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[PMID]:28453728
[Au] Autor:Vincent A; Sportouch C; Covinhes A; Barrère C; Gallot L; Delgado-Betancourt V; Lattuca B; Solecki K; Boisguérin P; Piot C; Nargeot J; Barrère-Lemaire S
[Ad] Endereço:IGF, CNRS, INSERM, Univ. Montpellier, F-34094 Montpellier, France.
[Ti] Título:Cardiac mGluR1 metabotropic receptors in cardioprotection.
[So] Source:Cardiovasc Res;113(6):644-655, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: In a previous study using a genome-wide microarray strategy, we identified metabotropic glutamate receptor 1 (mGluR1) as a putative cardioprotective candidate in ischaemic postconditioning (PostC). In the present study, we investigated the role of cardiac mGluR1 receptors during cardioprotection against myocardial ischaemia-reperfusion injury in the mouse myocardium. Methods and results: mGluR1 activation by glutamate administered 5 min before reperfusion in C57Bl/6 mice subjected to a myocardial ischaemia protocol strongly decreased both infarct size and DNA fragmentation measured at 24 h reperfusion. This cardioprotective effect was mimicked by the mGluR1 agonist, DHPG (10 µM), and abolished when glutamate was coinjected with the mGluR1 antagonist YM298198 (100 nM). Wortmannin (100 nM), an inhibitor of PI3-kinase, was able to prevent glutamate-induced cardioprotection. A glutamate bolus at the onset of reperfusion failed to protect the heart of mGluR1 knockout mice subjected to a myocardial ischaemia-reperfusion protocol, although PostC still protected the mGluR1 KO mice. Glutamate-treatment improved post-infarction functional recovery as evidenced by an echocardiographic study performed 15 days after treatment and by a histological evaluation of fibrosis 21 days post-treatment. Interestingly, restoration of functional mGluR1s by a PostC stimulus was evidenced at the transcriptional level. Since mGluR1s were localized at the surface membrane of cardiomyocytes, they might contribute to the cardioprotective effect of ischaemic PostC as other Gq-coupled receptors. Conclusion: This study provides the first demonstration that mGluR1 activation at the onset of reperfusion induces cardioprotection and might represent a putative strategy to prevent ischaemia-reperfusion injury.
[Mh] Termos MeSH primário: Agonistas de Aminoácidos Excitatórios/administração & dosagem
Glutamina/administração & dosagem
Infarto do Miocárdio/prevenção & controle
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Miocárdio/metabolismo
Receptores de Glutamato Metabotrópico/agonistas
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Antagonistas de Aminoácidos Excitatórios/farmacologia
Predisposição Genética para Doença
Camundongos Endogâmicos C57BL
Camundongos Knockout
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Miocárdio/patologia
Fenótipo
Fosfatidilinositol 3-Quinase/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de Glutamato Metabotrópico/deficiência
Receptores de Glutamato Metabotrópico/genética
Transdução de Sinais
Fatores de Tempo
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Agonists); 0 (Excitatory Amino Acid Antagonists); 0 (Receptors, Metabotropic Glutamate); 0 (metabotropic glutamate receptor type 1); 0RH81L854J (Glutamine); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx024


  2 / 15491 MEDLINE  
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[PMID]:27770401
[Au] Autor:Schulte ML; Hight MR; Ayers GD; Liu Q; Shyr Y; Washington MK; Manning HC
[Ad] Endereço:Vanderbilt Center for Molecular Probes, Vanderbilt University Medical Center, Nashville, TN, 37232, USA.
[Ti] Título:Non-Invasive Glutamine PET Reflects Pharmacological Inhibition of BRAF In Vivo.
[So] Source:Mol Imaging Biol;19(3):421-428, 2017 06.
[Is] ISSN:1860-2002
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: This study aimed to study whether cancer cells possess distinguishing metabolic features compared with surrounding normal cells, such as increased glutamine uptake. Given this, quantitative measures of glutamine uptake may reflect critical processes in oncology. Approximately, 10 % of patients with colorectal cancer (CRC) express BRAF , which may be actionable with selective BRAF inhibitors or in combination with inhibitors of complementary signaling axes. Non-invasive and quantitative predictive measures of response to these targeted therapies remain poorly developed in this setting. The primary objective of this study was to explore 4-[ F]fluoroglutamine (4-[ F]F-GLN) positron emission tomography (PET) to predict response to BRAF -targeted therapy in preclinical models of colon cancer. PROCEDURES: Tumor microarrays from patients with primary human colon cancers (n = 115) and CRC liver metastases (n = 111) were used to evaluate the prevalence of ASCT2, the primary glutamine transporter in oncology, by immunohistochemistry. Subsequently, 4-[ F]F-GLN PET was evaluated in mouse models of human BRAF -expressing and BRAF wild-type CRC. RESULTS: Approximately 70 % of primary colon cancers and 53 % of metastases exhibited positive ASCT2 immunoreactivity, suggesting that [ F]4-F-GLN PET could be applicable to a majority of patients with colon cancer. ASCT2 expression was not associated selectively with the expression of mutant BRAF. Decreased 4-[ F]F-GLN predicted pharmacological response to single-agent BRAF and combination BRAF and PI3K/mTOR inhibition in BRAF -mutant Colo-205 tumors. In contrast, a similar decrease was not observed in BRAF wild-type HCT-116 tumors, a setting where BRAF -targeted therapies are ineffective. CONCLUSIONS: 4-[ F]F-GLN PET selectively reflected pharmacodynamic response to BRAF inhibition when compared with 2-deoxy-2[ F]fluoro-D-glucose PET, which was decreased non-specifically for all treated cohorts, regardless of downstream pathway inhibition. These findings illustrate the utility of non-invasive PET imaging measures of glutamine uptake to selectively predict response to BRAF-targeted therapy in colon cancer and may suggest further opportunities to inform colon cancer clinical trials using targeted therapies against MAPK activation.
[Mh] Termos MeSH primário: Glutamina/química
Mutação/genética
Tomografia por Emissão de Pósitrons
Proteínas Proto-Oncogênicas B-raf/antagonistas & inibidores
Proteínas Proto-Oncogênicas B-raf/genética
[Mh] Termos MeSH secundário: Sistema ASC de Transporte de Aminoácidos/metabolismo
Animais
Linhagem Celular Tumoral
Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/metabolismo
Neoplasias do Colo/patologia
Feminino
Seres Humanos
Neoplasias Hepáticas/secundário
Camundongos Nus
Antígenos de Histocompatibilidade Menor/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Inibidores de Proteínas Quinases/uso terapêutico
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acid Transport System ASC); 0 (Minor Histocompatibility Antigens); 0 (Protein Kinase Inhibitors); 0 (SLC1A5 protein, human); 0RH81L854J (Glutamine); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s11307-016-1008-z


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[PMID]:29416026
[Au] Autor:Wang YQ; Wang HL; Xu J; Tan J; Fu LN; Wang JL; Zou TH; Sun DF; Gao QY; Chen YX; Fang JY
[Ad] Endereço:Division of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai, 200001, China.
[Ti] Título:Sirtuin5 contributes to colorectal carcinogenesis by enhancing glutaminolysis in a deglutarylation-dependent manner.
[So] Source:Nat Commun;9(1):545, 2018 02 07.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Reversible post-translational modifications represent a mechanism to control tumor metabolism. Here we show that mitochondrial Sirtuin5 (SIRT5), which mediates lysine desuccinylation, deglutarylation, and demalonylation, plays a role in colorectal cancer (CRC) glutamine metabolic rewiring. Metabolic profiling identifies that deletion of SIRT5 causes a marked decrease in C-glutamine incorporation into tricarboxylic-acid (TCA) cycle intermediates and glutamine-derived non-essential amino acids. This reduces the building blocks required for rapid growth. Mechanistically, the direct interaction between SIRT5 and glutamate dehydrogenase 1 (GLUD1) causes deglutarylation and functional activation of GLUD1, a critical regulator of cellular glutaminolysis. Consistently, GLUD1 knockdown diminishes SIRT5-induced proliferation, both in vivo and in vitro. Clinically, overexpression of SIRT5 is significantly correlated with poor prognosis in CRC. Thus, SIRT5 supports the anaplerotic entry of glutamine into the TCA cycle in malignant phenotypes of CRC via activating GLUD1.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Neoplasias Colorretais/metabolismo
Regulação Neoplásica da Expressão Gênica/fisiologia
Glutamato Desidrogenase/metabolismo
Glutamina/metabolismo
Sirtuínas/metabolismo
[Mh] Termos MeSH secundário: Proliferação Celular
Ciclo do Ácido Cítrico/fisiologia
Regulação Enzimológica da Expressão Gênica/fisiologia
Glutamato Desidrogenase/genética
Células HCT116
Seres Humanos
Interferência de RNA
Sirtuínas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0RH81L854J (Glutamine); EC 1.4.1.2 (Glutamate Dehydrogenase); EC 1.4.1.3 (GLUD1 protein, human); EC 3.5.1.- (SIRT5 protein, human); EC 3.5.1.- (Sirtuins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02951-4


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[PMID]:29390267
[Au] Autor:Delli Pizzi S; Bellomo RG; Carmignano SM; Ancona E; Franciotti R; Supplizi M; Barassi G; Onofrj M; Bonanni L; Saggini R
[Ad] Endereço:Department of Neuroscience, Imaging and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara.
[Ti] Título:Rehabilitation program based on sensorimotor recovery improves the static and dynamic balance and modifies the basal ganglia neurochemistry: A pilot 1H-MRS study on Parkinson's disease patients.
[So] Source:Medicine (Baltimore);96(50):e8732, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rehabilitation interventions represent an alternative strategy to pharmacological treatment in order to slow or reverse some functional aspects of disability in Parkinson's disease (PD). To date, the neurophysiological mechanisms underlying rehabilitation-mediated improvement in PD patients are still poorly understood. Interestingly, growing evidence has highlighted a key role of the glutamate in neurogenesis and brain plasticity. The brain levels of glutamate, and of its precursor glutamine, can be detected in vivo and noninvasively as "Glx" by means of proton magnetic resonance spectroscopy (H-MRS). In the present pilot study, 7 PD patients with frequent falls and axial dystonia underwent 8-week rehabilitative protocol focused on sensorimotor improvement. Clinical evaluation and Glx quantification were performed before and after rehabilitation. The Glx assessment was focused on the basal ganglia in agreement with their key role in the motor functions. We found that the rehabilitation program improves the static and dynamic balance in PD patients, promoting a better global motor performance. Moreover, we observed that the levels of Glx within the left basal ganglia were higher after rehabilitation as compared with baseline. Thus, we posit that our sensorimotor rehabilitative protocol could stimulate the glutamate metabolism in basal ganglia and, in turn, neuroplasticity processes. We also hypothesize that these mechanisms could prepare the ground to restore the functional interaction among brain areas deputed to motor controls, which are affected in PD.
[Mh] Termos MeSH primário: Gânglios da Base/metabolismo
Doença de Parkinson/reabilitação
Equilíbrio Postural/fisiologia
[Mh] Termos MeSH secundário: Idoso
Feminino
Ácido Glutâmico/metabolismo
Glutamina/metabolismo
Seres Humanos
Masculino
Doença de Parkinson/fisiopatologia
Projetos Piloto
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0RH81L854J (Glutamine); 3KX376GY7L (Glutamic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008732


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[PMID]:29305868
[Au] Autor:Tominaga A; Sato M; Takahashi T; Toyoda E; Toyoda K; Suzuki T; Takahashi M; Watanabe M; Okazaki K
[Ad] Endereço:Department of Orthopaedic Surgery, Tokyo Women's Medical University, 8-1 Kawadacho, Shinjuku-ku, Tokyo, 162-8666, Japan.
[Ti] Título:Quality assessment of cellular and tissue-based products using liquid chromatography-tandem mass spectrometry.
[So] Source:Biochem Biophys Res Commun;496(2):429-435, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We are currently conducting clinical research on cell sheets for cartilage regeneration. One issue with the future use of chondrocyte sheets as cellular and tissue-based products is quality assessment. Currently, chondrocyte sheets are evaluated using invasive methods that cannot be performed on every sheet produced. We report here on our liquid chromatography-tandem mass spectrometry (LC-MS/MS) technique that allows the noninvasive assessment of every sheet using only 50 µl of culture medium. We found that LC-MS/MS could be used to confirm cell sheet viability through the measurement of glucose and glutamine uptake, to estimate extracellular matrix production by measuring serine consumption, to estimate cell kinetics by measuring cytidine and uracil concentrations, and to estimate melanoma inhibitory activity level by measuring pyridoxal concentration. LC-MS/MS may be useful for the noninvasive assessment of products to be used in regenerative medicine.
[Mh] Termos MeSH primário: Cartilagem/metabolismo
Condrócitos/metabolismo
Cromatografia Líquida/normas
Regeneração/fisiologia
Espectrometria de Massas em Tandem/normas
[Mh] Termos MeSH secundário: Transporte Biológico
Cartilagem/patologia
Cartilagem/cirurgia
Citidina/metabolismo
Matriz Extracelular
Glucose/metabolismo
Glutamina/metabolismo
Seres Humanos
Controle de Qualidade
Medicina Regenerativa/métodos
Serina/metabolismo
Uracila/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0RH81L854J (Glutamine); 452VLY9402 (Serine); 56HH86ZVCT (Uracil); 5CSZ8459RP (Cytidine); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:28462779
[Au] Autor:Burns JA; Zhang H; Hill E; Kim E; Kerney R
[Ad] Endereço:Division of Invertebrate Zoology, American Museum of Natural History, New York, United States.
[Ti] Título:Transcriptome analysis illuminates the nature of the intracellular interaction in a vertebrate-algal symbiosis.
[So] Source:Elife;6, 2017 05 02.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During embryonic development, cells of the green alga enter cells of the salamander forming an endosymbiosis. Here, using dual-RNA seq, we compared the host salamander cells that harbored intracellular algae to those without algae and the algae inside the animal cells to those in the egg capsule. This two-by-two-way analysis revealed that intracellular algae exhibit hallmarks of cellular stress and undergo a striking metabolic shift from oxidative metabolism to fermentation. Culturing experiments with the alga showed that glutamine may be utilized by the algal as a primary nitrogen source. Transcriptional changes in salamander cells suggest an innate immune response to the alga, with potential attenuation of NF-κB, and metabolic alterations indicative of modulation of insulin sensitivity. In stark contrast to its algal endosymbiont, the salamander cells did not exhibit major stress responses, suggesting that the host cell experience is neutral or beneficial.
[Mh] Termos MeSH primário: Ambystoma/fisiologia
Simbiose
Volvocida/fisiologia
[Mh] Termos MeSH secundário: Ambystoma/genética
Animais
Perfilação da Expressão Gênica
Glutamina/metabolismo
Imunidade Inata
Redes e Vias Metabólicas/genética
Volvocida/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0RH81L854J (Glutamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180211
[Lr] Data última revisão:
180211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:29235329
[Au] Autor:Minchenko OH; Kharkova AP; Minchenko DO; Karbovskyi LL
[Ti] Título:Expression of IGFBP6, IGFBP7, NOV, CYR61, WISP1 and WISP2 genes in U87 glioma cells in glutamine deprivation condition.
[So] Source:Ukr Biochem J;88(3):66-77, 2016 May-Jun.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:We have studied gene expression of insulin-like growth factor binding proteins in U87 glioma cells upon glutamine deprivation depending on the inhibition of IRE1 (inositol requiring enzyme-1), a central mediator of endoplasmic reticulum stress. We have shown that exposure of control glioma cells upon glutamine deprivation leads to down-regulation of NOV/IGFBP9, WISP1 and WISP2 gene expressions and up-regulation of CYR61/IGFBP10 gene expression at the mRNA level. At the same time, the expression of IGFBP6 and IGFBP7 genes in control glioma cells was resistant to glutamine deprivation. It was also shown that the inhibition of IRE1 modifies the effect of glutamine deprivation on the expression of all studied genes. Thus, the inhibition of IRE1 signaling enzyme enhances the effect of glutamine deprivation on the expression of CYR61 and WISP1 genes and suppresses effect of the deprivation on WISP2 gene expression in glioma cells. Moreover, the inhibition of IRE1 introduces sensitivity of the expression of IGFBP6 and IGFBP7 genes to glutamine deprivation and removes this sensitivity to NOV gene. We have also demonstrated that the expression of all studied genes in glioma cells growing with glutamine is regulated by IRE1 signaling enzyme, because the inhibition of IRE1 significantly down-regulates IGFBP6 and NOV genes and up-regulates IGFBP7, CYR61, WISP1, and WISP2 genes as compared to control glioma cells. The present study demonstrates that glutamine deprivation condition affects most studied IGFBP and WISP gene expressions in relation to IRE1 signaling enzyme function and possibly contributes to slower glioma cell proliferation upon inhibition of IRE1.
[Mh] Termos MeSH primário: Proteínas de Sinalização Intercelular CCN/genética
Endorribonucleases/genética
Regulação Neoplásica da Expressão Gênica
Glutamina/deficiência
Proteína 6 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
Neuroglia/enzimologia
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas/genética
[Mh] Termos MeSH secundário: Proteínas de Sinalização Intercelular CCN/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Proteína Rica em Cisteína 61/genética
Proteína Rica em Cisteína 61/metabolismo
Endorribonucleases/deficiência
Seres Humanos
Proteína 6 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/genética
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/genética
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Neuroglia/patologia
Proteínas Serina-Treonina Quinases/deficiência
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (CYR61 protein, human); 0 (Cysteine-Rich Protein 61); 0 (Insulin-Like Growth Factor Binding Protein 6); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (NOV protein, human); 0 (Nephroblastoma Overexpressed Protein); 0 (Proto-Oncogene Proteins); 0 (Repressor Proteins); 0 (WISP1 protein, human); 0 (WISP2 protein, human); 0 (insulin-like growth factor binding protein-related protein 1); 0RH81L854J (Glutamine); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.1.- (Endoribonucleases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.03.066


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[PMID]:29215843
[Au] Autor:Savilov PN
[Ti] Título:[Influence of partial hepatectomie on ammoniumdetoxications function of liver at chronic tetrachlorcarbon hepatitis].
[So] Source:Patol Fiziol Eksp Ter;61(2):61-6, 2017 Apr-Jun.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The purpose. To study the effect of partial hepatectomy (PH) on the main ways of ammonia detoxication in the liver (synthesis of urea and glutamine) in chronic tetrachlorcarbon (CCl4) hepatitis. Methods. The experiments were performed on 165 white outbred rats (females) weighing 180-220 g Chronic CCl4-hepatitis was reproduced by subcutaneous injection of 50% CCl4 solution in olive oil (0.1 ml/100g of body weight,65 days, through the day with two two-week breaks between 6-7 and 13-14 injections). PH conducted electrocautery, removing part of the left lobe of the liver (15-20% by weight of the body) to 65th (and last) day of the introduction of the CCl4. Animals were studied after 65 days of development of CCl4-hepatitis on day 3, 7 and 14 days after laparotomy («falsely operated¼ animals) and partial hepatectomy. In subcellular fractions of the liver investigated the activity of phosphatdependent glutaminase (FDG), glutamatdehydrogenaze (GDG), glutaminsintetaze (GS), arginase. In the liver tissue investigated the content of ammonia, glutamine, glutamate and urea. Results. Found that on 65-th day of the development of CCl4 in the liver decreases the concentration of ammonia, glutamine, glutamate, urea, and activity of GS, GDG and arginase. Activity FDG was not changed. The use of PH on the background of chronic CCl4-hepatitis has a short-term (3 days) a stimulating effect on the activity FDG, GS, postponed (14 days) the inhibitory effect on the activity of GDG. This was accompanied by an increase in the concentration in the liver of ammonia within 14 days of the postoperative period on the background of maintaining reduced concentrations of glutamine and glutamate it. The stimulatory effect of CHA on the activity of arginase is saved to the 14th day of the postoperative period, however, the concentration of urea in the liver remained below normal. Conclusions. The obtained results show that CGA on the background of chronic hepatitis increases the pathological impact of CCl4 on amniocentesis liver function.
[Mh] Termos MeSH primário: Amônia/metabolismo
Intoxicação por Tetracloreto de Carbono/metabolismo
Tetracloreto de Carbono
Doença Hepática Induzida por Substâncias e Drogas/metabolismo
Hepatectomia
Fígado/metabolismo
[Mh] Termos MeSH secundário: Animais
Intoxicação por Tetracloreto de Carbono/patologia
Doença Hepática Induzida por Substâncias e Drogas/patologia
Doença Crônica
Feminino
Ácido Glutâmico/metabolismo
Glutamina/metabolismo
Fígado/patologia
Ratos
Ureia/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0RH81L854J (Glutamine); 3KX376GY7L (Glutamic Acid); 7664-41-7 (Ammonia); 8W8T17847W (Urea); CL2T97X0V0 (Carbon Tetrachloride)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171221
[Lr] Data última revisão:
171221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE


  9 / 15491 MEDLINE  
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[PMID]:29180187
[Au] Autor:Li W; Tao S; Wu Q; Wu T; Tao R; Fan J
[Ad] Endereço:Department of Health, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
[Ti] Título:Glutamine reduces myocardial cell apoptosis in a rat model of sepsis by promoting expression of heat shock protein 90.
[So] Source:J Surg Res;220:247-254, 2017 Dec.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Myocardial cell injury and cardiac myocyte apoptosis are associated with sepsis. Glutamine (Gln) has been reported to repair myocardial cell injury. The aim of this study was to explore the role of Gln on cardiac myocytes in a cecal ligation and puncture (CLP) model of sepsis in Wistar rats. MATERIALS AND METHODS: Following induction of sepsis in a CLP rat model, viral encoding heat shock protein 90 (Hsp90) gene and Hsp90dsDNA were designed to express and knockdown Hsp90, respectively. Rat cardiac tissues were examined histologically, and apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The expression of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, Hsp90, p53 upregulated modulator of apoptosis, and p53 was measured by western blotting and real-time polymerase chain reaction. Caspase-3, caspase-8, and caspase-9 were detected by enzyme-linked immunosorbent assay. RESULTS: Rat cardiac myocyte damage induced by CLP was reduced by Gln treatment and Hsp90 overexpression, and these changes were reversed by Hsp90 knockdown. Bcl-2 expression, Bcl-2-associated X protein, p53, p53 upregulated modulator of apoptosis, caspase-8, caspase-9, and caspase-3 activities were significantly upregulated in the CLP model, which were reduced by Gln treatment and Hsp90 overexpression. CONCLUSIONS: Gln reduced apoptosis of cardiac myocytes in a rat model of sepsis, by promoting Hsp90 expression. Further studies are needed to determine the possible therapeutic action of Gln in sepsis in human tissue.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Glutamina/metabolismo
Proteínas de Choque Térmico HSP90/metabolismo
Miócitos Cardíacos/fisiologia
Sepse/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Caspases/metabolismo
Ratos Wistar
Sepse/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HSP90 Heat-Shock Proteins); 0RH81L854J (Glutamine); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


  10 / 15491 MEDLINE  
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[PMID]:27770643
[Au] Autor:Kubo H; Nakataki M; Sumitani S; Iga JI; Numata S; Kameoka N; Watanabe SY; Umehara H; Kinoshita M; Inoshita M; Tamaru M; Ohta M; Nakayama-Yamauchi C; Funakoshi Y; Harada M; Ohmori T
[Ad] Endereço:Department of Psychiatry, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
[Ti] Título:1H-magnetic resonance spectroscopy study of glutamate-related abnormality in bipolar disorder.
[So] Source:J Affect Disord;208:139-144, 2017 Jan 15.
[Is] ISSN:1573-2517
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Previous studies of patients with bipolar disorder (BD) using magnetic resonance spectroscopy (MRS) have shown neurophysiological abnormalities related to the glutamate (Glu)-glutamine (Gln) cycle, membrane turnover, and neuronal integrity, although the results were neither consistent nor conclusive. Recently it has been reported the Gln/Glu ratio is the most useful index, quantifying neuronal-glial interactions and the balance of glutamatergic metabolites In this MRS study, we elucidated the abnormalities of metabolites in a larger sample of patients with BD with a high-field MRI system. METHODS: Sixty-two subjects (31 patients with BD and 31 healthy controls [HC]) underwent 3T proton MRS (1H-MRS) of the anterior cingulate cortex (ACC) and left basal ganglia (ltBG) using a stimulated echo acquisition mode (STEAM) sequence. RESULTS: After verifying the data quality, 20 patients with BD and 23 age- and gender-matched HCs were compared using repeated-measures analysis of covariance (ANCOVA). Compared to the HC group, the BD group showed increased levels of Gln, creatine (Cr), N-acetyl aspartate (NAA), choline (Cho), and an increased ratio of Gln to Glu in the ACC, and increased Gln and Cho in the ltBG. These findings remained after the participants with BD were limited to only euthymic patients. After removing the influence of lithium (Li) and sodium valproate (VPA), we observed activated glutamatergic neurotransmission in the ACC but not in the ltBG. LIMITATIONS: The present findings are cross-sectional and metabolites were measured in only two regions. CONCLUSIONS: Our results support a wide range of metabolite changes in patients with BD involved in glutamatergic neurotransmission, membrane turnover, and neuronal integrity. Moreover, the elevation of Gln/Glu ratio suggested that hyperactivity of glutamatergic neurotransmission in the ACC is a disease marker for BD.
[Mh] Termos MeSH primário: Gânglios da Base/metabolismo
Transtorno Bipolar/diagnóstico
Ácido Glutâmico/metabolismo
Glutamina/metabolismo
Giro do Cíngulo/metabolismo
Espectroscopia de Ressonância Magnética
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/metabolismo
Transtorno Bipolar/metabolismo
Estudos de Casos e Controles
Estudos Transversais
Feminino
Seres Humanos
Espectroscopia de Ressonância Magnética/métodos
Masculino
Meia-Idade
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0RH81L854J (Glutamine); 3KX376GY7L (Glutamic Acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE



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