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A diamond-like amorphous Fe-Co-PO x catalyst is created through a controllable amorphization engineering. It showcases wonderful OER activity, reaching a potential of 270 mV at 10 mA cm−2, and can operate as an anode stably at 200 mA cm−2 for 300 h with little degradation in overall water splitting. Studies observe that the unique amorphous structure, abundant oxygen vacancies, and the synergistic effect of Fe and Co species are the keys to gain excellent water splitting performance. [Display omitted] • An amorphous FeCo-PO x is constructed by hydrothermal and phosphating treatments. • The catalyst owns a diamond-like morphology and abundant oxygen vacancies. • The catalyst exhibits excellent OER and overall water splitting activity and stability. • The synergy of rich oxygen vacancy and amorphous structure are the key to improve performance. Strategically tuning the composition and structure of transition metal phosphates (TMPs) holds immense promise in the development of efficient oxygen evolution reaction (OER) electrocatalysts. However, the effect of crystalline phase transformation for TMPs on the catalytic OER activity remains relatively uncharted. In this study, we have deftly orchestrated the reaction process of anion-etched precursor to induce the amorphization process of FeCo-PO x from crystalline to amorphous states. The as-obtained amorphous FeCo-PO x (A-FeCo-PO x) exhibited an optimized OER performance with a low overpotential of 270 mV at a current density of 10 mA cm−2, which could be attributed to the flexibility of its amorphous structure and the synergistic effect of oxygen vacancies. Moreover, when incorporated into an overall water splitting (OWS) device configured as A-FeCo-POx(+)||Pt/C(–), it displayed long-term solid stability, sustaining operation for 300 h at a current density of 200 mA cm−2. This work not only provides valuable insights into understanding the transformation from crystalline to amorphous states, but also establishes the groundwork for the practical utilization of amorphous nanomaterials in the field of water splitting. [ABSTRACT FROM AUTHOR]

Huntington's disease (HD) is a progressive genetic neurodegenerative disease caused by an abnormal expansion of a cytosine-adenine-guanine trinucleotide repeat in the huntingtin gene. One pathological feature of HD is neuronal loss in the striatum. Despite many efforts, mechanisms underlying neuronal loss in HD striatum remain elusive. It was suggested that the mutant huntingtin protein interacts mitochondrial proteins and causes mitochondrial dysfunction in striatal neurons. However, whether axonal transport of mitochondria is altered in HD striatal neurons remains controversial. Here, we examined axonal transport of single mitochondria labelled with Mito-DsRed2 in cultured striatal neurons of zQ175 knock-in mice (a knock-in mouse model of HD). We observed decreased anterograde axonal transport of proximal mitochondria in HD striatal neurons compared with wild-type (WT) striatal neurons. Decreased anterograde transport in HD striatal neurons was prevented by overexpressing mitochondrial Rho GTPase 1 (Miro1). Our results offer a new insight into mechanisms underlying neuronal loss in the striatum in HD. • Cultured striatal neurons were mainly MSNs that are the most vulnerable neurons in HD. • Anterograde axonal transport of proximal mitochondria was altered in HD striatal neurons. • Overexpressing Miro1 prevented altered mitochondrial transport in HD striatal neurons. [ABSTRACT FROM AUTHOR]

Graphical abstract Abstract The mixing of binary droplets is of paramount importance in microfluidic systems. In order to reveal the mixing mechanism of two free droplets suspended in the immiscible phase, we have developed a novel experimental setup to study the internal mixing in coalescing droplets with varying interfacial tension differences and droplet sizes. It is confirmed that the interfacial energy of droplets supports the jet flow and liquid bridge expansion during the coalescence of droplets. The increase of interfacial tension difference can increase the intensity of jet flow accompanied with slower liquid bridge expansion, which enhances the mixing of droplets. The decrease of droplet size can increase the initial velocity of jet flow. However, the intensity of jet flow decreases due to the rapid expansion of the liquid bridge, which results in weaker internal mixing. On this basis, a Reynolds number incorporating the jet velocity and droplet size is proposed to characterize the vortex size, which represents the degree of droplet mixing. This study presents an effective approach for enhancing the mixing of droplets. [ABSTRACT FROM AUTHOR]

Glioblastoma (GBM) is the deadliest primary brain tumor that is highly resistant to current treatments. Polo-like kinase 1 (PLK1) and signal transducer and activator of transcription 3 (STAT3) are highly expressed in gliomas, especially GBM. Previous studies have shown reciprocal activation between PLK1 and STAT3 and that they regulate the same pools of MYC downstream. We have demonstrated that PLK1 and STAT3 levels are elevated in gliomas compared with those in normal brain tissues, and high expression of both PLK1 and STAT3 is associated with poor prognosis in TCGA. Moreover, there was direct or indirect reciprocal regulation between PLK1 and STAT3. Furthermore, we found that PLK1 and STAT3 can regulate the same pools of MYC downstream. Compared to monotherapy, combined treatment of glioma cells with PLK1 and STAT3 inhibitors, BI2536 and Stattic, respectively, showed lower expression of MYC, synergistic induction of cell invasion and apoptosis in vitro, and tumor inhibition in xenografts. PLK1 and STAT3 were able to directly regulate the expression of MYC and induce apoptosis of glioma cells through the regulation of MYC. These findings may help develop a therapeutic strategy for dual inhibition of PLK1 and STAT3 against the tumorigenesis of glioma. • PLK1 and STAT3 expression increased in GBM tissues. • PLK1 interacts with STAT3 in GBM. • PLK1 and STAT3 were able to directly regulate the expression of MYC. • Dual pLK1 and STAT3 inhibition promotes glioblastoma cells apoptosis via MYC. [ABSTRACT FROM AUTHOR]

Development of the strategy to regulate the acidic properties of solid superacids had been attracting widespread attention in the acidic catalysis-related fields. In the present work, an HCl-promoted SO 4 2−/TiO 2 solid composite superacid was synthesized by incorporation of hydrogen chloride into sulfated titania (SO 4 2−/TiO 2). The Brønsted acid strength of HCl-promoted SO 4 2−/TiO 2 was significantly increased compared with that of SO 4 2−/TiO 2. Friedel-Crafts alkylation reaction results of HCl-promoted SO 4 2−/TiO 2 showed an increase by 27% in reaction rate and decreased byproduct selectivity (1% versus 10% for HCl-promoted SO 4 2−/TiO 2 and SO 4 2−/TiO 2 , respectively). Structural characterizations demonstrated that HCl had the synergetic effect with induced titanium ion of HCl-promoted SO 4 2−/TiO 2 to form a new type of Brønsted acidic site. The configuration of enhanced Brønsted acidic site verified by DFT calculations was more liable to release the proton than that of conventional Brønsted acidic site, consequently increasing the Brønsted acid strength of HCl-promoted SO 4 2−/TiO 2. Hydrogen chloride is incorporated into sulfated titania to synthesize a HCl-promoted SO 4 2−/TiO 2 solid composite super-strong acid. Synergistic effect of hydrogen chloride with induced titanium endows HCl-promoted SO 4 2−/TiO 2 with enhanced Brønsted acid strength. [Display omitted] • HCl was incorporated into sulfated titania to prepare a solid composite acid. • HCl-promoted SO 4 2−/TiO 2 possessed the enhanced Brønsted acid strength. • Synergetic effect between HCl and induced titanium site was analyzed. • Configuration of a novel Brønsted acid site was proposed. [ABSTRACT FROM AUTHOR]