3D printing critical materials for rechargeable batteries: from materials, design and optimization strategies to applications

Three-dimensional (3D) printing, an additive manufacturing technique, is widely employed for the fabrication of various electrochemical energy storage devices (EESDs), such as batteries and supercapacitors, ranging from nanoscale to macroscale. This technique offers excellent manufacturing flexibility, geometric designability, cost-effectiveness, and eco-friendliness. Recent studies have focused on the utilization of 3D-printed critical materials for EESDs, which have demonstrated remarkable electrochemical performances, including high energy densities and rate capabilities, attributed to improved ion/electron transport abilities and fast kinetics. However, there is a lack of comprehensive reviews summarizing and discussing the recent advancements in the structural design and application of 3D-printed critical materials for EESDs, particularly rechargeable batteries. In this review, we primarily concentrate on the current progress in 3D printing (3DP) critical materials for emerging batteries. We commence by outlining the key characteristics of major 3DP methods employed for fabricating EESDs, encompassing design principles, materials selection, and optimization strategies. Subsequently, we summarize the recent advancements in 3D-printed critical materials (anode, cathode, electrolyte, separator, and current collector) for secondary batteries, including conventional Li-ion (LIBs), Na-ion (SIBs), K-ion (KIBs) batteries, as well as Li/Na/K/Zn metal batteries, Zn-air batteries, and Ni–Fe batteries. Within these sections, we discuss the 3DP precursor, designprinciples of 3D structures, and working mechanisms of the electrodes. Finally, we address the major challenges and potential applications in the development of 3D-printed critical materials for rechargeable batteries

Associations of serum DNA methylation levels of chemokine signaling pathway genes with mild cognitive impairment (MCI) and Alzheimer's disease (AD).

ObjectiveTo investigate the associations of serum DNA methylation levels of chemokine signaling pathway genes with Alzheimer's disease (AD) and mild cognitive impairment (MCI) in elderly people in Xinjiang, China, and to screen out genes whose DNA methylation could distinguish AD and MCI.Materials and methods37 AD, 40 MCI and 80 controls were included in the present study. DNA methylation assay was done using quantitative methylation-specific polymerase chain reaction (qMSP). Genotyping was done using Sanger sequencing.ResultsDNA methylation levels of ADCY2, MAP2K1 and AKT1 were significantly different among AD, MCI and controls. In the comparisons of each two groups, AKT1 and MAP2K1's methylation was both significantly different between AD and MCI (p ConclusionThis study found that the serum of AKT1 hypermethylation is related to AD independently of APOE ε4, which was differentially expressed in the Entorhinal Cortex of the brain and was an independent risk factor for AD. It could be used as one of the candidate serum markers to distinguish AD and MCI. Serum of MAP2K1 hypomethylation is an independent risk factor for MCI

LncRNA Expression Profile of Human Thoracic Aortic Dissection by High-Throughput Sequencing

Background/Aims: In this study, the long non-coding RNA (lncRNA) expression profile in human thoracic aortic dissection (TAD), a highly lethal cardiovascular disease, was investigated. Methods: Human TAD (n=3) and normal aortic tissues (NA) (n=3) were examined by high-throughput sequencing. Bioinformatics analyses were performed to predict the roles of aberrantly expressed lncRNAs. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to validate the results. Results: A total of 269 lncRNAs (159 up-regulated and 110 down-regulated) and 2, 255 mRNAs (1 294 up-regulated and 961 down-regulated) were aberrantly expressed in human TAD (fold-change> 1.5, P< 0.05). QRT-PCR results of five dysregulated genes were consistent with HTS data. A lncRNA-mRNA coexpression analysis showed positive correlations between the up-regulated lncRNA (ENSG00000269936) and its adjacent up-regulated mRNA (MAP2K6, R=0.940, P< 0.01), and between the down-regulated lncRNA_1421 and its down-regulated mRNAs (FBLN5, R=0.950, P< 0.01; ACTA2, R=0.96, P< 0.01; TIMP3, R=0.96, P< 0.05). The lncRNA-miRNA-mRNA network indicated that the up-regulated lncRNA XIST and p21 had similar sequences targeted by has-miR-17-5p. The results of luciferase assay and fluorescence immuno-cytochemistry were consistent with that. And qRT-PCR results showed that lncRNA XIST and p21 were expressed at a higher level and has-miR-17-5p was expressed at a lower level in TAD than in NA. The predicted binding motifs of three up-regulated lncRNAs (ENSG00000248508, ENSG00000226530, and EG00000259719) were correlated with up-regulated RUNX1 (R=0.982, P< 0.001; R=0.967, P< 0.01; R=0.960, P< 0.01, respectively). Conclusions: Our study revealed a set of dysregulated lncRNAs and predicted their multiple potential functions in human TAD. These findings suggest that lncRNAs are novel potential therapeutic targets for human TAD

Galphai1 and Galphai3 regulate macrophage polarization by forming a complex containing CD14 and Gab1

Heterotrimeric G proteins have been implicated in Toll-like receptor 4 (TLR4) signaling in macrophages and endothelial cells. However, whether guanine nucleotide-binding protein G(i) subunit alpha-1 and alpha-3 (Gαi1/3) are required for LPS responses remains unclear, and if so, the underlying mechanisms need to be studied. In this study, we demonstrated that, in response to LPS, Gαi1/3 form complexes containing the pattern recognition receptor (PRR) CD14 and growth factor receptor binding 2 (Grb2)-associated binding protein (Gab1), which are required for activation of PI3K-Akt signaling. Gαi1/3 deficiency decreased LPS-induced TLR4 endocytosis, which was associated with decreased phosphorylation of IFN regulatory factor 3 (IRF3). Gαi1/3 knockdown in bone marrow-derived macrophage cells (Gαi1/3 KD BMDMs) exhibited an M2-like phenotype with significantly suppressed production of TNF-α, IL-6, IL-12, and NO in response to LPS. The altered polarization coincidedwith decreased Akt activation. Further, Gαi1/3 deficiency caused LPS tolerance in mice. In vitro studies revealed that, in LPS-tolerant macrophages, Gαi1/3 were down-regulated partially by the proteasome pathway. Collectively, the present findings demonstrated that Gαi1/3 can interact with CD14/Gab1, which modulates macrophage polarization in vitro and in vivo.Fil: Li, Xiaolin. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Wang, Duowei. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Chen, Zen. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Lu, Ermei. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Wang, Zhuo. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Duan, Jingjing. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Tian, Wei. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Wang, Yun. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: You, Linjun. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Zou, Yulian. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Cheng, Yan. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Zhu, Qingyi. Jiangsu Province Hospital of Traditional Chinese Medicine. Departament of Urology; ChinaFil: Wan, Xiaojian. Second Military Medical University. Department of Anesthesiology and Intensive Care Medicine, Changhai Hospita; ChinaFil: Xia, Tao. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; ChinaFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences. Laboratory of Neurobiology, ; Estados UnidosFil: Yang, Yong. China Pharmaceutical University. Center for New Drug Safety Evaluation and Research; Chin