Irish
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
arachidonate/necrosis
Sábháiltear an nasc chuig an gearrthaisce
Leathanach 1 ó 137 torthaí
Gene expression of isoformic enzymes in arachidonate cyclooxygenase pathway and the regulation by tumor necrosis factor alpha during life cycle of adipocytes.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Adipocytes serve not only as a storage depot of fats but also as endocrine cells secreting adipocytokines including tumor necrosis factor alpha (TNFalpha). Using preadipogenic 3T3-L1 cells, we attempt to determine the response of adipocytes at different stages of the life cycle to TNFalpha with
Involvement of calcium and arachidonate metabolism in acetylated-low-density-lipoprotein-stimulated tumor-necrosis-factor-alpha production by rat peritoneal macrophages.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
We show that lipopolysaccharide-free actetylated low-density lipoprotein (LDL), but not native LDL, stimulates tumor-necrosis factor-alpha (TNF-alpha) secretion by rat peritoneal macrophages and the signal-transduction pathways involved. The role of the scavenger receptor (SR) in this response was
Tumor necrosis factor-alpha increases release of arachidonate and prolactin from rat anterior pituitary cells.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
We investigated the effect of tumor necrosis factor-alpha (TNF alpha), a product of activated macrophages, on the release of arachidonate from dispersed anterior pituitary cells. Primary cultures of anterior pituitary cells from rats were preincubated with [3H]arachidonate to label their
Tumour cell killing by tumour necrosis factor: inhibition by anaerobic conditions, free-radical scavengers and inhibitors of arachidonate metabolism.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Previous work on the mechanism of tumour-cell killing by the macrophage product tumour necrosis factor (TNF) is consistent with a free radical-induced process. In this study, free-radical involvement was sought by (i) investigating the effects on TNF cytolysis of anaerobic conditions, free-radical
U937 cell necrosis mediated by peroxynitrite is not caused by depletion of ATP and is prevented by arachidonate via an ATP-dependent mechanism.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Exposure of U937 cells to an otherwise nontoxic concentration of peroxynitrite promotes a rapid necrotic response in the presence of pharmacological inhibitors of phospholipase A2. A 12-fold higher concentration of the oxidant, in the absence of additional treatments, caused remarkably greater DNA
Role of Bcl-2 in the arachidonate-mediated survival signaling preventing mitochondrial permeability transition-dependent U937 cell necrosis induced by peroxynitrite.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Antisense technology was successfully employed to selectively reduce the expression of Bcl-2 in U937 cells, while leaving their redox status intact. These cells displayed enhanced sensitivity to mitochondrial permeability transition (MPT)-dependent apoptosis induced by arsenite and underwent a
Long-term renal preservation and prevention of acute tubular necrosis by inhibition of arachidonate metabolism.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Experimental preservation time for pulsatile perfused dog kidneys was extended from three to five days by phospholipase A2 inhibition suggesting a pathomechanical role of products of phospholipolysis like thromboxane and leukotrienes in the development of acute graft failure after renal
Long-term renal preservation and prevention of acute tubular necrosis by inhibition of arachidonate metabolism.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Tumor necrosis factor-induced mortality is reversed with cyclooxygenase inhibition.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
OBJECTIVE
The authors hypothesized that TNF would induce eicosanoid synthesis, and a cyclooxygenase inhibitor would attenuate both eicosanoid synthesis and improve survival in an LD90 TNF-induced (150 ng/kg/i.v./5 min) mortality model.
BACKGROUND
Tumor necrosis factor is a cardinal mediator in
Intracerebroventricular injection of tumor necrosis factor-alpha induces thermal hyperalgesia in rats.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
To investigate the role of tumor necrosis factor-alpha (TNF-alpha) in the brain in nociception, we injected recombinant human TNF-alpha (rhTNF-alpha; 1 pg-10 ng/rat) into the lateral cerebroventricle (LVC) in rats and observed the changes in paw withdrawal latency to radiant heat by using the
Membrane-derived second messenger regulates x-ray-mediated tumor necrosis factor alpha gene induction.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Cells adapt to adverse environmental conditions through a wide range of responses that are conserved throughout evolution. Physical agents such as ionizing radiation are known to initiate a stress response that is triggered by the recognition of DNA damage. We have identified a signaling pathway
Regulation of interleukin-1 and tumor necrosis factor-alpha induced granulocyte-macrophage colony-stimulating factor gene expression: potential involvement of arachidonic acid metabolism.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Signal transduction pathways evoked by interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) to stimulate expression of other cytokines in mesenchymal cells are not clearly understood. Stimulation of the murine bone marrow stromal cell line +/(+)-1.LDA 11 with IL-1 (500 U/ml) in
Signaling mechanisms involved in the activation of arachidonic acid metabolism in human astrocytoma cells by tumor necrosis factor-alpha: phosphorylation of cytosolic phospholipase A2 and transactivation of cyclooxygenase-2.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Tumor necrosis factor-alpha (TNF-alpha) is a cytokine that elicits cell responses by activating the mitogen-activated protein kinase (MAP kinase) cascade and transcription factors such as nuclear factor-kappaB (NF-kappaB). As these elements play a central role in the mechanisms of signaling involved
Phospholipase A2 is necessary for tumor necrosis factor alpha-induced ceramide generation in L929 cells.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
The role of cytosolic phospholipase A2 (cPLA2) in the regulation of ceramide formation was examined in a cell line (L929) responsive to the cytotoxic action of tumor necrosis factor alpha (TNFalpha). In L929 cells, the addition of TNFalpha resulted in the release of arachidonate, which was followed
Different apoptotic pathways mediated by Fas and the tumor-necrosis-factor receptor. Cytosolic phospholipase A2 is not involved in Fas-mediated apoptosis.
Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
Fas is a cell-surface receptor that belongs to the tumor-necrosis factor (TNF)/nerve growth factor receptor family. Fas can transduce an apoptotic signal through the death domain in the cytoplasmic region, which has similarity with the corresponding region of the TNF type-I receptor. Here, we
An bunachar luibheanna míochaine is iomláine le tacaíocht ón eolaíocht
- Oibreacha i 55 teanga
- Leigheasanna luibhe le tacaíocht ón eolaíocht
- Aitheantas luibheanna de réir íomhá
- Léarscáil GPS idirghníomhach - clibeáil luibheanna ar an láthair (ag teacht go luath)
- Léigh foilseacháin eolaíochta a bhaineann le do chuardach
- Cuardaigh luibheanna míochaine de réir a n-éifeachtaí
- Eagraigh do chuid spéiseanna agus fanacht suas chun dáta leis an taighde nuachta, trialacha cliniciúla agus paitinní
Clóscríobh symptom nó galar agus léigh faoi luibheanna a d’fhéadfadh cabhrú, luibh a chlóscríobh agus galair agus comharthaí a úsáidtear ina choinne a fheiceáil.
* Tá an fhaisnéis uile bunaithe ar thaighde eolaíoch foilsithe
