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Thomas Simmet

Researcher at University of Ulm

Publications -  211
Citations -  15559

Thomas Simmet is an academic researcher from University of Ulm. The author has contributed to research in topics: Proinflammatory cytokine & Monocyte. The author has an hindex of 54, co-authored 202 publications receiving 13691 citations. Previous affiliations of Thomas Simmet include University of Freiburg & French Institute of Health and Medical Research.

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Effect of food intake on the bioavailability of boswellic acids from a herbal preparation in healthy volunteers.

TL;DR: Detailed kinetics of BAs after oral dosing of an extract are revealed and a profound effect of food intake on the pharmacokinetic profile of the BAs is demonstrated.
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Intracellular Interleukin-1α Functionally Interacts with Histone Acetyltransferase Complexes

TL;DR: The data provide the first solid evidence for the nuclear target of the IL-1α precursor and suggest its novel function in transcriptional control, as well as demonstrating that yeast strains expressing Gal4BD/IL-1NTP display a toxic phenotype that can be relieved by depletion of various components of the SAGA complex.
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Human B cells differentiate into granzyme B-secreting cytotoxic B lymphocytes upon incomplete T-cell help.

TL;DR: It is shown that in the absence of CD40L, CD4+ T cell‐derived IL‐21 induces differentiation of B cells into granzyme B (GzmB)‐secreting cytotoxic cells, which may have a role in early cellular immune responses including tumor immunosurveillance before fully activated, antigen‐specific cytot toxic T cells are on the spot.
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Thrombin and vascular inflammation

TL;DR: This review summarizes the existing evidence on the role of thrombin in vascular inflammation and shows an array of effects on endothelial cells, vascular smooth muscle cells, monocytes, and platelets, all of which participate in the vascular pathophysiology such as atherothrombosis.
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Targeting NF-kappa B with a natural triterpenoid alleviates skin inflammation in a mouse model of psoriasis.

TL;DR: It is demonstrated that NF-κB signaling is pivotal for the pathogenesis in the CD18hypo mouse model of psoriasis, and targeting NF-β kinase inhibitor might provide an effective strategy for the treatment of Psoriasis.