A highly porous NiO/polyaniline (PANI) composite film was prepared on ITO glass by combining the chemical bath deposition and electro-polymerization methods, successively. The porous NiO film acts as a template for the preferential growth of PANI along NiO flakes, and the NiO/PANI composite film has an intercrossing net-like morphology. The electrochromic performance of the NiO/PANI composite film was investigated in 1 M LiClO(4)+1 mM HClO(4)/propylene carbonate (PC) by means of transmittance, cyclic voltammetry (CV) and chronoamperometry (CA) measurements. The NiO/PANI thin film exhibits a noticeable electrochromism with reversible color changes from transparent yellow to purple and presents quite good transmittance modulation with a variation of transmittance up to 56% at 550 nm. The porous NiO/polyaniline (PANI) composite film also shows good reaction kinetics with fast switching speed, and the response time for oxidation and reduction is 90 and 110 ms, respectively.

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Epithelial–mesenchymal transition (EMT) was initially recognized during organogenesis and has recently been reported to be involved in promoting cancer invasion and metastasis. Cooperation of transforming growth factor-β (TGF-β) and other signaling pathways, such as Ras and Wnt, is essential to inducing EMT, but the molecular mechanisms remain to be fully determined. Here, we reported that insulin-like growth factor binding protein-related protein 1 (IGFBP-rP1), a potential tumor suppressor, controls EMT in colorectal cancer progression. We revealed the inhibitory role of IGFBP-rP1 through analyses of clinical colorectal cancer samples and various EMT and metastasis models in vitro and in vivo. Moreover, we demonstrated that IGFBP-rP1 suppresses EMT and tumor metastasis by repressing TGF-β-mediated EMT through the Smad signaling cascade. These data establish that IGFBP-rP1 functions as a suppressor of EMT and metastasis in colorectal cancer.

Blast crisis (BC) is the final deadly phase of chronic myeloid leukemia (CML), but its molecular basis remains poorly understood. Here, we show that CML BC is regulated by calcium-calmodulin-dependent kinase IIγ (CaMKIIγ). Genetic deletion of CaMKIIγ greatly inhibits disease progression via selectively impairing the self-renewal of leukemia stem cells (LSCs) in mouse models, whereas overexpression of CaMKIIγ has the opposite effects. In human CML, phosphorylated CaMKIIγ abundance is significantly associated with BC. Moreover, CaMKIIγ phosphorylates and reduces the nuclear cyclin-dependent kinase inhibitor p27Kip1, a critical brake that maintains LSC quiescence. These findings suggest that CaMKIIγ might be an important switch for the transition of CML BC and identify a unique mechanism by which CaMKIIγ promotes the self-renewal of LSCs by deceasing nuclear p27Kip1 to wake up dormant LSCs. Therefore, CaMKIIγ may provide a new therapeutic target to treat CML BC.