Amorphous Chloride Solid Electrolytes with High Li-Ion Conductivity for Stable Cycling of All-Solid-State High-Nickel Cathodes.

Solid electrolytes (SEs) are central components that enable high-performance, all-solid-state lithium batteries (ASSLBs). Amorphous SEs hold great potential for ASSLBs because their grain-boundary-free characteristics facilitate intact solid-solid contact and uniform Li-ion conduction for high-performance cathodes. However, amorphous oxide SEs with limited ionic conductivities and glassy sulfide SEs with narrow electrochemical windows cannot sustain high-nickel cathodes. Herein, we report a class of amorphous Li-Ta-Cl-based chloride SEs possessing high Li-ion conductivity (up to 7.16 mS cm-1) and low Young's modulus (approximately 3 GPa) to enable excellent Li-ion conduction and intact physical contact among rigid components in ASSLBs. We reveal that the amorphous Li-Ta-Cl matrix is composed of LiCl43-, LiCl54-, LiCl65- polyhedra, and TaCl6- octahedra via machine-learning simulation, solid-state 7Li nuclear magnetic resonance, and X-ray absorption analysis. Attractively, our amorphous chloride SEs exhibit excellent compatibility with high-nickel cathodes. We demonstrate that ASSLBs comprising amorphous chloride SEs and high-nickel single-crystal cathodes (LiNi0.88Co0.07Mn0.05O2) exhibit ∼99% capacity retention after 800 cycles at ∼3 C under 1 mA h cm-2 and ∼80% capacity retention after 75 cycles at 0.2 C under a high areal capacity of 5 mA h cm-2. Most importantly, a stable operation of up to 9800 cycles with a capacity retention of ∼77% at a high rate of 3.4 C can be achieved in a freezing environment of -10 °C. Our amorphous chloride SEs will pave the way to realize high-performance high-nickel cathodes for high-energy-density ASSLBs.

Unleashing the Potential of High-Capacity Anodes through an Interfacial Prelithiation Strategy.

The scalable development of an environmentally adaptive and homogeneous Li+ supplementary route remains a formidable challenge for the existing prelithiation technologies, restricting the full potential of high-capacity anodes. In this study, we present a moisture-tolerant interfacial prelithiation approach through casting a hydrophobic poly(vinylidene-co-hexafluoropropylene) membrane blended with a deep-lithiated alloy (Li22Si5@C/PVDF-HFP) onto Si based anodes. This strategy could not only extend to various high-capacity anode systems (SiOx@C, hard carbon) but also align with industrial roll-to-roll assembly processes. By carefully adjusting the thickness of the prelithiation layer, the densely packed Si@C electrode (4.5 mAh cm-2) exhibits significantly improved initial Coulombic efficiency until a close-to-unit value, as well as extreme moisture tolerance (60% relative humidity). Furthermore, it achieves more than 10-fold enhancement of ionic conductivity across the electrode. As pairing the prelithiated Si@C anode with the LiNi0.8Co0.1Mn0.1O2 cathode, the 2 Ah pouch-format prototype balances an energy density of ∼371 Wh kg-1 and an extreme power output of 2450 W kg-1 as well as 83.8% capacity retention for 1000 cycles. The combined operando phase tracking and spatial arrangement analysis of the intermediate alloy elucidate that the enhanced Li utilization derives from the gradient stress dissipation model upon a spontaneous Li+ redistribution process.

Application of a highly simulated and adaptable training system in the laparoscopic training course for surgical residents: Experience from a high-volume teaching hospital in China.

Objective: To explore the effectiveness, feasibility, and training effect of a highly simulated and adaptable laparoscopic training system in the advanced integrated two-stage laparoscopic simulation training course for surgical residents. Methods: This study prospectively took the surgical residents who received the advanced integrated two-stage laparoscopic simulation training course in our hospital from December 2019 to December 2021 as the research objects. In the stage one course, the trainees are randomly distributed into the dry simulation system group and Darwin laparoscopic training system group. The subjective assessment results of the trainees from the two groups are collected by questionnaires, and the simulation assessment results of the two groups are evaluated in a unified, objective, and standardized assessment form. The pre-course and post-course questionnaires were used to evaluate the feasibility and effectiveness of the Darwin system in the stage two course. Results: A total of 62 trainees completed the stage one and stage two courses. In the stage one course, the trainees were randomly distributed into the dry simulation trainer group (N = 19) and the Darwin group (N = 43). The results of the subjective assessment questionnaire showed that compared with the dry simulator group, the students in the Darwin group had higher subjective scores (P < 0.05). The objective assessment results for the 3 modules of "One Track Transfer", "One Tunnel Pass" and "High and Low Pillars" in the Darwin group were significantly better than those in the dry simulator group (P < 0.05). The trainees who received the stage two course completed the questionnaires before and after the course. The results showed that compared with pre-course evaluation, "basic theoretical knowledge of laparoscopy", "basic skills of laparoscopy", "laparoscopic suture technique" and "camera-holding technique" were significantly improved after training (P < 0.05). Conclusion: The highly simulated and adaptable laparoscopic training system is effective and feasible in the advanced integrated two-stage laparoscopic simulation training course for surgical residents.

PKCδ promotes the invasion and migration of colorectal cancer through c-myc/NDRG1 pathway.

Objective: Colorectal cancer (CRC) is the third cause of expected cancer deaths both in men and women in the U.S. and the third most commonly diagnosed cancer in China Targeted therapy has been proven to improve overall survival for unresectable metastatic CRC. But the location of the primary tumor or the presence of various core driver gene mutations that confer resistance may limit the utility of targeted therapy. Therefore, it is of great significance to further elucidate novel mechanisms of invasion and metastasis of CRC and find potential novel therapeutic targets. Protein Kinase C Delta (PKCδ) plays an important role in various diseases, including tumors. In CRC, the function of PKCδ on proliferation and differentiation is mostly studied but various research results were reported. Therefore, the role of PKCδ in CRC needs to be further studied, especially in tumor invasion and metastasis in CRC which few studies have looked into. Methods: The expression of PRKCD was analyzed by the Genotype-Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) databases and Immunohistochemical (IHC). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) enrichment analysis were used to explore the biological functions and pathways related to PRKCD. Lentivirus transfection was used to construct CRC cell lines with overexpression and knock-down of PKCδ or N-myc Downstream Regulated Gene 1 (NDRG1). Cell invasion and migration assay, wound healing assay were used to detect the function of PKCδ and NDRG1 in the invasion and migration of cells. Flow cytometry analysis was used to detect the influence of PKCδ on the CRC cell cycles .Immunofluorescence histochemistry ,Immunoprecipitation Assay and qPCR were used to detect the relationship of PKCδ and NDRG1. Xenograft model was used to verify the role of PKCδ in vivo. Results: PKCδ is overexpressed in CRC and could promote Epithelial-Mesenchymal Transition (EMT) and the invasion and migration of CRC in vitro. We confirmed that PKCδ and the tumor suppressor factor NDRG1 had a co-localization relationship in CRC. PKCδ inhibited NDRG1 transcription and protein expression. Overexpressing NDRG1 could inhibit the function of PKCδ in promoting tumor invasion and migration. PKCδ could regulate c-Myc, one transcription factor of NDRG1, to down-regulate NDRG1. In vivo, overexpressing PKCδ could promote xenograft growth and volume. Thus, our results showed that PKCδ reduced the expression of NDRG1 through c-Myc, promoting the invasion and migration of CRC through promoting EMT. Conclusion: The increased expression of PKCδ in CRC tumor tissue could promote the invasion and migration of tumor cells, and one of the mechanisms may be regulating c-Myc to inhibit the expression of NDRG1 and promote EMT.

Comprehensive exploration of tumor immune microenvironment feature and therapeutic response in colorectal cancer based on a novel immune-related long non-coding RNA prognostic signature.

Colorectal cancer (CRC) is one of the most common malignant tumors with a high incidence rate and mortality. LncRNA is an important regulator of the immune system. It is of great significance to study immune-related lncRNAs (IR-lncRNAs) for CRC. In this study, we screened IR-lncRNAs differentially expressed in normal and CRC tissues, and Univariate Cox regression and the Least Absolute Shrinkage and Selection Operator were applied to construct IR-lncRNA prognostic signature in TCGA training dataset, and its predictive capability for the prognosis of CRC patients was verified in GSE39582 validation dataset. The novel signature was identified as an independent predictor of prognosis in CRC patients. In addition, the signature could accurately predict the feature of the immune microenvironment and therapeutic response in CRC patients. The CMap database was adopted to screen for small molecule candidate drugs that can reverse and treat high-risk CRC patients. Finally, the expression of six IR-lncRNAs were verified by qRT-PCR in clinical specimens from our patient cohort. In conclusion, we construct an IR-lncRNA prognostic signature, which is a powerful biomarker of CRC and can accurately predict the prognosis, immune microenvironment feature, and therapeutic response of CRC patients.

SFMBT1 facilitates colon cancer cell metastasis and drug resistance combined with HMG20A.

In colorectal cancer (CRC), the development of reagents that increase sensitivity to chemotherapeutic agents could prevent drug resistance and improve patient survival. Scm-like with four malignant brain tumor domains 1 (SFMBT1) is up-regulated in CRC tumor tissues and cells and may be associated with drug resistance. We detected the expression of SFMBT1 in CRC tissue microarrays by immunohistochemistry. The role of SFMBT1 in the migration, proliferation and invasion of CRC or resistance to 5-fluorouracil (5-FU) was determined using scratch assay, colony formation and Transwell assay. Fluorescence co-localization and immunoprecipitation were used to analyze the correlation between SFMBT1 and high mobility group domain-containing protein 20 A (HMG20A). Xenograft experiments were conducted to investigate the role of SFMBT1 and HMG20A in tumor growth and metastasis in vivo. We found that SFMBT1 is up-regulated in CRC and its expression is further amplified in 5-FU resistance. SFMBT1 drives 5-FU resistance and CRC proliferation, migration and invasion. Correlation analysis shows that SFMBT1 and HMG20A are positively correlated. Mechanistically, fluorescence co-localization and immunoprecipitation assay indicate an interaction between SFMBT1 and HMG20A. Depletion of SFMBT1 down-regulates HMG20A downstream. These results were verified by murine xenograft and lung metastasis models. Our results indicate that the SFMBT1/HMG20A axis could be targeted to increase the resistance of CRC cells to 5-FU.

CAMTA1-PPP3CA-NFATc4 multi-protein complex mediates the resistance of colorectal cancer to oxaliplatin.

Colorectal cancer is a major contributor to the worldwide prevalence of cancer-related deaths. Metastasis and chemoresistance are the two main causes for colorectal cancer treatment failure, and thus, high mortality. Calmodulin-binding transcription activator 1 (CAMTA1) is involved in tumor growth and development, but its mechanisms of action in the development of colorectal cancer and chemoresistance are poorly understood. Here, we report that Camta1 is a tumor suppressor. Immunohistochemical staining and western blotting analyses of normal and colorectal cancer tissues showed a significantly low expression of Camta1 expression in colorectal cancer tissues, when compared to adjacent normal tissues. In functional in vitro experiments, we observed that Camta1 overexpression significantly decreased the proliferation and invasion capacity of SW620 and SW480 cells, whereas Camta1 knockdown displayed a significant increase in the proliferative and invasive ability of these cells. Subsequently, we examined the effects of Camta1 overexpression and knockdown on the resistance of colorectal cancer cells to oxaliplatin, a common chemotherapeutic drug. Interestingly, the sensitivity of Camta1-overexpressed cells to oxaliplatin was increased, whereas that of Camta1-silenced cells to the same chemotherapeutic drug was decreased. Furthermore, Camta1 knockdown upregulated nuclear factor of activated T cells, cytoplasmic 4 (Nfatc4) mRNA, and protein levels in colorectal cancer cells and downregulated the phosphorylated NFATc4 level. By contrast, Nfatc4 knockdown reversed the resistance of colorectal cancer cells to oxaliplatin caused by Camta1 knockdown. In addition, we show that protein phosphatase 3 catalytic subunit alpha (PPP3CA) is essential for the expression and phosphorylation of NFATc4 caused by Camta1 knockdown, as well as the proliferation, invasion, and chemoresistance of colorectal cancer cells. We show that PPP3CA and CAMTA1 competitively bind to NFATc4, and Camta1 knockdown promotes the dephosphorylation of PPP3CA and suppresses the phosphorylation of NFATc4. To verify the role of CAMTA1 in oxaliplatin resistance in colorectal cancer, we established a xenograft mouse model and show agreement between in vitro and in vivo results.

Identification of Key Genes and Pathways Involved in Circulating Tumor Cells in Colorectal Cancer.

BACKGROUND: Characterization of the features associated with circulating tumor cells (CTCs) is one of major interests for predicting clinical outcome of colorectal cancer (CRC) patients. However, the molecular features of CTCs remain largely unclear. METHODS: For identification of key genes and pathways, GSE31023, contained CTCs from six metastatic CRC patients and three controls, was retrieved for differentially expressed gene (DEG) analysis. Protein-protein interaction networks of DEGs were constructed. Hub genes from the network were prognostic analyzed, as well as the association with tumor-infiltrating immune cells. RESULTS: 1353 DEGs were identified between the CTC and control groups, with 403 genes upregulated and 950 downregulated. 32 pathways were significantly enriched in KEGG, with ribosome pathway as top. The top 10 hub genes were included, including eukaryotic translation elongation factor 2 (EEF2), ribosomal protein S2 (RPS2), ribosomal protein S5 (RPS5), ribosomal protein L3 (RPL3), ribosomal protein S3 (RPS3), ribosomal protein S14 (RPS14), ribosomal protein SA (RPSA), eukaryotic translation elongation factor 1 alpha 1 (EEF1A1), ribosomal protein S15a (RPS15A), and ribosomal protein L4 (RPL4). The correlation between CD4+ T cells and RPS14 (correlation = -0.5) was the highest in colon cancer while CD8+ T and RPS2 (correlation = -0.53) was the highest in rectal cancer. CONCLUSION: This study identified potential role of ribosome pathway in CTC, providing further insightful therapeutic targets and biomarkers for CRC.

A mechanistic investigation of the Li10GeP2S12|LiNi1-x-yCoxMnyO2 interface stability in all-solid-state lithium batteries.

All-solid-state batteries are intensively investigated, although their performance is not yet satisfactory for large-scale applications. In this context, the combination of Li10GeP2S12 solid electrolyte and LiNi1-x-yCoxMnyO2 positive electrode active materials is considered promising despite the yet unsatisfactory battery performance induced by the thermodynamically unstable electrode|electrolyte interface. Here, we report electrochemical and spectrometric studies to monitor the interface evolution during cycling and understand the reactivity and degradation kinetics. We found that the Wagner-type model for diffusion-controlled reactions describes the degradation kinetics very well, suggesting that electronic transport limits the growth of the degradation layer formed at the electrode|electrolyte interface. Furthermore, we demonstrate that the rate of interfacial degradation increases with the state of charge and the presence of two oxidation mechanisms at medium (3.7 V vs. Li+/Li < E < 4.2 V vs. Li+/Li) and high (E ≥ 4.2 V vs. Li+/Li) potentials. A high state of charge (>80%) triggers the structural instability and oxygen release at the positive electrode and leads to more severe degradation.

Super-Enhancer Induced IL-20RA Promotes Proliferation/Metastasis and Immune Evasion in Colorectal Cancer.

Unveiling key oncogenic events in malignancies is the key to improving the prognosis and therapeutic outcome of malignancies. Lines of evidence have shown that super-enhancers control the expression of genes that determine the cell fate, but the oncogenic super-enhancers in colorectal cancer (CRC) and their impact on carcinogens remain largely unexplored. Here, we identified a new oncogenic super-enhancer-regulated gene, IL-20RA, in CRC. Using the integrative analysis of H3K27ac ChIP-seq and RNA-seq in CRC tumors and normal colon tissues, we obtained a series of oncogenic super-enhancers in CRC. We found that super-enhancer inhibition by JQ-1 or iBET-151 suppressed the growth of tumor cells and inhibited the expression of IL-20RA. We found that IL-20RA was highly expressed in the tumor tissue of CRC and related to the advanced stage. Further functional studies showed that knockdown of IL-20RA inhibited the growth and metastasis of CRC. In addition, we found that IL-20RA was involved in regulating oncogenic and immune pathways and affecting the expression of genes related to cell proliferation and immune evasion in CRC. Together, our study demonstrated a novel oncogene in CRC and shed new light on oncogenic super-enhancer contributions to cell proliferation and immune escape.

Detection and Clinical Value of Circulating Tumor Cells as an Assisted Prognostic Marker in Colorectal Cancer Patients.

BACKGROUND: Circulating tumor cells (CTCs) are cells that have been shed into the vasculature from a primary tumor and circulate in the bloodstream. It has been suggested that detecting CTCs could help the clinician to detect early metastasis or recurrence more effectively. This trial sets out to assess the detection and clinical value of CTCs as an assisted prognostic marker in patients with colon cancer and rectal cancer. METHODS: A prospective cohort of patients with colorectal cancer (CRC) was enrolled from July 2015 to February 2018 in Shanghai Minimally Invasive Surgery Center, Shanghai, China. In this study, 149 patients with CRC were enrolled and underwent surgical treatment. There were 79 cases of colon cancer and 70 cases of rectal cancer, including 93 males and 56 females. To investigate the correlativity and clinical value of CTCs, the patients were statistically analyzed in different subgroups: colon cancer group vs rectal cancer group, and left hemicolon cancer group vs right hemicolon cancer group. RESULTS: The results of analysis comparing CTC counts and clinical pathological features in colon and rectal cancer indicated that with increased tumor stage, the number of CTCs also increased, with significant statistical differences. CTC counts in patients with colon and rectal cancer showed positive correlations with TNM staging (P=0.001, 0.013, respectively), T staging (P=0.021, 0.001), N staging (P=0.014, 0.035) and M staging (P=0.018, 0.203). Detection of serum biomarkers in CTC-positive and CTC-negative groups indicated a significantly increasing expression in the CTC-positive group. To confirm the correlations between CTCs and histoembryological differences, analysis was conducted with the patients in two subgroups: left hemicolon cancer group and right hemicolon cancer group. The results showed that the positive rate of CTCs increased in both groups with the increase in tumor stage. The survival analysis indicated that there was a steep gradient in survival in the follow-up period, particularly in the CTC-positive group (P=0.000). Risk assessment curves showed that the change escalated more rapidly in the CTC-positive group. Furthermore, with the increase in T stage, changes in the survival curve and risk curve escalated more rapidly in the CTC-positive group. CONCLUSION: It was confirmed that in the left hemicolon cancer group, a much higher coincidence rate could be found on CTC-positive rate and clinicopathological features, than in the right hemicolon cancer group. The sensitivity of CTCs may be related to the histoembryological location of the tumor, lymphatic metastasis and the depth of infiltration. Monitoring CTCs may have value in evaluating clinical staging and estimating clinical prognosis.

Ratiometric nanoprobe for circulating tumor cell detection and intracellular hydrogen peroxide evaluation in colorectal cancer patients.

The application of intensity-based H2O2-responsive fluorescence nanoprobe for circulating tumor cell detection was limited by the complex background and the nanoprobe uptake in each CTC. In this context, we developed a ratiometric fluorescence nanoprobe, on which a H2O2-responsive subunit and a stable subunit grafted working as a H2O2 detector and a reference, respectively. When responding to intracellular H2O2, the reference fluorescence (580 nm) maintained as a correction background while the detector fluorescence (450 nm) was turned on to conduct CTC enumeration and intracellular H2O2 evaluation. Two normal cells and three colon cancer cells were examined to evaluate their endogenous H2O2 with the ratiometric nanoprobe by flow cytometry and confocal laser scanning microscopy. CTC sample from colorectal cancer patients was used to validate the performance of the nanoprobe for CTC enumeration and H2O2 evaluation. The results indicated that not only CTC could be effectively identified based on the "turn on" fluorescence, but also the viability of the identified CTCs could be assessed with the intensity of the reference fluorescence to avoid the false-positive number. Moreover, the clinical results demonstrated that the viability CTC count combined with intracellular H2O2 content (described as I450/580)were related to the tumor TNM stage, which might provide significant guidance for clinical treatments.

Hydrogen peroxide-response nanoprobe for CD44-targeted circulating tumor cell detection and H2O2 analysis.

Circulating tumor cells (CTCs) represent the most common way of tumor metastasis and has been considered as a significant index for tumor diagnosis, staging and prognosis. However, CTC detection and analysis are always limited by the scarcity of CTC in the peripheral blood and the interference of blood cells. Therefore, here we presented with a hydrogen peroxide (H2O2)-response nanoprobes with CD44-targeted ability to reduce the interference of blood cells and improve the detection efficiency and accuracy and the pancreatic cancer cell was used to evaluate the feasibility of our probe. Shortly, hydrophobic H2O2-response naphthalimide-borate fluorophore was introduced onto the hydrophilic hyaluronic acid to form an amphiphilic complex, which could self-assemble into fluorescent nanoprobes in water. Our studies demonstrated that the nanoprobes were not only able to specifically recognize the pancreatic cancer cells with overexpressed CD44 proteins and reduce the influence of white blood cells in the peripheral blood, but also capable of semi-quantifying H2O2 content in CTCs, Which could be further used as a significant index for tumor clinical evaluation and therapy.

Inhibition of KHSRP sensitizes colorectal cancer to 5-fluoruracil through miR-501-5p-mediated ERRFI1 mRNA degradation.

K-homology (KH)-type splicing regulatory protein (KHSRP) is an RNA binding protein that participates in RNA variable splicing and stability, and facilitates the biogenesis of miRNAs that target mRNA. However, to date, the role of KHSRP in colorectal cancer (CRC) progression has not been reported. In this study, the function of KHSRP in CRC proliferation and 5-fluoruracil (5-FU) resistance was investigated. The upregulation of KHSRP expression was confirmed in CRC patient tissues and two CRC cell lines. Manipulating KHSRP expression altered cell proliferation and 5-FU resistance in CRC cells. ERRFI1, a downstream effector of KHSRP in CRC cells, reduced CRC cell proliferation. Sensitivity to 5-FU mediated by KHSRP knockdown was reversed by ERRFI1 knockdown. We found that KHSRP decreased ERRFI1 mRNA expression indirectly. By screening KHSRP-regulated miRNAs, we further found that miR-501-5p directly combines with KHSRP in CRC cells. Mechanistically, the results of a luciferase assay suggested that miR-501-5p directly binds to the ERRFI1 3'-untranslated region. Taken together, our data indicated that modification of ERRFI1 by KHSRP occurs through miR-501-5p, an essential mechanism driving CRC proliferation and 5-FU resistance. Insight into this mechanism may provide novel targets for overcoming drug resistance in CRC.

Prediction of key genes and pathways involved in trastuzumab-resistant gastric cancer.

BACKGROUND: Trastuzumab has been prevailingly accepted as a beneficial treatment for gastric cancer (GC) by targeting human epidermal growth factor receptor 2 (HER2)-positive. However, the therapeutic resistance of trastuzumab remains a major obstacle, restricting the therapeutic efficacy. Therefore, identifying potential key genes and pathways is crucial to maximize the overall clinical benefits. METHODS: The gene expression profile GSE77346 was retrieved to identify the differentially expressed genes (DEGs) associated with the trastuzumab resistance in GC. Next, the DEGs were annotated by the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The DEGs-coded protein-protein interaction (PPI) networks and the prognostic values of the 20 hub genes were determined. Correlation of the hub genes were analyzed in The Cancer Genome Atlas. The prognostic values of hub genes were further validated by Kaplan-Meier (KM) plotter. RESULTS: A total of 849 DEGs were identified, with 374 in upregulation and 475 in downregulation. Epithelium development was the most significantly enriched term in biological processes while membrane-bounded vesicle was in cellular compartments and cell adhesion molecular binding was in molecular functions. Pathways in cancer and ECM-receptor interaction were the most significantly enriched for all DEGs. Among the PPI networks, 20 hub genes were defined, including CD44 molecule (CD44), HER-2, and cadherin 1 (CDH1). Six hub genes were associated with favorable OS while eight were associated with poor OS. Mechanistically, 2'-5'-oligoadenylate synthetase 1, 3 (OAS1, OAS3) and CDH1 featured high degrees and strong correlations with other hub genes. CONCLUSIONS: This bioinformatics analysis identified key genes and pathways for potential targets and survival predictors for trastuzumab treatment in GC.

On the Stability of NaO2 in Na-O2 Batteries.

Na-O2 batteries are regarded as promising candidates for energy storage. They have higher energy efficiency, rate capability, and chemical reversibility than Li-O2 batteries; in addition, sodium is cheaper and more abundant compared to lithium. However, inconsistent observations and instability of discharge products have inhibited the understanding of the working mechanism of this technology. In this work, we have investigated a number of factors that influence the stability of the discharge products. By means of in operando powder X-ray diffraction study, the influence of oxygen, sodium anode, salt, solvent, and carbon cathode were investigated. The Na metal anode and an ether-based solvent are the main factors that lead to the instability and decomposition of NaO2 in the cell environment. This fundamental insight brings new information on the working mechanism of Na-O2 batteries.

Nanocellulose Modified Polyethylene Separators for Lithium Metal Batteries.

Poor cycling stability and safety concerns regarding lithium (Li) metal anodes are two major issues preventing the commercialization of high-energy density Li metal-based batteries. Herein, a novel tri-layer separator design that significantly enhances the cycling stability and safety of Li metal-based batteries is presented. A thin, thermally stable, flexible, and hydrophilic cellulose nanofiber layer, produced using a straightforward paper-making process, is directly laminated on each side of a plasma-treated polyethylene (PE) separator. The 2.5 µm thick, mesoporous (≈20 nm average pore size) cellulose nanofiber layer stabilizes the Li metal anodes by generating a uniform Li+ flux toward the electrode through its homogenous nanochannels, leading to improved cycling stability. As the tri-layer separator maintains its dimensional stability even at 200 °C when the internal PE layer is melted and blocks the ion transport through the separator, the separator also provides an effective thermal shutdown function. The present nanocellulose-based tri-layer separator design thus significantly facilitates the realization of high-energy density Li metal-based batteries.

Redox-Active Separators for Lithium-Ion Batteries.

A bilayered cellulose-based separator design is presented that can enhance the electrochemical performance of lithium-ion batteries (LIBs) via the inclusion of a porous redox-active layer. The proposed flexible redox-active separator consists of a mesoporous, insulating nanocellulose fiber layer that provides the necessary insulation between the electrodes and a porous, conductive, and redox-active polypyrrole-nanocellulose layer. The latter layer provides mechanical support to the nanocellulose layer and adds extra capacity to the LIBs. The redox-active separator is mechanically flexible, and no internal short circuits are observed during the operation of the LIBs, even when the redox-active layer is in direct contact with both electrodes in a symmetric lithium-lithium cell. By replacing a conventional polyethylene separator with a redox-active separator, the capacity of the proof-of-concept LIB battery containing a LiFePO4 cathode and a Li metal anode can be increased from 0.16 to 0.276 mA h due to the capacity contribution from the redox-active separator. As the presented redox-active separator concept can be used to increase the capacities of electrochemical energy storage systems, this approach may pave the way for new types of functional separators.

Hydrogen Peroxide-Responsive Nanoprobe Assists Circulating Tumor Cell Identification and Colorectal Cancer Diagnosis.

In the clinic, numeration of circulating tumor cells (CTCs) plays a critical role in cancer diagnosis and treatment, but conventional CTC identification and counting that rely on specific antibodies to characterize a cell's surface antigens are costive and with limitations. Importantly, false positive or negative results may occur due to the high heterogeneity and epithelial-mesenchymal transition (EMT) of CTCs. Herein we demonstrate a novel and effective CTC detecting nanoprobe that could rapidly respond to the high level of endogenous H2O2 of CTCs and report the signal through fluorescence emission. Briefly, a hydrophobic coumarin-benzene boronic acid pinacol ester (Cou-Bpin) was grafted onto hydrophilic glycol chitosan (GC) to form an amphiphilic molecule, which further assembled into micellar nanoparticles in aqueous solution. This new nanoprobe was highly sensitive to H2O2 with a detection limit of 0.1 µM and could rapidly enter the cells within 30 min. Upon exposure to intracellular H2O2, the nanoprobe exhibited remarkable one-photon and two-photon luminescent characteristics, which were suitable for imaging of endogenous H2O2 of various human colorectal cancer cells and assist the identification of CTCs. Compared to a conventional CTC counting assay, the nanoprobe-based CTC numeration could overcome the false-negative findings due to the low expression of cytokeratin 19 (CK19). In a clinic test, CTC counting results based on the new nanoprobe match better to the postoperative pathological results of four clinic patients who had colorectal cancer at different stages.

Tumor Localization for Laparoscopic Colorectal Resection Without Endoscopic Tattooing.

INTRODUCTION: Tumor localization is a key step in laparoscopic colorectal surgery. Endoscopic tattooing is widely practiced with a satisfactory accuracy, whereas few studies have investigated its shortcomings. The aim of our study is to assess the accuracy and efficiency of a tumor localization protocol without endoscopic tattooing. METHODS: The tumor localization protocol was performed for 788 colorectal cancer/polyp patients undergoing laparoscopic colorectal resection. The localization accuracy was evaluated by the intraoperative exploration and the anatomopathologic results. RESULTS: The localization accuracy was 100% in our study. The drawbacks of endoscopic tattooing were overcome. Only 16.6% of the patients underwent preoperative endoscopic clip placement. Intraoperative colonoscopy was performed as a planned and purposive procedure instead of a remedial measurement. The misplacement of the camera port for laparoscopy was avoided in 18 cases (2.3%) guided by this protocol. CONCLUSIONS: Colorectal tumor localization could be improved by this tumor localization protocol without endoscopic tattooing.