Y-shaped ZnO nanobelts are fabricated by a simple thermal evaporation method. Transmission Electron Microscopy (TEM) investigation shows that these ZnO nanobelts are crystals with twinned planes {11–21}. Convergent Beam Electron Diffraction studies show that the two sides of twinned nanobelts are O-terminated towards the twinned boundary and Zn-terminated outwards. The two branches of twinned ZnO nanobelts grow along [11–26] from the trunk and then turn to the polarization direction [0001]. The featured Y-shape morphology and TEM characterizations indicate that the growth of these novel nanostructures is driven by an unusual twinned dislocation growth mechanism.

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The superior performance of metal oxide nanocomposites has introduced them as excellent candidates for emerging energy sources, and attracted significant attention in recent years. The drawback of these materials is their inherent structural pulverization which adversely impacts their performance and makes the rational design of stable nanocomposites a great challenge. In this work, functional V2O5-C-SnO2 hybrid nanobelts (VCSNs) with a stable structure are introduced where the ultradispersed SnO2 nanocrystals are tightly linked with glucose on the V2O5 surface. The nanostructured V2O5 acts as a supporting matrix as well as an active electrode component. Compared with existing carbon-V2O5 hybrid nanobelts, these hybrid nanobelts exhibit a much higher reversible capacity and architectural stability when used as anode materials for lithium-ion batteries. The superior cyclic performance of VCSNs can be attributed to the synergistic effects of SnO2 and V2O5. However, limited data are available for V2O5-based anodes in lithium-ion battery design.

As a key regulator of the DNA translesion synthesis (TLS) pathway, RAD18 is error-prone and contributes to the accumulation of DNA mutations. Our previous study showed that it plays an essential role in the progression of multiple tumors. However, the mechanism through which RAD18 influences triple-negative breast cancer (TNBC), especially the interaction between tumor cells and the tumor microenvironment, remains elusive. In this study, we showed that RAD18 expression is markedly higher in patients with high T stage TNBC and inversely correlated with prognosis. High expression of RAD18 facilitated a highly stem-cell phenotype through the Hippo/YAP pathway, which supports the proliferation of TNBC. In addition, the cytokine byproduct TGF-β activates macrophages to have an M2-like tumor-associated macrophage (TAM) phenotype. Reciprocally, TGF-β from TAMs activated RAD18 in TNBC to enhance tumor stemness, forming a positive feedback loop. Inhibition of YAP or TGF-β breaks this loop and suppresses cancer stemness and proliferation In nude mice, RAD18 promoted subcutaneous transplanted tumor growth and M2-type TAM recruitment. Collectively, the RAD18-YAP-TGF-β loop is essential for the promotion of the stemness phenotype by TNBC and could be a potential therapeutic target for TNBC.