Tunable band gap of Bi3+-doped anatase TiO2 for enhanced photocatalytic removal of acetaminophen under UV-visible light irradiation

A series of Bi3+-doped TiO2 photocatalysts has been prepared via the propylene oxide (PO) assisted sol-gel method. The effect of Bi3+ doping on structural surface morphology and optical properties of the as-prepared photocatalysts was characterized using UV-Visible (UV-Vis) diffuse reflectance spectroscopy, X-ray diffraction, scanning electron microscopy, energy-dispersive X-ray spectroscopy, Brunauer-Emmett-Teller for determination of the specific surface area and porosity, and X-ray photoelectron spectroscopy. Increasing the Bi3+ doping percentage up to 10 mole percent, resulted in all as-prepared photocatalysts exhibiting pure anatase phase upon calcination at 400 °C for 3 hours. A red shift in optical band gap measurements was observed with increasing Bi3+ ion percent doping, which led to extension of the photocatalysts' activity to the visible region. The enhanced photocatalytic activity for removal of the pharmaceutical compound acetaminophen under UV-Vis light irradiation was demonstrated by comparing bismuth doped as-prepared photocatalysts with pure TiO2 photocatalysts prepared under the same conditions. Based on experimental conditions, the highest activity was achieved using 10 mole percent Bi3+-doped photocatalyst, where over a period of 4 hours more than 98% acetaminophen removal was achieved

Recessive mutations in EPG5 cause Vici syndrome, a multisystem disorder with defective autophagy

Vici syndrome is a recessively inherited multisystem disorder characterized by callosal agenesis, cataracts, cardiomyopathy, combined immunodeficiency and hypopigmentation. To investigate the molecular basis of Vici syndrome, we carried out exome and Sanger sequence analysis in a cohort of 18 affected individuals. We identified recessive mutations in EPG5 (previously KIAA1632), indicating a causative role in Vici syndrome. EPG5 is the human homolog of the metazoan-specific autophagy gene epg-5, encoding a key autophagy regulator (ectopic P-granules autophagy protein 5) implicated in the formation of autolysosomes. Further studies showed a severe block in autophagosomal clearance in muscle and fibroblasts from individuals with mutant EPG5, resulting in the accumulation of autophagic cargo in autophagosomes. These findings position Vici syndrome as a paradigm of human multisystem disorders associated with defective autophagy and suggest a fundamental role of the autophagy pathway in the immune system and the anatomical and functional formation of organs such as the brain and hear