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[PMID]:29203736
[Au] Autor:Lutsenko RV; Vlasova EV; Kolot EG; Gladka VM; Sidorenko AG
[Ad] Endereço:Higher State Educational Establishment Of Ukraine, "Ukrainian Medical Stomatological Academy", Poltava, Ukraine.
[Ti] Título:The exchange of monoamines during the experimental neurosis on the background of using of amide "2-hydroxy-n-naphthalen-1-yl-2-(2-oxo-,2-dihydroindol-3-ylidene)".
[So] Source:Wiad Lek;70(5):895-900, 2017.
[Is] ISSN:0043-5147
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Incessant increase in the frequency and distribution of anxiety disorders stipulates searching, research and study of the mechanism of action of new substances for their correction, including the group of 2-oxoindolin-3-glyoxylic acid derivatives. THE AIM: To research the effect of N-(1-naphthyl) amide-2-oxoindolin-3-glyoxylic acid on monoaminergic system of subjected to experimental neurosis of rats. MATERIALS AND METHODS: The experiments were performed on male Wistar rats, who have weight 180-220g and were researching the effect of 2-hydro-N-naphthalen-1-yl-2-(2-oxy-1,2-dihydroindol-3-ylidene)-acetamide (compound 18) at a dose (12 mg/kg), by intragastric drug injection of subjected to experimental neurosis rats, during 30 days (1 time in three days), for monoamines content (epinephrine, norepinephrine, dopamine and serotonin) in the blood, their decay products (homovanillic acid, vanillylmandelic acid and 5-oxyindolacetic acid) in the urine and the ratio of end products of the reaction to their predecessors. RESEARCH: It was established that during the preventive-therapeutic application of N-(1-naphthyl)amide-2-oxoindolin-3-glyoxylic acid, it effectively adjusts the level of monoamines, reducing the content of adrenaline and increasing the content of noradrenaline, dopamine and 5-HT in the blood. The compound also reduces the content of products exchange of mediators (HVA,VMA and 5-OIAA) in the urine. The 2-oxoindolin derivatives reduces the ratio between HVA/dopamine, VMA/(noradrenaline + adrenaline) and 5-OIAA/5-HT, it testifies about the normalizing of enzymes activity, which are involved in the process of exchange and maintaining the constancy of monoamines. The results show that in the mechanisms of anxiolytic action of compound 18, a significant role plays the normalization of content and exchange of neurotransmitters in the organism, which caused an experimental neurosis. CONCLUSION: Compound 2-hydro-N-naphthalen-1-yl-2-(2-oxo-1,2-dihydroindol-3-ylidene)-acetamide by the experimental 30-day neurosis, was reducing the expression of neurotransmitter imbalance in the blood, apparently due to correction of enzymatic synthesis links and biotransformation of monoamines.
[Mh] Termos MeSH primário: Adamantano/análogos & derivados
Ansiolíticos/farmacologia
Transtornos de Ansiedade/tratamento farmacológico
Benzimidazóis/farmacologia
Transtorno Depressivo/tratamento farmacológico
Morfolinas/farmacologia
[Mh] Termos MeSH secundário: Adamantano/farmacologia
Animais
Monoaminas Biogênicas/farmacologia
Seres Humanos
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-((2-morpholino)ethylthio)-5-ethoxybenzimidazole); 0 (Anti-Anxiety Agents); 0 (Benzimidazoles); 0 (Biogenic Monoamines); 0 (Morpholines); 0 (N-(2-adamantyl)-N-p-bromophenylamine); PJY633525U (Adamantane)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:29368823
[Au] Autor:Ritchie MK; Ellison M; Ranganathan P; Sizemore D; Vallejo MC
[Ti] Título:Aprepitant: A Novel Medicaton in the Prevention of Postoperative Nausea and Vomiting.
[So] Source:W V Med J;112(6):20-4, 2016 Nov-Dec.
[Is] ISSN:0043-3284
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Antieméticos/uso terapêutico
Morfolinas/uso terapêutico
Náusea e Vômito Pós-Operatório/tratamento farmacológico
Náusea e Vômito Pós-Operatório/prevenção & controle
[Mh] Termos MeSH secundário: Antieméticos/farmacologia
Seres Humanos
Incidência
Morfolinas/farmacologia
Náusea e Vômito Pós-Operatório/epidemiologia
Medição de Risco
Fatores de Risco
West Virginia/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiemetics); 0 (Morpholines); 1NF15YR6UY (aprepitant)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


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[PMID]:29368813
[Au] Autor:Matthews PRL; Horder J; Pearce M
[Ad] Endereço:North Kildare Mental Health Service, Kildare West Wicklow MHS, Celbridge Community Health Centre, Shackleton Road, Celbridge, Co. Kildare, Ireland.
[Ti] Título:Selective noradrenaline reuptake inhibitors for schizophrenia.
[So] Source:Cochrane Database Syst Rev;1:CD010219, 2018 Jan 25.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Schizophrenia is frequently a chronic and disabling illness with a heterogeneous range of symptoms. The positive symptoms usually respond to antipsychotics but the cognitive and negative symptoms of schizophrenia are difficult to treat with conventional antipsychotics and significantly impact on quality of life and social outcomes. Selective noradrenaline reuptake inhibitors (NRIs) increase prefrontal dopamine and noradrenaline levels without significantly affecting subcortical dopamine levels, making them an attractive candidate for treating cognitive and negative symptoms. OBJECTIVES: To investigate the effects of selective noradrenaline reuptake inhibitors (NRIs), compared with a placebo or control treatment, for people with schizophrenia. SEARCH METHODS: We searched the Cochrane Schizophrenia Group's Trials Register (up to 7 February 2017) which is based on regular searches of MEDLINE, Embase, CINAHL, BIOSIS, AMED, PubMed, PsycINFO, and registries of clinical trials. There are no language, date, document type, or publication status limitation for inclusion of records into the register. We inspected references of all included studies for further relevant studies. SELECTION CRITERIA: We included randomised controlled trials (RCTs) comparing NRIs with either a control treatment or placebo for people with schizophrenia or related disorders (such as schizoaffective disorder) by any means of diagnosis. We included trials that met our selection criteria and provided useable information. DATA COLLECTION AND ANALYSIS: We independently inspected all citations from searches, identified relevant abstracts, and independently extracted data from all included studies. For binary data we calculated risk ratio (RR), for continuous data we calculated mean difference (MD), and for cognitive outcomes we derived standardised mean difference (SMD) effect sizes, all with 95% confidence intervals (CI) and using a random-effects model. We assessed risk of bias for the included studies and used the GRADE approach to produce a 'Summary of findings' table which included our prespecified main outcomes of interest. MAIN RESULTS: Searching identified 113 records. We obtained the full text of 48 of these records for closer inspection. Sixteen trials, randomising a total of 919 participants are included. The majority of trials included adults with schizophrenia or similar illness who were inpatients, and while they were poorly characterised, most appeared to include patients with a chronic presentation. The intervention NRI in nine of the 16 trials was reboxetine, with atomoxetine and viloxazine used in the remaining trials. 14 trials compared NRIs with placebo. Only two trials provided data to compare NRIs against an active control and both compared reboxetine to citalopram but at 4 weeks and 24 weeks respectively so they could not be combined in a meta-analysis.One trial was described as 'open' and we considered it to be at high risk of bias for randomisation and blinding, three trials were at high risk of bias for attrition, six for reporting, and two for other sources of bias. Our main outcomes of interest were significant response or improvement in positive/negative mental state, global state and cognitive functioning, average cognitive functioning scores, significant response or improvement in quality of life and incidence of nausea. All data for main outcomes were short term.NRIs versus placeboMental state results showed significantly greater rates of improvement in negative symptoms scores (1 RCT, n = 50; RR 3.17, 95% CI 1.52 to 6.58; very low quality evidence) with NRIs on the PANSS negative. No data were reported for significant response or improvement in positive symptoms, but average endpoint PANSS positive scores were available and showed no difference between NRIs and placebo (5 RCTs, n = 294; MD -0.16, 95% CI -0.96 to 0.63; low-quality evidence). Improvement in clinical global status was similar between groups (1 RCT, n = 28; RR 0.99, 95% CI 0.45 to 2.20; very low quality evidence). Significant response or improvement in cognitive functioning data were not reported. Average composite cognitive scores showed no difference between NRIs and placebo (4 RCTs, n = 180; SMD 0.04, 95% CI -0.28 to 0.36; low-quality evidence). Significant response or improvement in quality of life data were not reported, however average endpoint scores from the GQOLI-74 were reported. Those receiving NRIs had better quality of life scores compared to placebo (1 RCT, n = 114; MD 9.36, 95% CI 7.89 to 10.83; very low quality evidence). All-cause withdrawals did not differ between the treatment groups (8 RCTs, n = 401, RR 0.94 95% CI 0.63 to 1.39; moderate-quality evidence). Rates of nausea were not greater with NRIs (3 RCTs, n = 176; RR 0.49, 95% CI 0.10 to 2.41; low-quality evidence). AUTHORS' CONCLUSIONS: Our results provide tentative very low quality evidence that compared to placebo, NRIs (specifically reboxetine) may have a benefit on the negative symptoms of schizophrenia. Limited evidence also suggests that NRIs have no effect on the positive symptoms of schizophrenia or cognitive functioning. NRIs appear generally well tolerated with no real differences in adverse effects such as nausea noted between NRIs and placebo. However, these results are based on short-term follow-up and are poor quality - there is need for more good-quality evidence. A large RCT of reboxetine over a longer period of time, focusing specifically on negative and cognitive symptoms as well as more detailed and comprehensive reporting of outcomes, including adverse events, is required.
[Mh] Termos MeSH primário: Inibidores da Captação Adrenérgica/uso terapêutico
Esquizofrenia/tratamento farmacológico
Inibidores da Recaptação de Serotonina e Norepinefrina/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Cloridrato de Atomoxetina/uso terapêutico
Citalopram/uso terapêutico
Cognição/efeitos dos fármacos
Seres Humanos
Morfolinas/uso terapêutico
Qualidade de Vida
Ensaios Clínicos Controlados Aleatórios como Assunto
Viloxazina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Adrenergic Uptake Inhibitors); 0 (Morpholines); 0 (Serotonin and Noradrenaline Reuptake Inhibitors); 0DHU5B8D6V (Citalopram); 57WVB6I2W0 (Atomoxetine Hydrochloride); 5I5Y2789ZF (Viloxazine); 947S0YZ36I (reboxetine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD010219.pub2


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[PMID]:28458167
[Au] Autor:Fan TT; Feng XY; Yang YZ; Gao F; Liu Q
[Ad] Endereço:Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China; Department of Emergency, Chengdu First People's Hospital, Sichuan 610016, PR China.
[Ti] Título:Downregulation of PI3K-γ in a mouse model of sepsis-induced myocardial dysfunction.
[So] Source:Cytokine;96:208-216, 2017 08.
[Is] ISSN:1096-0023
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A key component during sepsis is the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, of which the PI3K-γ isoform is a major regulator in many inflammatory responses. However, the role of PI3K-γ in the development of sepsis-induced myocardial dysfunction (SIMD) is unknown. In this study, we established a model of SIMD induced by lipopolysaccharide (LPS), subsequently used the selective inhibitor LY294002 and AS605240 to block the effect of PI3K and PI3K-γ, respectively. Cardiac function was evaluated by echocardiography, hearts were obtained for histological and protein expression examinations. ELISA was used to measure the serum levels of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), cardiac troponin I (cTnI) and heart-type fatty acid binding protein (H-FABP). LPS-treated mice showed an increase to cardiac inflammation, myocardial damage and production of TNF-α, IL-6, NF-κB, cTnI and H-FABP. Administration of AS605240 to LPS-treated mice reduced some patho-physiological characteristics of SIMD and reduced TNF-α, IL-6, cTnI and H-FABP production. However, administration of LY294002 did not improve those same conditions. The results showed that PI3K-γ is likely a crucial element in SIMD by regulating the PI3K/Akt pathway, and become a new marker of myocardial injury. Inhibition of PI3K-γ might be a potential therapeutic target in SIMD.
[Mh] Termos MeSH primário: Cardiomiopatias/metabolismo
Classe II de Fosfatidilinositol 3-Quinases/metabolismo
Sepse/complicações
[Mh] Termos MeSH secundário: Animais
Cardiomiopatias/genética
Cardiomiopatias/fisiopatologia
Cromonas/administração & dosagem
Classe II de Fosfatidilinositol 3-Quinases/genética
Citocinas/sangue
Modelos Animais de Doenças
Regulação para Baixo
Interleucina-6/biossíntese
Lipopolissacarídeos/administração & dosagem
Camundongos
Morfolinas/administração & dosagem
Miocárdio/patologia
Quinoxalinas/administração & dosagem
Quinoxalinas/uso terapêutico
Transdução de Sinais/efeitos dos fármacos
Tiazolidinedionas/administração & dosagem
Tiazolidinedionas/uso terapêutico
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-quinoxalin-6-ylmethylenethiazolidine-2,4-dione); 0 (Chromones); 0 (Cytokines); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (Morpholines); 0 (Quinoxalines); 0 (Thiazolidinediones); 0 (Tumor Necrosis Factor-alpha); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.137 (Class II Phosphatidylinositol 3-Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  5 / 13926 MEDLINE  
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[PMID]:29287093
[Au] Autor:Hossain ME; Matsuzaki K; Katakura M; Sugimoto N; Mamun AA; Islam R; Hashimoto M; Shido O
[Ad] Endereço:Department of Environmental Physiology, Faculty of Medicine, Shimane University, Enya-cho, Izumo, Japan.
[Ti] Título:Direct exposure to mild heat promotes proliferation and neuronal differentiation of neural stem/progenitor cells in vitro.
[So] Source:PLoS One;12(12):e0190356, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heat acclimation in rats is associated with enhanced neurogenesis in thermoregulatory centers of the hypothalamus. To elucidate the mechanisms for heat acclimation, we investigated the effects of direct mild heat exposure on the proliferation and differentiation of neural stem/progenitor cells (NSCs/NPCs). The NSCs/NPCs isolated from forebrain cortices of 14.5-day-old rat fetuses were propagated as neurospheres at either 37.0°C (control) or 38.5°C (mild heat exposure) for four days, and the effects on proliferation were investigated by MTS cell viability assay, measurement of neurosphere diameter, and counting the total number of cells. The mRNA expressions of heat shock proteins (HSPs) and brain-derived neurotrophic factor (BDNF), cAMP response element-binding (CREB) protein and Akt phosphorylation levels, and intracellular reactive oxygen species (ROS) levels were analyzed using real time PCR, Western blotting and CM-H2DCFDA assay respectively. Heat exposure under proliferation condition increased NSC/NPC viability, neurosphere diameter, and cell count. BDNF mRNA expression, CREB phosphorylation, and ROS level were also increased by heat exposure. Heat exposure increased HSP27 mRNA expression concomitant with enhanced p-Akt level. Moreover, treatment with LY294002 (a PI3K inhibitor) abolished the effects of heat exposure on NSC/NPC proliferation. Furthermore, heat exposure under differentiation conditions increased the proportion of cells positive for Tuj1 (a neuronal marker). These findings suggest that mild heat exposure increases NSC/NPC proliferation, possibly through activation of the Akt pathway, and also enhances neuronal differentiation. Direct effects of temperature on NSCs/NPCs may be one of the mechanisms involved in hypothalamic neurogenesis in heat-acclimated rats. Such heat-induced neurogenesis could also be an effective therapeutic strategy for neurodegenerative diseases.
[Mh] Termos MeSH primário: Diferenciação Celular
Proliferação Celular
Temperatura Alta
Células-Tronco Neurais/citologia
Neurônios/citologia
[Mh] Termos MeSH secundário: Animais
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Proteína de Ligação a CREB/metabolismo
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Cromonas/farmacologia
Proteínas de Choque Térmico/metabolismo
Morfolinas/farmacologia
Células-Tronco Neurais/metabolismo
Neurônios/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Ratos
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Chromones); 0 (Heat-Shock Proteins); 0 (Morpholines); 0 (Reactive Oxygen Species); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190356


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[PMID]:28743078
[Au] Autor:Rashid MM; Oh HA; Lee H; Jung BH
[Ad] Endereço:Molecular Recognition Research Center, Korea Institute of Science and Technology, Seoul 02792, Republic of Korea; Department of Biological Chemistry, Korea University of Science and Technology (UST), Daejeon 34113, Republic of Korea.
[Ti] Título:Metabolite identification of AZD8055 in Sprague-Dawley rats after a single oral administration using ultra-performance liquid chromatography and mass spectrometry.
[So] Source:J Pharm Biomed Anal;145:473-481, 2017 Oct 25.
[Is] ISSN:1873-264X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AZD8055 is an ATP-competitive specific dual mTOR inhibitor and exhibited potent antitumor activity on several types of solid tumors. However, the metabolism of AZD8055 in the body still remains unknown. In this study, metabolite identification of AZD8055 was performed using ultra high-performance liquid chromatography-ion trap mass spectrometry (UHPLC-IT-MS) through both in vitro and in vivo approaches using rat liver microsomes (RLMs) and rat plasma, urine and feces, respectively. A total of eight putative metabolites (five phase I and three phase II) were identified, and a tentative metabolic pathway was suggested for the first time. Considering the accurate mass and mass fragmentations of the detected metabolites, their plausible structures were suggested. Demethylation, hydroxylation, oxidation and morpholine ring opening were the major biotransformation processes for the phase-I metabolism, while phase-II metabolites were merely generated by the glucuronide conjugation reaction. The cumulative excretion of AZD8055 in urine and feces was 0.13% and 1.11% of the dose, respectively. When the semi-quantitative analysis of the metabolites was performed using UHPLC-MS/MS (ultra-performance liquid chromatography tandem mass spectrometry) to evaluate the overall trend of metabolites formation and excretion, AZD8055 was excreted more in the form of the metabolites than itself and their formation was very fast. Therefore it was presumed that biotransformation was playing a crucial role in its elimination. Ultimately, this study provides novel insights regarding the in vitro and in vivo biotransformations of AZD8055. Further investigations of metabolites of this potent anti-cancer compound could be beneficial for the antitumor drug design and development process.
[Mh] Termos MeSH primário: Morfolinas/análise
[Mh] Termos MeSH secundário: Administração Oral
Animais
Cromatografia Líquida de Alta Pressão
Ratos
Ratos Sprague-Dawley
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol); 0 (Morpholines)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28448439
[Au] Autor:Li TM; Liu SC; Huang YH; Huang CC; Hsu CJ; Tsai CH; Wang SW; Tang CH
[Ad] Endereço:School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan. leedemaw@mail.cmu.edu.tw.
[Ti] Título:YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 27.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:YKL-40, also known as human cartilage glycoprotein-39 or chitinase-3-like-1, is a pro-inflammatory protein that is highly expressed in rheumatoid arthritis (RA) patients. Angiogenesis is a critical step in the pathogenesis of RA, promoting the infiltration of inflammatory cells into joints and providing oxygen and nutrients to RA pannus. In this study, we examined the effects of YKL-40 in the production of the pro-inflammatory cytokine interleukin-18 (IL-18), and the stimulation of angiogenesis and accumulation of osteoblasts. We observed that YKL-40 induces IL-18 production in osteoblasts and thereby stimulates angiogenesis of endothelial progenitor cells (EPCs). We found that this process occurs through the suppression of miR-590-3p via the focal adhesion kinase (FAK)/PI3K/Akt signaling pathway. YKL-40 inhibition reduced angiogenesis in in vivo models of angiogenesis: the chick embryo chorioallantoic membrane (CAM) and Matrigel plug models. We report that YKL-40 stimulates IL-18 expression in osteoblasts and facilitates EPC angiogenesis.
[Mh] Termos MeSH primário: Proteína 1 Semelhante à Quitinase-3/metabolismo
Interleucina-18/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Animais
Antagomirs/metabolismo
Artrite Reumatoide/patologia
Sequência de Bases
Movimento Celular/efeitos dos fármacos
Células Cultivadas
Proteína 1 Semelhante à Quitinase-3/antagonistas & inibidores
Proteína 1 Semelhante à Quitinase-3/genética
Cromonas/farmacologia
Células Progenitoras Endoteliais/citologia
Células Progenitoras Endoteliais/efeitos dos fármacos
Células Progenitoras Endoteliais/metabolismo
Proteína-Tirosina Quinases de Adesão Focal/metabolismo
Seres Humanos
Interleucina-18/antagonistas & inibidores
Interleucina-18/genética
Camundongos
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Morfolinas/farmacologia
Neovascularização Fisiológica/efeitos dos fármacos
Osteoblastos/citologia
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/genética
Proteínas Recombinantes/farmacologia
Alinhamento de Sequência
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antagomirs); 0 (CHI3L1 protein, human); 0 (Chitinase-3-Like Protein 1); 0 (Chromones); 0 (Interleukin-18); 0 (MIRN590 microRNA, human); 0 (MicroRNAs); 0 (Morpholines); 0 (Recombinant Proteins); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


  8 / 13926 MEDLINE  
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[PMID]:29216640
[Au] Autor:Sun YZ; Cai N; Liu NN
[Ti] Título:Celecoxib Down-Regulates the Hypoxia-Induced Expression of HIF-1α and VEGF Through the PI3K/AKT Pathway in Retinal Pigment Epithelial Cells.
[So] Source:Cell Physiol Biochem;44(4):1640-1650, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The goal of this study was to detect the expression of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF) in human retinal pigmented epithelial (RPE) cells treated with celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, under hypoxic and normoxic conditions and to explore the signaling mechanism involved in regulating the hypoxia-induced expression of HIF-1α and VEGF in RPE cells. METHODS: D407 cells were cultured in normoxic or hypoxic conditions, with or without celecoxib or a PI3K inhibitor (LY294002). The anti-proliferative effect of celecoxib was assessed using the MTT assay. RT-PCR, Western blotting and ELISA were performed to detect the levels of PI3K, phosphorylated AKT (p-AKT), HIF-1α, VEGF and COX-2. RESULTS: Celecoxib inhibited the proliferation of RPE cells in a dose-dependent manner. Celecoxib suppressed the expression of VEGF at both the mRNA and protein levels and decreased HIF-1α protein expression. HIF-1α activation was regulated by the PI3K/AKT pathway. The celecoxib-induced down-regulation of HIF-1α and VEGF required the suppression of the hypoxia-induced PI3K/AKT pathway. However, the down-regulation of COX-2 did not occur in cells treated with celecoxib. CONCLUSIONS: The antiangiogenic effects of celecoxib in RPE cells under hypoxic conditions resulted from the inhibition of HIF-1α and VEGF expression, which may be partly mediated by a COX-2-independent, PI3K/AKT-dependent pathway.
[Mh] Termos MeSH primário: Celecoxib/farmacologia
Hipóxia Celular
Inibidores de Ciclo-Oxigenase 2/farmacologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Cromonas/farmacologia
Ciclo-Oxigenase 2/química
Ciclo-Oxigenase 2/metabolismo
Regulação para Baixo/efeitos dos fármacos
Células Epiteliais/citologia
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Morfolinas/farmacologia
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromones); 0 (Cyclooxygenase 2 Inhibitors); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Morpholines); 0 (RNA, Messenger); 0 (Vascular Endothelial Growth Factor A); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 1.14.99.1 (Cyclooxygenase 2); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); JCX84Q7J1L (Celecoxib)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1159/000485764


  9 / 13926 MEDLINE  
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[PMID]:29176314
[Au] Autor:Wang H; Deng X; Zhang J; Ou Z; Mai J; Ding S; Huo S
[Ad] Endereço:Department of Radiation Oncology, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
[Ti] Título:Elevated Expression of Zinc Finger Protein 703 Promotes Cell Proliferation and Metastasis through PI3K/AKT/GSK-3ß Signalling in Oral Squamous Cell Carcinoma.
[So] Source:Cell Physiol Biochem;44(3):920-934, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Zinc finger protein 703 (ZNF703), initially identified as a novel oncogene in human breast cancer, is a member of the NET/NlZ family of zinc finger transcription factors. It is recognized that the overexpression of ZNF703 is associated with various types of human cancers, but the role and molecular mechanism of ZNF703 in oral squamous cell carcinoma (OSCC) are unknown. METHODS: ZNF703 expression levels were examined in OSCC tissues and non-cancerous tissues by qRT-PCR and immunohistochemistry (IHC). The molecular mechanisms of ZNF703 and its effects on cell growth and metastasis were explored in vitro and in vivo using the CCK8 assay, colony formation assay, cell cycle analysis, migration and invasion assays, wound-healing assay, western blotting and xenograft experiments in nude mice. RESULTS: In this study, ZNF703 was found to be upregulated in OSCC tissues compared to that in normal tissues at both mRNA and protein levels, and its expression level was closely correlated with the overall survival of patients with OSCC. Silencing of the ZNF703 gene in OSCC cells significantly inhibited cell growth and metastasis in vitro and in vivo. Conversely, the overexpression of ZNF703 in OSCC cells promoted cancer growth and metastasis in vitro. Mechanistically, ZNF703 activated the PI3K/AKT/GSK-3ß signalling pathway and its downstream effectors, thus regulating the cell cycle and epithelial-mesenchymal transition (EMT). Furthermore, the promotive effects of ZNF703 on cellular proliferation and metastasis could be rescued by LY294002 (a PI3K-specific inhibitor) and MK2206 (an Akt-specific inhibitor). CONCLUSION: The results show that ZNF703 promotes cell growth and metastasis through PI3K/Akt/GSK-3ß signalling in OSCC and that it may be a promising target in the treatment of patients with OSCC.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Proteínas de Transporte/metabolismo
Glicogênio Sintase Quinase 3 beta/metabolismo
Neoplasias Bucais/patologia
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/mortalidade
Proteínas de Transporte/antagonistas & inibidores
Proteínas de Transporte/genética
Pontos de Checagem do Ciclo Celular
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Cromonas/farmacologia
Transição Epitelial-Mesenquimal
Feminino
Compostos Heterocíclicos com 3 Anéis/farmacologia
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Camundongos
Camundongos Nus
Microscopia de Fluorescência
Meia-Idade
Morfolinas/farmacologia
Neoplasias Bucais/metabolismo
Neoplasias Bucais/mortalidade
Imagem Óptica
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais
Transplante Heterólogo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Chromones); 0 (Heterocyclic Compounds, 3-Ring); 0 (MK 2206); 0 (Morpholines); 0 (RNA, Small Interfering); 0 (ZNF703 protein, human); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485360


  10 / 13926 MEDLINE  
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[PMID]:29253850
[Au] Autor:Li DY; Dai YK; Zhang YZ; Huang MX; Li RL; Ou-Yang J; Chen WJ; Hu L
[Ad] Endereço:Institute of Gastroenterology, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
[Ti] Título:Systematic review and meta-analysis of traditional Chinese medicine in the treatment of constipation-predominant irritable bowel syndrome.
[So] Source:PLoS One;12(12):e0189491, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: This meta-analysis analyzed the efficacy and safety of traditional Chinese medicine (TCM) for the treatment of irritable bowel syndrome with constipation (IBS-C). METHODS: We searched seven electronic databases for randomized controlled trials investigating the efficacy of TCM in the treatment of IBS-C. The search period was from inception to June 1, 2017. Eligible RCTs compared TCM with cisapride and mosapride. Article quality was evaluated with the Cochrane Risk Bias Tool in the Cochrane Handbook by two independent reviewers. Begg's test was performed to evaluate publication bias. Review Manager 5.3 and Stata 12.0 were used for analyses. RESULTS: Eleven eligible studies comprising a total of 906 participants were identified. In the primary outcome, TCM showed significant improvement in overall clinical efficacy compared with cisapride and mosapride (odds ratio [OR] = 4.00; 95% confidence interval [CI]: 2.74,5.84; P < 0.00001). In terms of secondary outcomes, TCM significantly alleviated abdominal pain (OR = 5.69; 95% CI: 2.35, 13.78; P = 0.0001), defecation frequency (OR = 4.38; 95% CI: 1.93, 9.93. P = 0.0004), and stool form (OR = 4.96; 95% CI: 2.11, 11.65; P = 0.0002) in the treatment group as compared to the control group. A lower recurrence rate was associated with TCM as compared to cisapride and mosapride (OR = 0.15; 95% CI: 0.08, 0.27; P < 0.00001). No adverse effects were observed during TCM treatment. CONCLUSIONS: TCM showed greater improvement in terms of clinical efficacy in the treatment of IBS-C than cisapride and mosapride, although it was not possible to draw a definitive conclusion due to the small sample size, high risk, and low quality of the studies. Large multi-center and long-term high-quality randomized control trials are needed.
[Mh] Termos MeSH primário: Constipação Intestinal/terapia
Síndrome do Intestino Irritável/terapia
Medicina Tradicional Chinesa
[Mh] Termos MeSH secundário: Benzamidas/administração & dosagem
Cisaprida/administração & dosagem
Seres Humanos
Morfolinas/administração & dosagem
Razão de Chances
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Benzamides); 0 (Morpholines); I8MFJ1C0BY (mosapride); UVL329170W (Cisapride)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189491



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