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Pesquisa : D12.644.400.250 [Categoria DeCS]
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  1 / 2696 MEDLINE  
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[PMID]:28470686
[Au] Autor:Sideras K; Biermann K; Yap K; Mancham S; Boor PPC; Hansen BE; Stoop HJA; Peppelenbosch MP; van Eijck CH; Sleijfer S; Kwekkeboom J; Bruno MJ
[Ad] Endereço:Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center, Rotterdam, The Netherlands.
[Ti] Título:Tumor cell expression of immune inhibitory molecules and tumor-infiltrating lymphocyte count predict cancer-specific survival in pancreatic and ampullary cancer.
[So] Source:Int J Cancer;141(3):572-582, 2017 08 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Understanding the mechanisms of immune resistance in pancreatic and ampullary cancers is crucial for the development of suitable biomarkers and effective immunotherapeutics. Our aim was to examine the expression of the immune inhibiting molecules PD-L1, Galectin-9, HVEM, IDO and HLA-G, as well as CD8+ and FoxP3+ tumor infiltrating lymphocytes (TIL), in pancreatic and ampullary cancers, and to relate their individual, as well as their combined expression, to cancer survival. Tumor tissue from 224 patients with resected pancreatic (n = 148) and ampullary (n = 76) cancer was used to construct tissue-microarrays. Expression of immune inhibitory molecules and TIL was examined by immunohistochemistry. We show that immune inhibitory molecules are prevalently expressed. Moreover, high tumor expression of PD-L1 (p = 0.002), Gal-9 (p = 0.003), HVEM (p = 0.001), IDO (p = 0.049), HLA-G (p = 0.004) and high CD8/FoxP3 TIL ratio (p = 0.006) were associated with improved cancer-specific survival. All immune biomarkers, with the exception of IDO, were individually predictive of cancer-specific survival when adjusted for clinicopathologic characteristics. For every additional immune biomarker present survival was almost two-fold prolonged (HR 0.57 95%CI 0.47-0.69, p < 0.0001). When patients with pancreatic and ampullary cancer were analyzed separately the results were similar. We conclude that pancreas and ampullary cancers are rich in expression of immune-inhibitory molecules. These molecules can be targets for future immunotherapeutics, as well as form powerful immunological biomarkers. We propose that such immune biomarker panels be included in future prospective immunotherapy trials.
[Mh] Termos MeSH primário: Antígeno B7-H1/metabolismo
Neoplasias do Ducto Colédoco/mortalidade
Galanina/metabolismo
Antígenos HLA-G/metabolismo
Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo
Linfócitos do Interstício Tumoral/imunologia
Neoplasias Pancreáticas/mortalidade
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Ampola Hepatopancreática/imunologia
Ampola Hepatopancreática/metabolismo
Biomarcadores Tumorais/metabolismo
Neoplasias do Ducto Colédoco/imunologia
Neoplasias do Ducto Colédoco/metabolismo
Feminino
Seres Humanos
Linfócitos do Interstício Tumoral/metabolismo
Linfócitos do Interstício Tumoral/patologia
Masculino
Meia-Idade
Neoplasias Pancreáticas/imunologia
Neoplasias Pancreáticas/metabolismo
Prognóstico
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (Biomarkers, Tumor); 0 (CD274 protein, human); 0 (GAL protein, human); 0 (HLA-G Antigens); 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (TNFRSF14 protein, human); 88813-36-9 (Galanin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30760


  2 / 2696 MEDLINE  
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[PMID]:28648499
[Au] Autor:Chen S; Reichert S; Singh C; Oikonomou G; Rihel J; Prober DA
[Ad] Endereço:Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
[Ti] Título:Light-Dependent Regulation of Sleep and Wake States by Prokineticin 2 in Zebrafish.
[So] Source:Neuron;95(1):153-168.e6, 2017 Jul 05.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Light affects sleep and wake behaviors by providing an indirect cue that entrains circadian rhythms and also by inducing a direct and rapid regulation of behavior. While circadian entrainment by light is well characterized at the molecular level, mechanisms that underlie the direct effect of light on behavior are largely unknown. In zebrafish, a diurnal vertebrate, we found that both overexpression and mutation of the neuropeptide prokineticin 2 (Prok2) affect sleep and wake behaviors in a light-dependent but circadian-independent manner. In light, Prok2 overexpression increases sleep and induces expression of galanin (galn), a hypothalamic sleep-inducing peptide. We also found that light-dependent, Prok2-induced sedation requires prokineticin receptor 2 (prokr2) and is strongly suppressed in galn mutants. These results suggest that Prok2 antagonizes the direct wake-promoting effect of light in zebrafish, in part through the induction of galn expression in the hypothalamus.
[Mh] Termos MeSH primário: Ritmo Circadiano/genética
Luz
Neuropeptídeos/genética
Sono/genética
Vigília/genética
Proteínas de Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Galanina/genética
Galanina/metabolismo
Hipotálamo/metabolismo
Mutação
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/metabolismo
Receptores de Peptídeos/genética
Receptores de Peptídeos/metabolismo
Peixe-Zebra
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Prokr2 protein, zebrafish); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Peptide); 0 (Zebrafish Proteins); 0 (prokineticin 2 protein, zebrafish); 88813-36-9 (Galanin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE


  3 / 2696 MEDLINE  
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[PMID]:28634715
[Au] Autor:Yao S; Guo Y; Dong SS; Hao RH; Chen XF; Chen YX; Chen JB; Tian Q; Deng HW; Yang TL
[Ad] Endereço:Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, People's Republic of China.
[Ti] Título:Regulatory element-based prediction identifies new susceptibility regulatory variants for osteoporosis.
[So] Source:Hum Genet;136(8):963-974, 2017 Aug.
[Is] ISSN:1432-1203
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Despite genome-wide association studies (GWASs) have identified many susceptibility genes for osteoporosis, it still leaves a large part of missing heritability to be discovered. Integrating regulatory information and GWASs could offer new insights into the biological link between the susceptibility SNPs and osteoporosis. We generated five machine learning classifiers with osteoporosis-associated variants and regulatory features data. We gained the optimal classifier and predicted genome-wide SNPs to discover susceptibility regulatory variants. We further utilized Genetic Factors for Osteoporosis Consortium (GEFOS) and three in-house GWASs samples to validate the associations for predicted positive SNPs. The random forest classifier performed best among all machine learning methods with the F1 score of 0.8871. Using the optimized model, we predicted 37,584 candidate SNPs for osteoporosis. According to the meta-analysis results, a list of regulatory variants was significantly associated with osteoporosis after multiple testing corrections and contributed to the expression of known osteoporosis-associated protein-coding genes. In summary, combining GWASs and regulatory elements through machine learning could provide additional information for understanding the mechanism of osteoporosis. The regulatory variants we predicted will provide novel targets for etiology research and treatment of osteoporosis.
[Mh] Termos MeSH primário: Osteoporose/genética
Polimorfismo de Nucleotídeo Único
Sequências Reguladoras de Ácido Nucleico
[Mh] Termos MeSH secundário: Algoritmos
Linhagem Celular
Galanina/genética
Galanina/metabolismo
Frequência do Gene
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Modelos Genéticos
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
Separase/genética
Separase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GAL protein, human); 88813-36-9 (Galanin); EC 3.4.22.49 (ESPL1 protein, human); EC 3.4.22.49 (Separase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1007/s00439-017-1825-4


  4 / 2696 MEDLINE  
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[PMID]:28539422
[Au] Autor:Qualls-Creekmore E; Yu S; Francois M; Hoang J; Huesing C; Bruce-Keller A; Burk D; Berthoud HR; Morrison CD; Münzberg H
[Ad] Endereço:Neurobiology of Nutrition and Metabolism, and Heike.Munzberg@pbrc.edu Emily.Qualls-Creekmore@pbrc.edu.
[Ti] Título:Galanin-Expressing GABA Neurons in the Lateral Hypothalamus Modulate Food Reward and Noncompulsive Locomotion.
[So] Source:J Neurosci;37(25):6053-6065, 2017 Jun 21.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The lateral hypothalamus (LHA) integrates reward and appetitive behavior and is composed of many overlapping neuronal populations. Recent studies associated LHA GABAergic neurons (LHA ), which densely innervate the ventral tegmental area (VTA), with modulation of food reward and consumption; yet, LHA projections to the VTA exclusively modulated food consumption, not reward. We identified a subpopulation of LHA neurons that coexpress the neuropeptide galanin (LHA ). These LHA neurons also modulate food reward, but lack direct VTA innervation. We hypothesized that LHA neurons may represent a subpopulation of LHA neurons that mediates food reward independent of direct VTA innervation. We used chemogenetic activation of LHA or LHA neurons in mice to compare their role in feeding behavior. We further analyzed locomotor behavior to understand how differential VTA connectivity and transmitter release in these LHA neurons influences this behavior. LHA or LHA neuronal activation both increased operant food-seeking behavior, but only activation of LHA neurons increased overall chow consumption. Additionally, LHA or LHA neuronal activation similarly induced locomotor activity, but with striking differences in modality. Activation of LHA neurons induced compulsive-like locomotor behavior; while LHA neurons induced locomotor activity without compulsivity. Thus, LHA neurons define a subpopulation of LHA neurons without direct VTA innervation that mediate noncompulsive food-seeking behavior. We speculate that the striking difference in compulsive-like locomotor behavior is also based on differential VTA innervation. The downstream neural network responsible for this behavior and a potential role for galanin as neuromodulator remains to be identified. The lateral hypothalamus (LHA) regulates motivated feeding behavior via GABAergic LHA neurons. The molecular identity of LHA neurons is heterogeneous and largely undefined. Here we introduce LHA neurons as a subset of LHA neurons that lack direct innervation of the ventral tegmental area (VTA). LHA neurons are sufficient to drive motivated feeding and locomotor activity similar to LHA neurons, but without inducing compulsive-like behaviors, which we propose to require direct VTA innervation. Our study integrates galanin-expressing LHA neurons into our current understanding of the neuronal circuits and molecular mechanisms of the LHA that contribute to motivated feeding behaviors.
[Mh] Termos MeSH primário: Galanina/biossíntese
Região Hipotalâmica Lateral/fisiologia
Atividade Motora/fisiologia
Neurônios/fisiologia
Recompensa
Ácido gama-Aminobutírico/fisiologia
[Mh] Termos MeSH secundário: Animais
Antipsicóticos/farmacologia
Clozapina/farmacologia
Comportamento Compulsivo
Condicionamento Operante/efeitos dos fármacos
Condicionamento Operante/fisiologia
Metabolismo Energético/fisiologia
Alimentos
Região Hipotalâmica Lateral/citologia
Região Hipotalâmica Lateral/metabolismo
Masculino
Camundongos
Atividade Motora/efeitos dos fármacos
Rede Nervosa/citologia
Rede Nervosa/fisiologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Neurotransmissores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Neurotransmitter Agents); 56-12-2 (gamma-Aminobutyric Acid); 88813-36-9 (Galanin); J60AR2IKIC (Clozapine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0155-17.2017


  5 / 2696 MEDLINE  
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[PMID]:28525358
[Au] Autor:Mei Z; Yang Y; Li Y; Yang F; Li J; Xing N; Xu ZD
[Ti] Título:Galanin suppresses proliferation of human U251 and T98G glioma cells via its subtype 1 receptor.
[So] Source:Biol Chem;398(10):1127-1139, 2017 Sep 26.
[Is] ISSN:1437-4315
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Galanin is a neuropeptide with a widespread distribution throughout the nervous and endocrine systems, and recent studies have shown an anti-proliferative effect of galanin on several types of tumors. However, whether and how galanin and its receptors are involved in the regulation of cell proliferation in glioma cells remains unclear. In this study, the roles of galanin and its subtype 1 receptor (GAL1) in the proliferation of human U251 and T98G glioma cells were investigated. We found that galanin significantly suppressed the proliferation of U251 and T98G cells as well as tumor growth in nude mice. However, galanin did not exert apoptotic or cytotoxic effects on these two cell lines. In addition, we showed that galanin decreased the proliferation of U251 and T98G cells via its GAL1 receptor. Finally, we found that the GAL1 receptor was involved in the suppressive effects of galanin by activating ERK1/2.
[Mh] Termos MeSH primário: Galanina/farmacologia
Glioma/tratamento farmacológico
Glioma/patologia
Receptor Tipo 1 de Galanina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Glioma/metabolismo
Seres Humanos
Receptor Tipo 1 de Galanina/metabolismo
Relação Estrutura-Atividade
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptor, Galanin, Type 1); 88813-36-9 (Galanin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE


  6 / 2696 MEDLINE  
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[PMID]:28478895
[Au] Autor:Yadav N; Gupta MN; Khare SK
[Ad] Endereço:Department of Chemistry, Indian Institute of Technology Delhi, India.
[Ti] Título:Three phase partitioning and spectroscopic characterization of bioactive constituent from halophilic Bacillus subtilis EMB M15.
[So] Source:Bioresour Technol;242:283-286, 2017 Oct.
[Is] ISSN:1873-2976
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the present study, a halophilic Bacillus subtilis subsp. spizizenii (NCBI GenBank accession number KX109607) was isolated from the Sambhar Salt Lake, Rajasthan India. This organism exhibited significance antibacterial and antifungal activity against Proteus vulgaris, Bacillus subtilis, Aspergillus niger, Rhizopus oligosporus and Penicillium chrysogenum respectively. The bioactive constituent responsible for it was extracted by three phase partitioning and purified by column chromatography. The purified compound was further characterized by FTIR-ATR, NMR and Mass spectrometry. The mass spectra show a molecular ion of m/z 301.14. The compound has very high antimicrobial activity showing 35mm zone of inhibition against Bacillus subtilis.
[Mh] Termos MeSH primário: Antibacterianos
Antifúngicos
Bacillus subtilis
[Mh] Termos MeSH secundário: Galanina/análogos & derivados
Índia
Substância P/análogos & derivados
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Antifungal Agents); 138579-66-5 (galantide); 33507-63-0 (Substance P); 88813-36-9 (Galanin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE


  7 / 2696 MEDLINE  
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[PMID]:28365702
[Au] Autor:Zhang Z; Fang P; Guo L; He B; Shi M; Zhu Y; Bo P
[Ad] Endereço:Department of Endocrinology, Clinical Medical College, Yangzhou, China.
[Ti] Título:Akt2-Dependent Beneficial Effect of Galanin on Insulin-Induced Glucose Uptake in Adipocytes of Diabetic Rats.
[So] Source:Cell Physiol Biochem;41(5):1777-1787, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Glucose uptake occurs via the activation of an insulin-signaling cascade, resulting in the translocation of glucose transporter 4 (GLUT4) to the plasma membrane of adipocytes and myocytes. Recent research found that galanin could boost insulin-induced glucose uptake. This study aimed to explore whether activation of Akt2 mediates the beneficial effects of galanin on insulin-induced glucose uptake in the adipocytes of diabetic rats. METHOD: In this experiment, insulin, galanin and MK-2206, an Akt inhibitor, were injected individually or in combination into diabetic rats once a day for ten days. Then, glucose uptake and pAkt2 and its downstream proteins were examined in adipocytes. RESULTS: Administration of galanin significantly enhanced insulin-induced 2-Deoxy-D-[3H]glucose uptake; GLUT4 and vesicle-associated membrane protein 2 contents in plasma membranes; and pAkt2Thr308/Ser473 and Akt2 mRNA expression levels in adipocytes. In addition, Akt2 downstream proteins including phosphorylated AS160 were increased, but the levels of phosphorylated forkhead box O1 and glycogen synthase kinase-3ß were reduced. Treatment with MK-2206 may block the beneficial effects of galanin on these insulin-induced events. CONCLUSIONS: The results of this study suggest that phosphorylation of Akt2 mediates the beneficial effects of galanin on insulin-induced glucose uptake in the adipocytes of diabetic rats.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Diabetes Mellitus Experimental/metabolismo
Galanina/metabolismo
Glucose/metabolismo
Insulina/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Experimental/tratamento farmacológico
Diabetes Mellitus Experimental/patologia
Transportador de Glucose Tipo 4/metabolismo
Compostos Heterocíclicos com 3 Anéis/farmacologia
Masculino
Proteínas do Tecido Nervoso/metabolismo
Fosforilação/efeitos dos fármacos
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transporter Type 4); 0 (Heterocyclic Compounds, 3-Ring); 0 (Insulin); 0 (MK 2206); 0 (Nerve Tissue Proteins); 0 (RNA, Messenger); 0 (Slc2a4 protein, rat); 147604-79-3 (Foxo1 protein, rat); 88813-36-9 (Galanin); EC 2.7.11.1 (Akt2 protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170403
[St] Status:MEDLINE
[do] DOI:10.1159/000471870


  8 / 2696 MEDLINE  
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[PMID]:28358321
[Au] Autor:Lepiarczyk E; Bossowska A; Kaleczyc J; Majewska M; Gonkowski S; Majewski M
[Ad] Endereço:Department of Human Physiology, Faculty of Medical Sciences, University of Warmia and Mazury in Olsztyn, 10-082 Olsztyn, Poland. ewa.lepiarczyk@uwm.edu.pl.
[Ti] Título:The Influence of Tetrodotoxin (TTX) on the Distribution and Chemical Coding of Caudal Mesenteric Ganglion (CaMG) Neurons Supplying the Porcine Urinary Bladder.
[So] Source:Mar Drugs;15(4), 2017 Mar 30.
[Is] ISSN:1660-3397
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The treatment of micturition disorders creates a serious problem for urologists. Recently, new therapeutic agents, such as neurotoxins, are being considered for the therapy of urological patients. The present study investigated the chemical coding of caudal mesenteric ganglion (CaMG) neurons supplying the porcine urinary bladder after intravesical instillation of tetrodotoxin (TTX). The CaMG neurons were visualized with retrograde tracer Fast blue (FB) and their chemical profile was disclosed with double-labeling immunohistochemistry using antibodies against tyrosine hydroxylase (TH), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), somatostatin (SOM), calbindin (CB), galanin (GAL) and neuronal nitric oxide synthase (nNOS). It was found that in both the control ( = 6) and TTX-treated pigs ( = 6), the vast majority (92.6% ± 3.4% and 88.8% ± 2%, respectively) of FB-positive (FB+) nerve cells were TH+. TTX instillation caused a decrease in the number of FB+/TH+ neurons immunopositive to NPY (88.9% ± 5.3% in the control animals vs. 10.6% ± 5.3% in TTX-treated pigs) or VIP (1.7% ± 0.6% vs. 0%), and an increase in the number of FB+/TH+ neurons immunoreactive to SOM (8.8% ± 1.6% vs. 39% ± 12.8%), CB (1.8% ± 0.7% vs. 12.6% ± 2.7%), GAL (1.7% ± 0.8% vs. 10.9% ± 2.6%) or nNOS (0% vs. 1.1% ± 0.3%). The present study is the first to suggest that TTX modifies the chemical coding of CaMG neurons supplying the porcine urinary bladder.
[Mh] Termos MeSH primário: Gânglios Simpáticos/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Neurotoxinas/farmacologia
Tetrodotoxina/farmacologia
Bexiga Urinária/inervação
[Mh] Termos MeSH secundário: Animais
Calbindinas/metabolismo
Feminino
Galanina/metabolismo
Gânglios Simpáticos/metabolismo
Neurônios/metabolismo
Neuropeptídeo Y/metabolismo
Óxido Nítrico Sintase Tipo I/metabolismo
Somatostatina/metabolismo
Suínos
Tirosina 3-Mono-Oxigenase/metabolismo
Bexiga Urinária/metabolismo
Peptídeo Intestinal Vasoativo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calbindins); 0 (Neuropeptide Y); 0 (Neurotoxins); 37221-79-7 (Vasoactive Intestinal Peptide); 4368-28-9 (Tetrodotoxin); 51110-01-1 (Somatostatin); 88813-36-9 (Galanin); EC 1.14.13.39 (Nitric Oxide Synthase Type I); EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE


  9 / 2696 MEDLINE  
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[PMID]:28288814
[Au] Autor:Flores-Burgess A; Millón C; Gago B; Narváez M; Borroto-Escuela DO; Mengod G; Narváez JA; Fuxe K; Santín L; Díaz-Cabiale Z
[Ad] Endereço:Universidad de Málaga, Instituto de Investigación Biomédica de Málaga, Facultad de Medicina, Campus de Teatinos s/n, 29071 Málaga, Spain.
[Ti] Título:Galanin (1-15) enhancement of the behavioral effects of Fluoxetine in the forced swimming test gives a new therapeutic strategy against depression.
[So] Source:Neuropharmacology;118:233-241, 2017 May 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The pharmacological treatment of major depression is mainly based on drugs elevating serotonergic (5-HT) activity. Specifically, selective 5-HT reuptake inhibitors, including Fluoxetine (FLX), are the most commonly used for treatment of major depression. However, the understanding of the mechanism of action of FLX beyond its effect of elevating 5-HT is limited. The interaction between serotoninergic system and neuropeptides signaling could be a key aspect. We examined the ability of the neuropeptide Galanin(1-15) [GAL(1-15)] to modulate the behavioral effects of FLX in the forced swimming test (FST) and studied feasible molecular mechanisms. The data show that GAL(1-15) enhances the antidepressant-like effects induced by FLX in the FST, and we demonstrate the involvement of GALR1/GALR2 heteroreceptor complex in the GAL(1-15)-mediated effect using in vivo rat models for siRNA GALR1 or GALR2 knockdown. Importantly, 5-HT1A receptors (5HT1A-R) also participate in the GAL(1-15)/FLX interactions since the 5HT1AR antagonist WAY100635 blocked the behavioral effects in the FST induced by the coadministration of GAL(1-15) and FLX. The mechanism underlying GAL(1-15)/FLX interactions affected the binding characteristics as well as the mRNA levels of 5-HT1A-R specifically in the dorsal hippocampus while leaving unaffected mRNA levels and affinity and binding sites of this receptor in the dorsal raphe. The results open up the possibility to use GAL(1-15) as for a combination therapy with FLX as a novel strategy for treatment of depression.
[Mh] Termos MeSH primário: Antidepressivos/uso terapêutico
Depressão/tratamento farmacológico
Depressão/fisiopatologia
Fluoxetina/uso terapêutico
Galanina/uso terapêutico
Fragmentos de Peptídeos/uso terapêutico
Natação/psicologia
[Mh] Termos MeSH secundário: Animais
Autorradiografia
Cicloexanos/uso terapêutico
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Sistemas de Liberação de Medicamentos
Quimioterapia Combinada
Hipocampo/efeitos dos fármacos
Hipocampo/metabolismo
Resposta de Imobilidade Tônica/efeitos dos fármacos
Masculino
Piperazinas/uso terapêutico
RNA Interferente Pequeno/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor Tipo 1 de Galanina/genética
Receptor Tipo 1 de Galanina/metabolismo
Receptor Tipo 2 de Galanina/genética
Receptor Tipo 2 de Galanina/metabolismo
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Cyclohexanes); 0 (Peptide Fragments); 0 (Piperazines); 0 (RNA, Small Interfering); 0 (Receptor, Galanin, Type 1); 0 (Receptor, Galanin, Type 2); 0 (WAY 101363); 01K63SUP8D (Fluoxetine); 112747-70-3 (galanin (1-15)); 88813-36-9 (Galanin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE


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[PMID]:28196718
[Au] Autor:McMillin M; Frampton G; Grant S; DeMorrow S
[Ad] Endereço:Central Texas Veterans Health Care System, Texas A&M Health Science Center, College of Medicine, Temple, Texas.
[Ti] Título:The Neuropeptide Galanin Is Up-Regulated during Cholestasis and Contributes to Cholangiocyte Proliferation.
[So] Source:Am J Pathol;187(4):819-830, 2017 Apr.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During the course of cholestatic liver diseases, mitotically dormant cholangiocytes proliferate and subsequently acquire a neuroendocrine phenotype. Galanin is a neuroendocrine factor responsible for regulation of physiological responses, such as feeding behavior and mood, and has been implicated in the development of fatty liver disease, although its role in biliary hyperplasia is unknown. Biliary hyperplasia was induced in rats via bile duct ligation (BDL) surgery, and galanin was increased in serum and liver homogenates from BDL rats. Treatment of sham and BDL rats with recombinant galanin increased cholangiocyte proliferation and intrahepatic biliary mass, liver damage, and inflammation, whereas blocking galanin expression with specific vivo-morpholino sequences inhibited hyperplastic cholangiocyte proliferation, liver damage, inflammation, and subsequent fibrosis. The proliferative effects of galanin were via activation of galanin receptor 1 expressed specifically on cholangiocytes and were associated with an activation of extracellular signal-regulated kinase 1/2, and ribosomal S6 kinase 1 signal transduction pathways and subsequent increase in cAMP responsive element binding protein DNA-binding activity and induction of Yes-associated protein expression. Strategies to inhibit extracellular signal-regulated kinase 1/2, ribosomal S6 kinase 1, or cAMP responsive element binding protein DNA-binding activity prevented the proliferative effects of galanin. Taken together, these data suggest that targeting galanin signaling may be effective for the maintenance of biliary mass during cholestatic liver diseases.
[Mh] Termos MeSH primário: Ductos Biliares/patologia
Colestase/metabolismo
Colestase/patologia
Galanina/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/metabolismo
Biomarcadores/metabolismo
Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
DNA/metabolismo
Inflamação/patologia
Ligadura
Masculino
Camundongos
Morfolinos/farmacologia
Fosforilação/efeitos dos fármacos
Ratos Sprague-Dawley
Receptores de Galanina/metabolismo
Transdução de Sinais/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Biomarkers); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Morpholinos); 0 (Receptors, Galanin); 0 (Yap protein, rat); 88813-36-9 (Galanin); 9007-49-2 (DNA)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE



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