Magnet-in-ferroelectric crystals exhibiting photomultiferroicity.

Growing crystallographically incommensurate and dissimilar organic materials is fundamentally intriguing but challenging for the prominent cross-correlation phenomenon enabling unique magnetic, electronic, and optical functionalities. Here, we report the growth of molecular layered magnet-in-ferroelectric crystals, demonstrating photomanipulation of interfacial ferroic coupling. The heterocrystals exhibit striking photomagnetization and magnetoelectricity, resulting in photomultiferroic coupling and complete change of their color while inheriting ferroelectricity and magnetism from the parent phases. Under a light illumination, ferromagnetic resonance shifts of 910 Oe are observed in heterocrystals while showing a magnetization change of 0.015 emu/g. In addition, a noticeable magnetization change (8% of magnetization at a 1,000 Oe external field) in the vicinity of ferro-to-paraelectric transition is observed. The mechanistic electric-field-dependent studies suggest the photoinduced ferroelectric field effect responsible for the tailoring of photo-piezo-magnetism. The crystallographic analyses further evidence the lattice coupling of a magnet-in-ferroelectric heterocrystal system.

Direct Observation of Circularly Polarized Nonlinear Optical Activities in Chiral Hybrid Lead Halides.

Circularly polarized light emission is a crucial application in imaging, sensing, and photonics. However, utilizing low-energy photons to excite materials, as opposed to high-energy light excitation, can facilitate deep-tissue imaging and sensing applications. The challenge lies in finding materials capable of directly generating circularly polarized nonlinear optical effects. In this study, we introduce a chiral hybrid lead halide (CHLH) material system, R/S-DPEDPb3Br8·H2O (DPED = 1,2-diphenylethylenediammonium), which can directly produce circularly polarized second harmonic generation (CP-SHG) through linearly polarized infrared light excitation, exhibiting a polarization efficiency as high as 37% at room temperature. To understand the spin relaxation mechanisms behind the high polarization efficiency, we utilized two models, so-called D'yakonov-Perel' (DP) and Bir-Aronov-Pikus (BAP) mechanisms. The unique zigzag inorganic frameworks within the hybrid structure are believed to reduce the dielectric confinement and exciton binding energy, thus enhancing spin polarization, especially in regions with a high excitation pump fluence based on the DP mechanism. In the case of low excitation pump fluence, the BAP mechanism dominates, as evidenced by the observed decrease in the polarization ratio from CP-SHG measurement. Using density functional theory analysis, we elucidate how the distinctive 8-coordination environment of lead bromide building blocks effectively suppresses spin-orbit coupling at the conduction band minimum. This suppression significantly diminishes spin-splitting, thereby slowing the spin relaxation rate.

Prognostic marker CD27 and its micro-environmental in multiple myeloma.

BACKGROUND: The Cluster of Differentiation 27 (CD27) is aberrantly expressed in multiple myeloma (MM) -derived. This expression facilitates the interaction between tumor and immune cells within TME via the CD27-CD70 pathway, resulting in immune evasion and subsequent tumor progression. The objective of this study is to investigate the correlation between CD27 expression and the prognosis of MM, and to elucidate its potential relationship with the immune microenvironment. METHODS: In this research, CD27 expression in T cells within the 82 newly diagnosed MM microenvironment was assessed via flow cytometry. We then examined the association between CD27 expression levels and patient survival. Subsequent a series of bioinformatics and in vitro experiments were conducted to reveal the role of CD27 in MM. RESULTS: Clinical evidence suggests that elevated CD27 expression in T cells within the bone marrow serves as a negative prognostic marker for MM survival. Data analysis from the GEO database has demonstrated a strong association between MM-derived CD27 and the immune response, as well as the hematopoietic system. Importantly, patients with elevated levels of CD27 expression were also found to have an increased presence of MDSCs and macrophages in the bone marrow microenvironment. Furthermore, the PERK-ATF4 signaling pathway has been implicated in mediating the effects of CD27 in MM. CONCLUSIONS: We revealed that CD27 expression levels serve as an indicative marker for the prognosis of MM patients. The CD27- PERK-ATF4 is a promising target for the treatment of MM.

Large exchange-driven intrinsic circular dichroism of a chiral 2D hybrid perovskite.

In two-dimensional chiral metal-halide perovskites, chiral organic spacers endow structural and optical chirality to the metal-halide sublattice, enabling exquisite control of light, charge, and electron spin. The chiroptical properties of metal-halide perovskites have been measured by transmissive circular dichroism spectroscopy, which necessitates thin-film samples. Here, by developing a reflection-based approach, we characterize the intrinsic, circular polarization-dependent complex refractive index for a prototypical two-dimensional chiral lead-bromide perovskite and report large circular dichroism for single crystals. Comparison with ab initio theory reveals the large circular dichroism arises from the inorganic sublattice rather than the chiral ligand and is an excitonic phenomenon driven by electron-hole exchange interactions, which breaks the degeneracy of transitions between Rashba-Dresselhaus-split bands, resulting in a Cotton effect. Our study suggests that previous data for spin-coated films largely underestimate the optical chirality and provides quantitative insights into the intrinsic optical properties of chiral perovskites for chiroptical and spintronic applications.

Supramolecular Metal Halide Complexes for High-Temperature Nonlinear Optical Switches.

Nonlinear optical (NLO) switching materials, which exhibit reversible intensity modulation in response to thermal stimuli, have found extensive applications across diverse fields including sensing, photoelectronics, and photonic applications. While significant progress has been made in solid-state NLO switching materials, these materials typically showcase their highest NLO performance near room temperature. However, this performance drastically deteriorates upon heating, primarily due to the phase transition undergone by the materials from noncentrosymmetric to centrosymmetric phase. Here, we introduce a new class of NLO switching materials, solid-state supramolecular compounds 18-Crown-6 ether@Cu2Cl4·4H2O (1·4H2O), exhibiting reversible and stable NLO switching when subjected to near-infrared (NIR) photoexcitation and/or thermal stimuli. The reversible crystal structure in response to external stimuli is attributed to the presence of a weakly coordinated bridging water molecule facilitated by hydrogen bonding/chelation interactions between the metal halide and crown-ether supramolecules. We observed an exceptionally high second-harmonic generation (SHG) signal under continuous photoexcitation, even at temperatures exceeding 110 °C. In addition, the bridging water molecules within the complex can be released and recaptured in a fully reversible manner, all without requiring excessive energy input. This feature allows for precise control of SHG signal activation and deactivation through structural transformations, resulting in a high-contrast off/on ratio, reaching values in the million-fold range.

Broadband Achromatic Quarter-Waveplate Using 2D Hybrid Copper Halide Single Crystals.

Achromatic quarter waveplates (A-QWPs), traditionally constructed from multiple birefringent crystals, can modulate light polarization and retardation across a broad range of wavelengths. This mechanism is inherently related to phase retardation controlled by the fast and slow axis of stacked multi-birefringent crystals. However, the conventional design of A-QWPs requires the incorporation of multiple birefringent crystals, which complicates the manufacturing process and raises costs. Here, we report the discovery of a broadband (540-1060 nm) A-QWP based on a two-dimensional (2D) layered hybrid copper halide (HCH) perovskite single crystal. The 2D copper chloride (CuCl6) layers of the HCH crystal undergo Jahn-Teller distortion and subsequently trigger the in-plane optical birefringence. Its broad range of the wavelength response as an A-QWP is a consequence of the out-of-plane mosaicity formed among the stacked inorganic layers during the single-crystal self-assembly process in the solution phase. Given the versatility of 2D hybridhalide perovskites, the 2D HCH crystal offers a promising approach for designing cost-effective A-QWPs and the ability to integrate other optical devices.

HNRNPA2B1-mediated m6A modification of TLR4 mRNA promotes progression of multiple myeloma.

BACKGROUND: Multiple myeloma (MM) is a malignancy of plasma cells that remains incurable. Toll-like receptor 4 (TLR4) acts as a stress-responsive signal, protecting mitochondria during proteasome inhibitor (PI) exposure, maintaining mitochondrial metabolism and increasing drug resistance in MM. However, the mechanism of TLR4 regulation remains elusive. AIMS: The purpose of this study was to investigate the methylation pattern of multiple myeloma and its effect on the expression of HNRNPA2B1 and downstream targets. METHODS: The methylation level in MM and normal bone marrow specimens was detected using a colorimetric assay. HNRNPA2B1 gene knockdown was achieved in RPMI 8226 MM cells via adenovirus transfection. CCK8 and flow cytometric assays were used to detect proliferation and apoptosis, respectively. Transcriptome sequencing and m6A methylation MeRIP sequencing were applied, and differentially expressed genes (DEGs) were detected. Three independent NCBI GEO datasets were applied to examine the effects of HNRNPA2B1 and TLR4 expression on MM patient survival. RESULTS: HNRNPA2B1 promoted MM progression. Clinical data from database revealed that HNRNPA2B1 was adverse prognostic factor for survival among MM patients. Furthermore, transcriptome sequencing and methylation sequencing showed that HNRNPA2B1 recognized and was enriched at the m6A sites of TLR4 and TLR4 was down-regulated of both the m6A level and transcription level in HNRNPA2B1-knockdown MM cells. Moreover, TLR4 was an adverse survival prognostic factor based on database analysis. CONCLUSION: Overall, our study implies that the RNA-binding protein HNRNPA2B1 increases cell proliferation and deregulates cell apoptosis in MM through TLR4 signaling. Our study suggests HNRNPA2B1 as a potential therapeutic target for MM.

Proteomics-Based Approach Reveals the Involvement of SERPINB9 in Recurrent and Relapsed Multiple Myeloma.

Multiple myeloma (MM) is a common hematological malignancy with poorly understood recurrence and relapse mechanisms. Notably, bortezomib resistance leading to relapse makes MM treatment significantly challenging. To clarify the drug resistance mechanism, we employed a quantitative proteomics approach to identify differentially expressed protein candidates implicated in bortezomib-resistant recurrent and relapsed MM (RRMM). Bone marrow aspirates from five patients newly diagnosed with MM (NDMM) were compared with those from five patients diagnosed with bortezomib-resistant RRMM using tandem mass tag-mass spectrometry (TMT-MS). Subcellular localization and functional classification of the differentially expressed proteins were determined by gene ontology, Kyoto Encyclopedia of Genes and Genomes pathway, and hierarchical clustering analyses. The top candidates identified were validated with parallel reaction monitoring (PRM) analysis using tissue samples from 11 NDMM and 8 RRMM patients, followed by comparison with the NCBI Gene Expression Omnibus (GEO) dataset of 10 MM patients and 10 healthy controls (accession no.: GSE80608). Thirty-four differentially expressed proteins in RRMM, including proteinase inhibitor 9 (SERPINB9), were identified by TMT-MS. Subsequent functional enrichment analyses of the identified protein candidates indicated their involvement in regulating cellular metabolism, apoptosis, programmed cell death, lymphocyte-mediated immunity, and defense response pathways in RRMM. The top protein candidate SERPINB9 was confirmed by PRM analysis and western blotting as well as by comparison with an NCBI GEO dataset. We elucidated the proteome landscape of bortezomib-resistant RRMM and identified SERPINB9 as a promising novel therapeutic target. Our results provide a resource for future studies on the mechanism of RRMM.

Study on the protective effects of danshen-honghua herb pair (DHHP) on myocardial ischaemia/reperfusion injury (MIRI) and potential mechanisms based on apoptosis and mitochondria.

CONTEXT: Danshen, the dried root and rhizome of Salvia miltiorrhiza Bunge (Labiatae) and honghua, the dried flower of Carthamus tinctorius L. (Compositae) as the herb pair was used to treat cardiovascular diseases (CVD). OBJECTIVE: To study the effects of DHHP on MIRI and mechanisms based on apoptosis and mitochondria. MATERIALS AND METHODS: 36 SD rats (n = 6) were randomly divided into control group (Con), the ischaemia-reperfusion group (IR), positive control (Xinning tablets, XNT, 1 g/kg/d) and DHHP (1.2, 2.4, and 4.8 g/kg/d). Except for Con, the other groups were intragastrically administrated for 5 d, the rat hearts were isolated to establish the MIRI model in vitro for evaluating the effects of DHHP on MIRI. 24 SD rats (n = 6) were randomly divided into Con, IR, DPPH2.4 (2.4 g/kg/d) and DPPH 2.4 + Atractyloside (ATR) (2.4 + 5 mg/kg/d), administered intragastrically for 5 d, then treated with ATR (5 mg/kg/d) by intraperitoneal injection in DPPH2.4 + ATR group, took rat hearts to establish MIRI model in vitro for revealing mechanism. RESULTS: Myocardial infarct sizes were, respectively, 0.35%, 40.09%, 15.84%, 30.13%, concentrations of NAD+ (nmol/gw/w) were 144, 83, 119, and 88, respectively, in Con, IR, DHHP2.4, DHHP2.4 + ATR group. Cleaved caspase-3 were 0.3, 1.6, 0.5 and 1.3% and cleaved caspase-9 were 0.2, 1.1, 0.4 and 0.8%, respectively, in Con, IR, DHHP2.4 and DHHP2.4 + ATR group. The beneficial effects of DHHP on MIRI were reversed by ATR. CONCLUSIONS: The improvement of MIRI by DHHP may be involved in inhibiting MPTP opening, decreasing oxidative damage, alleviating ischaemic injury and inhibiting cardiomyocyte apoptosis.

Investigating the effects and possible mechanisms of danshen- honghua herb pair on acute myocardial ischemia induced by isoproterenol in rats.

Danshen (salvia miltiorrhiza) and honghua(Carthamus tinctorius) were traditional herb pair with promoting blood circulation and removing blood stasis actions, in China. Both were widely used to treat cardiovascular diseases (CVD) for hundreds years, especially shown definite advantage in the treatment of ischemic heart disease (IHD). However, the mechanism of danshen-honghua herb pair (DHHP) in the treatment of IHD was still unclear. This study was focused on examining the effects and possible mechanisms of DHHP in rats with acute myocardial ischemia induced by isoproterenol (ISO). The results suggested that DHHP significantly ameliorated the myocardial tissue abnormalities, notablely inhibited the elevation of lactate dehydrogenase (LDH), creatine kinase (CK), aspartate aminotransferase (AST), creatinekinase isoenzyme (CK-MB) and cardiac troponin T (CTn-T) in plasma, obviously decreased the plasma levels of Tumor Necrosis Factor α (TNF-α), outstandingly inhibited the reduction of superoxide dismutase (SOD), catalase (CAT) caused by ISO, significantly inhibited the high expression of Bcl-2 assaciated X protein (Bax) and nuclear transcriptionfactor-κBP65 (NF-κBP65) protein, significantly induced the low expression of B-cell lymphoma-2 (Bcl-2) protein in acute myocardial ischemia rats. DHHP can obviously ameliorate hemodynamic parameters. In summary, DHHP can significantly improve myocardial ischemia in acute myocardial ischemia model rats caused by ISO. Anti-free radicals, anti-peroxidation, inhibition of cell apoptosis and anti- inflammation maybe are the potential mechanisms of DHHP anti-myocardial ischemia in acute myocardial ischemia rats in duced by ISO.

Structural Optimization and Structure-Activity Relationship of 4-Thiazolidinone Derivatives as Novel Inhibitors of Human Dihydroorotate Dehydrogenase.

Human dihydroorotate dehydrogenase (hDHODH), one of the attractive targets for the development of immunosuppressive drugs, is also a potential target of anticancer drugs and anti-leukemic drugs. The development of promising hDHODH inhibitors is in high demand. Based on the unique binding mode of our previous reported 4-thiazolidinone derivatives, via molecular docking method, three new series 4-thiazolidinone derivatives were designed and synthesized as hDHODH inhibitors. The preliminary structure-activity relationship was investigated. Compound 9 of biphenyl series and compound 37 of amide series displayed IC50 values of 1.32 µM and 1.45 µM, respectively. This research will provide valuable reference for the research of new structures of hDHODH inhibitors.

Significance of the microRNA­17­92 gene cluster expressed in B­cell non­Hodgkin's lymphoma.

To evaluate the prognostic value of the microRNA (miR)­17­92 gene cluster, the expression of miR­17­92 in B­cell non­Hodgkin's lymphoma (B­NHL) was examined. Patients with B­NHL, who received therapy in the Department of Hematology, Harbin Medical University Cancer Hospital between January 2012 and October 2014, were enrolled in the study. The expression of the miR­17­92 cluster in tumor tissue samples was detected by reverse transcription­quantitative polymerase chain reaction analysis. The overall survival (OS) and event­free survival (EFS) times were also investigated by the Kaplan­Meier method and comparisons between groups were estimated using a log­rank test. Three types of lymphoid cancer cells with wild­type (WT), knockout of miR­17­92 (KO), and overexpression of miR­17­92 (TG), were utilized to establish a tumor xenograft model, and a reactive hyperplasia lymph cell was used as a control. The tumor incubation times and weights were examined. A total of 71 patients with B­NHL were registered. No significant correlations were identified between the expression of miR­17­92 and clinical factors (P>0.05). Members of the miR­17­92 cluster exhibited various expression in the subtypes of B­NHL, and the difference between follicular lymphoma (FL) and germinal center B­cell like (GBC) was most marked. The overexpression of miR­18, miR­19a, and miR­92a induced a marked reduction in the OS of patients with B­NHL, and high­levels of miR­19a and miR­92a led to a decline in EFS. The overexpression of miR­17­92 shortened the duration of incubation required for visualization of the xenograft tumor, whereas knockout led to inhibition of tumor formation. The expression of miR­17­92 in FL differed significantly from that in GBC, and miR­19a may have a crucial effect on the OS and EFS of patients with B­NHL.

Ganoderic acid A exerts antitumor activity against MDA-MB-231 human breast cancer cells by inhibiting the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway.

Breast cancer is a common malignant tumor among females, with triple-negative breast cancer being an important type accounting for 15-20% of all breast cancer cases. Triple-negative breast cancer is one of the most aggressive types of cancer without standard adjuvant chemotherapy. Ganoderic acid A (GA-A) is one of the major bioactive Ganoderma triterpenoids isolated from Ganoderma, which are recognized for their preventative and therapeutic effects. In the present study, the antineoplastic effect of GA-A on human breast cancer was investigated and the pro-apoptotic function of Janus kinase (JAK)2 and signal transducer and activator of transcription (STAT)3 on the function of GA-A was revealed. GA-A treatment inhibited the invasion of MDA-MB-231 cells. In addition, GA-A exhibited significant antitumor activity by enhancing the apoptotic index and reactive oxygen species production. In the present study, GA-A was identified to directly inhibit JAK2 phosphorylation and STAT3 downstream activation. In addition, GA-A suppressed STAT3 target gene expression, including B cell lymphoma-extra-large and Myeloid cell leukemia 1, resulting in elevated levels of proteins associated with mitochondrial apoptosis in addition to inhibitors of cyclin-dependent kinase. GA-A, in combination with AG490, a JAK2/STAT3 inhibitor, further decreased MDA-MB-231 cell viability. In conclusion, GA-A treatment inhibited breast cancer cell viability via JAK2/STAT3 downregulation and may regulate associated targets to serve an anti-MDA-MB-231 role, including mitochondrial apoptosis and regulating the expression of cell-cycle-associated factors.

Enhanced antitumor effect of combination of annexin A1 knockdown and bortezomib treatment in multiple myeloma in vitro and in vivo.

Bortezomib (BTZ) is one of the most frequently used drugs in treatment of multiple myeloma (MM), but drug-resistance often occurs and limits its clinical efficacy. Annexin A1 (ANXA1) is upregulated in MM, and its knockdown enhances chemosensitivity in MM. However, whether ANXA1 inhibition can increase antitumor activity of BTZ in MM cells remains unknown. In the present study, Cell Counting Kit-8 (CCK-8) and colony formation assays showed that ANXA1 silencing combined with BTZ treatment led to a more significant inhibition of MM cell proliferation than each treatment alone. Cell apoptosis was dramatically promoted in MM cells following silencing of ANXA1 and BTZ administration versus that in ANXA1-silenced alone or BTZ-treated alone cells, as evidenced by decreased expression of phosphorylated signal transducers and activators of transcription 3 and BCL2, and increased expression of BAX. Moreover, we demonstrated that the levels of IL-6 and IL-23 were markedly downregulated in ANXA1-silenced and BTZ-treated MM cells. Furthermore, the combination of ANXA1 knockdown and BTZ treatment distinctly suppressed tumor growth in vivo compared with BTZ treatment alone. Taken together, our results show that downregulation of ANXA1 enhances antitumor activity of BTZ in MM in vitro and in vivo, indicating that ANXA1 may be a promising target for enhancing the chemosensitivity of MM to BTZ.

miR-26b-5p suppresses proliferation and promotes apoptosis in multiple myeloma cells by targeting JAG1.

BACKGROUND: Though the levels of diagnosis and treatment of multiple myeloma (MM) have been largely improved recent years, the prognosis of these patients remain unacceptable. It is urgent for us to discover the exact mechanism and determine some new indicators for MM. MiRNAs play a critical role in the occurrence and progression of cancers, including MM. MiR-26b-5p has been reported to be closely related to cells proliferation in human pulmonary cancer, hepatocellular carcinoma and so on. MATERIAL AND METHODS: Here, we measured the expression of miR-26b-5p in MM samples and cell lines by real-time PCR. Then, Kaplan-Meier Curves were applied to assess the effect of miR-26b-5p expression on MM patients prognosis. Functionally, MTT assay and Flow cytometry were conducted to explore the functions of miR-26b-5p in cells proliferation and apoptosis. Furthermore, bioinformatics tools, Pearson's correlation coefficient analysis, gain-and loss of-function experiments and rescue experiment were used to determine the relationship between JAG1 and miR-26b-5p in MM cells. In addition, we also confirmed the role of JAG1 in MM cells proliferation and apoptosis by gain-and loss of-function experiments. RESULTS: Here, we reported for the first time that miR-26b-5p was under-expressed in MM by real-time PCR. Clinically, Kaplan-Meier Curves showed that MM patients with lower miR-26b-5p expression had worse prognosis. Functionally, MTT assay revealed that miR-26b-5p inhibited cells proliferation. Flow cytometry indicated that miR-26b-5p accelerated tumor cells apoptosis. Furthermore, bioinformatics tools, Pearson's correlation coefficient analysis gain-and loss of-function experiments showed that JAG1 was the target of miR-26b-5p in MM cells. And, gain-and loss of-function experiments for JAG1 confirmed that JAG1 was an oncogene in MM cells. What's more, rescue experiment showed that JAG1 mediated the function of miR-26b-5p in MM cells. CONCLUSION: MiR-26b-5p acts as a tumor suppressor through suppressing cells proliferation and inducing cells apoptosis via directly targeting JAG1 in MM. MiR-26b-5p could be a potential and ponderable tumor target for MM in future.

Lentivirus-mediated down-regulation of CK2α inhibits proliferation and induces apoptosis of malignant lymphoma and leukemia cells.

Casein kinase II subunit alpha (CK2α) is highly expressed in many malignant tumor tissues, including lymphomas and leukemia. To investigate the role of CK2α in cell proliferation and apoptosis of malignant lymphomas and leukemia, 2 lymphoma cell lines and one leukemia cell line were infected with CK2α shRNA lentivirus or negative control shRNA lentivirus, and stably infected cell lines were established. Real-time PCR and Western blot results showed that the mRNA and protein levels of CK2α were significantly reduced in CK2α knockdown cells. The tetrazolium-based colorimetric (MTT) assay found that down-regulation of CK2α inhibited the proliferation of these cells. Flow cytometry analysis showed that inhibition of CK2α induced cell cycle arrest and apoptosis of lymphoma and leukemia cells. In accordance with these, down-regulation of CK2α also reduced the protein levels of proliferating cell nuclear antigen (PCNA), cyclinD1, and bcl-2, and increased the protein expression of bax, cleaved caspase-3, cleaved caspase-9, and cleaved poly(ADP ribose) polymerase (PARP). Moreover, knockdown of CK2α impeded the growth of xenograft tumors in vivo. In summary, our study revealed that CK2α may contribute to the development of malignant lymphoma and leukemia, and serve as the therapeutic target of these malignant tumors.

Highly Efficient Visible Colloidal Lead-Halide Perovskite Nanocrystal Light-Emitting Diodes.

Lead-halide perovskites have been attracting attention for potential use in solid-state lighting. Following the footsteps of solar cells, the field of perovskite light-emitting diodes (PeLEDs) has been growing rapidly. Their application prospects in lighting, however, remain still uncertain due to a variety of shortcomings in device performance including their limited levels of luminous efficiency achievable thus far. Here we show high-efficiency PeLEDs based on colloidal perovskite nanocrystals (PeNCs) synthesized at room temperature possessing dominant first-order excitonic radiation (enabling a photoluminescence quantum yield of 71% in solid film), unlike in the case of bulk perovskites with slow electron-hole bimolecular radiative recombination (a second-order process). In these PeLEDs, by reaching charge balance in the recombination zone, we find that the Auger nonradiative recombination, with its significant role in emission quenching, is effectively suppressed in low driving current density range. In consequence, these devices reach a maximum external quantum efficiency of 12.9% and a power efficiency of 30.3 lm W-1 at luminance levels above 1000 cd m-2 as required for various applications. These findings suggest that, with feasible levels of device performance, the PeNCs hold great promise for their use in LED lighting and displays.

2D matrix engineering for homogeneous quantum dot coupling in photovoltaic solids.

Colloidal quantum dots (CQDs) are promising photovoltaic (PV) materials because of their widely tunable absorption spectrum controlled by nanocrystal size1,2. Their bandgap tunability allows not only the optimization of single-junction cells, but also the fabrication of multijunction cells that complement perovskites and silicon 3 . Advances in surface passivation2,4-7, combined with advances in device structures 8 , have contributed to certified power conversion efficiencies (PCEs) that rose to 11% in 2016 9 . Further gains in performance are available if the thickness of the devices can be increased to maximize the light harvesting at a high fill factor (FF). However, at present the active layer thickness is limited to ~300 nm by the concomitant photocarrier diffusion length. To date, CQD devices thicker than this typically exhibit decreases in short-circuit current (JSC) and open-circuit voltage (VOC), as seen in previous reports3,9-11. Here, we report a matrix engineering strategy for CQD solids that significantly enhances the photocarrier diffusion length. We find that a hybrid inorganic-amine coordinating complex enables us to generate a high-quality two-dimensionally (2D) confined inorganic matrix that programmes internanoparticle spacing at the atomic scale. This strategy enables the reduction of structural and energetic disorder in the solid and concurrent improvements in the CQD packing density and uniformity. Consequently, planar devices with a nearly doubled active layer thicknesses (~600 nm) and record values of JSC (32 mA cm-2) are fabricated. The VOC improved as the current was increased. We demonstrate CQD solar cells with a certified record efficiency of 12%.

Over-activated PD-1/PD-L1 axis facilitates the chemoresistance of diffuse large B-cell lymphoma cells to the CHOP regimen.

Interaction between the programmed cell death ligand 1 (PD-L1) and programmed cell death 1 (PD-1) contributes to tumor cell resistance to chemotherapeutic agents. PD-L1 is expressed in the cells of diffuse large B-cell lymphoma (DLBCL), one common type of malignant non-Hodgkin lymphomas. However, little is known about how the PD-1/PD-L1 pathway functions in the pathogenesis of DLBCL. Therefore, the present study investigated whether and how the PD-1/PD-L1 axis is involved in regulating the sensitivity of CRL2631, a DLBCL cell line, to the CHOP (Cyclophosphamide, Hydroxydaunorubicin/adriamycin, Oncovin/vincristine and Prednisone) chemotherapeutic regimen. CHOP treatment significantly decreased cell survival rate and increased apoptosis in CRL2631 cells. The application of recombinant human PD-1 (rPD-1) significantly decreased the cytotoxic effects of the CHOP regimen in CRL2631 cells, but not in the CRL2631 cells with PD-L1 deficiency. In the CRL2631 cells, rPD-1 enhanced the activity of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt1) pathway. However, the activity level of the PI3K/Akt1 pathway was decreased in CHOP-treated CRL2631 cells. The selective PI3K inhibitor BKM120 significantly increased CHOP-induced apoptosis, but this effect was abolished by rPD-1 and aggravated by PD-L1 knockdown. In CHOP-treated PD-L1 knockdown cells, the increased apoptosis was markedly inhibited by the overexpression of constitutively active Akt1. Overall, the results demonstrate that the over-activated PD-1/PD-L1 axis is associated with chemotherapeutic resistance of DLBCL cells to the CHOP regimen, potentially through a PI3K-dependent mechanism.