Relevant bibliographies by topics / TNFα

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'TNFα'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 September 2023

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Journal articles on the topic "TNFα"

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Yang, Liyun, Yan Chen, Sainan Zhu, Dingfang Bu, Lixiang Wang, Xiaojie Jiao, Xuechun Lu, Hongxing Liu, and Ping Zhu. "Haploidentical Allogeneic Hematopoietic Stem Cell Transplantation Using the Donors with the HLA-B*5801-TNFα -308A Haplotype Produced Higher Frequency of Untoward Effects in Acute Lymphocytic Leukemia Patients." Blood 120, no. 21 (November 16, 2012): 2002. http://dx.doi.org/10.1182/blood.v120.21.2002.2002.

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Abstract Abstract 2002 In this study, we investigated the clinical characteristics of acute lymphoblastic leukemia (ALL) patients using sibling donors with HLA-B*5801-TNFα-308A haplotype (B5801-TNF2) for haploidentical or identical hematopoietic stem cell transplantation (HSCT). A total of 136 B-ALL cases and 29 T/NK-ALL cases were recruited. DNA samples from the patients and their siblings were assayed for genotyping of HLA and TNFα at -308 (rs1800629). B5801-TNF2 haplotype in donors was determined by analyzing TNFα -308 and HLA-B genotypes in patients and their family members. Outcomes within 2 years including overall mortality and non-relapse mortality, disease course and complications within 100 days were compared among patients using related donors with HLA-B*5801-TNFα-308A haplotype for haploidentical HSCT (B5801-TNF2+HID group), those using related donor without HLA-B*5801-TNFα-308A haplotype for haploidentical HSCT (B5801-TNF2-HID group), and those using related sibling either B5801-TNF2+ or B5801-TNF2- haplotype for identical HSCT (SID group). In the 165 sibling donors after HSCT, 35 were found to carry HLA-B*5801-TNFα-308A haplotype. There were 21 cases in B5801-TNF2+HID group, 100 cases in B5801-TNF2-HID group, and 44 cases in SID group. Compared patients in B5801-TNF2-HID and SID groups, patients in B5801-TNF2+HID group had higher overall mortality (adjusted P=0.039) and non-relapse mortality within 2 years (adjusted P=0.001), delayed platelet engraftment (adjusted P<0.0001), higher incidences of severe acute graft-versus-host disease (P=0.007), severe late onset hemorrhagic cystitis (P=0.002), blood stream infection (P=0.017), and invasive fungal disease (P=0.004) within 100 days. Therefore, sibling donors carrying HLA-B*5801-TNFα-308A haplotype for haploidentical HSCT caused higher mortality rate and higher frequency of severe complications in ALL recipients. Keywords: HLA-B*5801-TNFα-308A haplotype; acute lymphoblastic leukemia; allogeneic haploidentical hematopoietic stem cell transplantation; allogeneic identical hematopoietic stem cell transplantation Disclosures: No relevant conflicts of interest to declare.
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Ma, Li, Haiyan Gong, Haiyan Zhu, Pei Su, Shannan Cao, Peng Liu, Jianfeng Yao, et al. "Identification Of a Novel Small-Molecule TNFα Inhibitor With Activity Against Inflammation In a Hepatitis Mouse Model." Blood 122, no. 21 (November 15, 2013): 4229. http://dx.doi.org/10.1182/blood.v122.21.4229.4229.

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Abstract Over-expression of tumor necrosis factor α (TNFα) is a hallmark of many inflammatory diseases including rheumatoid arthritis, inflammatory bowel disease and septic shock and hepatitis, making it a potential therapeutic target for clinical interventions. To date, significant advances have been made in the development of biological agents targeting TNFα and its signaling components. There are several well known commercial TNFα inhibitors, such as infliximab, adalimumab and etanercept, all of which are TNFα antibodies or TNFR1-Fc chimeras and function to prevent TNFα from binding to its receptor. Those biomacromolecular agents have been proved to be effective in the treatment of inflammatory bowel disease and rheumatoid arthritis due to their unique superiorities such as high specificity. However, several severe limitations such as poor stability, cost-ineffective commercial-scale production and exclusion from blood/brain barrier have also emerged. Instead, small-molecule chemical compounds have been appreciated as appropriate alternatives for overcoming most disadvantages associated with macromolecular inhibitors. Furthermore, they offer additional clinical benefits such as simpler preparation for oral medicine. Now by the use of computer-aided drug design (CADD) and cell-based assays in vitro, several selective small-molecule antagonists of TNFα activity have been identified. They include broad-spectrum inhibitors targeting the key molecules of the intracellular TNFα pathway, functionally uncharacterized inhibitors of TNFα expression, inhibitors of the processing enzyme TNFα converting enzyme (TACE), and molecules that directly bind to TNFR or prevent TNFα-TNFR interactions. Although the small-molecule inhibitors are capable of blocking the biological activity of TNFα in vitro, few have been shown to abrogate or reduce TNFα-induced inflammatory responses in vivo and exhibit high IC50 and severe side effects. Also, none of the small-molecular inhibitors have been reported to successfully block TNFα’s interaction with TNFR through direct binding to TNFα. Thus, development of small molecules for TNFα therapy remains a major challenge. In this study, to explore chemical inhibitors against TNFα activity, we applied CADD combined with in vitro and cell-based assays and identified a lead chemical compound (named as C87 thereafter) from a compound library including about 90,000 small molecular compounds, which directly binds to TNFα indicated by SPR assay, and it potently inhibits TNFα-induced cytotoxicity (IC50=8.73μM) and effectively blocks TNFα–triggered signaling activities. More importantly, by using a murine acute hepatitis model, we showed that C87 attenuates TNFα-induced inflammation, thereby markedly reducing injuries to the liver and improving animal survival. Thus, our results lead to a novel and highly specific small-molecule TNFα inhibitor, which can be potentially used to treat TNFα mediated inflammatory diseases. Disclosures: No relevant conflicts of interest to declare.
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Gharamti, Amal, Omar Samara, Anthony Monzon, Lilian Vargas Barahona, Sias Scherger, Kristen DeSanto, Daniel B. Chastain, et al. "1003. Cytokine Levels in Sepsis and TNFα Association with Mortality but not Sepsis Severity or Infection Source: a Systematic Review and Meta-analysis." Open Forum Infectious Diseases 8, Supplement_1 (November 1, 2021): S592. http://dx.doi.org/10.1093/ofid/ofab466.1197.

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Abstract Background Sepsis is a global health problem associated with significant morbidity and mortality and is attributed to a “cytokine storm.”. However, anti-cytokine therapies have failed to lower sepsis mortality in clinical trials. Linking cytokine excess to sepsis pathogenesis requires quantification of cytokine levels in sepsis. This systematic review and meta-analysis characterizes levels of key cytokines in the circulation of sepsis patients and relates TNFα levels to mortality and patient characteristics. Methods Medline, Embase, Cochrane Library, and Web of Science Core Collection databases were searched from 1946 to May 2020 for studies in English disclosing cytokine levels in sepsis. Keywords included sepsis, septic shock, purpura fulminans, and tumor necrosis factor (TNF)α. We related cytokine amounts to 28-day mortality. Data analyses were performed using a random-effects model to estimate pooled odds ratios (OR) and 95% confidence intervals (CI). This systematic review is registered in PROSPERO under number CRD42020179800. Results A total of 3656 records were identified. After exclusions, 103 studies were included. Among these studies, 72 disclosed TNFα levels, 25 showed interleukin (IL)-1β levels, and 6 presented interferon (IFN)γ levels. The pooled estimate mean TNFα concentration in sepsis patients was 58.4 pg/ml (95% CI, 39.8-85.8 pg.ml; I2 = 99.4%). Pooled estimate means for IL-1α and IFNγ in sepsis patients were 21.8 pg/ml (95% CI, 12.6-37.8 pg.ml; I2 =99.8%) and 63.3 pg/ml (95% CI, 19.4-206.6 pg/ml; I2 = 99.7%), respectively. Elevated TNFα concentrations were associated with increased 28-day mortality (P=0.001). In a subgroup analysis, TNFα levels did not relate to sepsis source, sepsis severity, or sequential organ failure assessment (SOFA) score (figure 1). In a metaregression, TNFα associated with age, percentage of females and mortality at 28 days. Figure 1: A: TNFa levels according to sepsis source. B: TNFa levels according to measurement technique. C: TNFa levels according to presence or absence of cardiovascular disease. D: TNFa levels according to presence or absence of malignancy. E: TNFa levels according to sepsis severity. F: TNFa levels in fungal compared to other causes of sepsis (Yes=fungal sepsis; No= Other types of sepsis). G: TNFa levels according to SOFA score. H: TNFa levels and mortality at 28 days. Conclusion We presented levels of TNFα, IL-1β, and IFNγ in human sepsis and showed that TNFα elevations are associated with sepsis mortality. TNFα concentrations did not correlate with sepsis severity. We believe the concept that elevated cytokines cause sepsis should be revisited in the context of these data. Disclosures All Authors: No reported disclosures
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Bertolaccini, M. L., J. S. Lanchbury, A. R. Caliz, K. Katsumata, R. W. Vaughan, E. Kondeatis, M. A. Khamashta, T. Koike, G. R. V. Hughes, and T. Atsumi. "Plasma Tumor Necrosis Factor α Levels and the –238* A Promoter Polymorphism in Patients with Antiphospholipid Syndrome." Thrombosis and Haemostasis 85, no. 02 (2001): 198–203. http://dx.doi.org/10.1055/s-0037-1615676.

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Summary Objectives. To explore the possible involvement of the proinflammatory and prothrombotic cytokine TNFα in APS by determining the plasma levels in patients and to test for association of TNFA promoter polymorphisms and HLA class II genotypes with both plasma TNF and disease. Patients and Method. We studied 83 Caucasoid patients with APS and two groups of healthy controls. TNFα levels were determined in plasma from 35 patients’ and 21 controls using a highly sensitive sandwich ELISA. The full patient group was genotyped together with 95 ethnically matched healthy controls. -308 and -238 TNFA promoter polymorphisms were assessed by ARMS-PCR. HLA-DQB1, DQA1 and DRB1 genotypes were determined by PCR using sequence specific primers. Results. TNFα levels were significantly higher in patients with APS than healthy controls (median 2.95 pg/ml [range 0.51-10.75] vs. 0.95 pg/ml [0.51-1.6], respectively; p = 0.0001). Frequencies of TNFA-308*2 genotype did not differ between patients and controls. In contrast, TNFA-238*A positive genotype was more frequent in APS patients with arterial thrombosis and pregnancy loss than in controls (OR 3.7 [95% CI 1.37-10.1], p = 0.007 and OR 3.95 [95% CI 1.3-11.7], p = 0.01; respectively). DQB1*0303-DRB1*0701 haplotype was associated with TNFA-238*A in the control group (OR 96.0 [95% CI 9.6-959], p 0.0001) as well as in APS patient’s group (OR 54.2 [95% CI 9.6-306.5], p 0.0001). Conclusions. Raised plasma TNFα levels were found in patients with APS. As a prothrombotic and proinflammatory cytokine, TNFα may be involved in the development of clinical features of APS. The lack of correlation between the TNFA-238 polymorphism and plasma levels associated with disease suggests that the TNFα genetic marker may only indirectly relate to protein levels by virtue of allelic association with a functional marker which may reside in the HLA class II region.
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Tani-Ishii, N., A. Tsunoda, T. Teranaka, and T. Umemoto. "Autocrine Regulation of Osteoclast Formation and Bone Resorption by IL-1α and TNFα." Journal of Dental Research 78, no. 10 (October 1999): 1617–23. http://dx.doi.org/10.1177/00220345990780100601.

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Bone resorption is regulated by the cytokines within marrow cells that mediate osteoclast formation and activation. IL-1 and TNF induce bone resorption by stimulating the production of osteoclast-like multinucleated cells and by increasing the bone-resorbing activity of formed osteoclasts. This study was designed to detect IL-1 and TNF in osteoclasts in vitro and to determine whether these cytokines up-regulate osteoclast differentiation and bone resorption. The production of IL-1α, -β, and TNFa, β in osteoclasts was examined immunohistochemically and by in situ hybridization. In the co-culture of C57BL/6N mouse bone marrow and MC3T3-G2/PA6 cells, a colony of osteoclasts formed, and IL-1α and TNFa were detected. However, IL-1β and TNF β were not detected. To investigate the role of IL-1α and TNFα from osteoclasts, we enumerated TRAP-positive cells and measured the resorption pit areas in the presence of antibodies against IL-1α and TNFα. The addition of antibodies against IL-1α and TNFα to the co-culture system decreased the number of TRAP-positive colonies at seven days after incubation (anti-IL-1α, 25.0 ± 2.3%; anti-TNFα, 41.7 ± 3.7%; anti-IL-1α + anti-TNFα, 40.5 ± 1.3%; and control, 100%), and the ratio of mononuclear to multinuclear cells had changed (anti-IL-1α, 90:10; anti-TNFα, 75:25; anti-IL-1α+ anti-TNFα, 88:12; and control, 60:40). The total pit areas per dentin slice also decreased with the addition of antibodies (anti-IL-1α, 28,828; anti-TNFα, 49,249; anti-IL-1α + anti-TNFα, 30,685; and control, 303,139 mm2). These results suggest that local production of IL-la and TNFα by osteoclasts is an important mechanism for regulating the osteoclast differentiation and bone resorptive process.
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Rosenzweig, Holly L., Manabu Minami, Nikola S. Lessov, Sarah C. Coste, Susan L. Stevens, David C. Henshall, Robert Meller, Roger P. Simon, and Mary P. Stenzel-Poore. "Endotoxin Preconditioning Protects against the Cytotoxic Effects of TNFα after Stroke: A Novel Role for TNFα in LPS-Ischemic Tolerance." Journal of Cerebral Blood Flow & Metabolism 27, no. 10 (February 28, 2007): 1663–74. http://dx.doi.org/10.1038/sj.jcbfm.9600464.

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Lipopolysaccharide (LPS) preconditioning provides neuroprotection against subsequent cerebral ischemic injury. Tumor necrosis factor-α (TNFα) is protective in LPS-induced preconditioning yet exacerbates neuronal injury in ischemia. Here, we define dual roles of TNFα in LPS-induced ischemic tolerance in a murine model of stroke and in primary neuronal cultures in vitro, and show that the cytotoxic effects of TNFα are attenuated by LPS preconditioning. We show that LPS preconditioning significantly increases circulating levels of TNFα before middle cerebral artery occlusion in mice and show that TNFα is required to establish subsequent neuroprotection against ischemia, as mice lacking TNFα are not protected from ischemic injury by LPS preconditioning. After stroke, LPS preconditioned mice have a significant reduction in the levels of TNFα (~ threefold) and the proximal TNFα signaling molecules, neuronal TNF-receptor 1 (TNFR1), and TNFR-associated death domain (TRADD). Soluble TNFR1 (s-TNFR1) levels were significantly increased after stroke in LPS-preconditioned mice (~ 2.5-fold), which may neutralize the effect of TNFα and reduce TNFα-mediated injury in ischemia. Importantly, LPS-preconditioned mice show marked resistance to brain injury caused by intracerebral administration of exogenous TNFα after stroke. We establish an in vitro model of LPS preconditioning in primary cortical neuronal cultures and show that LPS preconditioning causes significant protection against injurious TNFα in the setting of ischemia. Our studies suggest that TNFα is a twin-edged sword in the setting of stroke: TNFα upregulation is needed to establish LPS-induced tolerance before ischemia, whereas suppression of TNFα signaling during ischemia confers neuroprotection after LPS preconditioning.
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Droessler, Linda, Valeria Cornelius, Alexander G. Markov, and Salah Amasheh. "Tumor Necrosis Factor Alpha Effects on the Porcine Intestinal Epithelial Barrier Include Enhanced Expression of TNF Receptor 1." International Journal of Molecular Sciences 22, no. 16 (August 14, 2021): 8746. http://dx.doi.org/10.3390/ijms22168746.

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Tumor necrosis factor alpha (TNFα) has been shown to impair the intestinal barrier, inducing and maintaining inflammatory states of the intestine. The aim of the current study was to analyze functional, molecular and regulatory effects of TNFα in a newly established non-transformed jejunal enterocyte model, namely IPEC-J2 monolayers. Incubation with 1000 U/mL TNFα induced a marked decrease in transepithelial electrical resistance (TEER), and an increase in permeability for the paracellular flux marker [3H]-D-mannitol compared to controls. Immunoblots revealed a significant decrease in tight junction (TJ) proteins occludin, claudin-1 and claudin-3. Moreover, a dose-dependent increase in the TNF receptor (TNFR)-1 was detected, explaining the exponential nature of pro-inflammatory effects, while TNFR-2 remained unchanged. Recovery experiments revealed reversible effects after the removal of the cytokine, excluding apoptosis as a reason for the observed changes. Furthermore, TNFα signaling could be inhibited by the specific myosin light chain kinase (MLCK) blocker ML-7. Results of confocal laser scanning immunofluorescence microscopy were in accordance with all quantitative changes. This study explains the self-enhancing effects of TNFα mediated by MLCK, leading to a differential regulation of TJ proteins resulting in barrier impairment in the intestinal epithelium.
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Li, Yusheng, Darrell L. Dinwiddie, Kevin S. Harrod, Yong Jiang, and K. Chul Kim. "Anti-inflammatory effect of MUC1 during respiratory syncytial virus infection of lung epithelial cells in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 4 (April 2010): L558—L563. http://dx.doi.org/10.1152/ajplung.00225.2009.

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MUC1 is a transmembrane glycoprotein expressed on the apical surface of airway epithelial cells and plays an anti-inflammatory role during airway bacterial infection. In this study, we determined whether the anti-inflammatory effect of MUC1 is also operative during the respiratory syncytial virus (RSV) infection. The lung epithelial cell line A549 was treated with RSV, and the production of TNFα and the levels of MUC1 protein were monitored temporally during the course of infection by ELISA and Western blot analysis. Small inhibitory RNA (siRNA) transfection was utilized to assess the role of MUC1 in regulating RSV-mediated inflammatory responses by lung epithelial cells. Our results revealed that: 1) following RSV infection, an increase in MUC1 level was preceded by an increase in TNFα production and completely inhibited by soluble TNF receptor (TNFR); and 2) knockdown of MUC1 using MUC1 siRNA resulted in a greater increase in TNFα level following RSV infection compared with control siRNA treatment. We conclude that the RSV-induced increase in the TNFα levels upregulates MUC1 through its interaction with TNFR, which in turn suppresses further increase in TNFα by RSV, thus forming a negative feedback loop in the control of RSV-induced inflammation. This is the first demonstration showing that MUC1 can suppress the virus-induced inflammatory responses.
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Kapás, L., A. B. Cady, M. R. Opp, A. E. Postlethwaite, J. M. Seyer, and J. M. Krueger. "Somnogenic and pyrogenic activity of TNFα, TNFβ and fragments of TNFα." International Journal of Immunopharmacology 13, no. 6 (January 1991): 717. http://dx.doi.org/10.1016/0192-0561(91)90210-x.

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Sanz, Maria-Jesus, Adele Hartnell, Patricia Chisholm, Cindy Williams, Dawn Davies, Vivian B. Weg, Marc Feldmann, Mark A. Bolanowski, Roy R. Lobb, and Sussan Nourshargh. "Tumor Necrosis Factor α-Induced Eosinophil Accumulation in Rat Skin Is Dependent on α4 Integrin/Vascular Cell Adhesion Molecule-1 Adhesion Pathways." Blood 90, no. 10 (November 15, 1997): 4144–52. http://dx.doi.org/10.1182/blood.v90.10.4144.

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Abstract Tumor necrosis factor α (TNFα) is a cytokine implicated in the pathogenesis of numerous chronic and acute inflammatory conditions. In the present study, we have characterized the ability of TNFα in inducing eosinophil accumulation in rat skin and have shown the inhibitory effects of anti-α4 integrin and anti–vascular cell adhesion molecule-1 (VCAM-1) antibodies on this response. The intradermal injection of recombinant human TNFα induced a slowly developing, dose-dependent accumulation of 111In-eosinophils in rat skin that was maximal at the dose of 10−11 mol/site. Coadministration of TNFα with the soluble TNFα receptor (p55)-IgG fusion protein (TNFR-IgG) totally inhibited the 111In-eosinophil accumulation induced by the cytokine. The TNFα-induced 111In-eosinophil accumulation was not affected after pretreatment of rats with the platelet-activating factor (PAF) receptor antagonist UK-74,505 or the antihuman interleukin-8 monoclonal antibody (MoAb) DM/C7. In contrast, the intravenous administration of an anti-α4 integrin MoAb, HP2/1 (3.5 mg/kg), or an anti–VCAM-1 MoAb, 5F10 (2 mg/kg), greatly inhibited the 111In-eosinophil accumulation induced by TNFα (the responses detected at 10−11 mol/site were inhibited by 78% and 50%, respectively). These results show that TNFα is an effective inducer of eosinophil accumulation in vivo, with this response being dependent on an interaction between α4 integrins and VCAM-1.
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Dissertations / Theses on the topic "TNFα"

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Oates, Anna. "Mapping of functional TNFα-ligand interactions." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615706.

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Orsini, Marion. "Inhibition de l’érythropoïèse par la voie TNFα/sphingomyélinase/céramide : rôle du réseau de régulation microARN/facteurs de transcription et impact sur l’autophagie." Thesis, Université de Lorraine, 2017. http://www.theses.fr/2017LORR0225/document.

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L’anémie est un symptôme fréquent chez les patients atteints de cancer. La libération de la cytokine pro-inflammatoire TNFα, un inhibiteur connu de l’érythropoïèse, en est l’une des causes. L’érythropoïèse est un processus nécessitant l’arrêt de la prolifération et l’autophagie. Les résultats précédents ont montré que le TNFα inhibe l’expression des marqueurs érythroïdes et module l’expression de facteurs de transcription (FT) hématopoïétiques. Notre objectif est d’étudier l’implication de la voie TNFα/sphingomyélinase (SMase)/céramide dans l’inhibition de l’érythropoïèse en utilisant des cellules souches hématopoïétiques CD34+ induites à se différencier par l’érythropoïétine recombinante (Epo). Par l’utilisation de céramides exogènes, de SMase bactérienne et d’inhibiteurs de SMases, nous montrons l’implication de la voie SMase/céramide dans l’inhibition de l’expression des marqueurs érythroïdes mais également dans l’induction de la différenciation myéloïde avec une augmentation de l’expression du CD11b. Cet effet sur la différenciation est corrélé à la modulation du réseau FT/miR impliquant GATA-1, GATA-2 et PU.1 et les miR-144, 451, 155, 146a et 223. De plus, l’analyse par microscopie électronique à transmission, l’absence de formation de punctae GFP-LC3 et l’accumulation de SQSTM1/p62 montrent que le TNFα et les céramides inhibent l’autophagie induite par l’Epo. L’analyse des protéines impliquées dans la régulation de l’autophagie montre que le TNFα et les céramides activent mTOR. Son implication est confirmée par l’utilisation de rapamycine et l’inhibition de ULK1 et Atg13. De plus, le TNFα et les céramides inhibent l’expression de bécline 1 et de la formation du complexe Atg5-Atg12. Ces résultats démontrent que la voie TNFα/SMase/céramide joue un rôle dans l’homéostasie hématopoïétique par l’inhibition de l’érythropoïèse au profit de la myélopoïèse, en impactant les réseaux de régulation FT/miR et le processus d’autophagie
Anemia is a common symptom in cancer patients. It can be caused by the release of pro-inflammatory cytokines such as TNFα, a known inhibitor of erythropoiesis. Erythropoiesis involves proliferation arrest and autophagy. Our previous studies showed that TNFα inhibits the expression of erythroid markers as well as hematopoietic transcription factors (TF) expression. The aim is to study the involvement of TNFα/sphingomyelinase (SMase)/ceramide pathway in erythropoiesis inhibition using recombinant erythropoietin (Epo)-induced CD34+ hematopoietic stem cells. Using exogenous ceramides, a bacterial SMase and sphingomyelinase inhibitors, we show the involvement of SMase/ceramide pathway in the inhibition of erythroid markers as well as the induction of myeloid differentiation as shown by the increase in CD11b expression. This effect is correlated to the modulation of the TF/miR network involving GATA-1, GATA-2 and PU.1 as well as miR-144, 451, 155, 146a and 223. We show that TNFα and ceramides inhibit Epo-induced autophagy through transmission electron microscopy analysis, the absence of GFP-LC3 punctae formation and SQSTM1/p62 accumulation. Analysis of proteins involved in autophagy regulation showed that TNFα and ceramides activate mTOR, which is confirmed using rapamycin as well as the inhibition of ULK1 and Atg13. Moreover, TNFα and ceramides inhibit Beclin 1 expression and Atg5-Atg12 complex formation. These results demonstrate the role of TNFα/SMase/ceramide pathway in hematopoietic homeostasis through an erythropoiesis-myelopoiesis switch resulting from perturbation of TF/miR network and autophagy
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Mouhsine, Hadley. "Développement de nouveaux inhibiteurs du TNFα identifiés par Drug Design." Thesis, Paris, CNAM, 2012. http://www.theses.fr/2012CNAM0842/document.

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Les anticorps monoclonaux ont constitué une révolution dans le traitement desmaladies inflammatoires chroniques, mais ils présentent des inconvénients majeurs (effetssecondaires, coûts élevés, résistances).Notre équipe développe des inhibiteurs du TNFα par deux approches : immunisationactive contre des peptides de cytokine pour générer des anticorps neutralisants et petitesmolécules chimiques pouvant inhiber directement le TNFα.J’ai évalué in vitro les meilleurs composés d’un criblage de chimiothèque in silico, etnotamment identifié une petite molécule qui a protégé les animaux dans deux modèles demaladies in vivo (choc septique et colite au DSS). J’ai aussi réalisé l’analyse d’analogueschimiques des meilleurs composés identifiés in vitro.J’ai également évalué l’immunogénicité de plusieurs peptides de TNFα mais lesanticorps générés n’étaient pas neutralisants in vitro et nous n’avons donc pas testé lespeptides in vivo.Mon travail s’est situé à l’interface de la bioinformatique, de la chimie, et de labiologie et m’a permis de bien comprendre les enjeux du développement moderne dumédicament
Monoclonal antibodies have been a revolution for the treatment of chronicinflammatory diseases but present several drawbacks (secondary effects, prohibitive costs,resistance)Our team develops TNFα inhibitors using two approaches : active immunizationagainst cytokine peptides and small compounds having a direct inhibition on TNFα.I have evaluated in vitro the best compounds selected after in silico screening of achemical library and I have identified a small molecule which was protective in two animalmodels (septic shock and DSS induced colitis). I have also analyzed chemical analogues ofthe best compounds found in vitro.I have also tested the immunogenicity of TNFα peptides but they did not yieldneutralizing antibodies in vitro, and we thus did not test them in vivo.My work was at the interface of bioinformatics, chemistry and biology, and this hasenabled me to understand the key issues in the modern development of drugs
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Fouche, Celeste. "Differential effects of TNfα on satellite cell differentiation." Thesis, Stellenbosch : Stellenbosch University, 2007. http://hdl.handle.net/10019.1/19596.

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Thesis (MSc)--University of Stellenbosch, 2007.
ENGLISH ABSTRACT: Tumour necrosis factor alpha (TNFα) is a pleiotropic cytokine and has a wide variety of dose dependent cellular effects ranging from cell growth and differentiation, to inducing apoptosis. It has long been implicated in muscle and non-muscle inflammatory disorders, such as muscle wasting in chronic disease states, and rheumatoid arthritis. However, a physiological role for TNFα in muscle regeneration has been proposed as elevated levels of the cytokine are present when muscle regeneration processes are initiated: TNFα is secreted by infiltrating inflammatory cells, and by injured muscle fibres. Adult skeletal muscle contains a population of resident stem cell-like cells called satellite cells, which become activated, proliferate and differentiate following muscle injury to bring about repair of damaged muscle. Much research on the effects of TNFα on satellite cell differentiation has been conducted in recent years. It is however difficult to get a complete characterisation of the cytokine’s action as all models used slightly differ. We aimed therefore at providing comprehensive assessment of the effects of increasing doses of chronically supplemented TNFα on differentiating C2C12 cells. Cells were allowed to differentiate with or without TNFα supplementation for 7 days. Differentiation was induced at day 0. The effect on differentiation was assessed at days 1, 3, 5, and 7 by western blot analysis, and supplementary immunohistochemical analysis at days 1, 4, and 7 of markers of differentiation - muscle regulatory factors: MyoD and myogenin, markers of the cell cycle p21, PCNA, and the integral signalling molecule, p38MAPK. TNFα supplementation at day 1 tended to positively regulate early markers of differentiation. With continued supplementation however, markers of differentiation decreased dose dependently in treated cultures as the initial effect appeared to be reversed: A trend towards a dose dependent decrease in MyoD, myogenin and p21 protein existed in treated cultures at days 3, 5, and 7. These findings were significant at day 5 (p21, p<0.05), and day 7 (myogenin, p<0.05). A significant dose dependent decrease in p38 phosphorylation was evident at day 3 (p<0.05), while phospho-p38 was dose dependently increased at day 7 (p<0.05). Taken together, these data show that TNFα supplementation for 24 hours following the induction of differentiation in vitro, tends to increase levels of early markers of differentiation, and with continued TNFα supplementation decrease markers of differentiation in a dose dependent fashion. This study provides a comprehensive characterisation of the dose and time dependent effects of TNFα on satellite cell differentiaton in vitro. The model system used in the current study, allows us to make conclusions on more chronic disease states.
AFRIKAANSE OPSOMMING: Tumor nekrose faktor alfa (TNFα) is ‘n pleiotropiese sitokien wat ‘n wye verskeidenheid, dosis afhanklike, sellulêre effekte te weeg bring. Hierdie sellulêre effekte sluit sel groei en differensiasie tot sel dood in. TNFα is by beide spier en niespier inflammatoriese stoornisse soos spier tering in kroniese siektetoestande, en rumatiese artritis betrek. ‘n Fisiologiese rol vir TNFα is egter voorgestel aangesien verhoogde vlakke van die sitokien tydens inisiasie van spier herstel meganismes teenwoordig is: TNFα word deur infiltrerende inflammatoriese selle, asook deur beseerde spier vesels afgeskei. Volwasse skeletspier bevat ‘n populasie stamselagtige selle, sogenoemde satelliet selle. Laasgenoemde word geaktiveer, prolifereer en differensieër volgende spierbesering, om sodoende herstel van beskadigde spier te weeg te bring. Baie navorsing op die effekte van TNFα op satelliet sel differensiasie is onlangs uitgevoer. Dit is egter aansienlik moeilik om volgens hierdie navorsing‘n algehele beeld van TNFα se aksies te vorm aangesien alle modelle wat gebruik word verskil. Ons doel was daarom om ‘n omvangryke assessering van toenemende konsentrasies kronies gesupplementeerde TNFα op differensieërende C2C12 selle op ‘n enkele model uit te voer. Selle was vir 7 dae met of sonder TNFα supplementasie gedifferentieër. Differensiasie was by Dag 0 geïnduseer. TNFα se effek op differensiasie is op dae 1, 3, 5, en 7 deur middel van western blot analise geassesseer. Aanvullende immunohistochemiese bepalings op dae 1, 4, en 7 is verder deurgevoer. Merkers vir differensiasie het die spier regulatoriese faktore MyoD en miogenien, sel siklus merkers p21 en PCNA, asook die integrale sein transduksie molekule p38MAPK ingesluit. TNFα supplementasie by dag 1 het geneig om vroeë merkers van differensiasie positief te reguleer. Met voortdurende supplementasie is die vroeë positiewe effekte (op ‘n dosis afhanklike manier) egter omgekeer: ‘n neiging teenoor (‘n dosis afhanklike) vermindering in MyoD, miogenien en p21 proteïen het in behandelde kulture op dae 3, 5, en 7 bestaan. Hierdie bevindinge was beduidend by dag 5 (p21, p<0.05), en dag 7 (miogenien, p<0.05). A beduidende dosis afhanklike afname in p38 fosforilasie was duidelik by dag 3 (p<0.05), terwyl fosfo-p38 by dag 7 verhoog het met verhoogde konsentrasie TNFα (p<0.05). Bogenoemde saamgevat, dui aan dat TNFα supplementasie 24h volgende die induksie van differensiasie in vitro, verhoogde vlakke van vroeë differnsiasie merkers te weeg bring. Met voortdurende TNFα supplementasie, word differensiasie merkers egter met toenemende dosis verminder. Hierdie studie voorsien ‘n omvattende karakterisering van die dosis- en tyd afhanklike effekte van TNFα op satelliet sel differesiasie in vitro. Die model sisteem in hierdie studie gebruik, maak afleidings oor meer kroniese siektetoestande moontlik.
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Zeiller, Caroline. "Phospholipase D, perméabilité endothéliale, et apoptose TNFα dépendante." Lyon, INSA, 2007. http://theses.insa-lyon.fr/publication/2007ISAL0087/these.pdf.

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La phospholipase D (PLD) est une enzyme membranaire qui intervient au cœur du métabolisme lipidique en générant un second messager, l’acide phosphatidique (PA) impliqué dans de nombreuses fonctions cellulaires. Deux isoformes PLD1 et PLD2 contribuent à sa synthèse chez les mammifères. Nous avons montré que la PLD augmente la perméabilité de monocouches de cellules endothéliales (lignée HUV-EC-C) aux macromolécules en permettant un remodelage du cytosquelette d’actine. L’isoforme PLD2 jouerait un rôle prépondérant via sa localisation au sein des cavéoles membranaires. Nous avons étudié le rôle de la PLD dans l’apoptose des cellules ECV304 induite par le TNFα, une cytokine activant à la fois des voies de survie et des voies pro-apoptotiques. Nous avons aussi étudié le rôle de la PLD dans l’apoptose des cellules ECV304 induite par le TNFα une cytokine activant à la fois des voies de survie et des voies pro-apoptotiques. Nous avons montré que la PLD a un rôle protecteur contre la mort cellulaire induite par TNFα en présence de cycloheximide, l’isoforme PLD1 étant plus spécifiquement mise en jeu. Divers mécanismes expliquant cet effet protecteur sont proposés
PLD is a membrane-bound enzyme which plays a key role in lipid metabolism by generating phosphatidic acid, an anionic phospholipid involved in many cellular functions. Two isoforms PLD 1 and PLD2 exist in mammals. We have shown that PLD enhances the permeability of endothelial cell monolayers (HUV-EC-C cells) through an actin reorganization which is characterized by synthesis of stress fibers. PLD2 might be more particularly implicated, because of its sub cellular localization to membrane caveolae. We also studied the role of PLD in Tumor Necrosis Factor alpha (TNFα)-induced apoptosis of ECV304 cells. TNFα, a pleiotropic cytokine, activates both apoptotic and pro-survival signals depending on the cell model. We showed that PLD exerts a protective effect against cell death induced by TNFα in the presence of an inhibitor of protein synthesis, cycloheximide. PLD 1 isoform plays a predominant role in this process. Different mechanisms explaining the protective role of PLD are proposed
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Fischer, Johannes. "Tierexperimentelle Untersuchungen zu Stress, Zytokinen und depressionsähnlichem Verhalten." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-169143.

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Die vorliegende publikationsbasierte Dissertationsschrift erörtert auf der Basis experimenteller Untersuchungen im Tiermodell die Auswirkungen von Stress auf die Zytokinproduktion und depressionsähnliches Verhalten. Außerdem wird getestet, ob die Blockade des Zytokins Tumornekrosefaktor-α (TNF‑α) eine Möglichkeit zur antidepressiven Intervention darstellt. Einleitend werden die Zusammenhänge von Stress, Zytokinen und Depression referiert sowie das hypothetische Modell erläutert, das den publizierten Untersuchungen zugrunde liegt. Es wird hypothetisiert, dass Stress zur Erhöhung der Produktion proinflammatorischer Zytokine führt und dass die vermehrte Zytokinproduktion depressive Verhaltensweisen hervorruft. Aus dieser Annahme leitet sich die Möglichkeit ab, durch Blockade der Wirkung des proinflammatorischen Zytokins TNF‑α antidepressive Effekte zu erzielen. In den beiden Arbeiten „The impact of social isolation on immunological parameters in rats“ (Archives of Toxicology) und „Stress-induced cytokine changes in rats“ (European Cytokine Network) wurde der Einfluss von sozialer Isolation, chronischem, milden und akutem Stress auf die Zytokinproduktion untersucht. In diesen Untersuchungen führten die verschiedenen Stressarten zu einer Modulation der Produktion proinflammatorischer Zytokine. Die dritte Publikation „Antidepressant effects of TNF‑α blockade in an animal model of depression“ (Journal of Psychiatric Research) berichtet von einem Experiment, in dem untersucht wurde, ob der TNF‑α-Inhibitor Etanercept antidepressive Effekte aufweist. Tatsächlich zeigte sich unter Etanercept ein Rückgang des depressionsähnlichen Verhaltens im forced swim test (FST) analog zu Verhaltensänderungen durch das in Tierversuchen als Standard-Antidepressivum geltende Imipramin. Die Autoren schlussfolgern, dass das Zytokinsystem durch Stress moduliert wird und so in die pathophysiologische Entwicklung einer Depression involviert sein könnte. Zytokininhibitoren könnten eine neue Klasse der Antidepressiva bei Therapieresistenz werden, wenn sich die Ergebnisse dieser Tierversuche in Studien an Probanden und an Patienten replizieren lassen.
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Faletti, Laura [Verfasser], and Christoph [Akademischer Betreuer] Borner. "Molecular mechanisms of TNFα sensitization to fasL-induced apoptosis." Freiburg : Universität, 2017. http://d-nb.info/1183569556/34.

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Marshall, Aiden Christopher James 1976. "The role of Fas and TNFα in experimental autoimmune gastritis." Monash University, Dept. of Pathology and Immunology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9413.

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Somers, Sarin J. "Role of nuclear factors kappa-B in TNFα-induced cytoprotection." Master's thesis, University of Cape Town, 2006. http://hdl.handle.net/11427/3466.

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SAITO, Kiyoshi, Jun YOSHIDA, Hisao SEO, Kenichi WAKABAYASHI, Fukushi KAMBE, Takashi NAGAYA, and Mihoko KATO. "Effect of PPARα Ligand on TNFα -Dependent Expression of EGF Receptor in Human Glioma Cell Line." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2776.

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Books on the topic "TNFα"

1

Sanjay, Khare, ed. TNF superfamily. Austin, Tex: Landes Bioscience, 2007.

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Sanjay, Khare, ed. TNF superfamily. Austin, Tex: Landes Bioscience, 2007.

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Weinberg, Jeffrey M., and Robin Buchholz, eds. TNF-alpha Inhibitors. Basel: Birkhäuser-Verlag, 2006. http://dx.doi.org/10.1007/3-7643-7438-1.

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Bayry, Jagadeesh, ed. The TNF Superfamily. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0669-7.

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Bayry, Jagadeesh, ed. The TNF Superfamily. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1130-2.

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Afya, Tanzania Wizara ya. TNF: Tanzania National Formulary. 2nd ed. [Dar es Salaam]: Ministry of Health, 2005.

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1946-, Wallach David, Kovalenko Andrew, and Feldmann Marc, eds. Advances in TNF family research: Proceedings of the 12th International TNF Conference, 2009. New York [N.Y.]: Springer, 2011.

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Wu, Hao, ed. TNF Receptor Associated Factors (TRAFs). New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-70630-6.

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Wallach, David, Andrew Kovalenko, and Marc Feldmann, eds. Advances in TNF Family Research. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6612-4.

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D, Wu Hao Ph, ed. TNF receptor associated factors (TRAFs). New York: Springer Science+Business Media, 2007.

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Book chapters on the topic "TNFα"

1

Ignatowski, Tracey A., Bernice K. Noble, John R. Wright, Janet L. Gorfien, and Robert N. Spengler. "TNFα." In Advances in Experimental Medicine and Biology, 219–24. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0407-4_28.

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Moss, Marcia, J. David Becherer, Marcos Milla, Gregory Pahel, Mill Lambert, Rob Andrews, Stephen Frye, et al. "TNFα converting enzyme." In Metalloproteinases as Targets for Anti-Inflammatory Drugs, 187–203. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8666-6_9.

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Girardin, E. "TNFα and Soluble TNF Receptors in Meningococcemia." In Update in Intensive Care and Emergency Medicine, 68–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84827-8_5.

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Toro, C. Marani, M. Mabilia, F. Mancini, M. Giannangeli, and C. Milanese. "Modeling of Suramin-TNFα Interactions." In Molecular Modeling and Prediction of Bioactivity, 359–60. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4141-7_76.

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Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "TNFα (Tumor Necrosis Factor α)." In Encyclopedia of Signaling Molecules, 1884. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101378.

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Najafi, Sheyda, Ehab M. Abo-Ali, and Vikas V. Dukhande. "Methods for Studying TNFα-Induced Autophagy." In Methods in Molecular Biology, 131–46. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0247-8_12.

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Van der Auwera, P. "Interactions between TNFα and Human Polymorphonuclear Leukocytes." In Yearbook of Intensive Care and Emergency Medicine, 49–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84734-9_6.

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Lin, Anning. "Temporal Control of TNFα Signaling by Miz1." In Advances in Experimental Medicine and Biology, 127–28. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6612-4_13.

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Lin, Tong-Jun, Antonio Enciso, Elyse Y. Bissonnette, Agnes Szczepek, and A. Dean Befus. "Cytokine and Drug Modulation of TNFα in Mast Cells." In Advances in Experimental Medicine and Biology, 279–85. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5855-2_40.

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Scherbel, U., R. Raghupat, M. Nakamura, M. McNamara, T. McIntosh, and E. Neugebauer. "Nachweis der Bedeutung von TNFα nach Schädel/Hirntrauma (Polytrauma) auf das neurologische Outcome durch Verwendung einer transgenen TNFα knock out Maus." In Hefte zur Zeitschrift „Der Unfallchirurg“, 815–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60913-8_295.

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Conference papers on the topic "TNFα"

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Wood, AM, SC Gough, and RA Stockley. "Sputum TNFα Levels Are Associated withTNFAGenotype." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2942.

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Reynaert, Niki, Irene Eurlings, Evi Mercken, Rafael De Cabo, Scott Aesif, Jos Van der Velden, Yvonne Janssen-Heininger, Emiel Wouters, and Mieke Dentener. "Involvement of JNK in TNFα driven remodelling." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa5058.

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Bevill, Scott L., and Thomas P. Andriacchi. "Dynamic Compression in the Presence of TNF-Alpha Differentially Effects Gene Expression in Tibial Plateau Cartilage Covered and Uncovered by the Meniscus." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192575.

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It has been suggested that altered joint loading may be a cause of the cartilage degeneration commonly observed following joint destabilizing events such as anterior cruciate ligament (ACL) injury [1]. Changes in the biochemical environment of the joint accompany these changes in joint loading, though, with acute and chronic increases in synovial concentrations of proinflammatory cytokines such as tumor necrosis factor-alpha (TNFα) [2, 3]. TNFα is a potent catabolic factor associated with increased expression [4] and synthesis [5] of matrix proteases in articular cartilage, and therefore may play in important role in the degenerative events following joint injury.
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Rowlands, DJ, J. Lindert, and J. Bhattacharya. "Mitochondria Determine TNFα Receptor Shedding in Lung Microvessels." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2348.

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Mercogliano, María F., Mara De Martino, Sofia Bruni, Leandro Venturutti, Martín Rivas, Matías Amasino, Cecilia J. Proietti, Patricia V. Elizalde, and Roxana Schillaci. "Abstract 1195: TNFα induces multiresistance to HER2-targeted TNFα induces multiresistance to HER2-targeted therapies in HER2-positive breast cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1195.

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Kindermann, Sophie, Anda Nodieva, Ingrida Sture, Anita Skangale, Anita Jagmane, Nailja Lukmanova, Gunta Kirvelaite, et al. "Tuberculosis in patients on TNFα inhibitor treatment in Latvia." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2684.

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Vestbo, J., E. Wouters, S. Rennard, B. Miller, L. Edwards, and R. Tal-Singer. "TNFα and Systemic Manifestations in COPD Patients and Controls." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3781.

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Marin Mathieu, N., X. Chen, P. Delmotte, and G. C. Sieck. "TNFα Increases Mitochondrial Biogenesis in Human Airway Smooth Muscle." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2172.

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Ramirez Ramirez, O. A., S. Mahadev Bhat, P. Delmotte, and G. C. Sieck. "TNFα Mediates Mitophagy in Human Airway Smooth Muscle Cells." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2331.

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Robinson, L., J. Plumb, A. Bizzi, F. Facchinetti, R. Patacchini, and D. Singh. "17-BMP Potently Suppresses TNFα Production from COPD Alveolar Macrophages." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4566.

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Reports on the topic "TNFα"

1

Grueso-Navarro, Elena, Leticia Rodríguez-Alcolado, Ángel Arias, Emilio J. Laserna-Mendieta, and Alfredo J. Lucendo. Influence of HLA-DQA1*05 allele in the response to anti-TNFα drugs in inflammatory bowel diseases. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0076.

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Review question / Objective: Do patients with inflammatory bowel disease and treated with any anti-TNFα drug who had the HLA-DQA1*05 allele (in heterozygosis or homozygosis) have lower response or persistence to those drugs than patients without HLA-DQA1*05 allele? Condition being studied: Inflammatory bowel diseases (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition that may affect any part of the digestive tract (CD) or be limited to the colon (UC). While the specific aetiology of IBD remains unknown, it is believed to involve a complex impairment in the immunity of the gut mucosa due to a combination of several genetic and environmental factors, being the microbiota one of the latest that more attraction has received in recent years. Symptoms of IBD (such as abdominal pain, diarrhoea, fever, tiredness or rectal bleeding) may be either constant or alternate between periods of limited disease activity and flares with remarkable presence of symptoms. As IBD is associated with significant morbidity and disability, pharmacological treatment is required in most cases, especially in CD, aimed at reducing the inflammatory response and attenuating the activity of the immune system. In the moderate and severe forms of the disease, therapy is usually based on immunosuppressant and/or biological drugs. Among the latest, anti-TNFα drugs (infliximab or adalimumab) are normally chosen as the initial biological therapy.
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Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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Li, Peng, and Junjun Liu. Effect of tumor necrosis factor inhibitors on the risk of adverse cardiovascular events in patients with psoriasis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0090.

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Review question / Objective: Previous studies have indicated a cardioprotective effect of tumor necrosis factor inhibitor (TNFi) therapy in adult patients with psoriasis (Pso). However, most were retrospective studies, and the association between cardiometabolic comorbidities and major adverse cardiovascular events (MACE) has not been validated in randomized controlled trials (RCTs). Condition being studied: Because the available evidence has recently increased, we performed the present updated meta-analysis and meta-regression of cohort studies and RCTs to evaluate whether TNFi therapy can decrease the risk of MACE among patients with Pso and to assess the associations between cardiometabolic comorbidities and MACE.
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Anders, Greg T. Induction of TNF-A and IL-1 in Human Tuberculosis (CIC3). Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada259308.

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Wang, Jun, Congcong Wang, Hongjuan Fu, Zezhong Liu, Yimin Zhang, and Tong Zhang. TNF alpha antagonists improve oxidative stress and atherosclerosis induced by rheumatoid arthritis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0033.

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Yang, Dajun. Testing Clinical Relevance and Therapeutic Potential of a Novel Secreted Ligand of TNF Family. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada424660.

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Lewis, James, Meenakshi Bewtra, Frank Scott, Colleen Brensinger, Shelby Reed, Jason Roy, Mark Osterman, et al. Patient Valued Comparative Effectiveness of Corticosteroids versus Anti-TNF Alpha Therapy for Inflammatory Bowel Disease. Patient-Centered Outcomes Research Institute (PCORI), November 2018. http://dx.doi.org/10.25302/11.2018.ce.12114143.

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Yu, Ling, Qiaojia Huang, and Bing Su. The Role of MEKK3 Signaling Pathway in the Resistance of Breast Cancer Cells to TNF-(alpha)-Mediated Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada443658.

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Yu, Ling, Qjaojia Huang, and Bing Su. The Role of MEKK3 Signaling Pathway in the Resistance of Breast Cancer Cells to TNF-Alpha-Mediated Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, May 2006. http://dx.doi.org/10.21236/ada456016.

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Varela, Linda M., and Margot M. Ip. The Role and Regulation of TNF-Alpha in Normal Rat Mammary Gland during Development and in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1997. http://dx.doi.org/10.21236/ada330243.

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