Matched Electron-Transport Materials Enabling Efficient and Stable Perovskite Quantum-Dot-Based Light-Emitting Diodes.

Light-emitting diodes (LEDs) based on perovskite quantum dots (QDs), abbreviated as P-QLEDs have been regarded as significantly crucial emitters for lighting and displays. Efficient and stable P-QLEDs still lack ideal electron transport materials (ETM), which could efficiently block hole, transport electron, reduce interface non-radiative recombination and possess high thermal stability. Here, we report 2,4,6-Tris(3'-(pyridine-3-yl) biphenyl-3-yl)-1,3,5-triazine (TmPPPyTz, 3P) with strong electron-withdrawing moieties of pyridine and triazine to modulate the performance of P-QLEDs. Compared with commonly used 1,3,5-Tris(1-phenyl-1H-benzimidazol-2-yl)benzene (TPBi), the pyridine in 3P have a strong interaction with perovskites, which can effectively suppress the interface non-radiative recombination caused by the Pb2+ defects on the surface of QDs. In addition, 3P have deep highest occupied molecular orbital (HOMO) (enhancing hole-blocking properties), matched lowest unoccupied molecular orbital (LUMO) and excellent electron mobility (enhancing electron transport properties), realizing the carrier balance and maximizing the exciton recombination. Furthermore, high thermal resistance of 3P obviously improves the stability of QDs under variable temperature, continuous UV illumination, and electric field excitation. Resultantly, the P-QLEDs using the 3P as ETM achieved an outstanding performance with a champion EQE of 30.2 % and an operational lifetime T50 of 3220 hours at an initial luminance of 100 cd m-2, which is 151 % and about 11-fold improvement compared to control devices (EQE=20 %, T50=297 hours), respectively. These results provide a new concept for constructing the efficient and stable P-QLEDs from the perspective of selective ETM.

Polymer-Surface-Mediated Mechanochemical Reaction for Rapid and Scalable Manufacture of Perovskite QD Phosphors.

Perovskite quantum dots (QDs) have been considered new-generation emitters for lighting and displays due to their high photoluminescence (PL) efficiency, and pure color. However, their commercialization process is currently hindered by the challenge of mass production in a quick and environmentally friendly manner. In this study, a polymer-surface-mediated mechanochemical reaction (PMR) is proposed to prepare perovskite QDs using a high-speed multifunction grinder for the first time. PMR possesses two distinctive features: i) The ultra-high rotating speed (>15 000 rpm) of the grinder facilitates the rapid conversion of the precursor to perovskite; ii) The surface-rich polymer particulate ensures QDs with high dispersity, avoiding QD aggregation-induced PL quenching. Therefore, PMR can successfully manufacture green perovskite QDs with a high PL quantum yield (PLQY) exceeding 90% in a highly material- (100% yield), time- (1 kg min-1), and effort- (solvent-free) efficient manner. Moreover, the PMR demonstrates remarkable versatility, including synthesizing by various polymers and producing diverse colored and Pb-free phosphors. Importantly, these phosphors featuring a combination of polymer and perovskite, are facilely processed into various solid emitters. The proposed rapid, green, and scalable approach has great potential to accelerate the commercialization of perovskite QDs.

A ligand strategy retarding monovalent copper oxidation toward achieving Cs3Cu2I5 perovskite emitters with enhanced stability for lighting.

0D copper-based perovskites (Cs3Cu2I5) have fascinating optical properties, such as strong exciton binding energy, high photoluminescence quantum yield (PLQY) and large Stokes shifts from self-trapped excitons (STEs), which make them highly considerable candidates in the field of lighting. However, the stability of Cs3Cu2I5 is compromised by the oxidation of Cu+ to Cu2+ during the storage or operation process. Here, we proposed a ligand engineering strategy to improve the stability of Cs3Cu2I5via an organic molecule (ethylenediaminetetraacetic acid, EDTA) with multiple functional groups. The strong interaction between carboxyl groups and Cu+ was evidenced through FTIR and XPS, and it could retard monovalent copper oxidation. After storing for 90 days, the EDTA-engineered Cs3Cu2I5 (EDTA-Cs3Cu2I5) maintained its original crystalline structure, while the control Cs3Cu2I5 exhibited an impurity phase. Through quantitative analysis, the content of Cu2+ in EDTA-Cs3Cu2I5 was found to be 83.9% lower than that in control Cs3Cu2I5. Benefiting from the inhibition of Cu+ oxidation, EDTA-Cs3Cu2I5 exhibited improved light emission stability. For example, the optimized EDTA-Cs3Cu2I5 retained 74.7% of the initial photoluminescence (PL) intensity after 90-day storage under ambient conditions, while the pure Cs3Cu2I5 retained only 41.7%. Furthermore, EDTA could passivate defects and enhance the PL properties of the optimized Cs3Cu2I5, which showed a PLQY of 94.7%, much higher than that of 71.4% for pure Cs3Cu2I5. We further constructed a WLED based on the EDTA-engineered Cs3Cu2I5, which showed CIE at (0.3238, 0.3354), a CRI of 91.7, and a T50 of 361 h. The proposed EDTA ligand strategy provides a new way to regulate the light-emitting properties and stabilities of Cs3Cu2I5 for future industrialization.

Ginsenoside Rg3 Ameliorates DSS-Induced Colitis by Inhibiting NLRP3 Inflammasome Activation and Regulating Microbial Homeostasis.

Ulcerative colitis (UC) is a recurrent inflammatory disease without a specific cure or treatment for improvement. Here, we investigated the potential therapeutic effect and mechanism of ginsenoside Rg3 (Gin Rg3) on UC. We constructed an in vitro cellular inflammatory model and a dextran sulfate sodium (DSS)-induced UC mouse model. We also used Gin Rg3, MCC950 (NLRP3 inhibitor), MSU (NLRP3 activator), and fecal transplantation (FMT) to intervene the model. The results showed that Gin Rg3 inhibited NLRP3 inflammasome activation, pyroptosis, and apoptosis in vitro and in vivo. DSS-induced changes in the abundance of gut microbiota at the phylum or genus level were partially restored by Gin Rg3. Furthermore, gin Rg3 affected intestinal metabolism in mice by inhibiting the activation of NLRP3 inflammasome. The gut microbiota treated with Gin Rg3 was sufficient to alleviate DSS-induced UC. In summary, Gin Rg3 alleviated DSS-induced UC by inhibiting NLRP3 inflammasome activation and regulating gut microbiota homeostasis.

Fiber Optic Plate Coupled Pb-Free Perovskite X-ray Camera Featuring Low-Dose-Rate Imaging toward Dental Diagnosis.

Copper-based halide perovskites have been considered as promising scintillators. However, they still cannot meet the requirement of low-dose-rate X-ray imaging in medical diagnosis. Herein, we design a fiber optic plate (FOP) coupled perovskite X-ray camera to reduce the dose rate toward dental X-ray imaging. Tl doped Cs3Cu2I5 prepared via molten salt reaction has a high light yield of 72,000 photons/MeV, resulting from Tl10/Tl20-self-trapped hole emissions. After FOP coupling, the pulp cavity, root canal, dentin and root canal file can be clearly observed under a low dose rate as low as 3 µGyair s-1, which is absolutely lower than the required 5.5 µGyair s-1 for commercial intraoral dental sensors. The realization of such a low dose rate is attributed to the high coupling efficiency of 75% for the FOP and the high brightness of 262 lm m-2 for the scintillation screen. This designed portable X-ray camera shows its huge potential in intraoral dental X-ray imaging.

Recent progress of single-halide perovskite nanocrystals for advanced displays.

Light-emitting diodes based on lead halide perovskite nanocrystals (LHP NCs) have shown an astonishing increase in efficiency in just several years of academic research, reaching high external quantum efficiencies exceeding 20%. The extensive color-tunability and narrow emission bandwidth of LHP NCs, in particular, are of great importance in the creation of the next generation of ultra-high-definition displays, as defined by the Rec. 2020 standard recommendation. In fact, whereas the colour of LHP NCs can be easily tuned by the compositions of halogens, the ion migration in mixed-halide perovskites under the electric field will seriously affect the spectral stability and operational lifetimes of perovskite light-emitting diodes (PeLEDs). Therefore, it is essential to realize efficient colour-saturated PeLEDs based on single-halide perovskite NCs. In this review, we focus on the recent progress in LHP NC-based PeLEDs and highlight the strategy of tuning the spectral emission based on quantum confinement or cation alloying/doping in single-halide perovskite NCs. Finally, we will give an outlook on future research avenues for preparing high-efficiency pure green, red and blue PeLEDs based on single-halide perovskite NCs.

LINC01915 Facilitates the Conversion of Normal Fibroblasts into Cancer-Associated Fibroblasts Induced by Colorectal Cancer-Derived Extracellular Vesicles through the miR-92a-3p/KLF4/CH25H Axis.

Increasing long non-coding RNAs are reported to regulate the cell growth, apoptosis, and metastasis of cancer-associated fibroblasts (CAFs).This study aimed to explore how LINC01915 influences the conversion of normal fibroblasts (NFs) into CAFs in colorectal cancer (CRC). LINC01915 expression was initially measured in clinical tissue samples and in NFs and CAFs. Identification of the interaction between LINC01915, miR-92a-3p, KLF4, and CH25H was done. The effects of LINC01915, miR-92a-3p, and KLF4 on the angiogenesis, extracellular vesicle (EV) uptake by NFs, and activation of stromal cells were assessed using gain- or loss-of-function approaches. Xenograft mouse models were established to validate these in vitro findings in vivo. EVs were shown to stimulate NF proliferation, migration, and angiogenesis, as well as facilitate NF conversion into CAFs. CRC tissues and CAFs showed downregulated expression of LINC01915, which was associated with poor prognosis of patients. Moreover, employed LINC01915 inhibited tumor angiogenesis, CAF activation, and the uptake of tumor-derived EVs by NFs. Mechanistically, LINC01915 could competitively bind to miR-92a-3p and caused upregulation of the miR-92a-3p target KLF4 which, in turn, promoted the transcription of CH25H, leading to the suppressed uptake of EVs by NFs. The in vivo and in vitro experimental results showed that LINC01915 inhibited the uptake of CRC-derived EVs by NFs through the miR-92a-3p/KLF4/CH25H axis, thus arresting the angiogenesis and the conversion of NFs into CAFs and in turn prevent tumor growth. These data together supported the inhibiting role of LINC01915 in the conversion of NFs into CAFs triggered by the CRC-derived EVs and the ensuing tumor growth, which may be related to its regulation on the miR-92a-3p/KLF4/CH25H axis.

Exosomal MicroRNA-181a Derived From Mesenchymal Stem Cells Improves Gut Microbiota Composition, Barrier Function, and Inflammatory Status in an Experimental Colitis Model.

Background: Mesenchymal stem cell (MSC)-derived exosomes (Exos) are recently proved to be a promising candidate for ulcerative colitis (UC), but the mechanism remains unclear. We investigated the effects of MSC-derived exosomal microRNA-181a (miR-181a) on gut microbiota, immune responses, and intestinal barrier function in UC. Methods: Human bone marrow MSC-derived Exos were extracted and identified via transmission electron microscopy (TEM), Nanoparticle Tracking Analysis (NTA), and Western blotting. Dextran sodium sulfate (DSS)-induced colitis model and lipopolysaccharide (LPS)-induced human colonic epithelial cell (HCOEPIC) model were established to determine the effect of MSC-Exos on gut microbiota, immune responses, and intestinal barrier function in vivo and in vitro. The relationship between miR-181a and UC was analyzed using the Gene Expression Omnibus (GEO) database. MSC-miR-181-inhibitor was used to reveal the role of exosomal miR-181a in DSS-induced colitis. Results: TEM and NTA results showed that Exos of a diameter of about 100 nm with the round and oval vesicle-like structure were successfully extracted. The expressions of the CD63, CD81, and TSG101 proteins were positive in these Exos. After MSC-Exo treatment, the colon length in colitis mice increased; colon inflammatory injury decreased; TNF-α, IL-6, IL-1ß, IL-17, and IL-18 levels decreased; and Claudin-1, ZO-1, and IκB levels increased. In addition, the structure of the gut microbiota in DSS-induced colitis mice was changed by MSC-Exos. MSC-Exos showed antiapoptotic effects on LPS-induced HCOEPIC. The protective effects decreased significantly by treatment with MSC-Exos interfered with miR-181a inhibitor in vivo and in vitro. Conclusion: MSC-derived exosomal miR-181a could alleviate experimental colitis by promoting intestinal barrier function. It exerted anti-inflammatory function and affected the gut microbiota. This indicated that MSC exosomal miR-181a may exhibit potential as a disease-modifying drug for UC.

Bovine Lactoferrin Protects Dextran Sulfate Sodium Salt Mice Against Inflammation and Impairment of Colonic Epithelial Barrier by Regulating Gut Microbial Structure and Metabolites.

Background: Ulcerative colitis is characterized by relapsing and remitting mucosal inflammation. Bovine lactoferrin (BL) is a multifunctional protein that could regulate the intestinal flora and has anti-inflammatory effects. The aim of this study was to investigate the therapeutic effect of BL on colitis. Methods: Dextran sulfate sodium salt (DSS) was utilized to establish a mouse model of colitis. BL was administered to treat DSS mice. The weight, the activity, and fecal status of the mice were recorded every day. Disease activity index was calculated. After the mice were euthanized, the colon length was measured. Hematoxylin and eosin staining was used to observe the pathological changes of the colon, and histological activity index was calculated. The myeloperoxidase (MPO) activity of colon tissue was measured. Western blot and immunohistochemistry were used to detect the expressions of Claudin-1, Occludin, and ZO-1. The expressions of IL-1ß, IL-6, IL-10, TNF-α, and TGF-ß in colon tissue were detected by ELISA. The protein expressions of MUC2, Reg3γ, ß-defensin (HBD-2), and cAMP were detected by immunofluorescence (IF). 16S rDNA sequencing determined the type and structure of intestinal flora. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) measured the metabolites of the intestinal flora. Results: Compared with the DSS group, the mice's weight in the BL group was higher and the length of the colon was longer. At the 14th day, MPO activity was higher in the BL group. The expressions of Claudin-1, Occludin, and ZO-1 in the colon were up-regulated in the BL group compared with the DSS group. The expressions of IL-1ß, IL-6, and TNF-α were lower. The expressions of IL-10 and TGF-ß were higher. IF showed that the expressions of MUC2 and ß-defensin (HBD-2) were down-regulated, and the expressions of Reg3γ and cAMP were up-regulated. The 16S rDNA sequencing results showed that the alpha diversity and beta diversity were notably changed in the DSS mice treated with BL. Metabolomics results showed that BL changed purine metabolism in the DSS mice. Conclusion: BL alleviated colitis in mice by improving the inflammatory response and the structure of the colon barrier in the colon. BL changed the composition and metabolites of the intestinal flora. Thus, BL might be an effective nutritional supplement for colitis treatment.

Inhibitor of apoptosis-stimulating p53 protein protects against inflammatory bowel disease in mice models by inhibiting the nuclear factor kappa B signaling.

Drugs and therapies available for the treatment of inflammatory bowel disease (IBD) are not satisfactory. Our previous study has established the inhibitor of apoptosis-stimulating p53 protein (iASPP) as an oncogenic regulator in colorectal cancer by forming a regulatory axis or feedback loop with miR-124, p53, or p63. As iASPP could target and inhibit nuclear factor kappa B (NF-κB) activation, in this study the role and mechanism of iASPP in IBD was investigated. The aberrant up-regulation of iASPP in IBD was subsequently confirmed, based on online data sets, clinical sample examinations and 2,4,6-trinitrobenzene sulfonic acid (TNBS)- and dextran sulfate sodium (DSS)-induced colitis mice models. TNBS or DSS stimulation successfully induced colon shortness, body weight loss, mice colon oxidative stress and inflammation. In both types of colitis mice models, iASPP over-expression improved, whereas iASPP knockdown aggravated TNBS or DSS stimulation-caused colon shortness, body weight loss and mice colon oxidative stress and inflammation. Meanwhile, in both types of colitis mice models, iASPP over-expression inhibited p65 phosphorylation and decreased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, C-X-C motif chemokine ligand (CXCL)1 and CXCL2 in mice colons, whereas iASPP knockdown exerted opposite effects.

NEK7 interacts with NLRP3 to modulate the pyroptosis in inflammatory bowel disease via NF-κB signaling.

Inflammatory bowel disease (IBD) is one of the most common diseases in the gastrointestinal tract related to aberrant inflammation. Pyroptosis, which is characterized by inflammasome formation, the activation of caspase-1, and the separation of the N- and C-terminals of GSDMD, might be related to IBD pathogenesis. NEK7 is an important component of the NLRP3 inflammasome in macrophages. We attempted to investigate the mechanism of NEK7 interacting with NLRP3 to modulate the pyroptosis in IBD. NEK7 mRNA and protein expression and pyroptosis-associated factors, including Caspase-1 (p45, p20), NLRP3, and GSDMD, were upregulated in IBD tissues. NEK7 knockdown abolish ATP + LPS-induced pyroptosis in vitro and improved DSS-induced chronic colitis in vivo. NEK7 interacted with NLRP3, as revealed by Co-IP and GST pull-down assays, to exert its effects. Moreover, short-term LPS treatment alone induced no significant changes in NEK7 protein level. TLR4/NF-κB signaling in MODE-K cells could be activated by LPS treatment. LPS-induced NEK7 upregulation could be significantly reversed by JSH-23, an inhibitor of p65. Furthermore, LUC and ChIP assays revealed that RELA might activate the transcription of NEK7 via targeting its promoter region. LPS-induced TLR4/NF-κB activation causes an increase in NEK7 expression by RELA binding NEK7 promoter region. In conclusion, NEK7 interacts with NLRP3 to modulate NLRP3 inflammasome activation, therefore modulating the pyroptosis in MODE-K cells and DSS-induced chronic colitis in mice. We provide a novel mechanism of NEK7-NLRP3 interaction affecting IBD via pyroptosis.

Long non-coding RNA SNHG12 promotes proliferation and invasion of colorectal cancer cells by acting as a molecular sponge of microRNA-16.

Long non-coding (lnc)RNA small nucleolar RNA host gene 12 (SNHG12) has an oncogenic role in various common human cancer types, including colorectal cancer (CRC). However, the detailed regulatory mechanisms of SNHG12 in CRC cells have remained largely elusive, and the investigation thereof was the purpose of the present study. Polymerase chain reaction analysis was performed to examine the expression of lncRNA and microRNA (miR). Cell Counting Kit-8 and Transwell assays were used to assess cell proliferation and invasion. A luciferase reporter assay was performed to confirm a predicted targeting association between lncRNA and miR. It was observed that SNHG12 was markedly upregulated in CRC tissues when compared with that in adjacent non-tumour tissues, and its high expression was associated with CRC progression, as well as poor prognosis of patients. In addition, the expression of SNHG12 was higher in CRC cell lines when compared with that in a normal intestinal epithelial cell line. Knockdown of SNHG12 significantly inhibited CRC cell proliferation and invasion, while ectopic overexpression of SNHG12 had the opposite effect. A Bioinformatics analysis predicted that SNHG12 and miR-16 have complementary binding sites, which was confirmed by a luciferase reporter gene assay. The expression levels of miR-16 were markedly decreased in CRC tissues and cell lines compared with those in normal tissues or cells, and were inversely correlated with the expression levels of SNHG12 in CRC tissues. Furthermore, silencing of miR-16 eliminated the suppressive effects of SNHG12 knockdown on CRC cell proliferation and invasion. In conclusion, the present study demonstrated that SNHG12 promotes CRC cell proliferation and invasion, at least in part, by acting as a molecular sponge of miR-16, suggesting that SNHG12 may be a promising therapeutic target for CRC.

Solution processed membrane-based wearable ZnO/graphene Schottky UV photodetectors with imaging application.

Flexible and wearable electrical devices have attracted extensive research attention in recent years. In the device fabrication process, the low-cost and compatibility with industrialized mass production are of great importance. Herein, membrane-based flexible photodetectors (PDs) based on Polyvinylidene Fluoride filter membrane with the structure of Ag nanowires (NWs)/ZnO NWs/graphene were fabricated by a full-solution method. The built-in electric field due to the ZnO/graphene Schottky junction is in favor of the separation and transport of photo-generated carriers, leading to enhanced device performance. The I light/I dark ratio was as high as ∼102, which is far superior to that of the reported ZnO-based fiber-shaped PDs. The PDs with remarkable flexibility can be easily attached to the human body and even can work steadily under serious bending conditions. Particularly, the photocurrent can keep 95% of the maximum value after the PD was bent 1000 times. In addition to the wearable applications, the membrane-based PD arrays can also be applied for imaging application.

Narrowband Perovskite Photodetector-Based Image Array for Potential Application in Artificial Vision.

Image sensor arrays are widely used in digital cameras, smartphones, and biorobots. However, most commercial image arrays rely on the dichroic prisms or a set of interference filters to distinguish characteristic color spectrum, which significantly increases the cost and fabrication processing complexity. In this work, an ultranarrow response photodetector with full-width at half-maximum being ∼12 nm and specific detectivity over 1011 Jones at 545 nm are successfully achieved in CsPbBr3 polycrystalline films using freeze-drying casting method to adjust the surface-charge recombination. To our best knowledge, this is the narrowest spectrum response for perovskite photodetectors in the visible light waveband. More importantly, a series of narrowband photodetectors are developed to enhance diverse selectivity for target signals covering from blue light to red light via bandgap tuning in CsPbX3 by tailoring the halide component. Finally, an integrated sensing array with CsPbX3 (X = Cl, Br, I) narrowband photodetectors acting as color recognition cones is constructed, which presents clear color and shape recognition paving the way for commercialization of perovskite photodetector in artificial vision.

Inflammatory caspase-related pyroptosis: mechanism, regulation and therapeutic potential for inflammatory bowel disease.

As an essential part of programmed cell death, pyroptosis is an inflammatory response that is elicited upon infection by intracellular pathogens. Metabolic diseases, atherosclerosis and vital organ damage occur if pyroptosis is over-activated. Macrophages are the main cells that induce pyroptosis with the help of intracellular pattern-recognition receptors stimulated by danger signals and pathogenic microorganisms in the cytosol of host cells. Activated inflammatory caspases induce pyroptosis and produce pro-inflammatory cytokines, such as interleukin-1ß and interleukin-18. Inflammatory programmed cell death is classified as canonical or non-canonical based on inflammatory caspases, which includes caspase-1 (in human and mouse) and caspase-11 (in mouse) or caspase-4 and -5 (in humans). Activated inflammatory caspases cleave the pore-forming effector protein, gasdermin-D, inducing osmotic pressure deregulation of internal fluids and subsequently rupturing the cell membranes. Inflammatory caspases could be attractive therapeutic targets for inflammatory bowel disease (IBD) in which pyroptosis may play an important role. This article reviews the current understanding of the mechanism of pyroptosis, focusing on the regulation of inflammatory caspases and therapeutic strategies for IBD.

Nanowire network-based photodetectors with imaging performance for omnidirectional photodetecting through a wire-shaped structure.

Wearable photodetectors (PDs) have attracted extensive attention from both scientific and industrial areas due to intrinsic detection abilities as well as promising applications in flexible, intelligent, and portable fields. However, most of the existing PDs have rigid planar or bulky structures which cannot fully meet the demands of these unique occasions. Here, we present a highly flexible, omnidirectional PD based on ZnO nanowire (NW) networks. ZnO NW network-based PDs exhibit the imageable level performance with an on/off ratio of about 104. Importantly, a ZnO NW network can be assembled onto wire-shaped substrates to construct omnidirectional PDs. As a result, the wire-shaped PDs have excellent flexibility, a large light on/off ratio larger than 103, and 360° no blind angle detecting. Besides, they exhibit extraordinary stability against bending and irradiation. These results demonstrate a novel strategy for building wire-shaped optoelectronic devices through a NW network structure, which is highly promising for future smart and wearable applications.

MicroRNA-520b Functions as a Tumor Suppressor in Colorectal Cancer by Inhibiting Defective in Cullin Neddylation 1 Domain Containing 1 (DCUN1D1).

MicroRNAs (miRs), a class of small noncoding RNAs, are important regulators for gene expression through directly binding to the 3'-untranslated region (3'-UTR) of their target mRNA. Recently, downregulation of miR-520b has been observed in several common human cancers. However, the exact role of miR-520b in colorectal cancer (CRC) has not previously been studied. In this study, our data showed that miR-520b was significantly downregulated in CRC and cell lines when compared with adjacent normal tissues and a normal intestinal epithelial cell line. Low expression of miR-520b was notably associated with the malignant progress and a shorter survival time for CRC patients. Restoration of miR-520b inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in CRC cells. Defective in cullin neddylation 1 domain containing 1 (DCUN1D1) was then identified as a novel target gene of miR-520b in CRC cells. The expression of DCUN1D1 was significantly increased in CRC, with a negative correlation to miR-520b expression in CRC tissues. Moreover, a high expression of DCUN1D1 was significantly associated with the malignant progress and a poor prognosis for CRC patients. Furthermore, overexpression of DCUN1D1 rescued the miR-520b-mediated malignant phenotypes and EMT in CRC cells. The data demonstrate that miR-520b functions as a tumor suppressor in CRC through targeting DCUN1D1, suggesting that miR-520b may become a potential therapeutic target for the treatment of CRC.

Assembling tungsten oxide hydrate nanocrystal colloids formed by laser ablation in liquid into fast-response electrochromic films.

High-performance electrochromic films based on tungsten oxide hydrate ([WO2(O2)H2O]·1.66H2O) colloidal nanocrystals with fast switching speed were fabricated by laser ablation in a mixture of water and hydrogen peroxide followed by electrophoretic methods. Through electrophoretic deposition, the nanoparticles in the colloids synthesized by laser ablation aggregated onto the FTO coated glass substrate forming a lager cell with a uniform size of around 200nm, which subsequently self-assembled into a porous tungsten oxide hydrate film. By optimizing the electrophoretic time (800s) and voltage (-0.5V), the mesh-like porous tungsten oxide hydrate film achieved a wide optical modulation of 32% at 632nm, fast coloration and bleaching response speed of 7.8 s and 1.7s respectively due to the synergetic effect of the unique atomic structure of [WO2(O2)H2O]·1.66H2O and porous structure with large surface area that facilitates the ion insertion/extraction. Thus the tungsten oxide hydrate can be a promising electrochromic material for practical applications.

Predictive biomarkers for targeted and cytotoxic agents in gastric cancer for personalized medicine.

Gastric cancer (GC) is the fourth most common cancer and the second leading cause of cancer. The treatment of GC remains challenging as the outcomes achieved with surgery alone or adjuvant or neoadjuvant chemotherapy and radiotherapy are relatively poor. New treatment strategies are emerging and are being tested in solid tumors including GC. Over the past few years, the treatment of metastatic colorectal cancer (CRC) has made great advances, but strategies to manage GC have improved little. Multiple drug resistance is common in GC chemotherapy and targeted therapy; some patients appear to receive treatment that is suboptimal or even inefficacious. Unfortunately, there are few validated predictive biomarkers to guide the tailored treatment of GC. ToGA and AVAGAST are two phase III trials that tested the efficacy and safety of targeted agents in advanced gastric cancer (AGC), and results clearly indicated that patients need to be selected and that targeted agents are the best hope for better results. This review aims to provide an overview of potential predictive biomarkers for cytotoxic and targeted agents in GC.

Endovascular aortic repair combined with chimney technique in the treatment of stanford type B aortic dissection involving aortic arch.

BACKGROUND: In this study, we sought to explore the efficacy of endovascular aortic repair combined with the chimney technique in the treatment of Stanford type B aortic dissection involving the aortic arch. METHODS: Between June 2009 and June 2012, 41 consecutive patients were treated with chimney technique at our institute for aortic arch dissection with the primary entry tear adjacent to the orifices of the supra-aortic arteries. The chimney technique was used to reconstruct the left subclavian artery (n = 5) and the left common carotid artery (n = 34). Additionally, in 2 cases, the double chimney technique was used to simultaneously reconstruct the innominate artery and the left common carotid artery. RESULTS: Eight of the 41 patients had undergone emergent surgery. All the patients survived the surgery, and the mean follow-up period was 17.3 ± 6.1 months. None of the patients had type I endoleak. Four patients had type II endoleak, and 3 of them underwent implantation of the patent ductus arteriosus occluder in the left subclavian artery. Among these 3 patients, one patient who was pregnant with Marfan syndrome and pregnancy-induced hypertension required additional medication for recovery. None of the patients had any severe neurological complications, left ischemia of the subclavian artery, migration of the stent graft, or occlusion of the stent grafts. CONCLUSIONS: Thus, endovascular aortic repair combined with the chimney technique appears to be a feasible, safe, and effective treatment option for the management of Stanford type B aortic dissection involving the aortic arch.