Hans P. Merkle
ETH Zurich
179 Papers
3K Citations
Hans P. Merkle is an academic researcher from ETH Zurich. The author has contributed to research in topics: PLGA & Chemistry. The author has an hindex of 73, co-authored 179 publications. Previous affiliations of Hans P. Merkle include École Polytechnique Fédérale de Lausanne & University of Bonn.
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Papers
Physico-chemical parameters governing protein microencapsulation into biodegradable polyesters by coacervation
TL;DR: In this article, the interfacial properties between coacervate, continuous liquid and solid or aqueous BSA and selected process parameters were studied for microencapsulation of BSA powder and BSA solution.
Release of tetanus toxoid from adjuvants and PLGA microspheres: how experimental set-up and surface adsorption fool the pattern.
TL;DR: The tetanus toxoid (Ttxd) in vitro release from alum, IFA formulations and MS in four different test systems showed a stronger Ttxd association to alum than to IFA, and the release from both formulations lasted between 3-9 days.
PEGylation as a tool for the biomedical engineering of surface modified microparticles
Uta Wattendorf,Hans P. Merkle +1 more
TL;DR: The unique physicochemical properties of PEG are discussed, which make it the polymer of choice to render the surfaces of microparticles repellent to the adsorption of proteins and resistant to cellular recognition.
Biopolymer-based growth factor delivery for tissue repair: from natural concepts to engineered systems.
TL;DR: The engineering of novel biopolymer platforms holds promise to enhance the biological performance of GF-loaded artificial tissue substitutes to replace autologous and allogenous tissue grafts for the treatment of critical tissue defects.
Modulation of allergic responses in mice by using biodegradable poly(lactide-co-glycolide) microspheres.
TL;DR: This is the first physiological demonstration that plain PLGA microspheres can induce tolerance in mice for as long as 6 months postsensitization, and suggests a dual mechanism that does initially rely on a TH2 to TH1 immune deviation and then on IL-10-mediated suppression.