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Using density functional theory combined with the first principles calculation method of non-equilibrium Green's function (NEGF-DFT), we studied the thermoelectric (TE) characteristics of one-dimensional γ-graphdiyne nanoribbons (γ-GDYNRs). The study found that the thermal conductivity of γ-GDYNRs has obvious anisotropy. At the same temperature and geometrical size, the lattice thermal conductivity of zigzag-edged γ-graphdiyne nanoribbons (γ-ZGDYNRs) is much lower than that of armchair-edged γ-graphdiyne nanoribbons (γ-AGDYNRs). We disclose the underlying mechanism for this intrinsic orientation. That is, γ-AGDYNRs have more phonon dispersion over the entire frequency range. Furthermore, the orientation dependence increases when the width of the γ-GDYNRs decreases. These excellent TE properties allow armchair-edged γ-graphdiyne nanoribbons with a planar width of 1.639 nm (γ-Z(2)GDYNRs) to have a higher power factor and lower thermal conductivity, ultimately resulting in a significantly higher TE conversion rate than other γ-GDYNR structures. [ABSTRACT FROM AUTHOR]

The electronic states of fullerene structures are modulated by external environments, such as magnetic fields, electric fields, and stress, which exhibit unique physical properties. Compression, i.e., the application of compressive stress to fullerene structures, plays an important role in modulating the optoelectronic properties of fullerene materials. Herein, we comprehensively investigate the stability, band structures, Bloch wave functions, and optical responses of two-dimensional quasi-tetragonal phase C60 (qTP C60) and quasi-hexagonal phase C60 (qHP C60) under external stress. The findings reveal that qTP C60 and qHP C60 can be stabilized within a certain range based on the regulation of external stress. This kind of stress can considerably alter the band structures of qTP C60 and qHP C60, thereby changing the positions of the highest occupied and lowest unoccupied molecular orbitals. The analysis of Bloch wave functions can help visualize the electronic density distribution of qTP C60 and qHP C60 structures, indicating a considerable influence of stress on the electronic state distribution of the system. This influence results in changes in the band structure, thus affecting the electronic distribution state and optical response. Furthermore, qTP C60 and qHP C60 exhibit surface plasmon effects within a specific wavelength range, suggesting their potential applications in optoelectronic devices. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a toxic metal pollutant that still exists in the environment. The microRNA (miRNA) is a type of noncoding RNA that plays an important role in gene posttranscriptional regulation and disease development. Although the toxic effects of Cd have been extensively studied, studies on the mechanism of Cd from the perspective of miRNA are still limited. So, we established a Cd‐exposure pig model, which confirmed that Cd exposure would cause pig artery damage. The miR‐210 with the most reduced expression and the nuclear factor kappa B (NF‐κB) that had a targeting relationship with miR‐210 were screened. The effect of miR‐210/NF‐κB on the artery damage induced by Cd exposure was investigated by acridine orange/ethidium bromide staining, reactive oxygen species (ROS) staining, quantitative PCR, and western blotting. The results showed that miR‐210 inhibitor, pcDNA‐NF‐κB could induce ROS overproduction in pig hip artery endothelial cells, thus inducing Th1/Th2 imbalance and necroptosis, leading to increased inflammation, while small interfering RNA‐NF‐κB played a mitigating role. In conclusion, Cd can induce artery necroptosis and Th1/Th2 imbalance by regulating the miR‐210/NF‐κB axis, so as to lead to artery inflammatory damage. In this study, we explored the way in which Cd exposure causes artery damage in pig, providing a new perspective on the regulatory damage of miR‐210/NF‐κB axis. [ABSTRACT FROM AUTHOR]

Thioredoxin reductase 3 (Txnrd3) plays a crucial role in antioxidant and anti‐cancer activities, and sperm maturation. The damage of heavy metals, including Nickel (Ni), is the most prominent harm in social development, and hampering Txnrd3 might exacerbate Ni‐induced cardiac damage. In this study, a total of 160 8‐week‐old C57BL/N male mice with 25–30 g weight of Txnrd3+/+ wild‐type and Txnrd3−/− homozygote‐type were randomly divided into eight groups. The mice in the control and Ni groups were gavaged with distilled water and a freshly prepared 10 mg/kg NiCl2 solution. Melatonin (Mel) groups were administered at a concentration of 2 mg/kg for 21 days at the mice's 0.1 ml/10 g body weight. Ni exposure up‐regulated the messenger RNA (mRNA) levels of mitochondrial apoptosis (caspase‐3, caspase‐9, cytochrome c, p53, and BAX), autophagy (LC3, ATG 1, ATG 7, and Beclin‐1), and inflammation (TNF‐α, COX 2, IL‐1β, IL‐2, IL‐6, and IL‐7)‐related markers, but down‐regulated the mRNA levels of BCL‐2, p62 and mTOR (p <.05). Ni exposure decreased the expression of BCL‐2 and p62 protein but increased the expression levels of caspase‐3, caspase‐9, cytochrome c, p53, BAX, ATG 7, Beclin‐1, TNF‐α, COX 2, IL‐1β and IL‐2 protein (p <.05). Ni increased the contents of glutathione disulfide (GSSG) and malondialdehyde (MDA) and decreased the activities of catalase (CAT) and total superoxide dismutase (T‐SOD) (p <.05). Decreased Txnrd3 expression significantly exacerbated changes compared to the Ni exposure (p <.05). Mel significantly attenuated these changes, but the effect decreased when Txnrd3 was inhibited (p <.05). In conclusion, decreased Txnrd3 expression promoted Ni‐induced mitochondrial apoptosis and inflammation via oxidative stress and aggravated heart damage in mice. Decreased Txnrd3 expression significantly reduced the protective effect of Mel to Ni exposure. [ABSTRACT FROM AUTHOR]

Introduction: Nickel (Ni) is widely used in industrial manufacturing and daily life due to its excellent physical and chemical properties. However, Ni has the potential to harm animals' immune system, and spleen is a typical immune organ. Therefore, it is crucial to understand the mechanism of NiCl 2 damage to the spleen. The purpose of this study is to investigate the effects of different concentrations of NiCl 2 exposure and intervening with strong antioxidants on spleen lymphocytes to better understand the damage mechanism of Ni on spleen lymphocytes., Methods: In this experiment, mice spleen lymphocytes were used as the research object. We first measured the degree of oxidative stress, inflammation, and necroptosis caused by different NiCl 2 concentrations. Subsequently, we added the powerful antioxidant N-acetyl-L-cysteine (NAC) and used hydrogen peroxide (H 2 O 2 ) as the positive control in subsequent experiments., Results: Our findings demonstrated that NiCl 2 could cause spleen lymphocytes to produce a large number of reactive oxygen species (ROS), which reduced the mRNA level of antioxidant enzyme-related genes, the changes in GSH-PX, SOD, T-AOC, and MDA, the same to the mitochondrial membrane potential. ROS caused the body to produce an inflammatory response, which was manifested by tumor necrosis factor (TNF-α) in an immunofluorescence experiment, and the mRNA level of related inflammatory genes significantly increased. In the case of caspase 8 inhibition, TNF-α could cause the occurrence of necroptosis mediated by RIP1, RIP3, and MLKL. AO/EB revealed that spleen lymphocytes exposed to NiCl 2 had significant necroptosis, and the mRNA and protein levels of RIP1, RIP3, and MLKL increased significantly. Moreover, the findings demonstrated that NAC acted as an antioxidant to reduce oxidative stress, inflammation, and necroptosis caused by NiCl 2 exposure., Discussion: Our findings showed that NiCl 2 could cause oxidative stress, inflammation, and necroptosis in mice spleen lymphocytes, which could be mitigated in part by NAC. The study provides a point of reference for understanding the toxicological effect of NiCl 2 . The study suggests that NAC may be useful in reducing the toxicological effect of NiCl 2 on the immune system. The research may contribute to the development of effective measures to prevent and mitigate the toxicological effects of NiCl 2 on the immune system., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Zhang, Xu, Ma, Shi, Liu, Song, Fang, Liu, Qiao, Cai and Zhang.)