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Lead-free Cs3Cu2I5 metal halides have garnered significant attention recently due to their non-toxic properties and deep-blue emission. However, their relatively low photoluminescence quantum efficiency and poor stability have limited their applications. In this work, sodium iodide (NaI) is used to facilitate the synthesis of Cs3Cu2I5 nanocrystals (NCs), demonstrating improved photoluminescence intensity, photoluminescence quantum yield, and stability. Systematic optoelectronic characterizations confirm that Na+ is successfully incorporated into the Cs3Cu2I5 lattice without altering its crystal structure. The improved Photoluminescence Quantum Yield (PLQY) and stability are attributed to the strengthened chemical bonding, which effectively suppresses vacancy defects in the lattice. Additionally, light-emitting diodes (LEDs) based on 10% NaI-doped Cs3Cu2I5 NCs were assembled, emitting vibrant blue light with a maximum radiant intensity of 82 lux and Commission Internationale de l'Eclairage (CIE) chromaticity coordinates of (0.15, 0.1). This work opens new possibilities for commercial lighting display applications. [ABSTRACT FROM AUTHOR]

The protein-protein interaction between menin and mixed lineage leukemia 1 (MLL1) plays a critical role in acute leukemias with translocations of the MLL1 gene or with mutations in the nucleophosmin 1 (NPM1) gene. As a step toward clinical translation of menin-MLL1 inhibitors, we report development of MI-3454, a highly potent and orally bioavailable inhibitor of the menin-MLL1 interaction. MI-3454 profoundly inhibited proliferation and induced differentiation in acute leukemia cells and primary patient samples with MLL1 translocations or NPM1 mutations. When applied as a single agent, MI-3454 induced complete remission or regression of leukemia in mouse models of MLLI-rearranged or NPMI-mutated leukemia, including patient-derived xenograft models, through downregulation of key genes involved in leukemogenesis. We also identified MEIS1 as a potential pharmacodynamic biomarker of treatment response with MI-3454 in leukemia, and demonstrated that this compound is well tolerated and did not impair normal hematopoiesis in mice. Overall, this study demonstrates, for the first time to our knowledge, profound activity of the menin-MLL1 inhibitor as a single agent in clinically relevant PDX models of leukemia. These data provide a strong rationale for clinical translation of MI-3454 or its analogs for leukemia patients with MLL1 rearrangements or NPM1 mutations., Introduction The development of acute leukemia is associated with heterogeneous genetic and epigenetic alterations (1, 2), making it difficult to identify new effective therapies for leukemia patients. Despite these challenges, [...]

Carbon dots have received much attention due to their unique physicochemical properties and diverse applications in bioimaging, optoelectronic devices, catalysis, and agriculture. Here, in this work, we report a simple hydrothermal synthesis of nitrogen and phosphorus−doped carbon dots (N, P−CDs). The optical and physical properties of the synthesized N, P−CDs are analyzed using systematical spectroscopy and electrical characterization. The synthesized N, P−CDs show strong photoluminescence at 626 nm and demonstrate high stability under UV light and other conditions. Moreover, we incorporate the synthesized N, P−CDs into water spinach by root spraying and leaf spraying. It is found that N, P−CDs could effectively promote the growth of water spinach by accelerating the photosynthetic rate, and increasing the content of total phenols, anthocyanins, and flavonoids in water spinach. [ABSTRACT FROM AUTHOR]

Lead halide perovskite has become a promising candidate for high-performance photodetectors (PDs) due to its attractive optical and electrical properties, such as high optical absorption coefficient, high carrier mobility, and long carrier diffusion length. However, the presence of highly toxic lead in these devices has limited their practical applications and even hindered their progress toward commercialization. Therefore, the scientific community has been committed to searching for low-toxic and stable perovskite-type alternative materials. Lead-free double perovskite, which is still in the preliminary stage of exploration, has achieved inspiring results in recent years. In this review, we mainly focus on two types of lead-free double perovskite based on different Pb substitution strategies, including A2M(I)M(III)X6 and A2M(IV)X6. We review the research progress and prospects of lead-free double perovskite photodetectors in the past three years. More importantly, from the perspective of optimizing the inherent defects in materials and improving device performance, we propose some feasible pathways and make an encouraging perspective for the future development of lead-free double perovskite photodetectors. [ABSTRACT FROM AUTHOR]

Nickel oxide (NiOx) is desirable hole selective material (HSMs) for perovskite photovoltaics because of the characteristic in stability and low cost. However, they deliver limited open‐circuit voltage (VOC) compared to some organic HSMs. As it is known, the performance of perovskite solar cells is predominantly limited by trap‐assisted non‐radiative recombination at the perovskite/hole‐selective layer interfaces. A typical lithium‐doping strategy leads to the valence‐band maximum shift and the electronic levels of NiOx can be tuned robustly to match perovskite active layer in perovskite solar cells. More critically, carrier dynamics studies demonstrate another critical PN4N interlayer strategy reduced interfacial density of defect sites and trap‐assisted recombination. These merits contribute coordinately to lower energy loss across the perovskite/NiOx interface and facilitate charge transport process through the relevant interface, yielding VOC values increase to 1.14 V and power conversion efficiencies over 20%. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) mostly arises from progressive accumulation of somatic mutations within cells. Most commonly mutated genes like TP53, APC and KRAS can promote survival and proliferation of cancer cells. Although the molecular alterations and landscape of some specific mutations in CRC are well known, the presence of a somatic mutation signature related to genomic regions and epigenetic markers remain unclear. To find the signatures from a random distribution of somatic mutations in CRCs, we carried out enrichment analysis in different genomic regions and identified peaks of epigenetic markers. We validated that the mutation frequency in miRNA is dramatically higher than in flanking genomic regions. Moreover, we observed that somatic mutations in CRC and colon cancer cell lines are significantly enriched in CTCF binding sites. We also found these mutations are enriched for H3K27me3 in both normal sigmoid colon and colon cancer cell lines. Taken together, our findings suggest that there are some common somatic mutations signatures which provide new directions to study CRC. [ABSTRACT FROM AUTHOR]

Sb2S3 solar cells are lagging behind conventional thin-film solar cells such as silicon solar cells and cadmium telluride solar cells in the power conversion efficiency (PCE). One of the most prominent problems is that the carrier concentration of Sb2S3 is relatively low. In order to increase the carrier concentration, elemental Cu was doped into Sb2S3 film by radio-frequency (RF) magnetron sputtering. We proved that Cu was doped into Sb2S3 films and mainly anchored with sulfur in the form of copper chalcogenide species at the surface and grain boundaries of Sb2S3. The doping of Cu essentially affects the physical and electrical properties of RF-sputtered Sb2S3 films such as the optical band gap, crystallinity, chemical composition, morphology, and carrier concentration. Specially, the electronic carrier concentration is remarkably increased from 6.28 × 109 to 6.06 × 1010 cm−3 and the Fermi level is also significantly uplifted after prudent doping with Cu. Planar solar cells based on RF-sputtered Cu-doped Sb2S3 absorber deliver an increased PCE of 1.13% and show good stability. This research proves that doping of Cu is an alternative and effective way to improve the electronic property of Sb2S3 films and enhance the performance of Sb2S3 solar cells. [ABSTRACT FROM AUTHOR]

Background: Breast cancer is one of the foremost threats to female health nowadays. Tamoxifen, an antagonist of estrogen receptor-α (ERα), is the first choice for endocrine-dependent breast cancer (ERα-positive breast cancer) treatment. However, ERα has an important function in the normal physical regulation of estrogen, and current oral administration of tamoxifen has potential side effects on normal endocrine secretion. In the present work, we aim to develop novel approaches to increase the antitumor effect of tamoxifen on breast cancer cells and decrease the potential side effects in the human body during treatment. Methods: A temperature-sensitive phase-change hydrogel for tamoxifen (Tam-Gel) was generated. After establishing subcutaneous tumors formed by MCF-7, an ERα-positive breast cancer cell line, in nude mice, an intratumoral injection of Tam-Gel was performed to examine whether Tam-Gel facilitated the slow-release or antitumor effect of tamoxifen. A metastatic breast cancer model was established using the intrahepatic growth of MCF-7 cells in immunodeficient rats. Results: Tam-Gel can transform from liquid to hydrogel at room temperature. An intratumoral injection of Tam-Gel facilitated the slow-release or antitumor effect of tamoxifen. Once Tam-Gel, but not Tam-Sol, was administered by intratumoral injection, it significantly decreased the uptake of radionuclide probes (18F-fluoroestradiol or 18F-fluorodeoxyglucose) by cells in rats' livers and the intrahepatic growth of MCF-7 cells in rats' livers. Conclusion: A novel slow-release system was successfully prepared to facilitate the long-term release of tamoxifen in breast cancer tissues, and achieved an antitumor effect in the long term. [ABSTRACT FROM AUTHOR]

Osteoarthritis is the most common chronic condition of the joint disease. Chondrocyte is the sole cell type in joint tissues. Senescence of chondrocytes is known to contribute to the causation of osteoarthritis. Local inflammatory cytokines- caused chondrocytes senescence is proposed to be one of the molecular mechanisms of osteoarthritis. In this study, we show that the bile acid receptor GPBAR1 (TGR5), a G protein couples bile acid receptor, plays important roles in protecting chondrocytes from interleukin 1β (IL-1β)- caused senescence. TGR5 is fairly expressed in cultured chondrocytes. Its expression is reduced in isolated chondrocytes from osteoarthritis patients, and IL-1β treatment suppresses TGR5 expression. Activation of TGR5 by its synthetic agonist, INT-777, dramatically reduces senescence associated β galactosidase activity by IL-1β. Mechanistically, the action of INT-777 ameliorates IL-1β- induced chondrocytes entry of G0/G1 arrest phase and exit of S and G2/M phases. INT-777 inhibits IL-1β- induced expression of p21, PAI-1, and K382 acetylation of p53 as well as reduction of Sirt1. The knockdown of TRG5 abolished the protective role of INT-777 on these molecules. Collectively, our data indicates that activation of TGR5 is necessary for protection of IL-1β- induced chondrocytes senescence. [ABSTRACT FROM AUTHOR]

A single epitope of Leishmania analog of the receptors for activated C kinase (LACK) from Leishmania major, the polypeptide LACK156–173, is recognized by Vβ4+/Vα8+ T cells, and activate these cells that drives the subsequent T helper (Th)2 response. This study was undertaken to investigate the therapeutic potential of the LACK156–173 epitope in murine autoimmune arthritis models. To explore the influence of the LACK156–173 epitope on murine collagen antibody-induced arthritis, as well as its immunological mechanism, we vaccinated or treated mice with a LACK156–173 epitope expression plasmid or polypeptide. The effect of LACK156–173 epitope was then evaluated by clinical scores, histopathology, and quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Using flow cytometry, we measured the subsets and maturity of CD11c+ dendritic cells (DCs), as well as T cell polarization, in co-culture experiments. We also measured cytokine gene expression and production. The murine macrophage-like cell line RAW264.7 was used to identify the receptor for the epitope. Vaccination or treatment of the mice with the LACK156–173 epitope expression plasmid or polypeptide ameliorated the severity of arthritis. qRT-PCR analysis revealed that the LACK156–173 epitope improved the balance of effector T cells in synovial tissue compared to that in untreated arthritis controls. Toll-like receptor (TLR) 4 expression was diminished by LACK156–173. The epitope also influenced T cell polarization by regulating the differentiation, maturation, and functions of CD11c+ DCs and upregulating Jagged1 ligand expression. Blocking the mannose receptor (MR) significantly attenuated LACK156–173 epitope-induced macrophage activation. Our data indicate that vaccination or treatment with a single microorganism epitope, LACK156–173, is a highly efficient therapy for murine autoimmune arthritis. The therapeutic effects are mediated by the regulation of the differentiation, maturation, and functions of DCs via MR, resulting in the upregulation of Jagged1 expression and Th2 cell polarization. Our results demonstrate the therapeutic potential of the LACK156–173 epitope in rheumatoid arthritis. [ABSTRACT FROM AUTHOR]

Reducing the energy loss and retarding the carrier recombination at the interface are crucial to improve the performance of the perovskite solar cell (PSCs). However, little is known about the recombination mechanism at the interface of anode and SnO2 electron transfer layer (ETL). In this work, an ultrathin wide bandgap dielectric MgO nanolayer is incorporated between SnO2:F (FTO) electrode and SnO2 ETL of planar PSCs, realizing enhanced electron transporting and hole blocking properties. With the use of this electrode modifier, a power conversion efficiency of 18.23% is demonstrated, an 11% increment compared with that without MgO modifier. These improvements are attributed to the better properties of MgO‐modified FTO/SnO2 as compared to FTO/SnO2, such as smoother surface, less FTO surface defects due to MgO passivation, and suppressed electron–hole recombinations. Also, MgO nanolayer with lower valance band minimum level played a better role in hole blocking. When FTO is replaced with Sn‐doped In2O3 (ITO), a higher power conversion efficiency of 18.82% is demonstrated. As a result, the device with the MgO hole‐blocking layer exhibits a remarkable improvement of all J–V parameters. This work presents a new direction to improve the performance of the PSCs based on SnO2 ETL by transparent conductive electrode surface modification. [ABSTRACT FROM AUTHOR]

Perovskite Solar Cells: In Situ Defect Passivation with Silica Oligomer for Enhanced Performance and Stability of Perovskite Solar Cells (Adv. In article number 1901716, Hongwei Lei, Song Zhang, Zuojun Tan, and co-workers report a novel and efficient perovskite defect passivation strategy using silica oligomer. Silica oligomer PA can enlarge perovskite grain sizes, prolong carrier lifetime, enhance charge carrier dynamics and reduce trap state densities, resulting in highly efficient PVSCs with good humid and thermal stability. [Extracted from the article]

Perovskite solar cells (PVSCs) have achieved excellent power conversion efficiency (PCE) but still suffer from instability issues. Defect passivation is an important route to simultaneously increase the efficiency and stability of PVSCs. Here, a strategy of incorporating silica oligomer in perovskite films for surface and grain boundary defect passivation is reported. Silica oligomer passivation agent (PA) is in situ formed through hydrolysis and condensation reaction of tetraethyl orthosilicate additive in perovskite precursor. The passivation mechanism is elucidated by density functional theory calculation, revealing stable chelating interaction and hydrogen bond interaction between PA and perovskite. Spectroscopic and electrical characterizations demonstrate that silica oligomer can enlarge grain sizes, prolong carrier lifetime, enhance charge carrier dynamics, and reduce trap state densities in perovskite films. Planar PVSCs with passivation achieve a highly improved PCE of 19.64% with a stabilized efficiency of 18.81%. More importantly, unencapsulated perovskite devices with passivation retain nearly 90% of original efficiency after 1000 h storage under ambient condition and sustained 87% of initial performance after high‐temperature (120 °C) thermal accelerated aging, showing highly enhanced moisture and thermal stability. Therefore, the present study provides a pathway to the future design and optimization of PVSCs with higher efficiency and greater stability. [ABSTRACT FROM AUTHOR]

There are still challenges in growth of transferable large area orientated ultrathin high‐melting‐point metal oxide single crystals with conventional methods. Herein, a new pathway to produce high quality single‐crystal ZnO nanoplates with more than 400 µm crystal size is revealed by using the van der Waals epitaxy (vdWE) combined with pulsed laser deposition (PLD) method on fluorophlogopite mica. The quasi‐2D ZnO plates as thin as 5 nm on fluorophlogopite mica without transition layer are achieved, showing an excellent thickness and orientation control while maintaining the excellent crystalline. ZnO nanoplates grown on conducting graphite and insulating hexagonal boron nitride (h‐BN) 2D substrates are also obtained through PLD assisted vdWE. The transfer of 15 nm thick quasi‐2D ZnO plates with 8 mm × 8 mm area onto a SiO2/Si substrate is successfully demonstrated. Based on the ZnO nanoplates, semitransparent self‐powered ultraviolet (UV) photodetectors and light‐emitting diodes centered at 400 nm UV region are demonstrated. This research highlights that the PLD assisted vdWE method is a fascinating way to fabricate high coverage ultrathin 2D ZnO plates with precisely thickness control for optoelectronic applications and may have enormous inspiration for other 2D nanomaterials growth. [ABSTRACT FROM AUTHOR]

Abstract: Background: Systemic lupus erythematosus (SLE) is an autoimmune disease, with multiple genetic and environmental factors involving in its etiology. The toll-like receptor 9 (TLR9) gene has been reported to have important roles in the development and progression of SLE. We performed a case–control study to investigate the effects of 4 SNPs in the TLR9 gene in the development of SLE in Northern Chinese population. Methods: Four SNPs including rs187084, rs5743836, rs352139 and rs352140 were genotyped using the SNaPshot® method. A group of 430 SLE patients were compared to 424 normal controls. Data were analyzed by SPSS 17.0 and HaploView v 4.1 software. Results: The frequency distributions of SNP rs351240 and haplotype H2 (TGCT) and H3 (CATT) were found to differ significantly between patient and control groups (p <0.05), while other SNPs and haplotypes showed no significant difference between the two cohorts (p >0.05). Conclusion: The results revealed that variations in the TLR9 gene are associated with SLE, indicating that TLR9 may play an important role in the pathogenesis of SLE in the northern Chinese Han population. [Copyright &y& Elsevier]

Background: Increasing radiosensitivity of cancer cells can enhance the efficacy of cervical cancer treatment., Objectives: This study evaluated the potential roles and mechanism of baicalein in regulating the radiosensitivity of cervical cancer cells in vitro., Material and Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) was used to assess miR-183 expression in End1/E6E7 cells, Hela cells and Hela cells irradiated with X-ray (0 Gy, 1 Gy, 3 Gy, 5 Gy, and 10 Gy). Cell Counting Kit-8 (CCK-8) method measured cell viability of Hela cells after miR-183 regulation, baicalein or RO8191 treatment. Apoptosis rates were detected using flow cytometry. Thereafter, expression of Bcl-2, Bax and caspase-3 RNA was also detected through RT-qPCR. Protein concentrations of E-cadherin, N-cadherin, Vimentin in epithelial-mesenchymal transition (EMT), phospho-JAK2/STAT3, and total Janus kinase 2/signal transducer and activator of transcription 3 STAT3 (JAK2/STAT3) were examined using enzyme-linked immunosorbent assay (ELISA) methods. RO8191, a JAK2/STAT3 activator, was used to activate the JAK2/STAT3 signaling pathway., Results: The miR-183 expression was significantly lower in Hela cells compared to End1/E6E7 cells. Following upregulation of miR-183 in Hela cells, cell viability was inhibited while apoptosis was promoted. Moreover, EMT was inhibited after miR-183 over-expression. X-ray treatment markedly reduced the cell survival rate and increased miR-183 RNA expression. Baicalein treatment severely reduced the cell viability of 10-Gy X-ray-irradiated Hela cells, partially reversing the effect of miR-183, and also increased apoptosis and prevented EMT in irradiated cells. Y1007/8 in JAK2 and tyrosine (Tyr) residue 705 of STAT3 were phosphorylated, resulting in high expression of JAK2/STAT3, which was decreased by irradiation and baicalein treatment. RO8191 activated JAK2/STAT3 signaling, promoted cell viability and EMT, and inhibited cell apoptosis, while baicalein partly reversed the functions of RO8191., Conclusions: Baicalein inhibited cell viability and EMT, and induced cell apoptosis of Hela cells, through upregulating miR-183 via inactivation of the JAK2/STAT3 signaling pathway.

Epigenetic mechanisms that alter heritable gene expression and chromatin structure play an essential role in many biological processes, including liver function. Human MOF (males absent on the first) is a histone acetyltransferase that is globally downregulated in human steatohepatitis. However, the function of MOF in the liver remains unclear. Here, we report that MOF plays an essential role in adult liver. Genetic deletion of Mof by Mx1-Cre in the liver leads to acute liver injury, with increase of lipid deposition and fibrosis akin to human steatohepatitis. Surprisingly, hepatocyte-specific Mof deletion had no overt liver abnormality. Using the in vitro coculturing experiment, we show that Mof deletion-induced liver injury requires coordinated changes and reciprocal signaling between hepatocytes and Kupffer cells, which enables feedforward regulation to augment inflammation and apoptotic responses. At the molecular level, Mof deletion induced characteristic changes in metabolic gene programs, which bore noticeable similarity to the molecular signature of human steatohepatitis. Simultaneous deletion of Mof in both hepatocytes and macrophages results in enhanced expression of inflammatory genes and NO signaling in vitro. These changes, in turn, lead to apoptosis of hepatocytes and lipotoxicity. Our work highlights the importance of histone acetyltransferase MOF in maintaining metabolic liver homeostasis and sheds light on the epigenetic dysregulation in liver pathogenesis., Competing Interests: Conflict of interests The authors declare no competing interests., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

A single epitope of Leishmania analog of the receptors for activated C kinase (LACK) from Leishmania major , the polypeptide LACK 156-173 , is recognized by Vβ4 + /Vα8 + T cells, and activate these cells that drives the subsequent T helper (Th)2 response. This study was undertaken to investigate the therapeutic potential of the LACK 156-173 epitope in murine autoimmune arthritis models. To explore the influence of the LACK 156-173 epitope on murine collagen antibody-induced arthritis, as well as its immunological mechanism, we vaccinated or treated mice with a LACK 156-173 epitope expression plasmid or polypeptide. The effect of LACK 156-173 epitope was then evaluated by clinical scores, histopathology, and quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Using flow cytometry, we measured the subsets and maturity of CD11c + dendritic cells (DCs), as well as T cell polarization, in co-culture experiments. We also measured cytokine gene expression and production. The murine macrophage-like cell line RAW264.7 was used to identify the receptor for the epitope. Vaccination or treatment of the mice with the LACK 156-173 epitope expression plasmid or polypeptide ameliorated the severity of arthritis. qRT-PCR analysis revealed that the LACK 156-173 epitope improved the balance of effector T cells in synovial tissue compared to that in untreated arthritis controls. Toll-like receptor (TLR) 4 expression was diminished by LACK 156-173 . The epitope also influenced T cell polarization by regulating the differentiation, maturation, and functions of CD11c + DCs and upregulating Jagged1 ligand expression. Blocking the mannose receptor (MR) significantly attenuated LACK 156-173 epitope-induced macrophage activation. Our data indicate that vaccination or treatment with a single microorganism epitope, LACK 156-173 , is a highly efficient therapy for murine autoimmune arthritis. The therapeutic effects are mediated by the regulation of the differentiation, maturation, and functions of DCs via MR, resulting in the upregulation of Jagged1 expression and Th2 cell polarization. Our results demonstrate the therapeutic potential of the LACK 156-173 epitope in rheumatoid arthritis.

Inorganic p-type films with high mobility are very important for opto-electronic applications. It is very difficult to synthesize p-type films with a wider, tunable band gap energy and suitable band energy levels. In this research, p-type copper aluminum sulfide (Cu x Al 1- x S y ) films with tunable optical band gap, carrier density, hole mobility and conductivity were first synthesized using a simple, low cost and low temperature chemical bath deposition method. These in situ fabricated Cu x Al 1- x S y films were deposited at 60 °C using an aqueous solution of copper(ii) chloride dihydrate (CuCl 2 ·2H 2 O), aluminium nitrate nonohydrate [Al(NO 3 ) 3 ·9H 2 O], thiourea [(NH 2 ) 2 CS], and ammonium hydroxide, with citric acid as the complexing agent. Upon varying the ratio of the precursor, the band gap of the Cu x Al 1- x S y films can be tuned from 2.63 eV to 4.01 eV. The highest hole mobility obtained was 1.52 cm 2 V -1 s -1 and the best conductivity obtained was 546 S cm -1 . The Cu x Al 1- x S y films were used as a hole transporting layer (HTL) in organic solar cells (OSCs), and a good performance of the OSCs was demonstrated using the Cu x Al 1- x S y films as the HTL. These results demonstrate the remarkable potential of Cu x Al 1- x S y as hole transport material for opto-electronic devices., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

Rheumatoid arthritis (RA) is one of the most frequently occurring autoimmne diseases, with symptoms including synovium hyperplasia, immune disorder, cartilage damage and bone resorption. It has previously been demonstrated that microRNA-34a (miR-34a) may participate in cell apoptosis, immune activation and bone metabolism, therefore the present study investigated the effects of miR-34a on RA. Collagen-induced arthritic (CIA) mice were employed as a murine model of experimental arthritis, and it was demonstrated that the level of miR-34a in the spleens, lymph nodes and synovium was increased in the CIA mice compared with normal DBA/1j mice. Administration of miR-34a antagomir, the chemically modified inhibitor, ameliorated CIA and delayed the onset of symptoms. Arthritis scores decreased and joint swelling was alleviated with the miR-34a antagomir treatment and the expression of inflammatory cytokines was decreased. miR-34a antagomir delivery significantly decreased the percentage of T cells present including T helper (Th) 1, Th2, Th17 and regulatory T cells. Furthermore miR-34a antagomir-treated CIA mice demonstrated decreased inflammatory-induced bone loss. Overall, it was observed that inhibition of miR-34a ameliorated murine arthritis, downregulated T cell percentage and cytokine expression, and suppressed bone loss. The experimental results suggest that inhibition of miR-34a may offer a novel alternative for the treatment of RA.

LncRNA TUG1, a tumor oncogene associated with various human cancers, has been reported to be involved in regulating various cellular processes, such as proliferation, apoptosis and invasion through targeting multiple genes. However, its biological function in thyroid cancer cells has not been elucidated. The aim of this study is to measure TUG1 expression level and evaluate its function in thyroid cancer cells. LncRNA TUG1 expression levels in thyroid cancer tissues and three thyroid cancer cell lines (the ATC cell lines SW1736 and KAT18 and the FTC cell line FTC133) were assessed by qRT-PCR and compared with that of the human normal breast epithelial cell HGC-27. MTT assay, colony formation assay, transwell assay and western blot analysis were performed to assess the effects of TUG1 on proliferation, metastasis and EMT formation in thyroid cancer cells in vitro. Rescue assay was performed to further confirm that TUG1 contributes to the progression of thyroid cancer cells through regulating miR-145/ZEB1 signal pathway. LncRNA TUG1 was found to be up-regulated in thyroid cancer tissues and thyroid cancer cells compared with that in the human normal breast epithelial cell HGC-27. Increased lncRNA TUG1 expression was found to significantly promote tumor cell proliferation, and facilitate cell invasion, while down-regulated TUG1 could obviously inhibit cell proliferation, migration/invasion and reverse EMT to MET. These results indicated that TUG1 may contribute to the progression of thyroid cancer cells by function as a ceRNA competitive sponging miR-145, and that lncRNA TUG1 is associated with tumor progression in thyroid cancer cells., (© The Author 2017. Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Reducing the energy loss and retarding the carrier recombination at the interface are crucial to improve the performance of the perovskite solar cell (PSCs). However, little is known about the recombination mechanism at the interface of anode and SnO 2 electron transfer layer (ETL). In this work, an ultrathin wide bandgap dielectric MgO nanolayer is incorporated between SnO 2 :F (FTO) electrode and SnO 2 ETL of planar PSCs, realizing enhanced electron transporting and hole blocking properties. With the use of this electrode modifier, a power conversion efficiency of 18.23% is demonstrated, an 11% increment compared with that without MgO modifier. These improvements are attributed to the better properties of MgO-modified FTO/SnO 2 as compared to FTO/SnO 2 , such as smoother surface, less FTO surface defects due to MgO passivation, and suppressed electron-hole recombinations. Also, MgO nanolayer with lower valance band minimum level played a better role in hole blocking. When FTO is replaced with Sn-doped In 2 O 3 (ITO), a higher power conversion efficiency of 18.82% is demonstrated. As a result, the device with the MgO hole-blocking layer exhibits a remarkable improvement of all J-V parameters. This work presents a new direction to improve the performance of the PSCs based on SnO 2 ETL by transparent conductive electrode surface modification.