Targeting Phactr4 to rescue chronic stress-induced depression-like behavior in rats via regulating neuroinflammation and neuroplasticity.

Depression is a neuropsychiatric disorder characterized by persistent pleasure loss and behavioral despair. However, the potential mechanisms and therapeutic targets for depression treatment remain unclear. Therefore, identifying the underlying pathogenesis of depression would promote the development of novel treatment and provide effective targets for antidepressant drugs. In this study, proteomics analysis showed that the expression level of phosphatase and actin regulator 4 (Phactr4) was significantly increased in the CA1 hippocampus of depressed rats. The upregulated Phactr4 might induce dysfunction of the synaptic structure via suppressing the p-LIMK/p-Cofilin signaling pathway, and promote neuroinflammation via activating the NF-κB/NLRP3 pathway, which ultimately contributes to the pathogenesis of depression. In contrast, the downregulation of Phactr4 in hippocampal CA1 of depressed rats alleviated depression-like behaviors, along with reducing neuroinflammation and improving synaptic plasticity. In conclusion, these findings provide evidence that Phactr4 plays an important role in regulating neuroinflammatory response and impairment of synaptic plasticity, effects seem to involve in the pathogenesis of depression, and Phactr4 may serve as a potential target for antidepressant treatment.

The Value of Combined Detection of Serum BNP, Cardiac Troponin-I and Dynamic Electrocardiogram in Early Clinical Diagnosis and Prognosis of Patients with Acute Myocardial Infarction.

BACKGROUND: Acute myocardial infarction (AMI) is a prevalent cardiovascular disease resulting from myocardial ischemia and necrosis due to coronary artery occlusion. AMI is characterized by a sudden onset and high mortality, underscoring the significance of early diagnosis and treatment for improving patient prognosis. This study endeavors to assess the utility of a combined assessment involving serum brain natriuretic peptide (BNP), cardiac troponin-I (cTnI), and dynamic electrocardiogram (ECG) in the early clinical diagnosis and prognosis prediction of AMI. METHODS: This paper constitutes a retrospective study. All enrolled patients underwent dynamic ECG examination. The study compared the serum levels of BNP and cTnI, along with pertinent dynamic ECG parameters [turbulence slope (TS) and standard deviation (SDNN) of the 24-hour interval between normal atrial depolarization and ventricular depolarization (R-R)], between the observation group (AMI patients) and the control group (patients with unstable angina (UA)). To evaluate the early diagnostic potential of AMI, we utilized receiver operating characteristic (ROC) curves to analyze serum BNP, cTnI, dynamic ECG, and their combined utility. Furthermore, a follow-up period of 6 months was conducted for AMI patients to record major adverse cardiovascular events (MACE). RESULTS: In the observation group, the serum levels of BNP and cTnI were significantly higher than those in the control group (p < 0.001), while dynamic ECG parameters, specifically TS and SDNN, were significantly lower in the observation group compared to the control group (p < 0.001). The results obtained from the ROC curve analysis revealed that the area under the curve (AUC) for BNP, cTnI, dynamic ECG, and their combination in early AMI diagnosis were 0.838, 0.887, 0.874, and 0.974, respectively. The 95% confidence intervals (CI) were 0.781~0.884, 0.836~0.926, 0.822~0.915, and 0.942~0.991, respectively. Sensitivity values were 64.29%, 82.14%, 91.07%, and 88.39%, and specificity values were 91.00%, 88.00%, 70.00%, and 98.00%, respectively. Significantly, the combination of all three markers demonstrated superior efficacy in early AMI diagnosis compared to any single index (p < 0.05). During the 6-month follow-up of 112 AMI patients, 22 experienced MACE. The MACE group exhibited notably higher serum BNP and cTnI levels compared to the non-MACE group. Additionally, dynamic electrocardiogram parameters TS and SDNN demonstrated a significant decrease (p < 0.05) in the MACE group. CONCLUSIONS: The combined assessment of serum BNP, cTnI, and dynamic electrocardiogram enhances the early clinical diagnostic potential for AMI and holds value in assessing the prognosis of AMI patients.

FBXL20 promotes synaptic impairment in depression disorder via degrading vesicle-associated proteins.

BACKGROUND: Synaptic plasticity changes in presynaptic terminals or postsynaptic membranes play a critical role in cognitive impairments and emotional disorders, but the underlying molecular mechanisms in depression remain largely unknown. METHODS: The regulation effects of F-box and leucine-rich repeat protein 20 (FBXL20), vesicular glutamate transporter 1 (VGLUT1) and vesicle-associated membrane protein 1 (VAMP1) on synaptic plasticity and depressive-like behaviors examined by proteomics analysis, viral stereotaxic injection, transmission electron microscope and biochemical methods. The glutamate release detected by fluorescent probe in cultured primary pyramidal neurons. RESULTS: We found that chronic unpredictable mild stress (CUMS) induced significant synaptic deficits within hippocampus of depressed rats, accompanied with the decreased expression of VGLUT1 and VAMP1. Moreover, knockdown of VGLUT1 or VAMP1 in hippocampal pyramidal neurons resulted in abnormal glutamatergic neurotransmitter release. In addition, we found that the E3 ubiquitin ligase FBXL20 was increased within hippocampus, which may promote ubiquitination and degradation of VGLUT1 and VAMP1, and thus resulted in the reduction of glutamatergic neurotransmitter release, the disruptions of synaptic transmission and the induction of depression-like behaviors in rats. In contrast, shRNA knockdown of FBXL20 within the hippocampus of depressed rats significantly ameliorated synaptic damage and depression-like behaviors. LIMITATION: Only one type of depression model was used in the present study, while other animal models should be used in the future to confirm the underlying mechanisms reported here. CONCLUSIONS: This study provides new insights that inhibiting FBXL20 pathway in depressed rats may be an effective strategy to rescue synaptic transmission and depression-like behaviors.

First-in-human study to evaluate the safety, tolerability, and population pharmacokinetic/pharmacodynamic target attainment analysis of FL058 alone and in combination with meropenem in healthy subjects.

FL058 is a novel diazabicyclooctane ß-lactamase inhibitor. This first-in-human study evaluated the safety, tolerability, and population pharmacokinetic (PK)/pharmacodynamic target attainment analysis of FL058 alone and in combination with meropenem in healthy subjects. The results showed that the maximum tolerated dose of FL058 was 3,000 mg after single-dose infusion. FL058 in combination with meropenem did not cause any grade 3 or higher adverse event when the dose was escalated up to 1,000 mg/2,000 mg. FL058 exposure PK parameters showed dose proportionality. FL058 was excreted primarily in urine. No significant PK interaction was found between FL058 and meropenem. Population PK model analysis indicated that the PK profiles of FL058 and meropenem were consistent with the two-compartment model. The impact of covariates, creatinine clearance, concomitant use of meropenem, body weight, sex, and FL058 dose, on FL058 exposure was less than 10%. FL058/meropenem combination was safe and well tolerated up to a 1,000-mg/2,000-mg dose in healthy adults. The recommended minimum dose of FL058/meropenem combination was 500 mg/1,000 mg by intravenous infusion over 2 h every 8 h based on target attainment analysis. The good safety, tolerability, and satisfactory PK profiles of FL058 alone and in combination with meropenem in this first-in-human study will support further clinical development of FL058 in combination with meropenem in patients with target infections (ClinicalTrials.gov identifiers: NCT05055687, NCT05058118, and NCT05058105).

Enhanced electrocatalytic degradation of tetracycline by ZIF-67@CNT coupled with a self-standing aligned carbon nanofiber anodic membrane.

Due to the misuse and overuse of the antibiotic tetracycline (TC), as well as its refractory degradability, it has become a stubborn environmental contaminant. In this study, a self-standing polyacrylonitrile-based ZIF-67@CNT/ACF aligned anodic membrane was fabricated by innovatively incorporating ZIF-67@CNT nanoparticles into an aligned carbon nanofiber (ACF) membrane to treat the TC. The flow-through nanoporous construction of the ZIF-67@CNT/ACF membrane reactor can compress the diffusion boundary layer on the electrode surface to enhance mass transfer under microscopic laminar flow, which can further enhance the degradation rate. In addition, the enhanced degradation performance also benefited from the significant electrooxidation capacity of the ZIF-67@CNT/ACF membrane. At the optimal electrocatalytic condition of 3.0 V applied potential and pH 6, the degradation rate reached 81% in 1 h for an initial TC concentration of 10 mg l-1. The refractory and highly toxic TC was electrochemically degraded into small non-toxic molecules. Our results indicate that electrocatalytic TC degradation can be enhanced by ZIF-67@CNT/ACF membrane.

Phosphatidate phosphatase Lipin1 involves in diabetic encephalopathy pathogenesis via regulating synaptic mitochondrial dynamics.

Diabetic encephalopathy (DE) is a common central nervous system complication of diabetes mellitus without effective therapy currently. Recent studies have highlighted synaptic mitochondrial damages as a possible pathological basis for DE, but the underlying mechanisms remain unclear. Our previous work has revealed that phosphatidate phosphatase Lipin1, a critical enzyme involved with phospholipid synthesis, is closely related to the pathogenesis of DE. Here, we demonstrate that Lipin1 is significantly down-regulated in rat hippocampus of DE. Knock-down of Lipin1 within hippocampus of normal rats induces dysregulation of homeostasis in synaptic mitochondrial dynamics with an increase of mitochondrial fission and a decrease of fusion, then causes synaptic mitochondrial dysfunction, synaptic plasticity deficits as well as cognitive impairments, similar to that observed in response to chronic hyperglycemia exposure. In contrast, an up-regulation of Lipin1 within hippocampus in the DE model ameliorates this cascade of dysfunction. We also find that the effect of Lipin1 that regulating mitochondrial dynamics results from maintaining appropriate phospholipid components in the mitochondrial membrane. In conclusion, alterations in hippocampal Lipin1 contribute to hippocampal synaptic mitochondrial dysfunction and cognitive deficits observed in DE. Targeting Lipin1 might be a potential therapeutic strategy for the clinical treatment of DE.

Levomilnacipran Improves Lipopolysaccharide-Induced Dysregulation of Synaptic Plasticity and Depression-Like Behaviors via Activating BDNF/TrkB Mediated PI3K/Akt/mTOR Signaling Pathway.

Depression is a common psychological disease with high morbidity and mortality. Recently, the involvement of synaptic plasticity in the pathogenesis of depression has shed light on the direction of developing novel antidepressants. Levomilnacipran is a newly approved medication for the treatment of adult major depressive disorder. However, the detailed mechanisms underlying its antidepressant-like effects have yet to be illuminated. In this study, we aimed to investigate the role of levomilnacipran in regulating synaptic plasticity and explore the possible molecular mechanisms of its antidepressant effects using a rat model of depression induced by lipopolysaccharide (LPS). The results demonstrated that levomilnacipran (30 mg/kg, i.p.) significantly ameliorated depression-like behaviors in rats, alleviated the dysregulation of synaptic plasticity, and suppressed neuroinflammation within hippocampus induced by LPS-treatment. Levomilnacipran increased the expression of postsynaptic dense 95 (PSD-95) and synaptophysin (Syn) and reversed the imbalance between pro- and anti-inflammatory cytokines within hippocampus of depressed rats. Additionally, levomilnacipran elevated expression level of brain-derived neurotrophic factor (BDNF), accompanied by increased tyrosine kinase B (TrkB), phosphorylated phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-Akt), and phosphorylated mammalian target of rapamycin (p-mTOR). Taken together, these results suggest that levomilnacipran may exert antidepressant effects via upregulating BDNF/TrkB mediated PI3K/Akt/mTOR signaling pathway to improve synaptic plasticity. These findings reveal potential mechanisms for the antidepressant effects of levomilnacipran and offer new insights into the treatments for depression.

Synthesis, anti-inflammatory activity, and conformational relationship studies of chromone derivatives incorporating amide groups.

Inflammation is the initial biological reaction of the immune system to various stimuli such as infection, injury, or irritation. Extensive research has demonstrated that a growing array of diseases are triggered by inflammatory mechanisms. Currently, anti-inflammatory drugs are widely utilized in clinical practice due to their therapeutic advantages; however, the potential side effects cannot be ignored by us. In our work, a series of amide compounds with chromones as the parent nucleus were designed and synthesized using the principle of colligated drug design. The results of the biological evaluation indicated that four compounds exhibited lower EC50 values compared to the positive drug ibuprofen. Notably, compound 5-9 showed optimal inhibitory activity (EC50 = 5.33 ± 0.57 µM) against the production of nitric oxide (NO) induced by lipopolysaccharide (LPS) in RAW264.7 cells. Structure-activity relationships (SAR) showed that the presence of electron-withdrawing groups at positions 5 and 8, or electron-donating groups at positions 6 and 7 of the parent nucleus of the chromones can enhance the anti-inflammatory activity of the chromones. The molecular docking studies predicted the mode of interaction between the compounds and protein. Additionally, these studies have demonstrated that the amide bond is the key radical to the anti-inflammatory effect. Based on the summary of the aforementioned studies, it can be inferred that compound 5-9 exhibit potential as an anti-inflammatory drug that deserves further investigation.

Preparation and Characterization of GX-50 and Vitamin C Co-encapsulated Microcapsules by a Water-in-Oil-in-Water (W1/O/W2) Double Emulsion-Complex Coacervation Method.

Co-encapsulated xanthoxylin (GX-50) and vitamin C (Vc) microcapsules (GX-50-Vc-M) were prepared by the combination of a water-in-oil-in-water (W1/O/W2) double emulsion with complex coacervation. The W1/O/W2 double emulsion was prepared by two-step emulsification, and it has a uniform particle size of 8.388 µm and high encapsulation efficiencies of GX-50 (85.95%) and Vc (67.35%) under optimized process conditions. Complex coacervation occurs at pHs 4.0-4.7, which has the highest encapsulation efficiency of GX-50 and Vc at pH 4.5. The complex coacervate with tannic acid solidifying (namely, wet microcapsules) has better mechanical properties and also enhances the ability of co-encapsulation of active ingredients. The resulting microcapsules by freeze-drying of wet microcapsules were characterized by UV-vis absorbance spectroscopy (UV-vis), Fourier infrared spectroscopy (FI-IR), confocal laser scanning microscopy (CLSM), scanning electron microscopy (SEM), X-ray diffraction (XRD), 2,2-diphenyl-1-picrylhydrazyl (DPPH·) radical scavenging, and in vitro permeation measurements. Under optimal conditions, the encapsulation efficiency and drug loading of GX-50-Vc-M for GX-50 and Vc are, respectively, 78.38 ± 0.51 and 59.34 ± 0.56%, and 35.6 ± 0.68 and 29.8 ± 0.92%. A slight shift in the FTIR peak between single GX-50 or Vc and GX-50-Vc-M confirmed the successful co-encapsulation of GX-50 and Vc in microcapsules. GX-50-Vc-M has bridged irregular spherical aggregates, while GX-50 and Vc are, respectively, encapsulated in hydrophobic and hydrophilic cavities of microcapsules in an amorphous dissolved state. GX-50-Vc-M has the highest DPPH· radical scavenging rate of 62.51%, and the scavenging process of GX-50-Vc-M on DPPH· radicals is more in line with the pseudo-second-order kinetic equation model. Moreover, the in vitro permeation of GX-50 and Vc in GX-50-Vc-M can reach maximum values of 40 and 60%, respectively. This concludes that GX-50-Vc-M is a promising delivery system for the penetration of the antioxidant into the deeper layers of the skin for the antioxidant effect.

The STING inhibitor C-176 attenuates MPTP-induced neuroinflammation and neurodegeneration in mouse parkinsonian models.

Recent emerging evidence reveals that cGAS-STING-mediated Type I interferon (IFN) signaling axis takes part in the microglial-associated neuroinflammation. However, the potential role of pharmacological inhibition of STING on neuroinflammation and dopaminergic neurodegeneration remains unknown. In the present study, we investigated whether pharmacological inhibition of STING attenuates neuroinflammation and neurodegeneration in experimental models of Parkinson's disease. We report that therapeutic inhibition of STING with C-176 significantly inhibited the activation of downstream signaling pathway, suppressed neuroinflammation, and ameliorated MPTP-induced dopaminergic neurotoxicity and motor deficit. Furthermore, pharmacological inhibition of STING with C-176 attenuated proinflammatory response in BV2 microglial cells exposed to LPS/MPP+. More importantly, C-176 also reduced NLRP3 inflammasome activation both in vitro and in vivo. The results of our study suggest that pharmacologic inhibition of STING protects against dopaminergic neurodegeneration and neuroinflammation that may act at least in part through suppressing NLRP3 inflammasome activation. STING signaling may hold great promise for the development of new treatment strategy for PD.

Reversible and Turn-On Fluorescence Detection of Phosphate in Aqueous Solution and Living Cell Imaging by Supramolecular Metallacycles with AIE-Active Ligands.

Luminescent supramolecular metallacycles have attracted great interest as a new promising class of sensing substrates. In this work, two tetraphenylethene (TPE)-based diimidazole and dipyrazole ligands with the aggregation-induced emission (AIE) feature were designed for the construction of supramolecular tetragonal metallacycles 1-4 with two 90° mononuclear [(bpy)M]2+ or dinuclear [(bpy)2M2]4+ acceptors (bpy = 2,2'-dipyridine; M = Pd, Pt), in which the fluorescence can be quenched to an "off" state due to the ligand-to-metal charge transfer (LMCT). Metallacycle 1 was utilized as a fluorescence sensor for phosphate (PO43-) detection in aqueous solution by means of disassembly, leading to the release of the ligand. Additionally, the metallacycle can be regenerated through self-assembly via the introduction of Pd(II) acceptors. PO43- was detected using TPE-based metallacycles over a wide concentration range, with a detection limit as low as 2.1 × 10-8 M. Furthermore, sensor 1 also presented the semiquantitative visual detection ability for PO43- in the test paper mode via fluorescence changes. The aforementioned studies not only enhance the current research on fluorescent materials but also offer a strategy for the creation of stimuli-responsive supramolecular coordination complexes.

Direct methanol fuel cell with enhanced oxygen reduction performance enabled by CoFe alloys embedded into N-doped carbon nanofiber and bamboo-like carbon nanotube.

The exploration of cost-effective electrocatalysts with high catalytic activity and methanol tolerance to replace precious metal catalysts in the oxygen reduction reaction (ORR) is highly desirable for direct methanol fuel cells (DMFCs). Herein, we report a novel complex composed of a CoFe alloy with a modulated electronic structure confined to nitrogen-doped carbon nanofiber (NCNF) and bamboo-like carbon nanotube (BCNT) by tuning the molar ratio of Co and Fe (CoFe@NCNF/BCNT). The synthetized catalysts possess one-dimensional (1D) mesoporous structure, high specific surface area, and rich pyridinic-N content. Notably, the Co1Fe1@NCNF/BCNT and Co1Fe3@NCNF/BCNT (Co:Fe ≈ 1:1 and 1:3) exhibited enhanced oxygen reduction activity and methanol tolerance, compared to unmodified samples. In addition, alkaline DMFCs containing Co1Fe1@NCNF/BCNT and Co1Fe3@NCNF/BCNT presented high power density (29.10 and 31.11 mW cm-2), exceeding that of Pt/C-modified DMFC (27.23 mW cm-2). Furthermore, the Co1Fe1@NCNF/BCNT-catalyzed DMFC exhibited high stability. This improved catalytic activity can be attributed to the rich surface area, controllable alloy composition, optimized N configuration, and favorable electronic interaction. The as-developed CoFe@NCNF/BCNT with multifunctional components may open a new avenue for designing highly active cathode catalysts for various fuel cells.

Research progress of MOFs/carbon nanocomposites on promoting ORR in microbial fuel cell cathodes.

With the rapid development of the economy, energy demand is more urgent. Microbial fuel cells (MFCs) have the advantages of non-toxic, safety, and environmental protection, and are considered the ideal choice for the next generation of energy storage equipment. However, the slow kinetics of oxygen reduction reaction (ORR) on MFC air cathodes and the high cost of traditional platinum (Pt) catalysts hinder their practical application, so there is a need to develop efficient, low-cost, and stable electrocatalysts as alternatives. Recently, metal-organic framework (MOFs) has attracted wide attention in electrocatalysis. Electrocatalysts prepared by the nanocomposite of MOFs and carbon nanomaterials have multiple advantages, such as adjustable chemical properties, high specific surface area, and good electrical conductivity, which have been proven to be a promising electrocatalytic material. In this paper, the latest research progress of metal-organic frames (MOFs) and carbon nanocomposites is reviewed, and the preparation methods and modification of MOFs and carbon nanofibers, carbon nanotubes, and graphene composites are introduced, respectively, as well as their applications in MFC cathode. Finally, the main prospects of MOFs/carbon nanocomposite catalysts are put forward.

Ginsenoside-Rg1 synergized with voluntary running exercise protects against glial activation and dysregulation of neuronal plasticity in depression.

Depression is a common psychological disease accompanied by mental disorders and somatic symptoms. However, the underlying mechanisms regarding the pathogenesis of depression are still not clear. Neuronal damage resulting from inflammation is considered to be one of the important risk factors for depression. Ginsenoside-Rg1, a sterol extract extracted from ginseng herbs, has been shown to have neuroprotective effects against neurodegenerative diseases. Moreover, running exercise, a simple behavioral therapy, has been recently shown to have antidepressant effects. However, whether these two synergized strategies are more efficient in depression treatment, especially the neural mechanisms underlying this practical and interesting treatment is unknown. In this study, we have shown that ginsenoside-Rg1 synergized with voluntary running exercise exerts more efficiency on suppressing neuroinflammation, up-regulating expression of neurotrophic factors, and synaptic-related proteins, ameliorating neuronal structural damages than that of ginsenoside-Rg1 or voluntary exercise alone, suggesting its better neuroprotective effects. More importantly, the antidepressant-like effect of this synergistic treatment was also significantly better than either of these two treatments. These results suggest that ginsenoside-Rg1, synergized with voluntary running, may have higher efficacy in the treatment of depression through anti-inflammation and the improvement of neuroplasticity. These findings may provide a new perspective for the development of a therapeutic strategy for depression.

[M8L4]8+-Type Squares Self-Assembled by Dipalladium Corners and Bridging Aromatic Dipyrazole Ligands for Iodine Capture.

Square-like metallamacrocyclic palladium(II) complexes [M8L4]8+ (1-7) were synthesized by reacting aromatic dipyrazole ligands (H2L1-H2L3 with pyromellitic arylimide-, 1,4,5,8-naphthalenetetracarboxylic arylimide-, and anthracene-based aromatic groups, respectively) with dipalladium corners ([(bpy)2Pd2(NO3)2](NO3)2, [(dmbpy)2Pd2(NO3)2](NO3)2, or [(phen)2Pd2(NO3)2](NO3)2, where bpy = 2,2'-bipyridine, dmbpy = 4,4'-dimethyl-2,2'-bipyridine, and phen = 1,10-phenanthroline) in aqueous solutions via metal-directed self-assembly. Metallamacrocycles 1-7 were fully characterized by 1H and 13C nuclear magnetic resonance spectroscopy and electrospray ionization mass spectrometry, and the square structure of 7·8NO3- was further confirmed via single crystal X-ray diffraction. These square-like metallamacrocycles exhibit effective performance for iodine adsorption.

Hierarchical N-doped carbon nanofiber-loaded NiCo alloy nanocrystals with enhanced methanol electrooxidation for alkaline direct methanol fuel cells.

The high catalytic activity of non-precious metals in alkaline media opens a new direction for the development of alkaline direct methanol fuel cell (ADMFC) electrocatalysts. Herein, a highly dispersed N-doped carbon nanofibers (CNFs) -loaded NiCo non-precious metal alloy electrocatalyst based on metal-organic frameworks (MOFs) was prepared, which conferred excellent methanol oxidation activity and resistance to carbon monoxide (CO) poisoning through a surface electronic structure modulation strategy. The porous electrospun polyacrylonitrile (PAN) nanofibers and the P-electron conjugated structure of polyaniline chains provide fast charge transfer channels, enabling electrocatalysts with abundant active sites and efficient electron transfer. The optimized NiCo/N-CNFs@800 was tested as an anode catalyst for ADMFC single cell and exhibited a power density of 29.15 mW cm-2. Due to the fast charge transfer and mass transfer brought by its one-dimensional porous structure and the synergistic effect between NiCo alloy, NiCo/N-CNFs@800 is expected to be an economical, efficient and CO-resistant methanol oxidation reaction (MOR) electrocatalyst.

Energy-efficient reuse of bio-treated textile wastewater by a porous-structure electrochemical PbO2 filter: Performance and mechanism.

In this work, a novel porous-structure electrochemical PbO2 filter (PEF-PbO2) was developed to achieve the reuse of bio-treated textile wastewater. The characterization of PEF-PbO2 confirmed that its coating has a variable pore size that increases with depth from the substrate, and the pores with a size of 5 µm account for the largest proportion. The study on the role of this unique structure illustrated that PEF-PbO2 possesses a larger electroactive area (4.09 times) than the conventional electrochemical PbO2 filter (EF-PbO2) and enhanced mass transfer (1.39 times) in flow mode. The investigation of operating parameters with a special discussion of electric energy consumption suggested that the optimal conditions were a current density of 3 mA cm-2, Na2SO4 concentration of 10 g L-1 and pH value of 3, which resulted in 99.07% and 53.3% removal of Rhodamine B and TOC, respectively, together with an MCETOC of 24.6%. A stable removal of 65.9% COD and 99.5% Rhodamine B with a low electric energy consumption of 5.19 kWh kg-1 COD under long-term reuse of bio-treated textile wastewater indicated that PEF-PbO2 was durable and energy-efficient in practical applications. Mechanism study by simulation calculation illustrated that the part of the pore of the PEF-PbO2's coating with small size (5 µm) plays an important role in this excellent performance which provides the advantage of rich ·OH concentration, short pollutant diffusion distance and high contact possibility.

Correction: Self-assembly of tripyrazolate-linked [M6L2] cages for the selective sensing of HSO3- and gaseous SO2 by turn-on fluorescence.

Correction for 'Self-assembly of tripyrazolate-linked [M6L2] cages for the selective sensing of HSO3- and gaseous SO2 by turn-on fluorescence' by Peipei Wang et al., Dalton Trans., 2023, https://doi.org/10.1039/d3dt00083d.

Self-assembly of tripyrazolate-linked [M6L2] cages for the selective sensing of HSO3- and gaseous SO2 by turn-on fluorescence.

Owing to their structural designability and tuneable properties, supramolecular metal-organic complexes have recently emerged as promising candidates for the sensing and detection of molecules and anions. Herein, we synthesised three tripyrazolate-linked [M6L2] metallocages with the formulas [(bpyPd)6L2](NO3)6 (1), [(dmbpyPd)6L2](NO3)6 (2), and [(phenPd)6L2](NO3)6 (3) (H3L = tris(4-(5-(trifluoromethyl)-1H-pyrazol-3-yl)phenyl)amine, bpy = 2,2'-bipyridine, dmbpy = 4,4'-dimethylbipyridine, phen = 1,10-phenanthroline). Crystallography revealed that metal-directed coordination and the bidentate chelate behaviour of the ligand induced the self-assembly of supramolecular metal-organic cages. Notably, these cages were employed as turn-on fluorescence sensors for SO2 and its derivative (HSO3-) through a disassembly mechanism. Cages 1, 2, and 3 showed a highly selective and sensitive detection of HSO3- over other common anions in aqueous solutions and of SO2 gas over other common gasses, with an excellent anti-interference ability. These metallocages were subsequently applied as sensors in environmental and biological samples. This study not only enriches the ongoing research on metal-organic supramolecular materials but also facilitates the future preparation of stimuli-responsive supramolecular coordination complexes.

Lipin2 ameliorates diabetic encephalopathy via suppressing JNK/ERK-mediated NLRP3 inflammasome overactivation.

OBJECTIVES: Diabetic encephalopathy (DE) is a common complication of diabetes in the central nervous system, which can cause cognitive dysfunction in patients. However, its pathophysiological mechanism has not been elucidated, and thus effective prevention and treatment methods are still lacking.Previous studies reported that neuroinflammation involved in the central neuropathy, while lipin2 plays an important role in inflammatory response.Therefore, we aimed to investigate the effects of lipin2 on regulating inflammatory response in the pathogenesis of DE. METHODS: BV2 cells were treated with high glucose and infected with lipin2 overexpression or knockdown virus to observe the cell viability. Then, we constructed a mouse model of DE, and constructed a lipin2 knockdown or overexpression model by injecting lentivirus into the brain with stereotaxis. The expression of lipin2 in inflammatory bodies and related inflammatory factor signaling pathway-related proteins were examined by western blot and quantitative real-time PCR. Morris water maze was used to evaluate the spatial learning and memory of mice. RESULTS: High glucose decreased the expression of lipin2 in BV2 cells, while overexpression of lipin2 in BV2 cells significantly suppressed the inflammatory response and apoptosis induced by high glucose. Meanwhile, the expression of lipin2 was down-regulated in the hippocampus in a DE mice model. Up-regulation of lipin2 in the hippocampus of DE mice inhibited JNK/ERK signaling pathway, reduced NLRP3 inflammasome-mediated inflammatory response, down-regulated IL-1/TNF-α expression, and improved synaptic plasticity and cognitive dysfunction in mice. Conversely, knockdown of lipin2 increased NLRP3 inflammasome overactivation, caused neuronal abnormalities and cognitive impairment in mice. CONCLUSIONS: Lipin2 may play a neuroprotective role in DE by inhibiting JNK/ERK-mediated NLRP3 inflammasome overactivation and subsequent inflammatory responses. It may be a potential therapeutic target for DE therapy.