https://www.selleckchem.com/products/esi-09.html In preeclampsia (PE), preexistent maternal endothelial dysfunction leads to impaired placentation and vascular maladaptation. Long noncoding RNAs (lncRNAs) have been shown to participate in the placentation process. LncRNA fms-related tyrosine kinase 1 pseudogene 1 (FLT1P1) was previously reported to be upregulated in PE. In this study, we verified the effect of FLT1P1 and its cognate gene FLT1 on trophoblast cell proliferation and angiogenesis by using Cell Counting Kit-8 (CCK-8) assay, tube formation assay, and western blot analysis. Their binding to RNA binding protein dyskeratosis congenita 1 (DKC1) was validated by conducting RNA immunoprecipitation (RIP) and RNA pulldown assays. In this study, knockdown of FLT1P1 or FLT1 was found to promote cell proliferation and angiogenesis in trophoblasts. In addition, FLT1P1 recruited DKC1 to stabilize FLT1. Importantly, silencing FLT1P1 or DKC1 decreased the stability of FLT1. Rescue assays revealed that FLT1 overexpression reversed the effect of silenced FLT1P1. Overall, FLT1P1 cooperates with DKC1 to restrain trophoblast cell proliferation and angiogenesis by targeting FLT1. A detonation of nuclear weapon (NW) is considered as one of the most devastating radiological scenarios in the list of modern global threats. An essential proportion of victims in a mass casualty radiation event may require an immediate medical care due to radiation combined injuries (RCI). Surprisingly, there is a lack of clear guidance for quantitative prognosis of the spatial distribution of expected RCI casesin a given nuclear explosion scenario. This work is aimed at the presentation of a new, improved model, allowing more confident evaluation of the contributions from different NW destructive forces to RCI formation, thus leading to more accurate approximation of the zone around the epicentre for a guided search for RCI cases. The model is made compatible with a classic approach and provides th