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Nieves Olmo

Researcher at Complutense University of Madrid

Publications -  73
Citations -  2575

Nieves Olmo is an academic researcher from Complutense University of Madrid. The author has contributed to research in topics: Butyrate & Cell culture. The author has an hindex of 27, co-authored 72 publications receiving 2368 citations.

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Annexin-Phospholipid Interactions. Functional Implications

TL;DR: The in vivo physiological functions of annexins are just beginning to be established, most of them directly related with the conserved ability to bind to phospholipid bilayers: membrane trafficking, membrane-cytoskeleton anchorage, ion channel activity and regulation, as well as antiinflammatory and anticoagulant activities.
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Influence of different chemical cross-linking treatments on the properties of bovine pericardium and collagen.

TL;DR: The effects of alternative chemical treatments: diphenylphosphorylazide (DPPA) and ethyldimethylaminopropyl carbodiimide (EDAC) are studied, which show the mechanism of action is based on the activation of the carboxyl groups, which permits their cross-linking to amino groups.
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Bioactive sol-gel glasses with and without a hydroxycarbonate apatite layer as substrates for osteoblast cell adhesion and proliferation.

TL;DR: These bioactive glasses can be considered biocompatible and is greatly enhanced after induction of the formation of an HCA layer, being this process 2-4-fold higher when the apatite-like layer is already formed.
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Cytotoxic mechanism of the ribotoxin α‐sarcin

TL;DR: Data suggest that α-sarcin-induced caspase activation is a pathway downstream of the 28S rRNA catalytic cleavage and consequent protein biosynthesis inhibition, and that induced apoptosis is directly related to the effects of catalytic activity of the toxin on the ribosomes.
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Bile acids in the colon, from healthy to cytotoxic molecules.

TL;DR: There is increasing evidence that the continuous exposure to certain hydrophobic bile acids, due to a fat-rich diet or pathological conditions, may induce oxidative DNA damage that may lead to colorectal carcinogenesis as a consequence of the appearance of cell populations resistant to bile acid-induced apoptosis.