Base de dados : MEDLINE
Pesquisa : C06.552.380 [Categoria DeCS]
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[PMID]:28743082
[Au] Autor:Rodrigues GB; Oliveira EE; Junior FJBM; Santos LAMD; Oliveira WH; França MER; Lós DB; Gabínio BM; de Lira FCML; Peixoto CA
[Ad] Endereço:Laboratório de Ultraestrutura, Instituto Aggeu Magalhães - FIOCRUZ, Recife, Brazil; Programa de Pós-graduação em Ciências Biológicas, Centro de Biociências, Universidade Federal de Pernambuco - UFPE, Recife, Brazil.
[Ti] Título:Characterization and evaluation of nanoencapsulated diethylcarbamazine in model of acute hepatic inflammation.
[So] Source:Int Immunopharmacol;50:330-337, 2017 Sep.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Previous studies from our laboratory have demonstrated that Diethylcarbamazine (DEC) is a potent anti-inflammatory drug. The aim of the present study was to characterize the nanoencapsulation of DEC and to evaluate its effectiveness in a model of inflammation for the first time. C57BL/6 mice were divided into six groups: 1) Control; 2) Carbon tetrachloride (CCl4); 3) DEC 25mg/kg+CCl4; 4) DEC 50mg/kg+CCl4; 5) DEC-NANO 05mg/kg+CCl4 and 6) DEC-NANO 12.5mg/kg+CCl4. Liver fragments were stained with hematoxylin-eosin, and processed for Western blot, ELISA and immunohistochemistry. Serum was also collected for biochemical measurements. Carbon tetrachloride induced hepatic injury, observed through increased inflammatory markers (TNF-α, IL-1ß, PGE2, COX-2 and iNOS), changes in liver morphology, and increased serum levels of total cholesterol, triglycerides, TGO and TGP, LDL, as well as reduced HDL levels. Nanoparticles containing DEC were characterized by diameter, polydispersity index and zeta potential. Treatment with 12.5 nanoencapsulated DEC exhibited a superior anti-inflammatory action to the DEC traditional dose (50mg/kg) used in murine assays, restoring liver morphology, improving serological parameters and reducing the expression of inflammatory markers. The present formulation of nanoencapsulated DEC is therefore a potential therapeutic tool for the treatment of inflammatory hepatic disorders, permitting the use of smaller doses and reducing treatment time, while maintaining high efficacy.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Cápsulas/administração & dosagem
Dietilcarbamazina/uso terapêutico
Hepatite/tratamento farmacológico
Nanoestruturas/administração & dosagem
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Citocinas/metabolismo
Modelos Animais de Doenças
Sistemas de Liberação de Medicamentos
Seres Humanos
Mediadores da Inflamação/metabolismo
Metabolismo dos Lipídeos
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Capsules); 0 (Cytokines); 0 (Inflammation Mediators); V867Q8X3ZD (Diethylcarbamazine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:29117589
[Au] Autor:Ma J; Li Y; Duan H; Sivakumar R; Li X
[Ad] Endereço:College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
[Ti] Título:Chronic exposure of nanomolar MC-LR caused oxidative stress and inflammatory responses in HepG2 cells.
[So] Source:Chemosphere;192:305-317, 2018 Feb.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Low dose but long-term exposure of microcystin-LR (MC-LR) could induce human hepatitis and promote liver cancer according to epidemiological investigation results, but the exact mechanism has not been completely elucidated. In the present study, a chronic toxicity test of MC-LR exposure on HepG2 cells at 0.1-30 nM for 83 d was conducted under laboratory conditions. The western blot assay result revealed that MC-LR entered HepG2 cells, even at the concentration of 0.1 nM, after 83 d of exposure, but no cytotoxicity was observed in the HepG2 cells, as determined by the CCK-8 and LDH tests. However, the results of the DCF fluorescence assay showed that the intracellular ROS level in the 30 nM MC-LR-treated cells was significantly higher than that of the control cells, and 5 and 10 nM of MC-LR exposure totally increased the activity of SOD in HepG2 cells. These results indicate that MC-LR exposure at low concentration also induced excessive ROS in HepG2 cells. Additionally, long-term exposure of MC-LR at low concentration remarkably promoted the expression of NF-κB p65, COX-2, iNOS, TNF-α, IL-1ß, and IL-6 in the cells, suggesting that long-term MC-LR exposure at low concentration can induce inflammatory reaction to HepG2 cells, which might account for MC-induced human hepatitis. Thus, we hypothesized that the pathogenesis of human hepatitis and hepatocarcinoma caused by MCs might be closely associated with oxidative stress and inflammation.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/patologia
Inflamação/induzido quimicamente
Neoplasias Hepáticas/induzido quimicamente
Microcistinas/toxicidade
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Toxinas Bacterianas/farmacologia
Carcinoma Hepatocelular/induzido quimicamente
Carcinoma Hepatocelular/metabolismo
Células Hep G2
Hepatite/etiologia
Hepatite/metabolismo
Hepatite/patologia
Seres Humanos
Interleucina-6/metabolismo
Microcistinas/farmacocinética
NF-kappa B/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Fator de Necrose Tumoral alfa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Toxins); 0 (Interleukin-6); 0 (Microcystins); 0 (NF-kappa B); 0 (Reactive Oxygen Species); 0 (Tumor Necrosis Factor-alpha); EQ8332842Y (cyanoginosin LR)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171109
[St] Status:MEDLINE


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[PMID]:29307523
[Au] Autor:Wu GJ; Lin YW; Chuang CY; Tsai HC; Chen RM
[Ad] Endereço:Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan; Department of Anesthesiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
[Ti] Título:Liver nitrosation and inflammation in septic rats were suppressed by propofol via downregulating TLR4/NF-κB-mediated iNOS and IL-6 gene expressions.
[So] Source:Life Sci;195:25-32, 2018 Feb 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Propofol can be applied as an anesthetic or sedative agent for septic patients. Our previous studies showed that propofol ameliorated inflammation- and nitrosative stress-induced cellular insults. This study further evaluated effects of propofol on cecal ligation and puncture (CLP)-induced septic insults to rats and its possible mechanisms. MAIN METHODS: Wistar rats were administered with CLP and effects of propofol on CLP-induced liver dysfunction and rat death were evaluated. Levels of hepatic or systemic nitrogen oxides (NOx) and interleukin (IL)-6 were quantified. Sequentially, inducible nitric oxide synthase (iNOS) and IL-6 gene expressions, toll-like receptor 4 (TLR4) protein levels, and nuclear factor (NF)-κB translocation were determined. KEY FINDINGS: Subjecting rats to CLP led to body weight loss, liver weight gain, and death. Administration of propofol lessened CLP-induced augmentations of serum and hepatic nitrosative stress and IL-6 levels. Additionally, propofol suppressed CLP-induced enhancements in levels of hepatic iNOS protein. Furthermore, the CLP-induced iNOS and IL-6 mRNA expressions in the liver were inhibited following propofol administration. Sequentially, subjecting rats to CLP enhanced hepatic TLR4 protein levels and NF-κB translocation to nuclei, but propofol inhibited these augmentations. SIGNIFICANCE: Consequently, exposure to propofol protected against CLP-induced liver dysfunction and increased the survival rates of the animals. This study shows that propofol can protect rats against septic insults through suppression of systemic and hepatic nitrosative and inflammatory stress due to inhibition of TLR4/NF-κB-mediated iNOS and IL-6 mRNA and protein expressions.
[Mh] Termos MeSH primário: Hepatite/tratamento farmacológico
Hipnóticos e Sedativos/uso terapêutico
Interleucina-6/biossíntese
Fígado/metabolismo
Fígado/patologia
NF-kappa B/efeitos dos fármacos
Óxido Nítrico Sintase Tipo II/biossíntese
Nitrosação/efeitos dos fármacos
Propofol/uso terapêutico
Sepse/tratamento farmacológico
Receptor 4 Toll-Like/efeitos dos fármacos
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Doenças do Ceco/metabolismo
Doenças do Ceco/patologia
Regulação para Baixo
Regulação da Expressão Gênica/efeitos dos fármacos
Hepatite/metabolismo
Hepatite/patologia
Interleucina-6/genética
Masculino
Óxido Nítrico Sintase Tipo II/genética
Ratos
Ratos Wistar
Sepse/metabolismo
Sepse/patologia
Translocação Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Hypnotics and Sedatives); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Tlr4 protein, rat); 0 (Toll-Like Receptor 4); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); YI7VU623SF (Propofol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


  4 / 14643 MEDLINE  
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[PMID]:27773660
[Au] Autor:Al-Harbi NO; Nadeem A; Al-Harbi MM; Zoheir KMA; Ansari MA; El-Sherbeeny AM; Alanazi KM; Alotaibi MR; Ahmad SF
[Ad] Endereço:Department of Pharmacology & Toxicology, College of Pharmacy, Riyadh, Saudi Arabia.
[Ti] Título:Psoriatic inflammation causes hepatic inflammation with concomitant dysregulation in hepatic metabolism via IL-17A/IL-17 receptor signaling in a murine model.
[So] Source:Immunobiology;222(2):128-136, 2017 02.
[Is] ISSN:1878-3279
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Psoriatic inflammation has been shown to be associated with cardiovascular dysfunction and systemic inflammation. Recently, psoriasis has also been linked to hepatic disorders, however underlying mechanism connecting the two are unknown. IL-17A being a central pro-inflammatory cytokine in the pathogenesis of psoriasis may be involved in hepatic inflammation through its receptor and downward signaling; however so far no study has investigated IL-17A related signaling in the liver during psoriasis in a murine model. Therefore, this study explored psoriasis-induced hepatic inflammation and concurrent metabolic changes. Mice were applied topically imiquimod (IMQ) to develop psoriatic inflammation. Additionally mice were also treated either with IL-17A or anti-IL17A antibody to explore the role of IL-17 related signaling in liver. Mice were then assessed for hepatic inflammation through assessment of inflammatory/oxidative stress markers (IL-17RC, NFκB, IL-6, MCP-1, IL-1ß, GM-CSF, ICAM-1, iNOS, lipid peroxides and myeloperoxidase activity) as well as hepatic injury (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) and protein/lipid metabolic biomarkers (total proteins, albumin, total bilirubin, triglycerides, HDL cholesterol, and total cholesterol). IMQ treatment led to hepatic inflammation as evidenced by increased pro-inflammatory cytokines and oxidative stress with concomitant dysregulation in hepatic protein/lipid metabolism. Treatment with IL-17A further aggravated, whereas treatment with anti-IL17A antibody ameliorated IMQ-induced changes in hepatic injury/inflammation and protein/lipid metabolism. Our study shows for the first time that psoriatic inflammation leads to hepatic inflammation which results in dysregulated protein/lipid metabolism through IL-17RC/NFκB signaling. This could result in increased risk of cardiovascular dysfunction in patients with psoriasis.
[Mh] Termos MeSH primário: Metabolismo Energético
Hepatite/etiologia
Hepatite/metabolismo
Interleucina-17/metabolismo
Psoríase/complicações
Receptores de Interleucina-17/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Citocinas/metabolismo
Modelos Animais de Doenças
Metabolismo dos Lipídeos
Peroxidação de Lipídeos
Masculino
Camundongos
NF-kappa B/metabolismo
Estresse Oxidativo
Peroxidase/metabolismo
Psoríase/imunologia
Psoríase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (Interleukin-17); 0 (NF-kappa B); 0 (Receptors, Interleukin-17); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  5 / 14643 MEDLINE  
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[PMID]:27770558
[Au] Autor:Labonte AC; Sung SJ; Jennelle LT; Dandekar AP; Hahn YS
[Ad] Endereço:Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, VA.
[Ti] Título:Expression of scavenger receptor-AI promotes alternative activation of murine macrophages to limit hepatic inflammation and fibrosis.
[So] Source:Hepatology;65(1):32-43, 2017 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The liver maintains an immunologically tolerant environment as a result of continuous exposure to food and bacterial constituents from the digestive tract. Hepatotropic pathogens can take advantage of this niche and establish lifelong chronic infections causing hepatic fibrosis and hepatocellular carcinoma. Macrophages (MÏ•) play a critical role in regulation of immune responses to hepatic infection and regeneration of tissue. However, the factors crucial for MÏ• in limiting hepatic inflammation or resolving liver damage have not been fully understood. In this report, we demonstrate that expression of C-type lectin receptor scavenger receptor-AI (SR-AI) is crucial for promoting M2-like MÏ• activation and polarization during hepatic inflammation. Liver MÏ• uniquely up-regulated SR-AI during hepatotropic viral infection and displayed increased expression of alternative MÏ• activation markers, such as YM-1, arginase-1, and interleukin-10 by activation of mer receptor tyrosine kinase associated with inhibition of mammalian target of rapamycin. Expression of these molecules was reduced on MÏ• obtained from livers of infected mice deficient for the gene encoding SR-AI (msr1). Furthermore, in vitro studies using an SR-AI-deficient MÏ• cell line revealed impeded M2 polarization and decreased phagocytic capacity. Direct stimulation with virus was sufficient to activate M2 gene expression in the wild-type (WT) cell line, but not in the knockdown cell line. Importantly, tissue damage and fibrosis were exacerbated in SR-AI mice following hepatic infection and adoptive transfer of WT bone-marrow-derived MÏ• conferred protection against fibrosis in these mice. CONCLUSION: SR-AI expression on liver MÏ• promotes recovery from infection-induced tissue damage by mediating a switch to a proresolving MÏ• polarization state. (Hepatology 2017;65:32-43).
[Mh] Termos MeSH primário: Hepatite/etiologia
Cirrose Hepática/etiologia
Ativação de Macrófagos
Receptores Depuradores Classe A/biossíntese
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Scavenger Receptors, Class A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28873


  6 / 14643 MEDLINE  
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[PMID]:27770461
[Au] Autor:Piao X; Yamazaki S; Komazawa-Sakon S; Miyake S; Nakabayashi O; Kurosawa T; Mikami T; Tanaka M; Van Rooijen N; Ohmuraya M; Oikawa A; Kojima Y; Kakuta S; Uchiyama Y; Tanaka M; Nakano H
[Ad] Endereço:Department of Biochemistry, Toho University School of Medicine, Tokyo, Japan.
[Ti] Título:Depletion of myeloid cells exacerbates hepatitis and induces an aberrant increase in histone H3 in mouse serum.
[So] Source:Hepatology;65(1):237-252, 2017 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue-resident macrophages and bone marrow (BM)-derived monocytes play a crucial role in the maintenance of tissue homeostasis; however, their contribution to recovery from acute tissue injury is not fully understood. To address this issue, we generated an acute murine liver injury model using hepatocyte-specific Cflar-deficient (Cflar ) mice. Cellular FLICE-inhibitory protein expression was down-regulated in Cflar-deficient hepatocytes, which thereby increased susceptibility of hepatocytes to death receptor-induced apoptosis. Cflar mice developed acute hepatitis and recovered with clearance of apoptotic hepatocytes at 24 hours after injection of low doses of tumor necrosis factor α (TNFα), which could not induce hepatitis in wild-type (WT) mice. Depletion of Kupffer cells (KCs) by clodronate liposomes did not impair clearance of dying hepatocytes or exacerbate hepatitis in Cflar mice. To elucidate the roles of BM-derived monocytes and neutrophils in clearance of apoptotic hepatocytes, we examined the effect of depletion of these cells on TNFα-induced hepatitis in Cflar mice. We reconstituted Cflar mice with BM cells from transgenic mice in which human diphtheria toxin receptor (DTR) was expressed under control of the lysozyme M (LysM) promoter. TNFα-induced infiltration of myeloid cells, including monocytes and neutrophils, was completely ablated in LysM-DTR BM-reconstituted Cflar mice pretreated with diphtheria toxin, whereas KCs remained present in the livers. Under these experimental conditions, LysM-DTR BM-reconstituted Cflar mice rapidly developed severe hepatitis and succumbed within several hours of TNFα injection. We found that serum interleukin-6 (IL-6), TNFα, and histone H3 were aberrantly increased in LysM-DTR BM-reconstituted, but not in WT BM-reconstituted, Cflar mice following TNFα injection. CONCLUSION: These findings indicate an unexpected role of myeloid cells in decreasing serum IL-6, TNFα, and histone H3 levels via the suppression of TNFα-induced hepatocyte apoptosis. (Hepatology 2017;65:237-252).
[Mh] Termos MeSH primário: Hepatite/sangue
Hepatite/etiologia
Histonas/sangue
Células Mieloides/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Progressão da Doença
Hepatócitos
Macrófagos do Fígado
Camundongos
Camundongos Transgênicos
Fator de Necrose Tumoral alfa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Histones); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28878


  7 / 14643 MEDLINE  
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[PMID]:29210250
[Au] Autor:Dute J
[Ti] Título:European Court of Human Rights.
[So] Source:Eur J Health Law;23(5):525-37, 2016 Dec.
[Is] ISSN:0929-0273
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Prisioneiros/legislação & jurisprudência
[Mh] Termos MeSH secundário: Internação Compulsória de Doente Mental/legislação & jurisprudência
Alemanha
Hepatite/tratamento farmacológico
Dependência de Heroína/tratamento farmacológico
Seres Humanos
Masculino
Tratamento de Substituição de Opiáceos
Federação Russa
Esquizofrenia Paranoide
Tuberculose/tratamento farmacológico
Ucrânia
[Pt] Tipo de publicação:JOURNAL ARTICLE; LEGAL CASES
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171228
[Lr] Data última revisão:
171228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


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[PMID]:28467181
[Au] Autor:Soto-Gutierrez A; Gough A; Vernetti LA; Taylor DL; Monga SP
[Ad] Endereço:1 Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15260, USA.
[Ti] Título:Pre-clinical and clinical investigations of metabolic zonation in liver diseases: The potential of microphysiology systems.
[So] Source:Exp Biol Med (Maywood);242(16):1605-1616, 2017 10.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The establishment of metabolic zonation within a hepatic lobule ascribes specific functions to hepatocytes based on unique, location-dependent gene expression patterns. Recently, there have been significant developments in the field of metabolic liver zonation. A little over a decade ago, the role of ß-catenin signaling was identified as a key regulator of gene expression and function in pericentral hepatocytes. Since then, additional molecules have been identified that regulate the pattern of Wnt/ß-catenin signaling within a lobule and determine gene expression and function in other hepatic zones. Currently, the molecular basis of metabolic zonation in the liver appears to be a 'push and pull' between signaling pathways. Such compartmentalization not only provides an efficient assembly line for hepatocyte functions but also can account for restricting the initial hepatic damage and pathology from some hepatotoxic drugs to specific zones, possibly enabling effective regeneration and restitution responses from unaffected cells. Careful analysis and experimentation have also revealed that many pathological conditions in the liver lobule are spatially heterogeneous. We will review current research efforts that have focused on examination of the role and regulation of such mechanisms of hepatocyte adaptation and repair. We will discuss how the pathological organ-specific microenvironment affects cell signaling and metabolic liver zonation, especially in steatosis, viral hepatitis, and hepatocellular carcinoma. We will discuss how the use of new human microphysiological platforms will lead to a better understanding of liver disease progression, diagnosis, and therapies. In conclusion, we aim to provide insights into the role and regulation of metabolic zonation and function using traditional and innovative approaches. Impact statement Liver zonation of oxygen tension along the liver sinusoids has been identified as a critical liver microenvironment that impacts specific liver functions such as intermediary metabolism of amino acids, lipids, and carbohydrates, detoxification of xenobiotics and as sites for initiation of liver diseases. To date, most information on the role of zonation in liver disease including, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC) have been obtained from animal models. It is now possible to complement animal studies with human liver, microphysiology systems (MPS) containing induced pluripotent stem cells engineered to create disease models where it is also possible to control the in vitro liver oxygen microenvironment to define the role of zonation on the mechanism(s) of disease progression. The field now has the tools to investigate human liver disease progression, diagnosis, and therapeutic development.
[Mh] Termos MeSH primário: Hepatócitos/metabolismo
Células-Tronco Pluripotentes Induzidas/citologia
Fígado/metabolismo
Fígado/patologia
Microfluídica/métodos
Via de Sinalização Wnt/fisiologia
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/metabolismo
Células Cultivadas
Fígado Gorduroso/metabolismo
Expressão Gênica
Hepatite/metabolismo
Hepatite/virologia
Seres Humanos
Neoplasias Hepáticas/metabolismo
Camundongos
Ratos
Proteínas Wnt/metabolismo
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Wnt Proteins); 0 (beta Catenin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171206
[Lr] Data última revisão:
171206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1177/1535370217707731


  9 / 14643 MEDLINE  
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[PMID]:28906367
[Au] Autor:Huang HS; Hsu CC; Ye JC; Su SB; Huang CC; Lin HJ
[Ad] Endereço:aDepartment of Emergency Medicine bDepartment of Occupational Medicine, Chi-Mei Medical Center cDepartment of Biotechnology, Southern Taiwan University of Science and Technology dBachelor Program of Senior Service eDepartment of Leisure, Recreation, and Tourism Management, Southern Taiwan University of Science and Technology fDepartment of Medical Research, Chi-Mei Medical Center, Liouying gDepartment of Environmental and Occupational Health, College of Medicine, National Cheng Kung University hDepartment of Geriatrics and Gerontology, Chi-Mei Medical Center iDepartment of Emergency Medicine, Taipei Medical University, Taipei, Taiwan.
[Ti] Título:Predicting the mortality in geriatric patients with dengue fever.
[So] Source:Medicine (Baltimore);96(37):e7878, 2017 Sep.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Geriatric patients have high mortality for dengue fever (DF); however, there is no adequate method to predict mortality in geriatric patients. Therefore, we conducted this study to develop a tool in an attempt to address this issue.We conducted a retrospective case-control study in a tertiary medical center during the DF outbreak in Taiwan in 2015. All the geriatric patients (aged ≥65 years) who visited the study hospital between September 1, 2015, and December 31, 2015, were recruited into this study. Variables included demographic data, vital signs, symptoms and signs, comorbidities, living status, laboratory data, and 30-day mortality. We investigated independent mortality predictors by univariate analysis and multivariate logistic regression analysis and then combined these predictors to predict the mortality.A total of 627 geriatric DF patients were recruited, with a mortality rate of 4.3% (27 deaths and 600 survivals). The following 4 independent mortality predictors were identified: severe coma [Glasgow Coma Scale: ≤8; adjusted odds ratio (AOR): 11.36; 95% confidence interval (CI): 1.89-68.19], bedridden (AOR: 10.46; 95% CI: 1.58-69.16), severe hepatitis (aspartate aminotransferase >1000 U/L; AOR: 96.08; 95% CI: 14.11-654.40), and renal failure (serum creatinine >2 mg/dL; AOR: 6.03; 95% CI: 1.50-24.24). When we combined the predictors, we found that the sensitivity, specificity, positive predictive value, and negative predictive value for patients with 1 or more predictors were 70.37%, 88.17%, 21.11%, and 98.51%, respectively. For patients with 2 or more predictors, the respective values were 33.33%, 99.44%, 57.14%, and 98.51%.We developed a new method to help decision making. Among geriatric patients with none of the predictors, the survival rate was 98.51%, and among those with 2 or more predictors, the mortality rate was 57.14%. This method is simple and useful, especially in an outbreak.
[Mh] Termos MeSH primário: Dengue/diagnóstico
Dengue/mortalidade
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Estudos de Casos e Controles
Coma/complicações
Coma/mortalidade
Dengue/complicações
Feminino
Escala de Coma de Glasgow
Hepatite/complicações
Hepatite/mortalidade
Seres Humanos
Modelos Logísticos
Masculino
Análise Multivariada
Razão de Chances
Insuficiência Renal/complicações
Insuficiência Renal/mortalidade
Estudos Retrospectivos
Sensibilidade e Especificidade
Análise de Sobrevida
Taiwan
Centros de Atenção Terciária
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007878


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[PMID]:28808122
[Au] Autor:Webster P
[Ad] Endereço:Toronto, Ont.
[Ti] Título:Dramatic budget increase for hepatitis treatment in federal prisons.
[So] Source:CMAJ;189(32):E1052, 2017 08 14.
[Is] ISSN:1488-2329
[Cp] País de publicação:Canada
[La] Idioma:eng
[Mh] Termos MeSH primário: Orçamentos/tendências
Assistência à Saúde/economia
Financiamento Governamental
Hepatite/economia
Hepatite/terapia
Prisões/economia
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:NEWS
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1503/cmaj.1095468



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