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‣ Tumor necrosis factor-alpha modulates survival, proliferation, and neuronal differentiation in neonatal subventricular zone cell cultures

Bernardino, Liliana; Agasse, Fabienne; Silva, Bruno; Ferreira, Raquel; Grade, Sofia; Malva, João O.
Fonte: AlphaMed Press Publicador: AlphaMed Press
Tipo: Artigo de Revista Científica
Português
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Tumor necrosis factor (TNF)- has been reported to modulate brain injury, but remarkably, little is known about its effects on neurogenesis. We report that TNF- strongly influences survival, proliferation, and neuronal differentiation in cultured subventricular zone (SVZ) neural stem/progenitor cells derived from the neonatal P1-3 C57BL/6 mice. By using single-cell calcium imaging, we developed a method, based on cellular response to KCl and/or histamine, that allows the functional evaluation of neuronal differentiation. Exposure of SVZ cultures to 1 and 10 ng/ml mouse or 1 ng/ml human recombinant TNF- resulted in increased differentiation of cells displaying a neuronal-like profile of [Ca2+]i responses, compared with the predominant profile of immature cells observed in control, nontreated cultures. Moreover, by using neutralizing antibodies for each TNF- receptor, we found that the proneurogenic effect of 1 ng/ml TNF- is mediated via tumor necrosis factor receptor 1 activation. Accordingly, the percentage of neuronal nuclear protein-positive neurons was increased following exposure to mouse TNF-. Interestingly, exposure of SVZ cultures to 1 ng/ml TNF- induced cell proliferation, whereas 10 and 100 ng/ml TNF- induced apoptotic cell death. Moreover...

‣ Tumor necrosis factor-alpha-308G/A single nucleotide polymorphism and red-complex periodontopathogens are independently associated with increased levels of tumor necrosis factor-alpha in diseased periodontal tissues

TROMBONE, A. P. F.; CARDOSO, C. R.; REPEKE, C. E.; FERREIRA JR., S. B.; MARTINS JR., W.; CAMPANELLI, A. P.; AVILA-CAMPOS, M. J.; TREVILATTO, P. C.; SILVA, J. S.; GARLET, G. P.
Fonte: WILEY-BLACKWELL PUBLISHING, INC Publicador: WILEY-BLACKWELL PUBLISHING, INC
Tipo: Artigo de Revista Científica
Português
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Background and Objective: Inflammatory cytokines such as tumor necrosis factor-alpha are involved in the pathogenesis of periodontal diseases. A high between-subject variation in the level of tumor necrosis factor-alpha mRNA has been verified, which may be a result of genetic polymorphisms and/or the presence of periodontopathogens such as Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola (called the red complex) and Aggregatibacter actinomycetemcomitans. In this study, we investigated the effect of the tumor necrosis factor-alpha (TNFA) -308G/A gene polymorphism and of periodontopathogens on the tumor necrosis factor-alpha levels in the periodontal tissues of nonsmoking patients with chronic periodontitis (n = 127) and in control subjects (n = 177). Material and Methods: The TNFA-308G/A single nucleotide polymorphism was investigated using polymerase chain reaction-restriction fragment length polymorphism analysis, whereas the tumor necrosis factor-alpha levels and the periodontopathogen load were determined using real-time polymerase chain reaction. Results: No statistically significant differences were found in the frequency of the TNFA-308 single nucleotide polymorphism in control and chronic periodontitis groups...

‣ Níveis de interleucina-6 e fator de necrose tumoral-alfa no liquor de recém-nascidos a termo com encefalopatia hipóxico-isquêmica; Levels of interleukin-6 and tumor necrosis factor-alpha in the cerebrospinal fluid of full-term newborns with hypoxic-ischemic encephalopathy

Silveira, Rita de Cássia dos Santos; Procianoy, Renato Soibelmann
Fonte: Universidade Federal do Rio Grande do Sul Publicador: Universidade Federal do Rio Grande do Sul
Tipo: Artigo de Revista Científica Formato: application/pdf
Português
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Objetivo: avaliar os níveis liquóricos de IL-6 e TNF-a em recém-nascidos a termo com encefalopatia hipóxico-isquêmica (EHI), comparando-os com os de recém-nascidos controles. Metodologia: estudo caso-controle realizado no período de julho de 1999 a outubro de 2001, incluindo dois grupos de recémnascidos a termo: controle, com 20 recém-nascidos sem sepse e/ou meningite e com escore de Apgar > 9 no primeiro e quinto minutos de vida; e casos, com 15 recém-nascidos asfixiados, caracterizados pelo escore de Apgar < 4 e < 6 no primeiro e quinto minutos de vida, respectivamente, pH umbilical < 7,20 e/ou lactato arterial umbilical > 3,0 mmol/l e necessidade de ventilação com pressão positiva pelo menos durante 2 minutos após o nascimento. Foram coletadas amostras de liquor nas primeiras 48 horas de vida, para determinação dos níveis de IL-6 e TNF-a pelo método de enzimoimunoensaio. Resultados: os grupos não diferiram quanto ao peso de nascimento, idade gestacional, classificação quanto ao peso e idade gestacional, tipo de parto e tempo médio de obtenção do liquor; seus exames foram obtidos em média com 17 horas de vida. Nos recémnascidos asfixiados, as medianas dos níveis liquóricos foram: 157,5 pg/ml para IL-6 e 14...

‣ Tumor necrosis factor-alpha in gestation and puerperium of women with gestational hypertension and pre-eclampsia

Peraçoli, José Carlos; Rudge, Marilza Vieira Cunha; Serrao Peracoli, Maria Terezinha
Fonte: Blackwell Publishing Publicador: Blackwell Publishing
Tipo: Artigo de Revista Científica Formato: 177-185
Português
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Problem High plasma levels of tumor necrosis factor-alpha (TNF-alpha) in pregnant women have been associated with the pathogenesis of pre-eclampsia (PE). This study evaluated TNF-alpha plasma levels and monocyte production in gestational hypertension (GH) and PE during gestation and at puerperium.Method of study This study included 128 women, of whom 20 were non-pregnant (NP) normotensive (NT), and 108 were pregnant: 36 NT, 27 with GH, and 45 with PE. Peripheral blood plasma was used for TNF-alpha and uric acid determination. TNF-alpha was determined in plasma and lipopolysaccharide (LPS)-stimulated and non-stimulated monocyte supernatants by L929 bioassay.Results Tumor necrosis factor-alpha and uric acid plasma levels were higher in PE than in GH pregnancies. In both hypertensive groups, these parameters positively correlated and were significantly more elevated than in NT and NP women. TNF-alpha plasma levels and monocyte production were higher in hypertensive than in NT women during gestation, and significantly decreased at puerperium. Although decreased, TNF-alpha release in LPS-stimulated PE monocytes, was still significantly higher than in the other pregnant groups.Conclusion In vivo monocyte activation in GH and PE pregnant women was characterized by in vitro TNF-alpha production. The fact that higher circulating concentrations of TNF-alpha and uric acid were observed in PE than in GH suggests an association with disease severity.

‣ Secretion of tumor necrosis factor-alpha by mouse peritoneal macrophages in the presence of dental sealers, sealapex and endomethasone

Perassi, Fábio Tobias; Bonetti Filho, Idomeo; Berbert, Fábio Luis Camargo Villela; Carlos, Iracilda Zeppone; Leonardo, Renato de Toledo
Fonte: Universidade Estadual Paulista Publicador: Universidade Estadual Paulista
Tipo: Artigo de Revista Científica Formato: 534-537
Português
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After filling root canals, the healing process depends on the chemical composition or physical-chemical properties of the material used, among other factors. All root canal sealers, whether solid or plastic, are foreign matter for the body if they remain in permanent contact with apical and periapical tissues. As a result, the first organic reaction that occurs is an attempt to phagocytize the material. During phagocytosis, macrophages release a large number of cell mediators into the area, among which are cytokines that are essential in intercellular communication and in many physiological and pathophysiological processes. One of these cytokines is tumor necrosis factor-alfa (TNF-α), which acts through links to specific receptors on the cell membrane initiating a cascade of events leading to induction, activation, or inhibition of numerous cytokine-regulated genes in the cell nucleus. The release of TNF-α in a cell culture of mouse peritoneal macrophages incubated with three concentrations (25, 50, and 100 mg/ml) of two endodontic sealers was measured. The solutions containing the calcium hydroxide-based root canal sealer (Sealapex) released fewer units of TNF-α than solutions containing the zinc oxide and eugenol-based sealer (Endomethasone).

‣ Non-tumor necrosis factor-based biologic therapies for rheumatoid arthritis: present, future, and insights into pathogenesis.

Paula, F; Alves, J
Fonte: Dove Medical Press Publicador: Dove Medical Press
Tipo: Artigo de Revista Científica
Publicado em //2014 Português
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Therapeutic options for patients suffering from the more severe forms of spondyloarthritis have been rather limited in the last decades. There is now accumulating evidence that antitumor necrosis factor therapy is highly effective in spondyloarthritis, especially in ankylosing spondylitis and psoriatic arthritis. Based on the data recently published on more than 500 patients with ankylosing spondylitis and psoriatic arthritis, this treatment seems to be even more effective than in rheumatoid arthritis. The antitumor necrosis factor-alpha agents currently available, infliximab (Remicade), etanercept (Enbrel), and adalimumab (Humira), are approved for the treatment of rheumatoid arthritis in the United States and partly in Europe. The situation in spondyloarthritis is different from that of rheumatoid arthritis because there is an unmet medical need, especially in ankylosing spondylitis: no therapies with disease-modifying antirheumatic drugs are available for severely affected patients, especially with spinal disease. Thus, tumor necrosis factor blockers may even be considered a first-line treatment in a patient with active ankylosing spondylitis and psoriatic arthritis whose condition is not sufficiently controlled with nonsteroidal antiinflammatory drugs in the case of axial disease...

‣ Role of nuclear factor kappa B and reactive oxygen species in the tumor necrosis factor-a-induced epithelial-mesenchymal transition of MCF-7 cells

Dong,R.; Wang,Q.; He,X.L.; Chu,Y.K.; Lu,J.G.; Ma,Q.J.
Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/08/2007 Português
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The microenvironment of the tumor plays an important role in facilitating cancer progression and activating dormant cancer cells. Most tumors are infiltrated with inflammatory cells which secrete cytokines such as tumor necrosis factor-a (TNF-a). To evaluate the role of TNF-a in the development of cancer we studied its effects on cell migration with a migration assay. The migrating cell number in TNF-a -treated group is about 2-fold of that of the control group. Accordingly, the expression of E-cadherin was decreased and the expression of vimentin was increased upon TNF-a treatment. These results showed that TNF-a can promote epithelial-mesenchymal transition (EMT) of MCF-7 cells. Further, we found that the expression of Snail, an important transcription factor in EMT, was increased in this process, which is inhibited by the nuclear factor kappa B (NFkB) inhibitor aspirin while not affected by the reactive oxygen species (ROS) scavenger N-acetyl cysteine. Consistently, specific inhibition of NFkB by the mutant IkBa also blocked the TNF-a-induced upregulation of Snail promoter activity. Thus, the activation of NFkB, which causes an increase in the expression of the transcription factor Snail is essential in the TNF-a-induced EMT. ROS caused by TNF-a seemed to play a minor role in the TNF-a-induced EMT of MCF-7 cells...

‣ Influence of ?S-globin haplotypes and hydroxyurea on tumor necrosis factor-alpha levels in sickle cell anemia

Laurentino,Marília Rocha; Maia Filho,Pedro Aurio; Barbosa,Maritza Cavalcante; Bandeira,Izabel Cristina Justino; Rocha,Lilianne Brito da Silva; Gonçalves,Romelia Pinheiro
Fonte: Associação Brasileira de Hematologia e Hemoterapia e Terapia Celular Publicador: Associação Brasileira de Hematologia e Hemoterapia e Terapia Celular
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/04/2014 Português
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Background: Sickle cell anemia is a chronic inflammatory disease characterized by an increased production of proinflammatory cytokines including tumor necrosis factor-alpha. Hydroxyurea, by decreasing the polymerization of hemoglobin, reduces inflammatory states. The effect of the genetic polymorphisms of sickle cell patients on tumor necrosis factor-alpha levels remains unknown. Objective: The aim of this study was to investigate the association of tumor necrosis factor-alpha levels with β-globin haplotypes and the use of hydroxyurea. Methods: A cross-sectional study was performed of 67 patients with sickle cell anemia diagnosed at steady-state in a referral hospital in Fortaleza, Ceará, Brazil. A group of 26 healthy individuals was used as control. βS-haplotype analysis was performed by restriction fragment length polymorphism-polymerase chain reaction. The tumor necrosis factor-alpha levels were measured by the enzyme-linked immunosorbent assay test. Laboratory data (complete blood count and fetal hemoglobin) and information regarding the use of hydroxyurea were obtained from medical records. Statistical analysis was performed using R software with the Kruskal-Wallis and Mann-Whitney tests. Statistical significance was established for p-values < 0.05 for all analyses. Results: The mean age of the participants was 35.48 years. Patients with sickle cell anemia had significantly higher tumor necrosis factor-alpha levels than controls (p-values < 0.0001). Tumor necrosis factor-alpha levels were lower in sickle cell anemia patients who were receiving hydroxyurea treatment than those who were not (p-value = 0.1249). Sickle cell anemia patients with Bantu/n genotype had significantly higher levels than patients with the Bantu/Benin genotype (p-value = 0.0021). Conclusion: In summary...

‣ A randomized trial of supplementation with docosahexaenoic acid-rich tuna oil and its effects on the human milk cytokines interleukin 1beta, interleukin 6, and tumor necrosis factor alpha

Hawkes, J.; Bryan, D.L.; Makrides, M.; Neumann, M.; Gibson, R.
Fonte: Amer Soc Clinical Nutrition Publicador: Amer Soc Clinical Nutrition
Tipo: Artigo de Revista Científica
Publicado em //2002 Português
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Background: Increased consumption of n-3 long-chain polyunsaturated fatty acids (PUFAs) has been recommended during pregnancy and lactation. The production of proinflammatory cytokines by human peripheral blood mononuclear cells (PBMCs) can be modified by dietary n-3 PUFAs. Objective: We sought to determine whether dietary supplementation of lactating women with docosahexaenoic acid (DHA) can modulate the concentration of cytokines in the aqueous phase of human milk and the production of cytokines by human milk cells (HMCs) and PBMCs. Design: In this double-blind, prospective, randomized trial, mothers of healthy full-term infants were asked to consume daily a nutritional supplement of 2000 mg oil containing either placebo (n = 40), 300 mg DHA + 70 mg eicosapentaenoic acid (EPA; n = 40), or 600 mg DHA + 140 mg EPA (n = 40). The fatty acid composition of plasma, PBMCs, milk, and HMCs from lactating mothers at 4 wk postpartum was measured by gas chromatography. The concentration of interleukin 6 and tumor necrosis factor in milk and the production of interleukin 1ß, tumor necrosis factor , and interleukin 6 by PBMCs and HMCs after stimulation with lipopolysaccharide was measured by enzyme-linked immunosorbent assay. Results: At 4 wk postpartum...

‣ Activation of the neutrophil bactericidal activity for non-typable Haemophilus influenzae by tumor necrosis factor and lymphotoxin

Tan, A.M.; Ferrante, A.; Goh, D.; Roberton, D.; Cripps, A.
Fonte: S. Karger Publicador: S. Karger
Tipo: Artigo de Revista Científica
Publicado em //1995 Português
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Previous studies have suggested that, in vivo, activated T lymphocytes and neutrophils are important in immunity to non-typable Haemophilus influenzae. We now extend this work by showing that neutrophils pretreated with products of activated T lymphocytes or activated macrophages show significantly enhanced killing of nontypable H. influenzae. Lymphotoxin, a product of activated T lymphocytes, significantly enhanced the neutrophil-mediated killing of nontypable H. influenzae, and tumor necrosis factor, produced by activated T lymphocytes as well as macrophages stimulated by activated T lymphocytes, also significantly increased the bactericidal activity of neutrophils. These cytokine-induced effects were seen with short pretreatment times of neutrophils and were maximal by 30 min. The killing of H. influenzae by neutrophils required the presence of heat-labile opsonins. In the absence of these opsonins, both tumor necrosis factor and lymphotoxin were unable to promote the killing of the bacteria by neutrophils. Furthermore, the results showed that tumor necrosis factor-primed neutrophils displayed significantly increased expression of CR3 and CR4 that was associated with increased phagocytosis of complement-opsonized nontypable H. influenzae. These cytokines may play an important role in immunity toward nontypable H. influenzae by stimulating neutrophil bactericidal activity.; Anne-Marie Tan...

‣ Tumor necrosis factor-α induces adhesion molecule expression through the sphingosine kinase pathway; Tumor necrosis factor-alpha induces adhesion molecule expression through the sphingosine kinase pathway

Xia, P.; Gamble, J.; Rye, K.A.; Wang, L.; Hii, C.; Cockerill, P.; Khew-Goodall, Y.; Bert, A.; Barter, P.; Vadas, M.
Fonte: National Academy of Sciences Publicador: National Academy of Sciences
Tipo: Artigo de Revista Científica
Publicado em //1998 Português
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The signaling pathways that couple tumor necrosis factor-α (TNFα) receptors to functional, especially inflammatory, responses have remained elusive. We report here that TNFα induces endothelial cell activation, as measured by the expression of adhesion protein E-selectin and vascular adhesion molecule-1, through the sphingosine kinase (SKase) signaling pathway. Treatment of human umbilical vein endothelial cells with TNFα resulted in a rapid SKase activation and sphingosine 1-phosphate (S1P) generation. S1P, but not ceramide or sphingosine, was a potent dose-dependent stimulator of adhesion protein expression. S1P was able to mimic the effect of TNFα on endothelial cells leading to extracellular signal-regulated kinases and NF-κB activation, whereas ceramide or sphingosine was not. Furthermore, N,N-dimethylsphingosine, an inhibitor of SKase, profoundly inhibited TNFα-induced extracellular signal-regulated kinases and NF-κB activation and adhesion protein expression. Thus we demonstrate that the SKase pathway through the generation of S1P is critically involved in mediating TNFα-induced endothelial cell activation.; Xia, Pu ; Gamble, Jennifer R. ; Rye, Kerry-anne ; Wang, Lijun ; Cockerill, Peter ; Khew-goodall, Yeesim ; Bert...

‣ Early expression and cellular localization of proinflammatory cytokines interleukin-1[beta], interleukin-6, and tumor necrosis factor-[alpha] in human traumatic spinal cord injury

Yang, L.; Blumbergs, P.; Jones, N.; Manavis, J.; Sarvestani, G.; Ghabriel, M.
Fonte: Lippincott Williams & Wilkins Publicador: Lippincott Williams & Wilkins
Tipo: Artigo de Revista Científica
Publicado em //2004 Português
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Study Design. Post-traumatic inflammatory response was studied in 11 human cases of acute spinal cord contusion injury. Objectives. To examine the inflammatory cellular response and the immunocytochemical expression and localization of interleukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha]in human spinal cord after contusion injury. Summary of Background Data. The post-traumatic inflammatory response plays an important role in secondary injury mechanisms after spinal cord injury, and inter-leukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha] are key inflammatory mediators. Methods. The study group comprised 11 patients with spinal cord contusion injury and 2 normal individuals. Histologic and immunocytochemical assessments were undertaken to evaluate the inflammatory cellular response and the immunoexpression of interleukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha] in the injured human spinal cord. The cellular sources of interleukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha] were elucidated by immunofluorescence double-labeled confocal imaging. Results. Increased immunoreactivity of interleukin-1[beta], internleukin-6, and tumor necrosis factor-[alpha]was detected in neurons 0.5 hour after injury...

‣ Etanercept decreases tumor necrosis factor-alpha activity in chronic wound fluid

Cowin, A.; Hatzirodos, N.; Rigden, J.; Fitridge, R.; Belford, D.
Fonte: Blackwell Publishing Inc Publicador: Blackwell Publishing Inc
Tipo: Artigo de Revista Científica
Publicado em //2006 Português
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High levels of tumor necrosis factor-α (TNF-α), a pro-inflammatory cytokine, are present in the wound fluid of chronic nonhealing wounds. This leads to increased inflammation, cytokine expression, and ultimately results in impaired wound healing and tissue destruction. Etanercept is a recombinant fusion protein that consists of the soluble TNF receptor (p75) linked to the Fc portion of human IgG1. It is an effective inhibitor of TNF-α and has been shown to provide rapid and sustained improvement in rheumatoid arthritis by acting as a soluble receptor binding TNF-α and preventing its proinflammatory activities. Therefore, the aim of this study was to determine whether Etanercept could inhibit TNF-α activity in chronic wound fluid. Wound fluid was collected from the venous leg ulcers of 16 different patients. The effect of Etanercept on TNF-α activity was evaluated using both a TNF-α bioassay and an enzyme-linked immunoassay. Etanercept was found to reduce the cytotoxic effect of chronic wound fluid on L929 fibroblasts by approximately 30% and neutralized TNF-α binding in the enzyme-linked immunoassay by up to 80%. Direct application of Etanercept to chronic wounds may therefore reduce the inflammatory activity of TNF-α, which could reduce the chronicity of venous leg ulcers and thus aid in the healing of these wounds.; Allison J. Cowin...

‣ Tumor necrosis factor-induced neutrophil adhesion occurs via sphingosine kinase-1-dependent activation of endothelial α₅β₁ integrin; Tumor necrosis factor-induced neutrophil adhesion occurs via sphingosine kinase-1-dependent activation of endothelial alpha(5)beta(1) integrin

Sun, W.; Pitson, S.; Bonder, C.
Fonte: Amer Soc Investigative Pathology Inc Publicador: Amer Soc Investigative Pathology Inc
Tipo: Artigo de Revista Científica
Publicado em //2010 Português
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Leukocyte recruitment plays a major role in the immune response to infectious pathogens, as well as during inflammatory and autoimmune disorders. The process of leukocyte extravasation from the blood requires a complex cascade of adhesive events between the leukocytes and the endothelium, including initial leukocyte rolling, adhesion, and finally transendothelial migration. Current research in this area aims to identify the key leukocyte subsets that initiate a given disease and to identify the trafficking molecule(s) that will most specifically inhibit those cells. Herein we demonstrate that tumor necrosis factor (TNF)α activates the integrin α5β1 without altering total expression levels of β1 integrin on human umbilical vein endothelial cells. Moreover, our studies suggest that TNFα-induced β1 activation is dependent on sphingosine kinase-1, but independent of the sphingosine-1-phosphate family of G protein-coupled receptors. We also show, using a parallel plate flow chamber assay, that neutrophil adhesion to TNFα-activated endothelium can be attenuated by blocking α5β1 or its ligand angiopoietin-2. These observations add new complexities that broaden the accepted concept of cellular trafficking with neutrophil adhesion to TNFα activated endothelial cells being sphingosine kinase-1...

‣ The PSF·p54nrb complex is a novel Mnk substrate that binds the mRNA for tumor necrosis factor α; The PSF(.) p54(nrb) complex is a novel Mnk substrate that binds the mRNA for tumor necrosis factor alpha

Buxade, M.; Morrice, N.; Krebs, D.; Proud, C.
Fonte: Amer Soc Biochemistry Molecular Biology Inc Publicador: Amer Soc Biochemistry Molecular Biology Inc
Tipo: Artigo de Revista Científica
Publicado em //2008 Português
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To identify new potential substrates for the MAP kinase signal-integrating kinases (Mnks), we employed a proteomic approach. The Mnks are targeted to the translational machinery through their interaction with the cap-binding initiation factor complex. We tested whether proteins retained on cap resin were substrates for the Mnks in vitro, and identified one such protein as PSF (the PTB (polypyrimidine tract-binding protein)-associated splicing factor). Mnks phosphorylate PSF at two sites in vitro, and our data show that PSF is an Mnk substrate in vivo. We also demonstrate that PSF, together with its partner, p54nrb, binds RNAs that contain AU-rich elements (AREs), such as those for proinflammatory cytokines (e.g. tumor necrosis factor α (TNFα)). Indeed, PSF associates specifically with the TNFα mRNA in living cells. PSF is phosphorylated at two sites by the Mnks. Our data show that Mnk-mediated phosphorylation increases the binding of PSF to the TNFα mRNA in living cells. These findings identify a novel Mnk substrate. They also suggest that the Mnk-catalyzed phosphorylation of PSF may regulate the fate of specific mRNAs by modulating their binding to PSF·p54nrb.; Maria Buxadé, Nick Morrice, Danielle L. Krebs and Christopher G. Proud

‣ Uso da nanopartícula de ouro ligada a moléculas de fator alfa de necrose tumoral como adjuvante da termoablação por radiofrequência de tumores renais : modelo animal experimental; Use of tumor necrosis factor alpha-coated nanoparticles to enhance radiofrequency ablation in a translational model of renal tumor

Renato Nardi Pedro
Fonte: Biblioteca Digital da Unicamp Publicador: Biblioteca Digital da Unicamp
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 06/10/2010 Português
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98.4329%
O tratamento definitivo das massas renais malignas é primordialmente cirúrgico, sendo a nefrectomia radical eleita por muitos anos a cirurgia padrão para o tratamento do câncer renal localizado. Entretanto, com o envelhecimento populacional, maiores são as preocupações em se manter a capacidade funcional dos órgãos e sistemas do corpo humano. Portanto, a necessidade de se preservar tecido renal sadio durante o tratamento do câncer renal localizado, com auxílio de cirurgias parciais poupadoras de néfrons, se tornou imperativa. O tratamento de lesões renais sólidas pequenas passou a ter diferentes formas de abordagem, que variam desde técnicas de termoablação percutânea ou laparoscópica, nefrectomia parcial laparoscópica e aberta à até tradicional nefrectomia radical aberta. O uso de modalidades de tratamento cirúrgico com mínimo grau de agressão passou a ganhar atenção, devido à rápida recuperação do paciente, ao menor risco de complicações cirúrgicas e aos bons resultados oncológicos. Ablação por radiofreqüência (ARF) tem se mostrado um meio eficiente no tratamento de tumores renais pequenos e exofiticos. Atualmente, sua indicação é restrita a lesões de até 4 cm. O presente estudo foi montado para avaliar o uso conjunto da nanopartícula de ouro e fator alfa de necrose tumoral (TNF alfa) à ARF no tratamento de um modelo experimental de tumor renal. Materiais e Métodos: Trinta e sete coelhos brancos da raça New Zealand tiveram implantados em seus rins...

‣ La sobre-expresión crónica del factor de necrosis tumoral alfa en la substantia nigra induce neurodegeneración y síntomas motores; Chronic overexpression of tumor necrosis factor alpha in the substantia nigra elicits progressive neurodegeneration and motor symptoms

De Lella Ezcurra, Ana Laura
Fonte: Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires Publicador: Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires
Tipo: info:eu-repo/semantics/doctoralThesis; tesis doctoral; info:eu-repo/semantics/publishedVersion Formato: application/pdf
Publicado em //2010 Português
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La neuroinflamación es considerada una característica neuropatológica de la enfermedad de Parkinson. Se ha observado activación de microglía y niveles elevados de citoquinas pro-inflamatorias, entre las que se encuentra el factor de necrosis tumoral alfa (TNF-α), en la substantia nigra, una de las principales regiones del cerebro afectadas en esta enfermedad. Sin embargo, el rol funcional de la activación microglial y la sobre-expresión de TNF-α no es claro en la enfermedad de Parkinson. El objetivo de este trabajo fue determinar los efectos de la sobre-expresión crónica de TNF-α en la substantia nigra, e identificar moléculas candidatas a mediar ese efecto. Para ello, se inyectó en la substantia nigra de ratas adultas un adenovector que expresa TNF-α (AdTNFα), pudiendo detectarse la citoquina recombinante hasta 14 días p.i. La expresión crónica de TNF-α indujo una pérdida progresiva de neuronas en la substantia nigra, que comenzó el día 14 y se acentuó a los 21 y 28 días p.i., comparado con animales controles inyectados con un adenovector que expresa β- galactosidasa (Adβgal). La sobre-expresión de TNF-α produjo la aparición de síntomas motores a los 14 días p.i.; y la activación de la microglía y/o reclutamiento de macrófagos de la periferia desde el día 7 luego de la inoculación. No se pudo detectar inducción de IL-1β ni evidencias de apoptosis. En cambio...

‣ Participación del factor de necrosis tumoral alfa en la proliferación de carcinomas mamarios; Tumor necrosis factor alpha involvement in breast cancer cell proliferation

Rivas, Martín Alfredo
Fonte: Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires Publicador: Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires
Tipo: info:eu-repo/semantics/doctoralThesis; tesis doctoral; info:eu-repo/semantics/publishedVersion Formato: application/pdf
Publicado em //2010 Português
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El factor de necrosis tumoral alfa (TNFα) es una citoquina pro-inflamatoria implicada en promover el crecimiento de ciertos tipos de cánceres. En el presente trabajo de Tesis se exploraron los caminos de señalización intracelulares que llevan al crecimiento de las células de cáncer de mama inducido por TNFα y su interacción con el receptor tirosina quinasa tipo I, ErbB-2. Nuestros resultados indicaron que el TNFα, actuando a través del receptor de TNFα tipo 1 (TNFR1), indujo la activación de las quinasas activadas por mitógenos p42 y p44 (p42/p44 MAPK), la quinasa del amino terminal de c-jun (JNK) y la fosfatidilinositol 3-fosfato quinasa / Akt (PI3-K/Akt), la activación del factor de transcripción Factor Nuclear κB (NF-κB) y la proliferación celular. También comprobamos que la administración de TNFα in vivo indujo el crecimiento del tumor C4HD en ratones Balb/c y que el tratamiento con un inhibidor selectivo de NF-κB, Bay 11-7082, resultó en la regresión parcial de dicho tumor de mama. Asimismo, el Bay 11-7082 bloqueó la capacidad del TNFα de inducir el aumento de la proteína promotora del ciclo celular ciclina D1 y de la proteína antiapoptótica Bcl-XL. Un importante hallazgo fue demostrar que el TNFα indujo la transactivación de ErbB-2 en células de cáncer de mama que sobreexpresan ErbB-2. En estas células...

‣ Therapeutic approaches for tumor necrosis factor inhibition

Barbosa, Maria Letícia de Castro; Fumian, Milla Machado; Miranda, Ana Luísa Palhares de; Barreiro, Eliezer J.; Lima, Lídia Moreira
Fonte: Universidade de São Paulo. Faculdade de Ciências Farmacêuticas Publicador: Universidade de São Paulo. Faculdade de Ciências Farmacêuticas
Tipo: info:eu-repo/semantics/article; info:eu-repo/semantics/publishedVersion; ; ; ; ; Formato: application/pdf
Publicado em 01/09/2011 Português
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O fator de necrose tumoral (do inglês, tumor necrosis factor - TNF) consiste em uma citocina inflamatória essencial para a homeostase e defesa do organismo. A despeito de sua relevância fisiológica, o aumento da biossíntese e liberação do TNF conduzem à exacerbação das respostas inflamatória e oxidativa, as quais estão relacionadas à patogênese de várias doenças de natureza inflamatória, auto-imune e/ou infecciosa. A busca por abordagens terapêuticas eficientes na modulação do TNF tem sido alvo de diversos esforços de pesquisa. Aproximadamente um milhão de pessoas ao redor do mundo já foi tratado com inibidores biotecnológicos desta citocina, os chamados biofármacos anti-TNF. Entretanto, em face ao elevado risco de infecções e as limitações relacionadas ao custo e a via de administração, novas abordagens terapêuticas com foco em alvos que modulem, de forma direta ou indireta, a produção e/ou ativação do TNF surgem como alternativas promissoras para a descoberta de novos fármacos antiinflamatórios e imunomoduladores ativos por via oral e serão discutidas neste trabalho.; Tumor necrosis factor (TNF) consists of an inflammatory cytokine essential for homeostasis and organism defense. Despite its physiological relevance...

‣ Tumor necrosis factor receptor 2 mRNA in rat models of hypertension

Lin, Ruby; Schyvens, Chris; Zhang, Yi; Whitworth, Judith; Morris, Brian
Fonte: Elsevier Publicador: Elsevier
Tipo: Artigo de Revista Científica
Português
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In human hypertension (HT) plasma tumor necrosis factor (TNF-α) and soluble TNF receptor 2 fragment (sTNF-R2) are increased, and the TNF-R2 gene (TNFRSF1B) has been implicated. Therefore, we measured Tnfr2 mRNA in kidney, adrenal, heart, and aorta from r