Control of Biological Surface States on Chlorine-Doped Amorphous Silica Particles and Their Effective Absorptive Ability for Antibody Protein.

Amorphous silica particles (ASPs) have low biotoxicity and are used in foodstuffs; however, the adsorption states of proteins on their surfaces have not yet been clarified. If the adsorption states can be clarified and controlled, then a wide range of biological and medical applications can be expected. The conventional amorphous silica particles have the problem of protein adsorption due to the strong interaction with their dense silanol groups and denaturation. In this study, the surfaces of amorphous silica particles with a lower silanol group density were modified with a small amount of chlorine during the synthesis process to form a specific surface layer by adsorbing water molecules and ions in the biological fluid, thereby controlling the protein adsorption state. Specifically, the hydration state on the surface of the amorphous silica particles containing trace amounts of chlorine was evaluated, and the surface layer (especially the hydration state) for the adsorption of antibody proteins while maintaining their steric structures was evaluated and discussed. The results showed that the inclusion of trace amounts of chlorine increased the silanol groups and Si-Cl bonds in the topmost surface layer of the particles, thereby inducing the adsorption of ions and water molecules in the biological fluid. Then, it was found that a novel surface layer was formed by the effective adsorption of Na and phosphate ions, which would change the proportion of the components in the hydration layer. In particular, the proportion of the free water component increased by 21% with the doping of chlorine. Antibody proteins were effectively adsorbed on the particles doped with trace amounts of chlorine, and their steric adsorption states were evaluated. It was found that the proteins were clearly adsorbed and maintained the steric state of their secondary structure. In the immunoreactivity tests using streptavidin and biotin, biotin bound to the chlorine-doped particles showed efficient reactivity. In conclusion, this study is the first to discover the surface layer of the amorphous silica particles to maintain the steric structures of adsorbed proteins, which is expected to be used as a carrier particle for antibody test kits and immunochromatography.

NMDAR (2C) deletion in astrocytes relieved LPS-induced neuroinflammation and depression.

The link between neuroinflammation and depression is a subject of growing interest in neuroscience and psychiatry; meanwhile, the precise mechanisms are still being unrevealed. However, glial cell activation, together with cytokine level elevation, suggests a connection between neuroinflammation and the development or exacerbation of depression. Glial cells (astrocytes) communicate with neurons via their extracellular neurotransmitter receptors, including glutamate receptors NMDARs. However, these receptor roles are controversial and enigmatic in neurological disorders, including depression. Therefore, we hypothesized whether NMDAR subnit NR2C deletion in the astrocytes exhibited anti-depressive effects concurrent with neuroinflammation prevention. To assess, we prepared astrocytic-NR2C knockout mice (G-2C: GFAPCre+Grin2Cflox/flox), followed by LPS administration, behavior tests, and biochemical analysis. Stimulatingly, astrocytic-NR2C knockout mice (G-2C) did not display depressive-like behaviors, neuroinflammation, and synaptic deficits upon LPS treatment. PI3K was impaired upon LPS administration in control mice (Grin2Cflox/flox); however, they were intact in the hippocampus of LPS-treated G-2C mice. Further, PI3K activation (via PTEN inhibition by BPV) restored neuroinflammation and depressive-like behavior, accompanied by altered synaptic protein and spine numbers in G-2C mice in the presence of LPS. In addition, NF-κB and JNK inhibitor (BAY, SP600125) treatments reversed the effects of BPV. Moreover, these results were further validated with an NR2C antagonist DQP-1105. Collectively, these observations support the astrocytic-NR2C contribution to LPS-induced neuroinflammation, depression, and synaptic deficits.

Exhaustive exercise decreases tau phosphorylation and modifies biological processes associated with the protein translation and electron transport chain in P301L tau transgenic mice.

Stress response is a fundamental mechanism for cell survival, providing protection under unfavorable conditions. Mitochondrial stress, in particular, can trigger mitophagy, a process that restores cellular health. Exhaustive exercise (EE) is a form of acute mitochondrial stress. The objective of this current study is to investigate the impact of EE on tau pathology in pR5 mice, as well as the potential underlying mechanisms. To evaluate this, we examined the levels of total and phosphorylated tau in the hippocampus of pR5 mice, both with and without EE treatment. Furthermore, the application of weighted correlation network analysis (WGCNA) was employed to identify protein modules associated with the phenotype following the proteomic experiment. The findings of our study demonstrated a significant decrease in tau phosphorylation levels upon EE treatment, in comparison to the pR5 group. Moreover, the proteomic analysis provided additional insights, revealing that the mitigation of tau pathology was primarily attributed to the modulation of various pathways, such as translation factors and oxidative phosphorylation. Additionally, the analysis of heatmaps revealed a significant impact of EE treatment on the translation process and electron transport chain in pR5 mice. Furthermore, biochemical analysis provided further confirmation that EE treatment effectively modulated the ATP level in pR5 mice. In conclusion, our study suggests that the observed decrease in tau phosphorylation resulting from EE treatment may primarily be attributed to its regulation of the translation process and enhancement of mitochondrial function.

Ceftriaxone averts neuroinflammation and relieves depressive-like behaviors via GLT-1/TrkB signaling.

The beneficial effect of a beta-lactam antibiotic, Ceftriaxone (CEF), to improve depressive-like symptoms has been documented previously, attributed to its modulation of glutamate neurotransmission. Here, we aimed to determine whether CEF could improve LPS-altered glutamatergic signaling associated with neuroinflammation-allied depression. To assess our goals, we established a neuroinflammation-allied depression mice model by injecting lipopolysaccharides (LPS), followed by behavioral and biochemical analysis. LPS-treated mice displayed depressive symptoms, neuroinflammation, dysregulated glutamate and its transporter (GLT-1) expression, altered expression of astrocyte reactive markers (GFAP, cxcl10, steap4, GBP2, and SRGN), and dysregulated BDNF/TrkB signaling. However, these changes were rescued by CEF treatment, as we found decreased neuroinflammation, relief of depression symptoms, and improved GLT-1 and BDNF/TrkB signaling upon CEF treatment. Moreover, GLT-1 and BDNF/TrkB regulation role of CEF was validated by K252a and DHK treatment. In summary, the anti-depressive effects of glutamate modulators, like CEF, are closely related to their anti-inflammatory role.

A novel dopamine D2 receptor-NR2B protein complex might contribute to morphine use disorders.

Dopamine receptors can form heteromeric interactions with other receptors, including glutamate receptors, and present a novel pharmacological target because it contribute to dopamine-dysregulated brain disorders such as addiction and other motor-related diseases. In addition, dopamine receptors D2 (D2Rs) and glutamate NMDA receptors subtype-NR2B have been implicated in morphine use disorders; however, the molecular mechanism underlying the heteromeric complex of these two receptors in morphine use disorders is unclear. Herein, we focus on interactions between D2R and NR2B in morphine-induced conditioned place preference (CPP) and hyperlocomotion mice models. We found that the D2R-NR2B complex significantly increases in morphine-induced mice models, accompanied by ERK signaling impairment, implying the complex could contribute to the morphine addiction pathophysiological process. Further, we design a brain-penetrant interfering peptide (TAT-D2-KT), which could disrupt interactions of D2R-NR2B and decrease addictive-like behaviors concurrent to ERK signaling improvement. In summary, our data provided the first evidence for a D2R-NMDAR complex formation in morphine use disorders and its underlying mechanism of ERK signaling, which could present a novel therapeutic target with direct implications for morphine acquisition and relapse treatment.

eIF4E phosphorylation mediated LPS induced depressive-like behaviors via ameliorated neuroinflammation and dendritic loss.

The translational defect has emerged as a common feature of neurological disorders. Studies have suggested that alterations between opposing and balanced synaptic protein synthesis and turnover processes could lead to synaptic abnormalities, followed by depressive symptoms. Further studies link this phenomenon with eIF4E and TrkB/BDNF signaling. However, the interplay between the eIF4E and TrkB/BDNF signaling in the presence of neuroinflammation is yet to be explored. To illuminate the role of eIF4E activities within LPS-induced neuroinflammation and depression symptomology, we applied animal behavioral, biochemical, and pharmacological approaches. In addition, we sought to determine whether eIF4E dysregulated activities correlate with synaptic protein loss via the TrkB/BDNF pathway. Our results showed that LPS administration induced depressive-like behaviors, accompanied by neuroinflammation, reduced spine numbers, and synaptic protein dysregulation. Concurrently, LPS treatment enhanced eIF4E phosphorylation and TrkB/BDNF signaling defects. However, eFT508 treatment rescued the LPS-elicited neuroinflammation and depressive behaviors, as well as altered eIF4E phosphorylation, synaptic protein expression, and TrkB/BDNF signaling. The causal relation of eIF4E with BDNF signaling was further explored with TrkB antagonist K252a, which could reverse the effects of eFT508, validating the interplay between the eIF4E and TrkB/BDNF signaling in regulating depressive behaviors associated with neuroinflammation via synaptic protein translational regulation. In conclusion, our results support the involvement of eIF4E-associated translational dysregulation in synaptic protein loss via TrkB/BDNF signaling, eventually leading to depressiven-like behaviors upon inflammation-linked stress.

Electrophysiological mechanisms of motion-style scalp acupuncture for treating poststroke spasticity in rats. / è¿åŠ¨å¤´é’ˆæ³•æŠ—å’ä¸­åŽç—‰æŒ›æ•ˆåº”çš„ç”µç”Ÿç†æœºåˆ¶ç ”ç©¶.

OBJECTIVES: To observe the effect of motion-style scalp acupuncture (MSSA) on H-reflex in rats with post-stroke spasticity (PSS), so as to explore the electrophysiological mechanisms of MSSA against spasticity. METHODS: A total of 36 male SD rats were randomly divided into sham operation, model and MSSA groups, with 12 rats in each group. The stroke model was established by occlusion of the middle cerebral artery. After modeling, rats in the MSSA group were treated by scalp acupuncture (manipulated every 15 min, 200 r/min) at ipsilesional "parietal and temporal anterior oblique line" (MS6) for a total of 30 min, the treadmill training (10 m/min) was applied during the needling retention, once daily for consecutive 7 days. The neurological deficits, muscle tone and motor function were assessed by Zea Longa score, modified modified Ashworth scale (MMAS) score and screen test score before and after treatment, respectively. The H-reflex of spastic muscle was recorded by electrophysiological recordings and the frequency dependent depression (FDD) of H-reflex was also recorded. The cerebral infarction volume was evaluated by TTC staining. RESULTS: Compared with the sham operation group, the Zea longa score, MMAS score, cerebral infarction volume, motion threshold, Hmax/Mmax ratio and FDD of H-reflex were significantly increased (P<0.01), while the screen test score was significantly decreased (P<0.01) in the model group. Intriguingly, compared with the model group, the above results were all reversed (P<0.01) in the MSSA group. CONCLUSIONS: MSSA could exert satisfactory anti-spastic effects in rats with PSS, the underlying mechanism may be related to the improvement of nerve function injury, the reduction of spastic muscle movement threshold, Hmax/Mmax ratio and H-reflex FDD.

EPO prevents neuroinflammation and relieves depression via JAK/STAT signaling.

AIMS: Erythropoietin (EPO) is a glycoprotein cytokine that exerts therapeutic potential on neurological disorders by promoting neurogenesis and angiogenesis. However, its role as an antidepressant via anti-inflammatory axes is poorly explored. Furthermore, chronic inflammation can induce neuroinflammation, concurrent with depressive-like behaviors that anti-inflammatory and antidepressant agents could avert. Here, we aimed to elucidate the antidepressant potential of Erythropoietin (EPO) in the LPS-induced depression model. MAIN METHODS: For in vivo analysis, mice were treated with LPS (2 mg/kg BW), Erythropoietin (EPO) (5000 U/kg/day), (Ruxolitinib,15 mg/kg), and K252a (25 µg/kg). Depressive-like behaviors were confirmed via behavior tests, including OFT, FST, SPT, and TST. Cytokines were measured via ELISA, while IBA-1/GFAP expression was determined by immunofluorescence. Further, the desired gene expression was measured by immunoblotting. For in vitro analysis, BV2 and N2a cell lines were cultured, treated with LPS, EPO, Ruxolitinib, and K252a, collected, and analyzed. KEY FINDINGS: LPS treatment significantly induced neuroinflammation accompanied by depression-like behaviors in mice. However, EPO treatment rescued LPS-induced changes by averting cytokine production, secretion, and glial cell activation and reducing depressive-like behaviors in mice. Surprisingly, EPO treatment ameliorated LPS-induced JAK2/STAT5 signaling impairment, as validated by JAK2-antagonism. Furthermore, synaptic and dendritic spine defects and BNDF/TrkB signaling upon LPS administration could be prevented by EPO treatment. SIGNIFICANCE: EPO could act as an antidepressant via its anti-inflammatory potential by regulating JAK2/STAT5 signaling.

Adiponectin deficiency accelerates brain aging via mitochondria-associated neuroinflammation.

BACKGROUND: A wide spectrum of changes occurs in the brain with age, from molecular to morphological aspects, and inflammation accompanied by mitochondria dysfunction is one of the significant factors associated with age. Adiponectin (APN), an essential adipokine in glucose and lipid metabolism, is involved in the aging; however, its role in brain aging has not been adequately explored. Here, we aimed to explore the relationship between APN deficiency and brain aging using multiple biochemical and pharmacological methods to probe APN in humans, KO mice, primary microglia, and BV2 cells. RESULTS: We found that declining APN levels in aged human subjects correlated with dysregulated cytokine levels, while APN KO mice exhibited accelerated aging accompanied by learning and memory deficits, anxiety-like behaviors, neuroinflammation, and immunosenescence. APN-deficient mice displayed aggravated mitochondrial dysfunction and HDAC1 upregulation. In BV2 cells, the APN receptor agonist AdipoRon alleviated the mitochondrial deficits and aging markers induced by rotenone or antimycin A. HDAC1 antagonism by Compound 60 (Cpd 60) improved mitochondrial dysfunction and age-related inflammation, as validated in D-galactose-treated APN KO mice. CONCLUSION: These findings indicate that APN is a critical regulator of brain aging by preventing neuroinflammation associated with mitochondrial impairment via HDAC1 signaling.

Roxadustat (FG-4592) abated lipopolysaccharides-induced depressive-like symptoms via PI3K signaling.

Background: Despite its role in inflammation and the redox system under hypoxia, the effects and molecular mechanisms of hypoxia-inducible factor (HIF) in neuroinflammation-associated depression are poorly explored. Furthermore, Prolyl hydroxylase domain-containing proteins (PHDs) regulate HIF-1; however, whether and how PHDs regulate depressive-like behaviors under Lipopolysaccharides (LPS)-induced stress conditions remain covered. Methods: To highlight the roles and underlying mechanisms of PHDs-HIF-1 in depression, we employed behavioral, pharmacological, and biochemical analyses using the LPS-induced depression model. Results: Lipopolysaccharides treatment induced depressive-like behaviors, as we found, increased immobility and decreased sucrose preference in the mice. Concurrently, we examined increased cytokine levels, HIF-1 expression, mRNA levels of PHD1/PHD2, and neuroinflammation upon LPS administration, which Roxadustat reduced. Furthermore, the PI3K inhibitor wortmannin reversed Roxadustat-induced changes. Additionally, Roxadustat treatment attenuated LPS-induced synaptic impairment and improved spine numbers, ameliorated by wortmannin. Conclusion: Lipopolysaccharides-dysregulates HIF-PHDs signaling may contribute to neuroinflammation-coincides depression via PI3K signaling.

Analytical investigation of nano-bio interfacial protein mediation for fibroblast adhesion on hydroxyapatite nanoparticles.

A quartz crystal microbalance with dissipation (QCM-D) analysis was used to investigate fetal bovine serum (FBS) protein preadsorption on a hydroxyapatite (HAp) surface and the subsequent adhesion process of fibroblasts as compared with the case of oxidized poly(styrene) (PSox). The results showed that the preadsorption of FBS proteins on HAp promoted the subsequent initial cell adhesion ability. Moreover, the measured frequency (Δf) and dissipation shift (ΔD) curves, ΔD-Δf plots and viscoelastic analysis were used to study the initial cell adhesion process in real time. It was suggested that FBS-HAp showed sensitive changes in mass and viscoelasticity as compared with FBS-PSox, which realized the in situ reflection of the cell adhesion state, and the interfacial reactions between the cells and FBS-HAp surfaces such as dehydration and binding occurred to promote the initial cell adhesion and spreading. The viscoelastic analysis of the interface layer showed that the adhered cells on FBS-HAp could secrete some viscous substances such as extracellular matrix (ECM) proteins at the interfaces to provide good adhesion behaviors, and the Voigt-based viscoelastic model could clearly reveal the cellular interfacial viscoelasticity depending on the substrate surface. In addition, the morphology of cells was observed by confocal laser scanning microscopy (CLSM) and atomic force microscopy (AFM), and it was found that the pseudopodia were more uniformly stretched on FBS-HAp than on FBS-PSox. Furthermore, the state of the interfacial protein layer was analyzed by localized Fourier-transform infrared (FT-IR) spectroscopy and fluorescence microscopy (FLM), and it was indicated that the type of substrate affects the formation state of ECM proteins, resulting in changes in cell adhesion properties and morphology. The abundant formation of connective proteins (i.e., collagen type I) on FBS-HAp promoted subsequent pseudopodia formation and cell spreading. Therefore, the initial adhesion properties of fibroblasts on the FBS-HAp surface were systematically studied, which is of great importance for understanding the interfacial interaction between biomaterials and cells, and has great application value in biomedical fields.

Neuronal lack of PDE7a disrupted working memory, spatial learning, and memory but facilitated cued fear memory in mice.

BACKGROUND: PDEs regulate cAMP levels which is critical for PKA activity-dependent activation of CREB-mediated transcription in learning and memory. Inhibitors of PDEs like PDE4 and Pde7 improve learning and memory in rodents. However, the role of PDE7 in cognition or learning and memory has not been reported yet. METHODS: Therefore, we aimed to explore the cognitive effects of a PDE7 subtype, PDE7a, using combined pharmacological and genetic approaches. RESULTS: PDE7a-nko mice showed deficient working memory, impaired novel object recognition, deficient spatial learning & memory, and contextual fear memory, contrary to enhanced cued fear memory, highlighting the potential opposite role of PDE7a in the hippocampal neurons. Further, pharmacological inhibition of PDE7 by AGF2.20 selectively strengthens cued fear memory in C57BL/6 J mice, decreasing its extinction but did not affect cognitive processes assessed in other behavioral tests. The further biochemical analysis detected deficient cAMP in neural cell culture with genetic excision of the PDE7a gene, as well as in the hippocampus of PDE7a-nko mice in vivo. Importantly, we found overexpression of PKA-R and the reduced level of pPKA-C in the hippocampus of PDE7a-nko mice, suggesting a novel mechanism of the cAMP regulation by PDE7a. Consequently, the decreased phosphorylation of CREB, CAMKII, eif2a, ERK, and AMPK, and reduced total level of NR2A have been found in the brain of PDE7a-nko animals. Notably, genetic excision of PDE7a in neurons was not able to change the expression of NR2B, BDNF, synapsin1, synaptophysin, or snap25. CONCLUSION: Altogether, our current findings demonstrated, for the first time, the role of PDE7a in cognitive processes. Future studies will untangle PDE7a-dependent neurobiological and molecular-cellular mechanisms related to cAMP-associated disorders.

Nanospacial effect of citric acid-coordinated hydroxyapatite nanoparticle films on protein adsorption and cell adhesion states.

Hydroxyapatite (HA) and citric acid (Cit)-coordinated HA (Cit/HA) nanoparticle films with different nanospaces were used to examine the nanospacial effect on the protein adsorption behavior and initial osteoblast-like cell adhesion ability through the premise of the stability and ionic dissociation characteristics of the films in biological solution. In particular, the Cit/HA nanoparticle film with a nanospace of 4.2 nm could realize massive and stereoscopic adsorption of proteins due to its larger specific surface area and smaller nanospace as compared with the case of the HA nanoparticle film. It was also found that the α-helix and (ß-sheet + ß-turn) component ratios of the adsorbed fetal bovine serum proteins on the Cit/HA nanoparticle films increased as compared with the case of the HA nanoparticle film through the secondary structure analysis of the adsorbed proteins, which contributed to the good initial cell culture properties on the film surfaces. Therefore, we successfully realized the control of protein adsorption states using different nanospacial HA and Cit/HA nanoparticle films to achieve excellent initial cell culture properties, which would provide new insights into the creation of novel cell culture substrate surfaces in the regenerative medicine fields.

Surface modification of hydroxyapatite nanoparticles for bone regeneration by controlling their surface hydration and protein adsorption states.

Autogenous bone and metallic implant grafting has been used to repair and regenerate bone defects. However, there are still many unresolved problems. It is suggested that bioceramic nanoparticles should be developed and designed to promote effective bone regeneration. In addition, it is necessary to synthesize bioceramic nanoparticles that can support proteins related to bone repair and regeneration such as collagen and albumin. As the protein-interactive bioceramic, hydroxyapatite (HA) deserves to be mentioned and has several attractive properties that are useful in biomedical fields (e.g., biocompatibility, protein adsorption capacity and stability in the physiological environment). In order to prepare novel HA nanoparticles with high biocompatibility, it can be considered that human bones are mainly composed of HA and contain a small amount of silicate, and therefore, the design of coexistence of HA with silicate can be focused. Moreover, it is proposed that the state of the hydration layer on the nanoparticle surfaces can be controlled by introducing heteroelements and polymer chains, which have a great influence on the subsequent protein adsorption and cell adhesion. In this perspective, in order to develop novel bioceramic nanoparticles for the treatment of bone defect, the design of highly biocompatible HA nanoparticles and the control of the hydration layer and protein adsorption states on the surfaces were systematically discussed based on their surface modification techniques, which are very important for the proper understanding of the interface between cells and bioceramics, leading to the further application in biomedical fields.

Investigation of Inclusion States of Silicate and Carbonate Ions in Hydroxyapatite Particles Prepared under the Presence of Sodium Silicate.

Biological hydroxyapatite (HA) contains the different minor ions which favour its bio-reactivity in vivo. In this study, the preparation of HA particles containing both silicate and carbonate ions under the presence of sodium silicate was investigated, and the physicochemical properties were evaluated according to the contents and states of silicate and carbonate ions. The increment in the silicate ion reduced the crystallinity and expanded the crystalline size along with a-axis. Solid-state 29Si-NMR spectra indicated the increase in the adsorption of oligomeric silicate species on the HA particle surfaces in addition to the substitution state of silicate ions, suggesting the occurrence of the surface coating of silicates on the surfaces. The possible states of carbonate and silicate ions at the HA surfaces will provide the bioactivity.

Nanostructural control of transparent hydroxyapatite nanoparticle films using a citric acid coordination technique.

Hydroxyapatite (HA), as the main mineral component in hard tissues, has good biocompatibility. In particular, HA films are widely used as bioactive coatings for artificial bones and dental implants in biomedical fields. However, it is currently difficult to prepare a nanostructure-controlled HA film by a wet process for further applications. Herein, we report the synthesis of HA nanoparticles coordinated by citric acid (Cit/HA) based on the interactions between carboxylate and calcium ions to control the sizes and shapes of the hybrid nanoparticles, to improve their dispersibility in water and to eventually form uniform transparent films with nanospaces, and investigated the film formation mechanism. As compared with the well-known rod-like HA nanoparticles (size: 48 × 15 nm2), we successfully synthesized spherical and negatively charged Cit/HA nanoparticles (size: 25 × 23 nm2) to achieve highly transparent Cit/HA films using the spin-coating technique. The Cit/HA films had uniform and crack-free appearance. About the nanostructures, we found that the Cit/HA film surfaces had meso-scaled nanospaces with a diameter of 4.2 nm based on the regular arrangement of spherical nanoparticles, instead of the HA film with a nanospace diameter of 24.5 nm formed by non-uniform accumulation. Therefore, we successfully achieved the control of the nanospace sizes of the films with the nanoparticle arrangement and realized transparent nanoparticle film formation in a very simple way, which will provide more convenient bioceramic films for biomedical applications.

Bismuth oxychloride nanostructure coated carbon sponge as flow-through electrode for highly efficient rocking-chair capacitive deionization.

Rocking-chair capacitive deionization (RCDI), as the next generation technique of capacitive deionization, has thrived to be one of the most promising strategies in the desalination community, yet was hindered mostly by its relatively low desalination rate and stability. Motivated by the goal of simultaneously enhancing the desalination rate and structural stability of the electrode, this paper reports an anion-driven flow-through RCDI (AFT-RCDI) system equipped with BiOCl nanostructure coated carbon sponge (CS@BiOCl for short; its backbone is derived from commercially available melamine foam with minimum capital cost) as the flow-through electrode. Owning to the rational design of the composite electrode material with minimum charge transfer resistance and ultrahigh structure stability as well as the superior flow-through cell architecture, the AFT-RCDI displays excellent desalination performance (desalination capacity up to 107.33 mg g-1; desalination rate up to 0.53 mg g-1s-1) with superior long-term stability (91.75% desalination capacity remained after 30 cycles). This work provides a new thought of coupling anion capturing electrode with flow-through cell architecture and employing a low-cost CS@BiOCl electrode with commercially available backbone material, which could shed light on the further development of low-cost electrochemical desalination systems.

Anti-depressive-like behaviors of APN KO mice involve Trkb/BDNF signaling related neuroinflammatory changes.

Major depression disorder is a severe mental illness often linked with metabolic disorders. Adiponectin is an adipocyte-secreted circulatory hormone with antidiabetic and glucose/lipid modulation capacities. Studies have demonstrated the pathophysiological roles of adiponectin involved in various neurological disorders, including depression. However, the underlying mechanisms are poorly understood. Here we showed that adiponectin deprivation enhanced antidepressive-like behaviors in the LPS-induced model of depression. APN KO mice displayed increased cytokines (both pro and anti-inflammatory), accompanied by an impaired expression of adiponectin receptors (mRNA/protein level) and decreasing IBA-1 level in the cortex and primary microglia of LPS treated APN KO mice. Further, LPS-treatment significantly reduced p-NFκB expression in the microglia of APN KO mice. However, the Bay11-7082 treatment recovered p-NFκB expression in the cortex of APN KO mice in the presence of LPS. Interestingly, the antidepressant potentials of APN KO mice were abolished by TrkB antagonist K252a, IKK inhibitor Bay11-7082, and AdipoRon suggesting crosstalk between TrkB/BDNF signaling and NFκB in depression. Furthermore, the effects of Bay11-7082 were abolished by a TrkB/BDNF activator (7,8-DHF), indicating a critical role of TrkB/BDNF signaling. Taken together, these findings showed that dysregulated neuroinflammatory status and BDNF signaling might underlie the antidepressive-like behaviors of APN KO mice. NFκB elicited BDNF changes may be accountable for the pathogenesis of LPS induced depression, where APN might present an alternative therapeutic target for depressive disorders.

Layered double hydroxide coated electrospun carbon nanofibers as the chloride capturing electrode for ultrafast electrochemical deionization.

Slow desalination kinetics and poor durability of the electrodes are two key limitations of electrochemical deionization (EDI) that are considered to be the next generation of capacitive desalination (CDI). Herein, we report the design of a high-efficiency chloride removal electrode material for accelerating the desalination kinetics and concurrently improving the durability of EDI, which is based on coating NiMn-Cl layered double hydroxides (LDHs) on the surface of electrospun carbon nanofibers (CNFs@LDHs). The salient features of the as-developed CNFs@LDHs are that applying layer-structured LDHs with abundant redox-active sites to accelerate the pseudo-capacitive ion storage via fast ion intercalation/deintercalation, and leveraging the rigid CNF backbone to strengthen its durability by preventing the potential aggregation of LDHs. As expected, the CNFs@LDH based EDI system displays an ultrafast desalination rate of 0.51 mg g-1 s-1 and outstanding long-term stability (only 10.66 % desalination capacity reduction after 35 cycles), which is achieved without sacrificing its excellent desalination capacity (72.04 mg g-1). This work could be inspirational for the future design of ultrafast yet durable EDI approaching industrial desalination applications.