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HighlightsInterfacial bonding strategy has been successfully applied to address the high overpotential issue of sacrificial additives, which reduced the decompositon potential of Na2C2O4 from 4.50 to 3.95 V.Ultra-low-dose technique assisted commercial sodium ion capacitor (AC//HC) could deliver a remarkable energy density of 118.2 Wh kg−1 as well as excellent cycle stability.In-depth decomposition mechanism of sacrificial compound and the relative influence after pre-metallation were revealed by advanced in situ and ex situ characterization approaches.Sacrificial pre-metallation strategy could compensate for the irreversible consumption of metal ions and reduce the potential of anode, thereby elevating the cycle performance as well as open-circuit voltage for full metal ion capacitors (MICs). However, suffered from massive-dosage abuse, exorbitant decomposition potential, and side effects of decomposition residue, the wide application of sacrificial approach was restricted. Herein, assisted with density functional theory calculations, strongly coupled interface (M–O–C, M = Li/Na/K) and electron donating group have been put forward to regulate the band gap and highest occupied molecular orbital level of metal oxalate (M2C2O4), reducing polarization phenomenon and Gibbs free energy required for decomposition, which eventually decrease the practical decomposition potential from 4.50 to 3.95 V. Remarkably, full sodium ion capacitors constituted of commercial materials (activated carbon//hard carbon) could deliver a prominent energy density of 118.2 Wh kg−1 as well as excellent cycle stability under an ultra-low dosage pre-sodiation reagent of 15–30 wt% (far less than currently 100 wt%). Noteworthily, decomposition mechanism of sacrificial compound and the relative influence on the system of MICs after pre-metallation were initially revealed by in situ differential electrochemical mass spectrometry, offering in-depth insights for comprehending the function of cathode additives. In addition, this breakthrough has been successfully utilized in high performance lithium/potassium ion capacitors with Li2C2O4/K2C2O4 as pre-metallation reagent, which will convincingly promote the commercialization of MICs.

Carbonaceous materials have been regarded as highly promising anode candidates for potassium storage with their cost‐effectiveness and environmental benignity. However, low specific capacity and difficulty in large‐scale synthesis largely hinder their further development. Herein, a thermal‐induced potassium–carbon alloy phase (KxCy) with the expanded interlayer spacing strategy is first put forward. Through in situ high‐temperature X‐ray diffraction, a K2C2 phase is evoked by thermal energy during the in‐situ carbonization process of carbon quantum dots intermediate derived from potassium‐containing precursors, whereas no lithium or sodium–carbon alloy phase is observed from lithium/sodium‐containing precursors. The as‐obtained ultra‐thin carbon nanosheets achieve adjustable layer spacing, preparation in bulk, delivering reversible potassium storage of 403.4 mAh g−1 at 100 mA g−1 and 161.2 mAh g−1 even at 5.0 A g−1, which is one of the most impressive K‐storage performances reported so far with great potential application. Furthermore, the assembled potassium‐ion hybrid capacitor by combining the impressive CFMs‐900 anode with the three‐dimensional framework‐activated carbon delivers a high energy‐power density of 251.7 Wh kg−1 at 250 W kg−1 with long‐term stability. This study opens a scalable avenue to realize the expanded interlayer spacing, which can be extended to other multicarboxyl potassium salts and can provide approach for the design of high‐performance carbon anode materials for potassium storage. A thermal‐induced KxCy with an expanded interlayer spacing strategy is first proposed in this manuscript, which enables highly reversible potassium‐storage capability with superior long‐term cycling stability. In situ high‐temperature X‐ray diffraction and high‐resolution transmission electron microscopy techniques have been utilized to demonstrate the existence of the K2C2 phase and the evoked carbon expanded interlayer, which successfully validates the feasibility of the offered strategy.

Carbonaceous materials have been regarded as highly promising anode candidates for potassium storage with their cost‐effectiveness and environmental benignity. However, low specific capacity and difficulty in large‐scale synthesis largely hinder their further development. Herein, a thermal‐induced potassium–carbon alloy phase (K x C y ) with the expanded interlayer spacing strategy is first put forward. Through in situ high‐temperature X‐ray diffraction, a K 2 C 2 phase is evoked by thermal energy during the in‐situ carbonization process of carbon quantum dots intermediate derived from potassium‐containing precursors, whereas no lithium or sodium–carbon alloy phase is observed from lithium/sodium‐containing precursors. The as‐obtained ultra‐thin carbon nanosheets achieve adjustable layer spacing, preparation in bulk, delivering reversible potassium storage of 403.4 mAh g −1 at 100 mA g −1 and 161.2 mAh g −1 even at 5.0 A g −1 , which is one of the most impressive K‐storage performances reported so far with great potential application. Furthermore, the assembled potassium‐ion hybrid capacitor by combining the impressive CFMs‐900 anode with the three‐dimensional framework‐activated carbon delivers a high energy‐power density of 251.7 Wh kg −1 at 250 W kg −1 with long‐term stability. This study opens a scalable avenue to realize the expanded interlayer spacing, which can be extended to other multicarboxyl potassium salts and can provide approach for the design of high‐performance carbon anode materials for potassium storage.

Mitochondrial ROS can facilitate the release of higher levels of cytochrome C by participating in the formation of apoptosome, leading to the decrease of enzyme activities of mitochondrial complexes I, IV and V, which may be associated with swelling of mitochondria and its depolarization.1 Moreover, mitochondria are closely related to programmed cell death, with mtDNA involved in apoptosis, Neutrophil extracellular traps (NETs) and pyroptosis can induce immune inflammation via the cGAS-Sting pathway.2 Mitochondrial dysfunction may cause abnormal redox reaction, decreased functioning of biogenesis-related enzymes, increased NETosis, harmful cytokine effects, and aberrant lymphocyte behavior.3 SLE is closely related to mitochondrial dysfunction and overproduction of ROS.4 The mitochondrial respiratory chain (RC) is the site of adenosine triphosphate (ATP) synthesis and ROS generation. The mitochondrially encoded cytochrome c oxidase 1 (MT-CO1) gene encodes a crucial subunit of the RC complex IV.5 Decreased complex IV activity is related to increased oxidative stress in MT-CO1 mutants.6 Our previous research revealed the high mutation rate of MT-CO1 and its low messenger ribonucleic acid (mRNA) and protein levels in blood samples from MRL/lpr mice were related to decreased antioxidant capacity, indicating that the MT-CO1 gene of the mitochondrial RC in MRL/lpr mice is susceptible to ROS-induced oxidative damage.7 SLE is an autoimmune disease that leads to damage in multiple organs and systems. The distribution of mitochondria in various organs and tissues depends on energetic demands and age-related changes. [...]in the present study, we aimed to investigate the distinct functional characteristics of MT-CO1 and MDA levels in nine organs/tissues of MRL/lpr mice at different ages and to examine the potential mechanisms of SLE. [...]the skin was cut away from the head of each mouse, and the brain tissue was subsequently dissected.

Microglia are resident macrophages within the central nervous system, serving as the first responders to neuroinflammation. Glucocorticoids (GCs) may cause damage to brain tissue, but the specific mechanism remains unclear. This study was divided into two parts: a glucocorticoid receptor (GR) mitochondrial translocation intervention experiment and a mitochondrial oxidative stress inhibition experiment. BV-2 microglia were stimulated with dexamethasone (DEX) and treated with either tubastatin-A or mitoquinone (MitoQ) for 24 h. Our results showed that DEX increased the translocation of GRs to mitochondria, and this effect was accompanied by decreases in the expression of mitochondrially encoded cytochrome c oxidase 1 (MT-CO1) and mitochondrially encoded cytochrome c oxidase 3 (MT-CO3) and increases in the expression of NOD-like receptor thermal protein domain–associated protein 3 (NLRP3), caspase-1, and Gasdermin D (GSDMD). The level of mitochondrial respiratory chain complex IV (MRCC IV) and adenosine triphosphate (ATP) was decreased. An elevation in the level of mitochondrial oxidative stress and the opening of the mitochondrial permeability transition pore (mPTP) was also observed. Mechanistically, tubastatin-A significantly suppressed the mitochondrial translocation of GRs, improved the expression of mitochondrial genes, promoted the restoration of mitochondrial function, and inhibited pyroptosis. MitoQ significantly prevented mitochondrial oxidative stress, improved mitochondrial function, and reduced apoptosis and pyroptosis. Both tubastatin-A and MitoQ suppressed DEX-induced pyroptosis. This study substantiates that the increase in the mitochondrial translocation of GRs mediated by GCs exacerbates oxidative stress and pyroptosis in microglia, which indicates that the regulation of mitochondrial pathways by GCs is pathogenic to microglia.The increase in mitochondrial translocation of GRs mediated by GCs aggravates mitochondrial dysfunction and oxidative stress, leading to pyroptosis in BV-2 microglia. Tubastatin-A and MitoQ can inhibit GR translocation and oxidative stress in mitochondria, respectively, and these effects can inhibit pyroptosis and other damage induced by GCs to microglia.

The aim of the present study was to investigate the direct effects of BMS-202 on melanoma cells. The small molecule programmed cell death ligand 1 (PD-L1) inhibitor BMS-202 was used to treat A375 melanoma cells. The cell distribution of BMS-202 was examined using low-power and high-resolution confocal microscopy, focusing on its localization in mitochondria. The impact of BMS-202 on mitochondrial gene expression levels, the activity of respiratory chain complexes, and the levels of reactive oxygen species and apoptosis-related genes, including Bax, Bcl-2, PARP and caspase-3, were assessed by quantitative PCR and western blotting. Additionally, tumor cell viability, proliferation, migration and invasion were evaluated in vitro, with in vivo experiments conducted through the construction of tumor-bearing mouse models and Ki-67 immunohistochemical staining to validate tumor proliferation. The function of mitochondria was inhibited using a pyruvate carrier inhibitor to examine how this affected the action of BMS-202. The results revealed that BMS-202 can inhibit tumor cell function and promote apoptosis. Furthermore, BMS-202 was shown to enter the mitochondria where it may bind to PD-L1 and improve mitochondrial function. By inhibiting mitochondrial function, the antitumor effects of BMS-202 can be enhanced. Overall, the present study provides information on the potential antitumor mechanisms of BMS-202 as well as a theoretical basis for its application in melanoma therapy.

Background Endometrial cancer (EC) is the most prevalent malignancy worldwide. Although several efforts had been made to explore the molecular mechanism responsible for EC progression, it is still not fully understood. Aim of the study To evaluate the clinical characteristics and prognostic factors of patients with EC, and further to search for novel genes associated with EC progression. Methods We recruited 328 patients with EC and analyzed prognostic factors using Cox proportional hazard regression model. Further, a gene expression profile of EC was used to identify the differentially expressed genes (DEGs) between normal samples and tumor samples. Subsequently, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis ( http://www.genome.jp/kegg/ ) for DEGs were performed, and then protein–protein interaction (PPI) network of DEGs as well as the subnetwork of PPI were constructed with plug-in, MCODE by mapping DEGs into the Search Tool for the Retrieval of Interacting Genes database. Results Our results showed that body mass index (BMI), hypertension, myometrial invasion, pathological type, and Glut4 positive expression were prognostic factors in EC ( P  < 0.05). Bioinformatics analysis showed that upregulated DEGs were associated with cell cycle, and downregulated DEGs were related to MAPK pathway. Meanwhile, PPI network analysis revealed that upregulated CDK1 and CCNA2 as well as downregulated JUN and FOS were listed in top two nodes with high degrees. Conclusions Patients with EC should be given more focused attentions in respect of pathological type, BMI, hypertension, and Glut4-positive expression. In addition, CDK1 , CCNA2 , JUN , and FOS might play important roles in EC development.

The S100/calgranulin gene appears to modulate neuroinflammation following cerebral ischemia and could be a valuable biomarker for stroke prognosis, according to growing research. This study aimed at evaluating the correlation between calgranulin gene variants and susceptibility to ischemic stroke (IS) in the Southern Chinese population. Using an enhanced multi-temperature ligase detection reaction genotyping, 310 IS patients and 324 age-matched healthy controls were genotyped to identify five calgranulin gene variants. According to the obtained results, the S100A8 rs3795391, rs3806232, and S100A12 rs2916191 variants were linked to a higher risk of IS, while the S100A9 rs3014866 variant was associated with a lower risk of IS. Moreover, the T-T-C-A-T, T-T-C-G-T, or C-C-C-G-C haplotypes have been linked to a greater risk of developing IS, according to haplotype analysis. The occurrence of the variant C allele there in S100A8 rs3795391, rs3806232, and S100A12 rs2916191 variants may impart a greater risk of stroke in the LAA subtype, according to further stratification by IS subtypes, while the T allele of the S100A9 rs3014866 variant may be linked to a reduced risk of stroke of all subtypes. Furthermore, patients with the variant C allele of the S100A8 rs3795391, rs3806232, and S100A12 rs2916191 variants presented with increased circulating S100A8 and S100A12 levels and larger infarct volumes relative to those with the major TT genotype. Our findings suggest that calgranulin gene variants are linked to IS susceptibility, implying that the calgranulin gene may be a potential biomarker for IS prevention and personalized treatment.