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Pesquisa : G10.261.360 [Categoria DeCS]
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  1 / 19955 MEDLINE  
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[PMID]:29320574
[Au] Autor:Inoue A; Furukawa A; Yamamoto H; Ohta S; Linh NDH; Syerikjan T; Kaida S; Yamaguchi T; Murata S; Obata T; Tani M; Murata K
[Ad] Endereço:Department of Radiology, Shiga University of Medical Science, Otsu, Shiga, Japan.
[Ti] Título:Acceleration of small bowel motility after oral administration of dai-kenchu-to (TJ-100) assessed by cine magnetic resonance imaging.
[So] Source:PLoS One;13(1):e0191044, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dai-kenchu-to (TJ-100) is an herbal medicine used to shorten the duration of intestinal transit by accelerating intestinal movement. However, intestinal movement in itself has not been evaluated in healthy volunteers using radiography, fluoroscopy, and radioisotopes because of exposure to ionizing radiation. The purpose of this study was to evaluate the effect of TJ-100 on intestinal motility using cinematic magnetic resonance imaging (cine MRI) with a steady-state free precession sequence. Ten healthy male volunteers received 5 g of either TJ-100 or lactose without disclosure of the identity of the substance. Each volunteer underwent two MRI examinations after taking the substances (TJ-100 and lactose) on separate days. They drank 1200 mL of tap water and underwent cine MRI after 10 min. A steady-state free precession sequence was used for imaging, which was performed thrice at 0, 10, 20, 30, 40, and 50 min. The bowel contraction frequency and distention score were assessed. Wilcoxon signed-rank test was used, and differences were considered significant at a P-value <0.05. The bowel contraction frequency tended to be greater in the TJ-100 group and was significantly different in the ileum at 20 (TJ-100, 8.95 ± 2.88; lactose, 4.80 ± 2.92; P < 0.05) and 50 min (TJ-100, 9.45 ± 4.49; lactose, 4.45 ± 2.65; P < 0.05) between the groups. No significant differences were observed in the bowel distention scores. Cine MRI demonstrated that TJ-100 activated intestinal motility without dependence on ileum distention.
[Mh] Termos MeSH primário: Motilidade Gastrointestinal
Intestino Delgado/fisiologia
Imagem Cinética por Ressonância Magnética/métodos
Extratos Vegetais/administração & dosagem
[Mh] Termos MeSH secundário: Administração Oral
Adulto
Método Duplo-Cego
Seres Humanos
Intestino Delgado/diagnóstico por imagem
Meia-Idade
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Extracts); 0 (dai-kenchu-to)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191044


  2 / 19955 MEDLINE  
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[PMID]:28463898
[Au] Autor:Gastaldelli A; Gaggini M; DeFronzo R
[Ad] Endereço:aCardiometabolic Risk Laboratory, Institute of Clinical Physiology, National Research Council, Pisa, Italy bUniversity of Texas Health Science Center at San Antonio, TX, USA.
[Ti] Título:Glucose kinetics: an update and novel insights into its regulation by glucagon and GLP-1.
[So] Source:Curr Opin Clin Nutr Metab Care;20(4):300-309, 2017 Jul.
[Is] ISSN:1473-6519
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Glucagon and GLP-1 share the same origin (i.e., proglucagon); primarily GLP-1 is generated from intestinal L-cells and glucagon from pancreatic α-cell, but intestinal glucagon and pancreatic GLP-1 secretion is likely. Glucose kinetics are tightly regulated by pancreatic hormones insulin and glucagon, but other hormones, including glucagon-like peptide-1 (GLP-1), also play an important role. The purpose of this review is to describe the recent findings on the mechanisms by which these two hormones regulate glucose kinetics. RECENT FINDINGS: Recent findings showed new important mechanisms of action of glucagon and GLP-1 in the regulation of glucose metabolism. Knock out of glucagon receptors protects against hyperglycemia without causing hypoglycemia. GLP-1 not only stimulates insulin secretion, but it has also an independent effect on the liver and inhibits glucose production. Moreover, when coinfused with glucagon, GLP-1 limits the hyperglycemic effects. Both hormones have also central effects on gastric emptying (delayed), intestinal motility (reduced), and satiety (increased). SUMMARY: The implications of these findings are very important for the management of type 2 diabetes given that GLP-1 receptor agonist are currently approved for the treatment of hyperglycemia and glucagon receptor antagonists and GLP-1/glucagon dual agonists are under development.
[Mh] Termos MeSH primário: Peptídeo 1 Semelhante ao Glucagon/fisiologia
Glucagon/fisiologia
Glucose/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Tipo 2/tratamento farmacológico
Jejum
Esvaziamento Gástrico/fisiologia
Motilidade Gastrointestinal/fisiologia
Glucagon/sangue
Glucagon/farmacologia
Peptídeo 1 Semelhante ao Glucagon/farmacologia
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Receptor do Peptídeo Semelhante ao Glucagon 1/fisiologia
Gluconeogênese/efeitos dos fármacos
Glucose/biossíntese
Homeostase
Seres Humanos
Hiperglicemia/tratamento farmacológico
Cinética
Fígado/efeitos dos fármacos
Fígado/metabolismo
Receptores de Glucagon/antagonistas & inibidores
Receptores de Glucagon/fisiologia
Saciação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 0 (Receptors, Glucagon); 89750-14-1 (Glucagon-Like Peptide 1); 9007-92-5 (Glucagon); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1097/MCO.0000000000000384


  3 / 19955 MEDLINE  
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[PMID]:27773805
[Au] Autor:Camilleri M; Sellin JH; Barrett KE
[Ad] Endereço:Clinical Enteric Neuroscience Translational and Epidemiological Research, Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic, Rochester, Minnesota. Electronic address: camilleri.michael@mayo.edu.
[Ti] Título:Pathophysiology, Evaluation, and Management of Chronic Watery Diarrhea.
[So] Source:Gastroenterology;152(3):515-532.e2, 2017 Feb.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic watery diarrhea poses a diagnostic and therapeutic challenge and is often a disabling condition for patients. Although acute diarrhea is likely to be caused by infection, the causes of chronic diarrhea (>4 weeks in duration) are more elusive. We review the pathophysiology, diagnosis, and treatment of chronic diarrhea. Drawing on recent insights into the molecular mechanisms of intestinal epithelial transport and barrier function, we discuss how diarrhea can result from a decrease in luminal solute absorption, an increase in secretion, or both, as well as derangements in barrier properties. We also describe the various extraepithelial factors that activate diarrheal mechanisms. Finally, clinical evaluation and tests used in the assessment of patients presenting with chronic diarrhea are reviewed, and an algorithm guiding therapeutic decisions and pharmacotherapy is presented.
[Mh] Termos MeSH primário: Diarreia/metabolismo
Absorção Intestinal
Secreções Intestinais
Intestinos/metabolismo
[Mh] Termos MeSH secundário: Proteína C-Reativa/metabolismo
Cromograninas/metabolismo
Doença Crônica
Diarreia/diagnóstico
Diarreia/fisiopatologia
Diarreia/terapia
Fezes/química
Motilidade Gastrointestinal
Seres Humanos
Inflamação
Intestinos/fisiopatologia
Síndrome do Intestino Irritável/metabolismo
Lactoferrina/metabolismo
Complexo Antígeno L1 Leucocitário/metabolismo
Concentração Osmolar
Permeabilidade
Prostaglandinas/metabolismo
Serotonina/metabolismo
Substância P/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chromogranins); 0 (Leukocyte L1 Antigen Complex); 0 (Prostaglandins); 333DO1RDJY (Serotonin); 33507-63-0 (Substance P); 9007-41-4 (C-Reactive Protein); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  4 / 19955 MEDLINE  
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[PMID]:28450068
[Au] Autor:Du P; O'Grady G; Cheng LK
[Ad] Endereço:Auckland Bioengineering Institute, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand. Electronic address: peng.du@auckland.ac.nz.
[Ti] Título:A theoretical analysis of anatomical and functional intestinal slow wave re-entry.
[So] Source:J Theor Biol;425:72-79, 2017 Jul 21.
[Is] ISSN:1095-8541
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Intestinal bioelectrical slow waves are a key regulator of intestinal motility. Peripheral pacemakers, ectopic initiations and sustained periods of re-entrant activities have all been experimentally observed to be important factors in setting the frequency of intestinal slow waves, but the tissue-level mechanisms underpinning these activities are unclear. This theoretical analysis aimed to define the initiation, maintenance, and termination criteria of two classes of intestinal re-entrant activities: anatomical re-entry and functional re-entry. Anatomical re-entry was modeled in a three-dimensional (3D) cylindrical model, and functional rotor was modeled in a 2D rectangle model. A single-pulse stimulus was used to invoke an anatomical re-entry and a prolonged refractory block was used to invoke the rotor. In both cases, the simulated re-entrant activities operated at frequencies above the baseline entrainment frequency. The anatomical re-entry simulation results demonstrated that a temporary functional refractory block would be required to initiate the re-entrant activity in a single direction around the cylindrical model. The rotor could be terminated by a single-pulse stimulus delivered around the core of the rotor. In conclusion, the simulation results provide the following new insights into the mechanisms of intestinal re-entry: (i) anatomical re-entry is only maintained within a specific range of velocities, outside of which the re-entrant activities become either an ectopic activity or simultaneous activations of the intestinal wall; (ii) a maintained rotor entrained slow waves faster in the antegrade direction than in the retrograde direction. Simulations are shown to be a valuable tool for achieving novel insights into the mechanisms of intestinal slow wave dysrhythmia.
[Mh] Termos MeSH primário: Motilidade Gastrointestinal/fisiologia
Intestinos/anatomia & histologia
Intestinos/fisiologia
Modelos Biológicos
[Mh] Termos MeSH secundário: Fenômenos Eletrofisiológicos/fisiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  5 / 19955 MEDLINE  
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[PMID]:28880927
[Au] Autor:Chen LL; Zhu J; Schumacher J; Wei C; Ramdas L; Prieto VG; Jimenez A; Velasco MA; Tripp SR; Andtbacka RHI; Gouw L; Rodgers GM; Zhang L; Chan BK; Cassidy PB; Benjamin RS; Leachman SA; Frazier ML
[Ad] Endereço:Department of Sarcoma, University of Texas M D Anderson Cancer Center, Houston, Texas, United States of America.
[Ti] Título:SCF-KIT signaling induces endothelin-3 synthesis and secretion: Thereby activates and regulates endothelin-B-receptor for generating temporally- and spatially-precise nitric oxide to modulate SCF- and or KIT-expressing cell functions.
[So] Source:PLoS One;12(9):e0184154, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We demonstrate that SCF-KIT signaling induces synthesis and secretion of endothelin-3 (ET3) in human umbilical vein endothelial cells and melanoma cells in vitro, gastrointestinal stromal tumors, human sun-exposed skin, and myenteric plexus of human colon post-fasting in vivo. This is the first report of a physiological mechanism of ET3 induction. Integrating our finding with supporting data from literature leads us to discover a previously unreported pathway of nitric oxide (NO) generation derived from physiological endothelial NO synthase (eNOS) or neuronal NOS (nNOS) activation (referred to as the KIT-ET3-NO pathway). It involves: (1) SCF-expressing cells communicate with neighboring KIT-expressing cells directly or indirectly (cleaved soluble SCF). (2) SCF-KIT signaling induces timely local ET3 synthesis and secretion. (3) ET3 binds to ETBR on both sides of intercellular space. (4) ET3-binding-initiated-ETBR activation increases cytosolic Ca2+, activates cell-specific eNOS or nNOS. (5) Temporally- and spatially-precise NO generation. NO diffuses into neighboring cells, thus acts in both SCF- and KIT-expressing cells. (6) NO modulates diverse cell-specific functions by NO/cGMP pathway, controlling transcriptional factors, or other mechanisms. We demonstrate the critical physiological role of the KIT-ET3-NO pathway in fulfilling high demand (exceeding basal level) of endothelium-dependent NO generation for coping with atherosclerosis, pregnancy, and aging. The KIT-ET3-NO pathway most likely also play critical roles in other cell functions that involve dual requirement of SCF-KIT signaling and NO. New strategies (e.g. enhancing the KIT-ET3-NO pathway) to harness the benefit of endogenous eNOS and nNOS activation and precise NO generation for correcting pathophysiology and restoring functions warrant investigation.
[Mh] Termos MeSH primário: Endotelina-3/secreção
Óxido Nítrico/metabolismo
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptor de Endotelina B/metabolismo
Fator de Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Aterosclerose/patologia
Linhagem Celular Tumoral
Endotélio Vascular/metabolismo
Ensaio de Imunoadsorção Enzimática
Motilidade Gastrointestinal
Tumores do Estroma Gastrointestinal/metabolismo
Tumores do Estroma Gastrointestinal/patologia
Tumores do Estroma Gastrointestinal/fisiopatologia
Homeostase
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Imuno-Histoquímica
Melanoma/patologia
Plexo Mientérico/metabolismo
Invasividade Neoplásica
Óxido Nítrico Sintase Tipo I/metabolismo
Óxido Nítrico Sintase Tipo III/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Transdução de Sinais
Pele/metabolismo
Luz Solar
Fatores de Tempo
Regulação para Cima/genética
Vasodilatação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-3); 0 (Receptor, Endothelin B); 0 (Stem Cell Factor); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type I); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184154


  6 / 19955 MEDLINE  
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[PMID]:28847163
[Au] Autor:Chedid V; Camilleri M
[Ad] Endereço:a Department of Medicine, Division of Gastroenterology and Hepatology , Mayo Clinic , Rochester , MN , USA.
[Ti] Título:Relamorelin for the treatment of gastrointestinal motility disorders.
[So] Source:Expert Opin Investig Drugs;26(10):1189-1197, 2017 Oct.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Current treatments for gastroparesis are limited. Chronic idiopathic constipation (CIC) has more treatment options, but none are efficacious for severe cases. Areas covered: Molecular targets to accelerate GI motility are being identified, and relamorelin, a synthetic ghrelin analog, has been promising. In humans, relamorelin increases growth hormone levels and accelerates gastric emptying. Relamorelin was superior to placebo for symptom relief in phase IIA studies for diabetic gastroparesis (DG) and CIC. In phase IIB studies in DG, relamorelin did not significantly reduce vomiting frequency when compared to placebo, but it reduced four symptoms of DG (nausea, fullness, bloating and abdominal pain) and accelerated gastric emptying. To date, relamorelin has been well tolerated and safe in humans without cardiac or neurologic adverse effects. It is still in clinical trial stages and not yet approved by the Food and Drug Administration. Phase III studies are underway. Expert opinion: Relamorelin shows promise in treating DG, with a reduction in core symptoms. Relative to available treatments, it appears to be efficacious and well tolerated. The absence of neurological or cardiovascular adverse effects places it at an advantage over other available therapies. Once approved, it will likely become the drug of first choice for DG.
[Mh] Termos MeSH primário: Constipação Intestinal/tratamento farmacológico
Gastroparesia/tratamento farmacológico
Oligopeptídeos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Doença Crônica
Constipação Intestinal/fisiopatologia
Complicações do Diabetes/tratamento farmacológico
Complicações do Diabetes/fisiopatologia
Desenho de Drogas
Motilidade Gastrointestinal/efeitos dos fármacos
Gastroparesia/fisiopatologia
Seres Humanos
Terapia de Alvo Molecular
Oligopeptídeos/efeitos adversos
Oligopeptídeos/farmacologia
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Oligopeptides); BIW199E18V (relamorelin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2017.1373088


  7 / 19955 MEDLINE  
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[PMID]:28815345
[Au] Autor:Xu H; Xiong J; Xu J; Li S; Zhou Y; Chen D; Cai X; Ping J; Deng M; Chen J
[Ad] Endereço:Department of Gastroenterology and Hepatology, Hangzhou Red Cross Hospital, 208 Huancheng Dong Road, Hangzhou, 310003, China.
[Ti] Título:Mosapride Stabilizes Intestinal Microbiota to Reduce Bacterial Translocation and Endotoxemia in CCl -Induced Cirrhotic Rats.
[So] Source:Dig Dis Sci;62(10):2801-2811, 2017 Oct.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Impaired intestinal motility may lead to the disruption of gut microbiota equilibrium, which in turn facilitates bacterial translocation (BT) and endotoxemia in cirrhosis. We evaluated the influence of mosapride, a prokinetic agent, on BT and DNA fingerprints of gut microbiota in cirrhotic rats. METHODS: A rat model of cirrhosis was set up via subcutaneous injection of carbon tetrachloride (CCl ). The portal pressure, liver and intestinal damage, plasma endotoxin, BT, and intestinal transit rate (ITR) of cirrhotic rats were determined. Fecal DNA fingerprints were obtained by ERIC-PCR. The expressions of tight junction proteins were evaluated by western blotting. RESULTS: Mosapride treatment to cirrhotic rats significantly reduced the plasma endotoxin level and incidence of BT, accompanied by increased ITR. Cirrhotic rats (including those treated with mosapride) suffered from BT exhibited significantly lower ITR than those who are free of BT. Pearson coefficient indicated a significant and negative correlation between the plasma endotoxin level and ITR. The genomic fingerprints of intestinal microbiota from the three groups fell into three distinctive clusters. In the mosapride-treated group, Shannon's index was remarkably increased compared to the model group. Significantly positive correlation was detected between Shannon's index and ITR. Mosapride did not improve hepatic and intestinal damages and ileal expressions of occludin and ZO-1. CONCLUSIONS: Mosapride significantly increases intestinal motility in cirrhotic rats, thus to recover the disordered intestinal microbiota, finally resulting in decreased plasma endotoxin and BT.
[Mh] Termos MeSH primário: Translocação Bacteriana/efeitos dos fármacos
Benzamidas/farmacologia
Tetracloreto de Carbono
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Endotoxemia/prevenção & controle
Fármacos Gastrointestinais/farmacologia
Microbioma Gastrointestinal/efeitos dos fármacos
Intestinos/efeitos dos fármacos
Cirrose Hepática Experimental/prevenção & controle
Fígado/efeitos dos fármacos
Morfolinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/sangue
Doença Hepática Induzida por Substâncias e Drogas/microbiologia
Doença Hepática Induzida por Substâncias e Drogas/patologia
DNA Bacteriano/genética
Endotoxemia/sangue
Endotoxemia/induzido quimicamente
Endotoxemia/microbiologia
Endotoxemia/patologia
Fezes/microbiologia
Motilidade Gastrointestinal/efeitos dos fármacos
Intestinos/metabolismo
Intestinos/microbiologia
Intestinos/patologia
Fígado/metabolismo
Fígado/microbiologia
Fígado/patologia
Cirrose Hepática Experimental/sangue
Cirrose Hepática Experimental/microbiologia
Cirrose Hepática Experimental/patologia
Masculino
Ratos Sprague-Dawley
Proteínas de Junções Íntimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (DNA, Bacterial); 0 (Gastrointestinal Agents); 0 (Morpholines); 0 (Tight Junction Proteins); CL2T97X0V0 (Carbon Tetrachloride); I8MFJ1C0BY (mosapride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4704-x


  8 / 19955 MEDLINE  
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[PMID]:28813225
[Au] Autor:Duggan CP; Jaksic T
[Ad] Endereço:From the Center for Advanced Intestinal Rehabilitation (C.P.D., T.J.), Division of Gastroenterology, Hepatology, and Nutrition (C.P.D.), and the Department of Surgery (T.J.), Boston Children's Hospital and Harvard Medical School, Boston.
[Ti] Título:Pediatric Intestinal Failure.
[So] Source:N Engl J Med;377(7):666-675, 2017 08 17.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Fármacos Gastrointestinais/uso terapêutico
Nutrição Parenteral
Síndrome do Intestino Curto/terapia
[Mh] Termos MeSH secundário: Criança
Nutrição Enteral
Motilidade Gastrointestinal
Seres Humanos
Enteropatias
Intestinos/fisiologia
Intestinos/cirurgia
Intestinos/transplante
Síndrome do Intestino Curto/tratamento farmacológico
Síndrome do Intestino Curto/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Gastrointestinal Agents)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMra1602650


  9 / 19955 MEDLINE  
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[PMID]:28774488
[Au] Autor:Ghodraty MR; Rokhtabnak F; Dehghan HR; Pournajafian A; Baghaee Vaji M; Koleini ZS; Porhomayon J; Nader ND
[Ad] Endereço:Iran University of Medical Sciences, Tehran, Iran.
[Ti] Título:Crystalloid versus colloid fluids for reduction of postoperative ileus after abdominal operation under combined general and epidural anesthesia.
[So] Source:Surgery;162(5):1055-1062, 2017 Nov.
[Is] ISSN:1532-7361
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The main objective of this study was to compare the effect of perioperative administration of crystalloid versus colloid solutions and its impact on reversal of ileus after resection with primary anastomosis of intestine. We hypothesized that inclusion of colloids will improve the return of intestinal motility. METHODS: In a double-blinded clinical trial, 91 the American Society of Anesthesiologists I to III patients undergoing abdominal operation for resection with anastomosis of small or large intestine were randomized to receive either lactated Ringer solution crystalloid group or 6% hydroxyethyl starch colloid group to replace intraoperative fluid loss (blood loss + third space). The time to resume normal intestinal motility was the primary end point and the prevalence of composite postoperative complications was the secondary end point. RESULTS: Average duration of ileus was 86.7 ± 23.6 hours in crystalloid group and it lasted 73.4 ± 20.8 hours in colloid group (P = .006). While there was no difference in the frequency of postoperative nausea and vomiting between the 2 groups (P = .3), the actual vomiting occurred less frequently in colloid group (P = .02). Serum concentrations of potassium ion decreased significantly in both groups, whereas the degree of potassium changes was more remarkable in colloid group compared with crystalloid group (P = .03). Postoperative ileus did not correlate with sex, age, and the duration of operation. Duration of hospital stay was similar between the 2 groups. CONCLUSION: We concluded that administration of colloids as a part of perioperative fluid management improves intestinal motility and shortens the duration of ileus after gastrointestinal operations. This may improve the tolerance for enteral feeding and reduce ileus-related symptoms.
[Mh] Termos MeSH primário: Anastomose Cirúrgica/efeitos adversos
Motilidade Gastrointestinal/efeitos dos fármacos
Trato Gastrointestinal/cirurgia
Íleus/prevenção & controle
Soluções Isotônicas/administração & dosagem
Soluções para Reidratação/administração & dosagem
[Mh] Termos MeSH secundário: Abdome/cirurgia
Adulto
Idoso
Anestesia Epidural
Anestesia Geral
Coloides/administração & dosagem
Coloides/farmacologia
Procedimentos Cirúrgicos do Sistema Digestório/efeitos adversos
Método Duplo-Cego
Feminino
Hidratação/métodos
Trato Gastrointestinal/efeitos dos fármacos
Seres Humanos
Derivados de Hidroxietil Amido/administração & dosagem
Derivados de Hidroxietil Amido/farmacologia
Íleus/etiologia
Intestinos/efeitos dos fármacos
Intestinos/cirurgia
Soluções Isotônicas/farmacologia
Laparotomia/efeitos adversos
Masculino
Meia-Idade
Substitutos do Plasma/administração & dosagem
Substitutos do Plasma/farmacologia
Soluções para Reidratação/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Colloids); 0 (Hydroxyethyl Starch Derivatives); 0 (Isotonic Solutions); 0 (Plasma Substitutes); 0 (Rehydration Solutions); 0 (crystalloid solutions); 8022-63-7 (Ringer's lactate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE


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[PMID]:28736498
[Au] Autor:Raffort J; Lareyre F; Massalou D; Fénichel P; Panaïa-Ferrari P; Chinetti G
[Ad] Endereço:Clinical Chemistry Laboratory, University Hospital of Nice, Nice, France.
[Ti] Título:Insights on glicentin, a promising peptide of the proglucagon family.
[So] Source:Biochem Med (Zagreb);27(2):308-324, 2017 Jun 15.
[Is] ISSN:1330-0962
[Cp] País de publicação:Croatia
[La] Idioma:eng
[Ab] Resumo:Glicentin is a proglucagon-derived peptide mainly produced in the L-intestinal cells. While the roles of other members of the proglucagon family including glucagon-like peptide 1, glucagon-like peptide 2 and oxyntomodulin has been well studied, the functions and variation of glicentin in human are not fully understood. Experimental and clinical studies have highlighted its role in both intestinal physiology and glucose metabolism, pointing to its potential interest in a wide range of pathological states including gastrointestinal and metabolic disorders. Due to its structure presenting many similarities with the other proglucagon-derived peptides, its measurement is technically challenging. The recent commercialization of specific detection methods has offered new opportunities to go further in the understanding of glicentin physiology. Here we summarize the current knowledge on glicentin biogenesis and physiological roles. In the limelight of clinical studies investigating glicentin variation in human, we discuss future directions for potential applications in clinical practice.
[Mh] Termos MeSH primário: Ácido Gástrico/secreção
Motilidade Gastrointestinal/fisiologia
Glicentina/fisiologia
Intestinos/fisiologia
Proglucagon/fisiologia
[Mh] Termos MeSH secundário: Animais
Expressão Gênica
Glicentina/biossíntese
Glicentina/genética
Glucose/metabolismo
Seres Humanos
Intestinos/metabolismo
Proglucagon/biossíntese
Proglucagon/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
55963-74-1 (Proglucagon); 71567-77-6 (Glicentin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.11613/BM.2017.034



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