Salt water intrusion through the New Sea Lock of IJmuiden, Netherlands requires mitigation to ensure availability of enough fresh water further inland. For this purpose, a salt screen has been proposed for selective withdrawal of salt water from the Noordzeekanaal in the vicinity of the lock complex. Formulas to assess the withdrawal rate of selective withdrawal are based on idealized layouts and conditions. In the case of IJmuiden, the flow surrounding a salt screen has a strong nonuniform character, such that these formulas are not applicable to predict the correct withdrawal rate and the effectiveness of selective withdrawal accurately. In this case physical scale modeling or computational fluid dynamics (CFD) modeling can be applied. This article discusses the limitations of the formulas for a three-dimensional (3D) flow application near the locks of IJmuiden and presents the use of CFD and physical scale model research to assess the flow patterns around the salt screen and the effectiveness of selective withdrawal. The CFD model was validated against the physical scale model and represented the complex flow fields around the salt screen to within acceptable deviations for both steady and transient states. This gives confidence in applying these more advanced modeling tools for the design and positioning of salt screens in confined complex 3D flow areas.

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Background & Aims The polycomb repressive complex 2 (PRC2) regulates differentiation by contributing to repression of gene expression and thereby stabilizing the fate of stem cells and their progeny. PRC2 helps to maintain adult stem cell populations, but little is known about its functions in intestinal stem cells. We studied phenotypes of mice with intestine-specific deletion of the PRC2 proteins embryonic ectoderm development (EED) (a subunit required for PRC2 function) and enhancer of zeste homolog 2 (EZH2) (a histone methyltransferase). Methods We performed studies of AhCre;EedLoxP/LoxP (EED knockout) mice and AhCre;Ezh2LoxP/LoxP (EZH2 knockout) mice, which have intestine-specific disruption in EED and EZH2, respectively. Small intestinal crypts were isolated and subsequently cultured to grow organoids. Intestines and organoids were analyzed by immunohistochemical, in situ hybridization, RNA sequence, and chromatin immunoprecipitation methods. Results Intestines of EED knockout mice had massive crypt degeneration and lower numbers of proliferating cells compared with wild-type control mice. Cdkn2a became derepressed and we detected increased levels of P21. We did not observe any differences between EZH2 knockout and control mice. Intestinal crypts from EED knockout mice had signs of aberrant differentiation of uncommitted crypt cells—these differentiated toward the secretory cell lineage. Furthermore, crypts from EED-knockout mice had impaired Wnt signaling and concomitant loss of intestinal stem cells, this phenotype was not reversed upon ectopic stimulation of Wnt and Notch signaling in organoids. Analysis of gene expression patterns from intestinal tissues of EED knockout mice showed dysregulation of several genes involved in Wnt signaling. Wnt signaling was regulated directly by PRC2. Conclusions In intestinal tissues of mice, PRC2 maintains small intestinal stem cells by promoting proliferation and preventing differentiation in the intestinal stem cell compartment. PRC2 controls gene expression in multiple signaling pathways that regulate intestinal homeostasis. Sequencing data are available in the genomics data repository GEO under reference series GSE81578; RNA sequencing data are available under subseries GSE81576; and ChIP sequencing data are available under subseries GSE81577. @en