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Pesquisa : D06.472.931.740 [Categoria DeCS]
Referências encontradas : 680 [refinar]
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[PMID]:28791911
[Au] Autor:Cichero E; Tonelli M
[Ad] Endereço:Department of Pharmacy, University of Genoa, Viale Benedetto XV n. 3, Genoa 16132, Italy.
[Ti] Título:Targeting species-specific trace amine-associated receptor 1 ligands: to date perspective of the rational drug design process.
[So] Source:Future Med Chem;9(13):1507-1527, 2017 Sep.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:G-protein-coupled receptors represent main targets of several clinically relevant drugs, playing nowadays a leading part for further drug discovery process. Trace amine-associated receptor's family (TAARs) assumed an intriguing role as druggable target in medicinal chemistry, being TAAR1 the most investigated. Indeed, related ligands proved to be intertwined in several circuits involved in pathological pathways or therapeutic routes. Herein, we highlight relevant efforts in the search of novel agonists, focusing on responsiveness featured by different chemotypes toward rodent and human TAAR1, in order to explore species-specificity preferences. We also discuss the main strategies guiding so far the design of new TAAR1 agonists, giving a perspective of the structure-based methodologies aimed at deriving new insights for more potent and selective derivatives.
[Mh] Termos MeSH primário: Desenho de Drogas
Ligantes
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Seres Humanos
Simulação de Acoplamento Molecular
Receptores Acoplados a Proteínas-G/agonistas
Relação Estrutura-Atividade
Tironinas/química
Tironinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Ligands); 0 (Receptors, G-Protein-Coupled); 0 (Thyronines); 0 (Trace amine-associated receptor 1); 500-78-7 (thyronamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0044


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[PMID]:28368510
[Au] Autor:Gachkar S; Oelkrug R; Martinez-Sanchez N; Rial-Pensado E; Warner A; Hoefig CS; López M; Mittag J
[Ad] Endereço:Center of Brain, Behavior and Metabolism, Medizinische Klinik I, University of Lübeck, 23562 Lübeck, Germany.
[Ti] Título:3-Iodothyronamine Induces Tail Vasodilation Through Central Action in Male Mice.
[So] Source:Endocrinology;158(6):1977-1984, 2017 Jun 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:3-Iodothyronamine (3-T1AM) is an endogenous thyroid hormone (TH)-derived metabolite that induces severe hypothermia in mice after systemic administration; however, the underlying mechanisms have remained enigmatic. We show here that the rapid 3-T1AM-induced loss in body temperature is a consequence of peripheral vasodilation and subsequent heat loss (e.g., over the tail surface). The condition is subsequently intensified by hypomotility and a lack of brown adipose tissue activation. Although the possible 3-T1AM targets trace amine-associated receptor 1 or α2a-adrenergic receptor were detected in tail artery and aorta respectively, myograph studies did not show any direct effect of 3-T1AM on vasodilation, suggesting that its actions are likely indirect. Intracerebroventricular application of 3-T1AM, however, replicated the phenotype of tail vasodilation and body temperature decline and led to neuronal activation in the hypothalamus, suggesting that the metabolite causes tail vasodilation through a hypothalamic signaling pathway. Consequently, the 3-T1AM response constitutes anapyrexia rather than hypothermia and closely resembles the heat-stress response mediated by hypothalamic temperature-sensitive neurons. Our results thus underline the well-known role of the hypothalamus as the body's thermostat and suggest an additional molecular link between TH signaling and the central control of body temperature.
[Mh] Termos MeSH primário: Encéfalo/fisiologia
Cauda/irrigação sanguínea
Tironinas/farmacologia
Vasodilatação/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Regulação da Temperatura Corporal/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Hipotálamo/efeitos dos fármacos
Hipotálamo/metabolismo
Infusões Intraventriculares
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Transdução de Sinais/efeitos dos fármacos
Cauda/efeitos dos fármacos
Tironinas/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-iodothyronamine); 0 (Thyronines)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1951


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[PMID]:28082426
[Au] Autor:Selen Alpergin ES; Bolandnazar Z; Sabatini M; Rogowski M; Chiellini G; Zucchi R; Assadi-Porter FM
[Ad] Endereço:Department of Biological Chemistry, Johns Hopkins University, Baltimore, Maryland.
[Ti] Título:Metabolic profiling reveals reprogramming of lipid metabolic pathways in treatment of polycystic ovary syndrome with 3-iodothyronamine.
[So] Source:Physiol Rep;5(1), 2017 Jan.
[Is] ISSN:2051-817X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Complex diseases such as polycystic ovary syndrome (PCOS) are associated with intricate pathophysiological, hormonal, and metabolic feedbacks that make their early diagnosis challenging, thus increasing the prevalence risks for obesity, cardiovascular, and fatty liver diseases. To explore the crosstalk between endocrine and lipid metabolic pathways, we administered 3-iodothyronamine (T1AM), a natural analog of thyroid hormone, in a mouse model of PCOS and analyzed plasma and tissue extracts using multidisciplinary omics and biochemical approaches. T1AM administration induces a profound tissue-specific antilipogenic effect in liver and muscle by lowering gene expression of key regulators of lipid metabolism, PTP1B and PLIN2, significantly increasing metabolites (glucogenic, amino acids, carnitine, and citrate) levels, while enhancing protection against oxidative stress. In contrast, T1AM has an opposing effect on the regulation of estrogenic pathways in the ovary by upregulating STAR, CYP11A1, and CYP17A1. Biochemical measurements provide further evidence of significant reduction in liver cholesterol and triglycerides in post-T1AM treatment. Our results shed light onto tissue-specific metabolic vs. hormonal pathway interactions, thus illuminating the intricacies within the pathophysiology of PCOS This study opens up new avenues to design drugs for targeted therapeutics to improve quality of life in complex metabolic diseases.
[Mh] Termos MeSH primário: Expressão Gênica/efeitos dos fármacos
Metabolismo dos Lipídeos/genética
Redes e Vias Metabólicas/efeitos dos fármacos
Síndrome do Ovário Policístico/tratamento farmacológico
Tironinas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Colesterol/metabolismo
Feminino
Expressão Gênica/genética
Fígado/metabolismo
Espectroscopia de Ressonância Magnética
Redes e Vias Metabólicas/genética
Metabolômica/métodos
Camundongos
Músculos/metabolismo
Obesidade/metabolismo
Ovário/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Síndrome do Ovário Policístico/sangue
Síndrome do Ovário Policístico/metabolismo
Síndrome do Ovário Policístico/fisiopatologia
Qualidade de Vida
Tironinas/metabolismo
Tironinas/farmacologia
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-iodothyronamine); 0 (Thyronines); 0 (Triglycerides); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE


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[PMID]:27863038
[Au] Autor:Cichero E; Tonelli M
[Ad] Endereço:Department of Pharmacy, University of Genoa, Genoa, Italy.
[Ti] Título:New insights into the structure of the trace amine-associated receptor 2: Homology modelling studies exploring the binding mode of 3-iodothyronamine.
[So] Source:Chem Biol Drug Des;89(5):790-796, 2017 May.
[Is] ISSN:1747-0285
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent studies have further investigated the trace amine-associated receptor type 2 (TAAR2) pharmacology, revealing its role not only at the olfactory sensory neurons but also at the immune system, being expressed in human leucocytes. In particular, the ability of this receptor to bind the unselective TAAR ligand 3-iodo-thyronamine (T AM) was elucidated, making in the meanwhile the discovery of selective compounds a urgent need to derive much more suitable tools for studying TAARs. In this context, we developed our work on TAAR2 applying a structure-based computational protocol, including TAAR2 homology modelling and T AM docking studies. The results were compared with those we previously obtained about TAAR1, in order to point out new insights guiding for selectivity between TAAR1 and TAAR2. The in silico strategy applied allowed us to provide for the first time thorough TAAR2 homology models, which are expected to be useful tools for a further design process of more selective TAAR ligands.
[Mh] Termos MeSH primário: Receptores Acoplados a Proteínas-G/química
Tironinas/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sítios de Ligação
Seres Humanos
Leucócitos/metabolismo
Ligantes
Camundongos
Simulação de Acoplamento Molecular
Dados de Sequência Molecular
Ligação Proteica
Estrutura Terciária de Proteína
Receptores Acoplados a Proteínas-G/metabolismo
Alinhamento de Sequência
Tironinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-iodothyronamine); 0 (Ligands); 0 (Receptors, G-Protein-Coupled); 0 (TAAR2 protein, human); 0 (Thyronines)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1111/cbdd.12903


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[PMID]:27795490
[Au] Autor:Ha K; Shin H; Ju H; Chung CM; Choi I
[Ad] Endereço:Division of Biological Science and Technology, College of Science and Technology, Yonsei University, Wonju, Gangwon-do, 26493, Republic of Korea.
[Ti] Título:Behavioral hypothermia of a domesticated lizard under treatment of the hypometabolic agent 3-iodothyronamine.
[So] Source:Exp Anim;66(2):99-105, 2017 May 03.
[Is] ISSN:1881-7122
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Ectothermic animals rely on behavioral thermoregulation due to low capacity of heat production and storage. Previously, lizards were shown to achieve 'fever' during microbial infection by increasing their preferred body temperature (PBT) behaviorally, thereby attaining a relatively high survival rate. The purpose of this study was to investigate whether domesticated lizards pursued 'behavioral hypothermia' induced by a hypometabolic agent 3-iodothyronamine (T1AM). We found that treatment with 8.0 mg/kg T1AM caused a lizard species, the leopard gecko (Eublepharis macularius), to decrease its ventilation and oxygen consumption rates 0.64- and 0.76-fold, respectively, compared to those of the control (P<0.05). The lizards, habituated at an ambient temperature of 30 ± 0.5°C, also showed a significant decrease in the PBT range over a freely accessible thermal gradient between 5°C and 45°C. The upper limit of the PBT in the treated lizards lowered from 31.9°C to 30.6°C, and the lower limit from 29.5°C to 26.3°C (P<0.001). These findings demonstrate that the treated lizards pursued behavioral hypothermia in conjunction with hypoventilation and hypometabolism. Because prior studies reported a similar hypometabolic response in T1AM-injected laboratory mice, the domesticated lizards, as a part of the vertebrate phylogeny, may be a useful laboratory model for biological and pharmacological researches such as drug potency test.
[Mh] Termos MeSH primário: Comportamento Animal/fisiologia
Regulação da Temperatura Corporal/efeitos dos fármacos
Regulação da Temperatura Corporal/fisiologia
Hipotermia
Lagartos/metabolismo
Lagartos/fisiologia
Tironinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Domésticos
Metabolismo Energético/efeitos dos fármacos
Camundongos
Consumo de Oxigênio/efeitos dos fármacos
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-iodothyronamine); 0 (Thyronines)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170720
[Lr] Data última revisão:
170720
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE
[do] DOI:10.1538/expanim.16-0070


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[PMID]:27815171
[Au] Autor:Laurino A; Matucci R; Vistoli G; Raimondi L
[Ad] Endereço:Dept. of NEUROFARBA, Section of Pharmacology, University of Florence, 50139 Florence, Italy.
[Ti] Título:3-iodothyronamine (T1AM), a novel antagonist of muscarinic receptors.
[So] Source:Eur J Pharmacol;793:35-42, 2016 Dec 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:3-iodothyronamine (T1AM) is a trace amine suspected to derive from thyroid hormone metabolism. T1AM was described as a ligand of G-protein coupled monoaminergic receptors, including trace amine associated receptors, suggesting the amine may exert a modulatory role on the monoaminergic transmission. Nothing is known on the possibility that T1AM could also modulate the cholinergic transmission interacting with muscarinic receptors. We evaluated whether T1AM (10nM-100µM) was able to i) displace [ H]-NMS (0.20nM) binding to membrane preparations from CHO cells stably transfected with human muscarinic receptor subtypes (M1-M5); ii) modify basal or acetylcholine induced pERK levels in CHO expressing the human muscarinic type 3 receptor subtype by Western blot iii) modify basal and carbachol-induced contraction of isolated rat urinary bladder. T1AM fitting within rat muscarinic type 3 receptor was simulated by Docking studies. T1AM recognized all muscarinic receptor subtypes (pKi values in the micromolar range). Interacting at type 3, T1AM reduced acetylcholine-increased pERK levels. T1AM reduced carbachol-induced contraction of the rat urinary bladder. The fenoxyl residue and the iodide ion were found essential for establishing contacts with the active site of the rat muscarinic type 3 receptor subtype. Our results indicate that T1AM binds at muscarinic receptors behaving as a weak, not selective, antagonist. This finding adds knowledge on the pharmacodynamics features of T1AM and it may prompt investigation on novel pharmacological effects of T1AM at conditions of hyper-activation of the muscarinic tone including the overactive urinary bladder.
[Mh] Termos MeSH primário: Antagonistas Muscarínicos/farmacologia
Receptor Muscarínico M3/antagonistas & inibidores
Tironinas/farmacologia
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Animais
Carbacol/farmacologia
Domínio Catalítico
Cricetinae
Seres Humanos
Masculino
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Simulação de Acoplamento Molecular
Antagonistas Muscarínicos/metabolismo
Contração Muscular/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Ratos
Receptor Muscarínico M3/química
Receptor Muscarínico M3/metabolismo
Tironinas/metabolismo
Bexiga Urinária/efeitos dos fármacos
Bexiga Urinária/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-iodothyronamine); 0 (Muscarinic Antagonists); 0 (Receptor, Muscarinic M3); 0 (Thyronines); 8Y164V895Y (Carbachol); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170327
[Lr] Data última revisão:
170327
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


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[PMID]:27555478
[Au] Autor:Li X; Augustine A; Sun D; Li L; Fliegel L
[Ad] Endereço:Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada. Electronic address: xjli@ualberta.ca.
[Ti] Título:Activation of the Na /H exchanger in isolated cardiomyocytes through ß-Raf dependent pathways. Role of Thr of the cytosolic tail.
[So] Source:J Mol Cell Cardiol;99:65-75, 2016 Oct.
[Is] ISSN:1095-8584
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mammalian Na /H exchanger isoform 1 (NHE1) is a ubiquitous plasma membrane protein that is a key regulator of intracellular pH in isolated cardiomyocytes. A 500 amino acid membrane domain removes protons and is regulated by a 315 amino acid cytosolic domain. In the myocardium, aberrant regulation of NHE1 contributes to ischemia reperfusion damage and to heart hypertrophy. We examined mechanisms of regulation of NHE1 in the myocardium by endothelin and ß-Raf. Endothelin stimulated NHE1 activity and activated Erk-dependent pathways. Inhibition of ß-Raf reduced NHE1 activity and Erk-pathway activation. We demonstrated that myocardial ß-Raf binds to the C-terminal 182 amino acids of the NHE1 protein and that ß-Raf is associated with NHE1 in intact cardiomyocytes. NHE1 was phosphorylated in vivo and the protein kinase inhibitor sorafenib reduced NHE1 phosphorylation levels. Immunoprecipitates of ß-Raf from cardiomyocytes phosphorylated the C-terminal 182 amino acids of NHE1 and mass spectrometry analysis showed that amino acid Thr was phosphorylated. Mutation of this amino acid to Ala resulted in defective activity while mutation to Asp restored the activity. The results demonstrate that Thr is an important regulatory amino acid of NHE1 that is activated through ß-Raf dependent pathways by phosphorylation either directly or indirectly by ß-Raf, and this affects NHE1 activity.
[Mh] Termos MeSH primário: Proteínas Proto-Oncogênicas B-raf/metabolismo
Transdução de Sinais
Trocadores de Sódio-Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Linhagem Celular
Membrana Celular/metabolismo
Concentração de Íons de Hidrogênio
Mutação
Miócitos Cardíacos/metabolismo
Fosforilação
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas/genética
Ratos
Trocadores de Sódio-Hidrogênio/química
Trocadores de Sódio-Hidrogênio/genética
Tironinas/genética
Tironinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sodium-Hydrogen Exchangers); 0 (Thyronines); 0 (growth factor-activatable Na-H exchanger NHE-1); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160825
[St] Status:MEDLINE


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[PMID]:27338438
[Au] Autor:Jocsak G; Kiss DS; Toth I; Goszleth G; Bartha T; Frenyo LV; Horvath TL; Zsarnovszky A
[Ad] Endereço:Department of Physiology and Biochemistry, Szent Istvan Faculty University of Veterinary Sciences, Budapest 1078, Hungary. jocsak.gergely@aotk.szie.hu.
[Ti] Título:Comparison of Individual and Combined Effects of Four Endocrine Disruptors on Estrogen Receptor Beta Transcription in Cerebellar Cell Culture: The Modulatory Role of Estradiol and Triiodo-Thyronine.
[So] Source:Int J Environ Res Public Health;13(6), 2016 Jun 22.
[Is] ISSN:1660-4601
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Humans and animals are continuously exposed to a number of environmental substances that act as endocrine disruptors (EDs). While a growing body of evidence is available to prove their adverse health effects, very little is known about the consequences of simultaneous exposure to a combination of such chemicals; METHODS: Here, we used an in vitro model to demonstrate how exposure to bisphenol A, zearalenone, arsenic, and 4-methylbenzylidene camphor, alone or in combination, affect estrogen receptor ß (ERß) mRNA expression in primary cerebellar cell cultures. Additionally, we also show the modulatory role of intrinsic biological factors, such as estradiol (E2), triiodo-thyronine (T3), and glial cells, as potential effect modulators; RESULTS: RESULTS show a wide diversity in ED effects on ERß mRNA expression, and that the magnitude of these ED effects highly depends on the presence or absence of E2, T3, and glial cells; CONCLUSION: The observed potency of the EDs to influence ERß mRNA expression, and the modulatory role of E2, T3, and the glia suggests that environmental ED effects may be masked as long as the hormonal milieu is physiological, but may tend to turn additive or superadditive in case of hormone deficiency.
[Mh] Termos MeSH primário: Células Cultivadas/efeitos dos fármacos
Células Cultivadas/metabolismo
Cerebelo/metabolismo
Disruptores Endócrinos/metabolismo
Receptor alfa de Estrogênio/metabolismo
Receptor beta de Estrogênio/metabolismo
Estrogênios não Esteroides/metabolismo
[Mh] Termos MeSH secundário: Animais
Compostos Benzidrílicos/metabolismo
Cânfora/análogos & derivados
Cânfora/metabolismo
Estradiol/metabolismo
Feminino
Seres Humanos
Masculino
Fenóis/metabolismo
Ratos Sprague-Dawley
Tironinas/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Endocrine Disruptors); 0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Estrogens, Non-Steroidal); 0 (Phenols); 0 (Thyronines); 4TI98Z838E (Estradiol); 76-22-2 (Camphor); 8I3XWY40L9 (enzacamene); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160625
[St] Status:MEDLINE


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[PMID]:27169745
[Au] Autor:Xu H; Zhang L; Kang H; Zhang J; Liu J; Liu S
[Ad] Endereço:Department of Clinical Laboratory, Tianjin Third Central Hospital, Tianjin, China.
[Ti] Título:Serum Metabonomics of Mild Acute Pancreatitis.
[So] Source:J Clin Lab Anal;30(6):990-998, 2016 Nov.
[Is] ISSN:1098-2825
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mild acute pancreatitis (MAP) is a common acute abdominal disease, and exhibits rising incidence in recent decades. As an important component of systemic biology, metabonomics is a new discipline developed following genomics and proteomics. In this study, the objective was to analyze the serum metabonomics of patients with MAP, aiming to screen metabolic markers with potential diagnostic values. METHODS: An analysis platform with ultra performance liquid chromatography-high-resolution mass spectrometry was used to screen the difference metabolites related to MAP diagnosis and disease course monitoring. RESULTS: A total of 432 endogenous metabolites were screened out from 122 serum samples, and 49 difference metabolites were verified, among which 12 difference metabolites were identified by nonparametric test. After material identification, eight metabolites exhibited reliable results, and their levels in MAP serum were higher than those in healthy serum. Four metabolites exhibited gradual downward trend with treatment process going on, and the differences were statistically significant (P < 0.05). CONCLUSION: Metabonomic analysis has revealed eight metabolites with potential diagnostic values toward MAP, among which four metabolites can be used to monitor the disease course.
[Mh] Termos MeSH primário: Amilases/sangue
Decanoatos/sangue
Lipase/sangue
Metabolômica/métodos
Pancreatite/sangue
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Idoso
Cromatografia Líquida
Feminino
Ácido Glicocólico/sangue
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Espectrometria de Massas
Meia-Idade
Pancreatite/diagnóstico por imagem
Análise de Componente Principal
Curva ROC
Esfingosina/análogos & derivados
Esfingosina/sangue
Máquina de Vetores de Suporte
Tironinas/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-tetradecanone); 0 (Decanoates); 0 (Thyronines); EC 3.1.1.3 (Lipase); EC 3.2.1.- (Amylases); G59NX3I3RT (Glycocholic Acid); NGZ37HRE42 (Sphingosine); OWA98U788S (safingol)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160513
[St] Status:MEDLINE
[do] DOI:10.1002/jcla.21969


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[PMID]:26808713
[Au] Autor:Shi ST; Wu XX; Hao W; Wang X; Miao HT; Zhen L; Nie SP
[Ad] Endereço:*Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China; and †Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing, China.
[Ti] Título:Triiodo-L-Thyronine Promotes the Maturation of Cardiomyocytes Derived From Rat Bone Marrow Mesenchymal Stem Cells.
[So] Source:J Cardiovasc Pharmacol;67(5):388-93, 2016 May.
[Is] ISSN:1533-4023
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone marrow mesenchymal stem cells (BMMSCs) can differentiate into cardiomyocytes and be used in cardiac tissue engineering for heart regeneration. However, the effective clinical application of cardiomyocytes derived from BMMSCs is limited because of their immature phenotype. The aim of this study was to investigate the potential of triiodo-L-thyronine (T3) to drive cardiomyocytes derived from BMMSCs to a more mature state. BMMSCs were divided into 3 groups: untreated controls, differentiated, and T3 treated. The differentiation potential was evaluated by immunofluorescence microscopy and flow cytometry. Data were represented as the numbers of cells positive for the troponin I (cTnI), α-actinin, GATA4, and the connexin-43 (Cx-43). The mRNA levels of these specific markers of cardiomyocytes were determined by quantitative real-time polymerase chain reaction. The levels of cardiomyocytes markers protein and octamer-binding transcription factor 4 (Oct-4) were determined by Western blot analyses. Our data demonstrate that T3 treatment leads to a significant increase in cells positive for cTnI, GATA4, Cx-43, and α-actinin. The mRNA and protein expression levels of these specific markers of cardiomyocytes were also increased after T3 treatment. At the same time, the protein expression level of Oct-4 was substantially downregulated in T3-treated cells. These results demonstrate that T3 treatment increases the differentiation of BMMSCs induced to cardiomyocytes and promotes their maturation.
[Mh] Termos MeSH primário: Medula Óssea
Células Mesenquimais Estromais/efeitos dos fármacos
Miócitos Cardíacos/efeitos dos fármacos
Tironinas/farmacologia
[Mh] Termos MeSH secundário: Actinina/biossíntese
Animais
Diferenciação Celular
Células Cultivadas
Conexina 43/biossíntese
Fator de Transcrição GATA4/biossíntese
RNA Mensageiro
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Troponina I/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (GATA4 Transcription Factor); 0 (RNA, Messenger); 0 (Thyronines); 0 (Troponin I); 11003-00-2 (Actinin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160126
[St] Status:MEDLINE
[do] DOI:10.1097/FJC.0000000000000363



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