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[PMID]: 26946164 [Au] Autor: Júnior MF; Batista SA; Barbuto RC; Gomes AD; Queiroz DM; Araújo ID; Caliari MV [Ad] Endereço: Department of General Pathology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. [Ti] Título: CagA-positive Helicobacter pylori strain containing three EPIYA C phosphorylation sites produces increase of G cell and decrease of D cell in experimentally infected gerbils (Meriones unguiculatus). [So] Source: Adv Med Sci;61(2):231-236, 2016 Sep. [Is] ISSN: 1898-4002 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: PURPOSE: Human infection by Helicobacter pylori is associated with an increase in the number of gastrin-producing G cells and a concomitant decrease of somatostatin-producing D cells. However, to our knowledge, changes in G and D cell numbers in response to infection with H. pylori CagA-positive strains containing different number of EPIYA-C phosphorylation sites have not been analyzed to date. Therefore, the aim of this study was to perform a quantitative analysis of the number of G and D cells in Mongolian gerbils challenged with H. pylori strains with different numbers of EPIYA-C motifs. MATERIALS AND METHODS: Mongolian gerbils were inoculated with isogenic H. pylori strains containing one to three phosphorylation sites. Mucosal fragments were evaluated by morphometry and immunohistochemistry using primary polyclonal rabbit anti-gastrin and anti-somatostatin antibodies. Positive cells were counted using an image analyzer. RESULTS: Forty-five days after infection, there was a decrease in the number of D cells and an increase in the G/D cell ratio in the group with three EPIYA-C. Six months after infection, there was a progressive and significant increase in the number of G cells and in the G/D cell ratio, with a concomitant decrease in the number of D cells, especially in the three EPIYA-C group. CONCLUSIONS: CagA-positive H. pylori strains containing a large number of EPIYA-C phosphorylation sites induce a decrease in D cell number and an increase in G cell number and G/D ratio, which were correlated with the number of inflammatory cells of the lamina propria. [Mh] Termos MeSH primário: Antígenos de Bactérias/química Antígenos de Bactérias/metabolismo Proteínas de Bactérias/química Proteínas de Bactérias/metabolismo Células Secretoras de Gastrina/microbiologia Células Secretoras de Gastrina/patologia Helicobacter pylori/fisiologia [Mh] Termos MeSH secundário: Motivos de Aminoácidos Animais Contagem de Células Feminino Gerbillinae Imuno-Histoquímica Membrana Mucosa/microbiologia Membrana Mucosa/patologia Fosforilação Antro Pilórico/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antigens, Bacterial); 0 (Bacterial Proteins); 0 (cagA protein, Helicobacter pylori) [Em] Mês de entrada: 1702 [Cu] Atualização por classe: 170227 [Lr] Data última revisão: 170227 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160307 [St] Status: MEDLINE

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[PMID]: 26879837 [Au] Autor: Craven CJ [Ad] Endereço: Queensland University of Technology, Brisbane, Australia. cj.craven@qut.edu.au. [Ti] Título: A hypothesis of couplet molecules and couplet cells in gastric function and an association with Helicobacter pylori. [So] Source: BMC Gastroenterol;16:16, 2016 Feb 16. [Is] ISSN: 1471-230X [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: BACKGROUND: Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL) cells, are two of the hormones that regulate gastric activity. DISCUSSION: It is proposed that the G-cells and the ECL cells are coupled by the couplet molecules gastrin and histamine and by a prior asymmetrical cell division. The gastrin (from G-cells) stimulates the ECL cells to produce and secrete histamine while, in a reciprocal way, this histamine (from ECL cells), stimulates the G-cells to produce and secrete gastrin. These molecules would also stimulate cell division - the gastrin would stimulate cell division of ECL cells while histamine would stimulate that of G-cells. A chemical complex of gastrin and histamine is postulated as is also the asymmetric cell divisions of precursor cells to produce the coupled G-cells and ECL cells. CONCLUSION: There is sufficient evidence to support the feasibility of the model in general, but more direct experimental evidence is required to validate the model as applied here to gastric function. [Mh] Termos MeSH primário: Celulas Tipo Enterocromafim/metabolismo Células Secretoras de Gastrina/metabolismo Helicobacter pylori/metabolismo Modelos Biológicos Estômago/citologia [Mh] Termos MeSH secundário: Animais Divisão Celular/fisiologia Digestão/fisiologia Gastrinas/secreção Liberação de Histamina/fisiologia Seres Humanos Ratos [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Gastrins) [Em] Mês de entrada: 1610 [Cu] Atualização por classe: 170220 [Lr] Data última revisão: 170220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160217 [St] Status: MEDLINE [do] DOI: 10.1186/s12876-016-0429-0

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[PMID]: 24713247 [Au] Autor: Chen G; Huang S [Ad] Endereço: E-mail: guangyongchen@yahoo.com. [Ti] Título: [Autoimmune metaplastic atrophic gastritis, G cell hyperplasia and neuroendocrine tumor of stomach]. [So] Source: Zhonghua Bing Li Xue Za Zhi;43(1):34-5, 2014 Jan. [Is] ISSN: 0529-5807 [Cp] País de publicação: China [La] Idioma: chi [Mh] Termos MeSH primário: Doenças Autoimunes/patologia Células Secretoras de Gastrina/patologia Gastrite Atrófica/patologia Tumores Neuroendócrinos/patologia Neoplasias Gástricas/patologia Estômago/patologia [Mh] Termos MeSH secundário: Doenças Autoimunes/metabolismo Doenças Autoimunes/cirurgia Cromogranina A/metabolismo Feminino Gastrectomia Mucosa Gástrica/patologia Células Secretoras de Gastrina/metabolismo Gastrinas/metabolismo Gastrite Atrófica/metabolismo Gastrite Atrófica/cirurgia Seres Humanos Hiperplasia Meia-Idade Mucina-6/metabolismo Tumores Neuroendócrinos/metabolismo Tumores Neuroendócrinos/cirurgia Estômago/cirurgia Neoplasias Gástricas/metabolismo Neoplasias Gástricas/cirurgia Sinaptofisina/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Chromogranin A); 0 (Gastrins); 0 (MUC6 protein, human); 0 (Mucin-6); 0 (Synaptophysin) [Em] Mês de entrada: 1409 [Cu] Atualização por classe: 160818 [Lr] Data última revisão: 160818 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140410 [St] Status: MEDLINE

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[PMID]: 22886351 [Au] Autor: Boj-Carceller D [Ad] Endereço: Endocrinology and Nutrition Unit, Hospital Miguel Servet, Paseo Isabel La Católica, 1-3, 50009, Zaragoza, Spain. dianna_bc@hotmail.com [Ti] Título: Proton pump inhibitors: impact on glucose metabolism. [So] Source: Endocrine;43(1):22-32, 2013 Feb. [Is] ISSN: 1559-0100 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Diabetes mellitus is a complex chronic disease associated with an absolute insulin deficiency in type 1 diabetes (T1D) and a progressive deterioration of ß-cell function in type 2 diabetes (T2D). T2D pathophysiology has numerous defects including incretin deficiency/resistance. Gastrin has demonstrated to be an islet growth factor (like glucagon-like peptide-1, epidermal growth factor, transforming growth factor-α,…) and be able to restore a functional ß-cell mass in diabetic animals. This hormone is likely to stimulate insulin secretion during an ordinary protein-rich meal, this is, to have an incretin-like effect. Proton pump inhibitors (PPIs) can raise serum gastrin concentration significantly and therefore, affect to glucose metabolism through promoting ß-cell regeneration/expansion and also enhancing insulin secretion. The present paper aims to review studies concerning the effect of PPIs on glucose metabolism. Several research groups have recently explored the potential role of this class of drugs on glycemic control, mainly in T2D. The results show antidiabetic properties for the PPIs with a global glucose-lowering power around 0.6-0.7 % points of HbA1c, but the level of evidence for the available literature is still not high. If these data start to become demonstrated in the ongoing clinical trials, PPIs could become a new antidiabetic agent with a good and safe profile for T2D and even useful for T1D, particularly in the area of islet transplantation to preserve ß-cell mass. [Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico Células Secretoras de Gastrina/efeitos dos fármacos Gastrinas/secreção Fármacos Gastrointestinais/uso terapêutico Hipoglicemiantes/uso terapêutico Células Secretoras de Insulina/efeitos dos fármacos Inibidores da Bomba de Prótons/uso terapêutico [Mh] Termos MeSH secundário: Animais Diabetes Mellitus Tipo 1/sangue Diabetes Mellitus Tipo 1/tratamento farmacológico Diabetes Mellitus Tipo 1/metabolismo Diabetes Mellitus Tipo 2/sangue Diabetes Mellitus Tipo 2/metabolismo Celulas Tipo Enterocromafim/efeitos dos fármacos Celulas Tipo Enterocromafim/metabolismo Celulas Tipo Enterocromafim/secreção Esvaziamento Gástrico/efeitos dos fármacos Células Secretoras de Gastrina/metabolismo Células Secretoras de Gastrina/secreção Gastrinas/sangue Fármacos Gastrointestinais/farmacologia Glucose/metabolismo Seres Humanos Hipoglicemia/prevenção & controle Hipoglicemiantes/farmacologia Insulina/secreção Células Secretoras de Insulina/metabolismo Células Secretoras de Insulina/secreção Células Parietais Gástricas/efeitos dos fármacos Células Parietais Gástricas/metabolismo Células Parietais Gástricas/secreção Inibidores da Bomba de Prótons/farmacologia Somatostatina/metabolismo Somatostatina/secreção Células Secretoras de Somatostatina/efeitos dos fármacos Células Secretoras de Somatostatina/metabolismo Células Secretoras de Somatostatina/secreção [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Gastrins); 0 (Gastrointestinal Agents); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Proton Pump Inhibitors); 51110-01-1 (Somatostatin); IY9XDZ35W2 (Glucose) [Em] Mês de entrada: 1306 [Cu] Atualização por classe: 171107 [Lr] Data última revisão: 171107 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 120814 [St] Status: MEDLINE [do] DOI: 10.1007/s12020-012-9755-3

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[PMID]: 22766853 [Au] Autor: Veniaminova NA; Hayes MM; Varney JM; Merchant JL [Ad] Endereço: Division of Gastroenterology, Department of Internal Medicine, University of Michigan, Ann Arbor, 48109-2200, USA. [Ti] Título: Conditional deletion of menin results in antral G cell hyperplasia and hypergastrinemia. [So] Source: Am J Physiol Gastrointest Liver Physiol;303(6):G752-64, 2012 Sep 15. [Is] ISSN: 1522-1547 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Antral gastrin is the hormone known to stimulate acid secretion and proliferation of the gastric corpus epithelium. Patients with mutations in the multiple endocrine neoplasia type 1 (MEN1) locus, which encodes the protein menin, develop pituitary hyperplasia, insulinomas, and gastrinomas in the duodenum. We previously hypothesized that loss of menin leads to derepression of the gastrin gene and hypergastrinemia. Indeed, we show that menin represses JunD induction of gastrin in vitro. Therefore, we examined whether conditional deletion of Men1 (Villin-Cre and Lgr5-EGFP-IRES-CreERT2), with subsequent loss of menin from the gastrointestinal epithelium, increases gastrin expression. We found that epithelium-specific deletion of Men1 using Villin-Cre increased plasma gastrin, antral G cell numbers, and gastrin expression in the antrum, but not the duodenum. Moreover, the mice were hypochlorhydric by 12 mo of age, and gastric somatostatin mRNA levels were reduced. However, duodenal mRNA levels of the cyclin-dependent kinase inhibitor p27(Kip1) were decreased, and cell proliferation determined by Ki67 staining was increased. About 11% of the menin-deficient mice developed antral tumors that were negative for gastrin; however, gastrinomas were not observed, even at 12 mo of age. No gastrinomas were observed with conditional deletion of Men1 in the Lgr5 stem cells 5 mo after Cre induction. In summary, epithelium-specific deletion of the Men1 locus resulted in hypergastrinemia due to antral G cell hyperplasia and a hyperproliferative epithelium, but no gastrinomas. This result suggests that additional mutations in gene targets other than the Men1 locus are required to produce gastrin-secreting tumors. [Mh] Termos MeSH primário: Células Secretoras de Gastrina/fisiologia Hiperplasia/patologia Proteínas Proto-Oncogênicas/metabolismo Antro Pilórico/citologia [Mh] Termos MeSH secundário: Animais Trato Gastrointestinal/metabolismo Deleção de Genes Regulação da Expressão Gênica/fisiologia Genótipo Hiperplasia/genética Hiperplasia/metabolismo Camundongos Camundongos Knockout Proteínas Proto-Oncogênicas/genética Somatostatina/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL [Nm] Nome de substância: 0 (Men1 protein, mouse); 0 (Proto-Oncogene Proteins); 51110-01-1 (Somatostatin) [Em] Mês de entrada: 1211 [Cu] Atualização por classe: 170516 [Lr] Data última revisão: 170516 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 120707 [St] Status: MEDLINE [do] DOI: 10.1152/ajpgi.00109.2012

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[PMID]: 22595991 [Au] Autor: Bitziou E; Patel BA [Ad] Endereço: Department of Chemistry, University of Warwick, Coventry, United Kingdom. [Ti] Título: Simultaneous detection of gastric acid and histamine release to unravel the regulation of acid secretion from the guinea pig stomach. [So] Source: Am J Physiol Gastrointest Liver Physiol;303(3):G396-403, 2012 Aug 01. [Is] ISSN: 1522-1547 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Gastric acid secretion is regulated by three primary components that activate the parietal cell: histamine, gastrin, and acetylcholine (ACh). Although much is known about these regulatory components individually, little is known on the interplay of these multiple activators and the degree of regulation they pose on the gastric acid secretion mechanism. We utilized a novel dual-sensing approach, where an iridium oxide sensor was used to monitor pH and a boron-doped diamond electrode was used for the detection of histamine from in vitro guinea pig stomach mucosal sections. Under basal conditions, gastrin was shown to be the main regulatory component of the total acid secretion and directly activated the parietal cell rather than by mediating gastric acid secretion through the release of histamine from the enterochromaffin-like cell, although both pathways were active. Under stimulated conditions with ACh, the gastrin and histamine components of the total acid secretion were not altered compared with levels observed under basal conditions, suggestive that ACh had no direct effect on the enterochromaffin-like cell and G cell. These data identify a new unique approach to investigate the regulation pathways active during acid secretion and the degree that they are utilized to drive total gastric acid secretion. The findings of this study will enhance our understanding on how these signaling mechanisms vary under pathophysiology or therapeutic management. [Mh] Termos MeSH primário: Ácido Gástrico/secreção Liberação de Histamina/efeitos dos fármacos Células Parietais Gástricas/secreção Estômago/fisiologia [Mh] Termos MeSH secundário: Acetilcolina/farmacologia Animais Celulas Tipo Enterocromafim/secreção Células Secretoras de Gastrina/secreção Gastrinas Cobaias Histamina/farmacologia Concentração de Íons de Hidrogênio Técnicas In Vitro Masculino Células Parietais Gástricas/efeitos dos fármacos Estômago/efeitos dos fármacos [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Gastrins); 820484N8I3 (Histamine); N9YNS0M02X (Acetylcholine) [Em] Mês de entrada: 1210 [Cu] Atualização por classe: 141120 [Lr] Data última revisão: 141120 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 120519 [St] Status: MEDLINE [do] DOI: 10.1152/ajpgi.00548.2011

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[PMID]: 22561140 [Au] Autor: Erlandsen SE; Qvigstad G; Fossmark R; Bakke I; Chen D; Sandvik AK [Ad] Endereço: Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Pb 8905, N-7491 Trondheim, Norway. sten.e.erlandsen@ntnu.no [Ti] Título: Regulated endocrine-specific protein 18 (RESP18) is localized to and regulated in A-like cells and G-cells in rat stomach. [So] Source: Regul Pept;177(1-3):53-9, 2012 Aug 20. [Is] ISSN: 1873-1686 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: The regulated endocrine-specific protein 18 (RESP18) has previously been localized to different endocrine cells and neurons, in particular the pituitary gland and hypothalamus. It is found in the lumen of the endoplasmic reticulum and is degraded at the post-ER pre-Golgi compartment, and a role in processing of secreted peptides has been hypothesized. The present study examines localization of RESP18 in the gastrointestinal mucosa of rats by immunohistochemistry, and expression and regulation in response to hypergastrinemia induced by acid inhibition (pantoprazole), gastrin antagonism (YF476), fasting-refeeding and octreotide by mRNA measurements. RESP18 was mainly found in the gastric mucosa, but could also be detected in a few, scattered cells in the lower small intestine and in colon. In the antral mucosa, all RESP18 immunoreactivity was localized to ghrelin-producing A-like cells and gastrin-producing G-cells. In the corpus mucosa, a significant fraction, but not all of the RESP18 immunoreactive cells, were A-like cells. In both antrum and corpus, Resp18 mRNA seemed to vary similarly with the activation of the A-like cells, and in the antrum also with stimulation of the G-cells. This study demonstrates, for the first time, the localization of RESP18 to specific neuroendocrine cells of the gastrointestinal mucosa and that it seems to be regulated synchronously with the peptides secreted from these cells. This suggests that Resp18 may indeed have a functional role in the synthesis or storage of these gastrointestinal peptides. [Mh] Termos MeSH primário: Células Secretoras de Gastrina/metabolismo Regulação da Expressão Gênica Proteínas do Tecido Nervoso/metabolismo Estômago/metabolismo [Mh] Termos MeSH secundário: 2-Piridinilmetilsulfinilbenzimidazóis/farmacologia Animais Benzodiazepinonas/farmacologia Jejum/metabolismo Comportamento Alimentar Gastrinas/antagonistas & inibidores Gastrinas/farmacologia Grelina/metabolismo Imuno-Histoquímica Intestino Delgado/metabolismo Proteínas do Tecido Nervoso/genética Octreotida/administração & dosagem Octreotida/farmacologia Compostos de Fenilureia/farmacologia Antro Pilórico/fisiologia RNA Mensageiro/análise RNA Mensageiro/metabolismo Ratos Ratos Sprague-Dawley Estômago/citologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (2-Pyridinylmethylsulfinylbenzimidazoles); 0 (Benzodiazepinones); 0 (Gastrins); 0 (Ghrelin); 0 (Nerve Tissue Proteins); 0 (Phenylurea Compounds); 0 (RNA, Messenger); 0 (YF 476); 0 (regulated endocrine secretory protein 18); D8TST4O562 (pantoprazole); RWM8CCW8GP (Octreotide) [Em] Mês de entrada: 1210 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 120508 [St] Status: MEDLINE [do] DOI: 10.1016/j.regpep.2012.04.008

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[PMID]: 21790222 [Au] Autor: Pirzadeh A; Doustmohammadian N; Khoshbaten M; Doustmohammadion S [Ad] Endereço: Otorhinolaryngology Dept, Ardebil University of Medical Sciences, Ardebil, Iran. [Ti] Título: Is there any association between Helicobacter Pylori infection and laryngeal carcinoma? [So] Source: Asian Pac J Cancer Prev;12(4):897-900, 2011. [Is] ISSN: 2476-762X [Cp] País de publicação: Thailand [La] Idioma: eng [Ab] Resumo: OBJECTIVE: To investigate the possible role of Helicobacter pylori as a cause of squamous cell carcinoma of larynx in a case-control study in an otolaryngology ward at an academic university. SUBJECTS AND METHODS: A total of 65 patients with laryngeal cancer and 65 matched cancer-free controls underwent esophagogastroduodenoscopy and biopsy of antral and body regions of the stomach for evaluation of Helicobacter pylori infection. RESULTS: The proportion of subjects with a positive rapid urease test for gastric infection was similar between the two groups (49.2 % in cases vs. 40% in controls). However, a positive rapid urease test for body was less frequently seen in patients with laryngeal cancer whereas a positive rapid urease test for antrum was significantly higher (P=0.04). CONCLUSION: Our study failed to show Helicobacter pylori as one of the etiologies of laryngeal cancer. However, it supported the hypothesis that colonization of Helicobacter pylori only in the gastric body might have a protective effect against laryngeal cancer with decreasing gastric acid while antral Helicobacter pylori, increasing gastric acid due to G cell hyperplasia, may be a predisposing factor for laryngeal cancer, with acid reflux as a possible underlying etiology. [Mh] Termos MeSH primário: Carcinoma de Células Escamosas/microbiologia Carcinoma de Células Escamosas/patologia Infecções por Helicobacter/patologia Helicobacter pylori/isolamento & purificação Neoplasias Laríngeas/microbiologia Neoplasias Laríngeas/patologia [Mh] Termos MeSH secundário: Consumo de Bebidas Alcoólicas/efeitos adversos Biópsia/métodos Carcinoma de Células Escamosas/etiologia Estudos de Casos e Controles Endoscopia do Sistema Digestório/métodos Feminino Ácido Gástrico/secreção Células Secretoras de Gastrina/microbiologia Células Secretoras de Gastrina/patologia Refluxo Gastroesofágico/microbiologia Refluxo Gastroesofágico/patologia Infecções por Helicobacter/microbiologia Seres Humanos Hiperplasia/microbiologia Hiperplasia/patologia Neoplasias Laríngeas/etiologia Masculino Meia-Idade Fumar/efeitos adversos Urease/análise Urease/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: EC 3.5.1.5 (Urease) [Em] Mês de entrada: 1207 [Cu] Atualização por classe: 170308 [Lr] Data última revisão: 170308 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 110728 [St] Status: MEDLINE

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[PMID]: 21691871 [Au] Autor: Niederle MB; Niederle B [Ad] Endereço: Sektion Chirurgische Endokrinologie, Klinische Abteilung für Allgemeinchirurgie, Universitätsklinik für Chirurgie, Medizinische Universität Wien, Währinger Gürtel 18-20, Vienna, Austria. martin.niederle@meduniwien.ac.at [Ti] Título: [Gastric neuroendocrine tumors. Endoscopic and surgical treatment]. [Ti] Título: Neuroendokrine Tumoren des Magens. Endoskopische und chirurgische Therapie.. [So] Source: Chirurg;82(7):574-82, 2011 Jul. [Is] ISSN: 1433-0385 [Cp] País de publicação: Germany [La] Idioma: ger [Ab] Resumo: Neuroendocrine tumors (NETs) of the stomach are the most frequent among all neuroendocrine neoplasms in the digestive tract. The diagnosis and classification are complicated by the fact that these tumors have to be categorized not only by common staging and grading but also according to their pathophysiological background (types). The types differ in their biological behaviour (aggressiveness) which influences therapeutic concepts. This article explains and summarizes the etiology and classification of gastric NETs and offers a precise concept for diagnosis and treatment to improve clinical outcome. [Mh] Termos MeSH primário: Gastroscopia Tumores Neuroendócrinos/cirurgia Neoplasias Gástricas/cirurgia [Mh] Termos MeSH secundário: Células Enterocromafins/patologia Celulas Tipo Enterocromafim/patologia Mucosa Gástrica/patologia Células Secretoras de Gastrina/patologia Seres Humanos Gradação de Tumores Invasividade Neoplásica Estadiamento de Neoplasias Tumores Neuroendócrinos/classificação Tumores Neuroendócrinos/diagnóstico Tumores Neuroendócrinos/patologia Prognóstico Células Secretoras de Somatostatina/patologia Estômago/patologia Neoplasias Gástricas/classificação Neoplasias Gástricas/diagnóstico Neoplasias Gástricas/patologia [Pt] Tipo de publicação: ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW [Em] Mês de entrada: 1201 [Cu] Atualização por classe: 170916 [Lr] Data última revisão: 170916 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 110622 [St] Status: MEDLINE [do] DOI: 10.1007/s00104-011-2068-x

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[PMID]: 21521750 [Au] Autor: Iwakura H; Ariyasu H; Hosoda H; Yamada G; Hosoda K; Nakao K; Kangawa K; Akamizu T [Ad] Endereço: Ghrelin Research Project, Translational Research Center, Kyoto University Hospital, Kyoto, Japan. hiwaku@kuhp.kyoto-u.ac.jp [Ti] Título: Oxytocin and dopamine stimulate ghrelin secretion by the ghrelin-producing cell line, MGN3-1 in vitro. [So] Source: Endocrinology;152(7):2619-25, 2011 Jul. [Is] ISSN: 1945-7170 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: To understand the physiological role of ghrelin, it is crucial to study both the actions of ghrelin and the regulation of ghrelin secretion. Although ghrelin actions have been extensively revealed, the direct factors regulating ghrelin secretion by ghrelin-producing cells (X/A-like cells), however, is not fully understood. In this study, we examined the effects of peptide hormones and neurotransmitters on in vitro ghrelin secretion by the recently developed ghrelin-producing cell line MGN3-1. Oxytocin and vasopressin significantly stimulated ghrelin secretion by MGN3-1 cells. Because MGN3-1 cells express only oxytocin receptor mRNA, not vasopressin receptor mRNA, oxytocin is the likely regulator, with the effect of vasopressin mediated by a cross-reaction. We also discovered that dopamine stimulates ghrelin secretion from MGN3-1 cells in a similar manner to the previously known ghrelin stimulators, epinephrine and norepinephrine. MGN3-1 cells expressed mRNA encoding dopamine receptors D1a and D2. The dopamine receptor D1 agonist fenoldopam stimulated ghrelin secretion, whereas the D2, D3 agonist bromocriptine did not. Furthermore, the D1 receptor antagonist SKF83566 attenuated the stimulatory effect of dopamine. These results indicate that the stimulatory effect of dopamine on ghrelin secretion is mediated by the D1a receptor. In conclusion, we identified two direct regulators of ghrelin, oxytocin and dopamine. These findings will provide new direction for further studies seeking to further understand the regulation of ghrelin secretion, which will in turn lead to greater understanding of the physiological role of ghrelin. [Mh] Termos MeSH primário: Dopamina/metabolismo Células Secretoras de Gastrina/secreção Grelina/secreção Ocitocina/metabolismo Receptores de Dopamina D1/metabolismo Receptores de Ocitocina/metabolismo [Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos beta 1/farmacologia Animais Linhagem Celular Agonistas de Dopamina/farmacologia Antagonistas de Dopamina/farmacologia Epinefrina/antagonistas & inibidores Epinefrina/metabolismo Células Secretoras de Gastrina/efeitos dos fármacos Células Secretoras de Gastrina/metabolismo Regulação da Expressão Gênica Grelina/genética Antagonistas de Hormônios/farmacologia Camundongos Norepinefrina/antagonistas & inibidores Norepinefrina/metabolismo Ocitocina/antagonistas & inibidores RNA Mensageiro/metabolismo Receptores Adrenérgicos beta 1/genética Receptores Adrenérgicos beta 1/metabolismo Receptores de Dopamina D1/agonistas Receptores de Dopamina D1/antagonistas & inibidores Receptores de Dopamina D1/genética Receptores de Ocitocina/antagonistas & inibidores Receptores de Ocitocina/genética Reação em Cadeia da Polimerase Via Transcriptase Reversa [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Adrenergic beta-1 Receptor Antagonists); 0 (Dopamine Agonists); 0 (Dopamine Antagonists); 0 (Ghrelin); 0 (Hormone Antagonists); 0 (RNA, Messenger); 0 (Receptors, Adrenergic, beta-1); 0 (Receptors, Dopamine D1); 0 (Receptors, Oxytocin); 0 (dopamine D1A receptor); 50-56-6 (Oxytocin); VTD58H1Z2X (Dopamine); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine) [Em] Mês de entrada: 1109 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 110428 [St] Status: MEDLINE [do] DOI: 10.1210/en.2010-1455

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