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In 2005, after a postdoc on protein crystallization at the University of Houston (Houston, TX, USA), I returned to the work on biointerfaces as the Alexander von Humboldt Research fellow, hosted by Diethelm Johannsmann at the Clausthal University of Technology in Germany. There, I started working on the shear-acoustic response from laterally heterogeneous ultrathin films. That work led to the identification of a new contrast mechanism by which shear resonators used in quartz crystal microbalances sense adsorbed nanoparticles. Later, this allowed me to study adsorbed liposome deformation and so to further advance the understanding of the interactions between lipids and surfaces of artificial materials. It was also a start of a tremendously exciting and fulfilling collaboration that continues to date.
In 2006, I joined CIC biomaGUNE, a new research institute in San Sebastian, Spain, as a groupleader. There, I had a chance to participate in the establishment of a new institute, and to continue my work on the interactions between artificial materials and biological systems ranging from lipids to thrombocytes (platelets) to blood. In particular, my group investigated the role of surface ion exchange in the activation of platelets on TiO2, and worked on the design of a new platelet activation assay based on the analysis of platelet surface glycosylation changes. We showed that platelet activation at biomaterial surfaces could be selective, and that platelet surface glycosylation differed between platelets activated with different agonists, yielding an agonist-specific fingerprint. Platelets are key coagulation effectors (thus the connection with the earlier work on phosphatidylserine) that are also responsible for the adverse reactions to the biomaterials—reactions that lead to the material-induced thrombosis, inflammation, and that can be fatal. I also embarked on neutron reflectometry studies for quantifying the asymmetry in TiO2-supported SLBs and characterizing the interactions between PS and calcium that are crucial to the role of PS in coagulation and its interactions with titania.
In 2006, I joined CIC biomaGUNE, a new research institute in San Sebastian, Spain, as a groupleader. There, I had a chance to participate in the establishment of a new institute, and to continue my work on the interactions between artificial materials and biological systems ranging from lipids to thrombocytes (platelets) to blood. In particular, my group investigated the role of surface ion exchange in the activation of platelets on TiO2, and worked on the design of a new platelet activation assay based on the analysis of platelet surface glycosylation changes. We showed that platelet activation at biomaterial surfaces could be selective, and that platelet surface glycosylation differed between platelets activated with different agonists, yielding an agonist-specific fingerprint. Platelets are key coagulation effectors (thus the connection with the earlier work on phosphatidylserine) that are also responsible for the adverse reactions to the biomaterials—reactions that lead to the material-induced thrombosis, inflammation, and that can be fatal. I also embarked on neutron reflectometry studies for quantifying the asymmetry in TiO2-supported SLBs and characterizing the interactions between PS and calcium that are crucial to the role of PS in coagulation and its interactions with titania.
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BIOINTERPHASESno. 1 (2024)
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