Long noncoding RNAs (lncRNAs) play important regulatory roles in a variety of diseases, including many tumors. However, the functional roles of these transcripts and mechanisms responsible for their deregulation in pancreatic ductal adenocarcinoma (PDAC) are not thoroughly understood. In this study, we discovered that lncRNA MIR31HG is markedly upregulated in PDAC. Knockdown of MIR31HG significantly suppressed PDAC cell growth, induced apoptosis and G1/S arrest, and inhibited invasion, whereas enhanced expression of MIR31HG had the opposite effects. Online database analysis tools showed that miR-193b could target MIR31HG and we found an inverse correlation between MIR31HG and miR-193b in PDAC specimens. Inhibition of miR-193b expression significantly upregulated the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b. Moreover, using luciferase reporter and RIP assays, we provide evidence that miR-193b directly targeted MIR31HG by binding to two microRNA binding sites in the MIR31HG sequence. On the other hand, MIR31HG may act as an endogenous ‘sponge' by competing for miR-193b binding to regulate the miRNA targets. Collectively, these results demonstrate that MIR31HG functions as an oncogenic lncRNA that promotes tumor progression, and miR-193b targets not only protein-coding genes but also the lncRNA, MIR31HG.

The dissolution of platinum (Pt) has been one of the heart issues in developing advanced dye-sensitized solar cells (DSSCs). We present here the experimental realization of stable counter-electrode (CE) electrocatalysts by alloying Pt with transition metals for enhanced dissolution resistance to state-of-the-art iodide/triiodide (I(-)/I3(-)) redox electrolyte. Our focus is placed on the systematic studies of dissolution engineering for PtM0.05 (M=Ni, Co, Fe, Pd, Mo, Cu, Cr, and Au) alloy CE electrocatalysts along with mechanism analysis from thermodynamical aspects, yielding more negative Gibbs free energies for the dissolution reactions of transition metals. The competitive reactions between transition metals with iodide species (I3(-), I2) could protect the Pt atoms from being dissolved by redox electrolyte and therefore remain the high catalytic activity of the Pt electrode.

Increasing evidence indicates that activated microglia play an important role in the inflammatory response following traumatic brain injury (TBI). Inhibiting M1 and stimulating M2 activated microglia have demonstrated protective effects in several animal models of central nervous system diseases. However, it is not clear whether the polarization of microglia to M2 attenuates axonal injury following TBI. In this study, we used a lateral fluid percussion injury device to induce axonal injury in mice. Mice were randomly assigned to the sham, TBI, TBI + rosiglitazone (peroxisome proliferator-activated receptor gamma [PPAR-γ] agonist), and TBI + GW9662 (PPAR-γ antagonist) groups. Axonal injury was assessed using immunohistochemical staining for beta amyloid precursor protein. The inflammatory response was assessed by enzyme-linked immunosorbent assay, microglia polarization was assessed using specific markers of M1 and M2 microglia, and neurological function was assessed using the neurological severity score. Following TBI, microglia of the M1 phenotype increased significantly, while those of the M2 phenotype decreased. Rosiglitazone-induced PPAR-γ activation promoted microglia polarization to the M2 phenotype, which reduced the inflammatory response, attenuated axonal injury in the cerebral cortex, and improved neurological function. Conversely, GW9662 inhibited the polarization of microglia to M2 and aggravated inflammation and axonal injury. Our in vitro findings in lipopolysaccharide-induced microglia were consistent with those of our in vivo experiments. In conclusion, the polarization of microglia to the M2 phenotype via PPAR-γ activation attenuated axonal injury following TBI in mice, which may be a potential therapeutic approach for TBI-induced axonal injury.

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Human flap endonuclease 1 (hFEN1) is instrumental in DNA replication and repair. It is able to cleave the 5′ single-stranded protrusion (also known as 5′ flap) resulting from strand displacement reactions. In light of its crucial functions, hFEN1 is now deemed as a nontrivial target in the DNA damage response system for anticancer drug development. Herein, we report that myricetin and some natural flavonoids are able to inhibit hFEN1. Structure–activity relationship, inhibitory mechanisms, molecular docking, and cancer cell-based assays have been performed. Our original findings expand the activity of flavonoids and may pave the way for flavonoid-assisted targeted cancer therapy.

Despite the great progress of flexible perovskite solar cells (f-PSCs), it still faces several challenges during the homogeneous fabrication of high-quality perovskite thin films, and overcoming the insufficient exciton dissociation. To the ends, we rationally design the ferroelectric two-dimensional (2D) perovskite based on pyridine heterocyclic ring as the organic interlayer. We uncover that incorporation of the ferroelectric 2D material into 3D perovskite induces an increased builtin electric field (BEF), which enhances the exciton dissociation efficiency in the device. Moreover, the 2D seeds could assist the 3D crystallization by forming more homogeneous and highly-oriented perovskite crystals. As a result, an impressive power conversion efficiency (PCE) over 23 % has been achieved by the f-PSCs with outstanding ambient stability. Moreover, the piezo/ ferroelectric 2D perovskite intrigues a decreased hole transport barriers at the ITO/perovskite interface under tensile stress, which opens new possibilities for developing highly-efficient f-PSCs.

This study shows for the first time that S1P protects primordial follicles in human ovarian grafts from a chemotherapy drug treatment via suppressing follicle apoptosis.