Binder, Lutz

[["dc.bibliographiccitation.firstpage","248"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Psychosomatics"],["dc.bibliographiccitation.lastpage","256"],["dc.bibliographiccitation.volume","51"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Stanske, Beate"],["dc.contributor.author","Kochen, Michael M."],["dc.contributor.author","Cordes, Andreas"],["dc.contributor.author","Yüksel, Iraz"],["dc.contributor.author","Wachter, Rolf"],["dc.contributor.author","Lüers, Claus"],["dc.contributor.author","Scherer, Martin"],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Herrmann-Lingen, Christoph"],["dc.date.accessioned","2019-07-09T11:52:56Z"],["dc.date.available","2019-07-09T11:52:56Z"],["dc.date.issued","2010"],["dc.description.abstract","BACKGROUND: Vital exhaustion, a psychological state characterized by unusual fatigue, irritability, and feelings of demoralization, has been identified as a risk factor for cardiovascular diseases and linked to elevated levels of pro-inflammatory cytokines. OBJECTIVE: The purpose of this study was to investigate the relationship between vital exhaustion and cytokine levels in patients with cardiovascular risk factors. METHOD: The entire cohort consisted of 356 primary-care patients with cardiovascular risk factors who participated in a study of early recognition of heart failure. All participants completed the Maastricht questionnaire (MQ) for assessing vital exhaustion. Cytokine serum levels were measured in all those subjects (N=178) who were assigned to the highest and lowest quartiles of the MQ, respectively. RESULTS: We found that elevated serum concentrations of IL-6, TNFα, and IL-10, but not IL-1β or natriuretic peptides were associated with high MQ scores indicative of vital exhaustion. Using logistic regression analyses controlling for clinical variables and Type D personality, both TNFα (multivariate odds ratio [OR] =1.86; 95%-confidence interval [CI] =1.30-2.68; p=0.001) and IL-10(OR=1.62; 95%-CI=1.15-2.28; p=0.006), but not other cytokines significantly predicted vital exhaustion independently of other clinical and laboratory parameters examined [corrected]. CONCLUSION: The subjective state of vital exhaustion is linked to a substantial alteration in the pattern of secreted cytokines. Data suggest that a disturbance in the levels of both pro-inflammatory and anti-inflammatory mediators, rather than isolated stimulation by pro-inflammatory cytokines, is associated with the mental and physical changes of vital exhaustion."],["dc.identifier.doi","10.1176/appi.psy.51.3.248"],["dc.identifier.fs","573439"],["dc.identifier.pmid","20484723"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6169"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60303"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1545-7206"],["dc.relation.orgunit","Institut für Allgemeinmedizin"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.mesh","Aged"],["dc.subject.mesh","Austria"],["dc.subject.mesh","Cardiovascular Diseases"],["dc.subject.mesh","Cohort Studies"],["dc.subject.mesh","Coronary Disease"],["dc.subject.mesh","Fatigue"],["dc.subject.mesh","Female"],["dc.subject.mesh","Heart Failure"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Interleukin-10"],["dc.subject.mesh","Interleukin-6"],["dc.subject.mesh","Irritable Mood"],["dc.subject.mesh","Male"],["dc.subject.mesh","Middle Aged"],["dc.subject.mesh","Morale"],["dc.subject.mesh","Personality Inventory"],["dc.subject.mesh","Primary Health Care"],["dc.subject.mesh","Psychometrics"],["dc.subject.mesh","Risk Factors"],["dc.subject.mesh","Tumor Necrosis Factor-alpha"],["dc.title","Elevated serum levels of interleukin-10 and tumor necrosis factor α [corrected] are both associated with vital exhaustion in patients with cardiovascular risk factors."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","438"],["dc.bibliographiccitation.journal","Frontiers in physiology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.affiliation","Khan, Niamat; 1Institute for Clinical Chemistry/UMG-Laboratories, University Medical Center Goettingen, Germany"],["dc.contributor.affiliation","Binder, Lutz; 1Institute for Clinical Chemistry/UMG-Laboratories, University Medical Center Goettingen, Germany"],["dc.contributor.affiliation","Pantakani, D. V. Krishna; 1Institute for Clinical Chemistry/UMG-Laboratories, University Medical Center Goettingen, Germany"],["dc.contributor.affiliation","Asif, Abdul R.; 1Institute for Clinical Chemistry/UMG-Laboratories, University Medical Center Goettingen, Germany"],["dc.contributor.author","Khan, Niamat"],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Pantakani, D. V. Krishna"],["dc.contributor.author","Asif, Abdul R."],["dc.date.accessioned","2019-07-09T11:43:35Z"],["dc.date.available","2019-07-09T11:43:35Z"],["dc.date.issued","2017"],["dc.date.updated","2022-09-05T20:55:41Z"],["dc.description.abstract","Mycophenolic acid (MPA) is prescribed to prevent allograft rejection in organ transplanted patients. However, its use is sporadically linked to leak flux diarrhea and other gastrointestinal (GI) disturbances in around 75% of patients through yet unknown mechanisms. Recently, we identified Midkine as a modulator of tight junctions (TJs) permeability in MPA treated Caco-2 monolayer. In the present study, we investigated the possible involvement of Midkine dependent PI3K pathway in alteration of TJs under MPA treatment. Caco-2 cells were grown as monolayer to develop TJs and were treated for 72 h with DMSO (control) or MPA in presence and absence of Midkine inhibitor (iMDK) or PI3K inhibitors (LY/AMG). Caco-2 monolayer integrity was assessed by transepithelial electrical resistance (TEER) and FITC-dextran assays. Our functional assays showed that PI3K inhibitors (LY/AMG) can significantly inhibit the compromised TJs integrity of MPA-treated Caco-2 cells monolayer. Chromatin immunoprecipitation analyses showed a significant epigenetic activation of Midkine, PI3K, Cdx-2, and Cldn-2 genes and epigenetic repression of Cldn-1 gene after MPA treatment. The MPA-induced epigenetic alterations were further confirmed by mRNA and protein expression analysis. Collectively, our data shows that PI3K pathway as the downstream target of Midkine which in turn modulates p38MAPK and pAKT signaling to alter TJs permeability in Caco-2 cell monolayers treated with MPA. These results highlight the possible use of either Midkine or PI3K inhibitors as therapeutic agents to prevent MPA induced GI disturbances."],["dc.identifier.doi","10.3389/fphys.2017.00438"],["dc.identifier.pmid","28694783"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14582"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58920"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-042X"],["dc.relation.issn","1664-042X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","MPA Modulates Tight Junctions' Permeability via Midkine/PI3K Pathway in Caco-2 Cells: A Possible Mechanism of Leak-Flux Diarrhea in Organ Transplanted Patients."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]