Solar energy is readily available in most climates and can be used for water purification. However, solar disinfection of drinking water mostly relies on ultraviolet light, which represents only 4% of the total solar energy, and this leads to a slow treatment speed. Therefore, the development of new materials that can harvest visible light for water disinfection, and so speed up solar water purification, is highly desirable. Here we show that few-layered vertically aligned MoS (FLV-MoS) films can be used to harvest the whole spectrum of visible light (∼50% of solar energy) and achieve highly efficient water disinfection. The bandgap of MoS was increased from 1.3 to 1.55 eV by decreasing the domain size, which allowed the FLV-MoS to generate reactive oxygen species (ROS) for bacterial inactivation in the water. The FLV-MoS showed a ∼15 times better log inactivation efficiency of the indicator bacteria compared with that of bulk MoS, and a much faster inactivation of bacteria under both visible light and sunlight illumination compared with the widely used TiO. Moreover, by using a 5 nm copper film on top of the FLV-MoS as a catalyst to facilitate electron-hole pair separation and promote the generation of ROS, the disinfection rate was increased a further sixfold. With our approach, we achieved water disinfection of >99.999% inactivation of bacteria in 20 min with a small amount of material (1.6 mg l) under simulated visible light.
Summary
Gene-editing technologies have made it feasible to create nonhuman
primate models for human genetic disorders. Here, we report detailed genotypes
and phenotypes of TALEN-edited MECP2 mutant cynomolgus monkeys
serving as a model for a neurodevelopmental disorder, Rett syndrome (RTT), which
is caused by loss-of-function mutations in the human MECP2
gene. Male mutant monkeys were embryonic lethal, reiterating that RTT is a
disease of females. Through a battery of behavioral analyses, including
primate-unique eye-tracking tests, in combination with brain imaging via MRI, we
found a series of physiological, behavioral, and structural abnormalities
resembling clinical manifestations of RTT. Moreover, blood transcriptome
profiling revealed that mutant monkeys resembled RTT patients in immune gene
dysregulation. Taken together, the stark similarity in phenotype and/or
endophenotype between monkeys and patients suggested that gene-edited RTT
founder monkeys would be of value for disease mechanistic studies as well as
development of potential therapeutic interventions for RTT.
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