Database : MEDLINE
Search on : Sepsis [Words]
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[PMID]: 25514427
[Au] Autor:Kraft R; Herndon DN; Finnerty CC; Cox RA; Song J; Jeschke MG
[Ad] Address:*Shriners Hospitals for Children, and †Department of Surgery, Shriners Hospitals for Children; ‡Institute for Translational Sciences and Sealy Center for Molecular Medicine, University of Texas Medical Branch; and §Department of Pathology, Shriners Hospitals for Children, Galveston; and ∥Department of Surgery, University of Texas Southwestern, Dallas, Texas; and ¶Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Department of Surgery, Division of Plastic Surgery, University of Toronto, Toronto, Ontario, Canada.
[Ti] Title:Predictive Value of IL-8 for Sepsis and Severe Infections After Burn Injury: A Clinical Study.
[So] Source:Shock;43(3):222-7, 2015 Mar.
[Is] ISSN:1540-0514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The inflammatory response induced by burn injury contributes to increased incidence of infections, sepsis, organ failure, and mortality. Thus, monitoring postburn inflammation is of paramount importance but, so far, there are no reliable biomarkers available to monitor and/or predict infectious complications after burn. As interleukin 8 (IL-8) is a major mediator for inflammatory responses, the aim of our study was to determine whether IL-8 expression can be used to predict postburn sepsis, infections, and mortality. Plasma cytokines, acute-phase proteins, constitutive proteins, and hormones were analyzed during the first 60 days after injury from 468 pediatric burn patients. Demographics and clinical outcome variables (length of stay, infection, sepsis, multiorgan failure [MOF], and mortality) were recorded. A cutoff level for IL-8 was determined using receiver operating characteristic analysis. Statistical significance is set at P < 0.05. Receiver operating characteristic analysis identified a cutoff level of 234 pg/mL for IL-8 for survival. Patients were grouped according to their average IL-8 levels relative to this cutoff and stratified into high (H) (n = 133) and low (L) (n = 335) groups. In the L group, regression analysis revealed a significant predictive value of IL-8 to percent of total body surface area burned and incidence of MOF (P < 0.001). In the H group, IL-8 levels were able to predict sepsis (P < 0.002). In the H group, elevated IL-8 was associated with increased inflammatory and acute-phase responses compared with the L group (P < 0.05). High levels of IL-8 correlated with increased MOF, sepsis, and mortality. These data suggest that serum levels of IL-8 may be a valid biomarker for monitoring sepsis, infections, and mortality in burn patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/SHK.0000000000000294

  2 / 91813 MEDLINE  
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[PMID]: 25980007
[Au] Autor:Condotta SA; Khan SH; Rai D; Griffith TS; Badovinac VP
[Ad] Address:Department of Pathology, University of Iowa Carver College of Medicine, Iowa City, IA 52242;...
[Ti] Title:Polymicrobial Sepsis Increases Susceptibility to Chronic Viral Infection and Exacerbates CD8+ T Cell Exhaustion.
[So] Source:J Immunol;195(1):116-25, 2015 Jul 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Patients who survive sepsis display suppressed immune functions, often manifested as an increased susceptibility to secondary infections. Recently, using a cecal-ligation and puncture (CLP) model of sepsis, we showed that sepsis induces substantial and long-lasting changes in the available naive CD8(+) T cell repertoire affecting the capacity of the host to respond to newly encountered acute infections. However, the extent to which sepsis changes the host susceptibility to chronic infection and affects CD8(+) T cell responses is currently unknown. In this study, we demonstrate that inbred and outbred mice recovering from a septic event are more susceptible to lymphocytic choriomeningitis virus (LCMV) clone-13 infection exhibited by mortality and viral burden. Primary virus-specific CD8(+) T cells in LCMV clone-13-infected septic mice displayed exacerbated CD8(+) T cell exhaustion illustrated by increased inhibitory molecule expression (e.g., programmed cell death 1, lymphocyte-activation gene 3, and 2B4) and diminished Ag-driven cytokine production (e.g., IFN-γ, TNF-α) compared with similarly infected sham-treated mice. Importantly, therapeutic inhibitory molecule dual blockade (anti-PD-L1 and anti-lymphocyte-activation gene 3) increased the number of circulating LCMV-specific CD8(+) T cells, and improved CD8(+) T cell function and pathogen control in chronically infected septic mice. Together, these results illustrate that polymicrobial sepsis compromises the overall health of the host leading to increased vulnerability to chronic infection and exacerbated CD8(+) T cell exhaustion. Collectively, our findings suggest that septic survivors may be more susceptible and at greater risk for developing exhaustible CD8(+) T cells upon encountering a subsequent chronic infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1402473

  3 / 91813 MEDLINE  
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[PMID]: 26085210
[Au] Autor:Medvedev AE; Murphy M; Zhou H; Li X
[Ad] Address:Department of Immunology, University of Connecticut Health Center, Farmington, CT, USA....
[Ti] Title:E3 ubiquitin ligases Pellinos as regulators of pattern recognition receptor signaling and immune responses.
[So] Source:Immunol Rev;266(1):109-22, 2015 Jul.
[Is] ISSN:1600-065X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Pellinos are a family of E3 ubiquitin ligases discovered for their role in catalyzing K63-linked polyubiquitination of Pelle, an interleukin-1 (IL-1) receptor-associated kinase homolog in the Drosophila Toll pathway. Subsequent studies have revealed the central and non-redundant roles of mammalian Pellino-1, Pellino-2, and Pelino-3 in signaling pathways emanating from IL-1 receptors, Toll-like receptors, NOD-like receptors, T- and B-cell receptors. While Pellinos ability to interact with many signaling intermediates suggested their scaffolding roles, recent findings in mice expressing ligase-inactive Pellinos demonstrated the importance of Pellino ubiquitin ligase activity. Cell-specific functions of Pellinos have emerged, e.g. Pellino-1 being a negative regulator in T lymphocytes and a positive regulator in myeloid cells, and details of molecular regulation of receptor signaling by various members of the Pellino family have been revealed. In this review, we summarize current information about Pellino-mediated regulation of signaling by pattern recognition receptors, T-cell and B-cell receptors and tumor necrosis factor receptors, and discuss Pellinos roles in sepsis and infectious diseases, as well as in autoimmune, inflammatory, and allergic disorders. We also provide our perspective on the potential of targeting Pellinos with peptide- or small molecule-based drug compounds as a new therapeutic approach for septic shock and autoimmune pathologies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/imr.12298

  4 / 91813 MEDLINE  
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[PMID]: 26085872
[Au] Autor:Malthouse T; Lam W; Brewin J; Watkin N; Ayres B; Nitkunan T
[Ad] Address:Epsom & St Helier University Hospitals NHS Trust, Surrey, United Kingdom;...
[Ti] Title:Penile lesion in end-stage renal failure - cancer or otherwise?: Calcific uremic arteriolopathy presenting with a penile lesion.
[So] Source:Can Urol Assoc J;9(3-4):136-7, 2015 Mar-Apr.
[Is] ISSN:1911-6470
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:Calcific uremic arteriolopathy or calciphylaxis is a rare condition that can present with clinical features similar to penile cancer. It is a diagnosis to consider in patients with end-stage renal failure (ESRF) presenting with a penile lesion. We describe one such case, where a patient with ESRF presented with a solid, tender penile mass and underwent surgery for presumed penile cancer. Histopathological analysis however confirmed a diagnosis of calcific uremic arteriolopathy, without evidence of malignancy. The clinical diagnosis of calcific uremic arteriolopathy relies on a high index of suspicion, and lesion biopsy is controversial due to a high risk of poor wound healing and sepsis. New treatment options are encouraging, and have been reported, albeit in small numbers. Delayed diagnosis can adversely affect both quality of life and prognosis in a condition with an extremely high mortality rate.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Da] Date of entry for processing:150618
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.5489/cuaj.2331

  5 / 91813 MEDLINE  
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[PMID]: 25998681
[Au] Autor:Wang H; Hong LJ; Huang JY; Jiang Q; Tao RR; Tan C; Lu NN; Wang CK; Ahmed MM; Lu YM; Liu ZR; Shi WX; Lai EY; Wilcox CS; Han F
[Ad] Address:1] Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, China [2] Key Laboratory of Carbohydrate and Lipid Metabolism Research, College of Life Science and Technology, Dalian University, Dalian, Liaoning 116622, China....
[Ti] Title:P2RX7 sensitizes Mac-1/ICAM-1-dependent leukocyte-endothelial adhesion and promotes neurovascular injury during septic encephalopathy.
[So] Source:Cell Res;25(6):674-90, 2015 Jun.
[Is] ISSN:1748-7838
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Septic encephalopathy (SE) is a critical factor determining sepsis mortality. Vascular inflammation is known to be involved in SE, but the molecular events that lead to the development of encephalopathy remain unclear. Using time-lapse in vivo two-photon laser scanning microscopy, we provide the first direct evidence that cecal ligation and puncture in septic mice induces microglial trafficking to sites adjacent to leukocyte adhesion on inflamed cerebral microvessels. Our data further demonstrate that septic injury increased the chemokine CXCL1 level in brain endothelial cells by activating endothelial P2RX7 and eventually enhanced the binding of Mac-1 (CD11b/CD18)-expressing leukocytes to endothelial ICAM-1. In turn, leukocyte adhesion upregulated endothelial CX3CL1, thereby triggering microglia trafficking to the injured site. The sepsis-induced increase in endothelial CX3CL1 was abolished in CD18 hypomorphic mutant mice. Inhibition of the P2RX7 pathway not only decreased endothelial ICAM-1 expression and leukocyte adhesion but also prevented microglia overactivation, reduced brain injury, and consequently doubled the early survival of septic mice. These results demonstrate the role of the P2RX7 pathway in linking neurovascular inflammation to brain damage in vivo and provide a rationale for targeting endothelial P2RX7 for neurovascular protection during SE.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/cr.2015.61

  6 / 91813 MEDLINE  
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[PMID]: 26021615
[Au] Autor:Liu W; Wu H; Chen L; Wen Y; Kong X; Gao WQ
[Ad] Address:State Key Laboratory for Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China....
[Ti] Title:Park7 interacts with p47(phox) to direct NADPH oxidase-dependent ROS production and protect against sepsis.
[So] Source:Cell Res;25(6):691-706, 2015 Jun.
[Is] ISSN:1748-7838
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Inappropriate inflammation responses contribute to mortality during sepsis. Through Toll-like receptors (TLRs), reactive oxygen species (ROS) produced by NADPH oxidase could modulate the inflammation responses. Parkinson disease (autosomal recessive, early onset) 7 (Park7) has a cytoprotective role by eliminating ROS. However, whether Park7 could modulate inflammation responses and mortality in sepsis is unclear. Here, we show that, compared with wild-type mice, Park7(-/-) mice had significantly increased mortality and bacterial burdens in sepsis model along with markedly decreased systemic and local inflammation, and drastically impaired macrophage phagocytosis and bacterial killing abilities. Surprisingly, LPS and phorbol-12-myristate-13-acetate stimulation failed to induce ROS and proinflammatory cytokine production in Park7(-/-) macrophages and Park7-deficient RAW264.7 cells. Through its C-terminus, Park7 binds to p47(phox), a subunit of the NADPH oxidase, to promote NADPH oxidase-dependent production of ROS. Restoration of Park7 expression rescues ROS production and improves survival in LPS-induced sepsis. Together, our study shows that Park7 has a protective role against sepsis by controlling macrophage activation, NADPH oxidase activation and inflammation responses.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/cr.2015.63

  7 / 91813 MEDLINE  
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[PMID]: 25912130
[Au] Autor:Wang C; Gui Q; Zhang K
[Ad] Address:Department of Emergency, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
[Ti] Title:Functional polymorphisms in CD86 gene are associated with susceptibility to pneumonia-induced sepsis.
[So] Source:APMIS;123(5):433-8, 2015 May.
[Is] ISSN:1600-0463
[Cp] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract:Sepsis is an illness in which the body has a severe response to bacteria or other germs. A bacterial infection in the body such as lungs may set off the response that leads to the disease. CD86 (B7-2) is expressed on various immune cells and plays critical roles in immune responses. Genetic polymorphisms in CD86 gene may affect the development of several diseases. Here, we evaluated the association between two CD86 polymorphisms (rs1915087C/T and rs2332096T/G) and susceptibility to pneumonia-induced sepsis. CD86 rs1915087C/T and rs2332096T/G were identified in 186 pneumonia-induced septic patients and 196 healthy controls in the Chinese population. Results revealed that subjects with rs1915087CT and TT genotypes had significantly lower risk of pneumonia-induced sepsis than those with CC genotype [odds ratio (OR) = 0.58, 95% confidence interval (CI), 0.37-0.91, p = 0.017, and OR = 0.40, 95%CI, 0.21-0.76, p = 0.005]. However, prevalence of rs2332096GG genotype and G allele were significantly increased in patients than in healthy controls (OR = 2.75, 95%CI, 1.46-5.16, p = 0.001, and OR = 1.65, 95%CI, 1.21-2.24, p = 0.001]. We further investigated functions of these two polymorphisms by assessing gene expression in peripheral blood mononuclear cells and in monocytes. Data showed subjects carrying rs2332096GG genotype had significantly decreased level of CD86 in monocytes than those carrying rs2332096TT genotype. These results indicate that CD86 polymorphisms are associated with susceptibility to pneumonia-induced sepsis and may affect gene expression in monocytes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1111/apm.12364

  8 / 91813 MEDLINE  
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[PMID]: 25475180
[Au] Autor:Drosatos K; Lymperopoulos A; Kennel PJ; Pollak N; Schulze PC; Goldberg IJ
[Ad] Address:Metabolic Biology Laboratory, Center for Translational Medicine, Department of Pharmacology, Temple University School of Medicine, 3500 N. Broad Street, MERB-951, Philadelphia, PA, 19140, USA, drosatos@temple.edu.
[Ti] Title:Pathophysiology of sepsis-related cardiac dysfunction: driven by inflammation, energy mismanagement, or both?
[So] Source:Curr Heart Fail Rep;12(2):130-40, 2015 Apr.
[Is] ISSN:1546-9549
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Sepsis is a systemic inflammatory response that follows bacterial infection. Cardiac dysfunction is an important consequence of sepsis that affects mortality and has been attributed to either elevated inflammation or suppression of both fatty acid and glucose oxidation and eventual ATP depletion. Moreover, cardiac adrenergic signaling is compromised in septic patients and this aggravates further heart function. While anti-inflammatory therapies are important for the treatment of the disease, administration of anti-inflammatory drugs did not improve survival in septic patients. This review article summarizes findings on inflammatory and other mechanisms that are triggered in sepsis and affect cardiac function and mortality. Particularly, it focuses on the effects of the disease in metabolic pathways, as well as in adrenergic signaling and the potential interplay of the latter with inflammation. It is suggested that therapeutic approaches should include combination of anti-inflammatory treatments, stimulation of energy production, and restoration of adrenergic signaling in the heart.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1503
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1007/s11897-014-0247-z

  9 / 91813 MEDLINE  
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[PMID]: 24970700
[Au] Autor:Ranjan R; Deng J; Chung S; Lee YG; Park GY; Xiao L; Joo M; Christman JW; Karpurapu M
[Ad] Address:Department of Medicine and Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Ill., USA.
[Ti] Title:The transcription factor nuclear factor of activated T cells c3 modulates the function of macrophages in sepsis.
[So] Source:J Innate Immun;6(6):754-64, 2014.
[Is] ISSN:1662-8128
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:The role of the transcription factor nuclear factor of activated T cells (NFAT) was initially identified in T and B cell gene expression, but its role in regulating gene expression in macrophages during sepsis is not known. Our data show that NFATc3 regulates expression of inducible nitric oxide synthase (iNOS) in macrophages stimulated with lipopolysaccharide. Selective inhibition of NFAT by cyclosporine A and a competitive peptide inhibitor 11R-VIVIT inhibited endotoxin-induced expression of iNOS and nitric oxide (NO) release. Macrophages from NFATc3 knockout (KO) mice show reduced iNOS expression and NO release and attenuated bactericidal activity. Gel shift and chromatin immunoprecipitation assays show that endotoxin challenge increases NFATc3 binding to the iNOS promoter, resulting in transcriptional activation of iNOS. The binding of NFATc3 to the iNOS promoter is abolished by NFAT inhibitors. NFATc3 KO mice subjected to sepsis show that NFATc3 is necessary for bacterial clearance in mouse lungs during sepsis. Our study demonstrates for the first time that NFATc3 is necessary for macrophage iNOS expression during sepsis, which is essential for containment of bacterial infections.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Em] Entry month:1410
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1159/000362647

  10 / 91813 MEDLINE  
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[PMID]: 25042793
[Au] Autor:Schneider AG; Bagshaw SM
[Ti] Title:Renal recovery after acute kidney injury: choice of initial renal replacement therapy modality still matters.
[So] Source:Crit Care;18(3):154, 2014.
[Is] ISSN:1466-609X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Renal replacement therapy can be applied either in an intermittent fashion or in a continuous fashion in severe acute kidney injury. To date, no modality has been shown to consistently improve patient survival. In the study recently reported by Sun and colleagues, continuous application of renal replacement therapy was associated with improved renal recovery, defined by lower risk of long-term need for chronic dialysis therapy. This association between nonrecovery and intermittent renal replacement therapy may be explained by a higher rate of hypotensive episodes and the lower capacity for fluid removal during the first 72 hours of therapy. Altogether, this study adds to the growing body of evidence to suggest improved likelihood of recovery of kidney function in critically ill survivors of AKI with continuous modalities for renal replacement therapy.
[Mh] MeSH terms primary: Acute Kidney Injury/epidemiology
Acute Kidney Injury/therapy
Hemofiltration/methods
Sepsis/epidemiology
Sepsis/therapy
[Mh] MeSH terms secundary: Female
Humans
Male
[Pt] Publication type:COMMENT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1505
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[Da] Date of entry for processing:140830
[St] Status:MEDLINE
[do] DOI:10.1186/cc13936


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