Ruddlesden-Popper Perovskite Nanocrystals as Interface Modification Layer for Efficient Perovskite Solar Cells.

Perovskite nanocrystals are advantageous for interfacial passivation of perovskite solar cells (PSCs), but the insulating long alkyl chain surface ligands impede the charge transfer, while the conventional ligand exchange would possibly introduce surface defects to the nanocrystals. In this work, we reported novel in situ modification of CsPbBr3 nanocrystals using a short chain conjugated molecule 2-methoxyphenylethylammonium iodide (2-MeO-PEAI) for interfacial passivation of PSCs. Transmission electron microscopy studies with atomic resolution unveil the transformation from cubic CsPbBr3 to Ruddlesden-Popper phase (RPP) nanocrystals due to halogen exchange. Synergic passivation by the RPP nanocrystals and 2-MeO-PEA+ has led to suppressed interface defects and enhanced charge carrier transport. Consequently, PSCs with in situ modified RPP nanocrystals achieved a champion power conversion efficiency of 24.39%, along with an improvement in stability. This work brings insights into the microstructural evolution of perovskite nanocrystals, providing a novel and feasible approach for interfacial passivation of PSCs.

DNA methylation of promoter region inhibits galectin-1 expression in BMSCs of aged mice.

Senile osteoporosis increases fracture risks. Bone marrow stromal cells (BMSCs) are sensitive to aging. Deep insights into BMSCs aging are vital to elucidate the mechanisms underlying age-related bone loss. Recent advances showed that osteoporosis is associated with aberrant DNA methylation of many susceptible genes. Galectin-1 (Gal-1) has been proposed as a mediator of BMSCs functions. In our previous study, we showed that Gal-1 was downregulated in aged BMSCs and global deletion of Gal-1 in mice caused bone loss via impaired osteogenesis potential of BMSCs. Gal-1 promoter is featured by CpG islands. However, there are no reports concerning the DNA methylation status in Gal-1 promoter during osteoporosis. In the current study, we sought to investigate the role of DNA methylation in Gal-1 downregulation in aged BMSCs. The potential for anti-bone loss therapy based on modulating DNA methylation is explored. Our results showed that Dnmt3b-mediated Gal-1 promoter DNA hypermethylation plays an important role in Gal-1 downregulation in aged BMSCs, which inhibited ß-catenin binding on Gal-1 promoter. Bone loss of aged mice was alleviated in response to in vivo deletion of Dnmt3b from BMSCs. Finally, when bone marrow of young wild-type (WT) mice or young Dnmt3bPrx1-Cre mice was transplanted into aged WT mice, Gal-1 level in serum and trabecular bone mass were elevated in recipient aged WT mice. Our study will benefit for deeper insights into the regulation mechanisms of Gal-1 expression in BMSCs during osteoporosis development, and for the discovery of new therapeutic targets for osteoporosis via modulating DNA methylation status.NEW & NOTEWORTHY There is Dnmt3b-mediated DNA methylation in Gal-1 promoter in aged bone marrow stromal cell (BMSC). DNA methylation causes Gal-1 downregulation and osteogenesis attenuation of aged BMSC. DNA methylation blocks ß-catenin binding on Gal-1 promoter. Bone loss of aged mice is alleviated by in vivo deletion of Dnmt3b from BMSC.

Long non-coding RNA linc00659 promotes tumour progression by regulating FZD6/Wnt/ß-catenin signalling pathway in colorectal cancer via m6A reader IGF2BP1.

BACKGROUND: Abnormal N6-methyladenosine (m6A) modification has become a driving factor in tumour development and progression. The linc00659 is abnormally highly expressed in digestive tract tumours and promotes cancer progression, but there is little research on the mechanism of linc00659 and m6A. METHODS: The expression of linc00659 in colorectal cancer (CRC) tissues and cells was assessed by a quantitative real-time PCR. The proliferative capacity of CRC cells was determined by colony formation, Cell Counting Kit-8 and 5-ethynyl-2 deoxyuridine assays, and the migratory capacity of CRC was determined by wound healing and transwell assays and tube formation. In vivo, a xenograft tumour model was used to detect the effect of linc00659 on tumour growth. The Wnt/ß-catenin signalling pathway and related protein expression levels were measured by western blotting. The binding of linc00659 to insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) was assessed by RNA pull-down and an immunoprecipitation assay. The effect of IGF2BP1 on FZD6 was detected by an RNA stability assay. RESULTS: The expression of linc00659 was abnormally elevated in CRC tissues and cells compared to normal colonic tissues and cells. We confirm that linc00659 promotes the growth of CRC cells both in vivo and in vitro. Mechanistically, linc00659 binds to IGF2BP1 and specifically enhances its activity to stabilize the target gene FZD6. Therefore, linc00659 and IGF2BP1 activate the Wnt/ß-catenin signalling pathway, promoting cell proliferation in CRC. CONCLUSIONS: Our results show that linc00659 and IGF2BP1 cooperate to promote the stability of the target FZD6 mRNA, thereby facilitating CRC progression, which may represent a potential diagnostic, prognostic and therapeutic target for CRC.

Conductive MXene/Polymer Composites for Transparent Flexible Supercapacitors.

Transparent flexible energy storage devices are limited by the trade-off among flexibility, transparency, and charge storage capability of their electrode materials. Conductive polymers are intrinsically flexible, but limited by small capacitance. Pseudocapacitive MXene provides high capacitance, yet their opaque and brittle nature hinders their flexibility and transparency. Herein, the development of synergistically interacting conductive polymer Ti3C2Tx MXene/PEDOT:PSS composites is reported for transparent flexible all-solid-state supercapacitors, with an outstanding areal capacitance of 3.1 mF cm-2, a high optical transparency of 61.6%, and excellent flexibility and durability. The high capacitance and high transparency of the devices stem from the uniform and thorough blending of PEDOT:PSS and Ti3C2Tx, which is associated with the formation of O─H…O H-bonds in the composites. The conductive MXene/polymer composite electrodes demonstrate a rational means to achieve high-capacity, transparent and flexible supercapacitors in an easy and scalable manner.

The mechanism of RGS5 regulating gastric cancer mismatch repair protein.

The incidence and mortality rates of gastric cancer (GC) remain alarmingly high worldwide, imposing a substantial healthcare burden. In this study, we utilized data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. A 4-gene prognostic model was developed to predict patient prognosis, and its accuracy was validated across multiple datasets. Patients with a low-risk score exhibited improved prognosis, elevated tumor mutation burden, heightened sensitivity to both immunotherapy and conventional chemotherapy. Notably, our investigation revealed that the key gene RGS5 positively modulates the expression of mismatch repair proteins via c-Myc. Furthermore, co-immunoprecipitation (COIP) assays demonstrated the interaction between RGS5 and c-Myc. Additionally, we confirmed that RGS5 regulates c-Myc through the ubiquitin-proteasome pathway. Moreover, RGS5 was identified as a positive regulator of PD-L1 expression and exhibited a negative correlation with the majority of immune cells. These findings underscore the potential of RGS5 as a novel biomarker and therapeutic target in the context of GC.

Protective role of arachidonic acid against diabetic myocardial ischemic injury: a translational study of pigs, rats, and humans.

AIM: Patients with diabetes mellitus have poor prognosis after myocardial ischemic injury. However, the mechanism is unclear and there are no related therapies. We aimed to identify regulators of diabetic myocardial ischemic injury. METHODS AND RESULTS: Mass spectrometry-based, non-targeted metabolomic approach was used to profile coronary sinus blood from diabetic and non-diabetic Bama-mini pigs at 0.5-h post coronary artery ligation. Six metabolites had a |log2 (Fold Change)|> 1.3. Among them, the most changed is arachidonic acid (AA), levels of which were 32 times lower in diabetic pigs than in non-diabetic pigs. The AA-derived products, PGI2 and 6-keto-PGF1α, were also significantly reduced. AA treatment of cultured cardiomyocytes protected against cell death by 30% at 48 h of high glucose and oxygen deprivation, which coincided with increased mitophagic activity (as indicated by increased LC3II/LC3I, decreased p62 and increased parkin & PINK1), improved mitochondrial renewal (upregulation of Drp1 and FIS1), reduced ROS generation and increased ATP production. These cardioprotective effects were abolished by PINK1(a crucial mitophagy protein) knockdown or the autophagy inhibitor 3-Methyladenine. The protective effect of AA was also inhibited by indomethacin and Cay10441, a prostacyclin receptor antagonist. Furthermore, diabetic Sprague Dawley rats were subjected to coronary ligation for 40 min and AA treatment (10 mg/day per animal gavaged) decreased myocardial infarct size, cell apoptosis index, inflammatory cytokines and improved heart function. Scanning electron microscopy showed more intact mitochondria in the border zone of infarcted myocardium in AA treated rats. Lastly, diabetic patients after myocardial infarction had lower plasma levels of AA and 6-keto-PGF1α and reduced cardiac ejection fraction, compared with non-diabetic patients after myocardial infarction. Plasma AA level was inversely correlated with fasting blood glucose. CONCLUSIONS: AA protects against diabetic ischemic myocardial damage by promoting mitochondrial autophagy and renewal, which is related to AA derived PGI2 signaling. AA may represent a new strategy to treat diabetic myocardial ischemic injury.

Understanding the Electronic Structure and Chemical Bonding in the 2D Fullerene Monolayer.

Recently synthesized two-dimensional (2D) monolayer quasi-hexagonal-phase fullerene (qHPC60) demonstrates excellent thermodynamic stability. Within this monolayer, each fullerene cluster is surrounded by six adjacent C60 cages along an equatorial plane and is connected by both C-C single bonds and [2 + 2] cycloaddition bonds that serve as bridges. In this study, we investigate the stability mechanism of the 2D qHPC60 monolayer by examining the electronic structure and chemical bonding through state-of-the-art theoretical methodologies. Density functional theory (DFT) studies reveal that 2D qHPC60 possesses a moderate direct electronic band gap of 1.46 eV, close to the experimental value (1.6 eV). It is found that the intermolecular bridge bonds play a crucial role in enhancing the charge flow and redistribution among C60 cages, leading to the formation of dual π-aromaticity within the C60 sphere and stabilizing the 2D framework structure. Furthermore, we identify a series of delocalized superatom molecular orbitals (SAMOs) within the 2D qHPC60 monolayer, exhibiting atomic orbital-like behavior and hybridization to form nearly free-electron (NFE) bands with σ/π bonding and σ*/π* antibonding properties. Our findings provide insights into the design and potential applications of NFE bands derived from SAMOs in 2D qHPC60 monolayers.

Chelating Effect of Siderophore Desferrioxamine-B on Uranyl Biomineralization Mediated by Shewanella putrefaciens.

In contaminated water and soil, little is known about the role and mechanism of the biometabolic molecule siderophore desferrioxamine-B (DFO) in the biogeochemical cycle of uranium due to complicated coordination and reaction networks. Here, a joint experimental and quantum chemical investigation is carried out to probe the biomineralization of uranyl (UO22+, referred to as U(VI) hereafter) induced by Shewanella putrefaciens (abbreviated as S. putrefaciens) in the presence of DFO and Fe3+ ion. The results show that the production of mineralized solids {hydrogen-uranium mica [H2(UO2)2(PO4)2·8H2O]} via S. putrefaciens binding with UO22+ is inhibited by DFO, which can both chelate preferentially UO22+ to form a U(VI)-DFO complex in solution and seize it from U(VI)-biominerals upon solvation. However, with Fe3+ ion introduced, the strong specificity of DFO binding with Fe3+ causes re-emergence of biomineralization of UO22+ {bassetite [Fe(UO2)2(PO4)2·8(H2O)]} by S. putrefaciens, owing to competitive complexation between Fe3+ and UO22+ for DFO. As DFO possesses three hydroxamic functional groups, it forms hexadentate coordination with Fe3+ and UO22+ ions via these functional groups. The stability of the Fe3+-DFO complex is much higher than that of U(VI)-DFO, resulting in some DFO-released UO22+ to be remobilized by S. putrefaciens. Our finding not only adds to the understanding of the fate of toxic U(VI)-containing substances in the environment and biogeochemical cycles in the future but also suggests the promising potential of utilizing functionalized DFO ligands for uranium processing.

Chitosan alleviates ovarian aging by enhancing macrophage phagocyte-mediated tissue homeostasis.

BACKGROUND: Age-related changes in the ovarian microenvironment are linked to impaired fertility in women. Macrophages play important roles in ovarian tissue homeostasis and immune surveillance. However, the impact of aging on ovarian macrophage function and ovarian homeostasis remains poorly understood. METHODS: Senescence-associated beta-galactosidase staining, immunohistochemistry, and TUNEL staining were used to assess senescence and apoptosis, respectively. Flow cytometry was employed to evaluate mitochondrial membrane potential (MMP) and apoptosis in granulosa cells lines (KGN), and macrophages phagocytosis. After a 2-month treatment with low molecular weight Chitosan (LMWC), ovarian tissues from mice were collected for comprehensive analysis. RESULTS: Compared with the liver and uterus, the ovary displayed accelerated aging in an age-dependent manner, which was accompanied by elevated levels of inflammatory factors and apoptotic cells, and impaired macrophage phagocytic activity. The aged KGN cells exhibited elevated reactive oxygen species (ROS) and apoptotic levels alongside decreased MMP. H2O2-induced aging macrophages showed reduced phagocytosis function. Moreover, there were excessive aging macrophages with impaired phagocytosis in the follicular fluid of patients with diminished ovarian reserve (DOR). Notably, LMWC administration alleviated ovarian aging by enhancing macrophage phagocytosis and promoting tissue homeostasis. CONCLUSIONS: Aging ovarian is characterized by an accumulation of aging and apoptotic granulosa cells, an inflammatory response and macrophage phagocytosis dysfunction. In turn, impaired phagocytosis of macrophage contributes to insufficient clearance of aging and apoptotic granulosa cells and the increased risk of DOR. Additionally, LMWC emerges as a potential therapeutic strategy for age-related ovarian dysfunction.

Clinical Implications of a New DDX58 Pathogenic Variant That Causes Lupus Nephritis due to RIG-I Hyperactivation.

BACKGROUND: Lupus nephritis (LN) is one of the most severe complications of systemic lupus erythematosus, with heterogeneous phenotypes and different responses to therapy. Identifying genetic causes of LN can facilitate more individual treatment strategies. METHODS: We performed whole-exome sequencing in a cohort of Chinese patients with LN and identified variants of a disease-causing gene. Extensive biochemical, immunologic, and functional analyses assessed the effect of the variant on type I IFN signaling. We further investigated the effectiveness of targeted therapy using single-cell RNA sequencing. RESULTS: We identified a novel DDX58 pathogenic variant, R109C, in five unrelated families with LN. The DDX58 R109C variant is a gain-of-function mutation, elevating type I IFN signaling due to reduced autoinhibition, which leads to RIG-I hyperactivation, increased RIG-I K63 ubiquitination, and MAVS aggregation. Transcriptome analysis revealed an increased IFN signature in patient monocytes. Initiation of JAK inhibitor therapy (baricitinib 2 mg/d) effectively suppressed the IFN signal in one patient. CONCLUSIONS: A novel DDX58 R109C variant that can cause LN connects IFNopathy and LN, suggesting targeted therapy on the basis of pathogenicity. PODCAST: This article contains a podcast at.

Genome-Wide Identification, Phylogenetic and Expression Analysis of Expansin Gene Family in Medicago sativa L.

Expansins, a class of cell-wall-loosening proteins that regulate plant growth and stress resistance, have been studied in a variety of plant species. However, little is known about the Expansins present in alfalfa (Medicago sativa L.) due to the complexity of its tetraploidy. Based on the alfalfa (cultivar "XinjiangDaye") reference genome, we identified 168 Expansin members (MsEXPs). Phylogenetic analysis showed that MsEXPs consist of four subfamilies: MsEXPAs (123), MsEXPBs (25), MsEXLAs (2), and MsEXLBs (18). MsEXPAs, which account for 73.2% of MsEXPs, and are divided into twelve groups (EXPA-I-EXPA-XII). Of these, EXPA-XI members are specific to Medicago trunctula and alfalfa. Gene composition analysis revealed that the members of each individual subfamily shared a similar structure. Interestingly, about 56.3% of the cis-acting elements were predicted to be associated with abiotic stress, and the majority were MYB- and MYC-binding motifs, accounting for 33.9% and 36.0%, respectively. Our short-term treatment (≤24 h) with NaCl (200 mM) or PEG (polyethylene glycol, 15%) showed that the transcriptional levels of 12 MsEXPs in seedlings were significantly altered at the tested time point(s), indicating that MsEXPs are osmotic-responsive. These findings imply the potential functions of MsEXPs in alfalfa adaptation to high salinity and/or drought. Future studies on MsEXP expression profiles under long-term (>24 h) stress treatment would provide valuable information on their involvement in the response of alfalfa to abiotic stress.

Comparison of patient-controlled epidural analgesia and epidural morphine for post-cesarean section analgesia: experience from a tertiary center in China.

PURPOSE: To compare patient-controlled epidural analgesia (PCEA) and epidural morphine (EM) for post-cesarean section analgesia in real-world experience from China. METHODS: Parturients receiving one dose of EM (1-2 mg), PCEA, or both EM and PCEA from Peking Union Medical College Hospital were retrospectively recruited. Logistic models were used to identify risk factors. RESULTS: Of 1079 parturients enrolled, 919 (85.2%) parturients received only EM, 105 (9.7%) parturients received PCEA, and 55 (5.1%) parturients received both EM and PCEA. Significantly more parturients from EM group requested supplementary analgesia than those from PCEA and PCEA + EM group (583, 63.4% vs 52, 49.5% vs 25, 45.5%, P = 0.001) with more times of supplementary analgesia (1, IQR: 0-2 vs 0, IQR: 0-1 vs 0, IQR: 0-1 times, P < 0.001) and larger amounts of nonsteroidal anti-inflammatory drugs (NSAIDs) (50, IQR: 0-100 mg vs 0, IQR: 0-50 mg vs 0, IQR: 0-50 mg, P < 0.001). In multivariable Logistic regression for the supplementary analgesia risk, the application of PCEA (OR: 0.557, 95%CI 0.396-0.783, P = 0.001) and the use of NSAIDs intraoperatively (OR: 2.996, 95%CI 1.811-4.957, P < 0.001) were identified as independent predictors. A total of 1040 (96.4%) patients received prophylactic antiemetic therapy during surgery. Only 13 (1.2%) and 7 (0.6%) patients in our cohort requested antiemetic and antipruritic drugs, respectively. CONCLUSION: The use of PCEA was an independent protective factor for supplementary analgesia during the post-cesarean section. Prophylactic antiemetic therapy may reduce the side effects of post-cesarean analgesia.

Occurrence and risk assessment of azole fungicides during the urban water cycle: A year-long study along the Yangtze River, China.

Azole fungicides (AFs) play an important role in the prevention and treatment of fungal diseases in agricultural crops. However, limited studies are addressing the fate and ecological risk of AFs in the urban water cycle at a large watershed scale. To address this gap, we investigated the spatiotemporal distribution and ecological risk of twenty AFs in the lower reaches of the Yangtze River across four seasons. Carbendazim (CBA), tebuconazole (TBA), tricyclazole (TCA), and propiconazole (PPA) were found to be the dominant compounds. Their highest concentrations were measured in January (188.3 ng/L), and November (2197.1 ng/L), July (162.0 ng/L), and November (1801.9 ng/L), respectively. The comparison between wastewater treatment plants (WWTPs) effluents and surface water suggested that industrial WWTPs are major sources of AFs in the Yangtze River. In particular, TBA and PPA were found to be the most recalcitrant AFs in industrial WWTPs, while difenoconazole (DFA) was found to be the most potent pollutant in municipal WWTPs, with an average removal rate of less than 60%. The average risk quotient (RQ) for the entire AFs was 6.45 in the fall, which was higher than in January (0.98), April (0.61), and July (0.40). This indicates that AFs in surface water posed higher environmental risks during the dry season. Additionally, the exposure risk of AFs via drinking water for sensitive populations deserves more attention. This study provides benchmark data on the occurrence of AFs in the lower reaches of the Yangtze River, and offers suggestions for better reduction of AFs.

Steering Geometric Reconstruction of Bismuth with Accelerated Dynamics for CO2 Electroreduction.

Bismuth-based materials have emerged as promising catalysts in the electrocatalytic reduction of CO2 to formate. However, the reasons for the reconstruction of Bi-based precursors to form bismuth nanosheets are still puzzling, especially the formation of defective bismuth sites. Herein, we prepare bismuth nanosheets with vacancy-rich defects (V-Bi NS) by rapidly reconstructing Bi19Cl3S27 under negative potential. Theoretical analysis reveals that the introduction of chlorine induces the generation of intrinsic electric field in the precursor, thereby increasing the electron transfer rate and further promoting the metallization of trivalent bismuth. Meanwhile, experimental tests verify that Bi19Cl3S27 has a faster reconstruction rate than Bi2S3. The formed V-Bi NS exhibits up to 96 % HCOO- Faraday efficiency and 400 mA cm-2 HCOO- partial current densities, and its electrochemical active surface area normalized formate current density and yield are 2.2 times higher than those of intact bismuth nanosheets (I-Bi NS). Density functional theory calculations indicate that bismuth vacancies with electron-rich aggregation reduce the activation energy of CO2 to *CO2 - radicals and stabilize the adsorption of the key intermediate *OCHO, thus facilitating the reaction kinetics of formate production.

circEIF3I facilitates the recruitment of SMAD3 to early endosomes to promote TGF-ß signalling pathway-mediated activation of MMPs in pancreatic cancer.

BACKGROUND: Among digestive tract tumours, pancreatic ductal adenocarcinoma (PDAC) shows the highest mortality trend. Moreover, although PDAC metastasis remains a leading cause of cancer-related deaths, the biological mechanism is poorly understood. Recent evidence demonstrates that circular RNAs (circRNAs) play important roles in PDAC progression. METHODS: Differentially expressed circRNAs in normal and PDAC tissues were screened via bioinformatics analysis. Sanger sequencing, RNase R and actinomycin D assays were performed to confirm the loop structure of circEIF3I. In vitro and in vivo functional experiments were conducted to assess the role of circEIF3I in PDAC. MS2-tagged RNA affinity purification, mass spectrometry, RNA immunoprecipitation, RNA pull-down assay, fluorescence in situ hybridization, immunofluorescence and RNA-protein interaction simulation and analysis were performed to identify circEIF3I-interacting proteins. The effects of circEIF3I on the interactions of SMAD3 with TGFßRI or AP2A1 were measured through co-immunoprecipitation and western blotting. RESULTS: A microarray data analysis showed that circEIF3I was highly expressed in PDAC cells and correlated with TNM stage and poor prognosis. Functional experiments in vitro and in vivo revealed that circEIF3I accelerated PDAC cells migration, invasion and metastasis by increasing MMPs expression and activity. Mechanistic research indicated that circEIF3I binds to the MH2 domain of SMAD3 and increases SMAD3 phosphorylation by strengthening the interactions between SMAD3 and TGFßRI on early endosomes. Moreover, AP2A1 binds with circEIF3I directly and promotes circEIF3I-bound SMAD3 recruitment to TGFßRI on early endosomes. Finally, we found that circEif3i exerts biological functions in mice similar to those of circEIF3I in humans PDAC. CONCLUSIONS: Our study reveals that circEIF3I promotes pancreatic cancer progression. circEIF3I is a molecular scaffold that interacts with SMAD3 and AP2A1 to form a ternary complex, that facilitates the recruitment of SMAD3 to early endosomes and then activates the TGF-ß signalling pathway. Hence, circEIF3I is a potential prognostic biomarker and therapeutic target in PDAC.

STAT2-induced linc02231 promotes tumorigenesis and angiogenesis through modulation of hnRNPA1/ANGPTL4 in colorectal cancer.

BACKGROUND: Long non-coding RNAs (lncRNAs) play a critical role in regulating various human diseases including cancer. In colorectal cancer (CRC), there are still some undervalued lncRNAs with potential functions and mechanisms that need to be clarified. The present study aimed to investigate the role of linc02231 in the progression of CRC. METHODS: The proliferation of CRC cells was evaluated using Cell Counting Kit-8, colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) assays. Cell migration was examined through wound healing and Transwell analyses. The impact of linc02231 on angiogenesis was determined through a tube formation assay. Western blotting was used to detect the expression of specific proteins. A mouse xenograft model is established to observe the effect of linc02231 on the in vivo growth of CRC cells. Target genes of linc02231 are screened using high-throughput sequencing. The transcriptional activity of STAT2 on linc02231 and the binding activity between linc02231/miR-939-5p/hnRNPA1 were analyzed by a luciferase assay. RESULTS: Based on public databases and comprehensive bioinformatics analysis, we found that lncRNA linc02231 was upregulated in CRC tumor tissues, which is consistent with our clinical results. linc02231 promoted the proliferation and migration of CRC cells in vitro and their tumorigenicity in vivo. Furthermore, linc02231 promotes the angiogenic ability of human umbilical vein endothelial cells. Mechanistically, the transcription factor STAT2 binds to the promoter region of linc02231 and activates its transcription. linc02231 also competes with miR-939-5p for binding to the pro-oncogenic target gene hnRNPA1, preventing its degradation. hnRNPA1 prevents the maturation of angiopoietin-like protein 4 (ANGPTL4) messenger RNA, leading to impaired tumor angiogenesis and increased metastasis of CRC. CONCLUSIONS: The expression of linc02231, which is induced by STAT2, has been found to enhance the proliferation, metastasis, and angiogenesis of CRC by binding to miR-939-5p and increasing the expression of hnNRPA1 at the same time as suppressing ANGPTL4. These findings suggest that linc02231 could serve as a potential biomarker and therapeutic target for CRC.

Selective Adsorption Behavior Modulation on Nickel Selenide by Heteroatom Implantation and Heterointerface Construction Achieves Efficient Co-production of H2 and Formate.

Glycerol-assisted hybrid water electrolysis is a potential strategy to achieve energy-efficient hydrogen production. However, the design of an efficient catalyst for the specific reaction is still a key challenge, which suffers from the barrier of regulating the adsorption characteristics of distinctive intermediates in different reactions. Herein, a novel rationale that achieves selective adsorption behavior modulation for self-supported nickel selenide electrode by heteroatom implantation and heterointerface construction through electrodeposition is developed, which can realize nichetargeting optimization on hydrogen evolution reaction (HER) and glycerol oxidation reaction (GOR), respectively. Specifically, the prepared Mo-doped Ni3 Se2 electrode exhibits superior catalytic activity for HER, while the NiSe-Ni3 Se2 electrode exhibits high Faradaic efficiency (FE) towards formate production for GOR. A two-electrode electrolyzer exhibits superb activity that only needs an ultralow cell voltage of 1.40 V to achieve 40 mA cm-2 with a high FE (97%) for formate production. Theoretical calculation unravels that the introduction of molybdenum contributes to the deviation of the d-band center of Ni3 Se2 from the Fermi level, which is conducive to hydrogen desorption. Meanwhile, the construction of the heterojunction induces the distortion of the surface structure of nickel selenide, which exposes highly active nickel sites for glycerol adsorption, thus contributing to the excellent electrocatalytic performance.

Activating Single-Atom Ni Site via First-Shell Si Modulation Boosts Oxygen Reduction Reaction.

Atomically dispersed nitrogen-coordinated 3d transition-metal site on carbon support (M-NC) are promising alternatives to Pt group metal-based catalysts toward oxygen reduction reaction (ORR). However, despite the excellent activities of most of M-NC catalysts, such as Fe-NC, Co-NC et al., their durability is far from satisfactory due to Fenton reaction. Herein, this work reports a novel Si-doped Ni-NC catalyst (Ni-SiNC) that possesses high activity and excellent stability. X-ray absorption fine structure and aberration-corrected transmission electron microscopy uncover that the single-atom Ni site is coordinated with one Si atom and three N atoms, constructing Ni-Si1 N3  moiety. The Ni-SiNC catalyst exhibits a half-wave potential (E1/2 ) of 0.866 V versus RHE, with a distinguished long-term durability in alkaline media of only 10 mV negative shift in E1/2  after 35 000 cycles, which is also validated in Zn-air battery. Density functional theory calculations reveal that the Ni-Si1 N3  moiety facilitates ORR kinetics through optimizing the adsorption of intermediates.

Anisotropic epitaxial stabilization of a low-symmetry ferroelectric with enhanced electromechanical response.

Piezoelectrics interconvert mechanical energy and electric charge and are widely used in actuators and sensors. The best performing materials are ferroelectrics at a morphotropic phase boundary, where several phases coexist. Switching between these phases by electric field produces a large electromechanical response. In ferroelectric BiFeO3, strain can create a morphotropic-phase-boundary-like phase mixture and thus generate large electric-field-dependent strains. However, this enhanced response occurs at localized, randomly positioned regions of the film. Here, we use epitaxial strain and orientation engineering in tandem-anisotropic epitaxy-to craft a low-symmetry phase of BiFeO3 that acts as a structural bridge between the rhombohedral-like and tetragonal-like polymorphs. Interferometric displacement sensor measurements reveal that this phase has an enhanced piezoelectric coefficient of ×2.4 compared with typical rhombohedral-like BiFeO3. Band-excitation frequency response measurements and first-principles calculations provide evidence that this phase undergoes a transition to the tetragonal-like polymorph under electric field, generating an enhanced piezoelectric response throughout the film and associated field-induced reversible strains. These results offer a route to engineer thin-film piezoelectrics with improved functionalities, with broader perspectives for other functional oxides.

Association of C-peptide level with bone mineral density in type 2 diabetes mellitus.

This study revealed that there was no significant linear relationship between fasting C-peptide (FCP) level and bone mineral density (BMD) or fracture risk in type 2 diabetes mellitus (T2DM) patients. However, in the FCP ≤ 1.14 ng/ml group, FCP is positively correlated with whole body (WB), lumbar spine (LS), and femoral neck (FN) BMD and negatively correlated with fracture risk. PURPOSE: To explore the relationship between C-peptide and BMD and fracture risk in T2DM patients. METHODS: 530 T2DM patients were enrolled and divided into three groups by FCP tertiles, and the clinical data were collected. BMD was measured by dual-energy X-ray absorptiometry (DXA). The 10-year probability of major osteoporotic fractures (MOFs) and hip fractures (HFs) was evaluated by adjusted fracture risk assessment tool (FRAX). RESULTS: In the FCP ≤ 1.14 ng/ml group, FCP level was positively correlated with WB, LS, and FN BMD, while FCP was negatively correlated with fracture risk and osteoporotic fracture history. However, FCP was not correlated with BMD and fracture risk and osteoporotic fracture history in the 1.14 < FCP ≤ 1.73 ng/ml and FCP > 1.73 ng/ml groups. The study has shown that FCP was an independent factor influencing BMD and fracture risk in the FCP ≤ 1.14 ng/ml group. CONCLUSIONS: There is no significant linear relationship between FCP level and BMD or fracture risk in T2DM patients. In the FCP ≤ 1.14 ng/ml group, FCP is positively correlated with WB, LS, and FN BMD and negatively correlated with fracture risk, and FCP is an independent influencing factor of BMD and fracture risk. The findings suggest that FCP may predict the risk of osteoporosis or fracture in some T2DM patients, which has a certain clinical value.