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Hemocompatibility study of surface-attached antibiofouling polymer monolayers
Author(s) -
Bidhari Pidhatika
Publication year - 2019
Publication title -
journal of physics. conference series
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.21
H-Index - 85
eISSN - 1742-6596
pISSN - 1742-6588
DOI - 10.1088/1742-6596/1282/1/012069
Subject(s) - biomaterial , surface modification , ethylene glycol , monolayer , materials science , polymer , polymer brush , adhesion , platelet activation , polyelectrolyte , protein adsorption , polymer chemistry , ethylene oxide , chemical engineering , nanotechnology , chemistry , platelet , organic chemistry , copolymer , polymerization , composite material , immunology , engineering , biology
The interface between biomaterials and body fluid such as blood is a critical concern, because biomaterial-centered protein fouling and infection adversely affects the quality of life of many patients and cause major health care costs. Our research focused on polymer functionalization on surfaces to create antibiofouling interfaces ( i.e. interfaces that repel the adhesion of proteins and microorganisms) in biomaterial-related applications, such as surgical instruments and blood-contacting biomedical devices. To this end, we have studied two hydrophilic polymers, namely poly(2-oxazoline) and poly(ethylene glycol), attached on metal oxide surfaces in brush configuration through a polyelectrolyte surface anchor, poly(L-lysine). Apart from antibiofouling properties, blood-contacting surfaces must also serve hemocompatibility. Here the hemocompatibility of antibiofouling monolayer on silicon oxide surfaces prepared from either poly(2-oxazoline) or poly(ethylene glycol) grafted on a main backbone poly(L-lysine), has been studied. The activation of C5a (complement system), TAT and kallikrein (coagulation cascade), PF4 and sP-selectin, (platelet activation) after incubation of the polymer-modified surfaces in whole blood was measured by means of ELISA kit. The results showed that in general, the contact between blood and polymer monolayer activated the complement system, but relatively did not activate the coagulation cascade and the platelet surface marker.

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