Littérature scientifique sur le sujet « Trasforming Growth Factor Beta TNF-α »

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Articles de revues sur le sujet "Trasforming Growth Factor Beta TNF-α"

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Porowski, Dawid, Agnieszka Wirkowska, Ewa Hryniewiecka, Janusz Wyzgał, Marek Pacholczyk, and Leszek Pączek. "Liver Failure Impairs the Intrahepatic Elimination of Interleukin-6, Tumor Necrosis Factor-Alpha, Hepatocyte Growth Factor, and Transforming Growth Factor-Beta." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/934065.

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The strategic location of the liver and its metabolic activity make it a key organ regulating homeostasis. Our purpose was to examine its participation in removal of cytokines: interleukin-6 (Il-6), tumor necrosis factor-alpha (TNF-α), hepatocyte growth factor (HGF), and transforming growth factor-beta (TGF-β) from the portal circulation in human. 20 liver donors and 20 patients with end-stage liver failure were included in the study. Their blood was collected during liver transplantation from the portal, hepatic, and peripheral vein, and the hepatic artery and cytokines’ concentrations were d
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Pfeilschifter, J., W. Pignat, J. Leighton, F. Märki, K. Vosbeck та S. Alkan. "Transforming growth factor β2 differentially modulates interleukin-1 β- and tumour-necrosis-factor-α-stimulated phospholipase A2 and prostaglandin E2 synthesis in rat renal mesangial cells". Biochemical Journal 270, № 1 (1990): 269–71. http://dx.doi.org/10.1042/bj2700269.

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Treatment of rat glomerular mesangial cells with transforming growth factor beta 2 (TGF beta 2) stimulates prostaglandin E2 (PGE2) synthesis. Actinomycin D, cycloheximide and diclofenac attenuate the TGF beta 2-induced PGE2 formation. As shown previously, two proinflammatory cytokines, interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF alpha), are potent stimuli for PGE2 and phospholipase A2 secretion from mesangial cells. We report here that, whereas TGF beta 2 potentiates the IL-1 β- and TNF alpha-evoked PGE2 production, it strongly inhibits the phospholipase A2 secretion i
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Faber, Milosz, Michael Bette, Mirjam A. R. Preuss, et al. "Overexpression of Tumor Necrosis Factor Alpha by a Recombinant Rabies Virus Attenuates Replication in Neurons and Prevents Lethal Infection in Mice." Journal of Virology 79, no. 24 (2005): 15405–16. http://dx.doi.org/10.1128/jvi.79.24.15405-15416.2005.

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ABSTRACT The effect of tumor necrosis factor alpha (TNF-α) on rabies virus (RV) infection of the mouse central nervous system (CNS) was studied, using recombinant RV engineered to express either soluble TNF-α [SPBN-TNF-α(+)] or insoluble membrane-bound TNF-α [SPBN-TNF-α(MEM)]. Growth curves derived from infections of mouse neuroblastoma NA cells revealed significantly less spread and production of SPBN-TNF-α(+) than of SPBN-TNF-α(MEM) or SPBN-TNF-α(−), which carries an inactivated TNF-α gene. The expression of soluble or membrane-bound TNF-α was not associated with increased cell death or indu
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Bachmann, Anastasia, Brigitte Hanke, Rainer Zawatzky, et al. "Disturbance of Tumor Necrosis Factor Alpha-Mediated Beta Interferon Signaling in Cervical Carcinoma Cells." Journal of Virology 76, no. 1 (2002): 280–91. http://dx.doi.org/10.1128/jvi.76.1.280-291.2002.

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ABSTRACT In the present study we show that malignant human papillomavirus (HPV)-positive cells lost their ability to synthesize endogenous beta interferon (IFN-β) upon tumor necrosis factor alpha (TNF-α) treatment. IFN-β transcription, however, was reinducible in nonmalignant HPV-positive cells, which was confirmed in functional protection assays against encephalomyocarditis virus or vesicular stomatitis virus infections. Addition of neutralizing antibodies against IFN-β blocked the antiviral effect, excluding the possibility that other IFN types were involved. Conversely, both malignant and i
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Fan, Huizhen, Chunyan Jiang, Baoyuan Zhong та ін. "Matrine Ameliorates Colorectal Cancer in Rats via Inhibition of HMGB1 Signaling and Downregulation of IL-6, TNF-α, and HMGB1". Journal of Immunology Research 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/5408324.

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Matrine may be protective against colorectal cancer (CRC), but how it may work is unclear. Thus, we explored the underlying mechanisms of matrine in CRC. Matrine-related proteins and CRC-related genes and therapeutic targets of matrine in CRC were predicted using a network pharmacology approach. Five targets, including interleukin 6 (IL-6), the 26S proteasome, tumor necrosis factor alpha (TNF-α), transforming growth factor beta 1 (TGF-β1) and p53, and corresponding high-mobility group box 1 (HMGB1) signaling and T helper cell differentiation were thought to be associated with matrine’s mechani
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Myskiw, Chad, Janilyn Arsenio, Rebekah van Bruggen, Yvon Deschambault та Jingxin Cao. "Vaccinia Virus E3 Suppresses Expression of Diverse Cytokines through Inhibition of the PKR, NF-κB, and IRF3 Pathways". Journal of Virology 83, № 13 (2009): 6757–68. http://dx.doi.org/10.1128/jvi.02570-08.

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ABSTRACT The vaccinia virus double-stranded RNA binding protein E3 has been demonstrated to inhibit the expression of cytokines, including beta interferon (IFN-β) and tumor necrosis factor alpha (TNF-α). However, few details regarding the molecular mechanisms of this inhibition have been described. Using real-time PCR arrays, we found that E3 suppressed the induction of a diverse array of cytokines representing members of the IFN, interleukin (IL), TNF, and transforming growth factor cytokine families. We discovered that the factor(s) responsible for the induction of IL-6, TNF-α, and inhibin b
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Fritzgerald, Richard, Cecilia Lunardhi, Ruslan Effendy та Tamara Yuanita. "EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR". Conservative Dentistry Journal 7, № 2 (2019): 66. http://dx.doi.org/10.20473/cdj.v7i2.2017.66-73.

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Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main medi
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Peresi, Eliana, Sônia Maria Usó Ruiz Silva, Sueli Aparecida Calvi, and Jussara Marcondes-Machado. "Citocinas e proteínas de fase aguda do soro como marcadores de regressão da resposta inflamatória ao tratamento da tuberculose pulmonar." Jornal Brasileiro de Pneumologia 34, no. 11 (2008): 942–49. http://dx.doi.org/10.1590/s1806-37132008001100009.

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OBJETIVO: Analisar o padrão de citocinas pró- e antiinflamatórias e da resposta de fase aguda (RFA) como marcadores de resposta ao tratamento da tuberculose pulmonar. MÉTODOS: Determinação dos níveis de interferon-gama (IFN-γ), tumor necrosis factor-alpha (TNF-α, fator de necrose tumoral-alfa), interleucina-10 (IL-10) e transforming growth factor-beta (TGF-β, fator transformador de crescimento-beta), pelo método ELISA, em sobrenadante de cultura de células mononucleares do sangue periférico e monócitos, assim como dos níveis de proteínas totais, albumina, globulinas, alfa-1-glicoproteína ácida
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Hsu, Li-Han, Thomas C. Soong, Nei-Min Chu, Chung-Yu Huang, Shu-Huei Kao, and Yung-Feng Lin. "The Inflammatory Cytokine Profile of Patients with Malignant Pleural Effusion Treated with Pleurodesis." Journal of Clinical Medicine 9, no. 12 (2020): 4010. http://dx.doi.org/10.3390/jcm9124010.

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Patients with malignant pleural effusion (MPE) who underwent successful pleurodesis survive longer than those for whom it fails. We hypothesize that the therapy-induced inflammatory responses inhibit the cancer progression, and thereby lead to a longer survival. Thirty-three consecutive patients with MPE that were eligible for bleomycin pleurodesis between September 2015 and December 2017 were recruited prospectively. Nineteen patients (57.6%) achieved fully or partially successful pleurodesis, while 14 patients either failed or survived less than 30 days after pleurodesis. Two patients withou
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Jelodar, Gholamali, Mansour Azimzadeh, Fatemeh Radmard та Narges Darvishhoo. "Alteration of intrapancreatic serotonin, homocysteine, TNF-α, and NGF levels as predisposing factors for diabetes following exposure to 900-MHz waves". Toxicology and Industrial Health 37, № 8 (2021): 496–503. http://dx.doi.org/10.1177/07482337211022634.

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Exposure to mobile phone radiation causes deleterious health effects on biological systems. The objects of this study were to investigate the effect of 900-MHz radiofrequency waves (RFW) emitted from base transceiver station antenna on intrapancreatic homocysteine (Hcy), tumor necrosis factor-α (TNF-α), and nerve growth factor (NGF) as predisposing factors involved in pancreatic beta cell damage. Thirty male rats (Sprague-Dawley, 200 ± 10 g) were randomly divided into the control (without any exposure) and exposed groups: short time (2 h/day), long time (4 h/day), and exposed to 900-MHz RFW fo
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Thèses sur le sujet "Trasforming Growth Factor Beta TNF-α"

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LOCATELLI, LUIGI. "Expression of aVB6 integrin by Pkhd1-defective cholangiocytes links enhanced ductal secretion of Macrophage chemokines to progressive portal fibrosis in Congenital Hepatic Fibrosis." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41733.

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BACKGROUND AND AIMS: Congenital Hepatic Fibrosis (CHF) is caused by mutations in PKHD1, a gene encoding for fibrocystin, a protein of unknown function, expressed in cholangiocyte cilia and centromers. In CHF, biliary dysgenesis is accompanied by severe progressive portal fibrosis and portal hypertension. The mechanisms responsible for portal fibrosis in CHF are unclear. The αvβ6 integrin mediates local activation of TGFβ1 and is expressed by reactive cholangiocytes during cholestasis. To understand the mechanisms of fibrosis in CHF we studied the expression of αvβ6 integrin and its regulation
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Kam, Siu-kei Christy, та 甘笑琪. "The role of TGF-{221} signaling in the initiation of TNF-α expression in human PBMC derived macrophages". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38746049.

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Freese, Christiane [Verfasser]. "Rolle der Plasmakonzentrationen von transforming growth factor-β1 [factor-beta1] (TGFβ1) [TGF beta 1], {Tumor necrosis factor α [Tumor necrosis factor alpha] {(TNF α) [TNF alpha] und Plasminogen-Activator-Inhibitor-(PAI-)-Antigen bei Patienten mit Diabetes Mellitus Typ 2 und koronarer Herzkrankheit / vorglegt von Christiane Freese". 2002. http://d-nb.info/97149200X/34.

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Suntharalingam, Gaayathiri. "Der Einfluss der Induktion von Tumornekrosefaktor α und Transforming-Growth-Factor β auf die epithelial-mesenchymale Transition oraler Plattenepithelkarzinome im CAM-Assay". Doctoral thesis, 2021. http://hdl.handle.net/21.11130/00-1735-0000-0005-1567-0.

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Chapitres de livres sur le sujet "Trasforming Growth Factor Beta TNF-α"

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El-Youssef, M., A. Hughes, K. J. Bloch, S. R. Martin, and P. R. Harmatz. "Identification of tumor necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β) in murine milk." In Advances in Mucosal Immunology. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_162.

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Lambert, Charles. "Attenuating Cancer Cachexia-Prolonging Life." In Frailty and Sarcopenia - Recent Evidence and New Perspectives. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101250.

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Death by cancer cachexia is dependent on the time allotted to cancer to cause muscle and fat wasting. If clinicians, nurses, researchers can prolong the life of a cancer patient other therapeutic interventions such as radiation and chemotherapy may be given the time to work and rid the cancer patient of tumors and save lives. Three areas by which cancer induces cachexia is through impaired insulin-like growth factor signaling, elevations in the proinflammatory cytokines TNF-α and IL-6 and subsequent reductions in muscle protein synthesis and increases in muscle protein degradation. Therefore, it is important to augment the IGF-1 signaling, block TNF-α and IL-6 in cancer cachexia and in other ways augment muscle protein synthesis or decrease muscle protein degradation. Ghrelin like growth hormone secretagogues, monoclonal antibodies to TNF-α and IL-6, testosterone, and anabolic steroids, the beta 2 agonist albuterol, resistance exercise, and creatine monohydrate (with resistance exercise) are beneficial in increasing muscle protein synthesis and/or reducing muscle protein breakdown. With these muscle augmenting agents/interventions, the duration that a cancer patient lives is prolonged so that radiation and chemotherapy as well as emerging technologies can rid the cancer patient of cancer and save lives.
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