Immobilization of cross-linked In-doped Mo(O,S)2 on cellulose nanofiber for effective organic-compound degradation under visible light illumination

Relatively small amounts of In-doped Mo(O,S)₂ (IMS) catalysts (10%, 20%, and 30%) were deposited on cellulose nanofiber (CNF) by cross-linking them with functional groups of siloxane and epoxy to form CNF-IMS hybrid composites. The as-prepared hybrid composites were characterized and tested their performances toward the photo degradations of cationic (MB and RhB) and anionic (MO) dyes. As indium was doped into Mo(O,S)₂ lattice to form solid-solution, the charge transfer and photocarrier separation during the catalytic reaction were simultaneously enhanced as probed with electrochemical impedance spectroscopy and photoluminescence measurements, respectively. To ensure the catalyst on CNF was well deposited and recyclable, the hybrid composite was evaluated with a reusability experiment to show the stability performance in degrading organic dyes. It was found the environmentally friendly CNF-IMS hybrid composite was relatively stable during the reusability experiment, indicating no catalyst powder was leached out during the photocatalytic reaction. The photoreaction mechanism was convinced by radical-scavenging experiments to show that hydroxyl and superoxide played essential roles for the organic dye degradations in visible-light illuminated conditions. The cross-linked organic/inorganic hybrid catalyst showed a prospective visible light active material not only to solve the environmental issue due to the leaching of nanoparticles but also to lower the post-treatment/recycling cost of photocatalyst in industrial application.     

Pericytes are required for blood-brain barrier integrity during embryogenesis

Vascular endothelial cells in the central nervous system (CNS) form a barrier that restricts the movement of molecules and ions between the blood and the brain. This blood-brain barrier (BBB) is crucial to ensure proper neuronal function and protect the CNS from injury and disease. Transplantation studies have demonstrated that the BBB is not intrinsic to the endothelial cells, but is induced by interactions with the neural cells. Owing to the close spatial relationship between astrocytes and endothelial cells, it has been hypothesized that astrocytes induce this critical barrier postnatally, but the timing of BBB formation has been controversial. Here we demonstrate that the barrier is formed during embryogenesis as endothelial cells invade the CNS and pericytes are recruited to the nascent vessels, over a week before astrocyte generation. Analysing mice with null and hypomorphic alleles of Pdgfrb, which have defects in pericyte generation, we demonstrate that pericytes are necessary for the formation of the BBB, and that absolute pericyte coverage determines relative vascular permeability. We demonstrate that pericytes regulate functional aspects of the BBB, including the formation of tight junctions and vesicle trafficking in CNS endothelial cells. Pericytes do not induce BBB-specific gene expression in CNS endothelial cells, but inhibit the expression of molecules that increase vascular permeability and CNS immune cell infiltration. These data indicate that pericyte-endothelial cell interactions are critical to regulate the BBB during development, and disruption of these interactions may lead to BBB dysfunction and neuroinflammation during CNS injury and disease.