipid mediators and other putative endocannabinoid receptors, such as transient receptor potential channels and other GPCRs, have been identified. Accumulating evidence indicates that the endocannabinoid system is a key modulator of gastrointestinal physiology, influencing satiety, emesis, immune function, mucosal integrity, motility, secretion, and visceral sensation. In light of therapeutic benefits of herbal and synthetic cannabinoids, the vast potential of the endocannabinoid system for the treatment of gastrointestinal diseases has been demonstrated. This review focuses on the role of the endocannabinoid system in gut homeostasis and in the pathogenesis of intestinal disorders associated with intestinal motility, inflammation, and cancer. Finally, links between gut microorganisms and the endocannabinoid system are briefly discussed.

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Plourde, Victor. "Stress-Induced Changes in the Gastrointestinal Motor System." Canadian Journal of Gastroenterology 13, suppl a (1999): 26A—31A. http://dx.doi.org/10.1155/1999/320626.

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Several autonomic, hormonal, behavioural and neuropeptidergic bodily responses to stressful stimuli have been described over the past few decades. Both animal models and human paradigms have been explored. It is acknowledged that stress modulates gastrointestinal (GI) motility through central mechanisms including corticotropin-releasing-factor. This process requires the integrity of autonomic neural pathways. It has become evident that the effects of stress on GI motility vary according to the stressful stimulus, its intensity, the animal species under study and the time course of the study. Recent evidence suggests that chronic or possibly permanent changes develop in enteric smooth muscle properties in response to stress. In animals, the most consistent findings include retardation of gastric emptying in response to various stressors; acceleration of gastric emptying upon cold stress, presumably through the secretion of brain thyroglobulin-hormone; acceleration of intestinal transit; and stimulation of colonic transit and fecal output. In humans, the cold water immersion test has been associated with an inhibition of gastric emptying, while labyrinthine stimulation induces the transition from postprandial to fasting motor patterns in the stomach and the small bowel. Psychological stress has been shown to induce a reduction in the number and amplitude of intestinal migrating motor complexes and to neither affect nor stimulate colonic motility. These various responses to stress are presumably attributed to the preferential activation of specific neuronal pathways under the influence of a given stimulus or its intensity. The significance of these findings and the directions of further studies are discussed.

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Milla, PJ. "Acquired Motility Disorders in Childhood." Canadian Journal of Gastroenterology 13, suppl a (1999): 76A—84A. http://dx.doi.org/10.1155/1999/610486.

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Acquired motility disorders in childhood cause a number of gastrointestinal symptoms – principally, recurrent vomiting, abdominal pain and distension, constipation and loose stools. Gastrointestinal motility disorders result from disturbances of the control mechanisms of gut motor activity, which may be produced by organic disease involving enteric nerves and muscle, perturbation of the humoral environment of the nerves and muscle, and altered central nervous system input. In children, both congenital and acquired disease processes may produce these pathogenetic mechanisms, resulting in syndromes that vary in severity from chronic intestinal pseudo-obstruction to the irritable bowel syndrome.

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López-Pingarrón, Laura, Henrique Almeida, Marisol Soria-Aznar, Marcos C. Reyes-Gonzales, Ana B. Rodríguez-Moratinos, Antonio Muñoz-Hoyos, and Joaquín J. García. "Interstitial Cells of Cajal and Enteric Nervous System in Gastrointestinal and Neurological Pathology, Relation to Oxidative Stress." Current Issues in Molecular Biology 45, no. 4 (April 18, 2023): 3552–72. http://dx.doi.org/10.3390/cimb45040232.

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The enteric nervous system (ENS) is organized into two plexuses—submucosal and myenteric—which regulate smooth muscle contraction, secretion, and blood flow along the gastrointestinal tract under the influence of the rest of the autonomic nervous system (ANS). Interstitial cells of Cajal (ICCs) are mainly located in the submucosa between the two muscle layers and at the intramuscular level. They communicate with neurons of the enteric nerve plexuses and smooth muscle fibers and generate slow waves that contribute to the control of gastrointestinal motility. They are also involved in enteric neurotransmission and exhibit mechanoreceptor activity. A close relationship appears to exist between oxidative stress and gastrointestinal diseases, in which ICCs can play a prominent role. Thus, gastrointestinal motility disorders in patients with neurological diseases may have a common ENS and central nervous system (CNS) nexus. In fact, the deleterious effects of free radicals could affect the fine interactions between ICCs and the ENS, as well as between the ENS and the CNS. In this review, we discuss possible disturbances in enteric neurotransmission and ICC function that may cause anomalous motility in the gut.

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Pan, H. L., Z. B. Zeisse, and J. C. Longhurst. "Mechanical stimulation is not responsible for activation of gastrointestinal afferents during ischemia." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 1 (January 1, 1997): H99—H106. http://dx.doi.org/10.1152/ajpheart.1997.272.1.h99.

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Abdominal ischemia reflexly excites the cardiovascular system through activation of visceral sympathetic afferents. Although a number of ischemic metabolites are known to stimulate sympathetic afferents, the contribution of mechanical stimulation to activation of afferents during abdominal ischemia remains uncertain. Thus the present study examined the role of changes in motility in activation of gastrointestinal afferents during ischemia. Single-unit activity of C fiber afferents located on the stomach, duodenum, jejunum, or colon was recorded from the right sympathetic chain of anesthetized cats during 15 min of ischemia. Intraluminal pressure, as a reflection of local mechanical activity, was measured by an open catheter placed in the lumen of the gastrointestinal tract. The results show that gastrointestinal motility was mainly inhibited during abdominal ischemia. Changes in intraluminal pressure did not correlate with afferent discharge activity during ischemia (r = -0.32, n = 10). Furthermore, discharge frequency of gastrointestinal afferents during ischemia was not altered significantly by topical application of 100 micrograms/ml of atropine (3.98 +/- 0.62 to 3.83 +/- 0.59 imp/s, n = 12), which profoundly inhibited local gastrointestinal motility. Collectively, these data indicate that gastrointestinal motility changes during abdominal ischemia do not contribute to activation of gastrointestinal sympathetic C fiber afferents.

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Thèses sur le sujet "Gastrointestinal system Motility"

Andrews, Jane Mary. "Relationships between motor and sensory function in the proximal gut, appetite, & nutrients in healthy human subjects." Title page, contents and summary only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09pha567.pdf.

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Bibliography: leaves 206-251. The motor and sensory interactions between nutrients and proximal gut in humans are not well understood, despite the pivotal importance of these interactions on appetite, absorption and thus, nutrition. In part, this lack of knowledge results from technical difficulties in studying motor function in the human gut. In particular, the inability to continuously measure intraluminal flow with any degree of temporal resolution, has impeded progress in this field. The studies described in this thesis focus on nutrient-gut interactions, and also on the development of novel methodologies aimed at advancing the understanding and interpretation of the relationships between intraluminal pressures and flows.

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Spear, Estelle Trego. "Altered Gastrointestinal Motility in Multiple Sclerosis." ScholarWorks @ UVM, 2018. https://scholarworks.uvm.edu/graddis/837.

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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system that causes motor, visual, and sensory symptoms. Patients also experience constipation, which is not yet understood, but could involve dysfunction of the enteric nervous system (ENS). Autoimmune targeting of the ENS occurs in other autoimmune diseases that exhibit gastrointestinal (GI) symptoms, and similar mechanisms could lead to GI dysfunction in MS. Here, we characterize GI dysmotility in the experimental autoimmune encephalomyelitis (EAE) model of MS and test whether autoantibodies targeting the ENS are present in the serum of MS patients. Male SJL or B6 mice were induced with EAE by immunization against PLP139-151, MOG35-55, or mouse spinal cord homogenate, and monitored daily for somatic motor symptoms. EAE mice developed GI symptoms consistent with those observed in MS. In vivo motility analysis demonstrated slower whole GI transit, and decreased colonic propulsive motility. EAE mice had faster rates of gastric emptying, with no changes in small intestinal motility. Consistent with these results, ex vivo evaluation of isolated colons demonstrated that EAE mice have slower colonic migrating myoelectric complexes and slow wave contractions. Immunohistochemistry of EAE colons exhibited a significant reduction in GFAP area of ENS ganglia, with no changes in HuD, S100, or neuron numbers. To test whether antibodies in MS bind to ENS structures, we collected serum samples from MS patients with constipation and without constipation, and healthy control patients without constipation. Immunoreactivity was tested using indirect immunofluorescence by applying serum samples to guinea pig ENS tissue. MS serum exhibited significantly higher immunoreactivity against guinea pig ENS than control patients, which was particularly evident in MS patients who did not experience constipation. There was no significant difference in immunoreactivity between MS patients with and without constipation. Targets of human MS and mouse EAE serum include enteric glia and neurons. Taken together, these data validate EAE as a model for constipation in MS, and support the concept that this symptom involves changes within the neuromuscular system of the colon. EAE mice develop symptoms consistent with constipation that affects functional ENS networks and may result in structural or phenotypic changes at the cellular level. Serum immunoreactivity suggests that autoantibodies could play a role in the development of constipation in MS by targeting the ENS itself.

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Jones, Karen Louise. "Studies of normal and disordered gastric motility in humans /." Title page, table of contents and summary only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phj777.pdf.

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Boillat, Carol Simone. "Investigation of gastrointestinal motility in dogs using a wireless capsule system /." [S.l.] : [s.n.], 2009. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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HIRNING, LANE DURAND. "MULTIPLE PEPTIDE RECEPTORS AND SITES OF ACTION IN THE CANINE SMALL INTESTINE (OPIOIDS, MOTILIN, TACHYKININS, INTESTINAL MOTILITY, SUBSTANCE P)." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/188150.

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Motility of the small intestine is a result of complex neurochemical and hormonal interactions within the intestine. The net motility (contraction) of the intestine is a balance of the influences from the central nervous system, enteric nervous system and hormonal changes in the body. Recently, the discovery of several peptide neurotransmitters common to the brain and the intestine has stimulated new research into the influence of these novel neurotransmitter candidates on intestinal motility at the level of the enteric (intestinal) nervous system. The present studies examined the contractile actions of three families of peptides, the opioids, tachykinins and motilin. Each of these peptide groups has been localized in the intestine, and suggested to function in the control of intestinal motility. The peptides were administered by intraarterial injection to isolated segments of canine small intestine and the resulting contractile activity measured. The results of these experiments demonstrate that all of these peptides may elicit contractile activity of the intestine in very low doses. These actions were further examined, using pharmacological antagonists, to determine the mechanism of action and the receptor types involved in the contractile actions. The opioid peptide induced responses were found to be mediated by two receptor types, mu and delta, located on the enteric nerve and smooth muscle, respectively. Similarly, the tachykinin induced contractions were also found to be due to actions on two receptor types, SP-P and SP-K, located on the nerve and muscle layers, respectively. These data suggest that the opioids and tachykinins may have multiple functions in the intestine dependent on the site of action and the receptor type involved in the response. Administration of motilin induced long-lasting contractile patterns in the intestine. The results also suggest that the actions of motilin are mediated by intermediate neurons of the enteric plexes which synapse on terminal cholinergic motor neurons.

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Lo, Wing-joe. "Effects of neurotransmitters and peptides on gastrointestinal motility in the shark, hemiscyllium plagiosum (Bennett) /." [Hong Kong : University of Hong Kong], 1993. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13597322.

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羅穎祖 and Wing-joe Lo. "Effects of neurotransmitters and peptides on gastrointestinal motilityin the shark, hemiscyllium plagiosum (Bennett)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1993. http://hub.hku.hk/bib/B3123382X.

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Zhao, Ling. "Increased bile acid-metabolizing bacteria contributes to enhanced gastrointestinal motility in irritable bowel syndrome." HKBU Institutional Repository, 2018. https://repository.hkbu.edu.hk/etd_oa/561.

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Irritable bowel syndrome (IBS), majorly characterized by irregular bowel movements and abdominal pain, is one of the most prevalent functional gastrointestinal disorders (FGIDs) in the world. Disturbance of gut microbiota, closely linking with gut dysfunction, has been regarded as one of important pathogenetic factors for IBS. However, gut microbiota-driven mechanism underlying IBS remains unclear, which leads to inefficient and non-specific effects of current microbiota-oriented therapy. In this thesis, function-based microbiota investigation with combination of metagenomic and metabolomic analyses was separately performed in IBS cohort and model to precisely link pathogenic species with disordered GI motor function. A series of microbiota manipulation studies in rodents were conducted to explore bacteria-driven molecular mechanism. Firstly, a pilot study with 'omics' analyses revealed fecal microbial structure significantly varied in IBS patients with disorder GI motility relative to healthy controls (HC). Such changed IBS enterotype was functionally characterized by disturbed metabolism of bile acids (BAs) that are previously proved to regulate GI motor function. It indicates microbiota-driven GI dysmotility relevant to disturbance of BA metabolism in IBS. Secondly, a systematic review with meta-analysis was performed to comprehensively understand existing findings related to BA metabolism and its linkage with IBS. Results showed that abnormal BA excretion, previously reported in at least one IBS subtype, is associated with dysregulation of BA synthesis, marked with abnormalities of circulating indices 7α-hydroxy-4-cholesten-3-one (C4) and fibroblast growth factor 19 (FGF19). However, what's the role of gut microbiota in abnormal BA excretion is undetermined. Thirdly, to explore possible role of gut microbiota in abnormal BA excretion in IBS, BA metabolites and BA-related microbiome were simultaneously analyzed in stools of recruited subjects. Results found that total BA and microbiota-derived BAs were remarkably elevated in a quarter of IBS-D patients (BA+IBS-D) who exhibited more frequent defecation, higher level of serum C4 but lower level of serum FGF19 than those with normal BA excretion (BA-IBS-D). In line with metabolic results, abundances of BA-metabolizing bacteria, particularly Clostridium scindens (C. scindens) simultaneously expressed hdhA and bais that are responsible for BA 7α oxidation and dehydroxylation, were highly enriched in fecal metagenomes of such particular IBS-D population. These findings suggest the increased BA-metabolizing microbiome is associated with the dysregulated host BA synthesis in the subgroup of BA+IBS-D patients. Fourthly, by analyzing metabolites and bacteria related to BA metabolism, a neonatal maternal separation (NMS)-induced IBS-D rat model characterized by accelerated GI motility and excessive BA excretion were found to largely mimic gut microbial BA metabolism in BA+IBS-D patients. Specifically, intraluminal total and secondary BAs were significantly elevated in the large intestinal lumens (cecum, proximal colon and feces) of NMS rats, together with increased abundances of hdhA- and bais-expressing Clostridium species, including C. scindens. Moreover, quantitative polymerase chain reaction (PCR) analysis showed upregulated mRNA expression of cholesterol 7 α-hydroxylase (CYP7A1) whereas downregulated mRNA expression of small heterodimer partner (SHP) in the liver of NMS rats, indicating enhanced hepatic BA synthetic level. These observations based on such IBS-D model suggest the association of excessive BA-metabolizing microbiome and increased hepatic BA synthesis. Fifthly, to further clarify whether excessive BA-metabolizing bacteria contribute to enhanced hepatic BA synthesis and to explore the underlying molecular mechanism, we performed bacterial intervention in pseudo germ-free (GF) or/and specific pathogen free (SPF) mice by transplantation of human fecal microbiota and the signal strain C. scindens. Compared with GF mouse recipients of HC and BA-IBS-D fecal microbiota, BA+IBS-D fecal microbial recipients displayed shorter GI transit and increased subsistence of C. scindens in the cecal contents. In line with higher level of serum C4, taurine-conjugated BA contents and mRNA expressions of BA synthetase CYP7A1 and sterol 12α-hydroxylase (CYP8B1) were significantly elevated in the liver of BA+IBS-D recipients. These findings showed bioactive effects of BA+IBS-D fecal microbiota with enrichment of C. scindens on hepatic BA synthesis. Next, to further confirm the effects of the species C. scindens on host BA synthesis, we individually colonized C. scindens strains (ATCC 37504) to pseudo GF and SPF mice. Results showed both mice models with single strain colonization exhibited accelerated GI transit and higher contents of hepatic total and taurine-conjugated BAs compared with individual vehicles treated with PBS. Combining metabolic changes, the upregulated expressions of hepatic CYP7A1 mRNA in colonized mice indicate that C. scindens substantially promote hepatic BA synthesis in colonized mice. Furthermore, contents of taurine-conjugated BAs, served as natural antagonists of farnesoid X receptor (FXR) that negatively control of new BA synthesis, were elevated in ileal lumens of colonized mice. Expressions of FXR-targeted genes SHP and fibroblast growth factor 15 (FGF15) were consistently reduced in the liver and ileum tissues of colonized mice, respectively. Results suggest that suppression of FXR-mediated feedback signaling is involved in Clostridium-driven hepatic BA oversynthesis, which deserve the further investigation. Collectively, the works of this thesis integrating clinical and animal studies indicate that BA-metabolizing bacteria, particularly C. scindens, enhance hepatic BA synthesis and consequently leads to BA overexcretion. It provides novel bacteria-driven mechanism for enhanced GI motility, and supply a direction in precise microbiota-related pathogenesis and medication for IBS-D population in future.

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Fone, David R. "Studies of the function of the human pylorus : and its role in the regulation of gastric emptying / David R. Fone." Title page, contents and summary only, 1990. http://web4.library.adelaide.edu.au/theses/09MD/09mdf673.pdf.

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Branstutter, Joseph W. "The role of nitric oxide in altering intestinal motility in lipopolysaccharide-injected rats : a morphological and functional assessment." Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1136700.

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Nitric oxide, a short-lived free radical and neurotransmitter, is responsible for decreased smooth muscle contractility in vitro. When in excess, NO can cause hypotension and is believed to mediate altered intestinal motility. Not enough evidence is available for morphological changes in gastrointestinal smooth muscle and its correlation with motility disorders caused by Escherichia coli-induced NO production. Male Lewis rats were treated with injections of 10 mg/kg LPS from E. coli with or without 12.5 mg/kg of NOS inhibitor, LNMMA. Eighteen to 24 hours following injection, duodenum, ileum, colon, liver, and spleen were harvested for histological analysis. Urine and fecal analysis assessed functional aspects in control and treatment groups. Muscularis externa measurements revealed significant increase in muscle thickness of LPS + LNMMA injected group compared to control and LPS group. However, the average values in control and LPS group were not significantly different. Fecal consistency was significant in all 3 groups. Mean urinary nitrite in the LPS group was 44 times higher than control and 52 times higher than the inhibitor-treated group.<br>Department of Physiology and Health Science

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Livres sur le sujet "Gastrointestinal system Motility"

W, Read N., ed. Gastrointestinal motility : which test? Peterfield: Wrightson Biomedical, 1989.

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Hongō, Michio, editor of compilation, ed. Functional and GI motility disorders. Basel: Karger, 2014.

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G, Schultz Stanley, Rauner Brenda B, Wood Jack D, and American Physiological Society (1887- ), eds. The Gastrointestinal system. Bethesda, Md: American Physiological Society, 1989.

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Devinder, Kumar, and Gustavsson Sven, eds. An Illustrated guide to gastrointestinal motility. 2nd ed. Edinburgh: Churchill Livingstone, 1993.

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Michael, Camillieri, and Stanghellini Vincenzo, eds. Manometric diagnosis of gastrointestinal motility disorders. New York: Thieme, 1986.

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S, Gaginella Timothy, ed. Regulatory mechanisms in gastrointestinal function. Boca Raton: CRC Press, 1995.

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Cheng, L. K. New Advances in Gastrointestinal Motility Research. Dordrecht: Springer Netherlands, 2013.

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S, Davison J., ed. Gastrointestinal secretion. London: Wright, 1989.

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International Workshop on Stress and Digestive Motility (1988 Mont Gabriel, Canada). Stress and digestive motility: Proceedings of the International Workshop on Stress and Digestive Motility. Edited by Bueno Lionel, Collins Stephen M, and Junien Jean-Louis. London: John Libbey, 1989.

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A, Kurygin A., ed. Motornai͡a︡ funkt͡s︡ii͡a︡ tonkoĭ kishki: V norme i pri nekotorykh patologicheskikh sostoi͡a︡nii͡a︡kh. Sankt-Peterburg: "Nauka", 1994.

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Chapitres de livres sur le sujet "Gastrointestinal system Motility"

Chang, Eugene B., and Po Sing Leung. "Gastrointestinal Motility." In The Gastrointestinal System, 35–62. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8771-0_2.

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Klaus, Jennifer. "Gastrointestinal system motility and integrity." In Monitoring and Intervention for the Critically Ill Small Animal, 267–83. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118923870.ch15.

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Bredenoord, Albert J., André Smout, and Jan Tack. "Biliary System." In A Guide to Gastrointestinal Motility Disorders, 103–7. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26938-2_9.

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Kini, Usha. "Pathology of the Gut Motility Disorders: Hirschsprung’s Disease." In Surgical Pathology of the Gastrointestinal System, 339–74. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-6395-6_10.

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Das, Prasenjit, and Prateek Kinra. "Pathology of Gut Motility Disorders: Chronic Intestinal Pseudoobstruction and Entities Other than Hirschsprung’s Disease." In Surgical Pathology of the Gastrointestinal System, 375–403. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-6395-6_11.

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Sanger, Gareth J., John Broad, Brid Callaghan, and John B. Furness. "Ghrelin and Motilin Control Systems in GI Physiology and Therapeutics." In Gastrointestinal Pharmacology, 379–416. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/164_2016_104.

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Pocock, Gillian, Christopher D. Richards, and David A. Richards. "Introduction to the gastrointestinal system." In Human Physiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/hesc/9780198737223.003.53.

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This chapter describes the gross anatomical organization of the gastrointestinal system, the internal structure of the gut wall, and its blood supply. It provides an overview of the nervous and hormonal mechanisms that regulate the motility and secretory activity of the gut. It also presents a detailed examination of the structure and functions of the mouth and oesophagus, the stomach, and the small and large intestine, together with the digestive functions of the pancreas. The chapter outlines key aspects of nutrition and energy balance, noting how food is required by the body both for the production of energy and for the growth and repair of tissues. Each day an average adult consumes around 1 kg of solid food and 1-2 litres of fluid. The majority of this material is in a form that first must be broken down into simple molecules.

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Mischopoulou, Magdalini, and Gianluca Cipriani. "Muscularis Macrophages in Healthy and Diseased Gut." In Phagocytosis - Main Key of Immune System [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.109889.

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Muscularis macrophages are a newly discovered population of macrophages distributed within the smooth muscle layers of the gastrointestinal tract. Muscularis macrophages are emerging as essential cell keepers of homeostatic gastrointestinal function, and when affected, can lead to functional gastrointestinal disorders. In this chapter, we briefly introduce the phenotype, the distribution of muscularis macrophages, and the difference compared with other tissue-resident macrophages. We next describe how they contribute to normal gastrointestinal function by interacting with cells required for gastrointestinal motility, such as enteric neurons. Finally, we highlight the increasing pieces of evidence suggesting the contribution of muscularis macrophages to gastrointestinal function diseases, such as gastrointestinal inflammation, gastroparesis and post operative ileus.

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Camilleri, Michael, and Adil E. Bharucha. "Disturbances of Gastrointestinal Motility and the Nervous System." In Neurology and General Medicine, 293–310. Elsevier, 2008. http://dx.doi.org/10.1016/b978-044306707-5.50019-5.

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Camilleri, Michael, and Adil E. Bharucha. "Disturbances of Gastrointestinal Motility and the Nervous System." In Aminoff's Neurology and General Medicine, 255–71. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-407710-2.00014-x.

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Actes de conférences sur le sujet "Gastrointestinal system Motility"

Yoshimoto, Kayo, Kenji Yamada, Kenji Watabe, Maki Takeda, Takahiro Nishimura, Michiko Kido, Toshiaki Nagakura, et al. "Evaluation of the three-dimensional endoscope system for assessing the gastrointestinal motility." In SPIE BiOS, edited by Tuan Vo-Dinh, Anita Mahadevan-Jansen, and Warren S. Grundfest. SPIE, 2014. http://dx.doi.org/10.1117/12.2041652.

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Pinheiro, Amanda Pereira Sindeaux, Pedro Vitor Ferreira Rodrigues, Raoni de Oliveira da Silva Domingues, and Leonardo José Rodrigues Araújo Melo. "Gastrointestinal dysmotility associated with Parkinson’s disease’s mechanism." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.461.

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Introduction: Parkinson’s Disease (PD) is a condition of the brain that consiste of the death of dopaminergic neurons in the substantia nigra, therefore causing dyskinesias and dystonias. Besides the motor symptoms, the neurogastro motility is affected by the disease, since gastrointestinal dysfunction is a frequent and clinically relevant symptom of PD. Objectives: To link the neural pathways and neurotransmitters that involve the neuroenteric system control and the PD’s pathology. Methods: A systematic literature review was performed based on data extraction through the advanced research engine from Pubmed. Publications with the descriptors “dysmotility” OR “gastro motility” AND “Parkinson” were selected. Results: Through clinical and pre-clinical studies on PD, there has been hypothesized a gut-brain axis that is connected through hormones, neurotransmitters and dopamanergic inputs. This hypothesis is supported by evidence in the showing of accumulation of alpha-synuclein in the vagal system and Enteric Nervous System, the use of drugs such as peripheral dopaminergic blockers and serotonin for gastroparesis, the ghrelin effects on the central dopaminergic system through modulation of the mesencephalic dopaminergic signaling tested on rats, the gastrointestinal autonomic neuropathy detected in PD patients and the establishment of gut dysmotility before motor onset symptoms. Therefore, dysmotility isues such as delayed gastric emptying may not only be a symptom of PD, but also contrubute to the pathogenesis itself through impaired signaling. Conclusion: The gut-brain axis can be not only a tool for PD diagnosis but also a treatment target to restrain the advance of the disease. Although many articles are related this subject, there is a lack of designed trials for atypical movement disorders. To explore the dysmotility in PD, there is a need for multi-modality standardized tests to evaluate severity and prevalence.

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Nobe, Kazuki, Kayo Yoshimoto, Kenji Yamada, and Hideya Takahashi. "3D registration method for assessing the gastrointestinal motility using spectral reflectance estimation." In Advanced Biomedical and Clinical Diagnostic and Surgical Guidance Systems XVI, edited by Tuan Vo-Dinh, Anita Mahadevan-Jansen, and Warren S. Grundfest. SPIE, 2018. http://dx.doi.org/10.1117/12.2288383.

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