Coordination Confined Silver-Organic Framework for High Performance Electrochemical Deionization.

Silver (Ag) is deemed a promising anode material for capacitive deionization (CDI) due to its high theoretical capacity and efficient selectivity to Cl-. However, the strong volume change during the conversion reaction significantly undermines the cycling performance of the Ag electrode. Additionally, achieving well-dispersed Ag in the active matrix is challenging, as Ag electrodes prepared by conventional thermal reduction tend to agglomerate. Herein, the organic linker confinement strategy is proposed, applying metal-organic framework (MOF) chemistry between Ag nodes and organic ligands to construct Ag-based MOF. The uniform dispersion of Ag at the molecular level, confined in the organic matrix, efficiently enhances the utilization of active sites, and strengthens the interfacial stability of Ag. Consequently, the Ag-MOF for the CDI anode exhibits an excellent Cl- removal capacity of 121.52 mg g-1 at 20 mA g-1 in 500 mg L-1 NaCl solution, and a high Ag utilization rate of 60.54%. After 100 cycles, a capacity retention of 96.93% is achieved. Furthermore, the Cl- capture mechanism of Ag-MOF is elucidated through density functional theory (DFT) calculations, ex situ XRD, ex situ Raman and XPS. This ingenious electrode design can offer valuable insights for the development of high-performance conversion electrodes for CDI applications.

A host-microbiota interactome reveals extensive transkingdom connectivity.

The myriad microorganisms that live in close association with humans have diverse effects on physiology, yet the molecular bases for these impacts remain mostly unknown1-3. Classical pathogens often invade host tissues and modulate immune responses through interactions with human extracellular and secreted proteins (the 'exoproteome'). Commensal microorganisms may also facilitate niche colonization and shape host biology by engaging host exoproteins; however, direct exoproteome-microbiota interactions remain largely unexplored. Here we developed and validated a novel technology, BASEHIT, that enables proteome-scale assessment of human exoproteome-microbiome interactions. Using BASEHIT, we interrogated more than 1.7 million potential interactions between 519 human-associated bacterial strains from diverse phylogenies and tissues of origin and 3,324 human exoproteins. The resulting interactome revealed an extensive network of transkingdom connectivity consisting of thousands of previously undescribed host-microorganism interactions involving 383 strains and 651 host proteins. Specific binding patterns within this network implied underlying biological logic; for example, conspecific strains exhibited shared exoprotein-binding patterns, and individual tissue isolates uniquely bound tissue-specific exoproteins. Furthermore, we observed dozens of unique and often strain-specific interactions with potential roles in niche colonization, tissue remodelling and immunomodulation, and found that strains with differing host interaction profiles had divergent interactions with host cells in vitro and effects on the host immune system in vivo. Overall, these studies expose a previously unexplored landscape of molecular-level host-microbiota interactions that may underlie causal effects of indigenous microorganisms on human health and disease.

In the View of Electrons Transfer and Energy Conversion: The Antimicrobial Activity and Cytotoxicity of Metal-Based Nanomaterials and Their Applications.

The global pandemic and excessive use of antibiotics have raised concerns about environmental health, and efforts are being made to develop alternative bactericidal agents for disinfection. Metal-based nanomaterials and their derivatives have emerged as promising candidates for antibacterial agents due to their broad-spectrum antibacterial activity, environmental friendliness, and excellent biocompatibility. However, the reported antibacterial mechanisms of these materials are complex and lack a comprehensive understanding from a coherent perspective. To address this issue, a new perspective is proposed in this review to demonstrate the toxic mechanisms and antibacterial activities of metal-based nanomaterials in terms of energy conversion and electron transfer. First, the antimicrobial mechanisms of different metal-based nanomaterials are discussed, and advanced research progresses are summarized. Then, the biological intelligence applications of these materials, such as biomedical implants, stimuli-responsive electronic devices, and biological monitoring, are concluded based on trappable electrical signals from electron transfer. Finally, current improvement strategies, future challenges, and possible resolutions are outlined to provide new insights into understanding the antimicrobial behaviors of metal-based materials and offer valuable inspiration and instructional suggestions for building future intelligent environmental health.

Vagal sensory pathway for the gut-brain communication.

The communication between the gut and brain is crucial for regulating various essential physiological functions, such as energy balance, fluid homeostasis, immune response, and emotion. The vagal sensory pathway plays an indispensable role in connecting the gut to the brain. Recently, our knowledge of the vagal gut-brain axis has significantly advanced through molecular genetic studies, revealing a diverse range of vagal sensory cell types with distinct peripheral innervations, response profiles, and physiological functions. Here, we review the current understanding of how vagal sensory neurons contribute to gut-brain communication. First, we highlight recent transcriptomic and genetic approaches that have characterized different vagal sensory cell types. Then, we focus on discussing how different subtypes encode numerous gut-derived signals and how their activities are translated into physiological and behavioral regulations. The emerging insights into the diverse cell types and functional properties of vagal sensory neurons have paved the way for exciting future directions, which may provide valuable insights into potential therapeutic targets for disorders involving gut-brain communication.

Propofol Suppresses LPS-induced BBB Damage by Regulating miR-130a-5p/ZO-1 Axis.

The blood-brain barrier (BBB) is a highly selective semi-permeable barrier that separates circulating blood from the extracellular fluid of the brain and central nervous system, which is crucial for maintaining brain homeostasis. This study aimed to explore the role of propofol in BBB damage and further evaluate the underlying molecular mechanism. Lipopolysaccharide (LPS) was administered to mice to create an in vivo BBB damage mice model. Additionally, hCMEC/D3 cells as brain microvascular endothelial cells (BMECs) were treated with LPS to establish the in vitro BBB damage cell model. Subsequently, propofol was used for the BBB damage model. Evans blue staining and fluorescein sodium were utilized in the in vivo experiments to demonstrate BBB leakage and BBB permeability. Cell counting kit-8 (CCK-8) assay was used to assess cell viability and the trans-endothelial electrical resistance (TEER) value was measured using an epithelial voltmeter. Furthermore, enzyme-linked immunosorbent assay was performed to measure the levels of the inflammatory cytokines such as interleukin-1ß (IL-1ß) and tumor necrosis factor-alpha (TNF-α). The levels of miR-130a-5p and zonula occludens-1 (ZO-1) in brain tissues and cells were detected using reverse transcription-quantitative polymerase chain reaction, western blot, or immunofluorescence staining. Furthermore, a dual-luciferase reporter assay was used to demonstrate the association between miR-130a-5p and ZO-1. Propofol treatment suppressed BBB leakage, the amount of fluorescein sodium, and the levels of IL-1ß and TNF-α in the LPS-induced BBB damage mice model. Meanwhile, propofol treatment increased the TEER value in the LPS-induced hCMEC/D3 cells. Additionally, propofol treatment significantly down-regulated miR-130a-5p and up-regulated ZO-1. More importantly, miR-130a-5p directly targeted ZO-1 and negatively regulated ZO-1 expression in hCMEC/D3 cells. Furthermore, miR-130a-5p mimic partially reversed the effect of propofol on the TEER value and the levels of inflammatory cytokines such as IL-1ß and TNF-α in the LPS-induced hCMEC/D3 cells. Propofol suppressed LPS-induced BBB damage by regulating miR-130a-5p/ZO-1 axis. These findings suggested a potentially effective treatment approach for BBB damage.

Boron-Modulated Electronic-Configuration Tuning of Cobalt for Enhanced Nitric Oxide Fixation to Ammonia.

Electrocatalytic nitric oxide reduction (eNORR) to ammonia (NH3) provides an environmental route to alleviate NO pollution and yield great-value chemicals. The evolution of eNORR has been primarily hindered, however, by the poor reaction kinetics and low solubility of the NO in aqueous electrolytes. Herein, we have rationally designed a cobalt-based composite with a heterostructure as a highly efficient eNORR catalyst. In addition, by integrating boron to modulate the electronic structure, the catalyst CoB/Co@C delivered a significant NH3 yield of 315.4 µmol h-1 cm-2 for eNORR and an outstanding power density of 3.68 mW cm-2 in a Zn-NO battery. The excellent electrochemical performance of CoB/Co@C is attributed to the enrichment of NO by cobalt and boron dual-site adsorption and fast charge-transfer kinetics. It is demonstrated that the boron is pivotal in the enhancement of NO, the suppression of hydrogen evolution, and Co oxidation to boost eNORR performance.

Enhanced Pseudo-Capacitance Process in Nanoarchitectural Layered Double Hydroxide Nanoarrays Hollow Nanocages for Improved Capacitive Deionization Performance.

Layered double hydroxides (LDHs) are perceived as a hopeful capacitive deionization (CDI) faradic electrode for Cl- insertion due to its tunable composition, excellent anion exchange capacity, and fast redox activity. Nevertheless, the self-stacking and inferior electrical conductivity of the two-dimensional structure of LDH lead to unsatisfactory CDI performance. Herein, the three-dimensional (3D) hollow nanocage structure of CoNi-layered double hydroxide/carbon composites is well designed as a CDI anode by cation etching of the pre-carbonized ZIF-67 template. C/CoNi-LDH has a unique 3D hollow nanocage structure and abundant pore features, which can effectively suppress the self-stacking of LDH sheets and facilitate the transport of ions. Moreover, the introduced amorphous carbon layer can act as a conductive network. When employed as the CDI anode, C/CoNi-LDH exhibited a high Cl- removal capacity of 60.88 mg g-1 and a fast Cl- removal rate of 18.09 mg g-1 min-1 at 1.4 V in 1000 mg L-1 NaCl solution. The mechanism of the Cl- intercalation pseudo-capacitance reaction of C/CoNi-LDH is revealed by electrochemical kinetic analysis and ex situ characterization. This study provides vital guidance for the design of high-performance electrodes for CDI.

Surface redox pseudocapacitance boosting Fe/Fe3C nanoparticles-encapsulated N-doped graphene-like carbon for high-performance capacitive deionization.

The practical application of carbon anode in capacitive deionization (CDI) is greatly hindered by their poor adsorption capacity and co-ion effect. Herein, an N-doped graphene-like carbon (NC) decorated with Fe/Fe3C nanoparticles composite (Fe/Fe3C@NC) with large specific surface area and plentiful porosity is fabricated via a facile and scalable method, namely sol-gel method combined with Fe-catalyzed carbonization. As expected, it exhibits superior CDI performance as a Cl-storage electrode, with Cl- adsorption capacity as high as 102.3 mg g-1 at 1000 mg L-1 Cl- concentration and 1.4 V voltage, and a stable capacity of 68.5 mg g-1 for 60 cycles in 500 mg L-1 Cl- concentration and 100 mA g-1 current density. More importantly, on the basis of electrochemical tests, ex-situ X-ray diffraction, ex-situ X-ray photoelectron spectroscopy (XPS), and XPS analysis with argon ion depth etching, it is revealed that the chlorine storage mechanism of the Fe/Fe3C@NC electrode is dominated by the surface-related redox pseudocapacitance behavior of Fe2+/Fe3+ couple occurring on or near the surface, enabling fast and reversible ion storage. This work proposes an economical and environmentally friendly general method for the design and development of high-performance Cl-storage electrodes for CDI, and offers an in-depth insight into the Cl- storage mechanism of Fe decorated carbon electrodes, further promoting the development of CDI technology.

Commensal microbiota from patients with inflammatory bowel disease produce genotoxic metabolites.

Microbiota-derived metabolites that elicit DNA damage can contribute to colorectal cancer (CRC). However, the full spectrum of genotoxic chemicals produced by indigenous gut microbes remains to be defined. We established a pipeline to systematically evaluate the genotoxicity of an extensive collection of gut commensals from inflammatory bowel disease patients. We identified isolates from divergent phylogenies whose metabolites caused DNA damage and discovered a distinctive family of genotoxins-termed the indolimines-produced by the CRC-associated species Morganella morganii. A non-indolimine-producing M. morganii mutant lacked genotoxicity and failed to exacerbate colon tumorigenesis in mice. These studies reveal the existence of a previously unexplored universe of genotoxic small molecules from the microbiome that may affect host biology in homeostasis and disease.

Interspecies commensal interactions have nonlinear impacts on host immunity.

The impacts of individual commensal microbes on immunity and disease can differ dramatically depending on the surrounding microbial context; however, the specific bacterial combinations that dictate divergent immunological outcomes remain largely undefined. Here, we characterize an immunostimulatory Allobaculum species from an inflammatory bowel disease patient that exacerbates colitis in gnotobiotic mice. Allobaculum inversely associates with the taxonomically divergent immunostimulatory species Akkermansia muciniphila in human-microbiota-associated mice and human cohorts. Co-colonization with A. muciniphila ameliorates Allobaculum-induced intestinal epithelial cell activation and colitis in mice, whereas Allobaculum blunts the A.muciniphila-specific systemic antibody response and reprograms the immunological milieu in mesenteric lymph nodes by blocking A.muciniphila-induced dendritic cell activation and T cell expansion. These studies thus identify a pairwise reciprocal interaction between human gut bacteria that dictates divergent immunological outcomes. Furthermore, they establish a generalizable framework to define the contextual cues contributing to the "incomplete penetrance" of microbial impacts on human disease.

Carbon Nanoarchitectonics with Bi Nanoparticle Encapsulation for Improved Electrochemical Deionization Performance.

Electrochemical deionization (EDI) is hopefully the next generation of water treatment technology. Bismuth (Bi) is a promising anode material for EDI, due to its high capacity and selectivity toward Cl-, but the large volume expansion and severe pulverization aggressively attenuated the EDI cycling performance of Bi electrodes. Herein, carbon-layer-encapsulated nano-Bi composites (Bi@C) were prepared by a simple pyrolysis method using a Bi-based metal-organic framework as a precursor. Bi nanoparticles are uniformly coated within the carbon layer, in which the Bi-O-C bond enhances the interaction between Bi and C. Such a structure effectively relieves the stress caused by volume expansion by the encapsulation effect of the carbon layer. Moreover, the introduction of a carbon skeleton provides a conductive network. As a consequence, the Bi@C composite delivered excellent electrochemical performance with a capacity of 537.6 F g-1 at 1 mV s-1. The Cl- removal capacity was up to 133.5 mg g-1 at 20 mA g-1 in 500 mg L-1 NaCl solution. After 100 cycles, the Bi@C electrode still maintains 71.8% of its initial capacity, which is much higher than the 26.3% of the pure Bi electrode. This study provides a promising strategy for improving EDI electrode materials.

Spinel LiMn2O4 as a Capacitive Deionization Electrode Material with High Desalination Capacity: Experiment and Simulation.

Capacitive deionization (CDI) is a newly developed desalination technology with low energy consumption and environmental friendliness. The surface area restricts the desalination capacities of traditional carbon-based CDI electrodes while battery materials emerge as CDI electrodes with high performances due to the larger electrochemical capacities, but suffer limited production of materials. LiMn2O4 is a massively-produced lithium-ion battery material with a stable spinel structure and a high theoretical specific capacity of 148 mAh·g-1, revealing a promising candidate for CDI electrode. Herein, we employed spinel LiMn2O4 as the cathode and activated carbon as the anode in the CDI cell with an anion exchange membrane to limit the movement of cations, thus, the lithium ions released from LiMn2O4 would attract the chloride ions and trigger the desalination process of the other side of the membrane. An ultrahigh deionization capacity of 159.49 mg·g-1 was obtained at 1.0 V with an initial salinity of 20 mM. The desalination capacity of the CDI cell at 1.0 V with 10 mM initial NaCl concentration was 91.04 mg·g-1, higher than that of the system with only carbon electrodes with and without the ion exchange membrane (39.88 mg·g-1 and 7.84 mg·g-1, respectively). In addition, the desalination results and mechanisms were further verified with the simulation of COMSOL Multiphysics.

Hundred most cited articles in perioperative neurocognitive disorder: a bibliometric analysis.

BACKGROUND: In line with aging populations and increased application of anesthesia and surgery, perioperative neurocognitive disorder (PND) has received growing attention worldwide. Considerable researches into PND are being conducted; however, the quantity and quality of such researches have not been reported. Through a retrospective bibliometric analysis, this study aims to identify and characterize the top 100 cited publications on PND. METHODS: We searched the Web of Science database to find the top 100 cited articles focusing on PND. We collected bibliographic information, including year of publication, country of origin, article type, published journal, citation count, and authorship. To determine changes with time, we compared older and newest articles. RESULTS: The top 100 cited articles were published between 1955 and 2016; the number of citations ranged from 111 to 1248. The United States had the most published papers; clinical trial was the most common article type. The specialty journals of Anesthesiology and Anesthesia & Analgesia were the two most cited journals. Newest articles had a comparable number of citations to older articles, but the former had higher annual citation rates, greater funding disclosures, more focus on basic research, and more open access publications. CONCLUSIONS: This study provides a comprehensive overview of the most cited articles and highlights the increasing attention on PND. High-quality clinical trials with a greater journal impact factor receive more citations. However, there has been a growth in the number of basic science studies as an area of research with respect to the pathogenesis of PND.

JNK inhibition alleviates delayed neurocognitive recovery after surgery by limiting microglia pyroptosis.

Delayed neurocognitive recovery (dNCR) is a prevalent complication after surgery in older adults. Neuroinflammation plays a pivotal role in the pathogenesis of dNCR. Recently,compelling evidence suggests that theinvolvement of microglia pyroptosis in the regulation of neuroinflammation in neurologicaldiseases. Nevertheless, the exact role of microglia pyroptosis in dNCR remains elusive. In the study, in vitro and in vivo models of dNCR were used to examine the potential effects of the mitogen­activated protein kinase signaling pathway on Nod-like receptor protein 3 (NLRP3) inflammasome-mediated microglia pyroptosis and cognitive deficits following surgery. In vivo, we observed surgery-induced upregulation of phosphorylated (p)-c-Jun N-terminal kinases (JNK) in microglia and subsequently NLRP3 inflammasome activation, pyroptosis, and inflammatory cytokines release in mice hippocampus. Interestingly, JNK inhibitor SP600125 significantly attenuated surgery-induced cognitive impairments through inhibiting pyroptosis, inflammatory responses, and reducing immunoreactivity of NLRP3 and gasdermin D N terminus (GSDMD-N) in hippocampal microglia. In vitro, NLRP3 inflammasome- and pyroptosis-associated proteins and immunoreactivity of NLRP3, GSDMD-N, and interleukin-1ß were activated in BV2 microglial cells following lipopolysaccharide (LPS) stimulation. These effects were significantly suppressed in BV2 cells by SP600125 treatment. Furthermore, treatment with NLRP3 specific inhibitor, MCC950, attenuated microglia pyroptosis induced by LPS, but did not rescue LPS-induced increased expression of p-JNK. These results indicate that the JNK pathway is largely upstream of the NLRP3 inflammasome, which exerts a crucial regulatory impact on microglia pyroptosis and inflammatory responses, thus providing a promising avenue to prevent dNCR.

The Non-peptide Angiotensin-(1-7) Mimic AVE 0991 Attenuates Delayed Neurocognitive Recovery After Laparotomy by Reducing Neuroinflammation and Restoring Blood-Brain Barrier Integrity in Aged Rats.

Delayed neurocognitive recovery (dNCR) after surgery is a common postoperative complication in older adult patients. Our previous studies have demonstrated that cognitive impairment after surgery involves an increase in the brain renin-angiotensin system (RAS) activity, including overactivation of the angiotensin 2/angiotensin receptor-1 (Ang II/AT1) axis, which provokes the disruption of the hippocampal blood-brain barrier (BBB). Nevertheless, the potential role of the counter-regulatory RAS axis, the Ang-(1-7)/Mas pathway, in dNCR remains unknown. Using an aged rat model of dNCR, we dynamically investigated the activity of both axes of the RAS following laparotomy. AVE 0991, a nonpeptide analog of Ang-(1-7), was administered intranasally immediately after laparotomy. We found that the elevation of Ang II, induced by surgery was accompanied by a decrease of Ang-(1-7) in the hippocampus, but not in the circulation. Surgery also significantly downregulated hippocampal Mas receptor expression at 24 h postsurgery. Mas activation with intranasal AVE 0991 treatment significantly improved hippocampus-dependent learning and memory deficits induced by surgery. Furthermore, it attenuated hippocampal neuroinflammation, as shown by the decreased level of the microglial activation marker cluster of differentiation 11b (CD11b) and the decreased production of several inflammatory molecules. Along with these beneficial effects, the AVE 0991 treatment also alleviated the imbalance between matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-3 (TIMP-3), modulated the expression of occludin, and alleviated the IgG extravasation, thereby restoring the integrity of the BBB. In conclusion, these data indicate that activation of Mas by AVE 0991 attenuates dNCR after surgery by reducing neuroinflammation and restoring BBB integrity. Our findings suggest that the Ang-(1-7)/Mas pathway may be a novel therapeutic target for treating dNCR after surgery in older adult patients.

Ketamine and Propofol Protect Neuron Cells from Oxygen-Glucose Deprivation-Induced Injury through SAPK/JNK Signalling Pathway.

Ketamine and propofol are commonly used anaesthetic reagents. Recent research revealed that ketamine and propofol have an important role in cell survival. However, it remains unknown whether they affect the outcome of hypoxic-ischemic brain injury. To address this issue, we in this study investigated the effects of ketamine and propofol on the survival and proliferation of neuronal PC12 cells after exposure to oxygen-glucose deprivation- (OGD-) induced injury. PC12 cells were maintained under a 3-dimensional (3D) culture system to mimic a real physiological microenvironment. The cell injury was induced by 5% CO2 and 95% N2 for a different time point. MTT assay was used for the cell proliferation assay. The cell apoptosis was evaluated by annexin V and propidium iodide (PI) labeling, immunofluorescence staining, transmission electron microscopy (TEM), flow cytometry, and Western blot, respectively. Our results showed that PC12 cell apoptosis was significantly increased for up to 70% after the cells were treated with OGD for 24 hours and reduced to baseline at the 72-hour time point. However, pretreatment with ketamine and propofol significantly protected the cells from OGD-induced cell apoptosis, as evidenced by more expression of antiapoptotic Bcl-2 and lower expression of proapoptotic cleaved caspase-3, phosphor-SAPK/JNK, and phosphor-c-Jun than those of untreated control cells. Thus, we conclude that ketamine and propofol protected PC12 cells from OGD-induced cell apoptosis, at least partially through the SAPK/JNK signalling pathway.

Neurofilament degradation is involved in laparotomy-induced cognitive dysfunction in aged rats.

Excessive neuroinflammatory responses play important roles in the development of postoperative cognitive dysfunction (POCD). Neurofilaments (NFs) were essential to the structure of axon and nerve conduction; and the abnormal degradation of NFs were always accompanied with degenerative diseases, which were also characterized by excessive neuroinflammatory responses in brain. However, it is still unclear whether the NFs were involved in the POCD. In this study, the LC-MS/MS method was used to explore the neuroinflammatory response and NFs of POCD in aged rats. Moreover, trichostatin A (TSA), an inflammation-related drug, was selected to test whether it could improve the surgery-induced cognitive dysfunction, inflammatory responses and NFs. Evident cognitive dysfunction, excessive microglia activation, neuroinflammatory responses and upregulated NFs in hippocampus were observed in the POCD group. TSA pretreatment could significantly mitigate these changes. The KEGG analysis revealed that nine pathways were enriched in the TSA + surgery group (versus the surgery group). Among them, two signaling pathways were closely related with the changes of NFs proteins. In conclusion, surgery could impair the cognitive function and aggravate neuroinflammation and NFs. The TSA could significantly improve these changes which might be related to the activation of the "focal adhesion" and "ECM-receptor interaction" pathways.

Autophagy prevents hippocampal α-synuclein oligomerization and early cognitive dysfunction after anesthesia/surgery in aged rats.

Stress-induced α-synuclein aggregation, especially the most toxic species (oligomers), may precede synaptic and cognitive dysfunction. Under pathological conditions, α-synuclein is degraded primarily through the autophagic/lysosomal pathway. We assessed the involvement of autophagy in α-synuclein aggregation and cognitive impairment following general anesthesia and surgical stress. Autophagy was found to be suppressed in the aged rat hippocampus after either 4-h propofol anesthesia alone or 2-h propofol anesthesia during a laparotomy surgery. This inhibition of autophagy was accompanied by profound α-synuclein oligomer aggregation and neurotransmitter imbalances in the hippocampus, along with hippocampus-dependent cognitive deficits. These events were not observed 18 weeks after propofol exposure with or without surgical stress. The pharmacological induction of autophagy using rapamycin markedly suppressed α-synuclein oligomerization, restored neurotransmitter equilibrium, and improved cognitive behavior after prolonged anesthesia or anesthesia combined with surgery. Thus, both prolonged propofol anesthesia alone and propofol anesthesia during surgery impaired autophagy, which may have induced abnormal hippocampal α-synuclein aggregation and neurobehavioral deficits in aged rats. These findings suggest that the activation of autophagy and the clearance of pathological α-synuclein oligomers may be novel strategies to ameliorate the common occurrence of postoperative cognitive dysfunction.

Green synthesis of reusable multifunctional γ-Fe2O3/bentonite modified by doped TiO2 hollow spherical nanocomposite for removal of BPA.

Eco-friendly treatment of refractory pollutants in wastewater is still full of challenge in catalytic oxidation and adsorption. In this study, based on the concept of green chemistry, sulfur-doped titanium dioxide hollow spheres modified by surfactant loaded on magnetic bentonite (CST/γ-Fe2O3-BT) is synthesized in two steps, and bisphenol A (BPA) was chosen as the representative organic pollutant. These materials were characterized by means of XRD, FTIR, SEM, EDS, TEM, XPS, BET, and VSM techniques. The adsorption and photodegradation behavior of CST/γ-Fe2O3-BT were examined. The Langmuir isotherm exhibited a better fit with a maximum adsorption capacity of 77.36 mg/g. At pH 7, the reaction rate constant (k) of the BPA photocatalytic degradation by product was 0.00104 min-1, and the adsorption equilibrium constant (K) was 0.04034L/mg. In addition, the composite can be recovered from the reaction mixture by applying an external magnetic field due to the existence of the superparamagnetic iron oxide nanoparticles in the construct. The recovered particles retained their catalytic activity which the catalytic activity of the material still reached 91% of the first catalytic experiment after 5 repetitive experiments. Results infer that the material has excellent reusability. Thus, CST/γ-Fe2O3-BT is a significant candidate for the treatment of recalcitrant organic pollutants in wastewater.

Isoflurane-Induced Postoperative Neurovascular and Cognitive Dysfunction Is Associated with VEGF Overexpression in Aged Rats.

Postoperative cognitive dysfunction (POCD) is a common complication in older adults; however, its aetiology remains unclear. Although vascular endothelial growth factor (VEGF) is associated with blood-brain barrier (BBB) disorders and neurological disease, its role in POCD is unknown. Here, we investigated the effect of brain VEGF inhibition on isoflurane-induced cognitive impairment in an aged rat model of POCD. VEGF protein expression was increased in the hippocampus after isoflurane exposure, suggesting that inhalation anaesthesia induces hippocampal VEGF protein overexpression in aged rats. Pretreatment with 2 mg/kg RB-222, an anti-VEGF neutralizing antibody, may partially abolish the degradation of occludin protein in cerebral capillaries, thereby maintaining the ultrastructural and functional integrity of the hippocampal BBB. Inhibition of VEGF also significantly attenuated the isoflurane-induced cognitive deficits in the Morris water maze task. Together, our findings show, for the first time, that elevated expression of brain VEGF after isoflurane exposure contributes to POCD in aged rats. Therefore, therapeutic strategies involving VEGF should take into consideration its role in the pathogenesis of POCD.