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Статті в журналах з теми "Gastrointestinal system Motility":

1

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

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2

BURKS, THOMAS F. "Central Nervous System Regulation of Gastrointestinal Motility." Annals of the New York Academy of Sciences 597, 1 Neurobiology (July 1990): 36–42. http://dx.doi.org/10.1111/j.1749-6632.1990.tb16156.x.

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3

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 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.
4

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.
5

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 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.
6

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.
7

Spencer, Nick J., and Hongzhen Hu. "Enteric nervous system: sensory transduction, neural circuits and gastrointestinal motility." Nature Reviews Gastroenterology & Hepatology 17, no. 6 (March 2020): 338–51. http://dx.doi.org/10.1038/s41575-020-0271-2.

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8

., Manojkumar, and Sangeeta Gehlot. "EFFECT OF SHARAPUNKHA (TEPHROSIA PURPUREA) ON GASTROINTESTINAL SYSTEM." International Journal of Research in Ayurveda and Pharmacy 11, no. 5 (October 2020): 60–63. http://dx.doi.org/10.7897/2277-4343.1105142.

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Sharapunkha (Tephrosia purpurea) is one of the important drugs in Ayurvedic system of medicine. The present study was undertaken to find out the action of Sharapunkha (Tephrosia purpurea) on Gastrointestinal System. During the passage of drug through oral route, it is probable that the active principle present in Sharapunkha, might act on gastrointestinal System. Albino rats were used in this study and divided into control and drug treated group. Drug treated group rats were feed with intragastric drug decoction, along with their normal water and food. Water intake, diet intake, weight of rats, gastrointestinal motility and serum bilirubin level were compared. Healthy human volunteers were selected, and prepared drug decoction was given for 7 days. Observations were done based on self-assessment of the volunteers about any significant physiological variation specially related to the G.I. System. After study, it was found that Sharapunkha enhances intestinal motility, decreases serum bilirubin in albino rats. Human volunteers had feeling of increase appetite, easy bowel motion and increase urge for micturition. These facts suggest that some ingredients of Sharapunkha are acting on the smooth muscles of the bowel and urinary bladder. So, it may be presumed that Sharapunkha influences the feeding and satiety center located in hypothalamus. Sharapunkha decoction preparation does influence the activity of the autonomic nervous system with consequent alterations in the functions of gastrointestinal tract and possibly the urinary system.
9

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 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.
10

Nakamura, Hiroyuki, Tadashi Asano, Koichi Haruta, and Keisuke Takeda. "Gastrointestinal motor inhibition by exogenous human, salmon, and eel calcitonin in conscious dogs." Canadian Journal of Physiology and Pharmacology 73, no. 1 (January 1995): 43–49. http://dx.doi.org/10.1139/y95-006.

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Effects of synthetic eel (E-), salmon (S-), and human (H-) calcitonin (CT) on gastrointestinal motility were studied in conscious beagle dogs, which had been implanted with strain gauge force transducers. Intramuscular administration of E-, S-, or H-CT interrupted gastric migrating motor complexes, digestive pattern, and gastric emptying. The order of potency was E-CT = S-CT > H-CT. Motor inhibition induced by CT occurred independently of plasma immunoreactive motilin levels or hypocalcemia. In addition, E-CT and S-CT induced vomiting without a retrograde giant contraction (RGC) during the postprandial state. Apomorphine or CuSO4initiated RGC prior to vomiting. RGC induced by apomorphine was inhibited by pretreatment with E-CT as well as hexamethonium, atropine, or surgical vagotomy. E-CT showed no inhibitory effect on nicotine stimulated contraction of isolated guinea-pig ileum. These results suggest that peripherally administered CT inhibits canine gastrointestinal motility at the central nervous system level by lowering vagal activity.Key words: gastric emptying, motilin, retrograde giant contraction, vagus, vomiting.

Дисертації з теми "Gastrointestinal system Motility":

1

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.
2

Spear, Estelle Trego. "Altered Gastrointestinal Motility in Multiple Sclerosis." Text, 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.
3

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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4

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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5

HIRNING, LANE DURAND. "MULTIPLE PEPTIDE RECEPTORS AND SITES OF ACTION IN THE CANINE SMALL INTESTINE (OPIOIDS, MOTILIN, TACHYKININS, INTESTINAL MOTILITY, SUBSTANCE P)." Dissertation-Reproduction (electronic), 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.
6

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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7

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

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8

Zhao, Ling. "Increased bile acid-metabolizing bacteria contributes to enhanced gastrointestinal motility in irritable bowel syndrome." Text, 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.
9

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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10

Jiang, Qi 1957. "Site of clonidine action to inhibit gut propulsion in mice: Demonstration of a central component." Thesis-Reproduction (electronic), The University of Arizona, 1989. http://hdl.handle.net/10150/291819.

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The role of supraspinal, spinal and peripheral alpha-2 adrenoceptors in the regulation of gastrointestinal motility in mice was investigated using anatomically site specific administration of clonidine and adrenoceptor antagonists. Clonidine produced a dose-dependent inhibition of gastrointestinal transit when given by the i.c.v., i.th., or s.c. routes, and was most potent when given i.c.v. Yohimbine, an alpha-2 adrenoceptor antagonist, but not the alpha-1 antagonist prazosin, antagonized the antitransit effects of clonidine. Yohimbine was most potent in antagonizing i.c.v. clonidine; increased doses of the i.c.v. antagonist were required when the agonist was given s.c. After transection of the spinal cord, i.th. clonidine failed to produce an antitransit effect. Additionally, the i.c.v. potency of clonidine decreased approximately 7-fold in spinally-transected mice. The data suggest that the antitransit effects of clonidine occur through actions at alpha-2 adrenoceptors located at both supraspinal and peripheral sites.

Книги з теми "Gastrointestinal system Motility":

1

Malagelada, J. R. Manometric diagnosis of gastrointestinal motility disorders. New York: Thieme, 1986.

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2

Grundy, David. Gastrointestinal motility: The integration of physiological mechanisms. Lancaster: MTP Press, 1985.

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3

Zenilman, Michael E. Abnormalities of intestinal motility. Austin: R.G. Landes, 1992.

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4

Smout, A. J. P. M. Normal and disturbed motility of the gastrointestinal tract. Petersfield: Wrightson Biomedical Pub., 1992.

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5

Soffer, Edy. Color Atlas of High Resolution Manometry. Boston, MA: Springer-Verlag US, 2009.

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6

McCallum, Richard W., Henry P. Parkman, and Satish S. C. Rao. GI motility testing: A laboratory and office handbook. Thorofare, NJ: SLACK, 2011.

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7

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. London: John Libbey, 1989.

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8

Gregersen, Hans. Biomechanics of the gastrointestinal tract: New perspectives in motility research and diagnostics. London: Springer, 2003.

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9

International, Symposium on Gastrointestinal Motility (10th 1985 Rochester Minn ). Cellular physiology and clinical studies of gastrointestinal smooth muscle: Proceedings of the 10th International Symposium on Gastrointestinal Motility, 8-11 September 1985, Rochester, MN, U.S.A. Amsterdam: Excerpta Medica, 1987.

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10

Sundqvist, Monika. Development of gastrointestinal motility and the enteric nervous system in the amphibian Xenopus laevis. Göteborg: Dept. of Zoology/Zoophysiology, 2007.

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Частини книг з теми "Gastrointestinal system Motility":

1

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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2

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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3

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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4

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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5

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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6

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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7

Camilleri, Michael. "Disturbances of Gastrointestinal Motility and the Nervous System." In Aminoff's Neurology and General Medicine, 217–34. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-819306-8.00014-9.

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8

"Digestive system." In Oxford Handbook of Medical Sciences, edited by Robert Wilkins, Ian Megson, and David Meredith, 535–612. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198789895.003.0008.

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Анотація:
The chapter entitled ‘Digestive system’ opens with an overview of the anatomy of the abdomen, including the abdominal wall and peritoneal cavity, and the structure and histology of the major structures found therein, namely the intestinal tract (oesophagus, stomach, duodenum, jejunum, ileum, large intestine, rectum), spleen, liver, and pancreas. The functions of the gastrointestinal tract are described, covering motility, secretion (saliva, gastric acid, pancreatic fluid, bile, fluid, and electrolytes) and digestion/absorption of nutrients. Pathologies such as gastric and duodenal ulcers, malabsorption, intestinal obstruction, diarrhoea, and inflammatory diseases of the gut are considered, as are the immune functions of the gut. Similarly, the roles of the liver are covered, including protein synthesis, iron transport and storage, and detoxification, along with the effects of hepatic diseases such as hepatitis and cirrhosis.
9

Au, Shiu-chung, and Amar Gupta. "Gastrointestinal Motility Online Educational Endeavor." In Developments in Healthcare Information Systems and Technologies, 14–34. IGI Global, 2011. http://dx.doi.org/10.4018/978-1-61692-002-9.ch002.

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Medical information has been traditionally maintained in books, journals, and specialty periodicals. A growing subset of patients and caregivers are now turning to diverse sources on the internet to retrieve healthcare related information. The next area of growth will be sites that serve specialty fields of medicine, characterized by high quality of data culled from scholarly publications and operated by eminent domain specialists. One such site being developed for the field of Gastrointestinal Motility provides authoritative and current information to a diverse user base that includes patients and student doctors. Gastrointestinal Motility Online leverages the strengths of online textbooks, which have a high degree of organization, in conjunction with the strengths of online journal collections, which are more comprehensive and focused. Gastrointestinal Motility Online also utilizes existing Web technologies such as Wiki-editing and Amazonstyle commenting, to automatically assemble information from heterogeneous data sources.
10

Wass, John A. H. "Somatostatinoma." In Oxford Textbook of Endocrinology and Diabetes, 929–31. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0657.

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Somatostatin was isolated in 1973 by Paul Brazeau in Roger Guillemin’s laboratory. It was found to have a widespread distribution, not only in the hypothalamus and brain but also in the gastrointestinal tract. Sixty-five per cent of the body’s somatostatin is in the gut, mostly in the D cells of the gastric and intestinal epithelium. It is also present in the myometric and submucosal plexuses. The highest concentration is in the antrum of the stomach and there is a gradual decrease of concentrations down the gastrointestinal tract. Five per cent of the body’s somatostatin is in the pancreas. Infused somatostatin, which has a short half-life of 3 min, has a large number of actions on the pituitary gland, the endocrine and exocrine pancreas, gastrointestinal tract, other hormones, and on the nervous system (Box 6.8.1). Among its various actions of importance in the gastrointestinal tract is the inhibition of gastrin and cholecystokinin (CCK). In the pancreas, insulin and glucagon are inhibited. Nonendocrine actions include inhibition of gastric acid secretion, pancreatic exocrine function, gall bladder contraction, and intestinal motility. Intestinal absorption of nutrients, including glucose, triglycerides, and amino acids, is also inhibited (1). Somatostatin exists in two main forms, as a 14-amino acid peptide (somatostatin 14) present mainly in the pancreas and the stomach, and as a 28-amino acid peptide present mainly in the intestine. Somatostatin 14 is the peptide present in enteric neurons. Somatostatin receptors are present on many cell types, including the parietal cells of the stomach, G cells, D cells themselves, and cells of the exocrine and endocrine pancreas. A large number of tumours also have somatostatin receptors and these include pituitary adenomas, endocrine pancreatic tumours, carcinoid tumours, paragangliomas, phaeochromocytomas, small cell lung carcinomas, lymphomas, and meningiomas. Five different somatostatin receptors (SSTRs) have been cloned (SSTR1–SSTR5) and all are on different chromosomes. These have a varying affinity for somatostatin 14 and somatostatin 28 and a varying tissue distribution with SSTR2 and 5 being predominant in the pituitary (2). Somatostatin can act either as an endocrine hormone or in a paracrine or autocrine way. It probably also has luminal effects in the gastrointestinal tract. Lastly, it can act as a neurotransmitter (3).

Тези доповідей конференцій з теми "Gastrointestinal system Motility":

1

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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2

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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