M
Manuel Fresno
Researcher at Spanish National Research Council
Publications - 277
Citations - 10839
Manuel Fresno is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: Trypanosoma cruzi & Tumor necrosis factor alpha. The author has an hindex of 55, co-authored 262 publications receiving 9894 citations. Previous affiliations of Manuel Fresno include Autonomous University of Madrid & University of Oviedo.
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The role of tumour necrosis factor, interleukin 6, interferon-γ and inducible nitric oxide synthase in the development and pathology of the nervous system
TL;DR: Understanding the dichotomy pathogenesis/neuroprotection of those cytokines may provide a rationale for better therapeutic strategies and apparently conflicting results may be reconciled.
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Synergism between tumor necrosis factor-alpha and interferon-gamma on macrophage activation for the killing of intracellular Trypanosoma cruzi through a nitric oxide-dependent mechanism.
TL;DR: Results suggest that IFN‐γ and TNF‐α, secreted by T. cruzi‐immune T cells, are involved in the activation of the trypanocidal activity of mouse macrophages through an NO‐dependent mechanism.
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Inhibition of Translation in Eukaryotic Systems by Harringtonine
TL;DR: The results suggest that the Cephalotaxus alkaloids inhibit the elongation phase of translation by preventing substrate binding to the acceptor site on the 60-S ribosome subunit and therefore block aminoacyl-tRNA binding and peptide bond formation.
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An Essential Role of the Nuclear Factor of Activated T Cells in the Regulation of the Expression of the Cyclooxygenase-2 Gene in Human T Lymphocytes
TL;DR: The results emphasize the central role that the Ca2+/calcineurin pathway plays in COX-2 transcriptional regulation in T lymphocytes pointing to NFAT/activator protein-1 transcription factors as essential for COx-2 promoter regulation in these cells.
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Cyclooxygenase-2: a therapeutic target in angiogenesis
TL;DR: Inhibition of COX-2 by non-steroidal anti-inflammatory drugs leads to restricted angiogenesis and downregulated production of pro-angiogenic factors, such as vascular endothelial growth factor and basic fibroblast growth factor.