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Endoplasmic reticulum stress (ER stress) plays a critical role in neuronal apoptosis along with the aggravation of Alzheimer's disease (AD). Nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-activated transcription factor that is involved in regulating ER stress in Alzheimer's disease (AD), therefore, this protein could be a promising therapeutic target for AD. Vanadium compounds, such as vanadyl acetylacetonate, sodium metavanadate and bis(maltolato)oxovanadium, are well-known as puissant PPARγ modulators. Thus, we are curious whether bis(ethylmaltolato)oxidovanadium (IV) (BEOV) can ameliorate ER stress and subsequent neuronal apoptosis by regulating PPARγ in AD models. To this end, we determined the effect of BEOV on behavioral performance, ER stress and neuronal apoptosis in the triple transgenic mouse AD model (3×Tg-AD). Our results showed that BEOV improved cognitive abilities and reduced the ER stress- and apoptosis-associated proteins in the brains of 3×Tg-AD mice. In vitro administration of BEOV in primary hippocampal neurons and N2asw cells achieved similar results in repressing ER stress. In addition, cotreatment with GW9662 (an antagonist of PPARγ) effectively blocked these neuroprotective effects of BEOV, which provided strong evidence that PPARγ-dependent signaling plays a key role in protecting against ER stress and neuronal apoptosis in AD. In conclusion, our data demonstrated that BEOV alleviated neuronal apoptosis triggered by ER stress by regulating PPARγ in a 3×Tg-AD model.

Anisotropy and inhomogeneity are ubiquitous in spark plasma sintered thermoelectric devices. However, the origin of inhomogeneity in thermoelectric nanocomposites has rarely been investigated so far. Herein, we systematically study the impact of inhomogeneity in spark plasma sintered bismuth antimony telluride (BiSbTe) thermoelectric nanocomposites fabricated from solution-synthesized nanoplates. The figure of merit can reach 1.18, which, however, can be overestimated to 1.88 without considering the inhomogeneity. Our study reveals that the inhomogeneity in thermoelectric properties is attributed to the non-uniformity of porosity, textures and elemental distribution from electron backscatter diffraction and energy-dispersive spectroscopy characterizations. This finding suggests that the optimization of bulk material homogeneity should also be actively pursued in any future thermoelectric material research.

We synthesized Cu3.8Ni/CoO and Cu3.8Ni/MnO nanoparticles via an easy and scalable solution synthesis. The synthesized Cu3.8Ni/CoO and Cu3.8Ni/MnO nanoparticles were annealed to remove the organic surfactants without phase transitions or side reactions. Electrons can be transferred via metallic Cu3.8Ni, which will not react with lithium ions. The heterogeneous structures of Cu3.8Ni/CoO and Cu3.8Ni/MnO nanoparticles could enhance the lithium ion mobility and improve the life cycle, and these materials are therefore promising candidates as high-power-density and high-energy-density anode materials for lithium-ion batteries in diverse applications, such as electrical vehicles.

We demonstrate an easy and scalable low-temperature process to convert porous ternary complex metal oxide nanoparticles from solution-synthesized core/shell metal oxide nanoparticles by thermal annealing. The final products demonstrate superior electrochemical properties with a large capacity and high stability during fast charging/discharging cycles for potential applications as advanced lithium-ion battery (LIB) electrode materials. In addition, a new breakdown mechanism was observed on these novel electrode materials.

Many studies have shown that imbalance of mineral metabolism may play an important role in Alzheimer’s disease (AD) progression. It was recently reported that selenium could reverse memory deficits in AD mouse model. We carried out multi-time-point ionome analysis to investigate the interactions among 15 elements in the brain by using a triple-transgenic mouse model of AD with/without high-dose sodium selenate supplementation. Except selenium, the majority of significantly changed elements showed a reduced level after 6-month selenate supplementation, especially iron whose levels were completely reversed to normal state at almost all examined time points. We then built the elemental correlation network for each time point. Significant and specific elemental correlations and correlation changes were identified, implying a highly complex and dynamic crosstalk between selenium and other elements during long-term supplementation with selenate. Finally, we measured the activities of two important anti-oxidative selenoenzymes, glutathione peroxidase and thioredoxin reductase, and found that they were remarkably increased in the cerebrum of selenate-treated mice, suggesting that selenoenzyme-mediated protection against oxidative stress might also be involved in the therapeutic effect of selenate in AD. Overall, this study should contribute to our understanding of the mechanism related to the potential use of selenate in AD treatment.