Showing papers by "Weijian Chen published in 2022"

Mechanism of Photoinduced Phase Segregation in Mixed-Halide Perovskite Microplatelets and Its Application in Micropatterning.

Abstract: Photoinduced phase segregation (PPS) is considered as a dominant factor that greatly deteriorates the performances of mixed-halide perovskite devices. However, the mechanism of PPS is still under fierce debate. Herein, CsPb(Brx/Cl1-x)3 microplatelets (MPs) with homogeneous and heterogeneous surfaces are obtained by controlling the growth conditions. Under continuous irradiation, a new photoluminescence (PL) band at 516 nm gradually appears in the heterogeneous MPs, accompanied with the decreased emission of the mixed phase at 480 nm, revealing the occurrence of PPS, while the photoirradiation only leads to slight PL dimming without PPS in the homogeneous MPs. The direct correlation between PPS and the structural heterogeneity indicates that the localized electric field-induced drift (LEFD) of halide ions/carriers is responsible for the PPS. In situ microfluorescence images evidence that the migration of halide ions is directed by the structural heterogeneity-induced localized electric field. Our refined model not only consolidates that PPS can be suppressed by eliminating the defects but also reveals that PPS can be directed by the distribution of defects. Therefore, a fluorescence micropatterning technique is developed based on PPS.

HBx inhibits DNA sensing signaling pathway via ubiquitination and autophagy of cGAS

Abstract: Cyclic GMP-AMP synthase (cGAS) is a crucial DNA sensor and plays an important role in host antiviral innate immune responses. During hepatitis B virus (HBV) infection, the cGAS signaling pathway can suppress HBV replication. As an important regulatory protein of HBV, hepatitis B virus X protein (HBx) may serve as an antagonistic character to the cGAS/STING signaling pathway. In this study, we aim to investigate the functional role of HBx in the cGAS/STING signaling pathway.The effects of HBx on IFN-β promoter activity were measured by Dual-luciferase reporter assays. Ubiquitination and autophagy were analyzed by Western-blot and Co-immunoprecipitation assays.Our results show that HBx down-regulates IFN-I production by directly promoting ubiquitination and autophagy degradation of cGAS.HBV can antagonize host cGAS DNA sensing to promote HBV replication and provide novel insights to develop novel approaches against HBV infection.

Valence-Regulated Metal Doping of Mixed-Halide Perovskites to Modulate Phase Segregation and Solar Cell Performance

Abstract: Electronic doping is a promising approach to modulating the optoelectronic properties of semiconductors, but its effect on optoelectronic behaviors of halide perovskites remains controversial. Here, we comprehensively investigate the impact of Pb substitution in n-type CsPbIBr2 perovskite by utilizing monovalent Ag, divalent Zn, and trivalent Sb. Our findings reveal that the trap densities in doped CsPbIBr2 films are in the order of Ag < Zn < Sb. Compared with the pristine CsPbIBr2, the Ag-doped perovskite features a significantly reduced phase separation; however, the Sb doping accelerates halide segregation, and Zn exerts a negligible influence. The p-doping effect from monovalent Ag can shift the Fermi level of CsPbIBr2 toward the intrinsic midgap, which helps prevent the formation of ionic defects and reduce the migration of halide ions in the perovskite lattice. Through combing the density functional theory simulation, this study discloses the correlation between valence-controlled metal doping and phase segregation, providing a guideline for judiciously doping mixed-halide perovskites for optoelectronic applications.

HBx inhibits DNA sensing signaling pathway via ubiquitination and autophagy of cGAS

Abstract: Cyclic GMP-AMP synthase (cGAS) is a crucial DNA sensor and plays an important role in host antiviral innate immune responses. During hepatitis B virus (HBV) infection, the cGAS signaling pathway can suppress HBV replication. As an important regulatory protein of HBV, hepatitis B virus X protein (HBx) may serve as an antagonistic character to the cGAS/STING signaling pathway. In this study, we aim to investigate the functional role of HBx in the cGAS/STING signaling pathway.The effects of HBx on IFN-β promoter activity were measured by Dual-luciferase reporter assays. Ubiquitination and autophagy were analyzed by Western-blot and Co-immunoprecipitation assays.Our results show that HBx down-regulates IFN-I production by directly promoting ubiquitination and autophagy degradation of cGAS.HBV can antagonize host cGAS DNA sensing to promote HBV replication and provide novel insights to develop novel approaches against HBV infection.

Dual Metal‐Assisted Defect Engineering towards High‐Performance Perovskite Solar Cells

Abstract: Perovskite solar cells (PSCs) have witnessed an unprecedentedly rapid development, especially in terms of power conversion efficiency (PCE). However, the solution‐processed perovskite films inevitably possess numerous crystallographic defects (e.g., halide vacancies), which has been shown to incur non‐radiative charge recombination and ion migration, thus limiting the enhancement of the PCE and stability of PSCs. Here, a novel dual metal (i.e., divalent and monovalent metal ions) modification strategy is reported for simultaneously reducing the defects, immobilizing the halide anions, and preventing ion loss from perovskite during post‐annealing process. Accordingly, this strategy significantly reduces non‐radiative recombination, enhancing the PCE by ≈12% and mitigating the current density‐voltage (J–V) hysteresis effect in resultant devices compared to undoped counterparts. As a result, a champion PCE exceeding 22% and a high open‐circuit voltage (Voc) of 1.16 V is obtained for dual metal ions‐modified PSCs. The optimized devices also exhibit extended lifespan upon the dual metal treatment. The study provides a new defect engineering strategy toward more efficient and stable perovskite photovoltaics.

Novel microRNA biomarkers of systemic lupus erythematosus in plasma: miR-124-3p and miR-377-3p.

Abstract: • Circulating miR-124-3p and miR-377-3p may constitute promising biomarkers for the diagnosis of SLE . • The levels of miRNA-124-3p and miRNA-377-3p in PBMCs were significantly upregulated. • miR-377-3p is independently correlated with SLE. • Plasma miR-124-3p is independently associated with the remission rate of SLE. To explore the clinical value of miR-124-3p and miR-377-3p in plasma, and to examine whether these microRNAs can serve as biomarkers for systemic lupus erythematosus. Samples from 50 patients with SLE and 47 healthy individuals were collected from the Rheumatology and Immunology Department at the Second Affiliated Hospital of Chongqing Medical University. The expression of miR-124-3p and miR-377-3p in peripheral blood mononuclear cells (PBMCs) and serum were determined by quantitative reverse-transcription PCR (RT-PCR). We then further analyzed the associations between these microRNAs and clinically relevant indicators. We employed receiver operating characteristic (ROC) curves and the area under the ROC curves (AUCs) to validate the diagnostic value of miR-124-3p and miR-377-3p. The expression of miR-124-3p and miR-377-3p was significantly upregulated in PBMCs and serum from SLE patients compared with the normal control group ( P < 0.05). ROC curve analysis indicated that plasma miR-124-3p and miR-377-3p were thus candidate diagnostic biomarkers for SLE, with AUCs of 0.714 (95% CI, 0.610 to 0.820, P < 0.05) and 0.705 (95% CI, 0.600 to 0.809, P < 0.05), respectively. Furthermore, the combined diagnostic efficiency of miR-124-3p and miR-377-3p was higher than that for miR-124-3p or miR-377-3p alone, and the AUCs for miR-124-3p and miR-377-3p in plasma were higher than in PBMCs. Plasma miR-124-3p expression was also associated with various clinicopathological parameters such as antiC1q and C3. Binary logistic regression analysis revealed that the expression of miR-377-3p was an independent predictor for SLE, and the plasma miR-124-3p was independently associated with the remission rate of SLE. Circulating miR-124-3p and miR-377-3p may constitute promising biomarkers for the diagnosis of SLE.

In Situ Bonding Regulation of Surface Ligands for Efficient and Stable FAPbI3 Quantum Dot Solar Cells

Abstract: Quantum dots (QDs) of formamidinium lead triiodide (FAPbI3) perovskite hold great potential, outperforming their inorganic counterparts in terms of phase stability and carrier lifetime, for high‐performance solar cells. However, the highly dynamic nature of FAPbI3 QDs, which mainly originates from the proton exchange between oleic acid and oleylamine (OAm) surface ligands, is a key hurdle that impedes the fabrication of high‐efficiency solar cells. To tackle such an issue, here, protonated‐OAm in situ to strengthen the ligand binding at the surface of FAPbI3 QDs, which can effectively suppress the defect formation during QD synthesis and purification processes is selectively introduced. In addition, by forming a halide‐rich surface environment, the ligand density in a broader range for FAPbI3 QDs without compromising their structural integrity, which significantly improves their optoelectronic properties can be modulated. As a result, the power conversion efficiency of FAPbI3 QD solar cells (QDSCs) is enhanced from 7.4% to 13.8%, a record for FAPbI3 QDSCs. Furthermore, the suppressed proton exchange and reduced surface defects in FAPbI3 QDs also enhance the stability of QDSCs, which retain 80% of the initial efficiency upon exposure to ambient air for 3000 hours.

CCL25/CCR9 interaction promotes the malignant behavior of salivary adenoid cystic carcinoma via the PI3K/AKT signaling pathway

Abstract: Background CC chemokine receptor 9 (CCR9), an organ-specific chemokine receptor, interacts with its exclusive ligand CCL25 to promote tumor proliferation and metastasis. However, the effect of CCR9 on salivary adenoid cystic carcinoma (SACC) malignant behavior remains unknown. This study aimed to investigate the specific molecular mechanism by which CCR9/CCL25 modulates malignant progression in SACC. Methods Immunohistochemistry staining and RT–qPCR analyses were performed to detect the correlation of CCR9 expression and tumor progression-associated markers in SACC. In vitro, SACC cell proliferation and apoptosis were evaluated using Cell Counting Kit-8 and colon formation, and cell migration and invasion were detected by wound healing and transwell assays. Vercirnon was used as an inhibitor of CCR9, and LY294002 was used as an inhibitor of the PI3K/AKT pathway in this study. Western blot and RT–qPCR assays were carried out to measure the downstream factors of the interaction of CCL25 and CCR9. The effect of CCL25 on the development of SACC in vivo was examined by a xenograft tumor model in nude mice following CCL25, Vercirnon and LY294002 treatment. Results CCR9 was highly expressed in SACC compared with adjacent salivary gland tissues, and its level was associated with tumor proliferation and metastases. CCL25 enhanced cell proliferation, migration, and invasion through its interaction with CCR9 and exerted an antiapoptotic effect on SACC cells. Targeting CCR9 via Vercirnon significantly reduced the phosphorylation level of AKT induced by CCL25. CCL25/CCR9 could activate its downstream factors through the PI3K/AKT signaling pathway, such as cyclin D1, BCL2 and SLUG, thus promoting SACC cell proliferation, antiapoptosis, invasion and metastasis. The in vivo data from the xenograft mouse models further proved that CCL25 administration promoted malignant tumor progression by activating the PI3K/AKT pathway. Conclusion The interaction of CCL25 and CCR9 promotes tumor growth and metastasis in SACC by activating the PI3K/AKT signaling pathway, offering a promising strategy for SACC treatment.

Reduced Circulating Soluble Receptor for Advanced Glycation End-products in Chronic Hepatitis B Are Associated with Hepatic Necroinflammation

Abstract: The diagnosis and disease management of chronic hepatitis B (CHB) remain challenging due to the elusive assessment of disease severity. Recently, soluble receptor for advanced glycation end-products (sRAGE) has been implicated in the inflammatory-immune response initiated by liver injury. Nonetheless, its natural behavior and clinical importance in CHB remain elusive. One hundred and twenty CHB patients and forty healthy controls (HCs) were enrolled, and the serum sRAGE as well as RAGE expression in biopsy specimens from these subjects was analyzed, and correlation of sRAGE with clinical features as well as its potential predictive value for monitoring the CHB was also evaluated. Reduced serum sRAGE levels and decreased tissular RAGE expression were observed in CHB patients. sRAGE and RAGE were inversely correlated with gradually increased grades of hepatic necroinflammation as well as the routine indicator ALT. Furthermore, receiver operating characteristic (ROC) analysis showed that combination of ALT and sRAGE exerted better predictive power (area under the ROC curve (AUC) of 0.86) for hepatic necroinflammation than that of ALT (AUC of 0.82), sRAGE (AUC of 0.81), or sRAGE-to-ALT ratio (sRAGE/ALT) (AUC of 0.85) alone. More importantly, circulating sRAGE alone exerted valuable predictive power for hepatic moderate-to-severe necroinflammation in CHB patients but with normal ALT (AUC of 0.81) or minimally elevated ALT (AUC of 0.85). In conclusion, reduced serum sRAGE levels may imply an increased severity for necroinflammation, and it may serve as a potential alternative biomarker for monitoring hepatic necroinflammation in CHB.

Serum soluble E-cadherin is a new potential marker for assessing the severity of gout.

Abstract: OBJECTIVES Currently, millions of people suffer from gout-related disorders, which cause a great economic and health burden worldwide. However, so far, there is no effective serum marker to evaluate the severity of gout. Over the years, more and more experimental data have demonstrated that soluble E-cadherin (sE-cadherin) may act as a pivotal regulator involving in the initiation and development of various types of diseases. Unfortunately, the precise role of sE-cadherin in gout-related complications remains to be investigated. METHODS In this work, we try to investigate the potential function of E-cadherin in patients with gout-related disorders. Serum sE-cadherin levels and other clinical parameters, from 37 patients with hyperuricaemia, 107 patients diagnosed with gout, 76 gout arthritis patients and 125 healthy adults were analysed in this study. RESULTS Here, we firstly show that sE-cadherin levels are significantly elevated in gout patients and gout are patients compared to those in healthy subjects, and that there is no significant difference between patients with hyperuricaemia and control group. Next, to further our understanding of how sE-cadherin acts as a new marker for assessing the severity of gout-related diseases, we nd that serum sE-cadherin values are signi cantly positively correlated with the serum in ammatory markers, including hsCRP and IL-1β in patients with gout and gout are. We also present evidence that serum sE-cadherin values are associated with oxidative stress in patients with gout-related complications. This is perhaps best illustrated by the observation that serum sE-cadherin values are significantly correlated with oxidative markers including SOD and soluble NOX2. CONCLUSIONS Taken together, our ndings strongly support the idea that serum sE-cadherin levels may be a new candidate biomarker for evaluating and stratifying the severity of gout-related complications.