Tetragonal CsPbBr nanosheets were obtained by an oriented attachment of orthorhombic CsPbBr nanocubes, involving a lateral shape evolution from octagonal to square. Meanwhile, the experimental results, together with DFT simulation results, indicated that the tetragonal CsPbBr is an indirect bandgap semiconductor that is PL-inactive with a bandgap of 2.979 eV.

Increasing evidence demonstrates that pyroptosis, pro-inflammatory programmed cell death, is linked to atherosclerosis; however, the underlying mechanisms remain to be elucidated. Dihydromyricetin (DHM), a natural flavonoid, was reported to exert anti-oxidative and anti-inflammatory bioactivities. However, the effect of DHM on atherosclerosis-related pyroptosis has not been studied. In the present study, palmitic acid (PA) treatment led to pyroptosis in human umbilical vein endothelial cells (HUVECs), as evidenced by caspase-1 activation, LDH release, and propidium iodide-positive staining; enhanced the maturation and release of proinflammatory cytokine IL-1β and activation of the NLRP3 inflammasome; and markedly increased intracellular reactive oxygen species (ROS) and mitochondrial ROS (mtROS) levels. Moreover, NLRP3 siRNA transfection or treatment with inhibitors efficiently suppressed PA-induced pyroptosis, and pretreatment with total ROS scavenger or mtROS scavenger attenuated PA-induced NLRP3 inflammasome activation and subsequent pyroptosis. However, DHM pretreatment inhibited PA-induced pyroptotic cell death by increasing cell viability, decreasing LDH and IL-1β release, improving cell membrane integrity, and abolishing caspase-1 cleavage and subsequent IL-1β maturation. We also found that DHM pre-treatment remarkably reduced the levels of intracellular ROS and mtROS and activated the Nrf2 signaling pathway. Moreover, knockdown of Nrf2 by siRNA abrogated the inhibitory effects of DHM on ROS generation and subsequent PA-induced pyroptosis. Together, these results indicate that the Nrf2 signaling pathway plays a role, as least in part, in the DHM-mediated improvement in PA-induced pyroptosis in vascular endothelial cells, which implies the underlying medicinal value of DHM targeting immune/inflammatory-related diseases, such as atherosclerosis. © 2017 BioFactors, 44(2):123-136, 2018.

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wileyonlinelibrary.comBr, and I), have been intensively explored as promising photovoltaic materials and a respectable certified power conversion efficiency exceeding 22% has been achieved so far. [14] This great success has motivated research on perovskite QDs. [15] Among the various kinds of perovskites, all-inorganic lead halide perovskites, CsPbX 3 (X = Cl, Br, I), have demonstrated distinct photophysical properties, such as narrow emission line width, high quantum yield (QY) of luminescence, and short radiative lifetimes; they have thus been emerging as promising materials for applications like QD light-emitting diodes (LEDs), lasing and photodetectors. [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32] The current synthetic procedures of CsPbX 3 (X = Cl, Br, I) QDs can be mainly sorted into three routes, i.e., the direct ion reaction synthesis, anion-exchange synthesis, and the room-temperature reprecipitation. Kovalenko and co-workers pioneered the direct ion reaction synthesis of highly-luminescent CsPbX 3 (X = Cl, Br, I) nanocrystals in cubic perovskite structure using octadecene (ODE) at 140-200 °C; and through the compositional modulation and quantum size-effect, the emission could be tuned over the entire visible spectral region of 410-700 nm. [15] Following this approach, the anion-exchange method was successfully developed to prepare inorganic CsPbX 3 perovskite QDs, in which the reaction was initiated by adding another halide precursor into the parent CsPbX 3 QDs or mixing two kinds of parent QDs with different X component. [21,24] For the above two synthesis methods, CsPbX 3 QDs with good crystallinity and high yield could be obtained, but high temperature is often required to promote the reactions. At this point, room-temperature-based reprecipitation method was developed. [28,29,[33][34][35] Zeng and co-workers dissolved CsX and PbX 2 (X = Cl, Br, I) precursors in dimethylformamide (DMF) (or dimethylsulfoxide) together with oleylamine and oleic acid, then transferred the mixture to toluene, and obtained CsPbX 3 QDs at room temperature. [29] Deng and co-workers prepared the Cs-Oleate at 150 °C and by mixing the precursor with the DMF solution of PbX 2 , they synthesized various CsPbX 3 nanostructures (nanorods, nanocubes, nanoplates, and QDs) Cesium lead halide quantum dots (QDs) have tunable photoluminescence that is capable of covering the entire visible spectrum and have high quantum yields, which make them a new fluorescent materials for various applications. Here, the synthesis of CsPbX 3 (X = Cl, Br, I, or mixed Cl/Br and Br/I) QDs by direct ion reactions in ether solvents is reported, and for the first time the synergetic effects of solvent polarity and reaction temperature on the nucleation and growth of QDs are demonstrated. The use of solvent with a low polarity enables controlled growth of QDs, which facilitates the synthesis of high-quality CsPbX 3 QDs with broadly tunable luminescence, narrow emission width, and high quantum yield. A QD white LED (WLED) is demon...

Knowledge of the relative abundance of primary organic aerosol (POA) and secondary organic aerosol (SOA) forms an important scientific basis for formulating particulate matter (PM) control policies. Taking advantage of a comprehensive chemical composition data set of PM2.5 including both POA and SOA tracers (most notably, SOA tracers of a few biogenic voltaic organic compound precursors), we investigate the impact of inclusion of SOA tracers on the source apportionment of organic carbon (OC) and PM2.5 in the Pearl River Delta region of China using positive matrix factorization (PMF). In PMF runs incorporating SOA tracers (PMFw), ten PMF factors were resolved including four secondary factors: (1) SOA I (α-pinene, β-caryophyllene, and naphthalene-derived SOA), (2) SOA II (isoprene-derived SOA), (3) a secondary sulfate factor, and (4) a secondary nitrate factor. In PMF tests without SOA tracers (PMFwo), the SOA I and SOA II factors could not be extracted, but the remaining eight source factors were resolved. Among the eight common source factors, the industrial emission factor, identified by high loadings of Zn and Pb, showed the largest variations between PMFw and PMFwo solutions. The source contributions of SOA I and SOA II resolved in PMFw were largely shifted to the industry emission source in PMFwo. Secondary organic carbon (SOC) summed from the four secondary factors in PMFw contributed ∼40% (4.47 μgC/m3), and the SOC estimate by PMFwo (3.51 μgC/m3) was 21% lower due to the inability to extract SOA I and SOA II. Secondary PM2.5 by PMFwo was 6% lower than that by PMFw (23.7 vs 25.2 μg/m3). The PMFw results indicated that SOC from specific precursors may have different formation pathways than secondary sulfate and nitrate formation processes, and their source contributions could not be properly resolved without the indicative tracers included in PMF. This study demonstrates the utility of biogenic SOA tracers in resolving isoprene-derived SOA and highlights the need for more SOA tracers, especially those specific to anthropogenic precursors, in improving the source apportionment for those broad OA sources such as industrial emissions.

Our previous study has shown that ampelopsin (AMP), a flavonol mainly found in Ampelopsis grossedentata, could induce cell death in human breast cancer cells via reactive oxygen species generation and endoplasmic reticulum (ER) stress pathway. Here, we examined whether autophagy is activated in AMP-treated breast cancer cells and, if so, sought to find the exact role and underlying molecular profile of autophagy in AMP-induced cell death. Our results showed that AMP treatment activated autophagy in MDA-MB-231 and MCF-7 breast cancer cells, as evidenced by the accumulation of autophagosomes, an increase of microtubule-associated protein 1 light chain 3 beta-2 (LC3B-II) and the conversion of LC3B-I to LC3B-II, the degradation of the selective autophagic target p62/SQSTM1, and the formation of green fluorescent protein (GFP)-LC3 puncta. Blockage of autophagy augmented AMP-induced cell death, suggesting that autophagy has cytoprotective effects. Meanwhile, AMP treatment suppressed Akt-mammalian target of rapamycin (mTOR) pathway as evidenced by dose- and time-dependent decrease of the phosphorylation of Akt, mTOR and ribosomal protein S6 kinase (p70S6K), whereas Akt activator insulin-like growth factor-1 (IGF-1) pretreatment partially restored Akt-mTOR pathway inhibited by AMP and decreased AMP-inuduced autophagy, signifying that AMP activated autophagy via inhibition of the Akt-mTOR pathway. Additionally, blocking ER stress not only reduced autophagy induction, but also alleviated inhibition of the Akt-mTOR pathway induced by AMP, suggesting that activation of ER stress was involved in induction of autophagy and inhibition of the Akt-mTOR pathway. Taken together, these findings indicate that AMP induces protective autophagy in human breast cancer cells through Akt-mTOR pathway via ER stress.

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Our data suggested that Dp protected HUVECs against oxLDL-induced injury by inducing autophagy via the adenosine monophosphate-activated protein kinase/SIRT1 signaling pathway. This new finding might shed light to the prevention and therapy of AS.