scispace - formally typeset
K

Kate Lykke Lambertsen

Researcher at University of Southern Denmark

Publications -  119
Citations -  4533

Kate Lykke Lambertsen is an academic researcher from University of Southern Denmark. The author has contributed to research in topics: Microglia & Tumor necrosis factor alpha. The author has an hindex of 31, co-authored 99 publications receiving 3621 citations. Previous affiliations of Kate Lykke Lambertsen include University of Miami & Odense University Hospital.

Papers
More filters
Journal ArticleDOI

Inflammatory cytokines in experimental and human stroke

TL;DR: The fact that TNF and IL-1, and suppossedly also IL-6, are produced by microglia within the therapeutic window place these cells centrally in potential future stroke therapy, in the context of suggestions that neuronal sensitivity to ischemia may be modulated by cytokines.
Journal ArticleDOI

Microglia and macrophages are the major source of tumor necrosis factor in permanent middle cerebral artery occlusion in mice

TL;DR: To a time-restricted microglial/macrophage production of TNF in focal cerebral ischemia in mice, nonradioactive in situ hybridization for murine TNF mRNA was performed and translation of T NF mRNA into bioactive protein was demonstrated in the neocortex of C57Bl/6 mice subjected to permanent middle cerebral artery occlusion.
Journal ArticleDOI

Interleukin-1beta and tumor necrosis factor-alpha are expressed by different subsets of microglia and macrophages after ischemic stroke in mice

TL;DR: The results show that IL-1β and TNF-α are produced by largely segregated populations of microglia and macrophages after ischemic stroke in mice, providing evidence of a functional diversity among different subsets of microGlia and Macrophages that is potentially relevant to future design of anti-inflammatory therapies in stroke.
Journal ArticleDOI

Post-stroke inflammation-target or tool for therapy?

TL;DR: The cell biology of the post-stroke inflammatory response is summarized and pharmacological interventions targeting inflammation in the acute phase after a stroke that may be used alone or in combination with recanalization therapies are discussed.