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Ben J. A. Janssen
Researcher at Maastricht University
Publications - 137
Citations - 6517
Ben J. A. Janssen is an academic researcher from Maastricht University. The author has contributed to research in topics: Blood pressure & Baroreflex. The author has an hindex of 43, co-authored 137 publications receiving 6027 citations. Previous affiliations of Ben J. A. Janssen include Maastricht University Medical Centre & Eindhoven University of Technology.
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Journal ArticleDOI
Comparison of various techniques used to estimate spontaneous baroreflex sensitivity (the EuroBaVar study)
Dominique Laude,Jean Luc Elghozi,Arlette Girard,Elisabeth Bellard,Malika Bouhaddi,Paolo Castiglioni,Catherine Cerutti,Andrei Cividjian,Marco Di Rienzo,Jacques Olivier Fortrat,Ben J. A. Janssen,John M. Karemaker,Georges Lefthériotis,Gianfranco Parati,Pontus B. Persson,Alberto Porta,Luc Quintin,Jacques Regnard,Heinz Rüdiger,Harald M. Stauss +19 more
TL;DR: The discrepancies between procedures show that the choice of parameters and data handling should be considered before BRS estimation, and new techniques with this set of results are needed.
Journal ArticleDOI
Effects of anesthetics on systemic hemodynamics in mice
Ben J. A. Janssen,Tijl De Celle,Jacques Debets,Agnieszka E. Brouns,Michael F. Callahan,Thomas L. Smith +5 more
TL;DR: It is indicated that the anesthetic Iso has fewer systemic hemodynamic effects in mice than the nonvolatile anesthetics.
Journal ArticleDOI
17β-Estradiol Attenuates the Development of Pressure-Overload Hypertrophy
Martin van Eickels,Christian Grohé,Jack P.M. Cleutjens,Ben J. A. Janssen,Hein J.J. Wellens,Pieter A. Doevendans +5 more
TL;DR: It is shown that E2 attenuates the hypertrophic response to pressure overload in mice, demonstrating that hormone replacement therapy with E2 has direct effects on the heart and may be beneficial in the treatment of postmenopausal women to reduce cardiac hypertrophy.
Journal ArticleDOI
Macrophage MicroRNA-155 Promotes Cardiac Hypertrophy and Failure
Stephane Heymans,Maarten F. Corsten,Wouter Verhesen,Paolo Carai,Rick van Leeuwen,Kevin Custers,Tim Peters,Mark R. Hazebroek,Lauran J. Stöger,Erwin Wijnands,Ben J. A. Janssen,Esther E. Creemers,Yigal M. Pinto,Dirk Grimm,Nina Schürmann,Elena Vigorito,Thomas Thum,Frank R. M. Stassen,Xiaoke Yin,Manuel Mayr,Leon J. De Windt,Esther Lutgens,Kristiaan Wouters,Menno P.J. de Winther,Serena Zacchigna,Mauro Giacca,Marc van Bilsen,Anna-Pia Papageorgiou,Blanche Schroen +28 more
TL;DR: The findings reveal that microRNA-155 expression in macrophages promotes cardiac inflammation, hypertrophy, and failure in response to pressure overload, which supports the causative significance of inflammatory signaling in hypertrophic heart disease and demonstrates the feasibility of therapeutic microRNA targeting of inflammation in heart failure.
Journal ArticleDOI
Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2
TL;DR: The results demonstrated the pathophysiological relevance of caspase-independent, ROS-mediated pathways in response to lethal TNF-induced shock in mice and suggested that survival of TNF toxicity seemed to require a casp enzyme-dependent protective feedback on excessive reactive oxygen species (ROS) formation and phospholipase A2 activation.