Soluble FLT1 binds lipid microdomains in podocytes to control cell morphology and glomerular barrier function.

Vascular endothelial growth factor and its receptors, FLK1/KDR and FLT1, are key regulators of angiogenesis. Unlike FLK1/KDR, the role of FLT1 has remained elusive. FLT1 is produced as soluble (sFLT1) and full-length isoforms. Here, we show that pericytes from multiple tissues produce sFLT1. To define the biologic role of sFLT1, we chose the glomerular microvasculature as a model system. Deletion of Flt1 from specialized glomerular pericytes, known as podocytes, causes reorganization of their cytoskeleton with massive proteinuria and kidney failure, characteristic features of nephrotic syndrome in humans. The kinase-deficient allele of Flt1 rescues this phenotype, demonstrating dispensability of the full-length isoform. Using cell imaging, proteomics, and lipidomics, we show that sFLT1 binds to the glycosphingolipid GM3 in lipid rafts on the surface of podocytes, promoting adhesion and rapid actin reorganization. sFLT1 also regulates pericyte function in vessels outside of the kidney. Our findings demonstrate an autocrine function for sFLT1 to control pericyte behavior.

Mitochondrial genome provides species-specific targets for the rapid detection of early invasive populations of Hylurgus ligniperda in China.

BACKGROUND: Hylurgus ligniperda, a major international forestry quarantine pest, was recently found to have invaded and posed a serious threat to the Pinus forests of the Jiaodong Peninsula in China. Continuous monitoring and vigilance of the early population is imperative, and rapid molecular detection technology is urgently needed. We focused on developing a single-gene-based species-specific PCR (SS-PCR) method. RESULTS: We sequenced and assembled the mitochondrial genome of H. ligniperda to identify suitable target genes. We identified three closely related species for detecting the specificity of SS-PCR through phylogenetic analysis based on 13 protein-coding genes (PCGs). Subsequently, we analyzed the evolution of 13 PCGs and selected four mitochondrial genes to represent slow-evolving gene (COI) and faster-evolving genes (e.g. ND2, ND4, and ND5), respectively. We developed four species-specific primers targeting COI, ND2, ND4, and ND5 to rapidly identify H. ligniperda. The results showed that the four species-specific primers exhibited excellent specificity and sensitivity in the PCR assays, with consistent performance across a broader range of species. This method demonstrates the ability to identify beetles promptly, even during their larval stage. The entire detection process can be completed within 2-3 h. CONCLUSIONS: This method is suitable for large-scale species detection in laboratory settings. Moreover, the selection of target genes in the SS-PCR method is not affected by the evolutionary rate. SS-PCR can be widely implemented at port and forestry workstations, significantly enhancing early management strategies and quarantine measures against H. ligniperda. This approach will help prevent the spread of the pest and effectively preserve the resources of Chinese pine forests.

Linking a cell-division gene and a suicide gene to define and improve cell therapy safety.

Human pluripotent cell lines hold enormous promise for the development of cell-based therapies. Safety, however, is a crucial prerequisite condition for clinical applications. Numerous groups have attempted to eliminate potentially harmful cells through the use of suicide genes1, but none has quantitatively defined the safety level of transplant therapies. Here, using genome-engineering strategies, we demonstrate the protection of a suicide system from inactivation in dividing cells. We created a transcriptional link between the suicide gene herpes simplex virus thymidine kinase (HSV-TK) and a cell-division gene (CDK1); this combination is designated the safe-cell system. Furthermore, we used a mathematical model to quantify the safety level of the cell therapy as a function of the number of cells that is needed for the therapy and the type of genome editing that is performed. Even with the highly conservative estimates described here, we anticipate that our solution will rapidly accelerate the entry of cell-based medicine into the clinic.

Indium Cyanamide for Industrial-Grade CO2 Electroreduction to Formic Acid.

Developing industrial-grade electroreduction of CO2 to produce formate (HCOO-)/formic acid (HCOOH) depends on highly active electrocatalysts. However, structural changes due to the inevitable self-reduction of catalysts result in severe long-term stability issues at industrial-grade current density. Herein, linear cyanamide anion ([NCN]2-)-constructed indium cyanamide nanoparticles (InNCN) were investigated for CO2 reduction to HCOO- with a Faradaic efficiency of up to 96% under a partial current density (jformate) of 250 mA cm-2. Bulk electrolysis at a jformate of 400 mA cm-2 requires only -0.72 VRHE applied potential with iR correction. It also achieves continuous production of pure HCOOH at ∼125 mA cm-2 for 160 h. The excellent activity and stability of InNCN are attributed to its unique structural features, including strongly σ-donating [NCN]2- ligands, the potential structural transformation of [N═C═N]2- and [N≡C-N]2-, and the open framework structure. This study affirms metal cyanamides as promising novel materials for electrocatalytic CO2 reduction, broadening the variety of CO2 reduction catalysts and the understanding of structure-activity relationships.

Common and discrete mechanisms underlying chronic pain and itch: peripheral and central sensitization.

Normally, an obvious antagonism exists between pain and itch. In normal conditions, painful stimuli suppress itch sensation, whereas pain killers often generate itch. Although pain and itch are mediated by separate pathways under normal conditions, most chemicals are not highly specific to one sensation in chronic pathologic conditions. Notably, in patients with neuropathic pain, histamine primarily induces pain rather than itch, while in patients with atopic dermatitis, bradykinin triggers itch rather than pain. Accordingly, repetitive scratching even enhances itch sensation in chronic itch conditions. Physicians often prescribe pain relievers to patients with chronic itch, suggesting common mechanisms underlying chronic pain and itch, especially peripheral and central sensitization. Rather than separating itch and pain, studies should investigate chronic itch and pain including neuropathic and inflammatory conditions. Here, we reviewed chronic sensitization leading to chronic pain and itch at both peripheral and central levels. Studies investigating the connection between pain and itch facilitate the development of new therapeutics against both chronic dysesthesias based on the underlying pathophysiology.

Context-dependent functions of angiopoietin 2 are determined by the endothelial phosphatase VEPTP.

The angiopoietin (ANGPT)-TIE2/TEK signaling pathway is essential for blood and lymphatic vascular homeostasis. ANGPT1 is a potent TIE2 activator, whereas ANGPT2 functions as a context-dependent agonist/antagonist. In disease, ANGPT2-mediated inhibition of TIE2 in blood vessels is linked to vascular leak, inflammation, and metastasis. Using conditional knockout studies in mice, we show TIE2 is predominantly activated by ANGPT1 in the cardiovascular system and by ANGPT2 in the lymphatic vasculature. Mechanisms underlying opposing actions of ANGPT2 in blood vs. lymphatic endothelium are poorly understood. Here we show the endothelial-specific phosphatase VEPTP (vascular endothelial protein tyrosine phosphatase) determines TIE2 response to ANGPT2. VEPTP is absent from lymphatic endothelium in mouse in vivo, permitting ANGPT2/TIE2-mediated lymphangiogenesis. Inhibition of VEPTP converts ANGPT2 into a potent TIE2 activator in blood endothelium. Our data support a model whereby VEPTP functions as a rheostat to modulate ANGPT2 ligand effect on TIE2.

[Correlation of B-type Natriuretic Peptide Level with Hemodynamic Parameters and Inflammatory Cytokines in Patients with Gram-negative Sepsis].

Objective To study the correlation of B-type natriuretic peptide(BNP)level with hemodynamic parameters and inflammatory cytokines in patients with Gram-negative sepsis,and further determine the main factors for the significant increase of BNP level. Methods The prospective study method was applied,and septic patients infected with Gram-negative bacteria from May 2017 to October 2019 were enrolled.The patients were divided into the BNP<2400 ng/L group and the BNP≥2400 ng/L group by taking the average value of BNP as the dividing point.The independent predictors of BNP≥2400 ng/L were analyzed by Logistic regression.Pearson correlation analysis was used to analyze the correlation between BNP and various indicators. Results A total of 106 patients with Gram-negative sepsis were included,among which 60 cases present with higher serum BNP levels than the average of(2398.45 ± 421.45)ng/L.Thus BNP≥2400 ng/L was considered as a significantly increased BNP level.Multiple logistic regression analysis showed that cardiac index(CI)[odds ratio (OR)=0.428,95% confidence interval (95%CI)=0.743-0.965,P=0.011],left ventricular ejection fraction(LVEF) (OR=0.394,95%CI=0.182-0.549,P=0.013),lactic acid (OR=1.983,95%CI=1.264-3.420,P=0.023),endotoxin (OR=6.146,95%CI=4.091-8.226,P=0.001),procalcitonin(PCT) (OR=6.513,95%CI=4.365-8.210,P=0.005) and cardiac troponin I(cTnI) (OR=1.144,95%CI=1.001-2.150,P=0.047) were independent predictors of BNP≥2400 ng/L in patients with Gram-negative sepsis.Pearson correlation analysis showed that BNP was negatively correlated with CI(R=-0.514,P<0.001)and LVEF (R=-0.552,P<0.001),whereas positively correlated with lactic acid (R=0.265,P=0.032),cTnI (R=0.204, P=0.036),PCT(R=0.801,P<0.001),and endotoxin(R=0.765,P<0.001). Conclusions In septic patients with Gram-negative bacterial infection,LVEF,CI,lactic acid,cTnI,endotoxin and PCT are all independent risk factors for the significant increase of BNP,and endotoxin and PCT were more significantly correlated with BNP increase.Endotoxin and inflammatory reaction may be the more important stimulators of BNP increase in septic patients with Gram-negative bacterial infection.

Forward genetic screen in human podocytes identifies diphthamide biosynthesis genes as regulators of adhesion.

Podocyte function is tightly linked to the complex organization of its cytoskeleton and adhesion to the underlying glomerular basement membrane. Adhesion of cultured podocytes to a variety of substrates is reported to correlate with podocyte health. To identify novel genes that are important for podocyte function, we designed an in vitro genetic screen based on podocyte adhesion to plates coated with either fibronectin or soluble Fms-like tyrosine kinase-1 (sFLT1)/Fc. A genome-scale pooled RNA interference screen on immortalized human podocytes identified 77 genes that increased adhesion to fibronectin, 101 genes that increased adhesion to sFLT1/Fc, and 44 genes that increased adhesion to both substrates when knocked down. Multiple shRNAs against diphthamide biosynthesis protein 1-4 (DPH1-DPH4) were top hits for increased adhesion. Immortalized human podocyte cells stably expressing these hairpins displayed increased adhesion to both substrates. We then used CRISPR-Cas9 to generate podocyte knockout cells for DPH1, DPH2, or DPH3, which also displayed increased adhesion to both fibronectin and sFLT1/Fc, as well as a spreading defect. Finally, we showed that Drosophila nephrocyte-specific knockdown of Dph1, Dph2, and Dph4 resulted in altered nephrocyte function. In summary, we report here a novel high-throughput method to identify genes important for podocyte function. Given the central role of podocyte adhesion as a marker of podocyte health, these data are a rich source of candidate regulators of glomerular disease.

Transcription Factor 21 Is Required for Branching Morphogenesis and Regulates the Gdnf-Axis in Kidney Development.

BACKGROUND: The mammalian kidney develops through reciprocal inductive signals between the metanephric mesenchyme and ureteric bud. Transcription factor 21 (Tcf21) is highly expressed in the metanephric mesenchyme, including Six2-expressing cap mesenchyme and Foxd1-expressing stromal mesenchyme. Tcf21 knockout mice die in the perinatal period from severe renal hypodysplasia. In humans, Tcf21 mRNA levels are reduced in renal tissue from human fetuses with renal dysplasia. The molecular mechanisms underlying these renal defects are not yet known. METHODS: Using a variety of techniques to assess kidney development and gene expression, we compared the phenotypes of wild-type mice, mice with germline deletion of the Tcf21 gene, mice with stromal mesenchyme-specific Tcf21 deletion, and mice with cap mesenchyme-specific Tcf21 deletion. RESULTS: Germline deletion of Tcf21 leads to impaired ureteric bud branching and is accompanied by downregulated expression of Gdnf-Ret-Wnt11, a key pathway required for branching morphogenesis. Selective removal of Tcf21 from the renal stroma is also associated with attenuation of the Gdnf signaling axis and leads to a defect in ureteric bud branching, a paucity of collecting ducts, and a defect in urine concentration capacity. In contrast, deletion of Tcf21 from the cap mesenchyme leads to abnormal glomerulogenesis and massive proteinuria, but no downregulation of Gdnf-Ret-Wnt11 or obvious defect in branching. CONCLUSIONS: Our findings indicate that Tcf21 has distinct roles in the cap mesenchyme and stromal mesenchyme compartments during kidney development and suggest that Tcf21 regulates key molecular pathways required for branching morphogenesis.

Electroacupuncture Enhances the Antiallodynic and Antihyperalgesic Effects of Milnacipran in Neuropathic Rats.

BACKGROUND: Milnacipran, a selective serotonin/norepinephrine-reuptake inhibitor, has been shown to elicit a beneficial effect in various models of neuropathic pain. Previously, we reported that repetitive electroacupuncture (EA) significantly ameliorates neuropathic pain induced by L5 spinal nerve ligation (SNL). In the present study, we sought to determine whether a single treatment with EA produces analgesia and whether EA in combination with a subeffective dosage of milnacipran exhibits an additive effect in SNL rats. METHODS: Mechanical allodynia and thermal hyperalgesia were assessed by measuring paw withdrawal thresholds and latencies in response to mechanical and thermal stimuli, respectively, 1 day before and 5 days after neuropathic surgery. In addition, on day 5 post-SNL, time courses of behaviors were assessed at 0, 1, 2, 4, 6, and 8 hours after intrathecal (i.t.) milnacipran (1, 5, and 20 µg) administration. EA (10 Hz/1 mA) was administered at the ST36 and GB34 acupoints for 30 minutes on day 5 and the time courses of behaviors were also assessed at 0, 1, 2, 4, 6, and 8 hours later. Similarly, when treated in combination (milnacipran [5 µg, i.t.] and EA [10 Hz/1 mA]), time courses of behaviors were assessed at the same time points. RESULTS: Intrathecal injection of milnacipran at 5 or 20 µg exerted dose-dependent effects on thermal hyperalgesia but had similar efficacies on mechanical allodynia. Furthermore, EA itself detectably attenuated hyperalgesia at 4 hours after the application, but no statistically significant difference was found in mechanical allodynia. Importantly, cotreatment with EA and milnacipran (5 µL) produced more potent antiallodynic and antihyperalgesic effects than those obtained from EA or milnacipran alone at 1, 2, and 4 hours after treatment, indicating an additive effect. In addition, the analgesic effect of EA plus milnacipran was almost completely abolished by the catecholamine neurotoxin 6-hydroxydopamine hydrobromide (25 µg), which depletes spinal norepinephrine, and by yohimbine (an α2-adrenoceptor antagonist, 30 µg, i.t.). Somewhat surprisingly, the analgesic effect of milnacipran plus EA lasted for 6 hours. CONCLUSIONS: The study shows that, in male rats with SNL, spinal administration of milnacipran effectively alleviates mechanical allodynia and thermal hyperalgesia, and that a single treatment of EA has an antihyperalgesic effect. Furthermore, our findings suggest that coapplication of EA and milnacipran enhanced antiallodynia and antihyperalgesia by activating spinal noradrenergic systems coupled with spinal α2-adrenoceptors and prolongs the duration of analgesia.

Antifibrogenic effects of B16 melanoma-conditioned medium.

BACKGROUND: Some malignant cancers show high levels of local invasiveness by the secretion of soluble factors that can degrade adjacent tissues and suppress surrounding cell growth. We investigated the possibility of treating fibroproliferative scars based on these properties of malignant melanoma. MATERIAL AND METHODS: B16 melanoma-conditioned medium (B16 M-CM) was added to keloid fibroblasts (KFs), and proliferation, migration, and type I collagen production were measured. The cell cycle and signaling pathways were also analyzed. Proteins associated with cell proliferation were measured with Western blot analysis. Animal experiments using a rabbit ear model was performed to confirm the effect of B16 M-CM in vivo. RESULTS: B16 M-CM reduced proliferation, migration, and type I collagen production of KFs. This treatment also increased the number of cells in the subG1 phase and decreased phosphorylation levels of AKT, extracellular signal-regulated kinase1/2, cyclin D1, and c-Myc of KFs. Additionally, B16 M-CM reduced the thickness of rabbit ear scars in the rabbit ear model in vivo. CONCLUSIONS: B16 M-CM can suppress proliferation, migration, and type I collagen production of KFs. In addition, concentrated B16 M-CM reduced scar thickness in the rabbit ear model. The specific proteins involved should be identified in a future study.

Loss of the podocyte-expressed transcription factor Tcf21/Pod1 results in podocyte differentiation defects and FSGS.

Podocytes are terminally differentiated cells with an elaborate cytoskeleton and are critical components of the glomerular barrier. We identified a bHLH transcription factor, Tcf21, that is highly expressed in developing and mature podocytes. Because conventional Tcf21 knockout mice die in the perinatal period with major cardiopulmonary defects, we generated a conditional Tcf21 knockout mouse to explore the role of this transcription factor in podocytes in vivo. Tcf21 was deleted from podocytes and podocyte progenitors using podocin-cre (podTcf21) and wnt4-cre (wnt4creTcf21) driver strains, respectively. Loss of Tcf21 from capillary-loop stage podocytes (podTcf21) results in simplified glomeruli with a decreased number of endothelial and mesangial cells. By 5 weeks of age, 40% of podTcf21 mice develop massive proteinuria and lesions similar to FSGS. Notably, the remaining 60% of mice do not develop proteinuria even when aged to 8 months. By contrast, earlier deletion of Tcf21 from podocyte precursors (wnt4creTcf21) results in a profound developmental arrest of podocyte differentiation and renal failure in 100% of mice during the perinatal period. Taken together, our results demonstrate a critical role for Tcf21 in the differentiation and maintenance of podocytes. Identification of direct targets of this transcription factor may provide new therapeutic avenues for proteinuric renal disease, including FSGS.

Development and validation of a radiomics-based model for predicting osteoporosis in patients with lumbar compression fractures.

BACKGROUND: Osteoporosis, a metabolic bone disorder, markedly elevates fracture risks, with vertebral compression fractures being predominant. Antiosteoporotic treatments for patients with osteoporotic vertebral compression fractures (OVCF) lessen both the occurrence of subsequent fractures and associated pain. Thus, diagnosing osteoporosis in OVCF patients is vital. PURPOSE: The aim of this study was to develop a predictive radiographic model using T1 sequence MRI images to accurately determine whether patients with lumbar spine compression fractures also have osteoporosis. STUDY DESIGN: Retrospective cohort study. PATIENT SAMPLE: Patients over 45 years of age diagnosed with a fresh lumbar compression fracture. OUTCOME MEASURES: Diagnostic accuracy of the model (area under the ROC curve). METHODS: The study retrospectively collected clinical and imaging data (MRI and DEXA) from hospitalized lumbar compression fracture patients (L1-L4) aged 45 years or older between January 2021 and June 2023. Using the pyradiomics package in Python, features from the lumbar compression fracture vertebral region of interest (ROI) were extracted. Downscaling of the extracted features was performed using the Mann-Whitney U test and the least absolute shrinkage selection operator (LASSO) algorithm. Subsequently, six machine learning models (Naive Bayes, Support Vector Machine [SVM], Decision Tree, Random Forest, Extreme Gradient Boosting [XGBoost], and Light Gradient Boosting Machine [LightGBM]) were employed to train and validate these features in predicting osteoporosis comorbidity in OVCF patients. RESULTS: A total of 128 participants, 79 in the osteoporotic group and 49 in the non-osteoporotic group, met the study's inclusion and exclusion criteria. From the T1 sequence MRI images, 1906 imaging features were extracted in both groups. Utilizing the Mann-Whitney U test, 365 radiologic features were selected out of the initial 1,906. Ultimately, the lasso algorithm identified 14 significant radiological features. These features, incorporated into six conventional machine learning algorithms, demonstrated successful prediction of osteoporosis in the validation set. The NaiveBayes model yielded an area under the receiver operating characteristic curve (AUC) of 0.84, sensitivity of 0.87, specificity of 0.70, and accuracy of 0.81. CONCLUSIONS: A NaiveBayes machine learning algorithm can predict osteoporosis in OVCF patients using t1-sequence MRI images of lumbar compression fractures. This approach aims to obviate the necessity for further osteoporosis assessments, diminish patient exposure to radiation, and bolster the clinical care of patients with OVCF.

Loss of the tumor suppressor Vhlh leads to upregulation of Cxcr4 and rapidly progressive glomerulonephritis in mice.

Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome characterized by loss of renal function within days to weeks and by glomerular crescents on biopsy. The pathogenesis of this disease is unclear, but circulating factors are believed to have a major role. Here, we show that deletion of the Von Hippel-Lindau gene (Vhlh) from intrinsic glomerular cells of mice is sufficient to initiate a necrotizing crescentic glomerulonephritis and the clinical features that accompany RPGN. Loss of Vhlh leads to stabilization of hypoxia-inducible factor alpha subunits (HIFs). Using gene expression profiling, we identified de novo expression of the HIF target gene Cxcr4 (ref. 3) in glomeruli from both mice and humans with RPGN. The course of RPGN is markedly improved in mice treated with a blocking antibody to Cxcr4, whereas overexpression of Cxcr4 alone in podocytes of transgenic mice is sufficient to cause glomerular disease. Collectively, these results indicate an alternative mechanism for the pathogenesis of RPGN and glomerular disease in an animal model and suggest novel molecular pathways for intervention in this disease.

Inhibition of MTOR disrupts autophagic flux in podocytes.

Inhibitors of the mammalian target of rapamycin (MTOR) belong to a family of drugs with potent immunosuppressive, antiangiogenic, and antiproliferative properties. De novo or worsening proteinuria can occur during treatment with these agents, but the mechanism by which this occurs is unknown. We generated and characterized mice carrying a podocyte-selective knockout of the Mtor gene. Although Mtor was dispensable in developing podocytes, these mice developed proteinuria at 3 weeks and end stage renal failure by 5 weeks after birth. Podocytes from these mice exhibited an accumulation of the autophagosome marker LC3 (rat microtubule-associated protein 1 light chain 3), autophagosomes, autophagolysosomal vesicles, and damaged mitochondria. Similarly, human podocytes treated with the MTOR inhibitor rapamycin accumulated autophagosomes and autophagolysosomes. Taken together, these results suggest that disruption of the autophagic pathway may play a role in the pathogenesis of proteinuria in patients treated with MTOR inhibitors.

Role of lncRNA MAGI2-AS3 in lipopolysaccharide-induced nucleus pulposus cells injury by regulating miR-374b-5p/interleukin-10 axis.

BACKGROUND: Intervertebral disc degeneration (IDD) is a pathological process that occurs during the natural aging of intervertebral discs. Accumulating evidence suggests that noncoding RNAs (ncRNAs), including microRNAs and long ncRNAs (lncRNAs), participate in the pathogenesis and development of IDD. Herein, we examined the role of lncRNA MAGI2-AS3 in the pathogenic mechanism of IDD. MATERIAL AND METHODS: To develop an IDD in vitro model, we treated human nucleus pulposus (NP) cells with lipopolysaccharide (LPS). Aberrant levels of lncRNA MAGI2-AS3, miR-374b-5p, interleukin (IL)-10 and extracellular matrix (ECM)-related proteins in NP cells were examined using reverse transcription-quantitative PCR and western blot analysis. LPS-induced NP cell injury and inflammatory response were confirmed using the MTT assay, flow cytometry, Caspase3 activity, and enzyme-linked immunosorbent assay. Dual-luciferase reporter assay and rescue experiments were performed to confirm targets between lncRNA MAGI2-AS3 and miR-374b-5p or miR-374b-5p and IL-10. RESULTS: LPS-induced NP cells exhibited low levels of lncRNA MAGI2-AS3 and IL-10 expression, along with high miR-374b-5p expression. miR-374b-5p was a target of lncRNA MAGI2-AS3 and IL-10. LncRNA MAGI2-AS3 ameliorated injury, inflammatory response, and ECM degradation in LPS-treated NP cells by downregulating miR-374b-5p to upregulate IL-10 expression. CONCLUSIONS: LncRNA MAGI2-AS3 increased IL-10 expression levels by sponging miR-374b-5p, which, in turn, alleviated LPS-triggered decreased NP cell proliferation and increased apoptosis, inflammatory response, and ECM degradation. Therefore, lncRNA MAGI2-AS3 may be a potential therapeutic target for IDD.

Daily loneliness and social media use: The role of fear of missing out.

This study explored the effect of daily loneliness on social media use and the mediating role of fear of missing out (FoMO). A total of 106 college students participated in a 2-week experience sampling study, yielding 1194 data points. The results showed that daily loneliness predicted social media use via FoMO.

General synthesis of CoCeMOx trimetallic oxides via a cation exchange reaction for the oxygen evolution reaction.

Cobalt-based spinel oxides are considered potential candidates for the oxygen evolution reaction (OER) due to their abundant valence changes and promising electrochemical activity, but their low intrinsic activity hinders their practical applications. Herein, we synthesize a series of CoCeMOx (M = Zn, Ni, Ru, Er, Mg, Mn, Sn) derived from CoCeM coordination-driven self-assembled aggregates (CDSAAs) using a general ion exchange and subsequent calcination method. Interestingly, CoCeMOx exhibit different morphologies from porous nanospheres, particle-stacked nanospheres, to hollow nanospheres as the third metal element is altered. Markedly, CoCeZnOx porous nanospheres (PNs) exhibit the best OER performance. The XPS results reveal that the existence of CeO2 and Zn2+ ions significantly increased the Co2+/Co3+ ratio and the content of oxygen vacancies in Co3O4. Furthermore, Co2+ can be used as highly reactive sites to form CoOOH and the high content of oxygen vacancies can optimize the oxygen-containing intermediate adsorption energy, both of which can effectively improve the OER performance. Therefore, well-designed CoCeZnOx PNs demonstrate high OER activity with a lower overpotential (η = 333 mV) than that of commercial RuO2 (344 mV) in 10 mA cm-2, a Tafel slope of 98 mV dec-1, and a long-term durability of 45 h. This work may provide some inspiration for the design of trimetallic oxide nanomaterials.

Rapid assay using recombinase polymerase amplification and lateral flow dipstick for identifying Agrilus mali (Coleoptera: Buprestidae), a serious wood-boring beetle of the western Tianshan Mountains in China.

Agrilus mali stands as a significant wood-boring pest prevalent in Northeast Asia. Identifying this pest beetle is often hindered by insufficient efficient, rapid, on-site discrimination methods beyond examining adult morphological features. As a result, an urgent need arises for developing and implementing a rapid and accurate molecular technique to distinguish and manage the beetle. This study presents a straightforward, swift, highly specific, and sensitive method built upon recombinase polymerase amplification combined with a lateral flow dipstick (RPA-LFD). This method demonstrates the capability to promptly identify the beetle, even during its larval stage. RPA primers and probes were designed using the internal transcribed spacer 1 region. Through probe optimization, false-positive signals were successfully eliminated, with an accompanying discussion on the underlying causes of such signals. The RPA-LFD assays exhibited remarkable specificity and sensitivity, requiring as little as 10-3 ng of purified DNA. Furthermore, the extraction of crude DNA was achieved through immersion in sterile distilled water, thus streamlining the assay process. Achievable at temperatures ranging from 30 to 50 °C, the RPA-LFD assay can be executed manually without specialized equipment. By merging the RPA-LFD assay with DNA coarse extraction, A. mali can be detected within just 30 min. This current study effectively demonstrates the immense potential of RPA-LFD in quarantine and pest management. Additionally, it presents a universal technique for the rapid on-site diagnosis of insects, showcasing the wide applicability of this method.