All-solution-processed pure formamidinium-based perovskite light-emitting diodes (PeLEDs) with record performance are successfully realized. It is found that the FAPbBr device is hole dominant. To achieve charge carrier balance, on the anode side, PEDOT:PSS 8000 is employed as the hole injection layer, replacing PEDOT:PSS 4083 to suppress the hole current. On the cathode side, the solution-processed ZnO nanoparticle (NP) is used as the electron injection layer in regular PeLEDs to improve the electron current. With the smallest ZnO NPs (2.9 nm) as electron injection layer (EIL), the solution-processed PeLED exhibits a highest forward viewing power efficiency of 22.3 lm W , a peak current efficiency of 21.3 cd A , and an external quantum efficiency of 4.66%. The maximum brightness reaches a record 1.09 × 10 cd m . A record lifetime T of 436 s is achieved at the initial brightness of 10 000 cd m . Not only do PEDOT:PSS 8000 HIL and ZnO NPs EIL modulate the injected charge carriers to reach charge balance, but also they prevent the exciton quenching at the interface between the charge injection layer and the light emission layer. The subbandgap turn-on voltage is attributed to Auger-assisted energy up-conversion process.

In all-solution processed inverted quantum dots based light emitting diodes (QLEDs), the solvent erosion on the quantum dot (QD) layer prevents devices from reaching high performance. By employing an orthogonal solvent 1,4-dioxane for the hole transport layer (HTL) poly(9-vinlycarbazole) (PVK), the external quantum efficiencies (EQE) of red QLED is increased 4-fold, while the luminous efficiencies (LE) of blue QLED is enhanced by 25 times, compared to the previous devices' record. To further improve the device efficiency and reduce the efficiency roll-off, solution processed PVK/poly [(9,9-dioctylfluorenyl-2,7-diyl)-co-(4,4'-(N-(p-butylphenyl))diphenylamine)] (TFB) double-layer HTL is introduced to facilitate hole injection with stepwise energy level. By reducing the hole injection barrier, the turn-on voltage of QLEDs decreases from 3.4 to 2.7 V for red, from 5.1 to 2.7 V for green, and from 5.3 to 4.1 V for blue. The peak LE reach 22.1 cd/A, 21.4 cd/A, and 1.99 cd/A, while the maximum EQE reach 12.7%, 5.29%, and 5.99%, for red, green, and blue QLEDs, respectively. To the best of our knowledge, the red and blue QLEDs exhibit the best device performance among all the all-solution processed inverted QLEDs. In addition, the blue QLED is the champion among all the inverted QLEDs, including the devices fabricated by thermal evaporation.

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Laser emission-based detection and imaging technology has attracted significant interest in biomedical research due to its high sensitivity, narrow linewidth, and superior spectral and spatial resolution. Recent advances have further revealed the potential to use laser emission to investigate chromatin dynamics, as well as to diagnose cancer tissues based on nuclear biomarkers. To move the laser emission based detection technology a step further towards practical use, in this work, we developed a highly robust tissue laser platform by microfabricating an SU8 spacer with a fixed height on the top mirror of the Fabry-Pérot (FP) cavity, which allows generation of reproducible and stable lasing results regardless of tissue thickness. Then we applied this platform to achieve lasing emission from formalin-fixed, paraffin-embedded (FFPE) lung tissues, which account for an overwhelming fraction of tissues collected for research and clinical use worldwide. We further showed that the cancer and normal FFPE lung tissues can be distinguished by their respective lasing thresholds. Two different tissue thicknesses (10 μm and 5 μm) commonly used in pathological labs were explored. Finally, we tested three additional types of tissues (colon, stomach, and breast) that were prepared independently by lab technicians in a pathology lab in China and shipped to the US in order to validate the general applicability and practicality of the laser emission-based technology as well as the corresponding sample preparation protocol and the tissue laser platform. Our work will not only vastly broaden the applications of laser emission-based detection/imaging technology but also help translate it from the laboratory to an automated system for clinical practice that may eventually benefit biomedicine and biological research.

microRNA-33a (miR-33a) belongs to the miR-33 family that is implicated in the progression of various types of cancers. Aberrant expression of miR-33a has been detected in several human cancers, and has been shown to regulate the migration and invasion as well as proliferation and apoptosis of tumor cells. However, the clinical significance and precise mechanisms underlying the dysfunction of miR-33a in glioma have not been well investigated in previous studies. In this study, overexpression of miR-33a was observed in clinical glioma specimens and cell lines. Clinicopathological detection revealed that miR-33a highly expressing patients showed large tumor sized and advanced World Health Organization (WHO) grade as well as reduced overall survival. Furthermore, the results of in vitro experiments confirmed that loss of miR-33a resulted in reduced proliferation and enhanced apoptosis in U251 cells, while miR-33a restoration showed opposite effects in U87 cells. Further studies indicated that miR-33a knockdown restrained tumor growth of glioma in vivo. miR-33a negatively regulated the expression of sirtuin 6 (SIRT6) at both mRNA and protein levels via targeting the 3'UTR of SIRT6 mRNA. SIRT6 was underexpressed and inversely correlated with miR-33a expression in the glioma tissues. Mechanistically, SIRT6 overexpression increased the levels of lactate dehydrogenase (LDH) and reactive oxygen species (ROS) while it reduced cell survival under H2O2 treatment. In addition, SIRT6 restoration led to apoptosis with alterative expression of Bax, Bcl-2, cleaved caspase-8, and inhibition of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway in glioma. Thus, our studies demonstrated that the deregulation of miR-33a may promote tumor development in human glioma by regulating the expression of its target gene, SIRT6.

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