Discovery of a novel mutation F184S (c.551T>C) in GATA4 gene causing congenital heart disease in a consanguineous Saudi family.

Background & Aim: Congenital heart disease (CHD) is the most common cause of non-infectious deaths in infants worldwide. However, the molecular mechanisms underlying CHD remain unclear. Approximately 30 % of the causes are believed to be genetic mutations and chromosomal abnormalities.

Monitoring Photo-Fenton and Photo-Electro-Fenton process of contaminants emerging concern by a gas diffusion electrode using CaFeW(PO)(OH) nanoparticles as heterogeneous catalyst.

The catalytic performance of modified hydroxyapatite nanoparticles, CaFeW(PO)(OH), was applied for the degradation of methylene blue (MB), fast green FCF (FG) and norfloxacin (NOR). XPS analysis pointed to the successful partial replacement of Ca by Fe. Under photo-electro-Fenton process, the catalyst CaFeWFe(PO)(OH) was combined with UVC radiation and electrogenerated HO in a Printex L6 carbon-based gas diffusion electrode.

Notch and EGFR regulate apoptosis in progenitor cells to ensure gut homeostasis in Drosophila.

The regenerative activity of adult stem cells carries a risk of cancer, particularly in highly renewable tissues. Members of the family of inhibitor of apoptosis proteins (IAPs) inhibit caspases and cell death, and are often deregulated in adult cancers; however, their roles in normal adult tissue homeostasis are unclear. Here, we show that regulation of the number of enterocyte-committed progenitor (enteroblast) cells in the adult Drosophila involves a caspase-mediated physiological apoptosis, which adaptively eliminates excess enteroblast cells produced by intestinal stem cells (ISCs) and, when blocked, can also lead to tumorigenesis.