Highly efficient and bright blue organic light-emitting devices based on solvent engineered, solution-processed thermally activated delayed fluorescent emission layer

In this work, we use an efficient blue TADF emitter, bis [4-(9,9-dimethyl-9,10-dihydroacridine) phenyl]solfone (DMAC-DPS), as EML and propose a solvent engineering strategy to achieve high efficiency and brightness. The strategy employs synergetic solvents to improve the film morphology of the solution-processed DMAC-DPS EML. The improved film quality enhances the carrier injectionwhile reduces the surface trap charges, as revealed by the hole-/ electron-only device performance and the transient electroluminescence measurements

High efficient all-solution OLEDs and their transient electroluminescence

Solution-processed OLEDs have always been the hot topic in the research of OLEDs. The electron-hole evolution in all solution processed OLEDs involves the carrier transportation, the exciton recombination and dissociation.The dynamic of excitons plays a crucial role in governing the ultimate device performance

Role of LECT2 in exacerbating atopic dermatitis: insight from in vivo and in vitro models via NF-κB signaling pathway

Leukocyte cell-derived chemotaxin 2 (LECT2) is linked to various immune diseases. Previously, we reported that serum LECT2 levels correlate with disease severity in atopic dermatitis (AD) patients. To investigate the role of LECT2 in AD and elucidate its potential mechanisms, we used LECT2 to treat an AD mouse model induced by 1-Chloro-2,4-dinitrobenzene (DNCB) in LECT2 knockout (KO) and wild-type (WT) mice, and an AD cell model using TNF-α/IFN-γ-induced HaCaT cells. Inflammatory factors and barrier proteins were analyzed by histology, immunohistochemistry, RT-qPCR, ELISA, and Western Blot. Activation of the NF-κB signaling pathway was evaluated by Western Blot and immunofluorescence. In the AD mouse model, LECT2 treatment increased epidermal and dermal thickness, mast cell infiltration, and downregulated barrier proteins. Inflammatory factors were increased in skin lesions and serum. In the AD cell model, LECT2 decreased barrier protein levels and increased inflammatory factor levels, enhancing NF-κB P65 nuclear translocation. These results indicate that LECT2 exacerbates AD-like responses by dysregulating the NF-κB signaling pathway, highlighting its potential as a therapeutic target for AD management

Regulation of energy band and luminescence properties in blue quasi-2D lead bromide perovskite via lattice strain

Development of blue quasi-2D lead halide perovskite LEDs is key to the perovskite based full-color displays and white-light illumination. It is still quite challenging to accurately enlarge the bandgap to achieve high performance and stable blue Quasi-2D perovskite LEDs. The lattice strain due to the deformation of lead-bromide octahedra is a critical factor leading to the energy band adjustment and stability optimization. In this Letter, the lattice strain is adjusted via three cations with different sizes, Cs+, CH3CH2NH2+(EA+), and Rb+, for sophisticatedly micro-tuning of the lattice strain to achieve overall lattice expansion and lattice contraction. A ternary quasi-2D blue bromide perovskite material PEA 2 (Cs xEAyRb1-x-yPbBr)2 PbBr 4 is specially designed. The crystal structure and energy band are studied by the first principles calculations using the Density Functional Theory method. The luminescence properties of blue quasi-2D lead bromide perovskite materials are analyzed with spectra regulation from 508 to 464 nm for photoluminescence and from 510 to 470 nm for electroluminescence. The thermal treatment is used to accelerate the release of residual strain due to mismatch and disorder in the lattice, leading to defects and degradation. The lattice strain is strongly correlated with the energy band, luminescence performance, and thermal stability of blue quasi-2D lead bromide perovskite. The study of lattice strain relaxation in blue quasi-2D lead bromide perovskite could open avenues for high-performance and stable blue quasi-2D perovskite LEDs

bSRWPSO-FKNN: A boosted PSO with fuzzy K-nearest neighbor classifier for predicting atopic dermatitis disease

IntroductionAtopic dermatitis (AD) is an allergic disease with extreme itching that bothers patients. However, diagnosing AD depends on clinicians’ subjective judgment, which may be missed or misdiagnosed sometimes.MethodsThis paper establishes a medical prediction model for the first time on the basis of the enhanced particle swarm optimization (SRWPSO) algorithm and the fuzzy K-nearest neighbor (FKNN), called bSRWPSO-FKNN, which is practiced on a dataset related to patients with AD. In SRWPSO, the Sobol sequence is introduced into particle swarm optimization (PSO) to make the particle distribution of the initial population more uniform, thus improving the population’s diversity and traversal. At the same time, this study also adds a random replacement strategy and adaptive weight strategy to the population updating process of PSO to overcome the shortcomings of poor convergence accuracy and easily fall into the local optimum of PSO. In bSRWPSO-FKNN, the core of which is to optimize the classification performance of FKNN through binary SRWPSO.ResultsTo prove that the study has scientific significance, this paper first successfully demonstrates the core advantages of SRWPSO in well-known algorithms through benchmark function validation experiments. Secondly, this article demonstrates that the bSRWPSO-FKNN has practical medical significance and effectiveness through nine public and medical datasets.DiscussionThe 10 times 10-fold cross-validation experiments demonstrate that bSRWPSO-FKNN can pick up the key features of AD, including the content of lymphocytes (LY), Cat dander, Milk, Dermatophagoides Pteronyssinus/Farinae, Ragweed, Cod, and Total IgE. Therefore, the established bSRWPSO-FKNN method practically aids in the diagnosis of AD

Modification of PEDOT: PSS to enhance device efficiency and stability of the Quasi-2D perovskite light-emitting diodes

Poly(3,4-ethylenedioxy thiophene): poly(styrene sulfonate) (PEDOT: PSS) is a hole transport layer (HTL) that is often employed in a diverse array of optoelectronic devices, such as perovskite solar cells and perovskite light-emitting diodes (PeLEDs). By simply doping lithium fluoride (LiF) into PEDOT: PSS, we demonstrate that the electrical characteristics of the HTL can be modified. Especially in quasi-2D perovskite LEDs, the crystallization process is regulated by LiF modification, leading to reduced phase impurity defects and improved carrier transport in the perovskite emission layer. Therefore, the luminance and efficiency of the quasi-2D PeLEDs are notably enhanced. The optimized PeLED with LiF modification exhibits a peak luminance of 21517 cd m−2 with 317% higher than the standard PeLED; and a high current efficiency of 39.8 cd A−1 with 237% higher than the standard PeLED. Moreover, the device stability is also improved with a nearly doubled half lifetime due to the reduced phase impurities. The work demonstrates a facile yet effective method for altering PEDOT: PSS hole transport layer, emphasizing the critical role of the underneath layer in the crystallization of quasi-2D perovskites

SHON expression predicts response and relapse risk of breast cancer patients after anthracycline-based combination chemotherapy or tamoxifen treatment

BACKGROUND: SHON nuclear expression (SHON-Nuc+) was previously reported to predict clinical outcomes to tamoxifen therapy in ERα+ breast cancer (BC). Herein we determined if SHON expression detected by specific monoclonal antibodies could provide a more accurate prediction and serve as a biomarker for anthracycline-based combination chemotherapy (ACT).METHODS: SHON expression was determined by immunohistochemistry in the Nottingham early-stage-BC cohort (n=1,650) who, if eligible, received adjuvant tamoxifen; the Nottingham ERα- early-stage-BC (n=697) patients who received adjuvant ACT; and the Nottingham locally advanced-BC cohort who received pre- operative ACT with/without taxanes (Neo-ACT, n=120) and if eligible, 5-year adjuvant tamoxifen treatment. Prognostic significance of SHON and its relationship with the clinical outcome of treatments were analysed.RESULTS: As previously reported, SHON-Nuc+ in high risk/ERα+ patients was significantly associated with a 48% death risk reduction after exclusive adjuvant tamoxifen treatment compared with SHON-Nuc- [HR(95%CI)=0.52(0.34-0.78), p=0.002]. Meanwhile, in ERα- patients treated with adjuvant ACT, SHON cytoplasmic expression (SHON-Cyto+) was significantly associated with a 50% death risk reduction compared with SHON-Cyto- [HR(95%CI)=0.50(0.34-0.73), p=0.0003]. Moreover, in patients received Neo-ACT, SHON-Nuc- or SHON-Cyto+ was associated with an increased pathological complete response (pCR) compared with SHON-Nuc+ [21% vs 4%; OR(95%CI)=5.88(1.28-27.03), p=0.012], or SHON-Cyto- [20.5% vs 4.5%; OR(95%CI)=5.43(1.18-25.03), p=0.017], respectively. After receiving Neo-ACT, patients with SHON-Nuc+ had a significantly lower distant relapse risk compared to those with SHON-Nuc- [HR(95%CI)=0.41(0.19-0.87), p=0.038], whereas SHON-Cyto+ patients had a significantly higher distant relapse risk compared to SHON-Cyto- patients [HR(95%CI)=4.63(1.05-20.39), p=0.043]. Furthermore, multivariate Cox regression analyses revealed that SHON-Cyto+ was independently associated with a higher risk of distant relapse after Neo-ACT and 5- year tamoxifen treatment [HR(95%CI)=5.08(1.13-44.52), p=0.037]. The interaction term between ERα status and SHON-Nuc+ (p=0.005), and between SHON-Nuc+ and tamoxifen therapy (p=0.007), were both statistically significant.CONCLUSION: SHON-Nuc+ in tumours predicts response to tamoxifen in ERα+ BC while SHON-Cyto+ predicts response to ACT

MicroRNA100 Inhibits Self-Renewal of Breast Cancer Stem–like Cells and Breast Tumor Development

miRNAs are essential for self-renewal and differentiation of normal and malignant stem cells by regulating the expression of key stem cell regulatory genes. Here, we report evidence implicating the miR100 in self-renewal of cancer stem-like cells (CSC). We found that miR100 expression levels relate to the cellular differentiation state, with lowest expression in cells displaying stem cell markers. Utilizing a tetracycline-inducible lentivirus to elevate expression of miR100 in human cells, we found that increasing miR100 levels decreased the production of breast CSCs. This effect was correlated with an inhibition of cancer cell proliferation in vitro and in mouse tumor xenografts due to attenuated expression of the CSC regulatory genes SMARCA5, SMARCD1, and BMPR2. Furthermore, miR100 induction in breast CSCs immediately upon their orthotopic implantation or intracardiac injection completely blocked tumor growth and metastasis formation. Clinically, we observed a significant association between miR100 expression in breast cancer specimens and patient survival. Our results suggest that miR100 is required to direct CSC self-renewal and differentiation