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Metal oxide has a high energy bandgap and passes the visible light to enlighten the vision to human eyes. However, the strong and harmful UV light is easily captured by large bandgap metal oxide materials. One of the promising applications of metal oxide manipulation would be the transparent solar cells for the transparent window, to guarantee the view of visible light and generate electric power from the invisible UV radiation. Herein, we demonstrate the all-transparent photovoltaics for see-through applications with the functional deployment of TiO2 layer. P-type NiO and n-type ZnO form a heterojunction to establish a photovoltage. TiO2 layer with donor concentration >1019 cm−3 has flat-band potential of 0.4 V vs reversible hydrogen electrode (RHE) and is significantly higher than that of the photoactive ZnO layer, TiO2 layer insertion enables the multifunctions of giving a back surface field and also serving as a carrier selective transport layer. The ultrathin TiO2 embedded ZnO/NiO device has Ag nanowire top electrode and is highly transparent (>50%) in the visible range. This transparent solar cell provides power conversion efficiency of 6.1% and incident photon to charge carrier efficiency of 79.5% under UV light illumination. Mott-Schottky analysis showed the flat band potential to be 0.9 V by using the TiO2 layer insertion to induce the significant higher photovoltage and photocurrent on/off ratio of higher than 5 × 105 and played a vital role in the enhanced performance of ZnO/NiO heterostructure. We demonstrated the enhancement of the minority carrier lifetime for a broadband of light illumination via back surface field formation and proposed the energy band-diagram. We may suggest that this high transparent photovoltaic device can be functionally applied on-demands of power generation windows of electronic devices, vehicles and buildings.

Reactive microglia are a major pathological feature of Alzheimer's disease (AD). However, the exact role of microglia in AD pathogenesis is still unclear. Here, using metabolic profiling, we found that exposure to amyloid-β triggers acute microglial inflammation accompanied by metabolic reprogramming from oxidative phosphorylation to glycolysis. It was dependent on the mTOR-HIF-1α pathway. However, once activated, microglia reached a chronic tolerant phase as a result of broad defects in energy metabolisms and subsequently diminished immune responses, including cytokine secretion and phagocytosis. Using genome-wide RNA sequencing and multiphoton microscopy techniques, we further identified metabolically defective microglia in 5XFAD mice, an AD mouse model. Finally, we showed that metabolic boosting with recombinant interferon-γ treatment reversed the defective glycolytic metabolism and inflammatory functions of microglia, thereby mitigating the AD pathology of 5XFAD mice. Collectively, metabolic reprogramming is crucial for microglial functions in AD, and modulating metabolism might be a new therapeutic strategy for AD.