Built-in Electric Field-Assisted Surface-Amorphized Nanocrystals for High-Rate Lithium-Ion Battery

High-power batteries require fast charge/discharge rates and high capacity besides safe operation. TiO₂ has been investigated as a safer alternative candidate to the current graphite or incoming silicon anodes due to higher redox potentials in effectively preventing lithium deposition. However, its charge/discharge rates are reluctant to improve due to poor ion diffusion coefficients, and its capacity fades quickly with rate as only thinner surface layers can be effectively used in faster charge/discharge processes. Here, we demonstrate that surface-amorphized TiO₂ nanocrystals greatly improve lithium-ion rechargeable battery performance: 20 times rate and 340% capacity improvement over crystalline TiO₂ nanocrystals. This improvement is benefited from the built-in electric field within the nanocrystals that induces much lower lithium-ion diffusion resistance and facilitates its transport in both insertion and extraction processes. This concept thus offers an innovative and general approach toward designing battery materials with better performance

Table1_The m6A-regulation and single cell effect pattern in sunitinib resistance on clear cell renal cell carcinoma: Identification and validation of targets.docx

Background: Sunitinib is the main target drug for clear cell renal cell carcinoma. However, the effect of sunitinib is often limited by acquired drug resistance.Methods: The open-accessed data used in this study were obtained from different online public databases, which were analyzed using the R software. The RNA level of specific genes was detected using quantitative Real-Time PCR. Sunitinib-resistant cell lines were constructed based on protocol get from the previous study. Colony formation and Cell Counting Kit-8 assays were applied to detect cell proliferation ability.Results: In this study, through publicly available data and high-quality analysis, we deeply explored the potential biological mechanisms that affect the resistance of sunitinib. Detailed, data from GSE64052, GSE76068 and The Cancer Genome Atlas were extracted. We identified the IFITM1, IL6, MX2, PCOLCE2, RSAD2 and SLC2A3 were associated with sunitinib resistance. Single-cell analysis, prognosis analysis and m6A regulatory network were conducted to investigate their role. Moreover, the MX2 was selected for further analysis, including its biological role and effect on the ccRCC microenvironment. Interestingly, we noticed that MX2 might be an immune-related gene that could affect the response rate of immunotherapy. Then, in vitro experiments validated the overexpression of MX2 in sunitinib-resistance cells. Colony formation assay indicated that the knockdown of MX2 could remarkably inhibit the proliferation ability of 786-O-Res and Caki-1-Res when exposed to sunitinib.Conclusion: In summary, through publicly available data and high-quality analysis, we deeply explored the potential biological mechanisms that affect the resistance of sunitinib. MX2 was selected for further analysis, including its biological role and effect on the ccRCC microenvironment. Finally, in vitro experiments were used to validate its role in ccRCC.</p

Image1_The m6A-regulation and single cell effect pattern in sunitinib resistance on clear cell renal cell carcinoma: Identification and validation of targets.TIF

Background: Sunitinib is the main target drug for clear cell renal cell carcinoma. However, the effect of sunitinib is often limited by acquired drug resistance.Methods: The open-accessed data used in this study were obtained from different online public databases, which were analyzed using the R software. The RNA level of specific genes was detected using quantitative Real-Time PCR. Sunitinib-resistant cell lines were constructed based on protocol get from the previous study. Colony formation and Cell Counting Kit-8 assays were applied to detect cell proliferation ability.Results: In this study, through publicly available data and high-quality analysis, we deeply explored the potential biological mechanisms that affect the resistance of sunitinib. Detailed, data from GSE64052, GSE76068 and The Cancer Genome Atlas were extracted. We identified the IFITM1, IL6, MX2, PCOLCE2, RSAD2 and SLC2A3 were associated with sunitinib resistance. Single-cell analysis, prognosis analysis and m6A regulatory network were conducted to investigate their role. Moreover, the MX2 was selected for further analysis, including its biological role and effect on the ccRCC microenvironment. Interestingly, we noticed that MX2 might be an immune-related gene that could affect the response rate of immunotherapy. Then, in vitro experiments validated the overexpression of MX2 in sunitinib-resistance cells. Colony formation assay indicated that the knockdown of MX2 could remarkably inhibit the proliferation ability of 786-O-Res and Caki-1-Res when exposed to sunitinib.Conclusion: In summary, through publicly available data and high-quality analysis, we deeply explored the potential biological mechanisms that affect the resistance of sunitinib. MX2 was selected for further analysis, including its biological role and effect on the ccRCC microenvironment. Finally, in vitro experiments were used to validate its role in ccRCC.</p

Image2_The m6A-regulation and single cell effect pattern in sunitinib resistance on clear cell renal cell carcinoma: Identification and validation of targets.TIF

Background: Sunitinib is the main target drug for clear cell renal cell carcinoma. However, the effect of sunitinib is often limited by acquired drug resistance.Methods: The open-accessed data used in this study were obtained from different online public databases, which were analyzed using the R software. The RNA level of specific genes was detected using quantitative Real-Time PCR. Sunitinib-resistant cell lines were constructed based on protocol get from the previous study. Colony formation and Cell Counting Kit-8 assays were applied to detect cell proliferation ability.Results: In this study, through publicly available data and high-quality analysis, we deeply explored the potential biological mechanisms that affect the resistance of sunitinib. Detailed, data from GSE64052, GSE76068 and The Cancer Genome Atlas were extracted. We identified the IFITM1, IL6, MX2, PCOLCE2, RSAD2 and SLC2A3 were associated with sunitinib resistance. Single-cell analysis, prognosis analysis and m6A regulatory network were conducted to investigate their role. Moreover, the MX2 was selected for further analysis, including its biological role and effect on the ccRCC microenvironment. Interestingly, we noticed that MX2 might be an immune-related gene that could affect the response rate of immunotherapy. Then, in vitro experiments validated the overexpression of MX2 in sunitinib-resistance cells. Colony formation assay indicated that the knockdown of MX2 could remarkably inhibit the proliferation ability of 786-O-Res and Caki-1-Res when exposed to sunitinib.Conclusion: In summary, through publicly available data and high-quality analysis, we deeply explored the potential biological mechanisms that affect the resistance of sunitinib. MX2 was selected for further analysis, including its biological role and effect on the ccRCC microenvironment. Finally, in vitro experiments were used to validate its role in ccRCC.</p

Directional Heat Dissipation across the Interface in Anatase–Rutile Nanocomposites

Understanding the structures and properties of interfaces in (nano-)­composites helps to reveal their important influence on reactivity and overall performance. TiO₂ is a technologically important material, and anatase/rutile TiO₂ composites have been shown to display enhanced photocatalytic performance over pure anatase or rutile TiO₂. This has been attributed to a synergistic effect between the two phases, but the origin of this effect as well as the structure of the interface has not been established. Using Raman spectroscopy, here we provide evidence of distinct differences in the thermal properties of the anatase and rutile moieties in the composite, with anatase becoming effectively much warmer than the rutile phase under laser irradiation. With the help of first-principles calculations, we analyze the atomic structure and unique electronic properties of the composite and infer possible reasons for the directional heat dissipation across the interface