New perspectives in prognostication of hepatocellular carcinoma: The role and clinical implications of transient receptor potential family genes.

The study titled "Transient receptor potential-related risk model predicts prognosis of hepatocellular carcinoma patients" is a significant contribution to hepatocellular carcinoma (HCC) research, highlighting the role of transient receptor potential (TRP) family genes in the disease's progression and prognosis. Utilizing data from The Cancer Genome Atlas database, it establishes a new risk assessment model, emphasizing the interaction of TRP genes with tumor proliferation pathways, key metabolic reactions like retinol metabolism, and the tumor immune microenvironment. Notably, the overexpression of the TRPC1 gene in HCC correlates with poorer patient survival outcomes, suggesting its potential as a prognostic biomarker and a target for personalized therapy, particularly in strategies combining immunotherapy and anti-TRP agents.

WTAP-induced N6-methyladenosine of PD-L1 blocked T-cell-mediated antitumor activity under hypoxia in colorectal cancer.

N6-Methyladenosine (m6A) is a important process regulating gene expression post-transcriptionally. Programmed death ligand 1 (PD-L1) is a major immune inhibitive checkpoint that facilitates immune evasion and is expressed in tumor cells. In this research we discovered that Wilms' tumor 1-associated protein (WTAP) degradation caused by ubiquitin-mediated cleavage in cancer cells (colorectal cancer, CRC) under hypoxia was inhibited by Pumilio homolog 1 (PUM1) directly bound to WTAP. WTAP enhanced PD-L1 expression in a way that was m6A-dependent. m6A "reader," Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) identified methylated PD-L1 transcripts and subsequently fixed its mRNA. Additionally, we found that T-cell proliferation and its cancer cell-killing effects were prevented by overexpression of WTAP in vitro and in vivo. Overexpression prevented T cells from proliferating and killing CRC by maintaining the expression of PD-L1. Further evidence supporting the WTAP-PD-L1 regulatory axis was found in human CRC and organoid tissues. Tumors with high WTAP levels appeared more responsive to anti-PD1 immunotherapy, when analyzing samples from patients undergoing treatment. Overall, our findings demonstrated a novel PD-L1 regulatory mechanism by WTAP-induced mRNA epigenetic regulation and the possible application of targeting WTAP as immunotherapy for tumor hypoxia.

The importance of preoperative T3 stage substaging by 3D endorectal ultrasonography for the prognosis of middle and low rectal cancer.

OBJECTIVE: The study aimed to validate the role of 3D-endorectal ultrasonography in prognosis and recurrence for patients with T3-stage rectal cancer by evaluating the preoperative extramural depth of tumor invasion. METHODS: In this study, we investigated the medical records of rectal cancer patients who were admitted to Changhai Hospital's Colorectal Surgery Division. The sample group was categorized into three subgroups (T3a, T3b, and T3c) based on the extent of tumor progression (<5 mm, 5-10 mm, and >10 mm) to assess the endorectal ultrasonography diagnostic performance. The 5-year disease-free survival and overall survival were assessed using the Kaplan-Meier method and a log rank test. Cox regression analysis verified the tumor invasion depth's significance as a prognostic predictor, and it was also utilized to evaluate other independent risk variables for recurrence after surgery. RESULTS: The study included 72 individuals with low and middle rectal cancer from January 2014 to November 2019. Twenty-two individuals had stage T3a, 22 had stage T3b, and 28 had stage T3c based on preoperative endorectal ultrasonography. Endorectal ultrasonography had 88.0%, 86.8%, and 76.2% overall accuracy for stratifying subgroups, respectively. According to the Kaplan-Meier curve, 5-year OS was 100%, 83.5%, and 92.9% for T3a, T3b, and T3c (p = 0.172), and 5-year disease-free survival was 100%, 80.8%, and 72.9% for T3a, T3b, and T3c, respectively (p = 0.014). A distinct risk factor for 5-year disease-free survival was the degree of tumor infiltration (p = 0.039). CONCLUSION: Preoperative T3 stage subdivision allows for categorization of prognosis and survival. Endorectal ultrasonography reports should make explicit declarations of T3a, T3b, and T3c scales.

EVOAC-HP: An Efficient and Verifiable Outsourced Access Control Scheme with Hidden Policy.

As medical data become increasingly important in healthcare, it is crucial to have proper access control mechanisms, ensuring that sensitive data are only accessible to authorized users while maintaining privacy and security. Ciphertext-Policy Attribute-Based Encryption (CP-ABE) is an attractive access control solution that can offer effective, fine-grained and secure medical data sharing, but it has two major drawbacks: Firstly, decryption is computationally expensive for resource-limited data users, especially when the access policy has many attributes, limiting its use in large-scale data-sharing scenarios. Secondly, existing schemes are based on data users' attributes, which can potentially reveal sensitive information about the users, especially in healthcare data sharing, where strong privacy and security are essential. To address these issues, we designed an improved CP-ABE scheme that provides efficient and verifiable outsourced access control with fully hidden policy named EVOAC-HP. In this paper, we utilize the attribute bloom filter to achieve policy hiding without revealing user privacy. For the purpose of alleviating the decryption burden for data users, we also adopt the technique of outsourced decryption to outsource the heavy computation overhead to the cloud service provider (CSP) with strong computing and storage capabilities, while the transformed ciphertext results can be verified by the data user. Finally, with rigorous security and reliable performance analysis, we demonstrate that EVOAC-HP is both practical and effective with robust privacy protection.

Up-regulation of PUM1 by miR-218-5p promotes colorectal tumor-initiating cell properties and tumorigenesis by regulating the PI3K/AKT axis.

Background: Colorectal cancer (CRC) is the third most common cancer and the fourth most common cause of cancer-related death worldwide. Advanced stage CRC, during the recent past, had a dismal prognosis and only a few available treatments. Pumilio homologous protein 1 (PUM1) is reportedly aberrant in human malignancies, including CRC. However, the role of PUM1 in the regulation of tumor-initiating cells (T-ICs) remains unknown. Methods: The levels of messenger RNAs (mRNAs) were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunoblot analyses. Statistical analyses were performed to determine the associations between the levels of PUM1 and tumor features and patient outcomes. Whether PUM1 is a downstream target of miR-218-5p was verified by bioinformatics target gene prediction and qRT-PCR. Results: Herein, it was found that T-ICs, chemoresistance, and recurrent CRC samples all manifest increased PUM1 expression. Functional investigations have shown that PUM1 increased the self-renewal, tumorigenicity, malignant proliferation, and chemoresistance of colorectal cells. PUM1 activates the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway biochemically. Furthermore, it was discovered that miR-218-5p specifically targets T-ICs' PUM1 3'-untranslated region (3'-UTR). More importantly, the PUM1/PI3K/AKT axis regulates CRC cells' responses to treatment with cetuximab, and PUM1 overexpression increased cetuximab resistance. More evidence points to the possibility that low PUM1 may predict cetuximab benefits in CRC patients after analysis of the patient cohort, patient-derived tumor organoids, and patient-derived xenografts (PDXs). Conclusions: Taken together, the result of this work points to the critical function of the miR-218-5p/PUM1/PI3K/AKT regulatory circuit in regulating T-ICs characteristics and thus suggests possible therapeutic targets for CRC.

Exploring the Potential Association between COVID-19 and Thyroid Cancer: A Mendelian Randomization Study.

In order to address the ongoing debate surrounding the potential link between COVID-19 and thyroid cancer, our study was specifically designed to investigate the association between these two factors. We acquired summary data from a genome-wide association study (GWAS) concerning COVID-19 susceptibility and severity of COVID-19 in the European population, with a focus on their relationship with thyroid cancer. We applied three distinct methodologies to evaluate the causality between COVID-19 and thyroid cancer, employing Mendelian randomization (MR)-Egger, weighted median (WM), and inverse variance-weighted (IVW) approaches. Furthermore, we utilized a variety of techniques to assess pleiotropy and heterogeneity, including the MR-Egger intercept, MR-pleiotropy residual sum and outlier method (PRESSO), and Cochran's Q test. The MR analysis revealed associations between the susceptibility of COVID-19 and thyroid cancer (IVW odds ratio [OR]: 2.826, 95% confidence interval [CI]: [0.842, 9.483], P = 0.093) as well as between the risk of COVID-19 hospitalization and thyroid cancer (IVW OR: 1.630, 95% CI: [1.050, 2.529], P = 0.029). However, the relationship between COVID-19 and the occurrence of severe thyroid cancer cases was less evident (IVW OR: 1.061, 95% CI: [0.575, 1.956], P = 0.850). Our sensitivity analyses did not reveal any signs of horizontal pleiotropy or heterogeneity. Our MR study provided compelling evidence supporting a causal connection between the risk of COVID-19 hospitalization and thyroid cancer. Nevertheless, the MR results derived from genetic data do not support a causal link between susceptibility to COVID-19 and the risk of thyroid cancer or between very severe cases of COVID-19 and the risk of thyroid cancer. These findings have significant implications for further investigations into the impact of COVID-19 on health and the etiology of thyroid cancer.

Development and validation of an epithelial-mesenchymal transition-related gene signature for predicting prognosis.

BACKGROUND: Currently, there are many therapeutic methods for lung adenocarcinoma (LUAD), but the 5-year survival rate is still only 15% at later stages. Epithelial- mesenchymal transition (EMT) has been shown to be closely associated with local dissemination and subsequent metastasis of solid tumors. However, the role of EMT in the occurrence and development of LUAD remains unclear. AIM: To further elucidate the value of EMT-related genes in LUAD prognosis. METHODS: Univariate, least absolute shrinkage and selection operator, and multivariate Cox regression analyses were applied to establish and validate a new EMT-related gene signature for predicting LUAD prognosis. The risk model was evaluated by Kaplan-Meier survival analysis, principal component analysis, and functional enrichment analysis and was used for nomogram construction. The potential structures of drugs to which LUAD is sensitive were discussed with respect to EMT-related genes in this model. RESULTS: Thirty-three differentially expressed genes related to EMT were found to be highly associated with overall survival (OS) by using univariate Cox regression analysis (log2FC ≥ 1, false discovery rate < 0.001). A prognostic signature of 7 EMT-associated genes was developed to divide patients into two risk groups by high or low risk scores. Kaplan-Meier survival analysis showed that the OS of patients in the high-risk group was significantly poorer than that of patients in the low-risk group (P < 0.05). Multivariate Cox regression analysis showed that the risk score was an independent risk factor for OS (HR > 1, P < 0.05). The results of receiver operator characteristic curve analysis suggested that the 7-gene signature had a perfect ability to predict prognosis (all area under the curves > 0.5). CONCLUSION: The EMT-associated gene signature classifier could be used as a feasible indicator for predicting OS.

Severe complications from anastomotic leakage after total mesorectal excision with the protective loop ileostomy in three patients.

INTRODUCTION AND IMPORTANCE: A protective loop ileostomy is recommended in ultra-low rectal cancer to reduce the complications associated with anastomotic leakage (AL), but there are few studies on the complications after AL. The purpose of this study was to outline our experience in the successful treatment of severe abdominal infection after AL in rectal cancer patients with the protective loop ileostomy. CASE PRESENTATION: In this report, we describe three cases of AL after standard total mesorectal excision with the protective loop ileostomy. Severe abdominal infection occurred postoperatively. The patients were successfully treated by surgical reintervention and had an uneventful recovery. No recurrence was observed after 2 years. CLINICAL DISCUSSION: We consider that pelvic floor reconstruction and extending the extubation time should be performed in patients with a high risk of AL. Moreover, when severe abdominal infection and early infectious shock occur after AL, immediate reoperation should be performed to minimize the complication. CONCLUSION: Protective loop ileostomy can't decrease the re-operation rate for patients with AL. We should take preventive measures during and after the operation, as well as early detection and early treatment.

LncRNA SOX2-OTinhibitionprotects against myocardialischemia/reperfusion-inducedinjury via themicroRNA-186-5p (miR-186-5p)/Yin Yang 1 (YY1)pathway.

Long noncoding RNAs (lncRNAs) exert essential effects in regulating myocardial ischemia/reperfusion (MI/R)-induced injury. This work intended to explore the functions of lncRNA SOX2-OT and its regulatory mechanism within MI/R-induced injury. In this study, gene expression was determined by RT-qPCR. Western blotting was applied for the detection of protein levels. Pro-inflammatory cytokine concentrations, cardiomyocyte viability, and apoptosis were detected via ELISA, CCK-8 and flow cytometry. In the in vitro model, SOX2-OT and YY1 were both upregulated, while miR-186-5p was downregulated. SOX2-OT knockdown attenuated oxygen-glucose deprivation/reoxygenation (OGD/R)-induced cardiomyocyte dysregulation through relieving inflammation, promoting proliferation, and reducing apoptosis in OGD/R-treated H2C9 cells. SOX2-OT positively regulated YY1 expression via miR-186-5p. Moreover, miR-186-5p inhibition or YY1 upregulation abolished the effects of SOX2-OT blocking on the inflammatory responses, proliferation, and apoptosis of OGD/R-challenged H2C9 cells. In conclusion, our results, for the first time, demonstrated that SOX2-OT inhibition attenuated MI/R injury in vitro via regulating the miR-186-5p/YY1 axis, offering potential therapeutic targets for MI/R injury treatment.

Differences in lipidomics may be potential biomarkers for early diagnosis of pancreatic cancer.

PURPOSE: To analyze the plasma lipid spectrum between healthy control and patients with pancreatic cancer and to select differentially expressed tumor markers for early diagnosis. METHODS: In total, 20 patents were divided into case group and healthy control group according to surgical pathology. Of almost 1206 plasma lipid molecules harvested from 20 patients were measured by HILIC using the normal phase LC/MS. Heat map presented the relative levels of metabolites and lipids in the healthy control group and patients with pancreatic cancer. The PCA model was constructed to find out the difference in lipid metabolites. The principal components were drawn in a score plot and any clustering tendency could be observed. PLS-DA were performed to distinguish the healthy control group and pancreatic cancer according to the identified lipid profiling datasets. The volcano plot was used to visualize all variables with VIP>1 and presented the important variables with P<0.01 and |FC|>2. RESULTS: The upregulated lipid metabolites in patients with pancreatic cancer contained 9 lipids; however, the downregulated lipid metabolites contained 79 lipids. CONCLUSION: There were lipid metabolomic differences in patients with pancreatic cancer, which could serve as potential tumor markers for pancreatic cancer.

Differences in lipidomics may be potential biomarkers for early diagnosis of pancreatic cancer

Abstract Purpose To analyze the plasma lipid spectrum between healthy control and patients with pancreatic cancer and to select differentially expressed tumor markers for early diagnosis. Methods In total, 20 patents were divided into case group and healthy control group according to surgical pathology. Of almost 1206 plasma lipid molecules harvested from 20 patients were measured by HILIC using the normal phase LC/MS. Heat map presented the relative levels of metabolites and lipids in the healthy control group and patients with pancreatic cancer. The PCA model was constructed to find out the difference in lipid metabolites. The principal components were drawn in a score plot and any clustering tendency could be observed. PLS-DA were performed to distinguish the healthy control group and pancreatic cancer according to the identified lipid profiling datasets. The volcano plot was used to visualize all variables with VIP>1 and presented the important variables with P<0.01 and -FC->2. Results The upregulated lipid metabolites in patients with pancreatic cancer contained 9 lipids; however, the downregulated lipid metabolites contained 79 lipids. Conclusion There were lipid metabolomic differences in patients with pancreatic cancer, which could serve as potential tumor markers for pancreatic cancer.

Roles and mechanisms of action of HNF­4α in the hepatic differentiation of WB­F344 cells.

Hepatocyte nuclear factor 4 α (HNF­4α) is a nuclear receptor and mediates hepatic genes. WB­F344 liver epithelial cells can differentiate into hepatocytes. The present study aimed to examine the roles and mechanisms of action of HNF­4α on the hepatic differentiation of WB­F344 cells. WB­F344 cells were divided into a normal cell group (WB­F344), empty vector group (PLKO), and gene silencing group (PLKO­SH). The expression levels of HNF­4α were measured using reverse transcription­quantitative polymerase chain reaction analysis. Proliferation of the cells was determined using a Cell Counting kit­8 assay. Based on western blot analysis, the protein levels of α­fetoprotein (AFP), albumin (ALB) and cytokeratin 19 (CK19) were determined. The positive cell rates of the three groups were assessed using periodic acid­Schiff (PAS) staining. Following construction of an RNA­sequencing library, differentially expressed genes (DEGs) between the HNF­4α­silenced and normal samples were screened using the limma package and enrichment analysis was conducted using the DAVID tool. Protein­protein interaction (PPI) and microRNA­targeted regulatory networks were constructed in Cytoscape software. The PLKO­SH group exhibited a lower mRNA level of HNF­4α, higher protein level of AFP, lower protein levels of ALB and CK19, increased cell proliferation, and a lower PAS­positive cell rate. The HNF­4α­silenced and normal samples differed in 499 DEGs. In the PPI network, matrix metallopeptidase 9 (MMP9), early growth response 1 (EGR1), SMAD family member 2 (SMAD2), and RAS­related C3 botulinum substrate 2 (RAC2) were key nodes. HNF­4α may promote the differentiation of WB­F344 cells into hepatocytes by targeting MMP9, EGR1, SMAD2 and RAC2.

BRAF V600E and RET/PTC Promote the Activity of Nuclear Factor-κB, Inflammatory Mediators, and Lymph Node Metastasis in Papillary Thyroid Carcinoma: A Study of 50 Patients in Inner Mongolia.

BACKGROUND The aim of this study was to investigate the expression of the BRAF V600E gene mutation and the RET/PTC gene rearrangement in the progression of papillary thyroid carcinoma (PTC) in 50 patients from Inner Mongolia. MATERIAL AND METHODS Clinical data, blood, and tissue samples were obtained from 50 patients with PTC and ten patients with benign thyroid adenoma. Expression of BRAF V600E, RET/PTC, nuclear factor-κB (NF-κB), interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-ß, C-X-C motif chemokine ligand (CXCL)1, CXCL2, C-C motif chemokine ligand (CCL)2, and CCL3 were measured using polymerase chain reaction (PCR), immunohistochemistry, and an enzyme-linked immunosorbent assay (ELISA). RESULTS Of the 50 patients with PTC, 37 patients expressed the BRAF V600E gene mutation, eight patients expressed RET/PTC, and five patients showed concomitant BRAF V600E and RET/PTC. Time to recurrence for patients with PTC with BRAF V600E was significantly increased compared with patients with concomitant BRAF V600E mutation and RET/PTC rearrangement (P<0.05). Expression of BRAF V600E, RET/PTC, and concomitant expression of BRAF V600E and RET/PTC were significantly associated with patient age and lymph node metastasis (P<0.05). Serum levels of NF-κB, IL-1ß, IL-6, TNF-α, TGF-ß and CCL3, and tumor tissue levels of IL-1ß, IL-6, TNF-α, TGF-ß, CXCL2 and CCL2 in patients with PTC were significantly increased compared with patients with benign thyroid adenoma, before and after surgery (P<0.05). CONCLUSIONS Expression of the BRAF V600E mutation and RET/PTC translocation promoted the activity of NF-κB, expression of inflammatory mediators, and lymph node metastases in patients with PTC.

Bioinformatics analysis to screen key genes implicated in the differentiation of induced pluripotent stem cells to hepatocytes.

Due to the lack of potential organs, hepatocellular transplantation has been considered for treating end-stage liver disease. Induced pluripotent stem cells (iPSCs) are reverted from somatic cells and are able to differentiate into hepatocytes. The present study aimed to investigate the mechanisms underlying iPSC differentiation to hepatocytes. GSE66076 was downloaded from the Gene Expression Omnibus; this database includes data from 3 undifferentiated (T0), 3 definitive endoderm (T5), and 3 early hepatocyte (T24) samples across hepatic­directed differentiation of iPSCs. Differentially expressed genes (DEGs) between T0 and T5 or T24 samples were identified using the linear models for microarray data package in Bioconductor, and enrichment analyses were performed. Using the weighted correlation network analysis package in R, clusters were identified for the merged DEGs. Cytoscape was used to construct protein­protein interaction (PPI) networks for DEGs identified to belong to significant clusters. Using the ReactomeFI plugin in Cytoscape, functional interaction (FI) networks were constructed for the common genes. A total of 433 and 1,342 DEGs were identified in the T5 and T24 samples respectively, compared with the T0 samples. Blue and turquoise clusters were identified as significant gene clusters. In the PPI network for DEGs in the blue cluster, the key node fibroblast growth factor 2 (FGF2) could interact with bone morphogenetic protein 2 (BMP2). Cyclin­dependent kinase 1 (CDK1) was demonstrated to have the highest degree (degree=71) in the PPI network for DEGs in the turquoise cluster. Enrichment analysis for the common genes, including hepatocyte nuclear factor 4α (HNF4A) and epidermal growth factor (EGF), in the FI network indicated that EGF and FGF2 were enriched in the Ras and Rap1 signaling pathways. The present results suggest that FGF2, BMP2, CDK1, HNF4A and EGF may participate in the differentiation of iPSCs into hepatocytes.

BRAFV600E and RET/PTC Promote Proliferation and Migration of Papillary Thyroid Carcinoma Cells In Vitro by Regulating Nuclear Factor-κB.

BACKGROUND Papillary thyroid carcinoma (PTC) is associated with mutations of BRAFV600E and RET/PTC and high levels of expression of nuclear factor-κB (NF-κB). However, few studies have focused on the association between NF-κB expression and mutations in BRAFV600E and RET/PTC, especially regarding PTC cell proliferation and migration. The aim of this in vitro study was to investigate the effect of BRAFV600E or RET/PTC on NF-κB expression, cell proliferation and cell migration in four established PTC cell lines. MATERIAL AND METHODS Four cell lines included TPC-1 (BRAFWT/WT), BCPAP (BRAFV600E/V600E), PCCL3, and PTC3-5 (RET/PTC), were grown in culture in vitro with or without suppression of NF-κB using pyrrolidine dithiocarbamate (PDTC), and cell proliferation, and cell migration were evaluated. RESULTS Expression of the BRAF gene was increased in the BCPAP cell line when compared with the TPC-1 cells. Expression of the RET gene was increased in the PTC3-5 cell line when compared with the PCCL3 cells. In the BCPAP and PTC3-5 cell lines, the relative expression of NF-κB protein, including phosphorylated p100/52, phosphorylated p65, phosphorylated IKKa/b, phosphorylated IκBα, and p65 nuclear translocation were increased compared with the TPC-1 and PCCL3 cells. Proliferation and migration of BCPAP and PTC3-5 cells were increased compared with the TPC-1 and PCCL3 cells. Suppression of NF-κB reduced NF-κB protein expression and inhibited the proliferation of cells in the TPC-1, BCPAP, PCCL3 and PTC3-5 cell lines, and migration of the BCPAP and PTC3-5 cells. CONCLUSIONS BRAFV600E and RET/PTC and the expression of NF-κB promote the proliferation and migration of papillary thyroid carcinoma cells in vitro.

Bundle-like α'-NaV2O5 mesocrystals: from synthesis, growth mechanism to analysis of Na-ion intercalation/deintercalation abilities.

Bundle-like α'-NaV2O5 mesocrystals were synthesized successfully by a two-step hydrothermal method. Observations using electron microscopy revealed that the obtained NaV2O5 mesocrystals were composed of nanobelts with the preferential growth direction of [010]. The precise crystal structure was further confirmed by Rietveld refinement and Raman spectroscopy. Based on analysis of crystal structure and microscopy, a reaction and growth mechanism, hydrolysis-condensation (oxolation and olation)-ion exchange-self-assembly, was proposed and described in detail. Furthermore, electrochemical measurements were used to analyze the Na-ions intercalation/deintercalation abilities in NaV2O5, and indicated that Na-ions were difficult to extract. Importantly, the DFT theoretical calculation results, which showed that the migration energy of Na-ions was so huge that migration of Na-ions was quite difficult, can explain and support well the results of the electrochemical measurements.

Nanostructured Layered Cathode for Rechargeable Mg-Ion Batteries.

Nanostructured bilayered V2O5 was electrochemically deposited within a carbon nanofoam conductive support. As-prepared electrochemically synthesized bilayered V2O5 incorporates structural water and hydroxyl groups, which effectively stabilizes the interlayers and provides coordinative preference to the Mg(2+) cation in reversible cycling. This open-framework electrode shows reversible intercalation/deintercalation of Mg(2+) ions in common electrolytes such as acetonitrile. Using a scanning transmission electron microscope we demonstrate that Mg(2+) ions can be effectively intercalated into the interlayer spacing of nanostructured V2O5, enabling electrochemical magnesiation against a Mg anode with a specific capacity of 240 mAh/g. We employ HRTEM and X-ray fluorescence (XRF) imaging to understand the role of environment in the intercalation processes. A rebuilt full cell was tested by employing a high-energy ball-milled Sn alloy anode in acetonitrile with Mg(ClO4)2 salt. XRF microscopy reveals effective insertion of Mg ions throughout the V2O5 structure during discharge and removal of Mg ions during electrode charging, in agreement with the electrode capacity. We show using XANES and XRF microscopy that reversible Mg intercalation is limited by the anode capacity.

Asynchronous Crystal Cell Expansion during Lithiation of K(+)-Stabilized α-MnO2.

α-MnO2 is a promising material for Li-ion batteries and has unique tunneled structure that facilitates the diffusion of Li(+). The overall electrochemical performance of α-MnO2 is determined by the tunneled structure stability during its interaction with Li(+), the mechanism of which is, however, poorly understood. In this paper, a novel tetragonal-orthorhombic-tetragonal symmetric transition during lithiation of K(+)-stabilized α-MnO2 is observed using in situ transmission electron microscopy. Atomic resolution imaging indicated that 1 × 1 and 2 × 2 tunnels exist along c ([001]) direction of the nanowire. The morphology of a partially lithiated nanowire observed in the ⟨100⟩ projection is largely dependent on crystallographic orientation ([100] or [010]), indicating the existence of asynchronous expansion of α-MnO2's tetragonal unit cell along a and b lattice directions, which results in a tetragonal-orthorhombic-tetragonal (TOT) symmetric transition upon lithiation. Such a TOT transition is confirmed by diffraction analysis and Mn valence quantification. Density functional theory (DFT) confirms that Wyckoff 8h sites inside 2 × 2 tunnels are the preferred sites for Li(+) occupancy. The sequential Li(+) filling at 8h sites leads to asynchronous expansion and symmetry degradation of the host lattice as well as tunnel instability upon lithiation. These findings provide fundamental understanding for appearance of stepwise potential variation during the discharge of Li/α-MnO2 batteries as well as the origin for low practical capacity and fast capacity fading of α-MnO2 as an intercalated electrode.

A XANES study of LiVPO4F: a factor analysis approach.

Evolving factor analysis (EFA) of X-ray absorption near-edge spectroscopy (XANES) data is shown to be a useful tool to understand the phase relationships and compositional ranges of stability in the LiVPO4F-VPO4F system. EFA was used to calculate the concentration of phases versus state-of-charge in a lithium-ion battery and true XANES spectra. The results of EFA showed that, indeed, three phases were present during cycling of a LiVPO4F∥Li cell: LiVPO4F, LixVPO4F, and VPO4F. In contrast to what was reported by others, the second phase was not a fixed composition with x = 0.67, but, instead, existed over a range of lithium stoichiometry, x = 0.25 to 0.80. EFA results also showed that the reactions leading to these phases are reversible.