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PMID:28727832
Autor:Alotaibi NM; Ibrahim GM; Wang J; Guha D; Mamdani M; Schweizer TA; Macdonald RL
Endereço:Division of Neurosurgery, Department of Surgery, University of Toronto, Toronto, Ontario, Canada.
Título:Neurosurgeon academic impact is associated with clinical outcomes after clipping of ruptured intracranial aneurysms.
Fonte:PLoS One; 12(7):e0181521, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:BACKGROUND: Surgeon-dependent factors such as experience and volume are associated with patient outcomes. However, it is unknown whether a surgeon's research productivity could be related to outcomes. The main aim of this study is to investigate the association between the surgeon's academic productivity and clinical outcomes following neurosurgical clipping of ruptured aneurysms. METHODS: We performed a post-hoc analysis of 3567 patients who underwent clipping of ruptured intracranial aneurysms in the randomized trials of tirilazad mesylate from 1990 to 1997. These trials included 162 centers and 156 surgeons from 21 countries. Primary and secondary outcomes were: Glasgow outcome scale score and mortality, respectively. Total publications, H-index, and graduate degrees were used as academic indicators for each surgeon. The association between outcomes and academic factors were assessed using a hierarchical logistic regression analysis, adjusting for patient covariates. RESULTS: Academic profiles were available for 147 surgeons, treating a total of 3307 patients. Most surgeons were from the USA (62, 42%), Canada (18, 12%), and Germany (15, 10%). On univariate analysis, the H-index correlated with better functional outcomes and lower mortality rates. In the multivariate model, patients under the care of surgeons with higher H-indices demonstrated improved neurological outcomes (p = 0.01) compared to surgeons with lower H-indices, without any significant difference in mortality. None of the other academic indicators were significantly associated with outcomes. CONCLUSION: Although prognostication following surgery for ruptured intracranial aneurysms primarily depends on clinical and radiological factors, the academic impact of the operating neurosurgeon may explain some heterogeneity in surgical outcomes.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Neuroprotective Agents); 0 (Pregnatrienes); YD064E883I (tirilazad)


  2 / 738 MEDLINE  
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PMID:27979473
Autor:Dedeilias P; Papalois A; Angelidis C; Giannopoulos G; Deftereos S; Chorti M; Apostolakis E; Kostopanagiotou G
Endereço:Cardiovascular and Thoracic Surgery Department, Evangelismos Hospital, Athens, Greece.
Título:Lazaroid U-74389G for cardioplegia-related ischemia-reperfusion injury: an experimental study.
Fonte:J Surg Res; 207:164-173, 2017 Jan.
ISSN:1095-8673
País de publicação:United States
Idioma:eng
Resumo:BACKGROUND: The adverse effects of myocardial ischemia and reperfusion during cardiopulmonary bypass (CPB) have been thoroughly described. Lazaroid U-74389G, a 21 aminosteroid, has been shown to attenuate ischemia and reperfusion injury and improve recovery in a variety of experimental models. METHODS: Sixteen male swine were randomly divided in two groups. All animals underwent 45 min of ischemic cardioplegic arrest, with U-74389G addition to the standard cardioplegic solution, whereas controls underwent the same procedure without U-74389G. Creatine kinase-MB isoenzyme (CK-MB) and cardiac troponin T levels were measured immediately before CPB (time point 0), during the ischemic period (time point 1) and 30 (time point 2), 60 (time point 3), and 120 (time point 4) min after reperfusion. Myocardial biopsies were obtained at time points 0 and 4. RESULTS: CK-MB levels (in U/L) at time points 0-4 were 205 (186-235) versus 219 (196-269; P = 0.72), 215 (167-248) versus 253 (193-339; P = 0.23), 234 (198-255) versus 338 (249-441; P = 0.02), 244 (217-272) versus 354 (269-496; P = 0.01), and 285 (230-321) versus 439 (432-530; P < 0.01) in lazaroid-treated animals versus controls, respectively. Cardiac troponin T levels (in ng/L) at time points 0-4 were 58 (26-287) versus 237 (26-395; P = 0.72), 129 (61-405) versus 265 (145-525; P = 0.23), 261 (123-467) versus 474 (427-1604; P = 0.04), 417 (204-750) versus 841 (584-1818; P = 0.11), and 643 (353-1259) versus 1600 (1378-2313; P < 0.01), respectively. Necrosis grades at time point 4 were 0.0 (0.0-1.0) versus 1.5 (1.0-2.0; P < 0.01) in lazaroid-treated animals versus controls, respectively. CONCLUSIONS: The present study, in addition to reconfirming the well-described adverse effects of CPB, demonstrates the efficacy of the newer generation lazaroid U-74389G in alleviating these effects.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Biomarkers); 0 (Cardiotonic Agents); 0 (Pregnatrienes); 111668-89-4 (U 74389F)


  3 / 738 MEDLINE  
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PMID:26848737
Autor:Gadgil P; Ibrahim F; Chow DS
Endereço:Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77030, USA. Electronic address: psgadgil@uh.edu.
Título:UPLC-MS/MS assay of 21-aminosteroid (lazaroid U74389G) for application in pharmacokinetic study.
Fonte:J Pharm Biomed Anal; 122:90-7, 2016 Apr 15.
ISSN:1873-264X
País de publicação:England
Idioma:eng
Resumo:Lazaroids are potent inhibitors of lipid peroxidation, both in vitro and in vivo. Additionally, a member of the lazaroid family, U-74389G (LAZ) has been shown to have specific radio-protective and anti-proliferative effects. However, there is no quantitative analytical method developed for measuring the therapeutic levels of LAZ for the aforementioned effects. This article highlights the development and validation of a sensitive UPLC-MS/MS method for the quantification of LAZ, and its subsequent application in pharmacokinetic studies in rats with the lower limit of quantification (LLOQ) of 1.95 ng/mL. LAZ and internal standard diadzein (IS) were separated using ACQUITY UPLC(®) BEH C18 column. Gradient elution was used at a flow rate of 0.45 mL/min with mobile phases consisting of 0.1% formic acid in water and 0.1% formic in acetonitrile. LAZ (m/z 612→260) and IS (m/z 255→199) were detected by electrospray ionization (ESI) using multiple reaction monitoring (MRM) in a positive mode on QTRAP(®) 5500 System. The UPLC-MS/MS method was validated as per the US FDA Guidelines for Bio-analytical Validation. LAZ was extracted from rat plasma (100 µL) using protein precipitation by acetonitrile with mean recovery and matrix factor in range of 47.7-56.1%, and 85.6-89.4%, respectively. The calibration curve for LAZ was linear in the range of 1.95-250 ng/mL. The inter-day and intra-day accuracy and precision values for LLOQ, low, medium, high and very high concentration QC samples were within ±15%. LAZ was tested under different storage conditions, for short-term bench-top stability (1h and 3h at 25°C), long-term stability (1 month at -80°C), freeze-thaw cycle stability (1 cycle and 3 cycles) and stability of processed samples in auto-sampler (24h at 10°C) with stability values within ±15% range of nominal concentrations. The validated UPLC-MS/MS method was further applied to a pharmacokinetic study in rats after a single intravenous dose of LAZ at 5 mg/kg.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Pregnatrienes); 111668-89-4 (U 74389F)


  4 / 738 MEDLINE  
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PMID:26745667
Autor:Hurt DE; Suzuki S; Mayama T; Charmandari E; Kino T
Endereço:Bioinformatics and Computational Biosciences Branch (D.E.H.), Office of Cyber Infrastructure and Computational Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852; Program in Reproductive and Adult Endocrinology (S.S., T.M., T.K.),
Título:Structural Analysis on the Pathologic Mutant Glucocorticoid Receptor Ligand-Binding Domains.
Fonte:Mol Endocrinol; 30(2):173-88, 2016 Feb.
ISSN:1944-9917
País de publicação:United States
Idioma:eng
Resumo:Glucocorticoid receptor (GR) gene mutations may cause familial or sporadic generalized glucocorticoid resistance syndrome. Most of the missense forms distribute in the ligand-binding domain and impair its ligand-binding activity and formation of the activation function (AF)-2 that binds LXXLL motif-containing coactivators. We performed molecular dynamics simulations to ligand-binding domain of pathologic GR mutants to reveal their structural defects. Several calculated parameters including interaction energy for dexamethasone or the LXXLL peptide indicate that destruction of ligand-binding pocket (LBP) is a primary character. Their LBP defects are driven primarily by loss/reduction of the electrostatic interaction formed by R611 and T739 of the receptor to dexamethasone and a subsequent conformational mismatch, which deacylcortivazol resolves with its large phenylpyrazole moiety and efficiently stimulates transcriptional activity of the mutant receptors with LBP defect. Reduced affinity of the LXXLL peptide to AF-2 is caused mainly by disruption of the electrostatic bonds to the noncore leucine residues of this peptide that determine the peptide's specificity to GR, as well as by reduced noncovalent interaction against core leucines and subsequent exposure of the AF-2 surface to solvent. The results reveal molecular defects of pathologic mutant receptors and provide important insights to the actions of wild-type GR.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Carrier Proteins); 0 (GRIP1 protein, human); 0 (Ligands); 0 (Mutant Proteins); 0 (Nerve Tissue Proteins); 0 (Peptides); 0 (Pregnatrienes); 0 (Receptors, Glucocorticoid); 3JO09QT49F (deacylcortivazol); 7S5I7G3JQL (Dexamethasone); GMW67QNF9C (Leucine)


  5 / 738 MEDLINE  
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PMID:27180351
Autor:Tsompos C; Panoulis C; Toutouzas K; Zografos G; Papalois A
Endereço:Department of Obstetrics & Gynecology, Mesologi County Hospital, Etoloakarnania, Greece
Título:The Acute Effect of the Antioxidant Drug U-74389G on Red Blood Cell Distribution Width Levels During Hypoxia Reoxygenation Injury in Rats.
Fonte:Folia Med (Plovdiv); 57(3-4):235-42, 2015 Jul-Dec.
ISSN:0204-8043
País de publicação:Germany
Idioma:eng
Resumo:UNLABELLED: The AIM of this experimental study was to evaluate the effect of the antioxidant drug "U-74389G" in a rat model of hypoxia reoxygenation (HR) using the previously established protocol. Effects of treatment were evaluated by mean red blood cell distribution width (RDW) levels. MATERIALS AND METHODS: 40 rats of a mean weight of 231.875 g were employed in the study. RDW levels were determined at 60 min (groups A and C) and at 120 min (groups B and D) after starting the reoxygenation. Groups A and B received no drugs, whereas rats from groups C and D were administered with U-74389G. RESULTS: demonstrated that U-74389G administration significantly decreased the RDW levels by 4.96% + 2.27% (p = 0.0175). Reoxygenation time non-significantly decreased the RDW levels by 0.27% + 2.41% (p = 0.8889). Together, U-74389G administration and reoxygenation time non-significantly decreased the RDW levels by 2.54% + 1.39% (p = 0.0679). CONCLUSIONS: U-74389G administration particulary in concert without reperfusion declines the RDW levels even within the short - time context of 1.5 hours reperfusion.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Antioxidants); 0 (Pregnatrienes); 111668-89-4 (U 74389F); S88TT14065 (Oxygen)


  6 / 738 MEDLINE  
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PMID:26774629
Autor:Tsompos C; Panoulis C; Toutouzas K; Zografos G; Papalois A
Endereço:Department of Obstetrics & gynecology, Mesologi County Hospital Nafpaktou, Mesolongi, Etoloakarnania, Greece. Constantinostsompos@yahoo.com.
Título:Antioxidant 21-aminosteroid "U-74389G" ameliorates the short-time effect of hypoxia-reoxygenation on the platelet count in rats.
Fonte:Folia Med Cracov; 55(1):25-34, 2015.
ISSN:0015-5616
País de publicação:Poland
Idioma:eng
Resumo:AIM: The aim of this experimental study was to examine the effect of the antioxidant drug "U-74389G", on rat model and particularly in a hypoxia-reoxygenation protocol. The beneficial effect or non-effectiveness of that molecule were studied hematologically using blood mean platelet count. Results were that U-74389G administration interacted or not with reoxygenation time decreased the platelet count by 6.12% ± 3.58% (p = 0.0857) and 12.83% ± 5.79% (p = 0.0303) respectively. CONCLUSIONS: U-74389G administration interacted or not with reoxygenation time decreases the platelet count within short-term time of 2 hours by different significance levels.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Antioxidants); 0 (Free Radical Scavengers); 0 (Pregnatrienes); 111668-89-4 (U 74389F)


  7 / 738 MEDLINE  
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PMID:26710522
Autor:Tsompos C; Panoulis C; Toutouzas K; Zografos G; Papalois A
Título:[The Effect of the Antioxidant Drug U-74389G on Magnesium Levels During Hypoxia-Reoxygenation Injury in Rats].
Fonte:Vestn Ross Akad Med Nauk; (4):408-12, 2015.
ISSN:0869-6047
País de publicação:Russia (Federation)
Idioma:rus
Resumo:OBJECTIVE: The aim of this experimental study was to examine the effect of the antioxidant drug U-74389G in a rat model of hypoxia-reoxygenation using the previously established protocol. Effects of treatments were evaluated by magnesium (Mg2+) levels in blood. METHODS: Non-randomized controlled study was performed. Mg2+ levels were determined in 60 min (groups A and C) and 120 min (groups B and D) after starting the reoxygenation. Groups A and B received no drugs, whereas rats from groups C and D were administered with U-74389G. RESULTS: 40 rats 16-18 weeks old of a mean weight of 2312 g were employed in the study. It is demonstrated that U-74389G administration did not alter the Mg2+ levels (decrease in Mg2+ concentration was 0.28±2.75%; p=0.917). Reoxygenation non-significantly increased the Mg2+ levels by 4.27±2.66% (p=0.107). Together, the U-74389G administration and reoxygenation non-significantly increased the Mg2+ levels by 0.36±1.64% (p=0.823). CONCLUSION: U-74389G administration, alone or in concert with reoxygenation did not significantly affect Mg2+ level in blood after experimental hypoxia in rats.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antioxidants); 0 (Pregnatrienes); 111668-89-4 (U 74389F); I38ZP9992A (Magnesium)


  8 / 738 MEDLINE  
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PMID:26359418
Autor:Bonatsos V; Kappas I; Birbas K; Vlachodimitropoulos D; Toutouzas K; Karampela E; Syrmos N; Bonatsos G; Papalois AE
Endereço:The Hillingdon Hospital NHS Trust, Imperial Lead Provider, London Deanery, London, U.K.
Título:Effects of U-74389G (21-Lazaroid) and Ascorbic Acid on Liver Recovery After Acute Ischemia and Reperfusion in Rats.
Fonte:In Vivo; 29(5):585-94, 2015 Sep-Oct.
ISSN:1791-7549
País de publicação:Greece
Idioma:eng
Resumo:BACKGROUND/AIM: The free radical-scavenging effects of the lazaroid U-74389G have been shown in several experimental models to protect the liver from ischemia/reperfusion (I/R), however, the mechanism of cytoprotection is not fully understood. Similar findings were observed when ascorbic acid was administered. This study investigates the effects of infusion of lazaroid U-74389G and ascorbic acid on cytokines and liver structure in a liver I/R rat model. MATERIALS AND METHODS: Sixty male Wistars rats, weighting 220-290 g, were used in the study. Six experimental groups were formed: Group 1 (control group): ischemia for 30 min and reperfusion for 60 min; group 2 (control group): ischemia for 30 min and reperfusion for 120 min; group 3: ischemia for 30 min, intraportal injection of ascorbic acid, and reperfusion for 60 min; group 4: ischemia for 30 min, ascorbic acid administration, and reperfusion for 120 min; group 5: ischemia for 30 min, U-74389G administration, and reperfusion for 60 min; and group 6: ischemia for 30 min, U-74389G administration, and reperfusion for 120 min. Tissue and blood sampling took place upon completion of each model's reperfusion. U-74389G was administered at 10 mg/kg animal body weight and ascorbic acid at 100 mg/kg. Anesthesia was induced with ketamine and xylazine. Surgery was performed through a midline laparotomy. The portal vein and the common hepatic artery were isolated and prepared for occlusion. Blood samples and wedge liver biopsies were taken to measure levels of liver enzymes, cytokines and for microscopic analysis upon completion of reperfusion once for each model. RESULTS: Histopathological evaluation revealed a statistically significant reduction in the degree of necrosis of liver tissue in the treated groups compared to the control groups 1 and 2 [groups 3, 5 (p=0.010) and 4, 6 (p<0.0005)]. On the other hand, tissue malondialdehyde levels (MDA) were statistically significantly increased only between control group 2 and groups 4, 6 (p<0.0005). There was no statistically significant difference in tumor necrosis factor-α between groups. As for liver enzymes, only alkaline phosphatase (ALP) and gamma-glutamyl transferase (gGT) were statistically significantly reduced in treated groups 3 and 5 (ALP: p=0.027, and gGT: p=0.002) and 4 and 6 (ALP: p=0.004, and gGT: p=0.015) compared to control groups 1 and 2. CONCLUSION: Based on histological data and the reduction of some of the liver enzymes, in spite of a rise of malondialdehyde, in this rat model, administration of U-74389G in liver ischemia/reperfusion (I/R) injury has potential in attenuating liver damage.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antioxidants); 0 (Biomarkers); 0 (Cytokines); 0 (Pregnatrienes); 0 (Reactive Oxygen Species); 111668-89-4 (U 74389F); 4Y8F71G49Q (Malondialdehyde); EC 2.6.1.1 (Aspartate Aminotransferases); PQ6CK8PD0R (Ascorbic Acid)


  9 / 738 MEDLINE  
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PMID:26168778
Autor:Sood PK; Verma S; Nahar U; Nehru B
Endereço:Biophysics Department, Panjab University, Chandigarh, 160014, India.
Título:Neuroprotective Role of Lazaroids Against Aluminium Chloride Poisoning.
Fonte:Neurochem Res; 40(8):1699-708, 2015 Aug.
ISSN:1573-6903
País de publicação:United States
Idioma:eng
Resumo:Aluminium (Al) is neurotoxic primarily because of its interference with biological enzymes in key mechanisms of metabolic pathways. Mitochondria being a major site of reactive oxygen species (ROS) production, it seems that the oxidative damage to mitochondrial proteins may underlie the pathogenesis of Al induced neurodegeneration. The present study investigates the effectiveness of the anti-oxidant property of lazaroids (U-74500A), a known lipid peroxidation inhibitor as neuroprotective agent against Al induced neurotoxicity. Al chloride was administered orally at a dose level of 100 mg/kg body wt/day in water and U-74500A was administered at a dose of 0.25 mg/kg body wt i.p. in citrate buffer for a period of 8 weeks on alternate days. Following Al exposure there was a significant increase in lipid peroxidation (LPO), ROS levels and reduction in the activity of mitochondrial complexes in all the three regions of rat brain, i.e., cerebral cortex, mid brain, and cerebellum. This decrease in the activities of electron transport complexes in turn affected the ATP synthesis and ATP levels adversely in the mitochondria. These alterations were also depicted in the histology which shows signs of hypoxia, paucity of neurons in cortical region and loosening of fibers in the white matter. U-74500A co-administration was able to restore alterations in the LPO, ROS levels as well as all the three mitochondrial complexes and caspase expression. Therefore, it is suggested that 21-aminosteroids (lazaroids), by attenuating LPO and mitochondrial dysfunction, holds a promise as an agent that can potentially reduce Al-induced adverse effects in brain.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Aluminum Compounds); 0 (Antioxidants); 0 (Chlorides); 0 (Neuroprotective Agents); 0 (Pregnatrienes); 0 (Reactive Oxygen Species); 3CYT62D3GA (aluminum chloride); IDW4RCM01L (U 74500A)


  10 / 738 MEDLINE  
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PMID:25957738
Autor:Sun F; Shi J; Chen S; Deng C; Hu X; Li H; Li G; Liu Y; Dong N
Endereço:Department of Cardiovascular surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China; Department of Cardiovascular surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. Electronic address: sfq1010@126.com.
Título:Lazaroid U-74389G inhibits the osteoblastic differentiation of IL-1ß-indcued aortic valve interstitial cells through glucocorticoid receptor and inhibition of NF-κB pathway.
Fonte:J Steroid Biochem Mol Biol; 152:114-23, 2015 Aug.
ISSN:1879-1220
País de publicação:England
Idioma:eng
Resumo:BACKGROUND: Aortic valve calcification is characterized as the active process of aortic valve interstitial cells (AVICs), and considered as an inflammatory disease. As an antioxidant, the anti-inflammatory activity of Lazaroid has been exhibited in various models. We hypothesized that Lazaroid U-74389G would inhibit the osteoblastic differentiation of AVICs induced by IL-1ß. METHODS: Normal tricuspid aortic valve leaflets were collected from patients with acute aortic dissection (Type A) undergoing the Bentall procedure. AVICs were isolated and stimulated with IL-1ß in presence or absence of U-74389G in culture. Cell lysates were analyzed for osteogenic markers and nuclear factor-κB using real-time PCR and Immunoblotting. Culture media was analyzed for IL-6 and IL-8 with enzyme-linked immunosorbent assay. Alizarin Red Staining was adopted to demonstrate the calcium deposition. RESULTS: The expression of alkaline phosphatase and bone morphogenetic protein, accompanied by the production of IL-6 and IL-8, was up-regulated in response to IL-1ß and was inhibited by the addition of U-74389G. The NF-κB pathway was activated by IL-1ß and involved in the suppression of U-74389G on osteoblastic differentiation in AVICs. The negative effects of U-74389G on ostengenic gene expression and mineralization of AVICs were blocked by glucocorticoid receptor antagonist mifepristone and the NF-κB inhibitor Bay 11-7082. CONCLUSIONS: U-74389G inhibits the pro-osteogenic response to IL-1ß stimulation in AVICs. The osteoblastic differentiation and mineralization of AVICs were inhabited by U-74389G though the modulation of NF-κB activation, and this pathway could be potential therapeutic targets for medical treatment of calcified aortic valve disease.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (3-(4-methylphenylsulfonyl)-2-propenenitrile); 0 (Bone Morphogenetic Proteins); 0 (IL1B protein, human); 0 (IL6 protein, human); 0 (IL8 protein, human); 0 (Inflammation Mediators); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Nitriles); 0 (Pregnatrienes); 0 (RELA protein, human); 0 (Receptors, Glucocorticoid); 0 (Sulfones); 0 (Transcription Factor RelA); 111668-89-4 (U 74389F); 320T6RNW1F (Mifepristone); EC 3.1.3.1 (Alkaline Phosphatase)



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