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Lithium-ion batteries (LIBs) has been developed over the last three decades. Increased amount of silicon (Si) is added into graphite anode to increase the energy density of LIBs. However, the amount of Si is limited, due to its structural instability and poor electronic conductivity so a novel approach is needed to overcome these issues. In this work, the synthesized chromium silicide (CrSi2) doped Si nanoparticle anode material achieves an initial capacity of 1729.3 mAh g-1 at 0.2C and retains 1085 mAh g-1 after 500 cycles. The new anode also shows fast charge capability due to the enhanced electronic conductivity provided by CrSi2 dopant, delivering a capacity of 815.9 mAh g-1 at 1C after 1000 cycles with a capacity degradation rate of <0.05% per cycle. An in situ transmission electron microscopy is used to study the structural stability of the CrSi2-doped Si, indicating that the high control of CrSi2 dopant prevents the fracture of Si during lithiation and results in long cycle life. Molecular dynamics simulation shows that CrSi2 doping optimizes the crack propagation path and dissipates the fracture energy. In this work a comprehensive information is provided to study the function of metal ion doping in electrode materials.
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INTRODUCTION: In women of childbearing age with epilepsy, 40% experience the comorbidity of polycystic ovary syndrome (PCOS), which is marked by a higher prevalence of hyperandrogenism. Our recent clinical observations indicate the potential contribution of hyperandrogenism-induced PCOS to epilepsy susceptibility, and this study aimed to unravel the underlying factors that increase the susceptibility of females to epilepsy. METHODS: A letrozole-induced PCOS rat model was employed to simulate endogenous hyperandrogenism. Susceptibility was assessed through seizure kindling rates using pentetrazol and electroencephalogram recordings. Additionally, the role of androgens in epilepsy was verified through interventions using Diane-35. RESULTS: This study revealed that letrozole induced elevated testosterone levels and PCOS-related changes in female rats. PCOS rats, through pentetrazol-kindling, exhibited a reduced seizure threshold compared with controls. Elevated testosterone levels were observed in both the hippocampal and frontal brain tissues, accompanied by changes in circulation. Two weeks of Diane-35 intervention showed a tendency to alleviate these changes, modifying testosterone levels in both the plasma and brain tissue. Western blotting and immunohistochemistry revealed increased expression of GABA-A receptor in the hippocampus and decreased AMPA receptor expression in the frontal cortex, correlating with anti-epileptic status in PCOS rats. CONCLUSION: This study delves into the impact of elevated androgen levels on seizure threshold, providing crucial insights into the underpinnings of the comorbidity between PCOS and epilepsy. These findings significantly contribute to the evolving field of epilepsy research, emphasizing the imperative consideration of hormonal influences for the development of targeted therapeutic interventions in individuals with epilepsy and PCOS.
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Metabolic reprogramming enables cancer cells to generate energy mainly through aerobic glycolysis, which is achieved by increasing the expression levels of glycolysis-related enzymes. Therefore, the development of drugs targeting aerobic glycolysis could be an effective strategy for cancer treatment. Icaritin (ICT) is an active ingredient from the Chinese herbal plant Epimedium with several biological activities, but its anti-cancer mechanism remains inconclusive. Using normal hepatocytes and hepatoma cells, our results showed that ICT suppressed cell proliferation and clonal formation and decreased glucose consumption and lactate production in liver cancer cells. In consistent, the mRNA and protein levels of several aerobic glycolysis-related genes were decreased upon ICT treatment. Furthermore, our results demonstrated that the expression levels of the aerobic glycolysis-related proteins were correlated with the p53 status in hepatoma cells. Using PFT-α or siRNA-p53, our results confirmed that ICT regulated aerobic glycolysis in a p53-dependent manner. In addition, ICT was found to stabilize p53 at the post-translational level which might be mediated by inhibiting MDM2 expression and affecting its interaction with p53. Finally, our results demonstrated that ICT increased the levels of ROS that activated p53 via the p38 MAPK pathway. In conclusion, ICT increased intracellular ROS levels in liver cancer cells, which promoted the stabilization and activation of p53, inhibiting the expression of aerobic glycolysis-related genes and glycolysis, and ultimately leading to the suppression of liver cancer development.
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Carcinoma Hepatocelular , Flavonoides , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/metabolismo , Proteína p53 Supresora de Tumor/genética , Proteína p53 Supresora de Tumor/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/metabolismo , Glucólisis , Proliferación Celular , Línea Celular TumoralRESUMEN
BACKGROUND: The energy supply of certain cancer cells depends on aerobic glycolysis rather than oxidative phosphorylation. Our previous studies have shown that withaferin A (WA), a lactone compound derived from Withania somnifera, suppresses skin carcinogenesis at least partially by stabilizing IDH1 and promoting oxidative phosphorylation. Here, we have extended our studies to evaluate the anti-tumor effect of WA in liver cancer. METHODS: Differential expression of glycolysis-related genes between liver cancer tissues and normal tissues and prognosis were verified using an online database. Glycolysis-related protein expression was detected using western blot after overexpression and knockdown of IDH1 and mitochondrial membrane potential assay based on JC-1, and mitochondrial complex I activity was also detected. The inhibitory effect of WA on the biological functions of HepG2 cells was detected along with cell viability using MTT assay, scratch assay, clone formation assay, glucose consumption and lactate production assay. Western blot and qRT-PCR were used to detect the expression of proteins and genes related to IDH1, p53 and HIF1α signaling pathways. RESULTS: We first identified that IDH1 expression was downregulated in human liver cancer cells compared to normal liver cells. Next, we found that treatment of HepG2 cells with WA resulted in significantly increased protein levels of IDH1, accompanied by decreased levels of several glycolytic enzymes. Furthermore, we found that WA stabilized IDH1 proteins by inhibiting the degradation by the proteasome. The tumor suppressor p53 was also upregulated by WA treatment, which played a critical role in the upregulation of IDH1 and downregulation of the glycolysis-related genes. Under hypoxic conditions, glycolysis-related genes were induced, which was suppressed by WA treatment, and IDH1 expression was still maintained at higher levels under hypoxia. CONCLUSION: Taken together, our results indicated that WA suppresses liver cancer tumorigenesis by p53-mediated IDH1 upregulation, which promotes mitochondrial respiration, thereby inhibiting the HIF-1α pathway and blocking aerobic glycolysis.
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Glucólisis , Subunidad alfa del Factor 1 Inducible por Hipoxia , Isocitrato Deshidrogenasa , Neoplasias Hepáticas , Transducción de Señal , Proteína p53 Supresora de Tumor , Witanólidos , Humanos , Witanólidos/farmacología , Proteína p53 Supresora de Tumor/metabolismo , Proteína p53 Supresora de Tumor/genética , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Subunidad alfa del Factor 1 Inducible por Hipoxia/genética , Glucólisis/efectos de los fármacos , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patología , Transducción de Señal/efectos de los fármacos , Isocitrato Deshidrogenasa/genética , Isocitrato Deshidrogenasa/metabolismo , Proliferación Celular/efectos de los fármacos , Células Hep G2 , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Carcinogénesis/efectos de los fármacosRESUMEN
Acute kidney injury (AKI) poses a significant global public health challenge. Current methods for detecting AKI rely on monitoring changes in serum creatinine (Scr), blood urea nitrogen (BUN), urinary output and some commonly employed biomarkers. However, these indicators are usually neither specific nor sensitive to AKI, especially in cases of mild kidney injury. AKI is accompanied by severe inflammatory reactions, resulting in the upregulation of numerous inflammation-associated proteins in the plasma. Plasma biomarkers are a noninvasive method for detecting kidney injury, and to date, plasma inflammation-associated cytokines have not been adequately studied in AKI patients. The objective of our research was to identify novel inflammatory biomarkers for AKI. We utilized Olink proteomics to analyze the alterations in plasma inflammation-related proteins in the serum of healthy mice (n = 2) or mice treated with cisplatin (n = 6). Additionally, transcriptome datasets for the lipopolysaccharide (LPS), cisplatin, and ischemiaâreperfusion injury (IRI) groups were obtained from the National Center of Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database. We calculated the intersection of differentially expressed proteins (DEPs) and genes (DEGs) from both datasets. In the Olink proteomics analysis, the AKI group had significantly greater levels of 11 DEPs than did the control group. In addition, 56 common upregulated DEGs were obtained from the transcriptome dataset. The expression of CXCL1 and TNFRSF12A overlapped across all the datasets. The transcription and protein expression levels of CXCL1 and TNFRSF12A were detected in vivo. The gene and protein levels of CXCL1 and TNFRSF12A were significantly increased in different AKI mouse models and clinical patients, suggesting that these genes and proteins could be potential specific biomarkers for the identification of AKI.
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With the annual increase in lithium-ion batteries (LIBs) disposal, valuable resources are being generated with worrying waste, so it is strategically important to recover the critical metals from them. Individual high temperature or leaching processes do not apparently achieve very satisfactory results. In the present work, the reduction with zinc powder was able to convert the lithium in LiNixCoyMnzO2 (NCM) to soluble LiOH, while the reduction and ammonia complexation environment generated by the decomposition of cysteine (Cys) achieved an efficient leaching of transition metals without additional additives. The leaching efficiency of Li can reach more than 92 %, while that of Ni/Co/Mn reaches more than 97 % through the regulation of the parameters of each process. In particular, an in-situ redox mechanism is proposed to explain the efficient leaching of transition metals, which further enriches the theory of spent LIBs recycling and provides a promising idea for various hydrometallurgical extraction systems.
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As the strategic importance of Li in the energy sector increases, selective Li extraction technology from spent lithium-ion batteries (LIBs) is attracting increasing attention. Current Li extraction processes typically suffer from lengthy procedures, high costs, and low efficiency. To improve the efficiency of Li extraction, a novel approach to achieve efficient Li recovery is proposed in this study, namely, reacting pyrite (FeS2) with LiNixCoyMnzO2 (NCM) powder in a subcritical water reduction (SWR) system. The reducing solvent environment created by the enhanced reaction of FeS2 with subcritical water converts the high-valent metals in NCM to a low-valent state, causing the collapse of the stable laminar structure and allowing Li+ to be released smoothly. After dual activation through mechanochemical and roasting processes, more than 99 % of Li is preferentially extracted under optimal conditions. Furthermore, Li+ in solution is converted into highly pure Li2CO3, while other metallic elements remain in the residue. Using inexpensive FeS2 for efficient Li extraction without adding additional chemical reagents is a promising approach for recovering spent LIBs.
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Immunotherapy has emerged as a promising modality for addressing advanced or conventionally drug-resistant malignancies. When it comes to lung adenocarcinoma (LUAD), T cells have demonstrated significant influence on both antitumor activity and the tumor microenvironment. However, their specific contributions remain largely unexplored. This investigation aimed to delineate molecular subtypes and prognostic indicators founded on T cell marker genes, thereby shedding light on the significance of T cells in LUAD prognosis and precision treatment. The cellular phenotypes were identified by scrutinizing the single-cell data obtained from the GEO repository. Subsequently, T cell marker genes derived from single-cell sequencing analyses were integrated with differentially expressed genes from the TCGA repository to pinpoint T cell-associated genes. Utilizing Cox analysis, molecular subtypes and prognostic signatures were established and subsequently verified using the GEO dataset. The ensuing molecular and immunological distinctions, along with therapy sensitivity between the two sub-cohorts, were examined via the ESTIMATE, CIBERSORT, and ssGSEA methodologies. Compartmentalization, somatic mutation, nomogram development, chemotherapy sensitivity prediction, and potential drug prediction analyses were also conducted according to the risk signature. Additionally, real-time qPCR and the HPA database corroborated the mRNA and protein expression patterns of signature genes in LUAD tissues. In summary, this research yielded an innovative T cell marker gene-based signature with remarkable potential to prognosis and anticipate immunotherapeutic outcomes in LUAD patients.
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Adenocarcinoma del Pulmón , Neoplasias Pulmonares , Humanos , Pronóstico , ARN , Secuencia de Bases , Adenocarcinoma del Pulmón/genética , Complejo CD3 , Neoplasias Pulmonares/genética , Microambiente Tumoral/genéticaRESUMEN
Smart responsive materials are capable of responding to external stimuli and, compared to traditional materials, can be effectively reused and reduce usage costs in applications. However, smart responsive materials often face challenges such as the inability to repair extensive damage, instability in long-term performance, and inapplicability in extreme environments. This study combines 2D diamond nanosheets with organic fluorinated molecules to prepare a smart nanofluid (fluorinated diamond nanosheets, F-DN) with self-healing and self-adhesion properties. This smart nanofluid can be used to design various coatings for different applications. For example, coatings prepared on textured steel plates using the drop-casting method have excellent superhydrophobic and high oleophobic properties; coatings on titanium alloy plates achieve low friction and wear in the presence of lubricating additives of F-DN in perfluoropolyether (PFPE). Most impressively, coatings on steel plates not only provide effective corrosion resistance but also have the ability to self-heal significant damage (approximately 2 mm in width), withstand extremely low temperatures (-64 °C), and resist long-term corrosion factors (immersion in 3.5 wt % NaCl solution for 35 days). Additionally, it can act as a "coating glue" to repair extensive damage to other corrosion-resistant organic coatings and recover their original protective properties. Therefore, the smart nanofluid developed in this study offers diverse applications and presents new materials system for the future development of smart responsive materials.