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[PMID]:29505522
[Au] Autor:Zhang BJ; Tian HT; Li HO; Meng J
[Ad] Endereço:Department of Anesthesia, Jining No. 1 People's Hospital, Jining City, Shandong Province, China.
[Ti] Título:The effects of one-lung ventilation mode on lung function in elderly patients undergoing esophageal cancer surgery.
[So] Source:Medicine (Baltimore);97(1):e9500, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The objective of the present study was to explore the effects of different one-lung ventilation (OLV) modes on lung function in elderly patients undergoing esophageal cancer surgery. A total of 180 consecutive elderly patients (ASA Grades I-II, with OLV indications) undergoing elective surgery were recruited in the study. Patients were randomly divided into 4 groups (n = 45). In Group A, patients received low tidal volume (VT < 8 mL/kg) + pressure controlled ventilation (PCV), low tidal volume (VT < 8 mL/kg) + volume-controlled ventilation (VCV) in Group B, high tidal volume (VT ≥ 8 mL/kg) + PCV in Group C and high tidal volume (VT ≥ 8 mL/kg) + VCV in Group D. Two-lung ventilation involved routine tidal volume (8-10 mL/kg) at a frequency of 12 to 18 times/min, and VCV mode. Clinical efficacy among 4 groups was compared. The partial pressure of end-tidal carbon dioxide (PetCO2) did not significantly differ among 4 groups (all P > .05), and the oxygenation index and SO2 in Group A were significantly higher than in the other groups (P < .05). The PetCO2, peak airway pressure (Ppeak), platform airway pressure (Pplat), and mean airway pressure (Pmean) in Group A were significantly lower than those in the other groups (all P < .05). However, airway resistance (Raw) among 4 groups did not significantly differ (all P > .05). The incidence of pulmonary infection, anastomotic fistula, ventilator-induced lung injury, lung dysfunction, difficulty weaning from mechanical ventilation, and multiple organ dysfunction in Groups A and B were lower than that in Groups C and D (all P < .05). The expression levels of IL-6, tumor necrosis factor-α, and C-reactive protein in lavage fluid in Group A were significantly lower than those in the other groups (all P < .05). OLV with low tidal volume (VT < 8 mL/kg) + PCV (5 cmH2O PEEP) improved lung function and mitigated inflammatory responses in elderly patients undergoing esophageal cancer surgery.
[Mh] Termos MeSH primário: Neoplasias Esofágicas/cirurgia
Ventilação Monopulmonar/métodos
[Mh] Termos MeSH secundário: Idoso
Líquido da Lavagem Broncoalveolar/química
Proteína C-Reativa/análise
Feminino
Seres Humanos
Interleucina-6/análise
Masculino
Meia-Idade
Testes de Função Respiratória
Fator de Necrose Tumoral alfa/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (IL6 protein, human); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009500


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[PMID]:29357800
[Au] Autor:Siverio-Mota D; Andujar I; Marrero-Ponce Y; Giner RM; Diaz-Mendoza C; Paba GM; Vicet-Muro L; Cordero-Maldonado ML; de Witte PAM; Crawford AD; Veitia MS; Perez-Jimenez F; Aran VJ
[Ad] Endereço:Laboratory for Molecular Biodiscovery, Department of Pharmaceutical and Pharmacological Sciences, University of Leuven, Herestraat 49, 3000 Leuven, Belgium.
[Ti] Título:Anti-Inflammatory Activity and Cheminformatics Analysis of New Poten t 2-Substituted 1-Methyl-5-Nitroindazolinones.
[So] Source:Curr Top Med Chem;17(30):3236-3248, 2018 Feb 09.
[Is] ISSN:1873-4294
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:After the identification of the anti-inflammatory properties of VA5-13l (2-benzyl-1- methyl-5-nitroindazolinone) in previous investigations, some of its analogous compounds were designed, synthesized and evaluated in two anti-inflammatory methods: LPS-enhanced leukocyte migration assay in zebrafish; and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear edema. The products evaluated (3, 6, 8, 9 and 10) showed the lower values of relative leukocyte migration at 30 µM (0.14, 0.07, 0.10, 0.13 and 0.07, respectively), while in ear edema and myeloperoxidase activity methods, all the compounds reduced inflammation, only 4 and 16 yielded unsatisfactory results. The relationship linking structure and activity (SAR analysis) was determinate by using SARANEA software. The importance of the 5-Nitro group of the indazole ring for the activity was evident, and showed modest reduction when benzyl (Bn) is changed by alkyl group. A substituted Bn moiety at N2 (R) is the best substituent (5-10); nevertheless, if methylene group of Bn is deleted, the activity is affected. Also, introduction of halogen atoms mainly at positions 3 or 4 of the benzyl moiety (6 and 10) leads in general to strong activities. In fact, compounds 7 and 8 (R = 4-FBn or 4-ClBn, respectively) exhibit satisfactory results in in vivo tests and appear promising. The production of IL-6 at all doses assayed was significantly reduced, except with 16. Nonetheless, the production of TNF-α was significantly inhibited only by this chemical (16) at concentration of 50 µM. On the other hand, compound 2 was the one that mostly inhibited the expression of COX-2 and iNOS. From these results, it can be concluded that the inhibition in the release of cytokines can be one of the mechanisms of action responsible for the anti-inflammatory effect for 2-benzyl derivates while other 2-alkyl derivatives can inhibit production of NO. Therefore, nitroindazolinone chemical prototype could be an interesting structural group with anti-inflammatory purposes in the therapeutic.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Inibidores de Ciclo-Oxigenase 2/farmacologia
Indazóis/farmacologia
Informática
Nitrocompostos/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/química
Ciclo-Oxigenase 2/metabolismo
Inibidores de Ciclo-Oxigenase 2/química
Relação Dose-Resposta a Droga
Seres Humanos
Indazóis/química
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Estrutura Molecular
Óxido Nítrico/antagonistas & inibidores
Óxido Nítrico/biossíntese
Óxido Nítrico Sintase Tipo II/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/metabolismo
Nitrocompostos/química
Relação Estrutura-Atividade
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cyclooxygenase 2 Inhibitors); 0 (Indazoles); 0 (Lipopolysaccharides); 0 (Nitro Compounds); 0 (Tumor Necrosis Factor-alpha); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.99.1 (Cyclooxygenase 2)
[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:180124
[St] Status:MEDLINE
[do] DOI:10.2174/1568026618666180119125255


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[PMID]:28462525
[Au] Autor:Tummers B; Green DR
[Ad] Endereço:Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.
[Ti] Título:Caspase-8: regulating life and death.
[So] Source:Immunol Rev;277(1):76-89, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Roles for cell death in development, homeostasis, and the control of infections and cancer have long been recognized. Although excessive cell damage results in passive necrosis, cells can be triggered to engage molecular programs that result in cell death. Such triggers include cellular stress, oncogenic signals that engage tumor suppressor mechanisms, pathogen insults, and immune mechanisms. The best-known forms of programmed cell death are apoptosis and a recently recognized regulated necrosis termed necroptosis. Of the two best understood pathways of apoptosis, the extrinsic and intrinsic (mitochondrial) pathways, the former is induced by the ligation of death receptors, a subset of the TNF receptor (TNFR) superfamily. Ligation of these death receptors can also induce necroptosis. The extrinsic apoptosis and necroptosis pathways regulate each other and their balance determines whether cells live. Integral in the regulation and initiation of death receptor-mediated activation of programmed cell death is the aspartate-specific cysteine protease (caspase)-8. This review describes the role of caspase-8 in the initiation of extrinsic apoptosis execution and the mechanism by which caspase-8 inhibits necroptosis. The importance of caspase-8 in the development and homeostasis and the way that dysfunctional caspase-8 may contribute to the development of malignancies in mice and humans are also explored.
[Mh] Termos MeSH primário: Caspase 8/imunologia
Inflamassomos/metabolismo
Mitocôndrias/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Homeostase
Seres Humanos
Necrose
Receptores de Morte Celular/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Inflammasomes); 0 (Receptors, Death Domain); 0 (Receptors, Tumor Necrosis Factor); 0 (Tumor Necrosis Factor-alpha); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12541


  4 / 111894 MEDLINE  
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[PMID]:28453766
[Au] Autor:Lim KJ; Lee SJ; Kim S; Lee SY; Lee MS; Park YA; Choi EJ; Lee EB; Jun HK; Cho JM; Lee S; Kwon KS; Lim BP; Jeon MS; Shin EC; Choi YS; Fudim E; Picard O; Yavzori M; Ben-Horin S; Chang SJ
[Ad] Endereço:R&D Division, Celltrion Inc., Incheon, Korea.
[Ti] Título:Comparable Immune Function Inhibition by the Infliximab Biosimilar CT-P13: Implications for Treatment of Inflammatory Bowel Disease.
[So] Source:J Crohns Colitis;11(5):593-602, 2017 May 01.
[Is] ISSN:1876-4479
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background and Aims: CT-P13 is the first biosimilar monoclonal antibody to infliximab, and was recently approved in the European Union, Japan, Korea, and USA for all six indications of infliximab. However, studies directly assessing the biologic activity of CT-P13 versus inflximab in the context of inflammatory bowel disease [IBD] are still scanty. In the present study, we aimed to compare the biological activities of CT-P13 and infliximab with specific focus on intestinal cells so as to gain insight into the potential biosimilarity of these two agents for treatment of IBD. Methods: CT-P13 and infliximab were investigated and compared by in vitro experiments for their neutralisation ability of soluble tumour necrosis factor alpha [sTNFα] and membrane-bound tumour necrosis factor alpha [mTNFα], suppression of cytokine release by reverse signalling, induction of regulatory macrophages and wound healing, and antibody-dependent cell cytotoxicity [ADCC]. Results: CT-P13 showed similar biological activities to infliximab as gauged by neutralisation of soluble TNFα, as well as blockade of apoptosis and suppression of pro-inflammatory cytokines in intestinal Caco-2 cells. Infliximab and CT-P13 equally induced apoptosis and outside-to-inside signals through transmembrane TNFα [tmTNFα]. Moreover, regulatory macrophage induction and ensuing wound healing were similarly exerted by CT-P13 and infliximab. However, neither CT-P13 nor infliximab exerted any significant ADCC of ex vivo-stimulated peripheral blood monocytes or lamina propria mononuclear cells from IBD patients. Conclusions: These findings indicate that CT-P13 and infliximab exert highly similar biological activities in intestinal cells, and further support a mechanistic comparability of these two drugs in the treatment of IBD.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Medicamentos Biossimilares/farmacologia
Fármacos Gastrointestinais/farmacologia
Doenças Inflamatórias Intestinais/tratamento farmacológico
Infliximab/farmacologia
Intestinos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/uso terapêutico
Medicamentos Biossimilares/uso terapêutico
Células CACO-2/efeitos dos fármacos
Citocinas/metabolismo
Fármacos Gastrointestinais/uso terapêutico
Seres Humanos
Técnicas In Vitro
Infliximab/uso terapêutico
Intestinos/citologia
Intestinos/imunologia
Macrófagos/efeitos dos fármacos
Fator de Necrose Tumoral alfa/metabolismo
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Biosimilar Pharmaceuticals); 0 (CT-P13); 0 (Cytokines); 0 (Gastrointestinal Agents); 0 (Tumor Necrosis Factor-alpha); B72HH48FLU (Infliximab)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1093/ecco-jcc/jjw183


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[PMID]:29397594
[Au] Autor:Wang W; Shi LP; Shi L; Xu L
[Ad] Endereço:Department of Gastroenterology, National Center of Gerontology, Beijing Hospital, Beijing 100730, China.
[Ti] Título:[Efficacy of probiotics on the treatment of non-alcoholic fatty liver disease].
[So] Source:Zhonghua Nei Ke Za Zhi;57(2):101-106, 2018 Feb 01.
[Is] ISSN:0578-1426
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To study the clinical effect of probiotics in the treatment of non-alcoholic fatty liver disease (NAFLD). A total of 200 patients with NAFLD were randomly divided into 4 groups: control group (routine treatment group) and combined treatment group A, B and C. Each group had equal patients. The control group received orally polyene phosphatidylcholine capsules; whereas combined group A, B and C were given orally the live "combined and powder" , "two live combined and " , and the both probiotics respectively. The duration of treatment was 1 month. Laboratory parameters were evaluated before treatment and thirtieth day after treatment, including cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol(LDL-C), alanine aminotransferase(ALT), aspartate aminotransferase (AST), fasting blood glucose (FPG), serum high molecular weight adiponectin (HMW-APN) and serum TNFα. Meanwhile the faece sample was collected for routine test and bacterial culture. Liver ultrasound scan was done in all patients. In terms of blood lipids and blood glucose, each group improved after treatment with significant differences ( 0.05) except for HDL-C. As for liver function, serum ALT and AST decreased after treatment in each group; especially in combined group C which were lower than those of control group [(33.7±7.6) U/L vs. (45.0±8.5) U/L; (22.0±1.6) U/L vs. (29.4±3.7) U/L; 0.05]. TNFα levels decreased after treatment in each group, in addition the values in combined group C was significantly lower than that of control group[(0.51±0.27) µg/L vs. (0.82±0.28) µg/L, 0.05]. Serum HMW-APN increased after treatment in each group, and the HMW-APN in combined C group was significantly higher than that of control group[(9.28±3.72) µg/L vs. (7.87±3.96)µg/L, 0.05]. (5) After treatment, all groups showed improvement of fatty liver by ultrasound, but the difference between groups was not statistically significant. (6) Compared with before treatment, fecal flora in combined groups was all reduced ( 0.01), but it was comparable before and after treatment in control group. Probiotics improve intestinal microecological system in NAFLD patients via inhibiting TNFα and enhancing adiponectin, possibly resulting in regulating blood glucose, lipid metabolism, and protecting liver injury from NAFLD.
[Mh] Termos MeSH primário: Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/terapia
Probióticos
[Mh] Termos MeSH secundário: Adiponectina
Alanina Transaminase/sangue
Alanina Transaminase/efeitos dos fármacos
Aspartato Aminotransferases/sangue
Aspartato Aminotransferases/efeitos dos fármacos
Glicemia
Colesterol/sangue
LDL-Colesterol/efeitos dos fármacos
LDL-Colesterol/metabolismo
Seres Humanos
Metabolismo dos Lipídeos
Lipídeos
Probióticos/uso terapêutico
Triglicerídeos/sangue
Triglicerídeos/metabolismo
Fator de Necrose Tumoral alfa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adiponectin); 0 (Blood Glucose); 0 (Cholesterol, LDL); 0 (Lipids); 0 (TNF protein, human); 0 (Triglycerides); 0 (Tumor Necrosis Factor-alpha); 97C5T2UQ7J (Cholesterol); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase)
[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:180206
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0578-1426.2018.02.004


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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


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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


  8 / 111894 MEDLINE  
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[PMID]:29180487
[Au] Autor:Pierog PL; Zhao Y; Singh S; Dai J; Yap GS; Fitzgerald-Bocarsly P
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103.
[Ti] Título: Inactivates Human Plasmacytoid Dendritic Cells by Functional Mimicry of IL-10.
[So] Source:J Immunol;200(1):186-195, 2018 01 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plasmacytoid dendritic cells (pDCs) are the major producers of IFN-α, an antiviral cytokine involved in immunomodulation and control of HIV type 1 replication, whereas is a life-threatening opportunistic infection in AIDS patients. During infection with HIV type 1, human pDCs decrease in circulation and remaining pDC produce lower amounts of IFN-α in response to viral stimulation. In this study, we investigated the impact of coinfection with on the innate virus-directed responses of human pDCs. Using intracellular flow cytometry and fluorescence microscopy, we determined that invaded but did not induce IFN-α or TNF-α in human pDC. However, inhibited IFN-α and TNF-α produced in response to HSV and HIV, thus functionally inactivating pDC. IFN-α production was inhibited only in cells infected by , which inhibited neither uptake of GFP-HSV nor localization of TLR9 in CD71 endosomes, directing us to investigate downstream events. Using imaging flow cytometry, we found that both and IL-10 inhibited virus-induced nuclear translocation, but not phosphorylation, of IFN response factor 7. Blockade of IFN response factor 7 nuclear translocation and inhibition of the IFN-α response was partially reversed by a deficiency in the -derived ROP16 kinase, known to directly phosphorylate STAT3, a critical mediator of IL-10's anti-inflammatory effects. Taken together, our results indicate that suppresses pDC activation by mimicking IL-10's regulatory effects through an ROP16 kinase-dependent mechanism. Our findings further imply a convergent mechanism of inhibition of TLR signaling by and IL-10 and suggest potential negative consequences of HIV/ coinfection.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Infecções por HIV/imunologia
HIV-1/imunologia
Interleucina-10/metabolismo
Infecções Oportunistas/imunologia
Proteínas Tirosina Quinases/metabolismo
Proteínas de Protozoários/metabolismo
Toxoplasma/imunologia
Toxoplasmose/imunologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Células Cultivadas
Coinfecção
Células Dendríticas/parasitologia
Seres Humanos
Imunidade Inata
Imunomodulação
Fator Regulador 7 de Interferon/metabolismo
Interferon-alfa/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Receptor Toll-Like 9/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (IRF7 protein, human); 0 (Interferon Regulatory Factor-7); 0 (Interferon-alpha); 0 (Protozoan Proteins); 0 (STAT3 Transcription Factor); 0 (Toll-Like Receptor 9); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Rop16 protein, Toxoplasma gondii)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1701045


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[PMID]:28747346
[Au] Autor:Nagalingam G; Vinuesa CG; Britton WJ; Saunders BM
[Ad] Endereço:Tuberculosis Research Program, Centenary Institute, Newtown, New South Wales 2042, Australia.
[Ti] Título:Modulation of Roquin Function in Myeloid Cells Reduces -Induced Inflammation.
[So] Source:J Immunol;199(5):1796-1804, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Damaging inflammation is a hallmark of infection, and understanding how this is regulated is important for the development of new therapies to limit excessive inflammation. The E3 ubiquitin ligase, Roquin, is involved in immune regulation; however, its role in immunity to is unknown. To address this, we infected mice with a point mutation in ( ). Aerosol-infected mice showed enhanced control of infection associated with delayed bacterial dissemination and upregulated TNF production in the lungs after 2 wk. However, this early control of infection was not maintained, and by 8 wk postinfection mice demonstrated an increased bacterial burden and dysregulated inflammation in the lungs. As the inflammation in the lungs of the mice could have been influenced by emerging autoimmune conditions that are characteristic of the mice aging, the function of Roquin was examined in immune cell subsets in the absence of autoimmune complications. bacillus Calmette-Guérin-primed T cells transferred into mice provided equivalent protection in the spleen and liver. Interestingly, the transfer of mycobacteria-specific (P25 CD4 TCR transgenic) wild-type spleen cells into mice actually led to enhanced protection with reduced bacterial load, decreased chemokine expression, and reduced inflammation in the lungs compared with transfers into mice expressing intact Roquin. These studies suggest that modulation of Roquin in myeloid cells may reduce both inflammation and bacterial growth during the chronic phase of infection.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Inflamação/imunologia
Pulmão/imunologia
Mycobacterium tuberculosis/fisiologia
Células Mieloides/imunologia
Tuberculose/imunologia
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Linfócitos T CD4-Positivos/microbiologia
Linfócitos T CD4-Positivos/transplante
Células Cultivadas
Pulmão/microbiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Mieloides/microbiologia
Quimeras de Transplante
Fator de Necrose Tumoral alfa/metabolismo
Ubiquitina-Proteína Ligases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Tumor Necrosis Factor-alpha); EC 2.3.2.27 (Rc3h1 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602069


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[PMID]:28456632
[Au] Autor:Laidlaw SM; Marukian S; Gilmore RH; Cashman SB; Nechyporuk-Zloy V; Rice CM; Dustin LB
[Ad] Endereço:Kennedy Institute of Rheumatology, The University of Oxford, Oxford, United Kingdom; Peter Medawar Building for Pathogen Research, The University of Oxford, Oxford, United Kingdom.
[Ti] Título:Tumor Necrosis Factor Inhibits Spread of Hepatitis C Virus Among Liver Cells, Independent From Interferons.
[So] Source:Gastroenterology;153(2):566-578.e5, 2017 Aug.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Tumor necrosis factor (TNF) is an inflammatory cytokine expressed by human fetal liver cells (HFLCs) after infection with cell culture-derived hepatitis C virus (HCV). TNF has been reported to increase entry of HCV pseudoparticles into hepatoma cells and inhibit signaling by interferon alpha (IFNα), but have no effect on HCV-RNA replication. We investigated the effects of TNF on HCV infection of and spread among Huh-7 hepatoma cells and primary HFLCs. METHODS: Human hepatoma (Huh-7 and Huh-7.5) and primary HFLCs were incubated with TNF and/or recombinant IFNA2A, IFNB, IFNL1, and IFNL2 before or during HCV infection. We used 2 fully infectious HCV chimeric viruses of genotype 2A in these studies: J6/JFH (clone 2) and Jc1(p7-nsGluc2A) (Jc1G), which encodes a secreted luciferase reporter. We measured HCV replication, entry, spread, production, and release in hepatoma cells and HFLCs. RESULTS: TNF inhibited completion of the HCV infectious cycle in hepatoma cells and HFLCs in a dose-dependent and time-dependent manner. This inhibition required TNF binding to its receptor. Inhibition was independent of IFNα, IFNß, IFNL1, IFNL2, or Janus kinase signaling via signal transducer and activator of transcription. TNF reduced production of infectious viral particles by Huh-7 and HFLC, and thereby reduced the number of infected cells and focus size. TNF had little effect on HCV replicons and increased entry of HCV pseudoparticles. When cells were incubated with TNF before infection, the subsequent antiviral effects of IFNs were increased. CONCLUSIONS: In a cell culture system, we found TNF to have antiviral effects independently of, as well as in combination with, IFNs. TNF inhibits HCV infection despite increased HCV envelope glycoprotein-mediated infection of liver cells. These findings contradict those from other studies, which have reported that TNF blocks signal transduction in response to IFNs. The destructive inflammatory effects of TNF must be considered along with its antiviral effects.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Hepacivirus/efeitos dos fármacos
Hepatite C/tratamento farmacológico
Interferons/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/virologia
Linhagem Celular Tumoral
Genótipo
Hepacivirus/genética
Hepatócitos/efeitos dos fármacos
Hepatócitos/virologia
Seres Humanos
Janus Quinases/metabolismo
Fígado/citologia
Neoplasias Hepáticas/virologia
Receptores do Fator de Necrose Tumoral/metabolismo
Replicon/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/metabolismo
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Receptors, Tumor Necrosis Factor); 0 (Tumor Necrosis Factor-alpha); 9008-11-1 (Interferons); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE



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