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  1 / 17423 MEDLINE  
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[PMID]:29374923
[Au] Autor:Bai XZ; He T; Zhang JL; Liu Y; Cao MY; Zhang JN; Cai WX; Jia YH; Shi JH; Su LL; Hu DH
[Ad] Endereço:Burn Center of PLA, Department of Burns and Cutaneous Surgery, Xijing Hospital, Air Force Medical University, Xi'an 710032, China.
[Ti] Título:[Effects of microRNA-34a on regulating silent information regulator 1 and influence of the factor on myocardial damage of rats with severe burns at early stage].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):21-28, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the effects of microRNA-34a on regulating silent information regulator 1 (SIRT1) and influence of SIRT1 on myocardial damage of rats with severe burns at early stage. (1) Twenty-four Sprague-Dawley (SD) rats were divided into sham injury (SI) group, simple burns (SB) group and SIRT1 agonist (SA) group according to the random number table (the same grouping method below), with 8 rats in each group. Rats in groups SB and SA were inflicted with 30% total body surface area full-thickness scald (hereinafter referred to as burns) on the back, and rats in group SI were sham injuried on the back. Immediately after injury, rats in groups SI and SB were intraperitoneally injected with normal saline of 50 mL/kg, and rats in group SA were intraperitoneally injected with normal saline of 50 mL/kg and 1 mg/mL resveratrol of 50 mg/kg. At 6 h post injury, abdominal aortic blood was collected to make serum and myocardial tissue of rats was collected. (2) Myocardial cells of twelve neonatal SD rats were collected and divided into microRNA-34a mimic control (MMC) group, microRNA-34a mimic (MM) group, microRNA-34a inhibitor control (MIC) group, and microRNA-34a inhibitor (MI) group, which were respectively transfected with gene sequences of mimic control, mimic, inhibitor control, and inhibitor of microRNA-34a. The microRNA-34a expression level and protein expression level of SIRT1 in myocardial cells were respectively detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Another batch of myocardial cells were divided into microRNA-34a inhibitor control+ burn serum (MCB) group, microRNA-34a inhibitor+ burn serum (MB) group, and microRNA-34a inhibitor+ burn serum + EX527 (MBE) group. Myocardial cells in group MCB were transfected with gene sequence of inhibitor control, and myocardial cells in the later groups were transfected with gene sequence of inhibitor of microRNA-34a. After transfection of 48 h, myocardial cells in group MBE were cultured in Dulbecco's modified Eagle's medium (DMEM) solution for 6 hours, with serum in group SB of volume fraction of 10% and final amount-of-substance concentration of 1 mol/L, and myocardial cells in the other 2 groups were cultured in DMEM solution with serum from rats of group SB of volume fraction of 10%. The protein expression levels of myocardial cells of SIRT1, cleaved-caspase-3, and Bax were detected by Western blotting. (3) Myocardial tissue from (1) was collected to detect expression levels of microRNA-34a and mRNA of SIRT1 in groups SI and SB by real-time fluorescence quantitative RT-PCR. Morphology of myocardial tissue of rats in groups SI, SB, and SA was observed with biological image navigator. The mRNA expression levels of interleukin 1ß (IL-1ß) and tumor necrosis factor (TNF-α) of rats in groups SI, SB, and SA were detected by real-time fluorescence quantitative RT-PCR. The expression levels of cleaved-caspase-3, and Bax of myocardial tissue of rats in groups SI, SB, and SA were detected by Western blotting. Data were processed with one-way analysis of variance and least-significant difference test. (1) After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MM was 4.67±0.92, significantly higher than 1.03±0.04 in group MMC ( <0.01); the protein expression level of SIRT1 of myocardial cells in group MM was 0.35±0.06, significantly lower than 1.12±0.11 in group MMC ( <0.01). After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MI was 0.26±0.07, significantly lower than 1.33±0.07 in group MIC ( <0.01); the protein expression level of SIRT1 of myocardial cells in group MIC was 1.12±0.16, significantly lower than 1.74±0.34 in group MI ( <0.01). At 6 h after culture, compared with those in group MCB, the SIRT1 protein expression level of myocardial cells in group MB was significantly increased ( <0.05), while cleaved-caspase-3 and Bax protein expression levels of myocardial cells in group MB were significantly decreased ( <0.05). Compared with those in group MB, the SIRT1 protein expression level of myocardial cells in group MBE was with no significantly statistical difference ( >0.05), and cleaved-caspase-3 and Bax protein expression levels were significantly increased ( <0.05). (2) At 6 h post injury, compared with that in group SI, the microRNA-34a expression level of myocardial tissue in group SB was significantly increased ( <0.01), and the mRNA expression level of SIRT1 of myocardial tissue in group SB was significantly decreased ( <0.01). At 6 h post injury, myocardial cells in group SI arranged neatly with normal nucleus and no inflammatory cells infiltration; myocardial cells in group SB arranged disorderly, with no abnormal nucleus, and obvious inflammatory cells infiltration; myocardial cells in group SA arranged neatly, with normal nucleus and little inflammatory cells infiltration. At 6 h post injury, compared with those in group SB, the mRNA expression levels of IL-1ß and TNF-α, and the protein expression levels of cleaved-caspase-3 and Bax of myocardial tissue in groups SI and SA were significantly decreased ( <0.01). The microRNA-34a expression level of myocardial tissue of rats with severe burns at early stage increases, which decreases the expression level of SIRT1, and increases the expression levels of IL-1ß, TNF-α, cleaved-caspase-3 and Bax, leading to obvious myocardial damage. Activation of SIRT1 can alleviate myocardial damage of rats with severe burns at early stage through decreasing expression levels of IL-1ß, TNF-α, cleaved-caspase-3, and Bax.
[Mh] Termos MeSH primário: Queimaduras
MicroRNAs/genética
Miocárdio/metabolismo
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Caspase 3/genética
Caspase 3/metabolismo
Interleucina-1beta
Miocárdio/patologia
Miócitos Cardíacos
RNA Mensageiro/genética
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Sirtuína 1/genética
Estilbenos
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (Stilbenes); 0 (Tumor Necrosis Factor-alpha); EC 3.4.22.- (Caspase 3); EC 3.5.1.- (Sirt1 protein, rat); EC 3.5.1.- (Sirtuin 1); Q369O8926L (resveratrol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.005


  2 / 17423 MEDLINE  
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[PMID]:29292899
[Au] Autor:Jonasson L; Hansson G
[Ad] Endereço:Universitetssjukhuset i Linköping Kardiologiska kliniken - Linköping, Sweden - Linköping, Sweden.
[Ti] Título:Inflammation och ateroskleros ­ sista pusselbiten är på plats - Inflammation är en aktör vid ateroskleros: nya fynd kan ge ny måltavla för effektiv läkemedelsterapi..
[So] Source:Lakartidningen;114, 2017 Oct 30.
[Is] ISSN:1652-7518
[Cp] País de publicação:Sweden
[La] Idioma:swe
[Ab] Resumo:Inflammation and atherosclerosis - last piece of the puzzle has fallen into place Inflammation is a major component of atherosclerotic lesions and inflammatory biomarkers can be used to predict cardiovascular disease. Still, it has been unclear whether inflammation is a driving force in atherosclerosis, or merely an epiphenomenon. The recently published results of the CANTOS trial shows that treatment with canacinumab, a monoclonal antibody to the proinflammatory cytokine interleukin-1ß, led to a significantly lower rate of recurrent cardiovascular events, compared to placebo. Thus, it establishes beyond doubt that inflammation is a treatable pathogenetic mechanism in atherosclerosis.
[Mh] Termos MeSH primário: Aterosclerose/patologia
Inflamação/patologia
[Mh] Termos MeSH secundário: Anti-Inflamatórios/administração & dosagem
Anticorpos Monoclonais/administração & dosagem
Aterosclerose/tratamento farmacológico
Doenças Cardiovasculares/prevenção & controle
LDL-Colesterol/sangue
Seres Humanos
Inflamação/tratamento farmacológico
Interleucina-1beta/antagonistas & inibidores
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antibodies, Monoclonal); 0 (Cholesterol, LDL); 0 (Interleukin-1beta); 37CQ2C7X93 (canakinumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE


  3 / 17423 MEDLINE  
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[PMID]:29268779
[Au] Autor:Patlán M; Sánchez-Muñoz F; Amezcua-Guerra LM; Granados A; Páez A; Massó F; Mejía AM; Soster A; Bojalil R; Pavón L; Jiménez-Zamudio LA; Márquez-Velasco R
[Ad] Endereço:Doctorado en Ciencias Quimicobiológicas, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City, Mexico.
[Ti] Título:Effect of fresh frozen plasma on the in vitro activation of U937 monocytes: a potential role for the age of blood donors and their underlying cytokine profile.
[So] Source:Biol Res;50(1):42, 2017 Dec 21.
[Is] ISSN:0717-6287
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Fresh frozen plasma (FFP) administration may increase the risk of nosocomial infections in parallel with the development of immune modulation. This could be driven by soluble mediators, possibly influencing the in vitro activation of human U937 monocyte cells, in a manner dependent on the age of the donors. METHODS: FFP donors were stratified into groups of 19-30 years, 31-40 years or 41-50 years, and U937 cells were cultured with FFP (alone or plus lipopolysaccharide-LPS) for 24 h. Both in FFP and supernatants, TNF, IL-1ß, IL-6, and IL-10 levels were measured by ELISA. Additionally, CD11B, TLR2, and CASP3 gene expression were measured by qtPCR in U937 cells. Total phagocytic activity was also assayed. RESULTS: Elevated IL-10, but low TNF and IL-1ß levels were measured in FFP from individuals aged 19-40 years, whereas in individuals aged 41-50 years FFP were characterized by equalized TNF and IL-10 levels. Elevated IL-6 levels were found in all FFP samples, especially in those from the oldest individuals. FFP stimulation was associated with striking modifications in cytokine production in an age-dependent way. Exposure to FFP attenuates the response to LPS. TLR2 and CD11B expression were enhanced regardless of the age of plasma donors, although CASP3 expression was increased only when FFP from individuals aged 19-40 years were tested. Phagocytosis decreased after exposure to FFP regardless of donor age. CONCLUSION: Our results suggest that soluble mediators in FFP may modulate the functioning of monocytes. Interestingly, this effect appears to be partially influenced by the age of donors.
[Mh] Termos MeSH primário: Doadores de Sangue
Citocinas/imunologia
Monócitos/imunologia
Plasma/imunologia
Células U937/imunologia
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Interleucina-10/metabolismo
Interleucina-1beta/metabolismo
Interleucina-6/metabolismo
Masculino
Meia-Idade
Monócitos/fisiologia
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL10 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1186/s40659-017-0146-3


  4 / 17423 MEDLINE  
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[PMID]:29241192
[Au] Autor:Mao G; Wu P; Zhang Z; Zhang Z; Liao W; Li Y; Kang Y
[Ad] Endereço:Department of Joint Surgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
[Ti] Título:MicroRNA-92a-3p Regulates Aggrecanase-1 and Aggrecanase-2 Expression in Chondrogenesis and IL-1ß-Induced Catabolism in Human Articular Chondrocytes.
[So] Source:Cell Physiol Biochem;44(1):38-52, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Aggrecanase-1 (ADAMTS-4) and aggrecanase-2 (ADAMTS-5) are secreted enzymes belonging to the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family that play significant roles in the progression of osteoarthritis (OA). Here, we aimed to determine whether the expression of ADAMTS-4/5 in chondrogenesis and inflammation is regulated by microRNA-92a-3p (miR-92a-3p). METHODS: MiR-92a-3p and ADAMTS-4/5 expressions were determined by quantitative polymerase chain reaction (qPCR). To investigate the repressive effect of miR-92a-3p on ADAMTS-4/5 expression, chondrogenic human mesenchymal stem cells (hMSCs) and human chondrocytes were transfected with mature miR-92a-3p or an antisense inhibitor (anti-miR-92a-3p), respectively. ADAMTS-4/5 protein production was quantified by enzyme-linked immunosorbent assay (ELISA), and miR-92a-3p involvement in IL-1ß-mediated catabolic effects was examined by immunoblotting. The roles of activated MAP kinases (MAPK) and nuclear factor (NF)-κB were evaluated by using specific inhibitors. Interaction between miR-92a-3p and its putative binding site in the 3'-untranslated region (3'-UTR) of ADAMTS-4/5 mRNA was confirmed by luciferase reporter assay. RESULTS: miR-92a-3p expression was elevated in chondrogenic hMSCs, with significantly lower expression in OA cartilage than in normal cartilage. Stimulation with IL-1ß significantly reduced miR-92a-3p expression in primary human chondrocytes (PHCs). Transfection of chondrocytes with miR-92a-3p downregulated IL-1ß-induced ADAMTS-4/5 expression, and the activity of a reporter construct containing the 3'-UTR of human ADAMTS-4/5 mRNA. MiR-92a-3p expression was suppressed upon IL-1ß-induced activation of MAPK and NF-κB in chondrocytes. CONCLUSION: MiR-92a-3p is an important regulator of ADAMTS-4/5 in human chondrocytes and may contribute to the development of OA.
[Mh] Termos MeSH primário: Proteína ADAMTS4/metabolismo
Proteína ADAMTS5/metabolismo
Condrogênese/efeitos dos fármacos
Condrogênese/genética
Interleucina-1beta/farmacologia
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS4/antagonistas & inibidores
Proteína ADAMTS4/genética
Proteína ADAMTS5/antagonistas & inibidores
Proteína ADAMTS5/genética
Adulto
Idoso
Antagomirs/metabolismo
Células da Medula Óssea/citologia
Cartilagem Articular/metabolismo
Cartilagem Articular/patologia
Células Cultivadas
Condrócitos/citologia
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Feminino
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/efeitos dos fármacos
Células Mesenquimais Estromais/metabolismo
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Meia-Idade
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/antagonistas & inibidores
NF-kappa B/metabolismo
Osteoartrite do Joelho/genética
Osteoartrite do Joelho/metabolismo
Osteoartrite do Joelho/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antagomirs); 0 (Interleukin-1beta); 0 (MIRN92 microRNA, human); 0 (MicroRNAs); 0 (NF-kappa B); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.- (ADAMTS5 Protein); EC 3.4.24.82 (ADAMTS4 Protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1159/000484579


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[PMID]:27776448
[Au] Autor:Ye C; Zhang W; Jiang S; Yu Y; Zhou X; Zhu L; Xue D; He R
[Ad] Endereço:a Department of Orthopedic Surgery , the Second Affiliated Hospital, School of Medicine, Zhejiang University , Hangzhou , Zhejiang , China.
[Ti] Título:Platelet-derived growth factor-BB attenuates titanium-particle-induced osteolysis in vivo.
[So] Source:Growth Factors;34(5-6):177-186, 2016 12.
[Is] ISSN:1029-2292
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inflammation and osteoclastogenesis play critical roles in wear-particle-induced periprosthetic osteolysis (WPO). Platelet-derived growth factor-BB (PDGF-BB) could promote osteogenesis and inhibit inflammatory response. The aim of this study was to investigate the impact of PDGF-BB on WPO. Mice were divided into four groups, namely, sham, vehicle, low-, and high-dose PDGF-BB groups. Mice in the rhPDGF-BB groups were treated with PDGF-BB at 0.25 or 1 mg/ml/kg/day. Mice in the sham and vehicle groups received PBS daily. Two weeks after surgery, calvariae were harvested. Immunohistochemical analysis and µ-CT showed that PDGF-BB significantly reduced osteoclast formation and bone resorption. ELISA showed that rhPDGF-BB decreased the secretion of TNF-α, IL-1ß, and IL-6. Western blotting revealed that rhPDGF-BB stimulated the expression of osteocalcin and osteoprotegerin. Furthermore, more VEGF and CD31 proteins were observed due to PDGF-BB by immunofluorescence. In conclusion, these findings suggest that rhPDGF-BB represents a potential treatment for WPO.
[Mh] Termos MeSH primário: Interface Osso-Implante/patologia
Osteólise/tratamento farmacológico
Proteínas Proto-Oncogênicas c-sis/uso terapêutico
Titânio/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Osteólise/etiologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Proteínas Proto-Oncogênicas c-sis/administração & dosagem
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Proto-Oncogene Proteins c-sis); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Endothelial Growth Factor A); 1B56C968OA (becaplermin); D1JT611TNE (Titanium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1080/08977194.2016.1240680


  6 / 17423 MEDLINE  
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[PMID]:29424990
[Au] Autor:Loskutov DV; Khamitova RY
[Ti] Título:[The genetic component of chronic respiratory diseases in workers of foundry productions].
[So] Source:Gig Sanit;95(7):623-6, 2016.
[Is] ISSN:0016-9900
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Review of the literature shows that currently there is an accumulation of data on the genetic determination of individual susceptibility to adverse industrial factors. Material of the research were high molecular DNA samples isolated from epithelial mouth scrapings in 99 foundry workers. Study of polymorphic variants of interleukin genes was performed by means of the analysis ofproducts of amplification of specific regions of the genome. Homozygous genotype TNF-a (-308A/G) was established to increase the relative risk of shaping of chronic respiratory diseases: with AA alleles - by 6.4 times and GG alleles - by 2.4 times, while the heterozygous genotype (AG) decreases - by 1. 9 times. Polymorphism of gene IL-1ß (+3953 T / C) had no significance for the development of respiratory disease. Genotyping interleukins, involved in the inflammatory responses of the bronchopulmonary tract, can be considered as an element ofprimary prevention in industries with a high risk for shaping of respiratory diseases.
[Mh] Termos MeSH primário: Metalurgia
Doenças Profissionais
Doenças Respiratórias
Fator de Necrose Tumoral alfa/genética
[Mh] Termos MeSH secundário: Adulto
Predisposição Genética para Doença
Seres Humanos
Hipersensibilidade/genética
Interleucina-1beta/genética
Masculino
Doenças Profissionais/epidemiologia
Doenças Profissionais/etiologia
Doenças Profissionais/genética
Polimorfismo Genético
Doenças Respiratórias/epidemiologia
Doenças Respiratórias/etiologia
Doenças Respiratórias/genética
Federação Russa/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL1B protein, human); 0 (Interleukin-1beta); 0 (Tumor Necrosis Factor-alpha)
[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:180210
[St] Status:MEDLINE


  7 / 17423 MEDLINE  
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[PMID]:28462597
[Au] Autor:Dias RD; Scalabrini Neto A
[Ad] Endereço:a STRATUS Center for Medical Simulation , Brigham and Women's Hospital, Harvard Medical School , Boston , MA , USA.
[Ti] Título:Acute stress in residents during emergency care: a study of personal and situational factors.
[So] Source:Stress;20(3):241-248, 2017 May.
[Is] ISSN:1607-8888
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Providing care for simulated emergency patients may induce considerable acute stress in physicians. However, the acute stress provoked in a real-life emergency room (ER) is not well known. Our aim was to assess acute stress responses in residents during real emergency care and investigate the related personal and situational factors. A cross-sectional observational study was carried out at an emergency department of a tertiary teaching hospital. All second-year internal medicine residents were invited to voluntarily participate in this study. Acute stress markers were assessed at baseline (T1), before residents started their ER shift, and immediately after an emergency situation (T2), using heart rate, systolic, and diastolic blood pressure, salivary α-amylase activity, salivary interleukin-1 ß, and the State-Trait Anxiety Inventory (STAI-s and STAI-t). Twenty-four residents were assessed during 40 emergency situations. All stress markers presented a statistically significant increase between T1 and T2. IL-1 ß presented the highest percent increase (141.0%, p < .001), followed by AA (99.0%, p = .002), HR (81.0%, p < .001), DBP (8.0%, p < .001), and SBP (3.0%, p < .001). In the multivariable analysis, time of residency had a negative correlation with HR during the emergency (adjusted R-square = .168; F = 8.69; p = .006), SBP response (adjusted R-square = .210; F = 6.19; p = .005) and DBP response (adjusted R-square = .293; F = 9.09; p = .001). Trait anxiety (STAI-t) was positively correlated with STAI-s (adjusted R-square = .326; F = 19.9; p < .001), and number of procedures performed during emergency care had a positive association with HR response (adjusted R-square = .241; F = 5.02; p = .005). In the present study, emergency care provoked substantial acute stress in residents. Resident experience, trait anxiety, and number of emergency procedures were independently associated with acute stress response.
[Mh] Termos MeSH primário: Ansiedade/fisiopatologia
Pressão Sanguínea
Serviço Hospitalar de Emergência
Frequência Cardíaca
Internato e Residência
Estresse Ocupacional/fisiopatologia
Médicos/psicologia
Estresse Psicológico/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Ansiedade/metabolismo
Ansiedade/psicologia
Estudos Transversais
Emergências
Feminino
Seres Humanos
Interleucina-1beta/metabolismo
Medicina Interna/educação
Masculino
Estresse Ocupacional/metabolismo
Estresse Ocupacional/psicologia
Saliva/química
alfa-Amilases Salivares/metabolismo
Estresse Psicológico/metabolismo
Estresse Psicológico/psicologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); EC 3.2.1.1 (Salivary alpha-Amylases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1080/10253890.2017.1325866


  8 / 17423 MEDLINE  
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[PMID]:29328647
[Au] Autor:Hsieh HL; Lee CH; Lin KC
[Ad] Endereço:Department of Life Science, National Dong Hwa University , Hualien County 974, Taiwan.
[Ti] Título:Development of Yam Dioscorin-Loaded Nanoparticles for Paracellular Transport Across Human Intestinal Caco-2 Cell Monolayers.
[So] Source:J Agric Food Chem;66(5):1175-1183, 2018 Feb 07.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dioscorins, the major storage proteins of yam tubers, exert immunomodulatory activities. To improve oral bioavailability of dioscorins in the intestine, recombinant dioscorin (rDioscorin) was coated with N,N,N-trimethyl chitosan (TMC) and tripolyphosphate (TPP), resulting in the formation of TMC-rDio-TPP nanoparticles (NPs). The loading capacity and entrapment efficiency of rDioscorin in the NPs were 26 ± 0.7% and 61 ± 1.4%, respectively. The NPs demonstrated a substantial release profile in the pH environment of the jejunum. The rDioscorin released from the NPs stimulated proliferation and phagocytosis of the macrophage RAW264.7 and activated the gene expression of IL-1ß and IL-6. Incubation of the NPs in the Caco-2 cell monolayer led to a 5.2-fold increase of P compared with rDioscorin alone, suggesting that rDioscorin, with the assistance of TMC, can be promptly transported across the intestinal epithelia. These results demonstrate that the TMC-rDio-TPP NPs can be utilized for elucidating the immunopharmacological effects of dioscorins through oral delivery.
[Mh] Termos MeSH primário: Dioscorea/química
Intestinos/metabolismo
Nanopartículas/metabolismo
Proteínas de Plantas/metabolismo
[Mh] Termos MeSH secundário: Administração Oral
Disponibilidade Biológica
Transporte Biológico
Células CACO-2
Proliferação Celular/efeitos dos fármacos
Quitosana
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Concentração de Íons de Hidrogênio
Interleucina-1beta/genética
Interleucina-6/genética
Mucosa Intestinal/metabolismo
Nanopartículas/administração & dosagem
Fagocitose/efeitos dos fármacos
Proteínas de Plantas/administração & dosagem
Proteínas de Plantas/farmacocinética
Tubérculos/química
Polifosfatos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Interleukin-6); 0 (N-trimethyl chitosan chloride); 0 (Plant Proteins); 0 (Polyphosphates); 0 (dioscorin protein, Dioscorea); 9012-76-4 (Chitosan); NU43IAG5BC (triphosphoric acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04150


  9 / 17423 MEDLINE  
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[PMID]:29443743
[Au] Autor:Chen BB; Li ZH; Gao S
[Ad] Endereço:Department of Respiratory, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Título:Circulating miR-146a/b correlates with inflammatory cytokines in COPD and could predict the risk of acute exacerbation COPD.
[So] Source:Medicine (Baltimore);97(7):e9820, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to investigate the predicting value of miR-146a/b for acute exacerbation chronic obstructive pulmonary disease (AECOPD) and COPD, and to explore their associations with inflammatory cytokines in AECOPD and stable COPD patients.One hundred six AECOPD, 122 stable COPD patients, and 110 health volunteers with age and sex matched to total COPD patients (AECOPD and stable COPD) were enrolled. Blood samples were collected from all participants. Relative expression of miR-146a/b was determined by real-time polymerase chain reaction. Tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-8 (IL-8), leukotriene B4 (LTB-4) expression in serum from AECOPD and stable COPD patients were assessed using commercial ELISA kit.Serum levels of miR-146a and miR-146b were down regulated in AECOPD patients compared with stable COPD patients and HCs. miR-146a and miR-146b are of good values for predicting the risk of AECOPD in HCs with AUC of 0.702 and 0.715. Additionally, miR-146a and miR-146b could distinguish AECOPD from stable COPD patients with AUC of 0.670 and 0.643. In AECOPD patients, levels of miR-146a in AECOPD patients were negatively associated with TNF-α, IL-6, IL-8, and LTE-4 expression. In stable COPD patients, miR-146a expressions were negatively correlated with TNF-α, IL-1ß, IL-6, IL-8, and LTE-4 levels. And, the expressions of miR-146b in AECOPD patients were negatively associated with IL-1ß and LTB-4 expression. While in stable COPD patients, miR-146b expressions were only negatively correlated with TNF-α level.In conclusion, miR-146a and miR-146b were negatively correlated with inflammatory cytokines, and could be promising biomarkers for predicting the risk of AECOPD in stable COPD patients and healthy individuals.
[Mh] Termos MeSH primário: Citocinas/sangue
Progressão da Doença
MicroRNAs/sangue
Doença Pulmonar Obstrutiva Crônica/sangue
[Mh] Termos MeSH secundário: Doença Aguda
Idoso
Biomarcadores/sangue
Estudos de Casos e Controles
Regulação para Baixo
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Interleucina-1beta/sangue
Interleucina-6/sangue
Interleucina-8/sangue
Leucotrieno B4/sangue
Masculino
Meia-Idade
Reação em Cadeia da Polimerase em Tempo Real
Fatores de Risco
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (IL6 protein, human); 0 (IL8 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Interleukin-8); 0 (MIRN146 microRNA, human); 0 (MicroRNAs); 0 (Tumor Necrosis Factor-alpha); 1HGW4DR56D (Leukotriene B4)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009820


  10 / 17423 MEDLINE  
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[PMID]:29217355
[Au] Autor:Wang X; Zhang G; Qiao Y; Feng C; Zhao X
[Ad] Endereço:Department of Anesthesiology, The Second Hospital of Shandong University, 247 Bei Yuan Street, Jinan 250033, China.
[Ti] Título:Crocetin attenuates spared nerve injury-induced neuropathic pain in mice.
[So] Source:J Pharmacol Sci;135(4):141-147, 2017 Dec.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Crocetin is the main component of saffron and exhibits anti-oxidative and anti-inflammatory effects. Neuroinflammation and oxidative stress have been recognized to play a crucial role in the pathogenesis of neuropathic pain. We investigated the effect of crocetin in a mouse model with neuropathic pain induced by spared nerve injury (SNI). Crocetin was intrathecally perfused at various doses for up to 12 days starting 3 days before the surgery. Behavioral tests were performed to determine pain sensitivity. The concentrations of proinflammatory cytokines tumor necrosis factor (TNF-α) and interleukin-1ß (IL-1ß) were measured to assess neuroinflammation. In addition, the enzymatic activity of superoxide dismutase (SOD) was measured to reveal the oxidative stress level. We found that repeated treatment with crocetin dose-dependently attenuated mechanical and thermal allodynia in SNI mice. In addition, treatment with high dose of crocetin reduced SNI-induced increase of TNF-α and IL-1ß. Crocetin also restored the activity of mitochondrial MnSOD which was reduced in the sciatic nerve and the spinal cord of SNI mice. Collectively, our data demonstrate that crocetin effectively attenuates the neuropathic pain and significantly suppresses oxidative stress and neuroinflammation in the SNI mouse model, supporting the potential of crocetin in the treatment against neuropathic pain.
[Mh] Termos MeSH primário: Carotenoides/administração & dosagem
Carotenoides/farmacologia
Neuralgia/tratamento farmacológico
Neuralgia/etiologia
Traumatismos dos Nervos Periféricos/complicações
Fitoterapia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios
Antioxidantes
Biomarcadores
Carotenoides/isolamento & purificação
Crocus/química
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Mediadores da Inflamação/metabolismo
Interleucina-1beta/metabolismo
Masculino
Camundongos Endogâmicos
Neuralgia/diagnóstico
Neuralgia/metabolismo
Estresse Oxidativo
Nervo Isquiático/metabolismo
Medula Espinal
Superóxido Dismutase
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Biomarkers); 0 (Inflammation Mediators); 0 (Interleukin-1beta); 0 (Tumor Necrosis Factor-alpha); 20TC155L9C (crocetin); 36-88-4 (Carotenoids); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE



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