Search

Climate change is intensifying extreme weather events in coastal areas, leading to more frequent discharge of untreated wastewater containing human viruses into coastal waters. This poses a health risk, especially during heatwaves when bathing activity increases. A study examined the survival and viability of seven common wastewater viruses in seawater at different temperatures. Viral genomes were quantified using direct qPCR, whilst viability was assessed using Capsid Integrity qPCR. Results showed that T90 values from direct qPCR were much higher than those from CI-qPCR, suggesting that risk mitigation should be based on viral integrity tests. All viruses remained potentially viable for at least 72 h in environmental seawater and longer in sterile artificial seawater, highlighting the importance of biotic processes in viral inactivation. Viral persistence decreased with increasing temperature. Whilst heatwaves may partially reduce risks from human viral pathogens in coastal waters, they do not eliminate them entirely., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The orphan nuclear receptor liver receptor homologue-1 (LRH-1) has roles in the development, cholesterol and bile acid homeostasis, and steroidogenesis. It also enhances proliferation and cell cycle progression of cancer cells. In breast cancer, LRH-1 expression is associated with invasive breast cancer; positively correlates with ERα status and aromatase activity; and promotes oestrogen-dependent cell proliferation. However, the mechanism of action of LRH-1 in breast cancer epithelial cells is still not clear. By silencing or over-expressing LRH-1 in ER-positive MCF-7 and ER-negative MDA-MB-231 breast cancer cells, we have demonstrated that LRH-1 promotes motility and cell invasiveness. Similar effects were observed in the non-tumourigenic mammary epithelial cell line, MCF-10A. Remodelling of the actin cytoskeleton and E-cadherin cleavage was observed with LRH-1 over-expression, contributing to increased migratory and invasive properties. Additionally, in LRH-1 over-expressing cells, the truncation of the 120 kDa E-cadherin to the inactive 97 kDa form was observed. These post-translational modifications in E-cadherin may be associated with LRH-1-dependent changes to matrix metalloproteinase 9 expression. These findings suggest a new role of LRH-1 in promoting migration and invasion in breast cancer, independent of oestrogen sensitivity. Therefore, LRH-1 may represent a new target for breast cancer therapeutics.