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Dick F. van Wichen

Researcher at Utrecht University

Publications -  20
Citations -  4102

Dick F. van Wichen is an academic researcher from Utrecht University. The author has contributed to research in topics: Heart failure & Heart transplantation. The author has an hindex of 16, co-authored 20 publications receiving 3978 citations.

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Constitutive Transcriptional Activation by a β-Catenin-Tcf Complex in APC−/− Colon Carcinoma

TL;DR: Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium.
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The Chemokine and Chemokine Receptor Profile of Infiltrating Cells in the Wall of Arteries With Cardiac Allograft Vasculopathy Is Indicative of a Memory T–Helper 1 Response

TL;DR: In coronary arteries with CAV, most T cells are CD4+ and express human leukocyte antigen DR, and activated TH cells are mainly memory TH1 cells on the basis of their C+CR profile and cytokine expression.
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Left ventricular assist device in end-stage heart failure: Persistence of structural myocyte damage after unloading: An immunohistochemical analysis of the contractile myofilaments

TL;DR: After LVAD support, during a period of 213 +/- 135 days in patients with end-stage HF, severe structural myocyte damage persisted, and this does not support complete recovery of myocyte histologic features.
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Brain natriuretic peptide is produced both by cardiomyocytes and cells infiltrating the heart in patients with severe heart failure supported by a left ventricular assist device.

TL;DR: A significant decrease in serum BNP concentration after LVAD support coincides with a decrease in BNP mRNA and protein expression in the heart, which may play an important role in the reverse remodeling process of the heart.
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Adhesion molecule expression on skin endothelia in atopic dermatitis: Effects of TNF-α and IL-4

TL;DR: Adhesion molecule expression is increased in the skin of patients with AD, and most probably, this increased expression is not a (direct) effect of IL-4 on skin endothelium, but other cytokines, such as TNF-α, might be responsible for this increased adhesion molecules expression.