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Yann Seimbille

Researcher at Erasmus University Rotterdam

Publications -  81
Citations -  1937

Yann Seimbille is an academic researcher from Erasmus University Rotterdam. The author has contributed to research in topics: Medicine & Chemistry. The author has an hindex of 15, co-authored 58 publications receiving 1532 citations. Previous affiliations of Yann Seimbille include University of Lausanne & Erasmus University Medical Center.

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Microbiota depletion promotes browning of white adipose tissue and reduces obesity

TL;DR: Insight is provided into the microbiota-fat signaling axis and beige-fat development in health and metabolic disease and the metabolic phenotype and the browning of the subcutaneous fat are impaired by the suppression of type 2 cytokine signaling and they are reversed by recolonization of the antibiotic-treated or germ-free mice with microbes.
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Monitoring Tumor Glucose Utilization by Positron Emission Tomography for the Prediction of Treatment Response to Epidermal Growth Factor Receptor Kinase Inhibitors

TL;DR: Glucose metabolic activity closely reflects response to gefitinib therapy, and may be a valuable clinical predictor, early in the course of treatment, for therapeutic responses to EGFR kinase inhibitors.
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Elevated endocannabinoid plasma levels are associated with coronary circulatory dysfunction in obesity

TL;DR: Increased EC plasma levels of AEA and 2-AG are associated with coronary circulatory dysfunction in obese individuals, and this observation might suggest increases inEC plasma levels as a novel endogenous cardiovascular risk factor in obesity, but needing further investigations.
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Evaluation of [ 18 F]gefitinib as a molecular imaging probe for the assessment of the epidermal growth factor receptor status in malignant tumors

TL;DR: The biodistribution of the drug analogue [18F]gefitinib suggests that it may be used to assess noninvasively the pharmacokinetics of gefitinib in patients by PET imaging, which is of clinical relevance, as insufficient intratumoral drug concentrations are considered to be a factor for resistance to gefITinib therapy.