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Hollandite-type crystals have unique and interesting physical and chemical properties. Here, we report the flux growth of hollandite-type single-crystalline potassium ferrotitanate (KFTO) with faceted surface features from a KCl flux. We varied the flux growth conditions, including the kind of flux, holding temperature, and solute concentration for growing faceted crystallites. KCl was found to be the best flux to grow the single-crystalline KFTO particles, while heating at or above 900°C was needed to yield the KFTO single crystals. The crystal growth was only weakly dependent on the solute concentration. Next, we characterized the grown single crystals and discussed the manner of their growth from the KCl flux. TEM images with clear electron diffraction spots indicated that the KFTO crystals grew along the direction to form microrods ~10 μm in size. DFT calculation results indicated that the surface energy of the (100) face is lower than that of the (001) face. Based on these characterization results, we proposed a possible growth mechanism of the KFTO crystals.

Tyrosine kinase inhibitors (TKIs) are widely utilized in clinical practice to treat carcinomas, but secondary tumor resistance during chronic treatment can be problematic. AKR1B1 and AKR1B10 of the aldo-keto reductase (AKR) superfamily are highly expressed in cancer cells and are believed to be involved in drug resistance. The aim of this study was to understand how TKI treatment of chronic myelogenous leukemia (CML) cells changes their glucose metabolism and if inhibition of AKRs can sensitize CML cells to TKIs. K562 cells were treated with the TKIs imatinib, nilotinib, or bosutinib, and the effects on glucose metabolism, cell death, glutathione levels, and AKR levels were assessed. To assess glucose dependence, cells were cultured in normal and low-glucose media. Pretreatment with AKR inhibitors, including epalrestat, were used to determine AKR-dependence. Treatment with TKIs increased intracellular glucose, AKR1B1/10 levels, glutathione oxidation, and nuclear translocation of nuclear factor erythroid 2-related factor 2, but with minimal cell death. These effects were dependent on intracellular glucose accumulation. Pretreatment with epalrestat, or a selective inhibitor of AKR1B10, exacerbated TKI-induced cell death, suggesting that especially AKR1B10 was involved in protection against TKIs. Thus, by disrupting cell protective mechanisms, AKR inhibitors may render CML more susceptible to TKI treatments.