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Reto A. Schwendener

Researcher at University of Zurich

Publications -  172
Citations -  12645

Reto A. Schwendener is an academic researcher from University of Zurich. The author has contributed to research in topics: Liposome & Cytotoxic T cell. The author has an hindex of 55, co-authored 171 publications receiving 11423 citations. Previous affiliations of Reto A. Schwendener include École Polytechnique Fédérale de Lausanne & Paul Scherrer Institute.

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Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation.

TL;DR: Transcriptional and functional data revealed that monocyte-derived macrophages coordinate cardiac inflammation, while playing redundant but lesser roles in antigen sampling and efferocytosis, and the presence of multiple cardiac macrophage subsets, with different functions, origins, and strategies to regulate compartment size.
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Clodronate-liposome-mediated depletion of tumour-associated macrophages: a new and highly effective antiangiogenic therapy approach.

TL;DR: Clodrolip therapy in combination with angiogenesis inhibitors as a promising novel strategy for an indirect cancer therapy aimed at the haematopoietic precursor cells that stimulate tumour growth and dissemination and as a tool to study the role of macrophages and dendritic cells in tumorigenesis are validated.
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Inflammation Is Necessary for Long-Term but Not Short-Term High-Fat Diet–Induced Insulin Resistance

TL;DR: Data suggest that the initial stage of HFD-induced insulin resistance is independent of inflammation, whereas the more chronic state of insulin resistance in established obesity is largely mediated by macrophage-induced proinflammatory actions.
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Antennapedia and HIV Transactivator of Transcription (TAT) “Protein Transduction Domains” Promote Endocytosis of High Molecular Weight Cargo upon Binding to Cell Surface Glycosaminoglycans

TL;DR: The data reported here support the idea that certain PTDs promote cellular uptake via endocytosis and require the expression of negatively charged glycosaminoglycans on the surface of the target cells, and support the view that PTD-mediated cellular uptake is energy-independent.