J
José María Gutiérrez
Researcher at University of Costa Rica
Publications - 645
Citations - 30336
José María Gutiérrez is an academic researcher from University of Costa Rica. The author has contributed to research in topics: Antivenom & Venom. The author has an hindex of 84, co-authored 607 publications receiving 26779 citations. Previous affiliations of José María Gutiérrez include Spanish National Research Council & Tecnológico de Antioquia.
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Phospholipase A2 myotoxins from Bothrops snake venoms
TL;DR: Current evidence suggests that these toxins interact with biological membranes via a molecular region distinct from their known catalytic site, which may lead to membrane destabilization and loss of selective permeability to ions such as calcium, both of which appear to be important mediators in the process of muscle necrosis.
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Snake venom metalloproteinases:Their role in the pathogenesis of local tissue damage
TL;DR: Owing to their protagonic role in the pathogenesis of local tissue damage, snake venom metalloproteinases constitute relevant targets for natural and synthetic inhibitors which may complement antivenoms in the neutralization of these effects.
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Confronting the Neglected Problem of Snake Bite Envenoming: The Need for a Global Partnership
TL;DR: An attempt is made to evaluate the phytochemical properties of the venomous materials used in the making of venomous snake venom, which have the potential to have a positive impact on human health.
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Hemorrhage induced by snake venom metalloproteinases: biochemical and biophysical mechanisms involved in microvessel damage.
TL;DR: It is proposed that SVMP-induced hemorrhage occurs in vivo by a 'two-step' mechanism, whereby SVMPs degrade basement membrane and adhesion proteins, thus weakening the capillary wall and perturbing the interactions between endothelial cells and the basement membrane.
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Skeletal muscle degeneration induced by venom phospholipases A2: insights into the mechanisms of local and systemic myotoxicity
TL;DR: A model is presented to explain the difference between PLA2s that induce predominantly local myonecrosis and those inducing both local and systemic myotoxicity, and the former bind not only to muscle cells, but also to other cell types, thereby precluding a systemic distribution of thesePLA2s.