In-situ synthesis Fe3C@C/rGO as matrix for high performance lithium-sulfur batteries at room and low temperatures.

People have been focusing on how to improve the specific capacity and cycling stability of lithium-sulfur batteries at room temperature, however, on some special occasions such as cold cities and aerospace fields, the operating temperature is low, which dramatically hinders the performance of batteries. Here, we report an iron carbide (Fe3C)/rGO composite as electrode host, the Fe3C nanoparticles in the composite have strong adsorption and high catalytic ability for polysulfide. The rGO makes the distribution of Fe3C nanoparticles more disperse, and this specific structure makes the deposition of Li2S more uniform. Therefore, it realizes the rapid transformation and high performance of lithium-sulfur batteries at both room and low temperatures. At room temperature, after 100 cycles at 1C current density, the reversible specific capacity of the battery can be stabilized at 889 ± 7.1 mAh/g. Even at -40 °C, in the first cycle battery still emits 542.9 ± 3.7 mAh/g specific capacity. This broadens the operating temperature for lithium-sulfur batteries and also provides a new idea for the selection of host materials for sulfur in low-temperature lithium-sulfur batteries.

Interannual precipitation variability dominates the growth of alpine grassland above-ground biomass at high elevations on the Tibetan Plateau.

The impact of global climate change on mountainous regions with significant elevational gaps is complex and often unpredictable. In particular, alpine grassland ecosystems, are experiencing changes in their spatial patterns along elevational gradients, which increases their vulnerability to degradation. Therefore, a more detailed understanding of spatiotemporal changes in alpine grassland productivity along elevational gradients and an elevation-dependent characterization of the effects of climatic variables on grassland productivity dynamics are essential. Thus, we conducted a study in the Tibetan Plateau, where we collected 2251 above-ground biomass (AGB) observations collected from 1986 to 2020. Mean annual temperature (TMP), annual precipitation (PRE), interannual precipitation variability (CVP), and snowmelt (SNMM) were chosen as influential variables. Using the Random Forest algorithm, we generated an AGB raster dataset covering the period 1989-2020 based on earth observation data at 30 m resolution to examine the dynamics of alpine grasslands and their response to climate change with respect to elevation. The results showed that the AGB of alpine grassland on the Tibetan Plateau was 49.17 g/m2. We observed an increasing trend in grassland AGB at high elevations, with a growth rate of about 0.28 g/m2 per year within the interval of 3100-4800 m. However, above the elevation of approximately 4400-4600 m, we observed a decoupling trend between grassland AGB and TMP. Moreover, at most elevations, the proportion of maximum partial correlation coefficients for CVP, PRE, and SNMM surpassed that of TMP. We found the dominant role of precipitation variability on grassland AGB dynamics, with 22.80 % and 18.86 % for CVP+ and CVP-, respectively. The proportion of CVP+ did not vary much at different elevations, whereas the proportion of CVP- increased with elevation, varying between 12.85 and 30.25 %. In the future, precipitation on the Tibetan plateau is expected to increase, potentially reversing its original positive impact.

Declined terrestrial ecosystem resilience.

Terrestrial ecosystem resilience is crucial for maintaining the structural and functional stability of ecosystems following disturbances. However, changes in resilience over the past few decades and the risk of future resilience loss under ongoing climate change are unclear. Here, we identified resilience trends using two remotely sensed vegetation indices, analyzed the relative importance of potential driving factors to resilience changes, and finally assessed the risk of future resilience loss based on the output data of eight models from CMIP6. The results revealed that more than 60% of the ecosystems experienced a conversion from an increased trend to a declined trend in resilience. Attribution analysis showed that the most important driving factors of declined resilience varied regionally. The declined trends in resilience were associated with increased precipitation variability in the tropics, decreased vegetation cover in arid region, increased temperature variability in temperate regions, and increased average temperature in cold regions. CMIP6 reveals that terrestrial ecosystems under SPP585 are expected to experience more intense declines in resilience than those under SSP126 and SSP245, particularly in cold regions. These results highlight the risk of continued degradation of ecosystem resilience in the future and the urgency of climate mitigation actions.

Thermally Activated Delayed Fluorescent Binuclear Copper(I) Alkynyl Complexes with Cuprophilic Interactions.

Copper(I)-based thermally activated delayed fluorescence (TADF) emitters have been conceived to be promising candidates for display and lighting applications because of their multifarious structures and strong photoluminescence. Herein a string of binuclear Cu(I) complexes bearing pronounced cuprophilic interactions have been designed and synthesized. [Cu2(dppb)2(µ2-η1-C≡C-Ph)2] (1 a) and [Cu2(dppb)2(µ2-η1-C≡C-PPXZ)2] (1 b) display photoluminescence quantum yields of up to 67 % in doped films and solid states via TADF and exhibit reversible bicolor luminescence switching upon mechanical stimuli. Computational studies manifest that the metal-to-ligand charge transfer predominant transitions ensure a small energy splitting (ΔEST) between the lowest singlet (S1) and triplet (T1) excited states and cuprophilic interactions promote the spin-orbit coupling (SOC), favoring the reverse intersystem crossing (RISC) process. This study provides a new strategy for the construction of stimuli-responsive metal-based TADF materials.

RORα is required for expansion and memory maintenance of ILC1s via a lymph node-liver axis.

Type 1 innate lymphoid cells (ILC1s) possess adaptive immune features, which confer antigen-specific memory responses against haptens and viruses. However, the transcriptional regulation of memory ILC1 responses is currently not known. We show that retinoic acid receptor-related orphan receptor alpha (RORα) has high expression in memory ILC1s in murine contact hypersensitivity (CHS) models. RORα deficiency diminishes ILC1-mediated CHS responses significantly but has no effect on memory T cell-mediated CHS responses. During sensitization, RORα promotes sensitized-ILC1 expansion by suppressing expression of cell-cycle repressors in draining lymph nodes. RORα programs gene-expression patterns related to cell survival and is required for the long-term maintenance of memory ILC1s in the liver. Our findings reveal RORα to be a key transcriptional factor for sensitized-ILC1 expansion and long-term maintenance of memory ILC1s.

Polysaccharides from Phellinus linteus attenuate type 2 diabetes mellitus in rats via modulation of gut microbiota and bile acid metabolism.

Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disorder. Polysaccharides from Phellinus linteus (PLP) have been found to have anti-diabetes effects, but the mechanism has not been elucidated. The purpose of this study was to investigate the mechanism of PLP on T2DM through the gut microbiota and bile acids metabolism. The T2DM rat model was induced by a high-fat high-carbohydrate (HFHC) diet and streptozocin (30 mg/kg). We found that PLP ameliorated diabetes symptoms. Besides, PLP intervention increased the abundance of g_Bacteroides, g_Parabacteroides, and g_Alistioes, which are associated with the biosynthesis of short-chain fatty acids (SCFAs) and bile acids (BAs) metabolism. Meanwhile, untargeted and targeted metabolomics indicated that PLP could regulate the composition of BAs and increase the levels of SCFAs. Real-time quantitative PCR (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA) were performed to analyze the expression levels of BAs metabolism enzymes in the liver. Finally, the results of correlation analysis and Glucagon-like peptide-1 (GLP-1) showed that PLP stimulated the release of GLP-1 by regulating SCFAs and BAs. In conclusion, this study demonstrated that PLP can regulate gut microbiota and BAs metabolism to promote GLP-1 secretion, thereby increasing insulin release, decreasing blood glucose and attenuating T2DM.

Baicalein ameliorates cognitive impairment of vascular dementia rats via suppressing neuroinflammation and regulating intestinal microbiota.

Neuroinflammation induced by chronic cerebral hypoperfusion (CCH) plays a crucial role in the pathophysiologic mechanisms of vascular dementia (VD). A growing body of research has found that intestinal microbiota is associated with a variety of central nervous system disorders and that there is a relationship between intestinal microbiota dysbiosis and cognitive dysfunction and inflammatory responses. Baicalein belongs to the class of flavonoids and has a variety of biological functions, including anti-inflammatory, antioxidant and anti-apoptotic. Baicalein has a significant improvement in memory and learning, and can be used as a potential drug for the protection and treatment of central nervous system disorders. Whether baicalein has an ameliorative effect on cognitive impairment in VD, and whether its mechanism is related to the inhibition of inflammatory response and regulation of intestinal microbiota has not been reported. We used bilateral common carotid artery occlusion (BCCAO) to establish a VD rat model. Morris water maze (MWM) test showed that baicalein improved cognitive dysfunction in VD rats. We applied HE staining, immunofluorescence and ELISA to observe that baicalein treatment significantly improved CCH-induced neuronal damage in the CA1 region of the hippocampus, and reduced glial cell activation and release of pro-inflammatory factors. Western blot showed that baicalein inhibited the activation of the TLR4/MyD88/NF-κB signaling pathway in VD rats. We applied 16 S rDNA sequencing to analyze the composition of the intestinal microbiota. The results showed that baicalein modulated the diversity and composition of the intestinal microbiota, and suppressed the relative abundance of inflammation-associated microbiota in VD rats. In conclusion, this study found that baicalein ameliorated cognitive impairment, attenuated hippocampal inflammatory responses, inhibited the TLR4/MyD88/NF-κB signaling pathway, and modulated intestinal microbiota in VD rats.

Mettl3-Mediated m6A Methylation Controls Pancreatic Bipotent Progenitor Fate and Islet Formation.

The important role of m6A RNA modification in ß-cell function has been established; however, how it regulates pancreatic development and endocrine differentiation remains unknown. Here, we generated transgenic mice lacking RNA methyltransferase-like 3 (Mettl3) specifically in Pdx1+ pancreatic progenitor cells and found the mice with the mutation developed hyperglycemia and hypoinsulinemia at age 2 weeks, along with an atrophic pancreas, reduced islet mass, and abnormal increase in ductal formation. At embryonic day 15.5, Mettl3 deletion had caused a significant loss of Ngn3+ endocrine progenitor cells, which was accompanied by increased Sox9+ ductal precursor cells. We identified histone deacetylase 1 (Hdac1) as the critical direct m6A target in bipotent progenitors, the degeneration of which caused abnormal activation of the Wnt/Notch signaling pathway and blocked endocrine differentiation. This transformation could be manipulated in embryonic pancreatic culture in vitro through regulation of the Mettl3-Hdac1-Wnt/Notch signaling axis. Our finding that Mettl3 determines endocrine lineage by modulating Hdac1 activity during the transition of bipotent progenitors might help in the development of targeted endocrine cell protocols for diabetes treatment.

Bile acids metabolism involved in the beneficial effects of Danggui Shaoyao San via gut microbiota in the treatment of CCl4 induced hepatic fibrosis.

ETHNOPHARMACOLOGICAL RELEVANCE: Danggui Shaoyao San (DSS) is a traditional Chinese medicine (TCM) first recorded in the Synopsis of the Golden Chamber. DSS has proven efficacy in treating hepatic fibrosis (HF). However, the effects and mechanisms of DSS on HF are not clear. AIM OF THE STUDY: To investigate the effect of DSS on HF via gut microbiota and its metabolites (SCFAs, BAs). MATERIALS AND METHODS: HF rats were induced with CCl4 and treated with DSS. Firstly, the therapeutic efficacy of DSS in HF rats and the protection of gut barrier were assessed. Then, 16S rRNA gene sequencing and untargeted fecal metabolomics preliminarily explored the mechanism of DSS in treating HF, and identified different microbiota and metabolic pathways. Finally, targeted metabolomics and RT-qPCR were used to further validate the mechanism of DSS for HF based on the metabolism of SCFAs and BAs. RESULTS: After 8 weeks of administration, DSS significantly reduced the degree of HF. In addition, DSS alleviated inflammation in the ileum and reduced the levels of LPS and D-lactate. Furthermore, DSS altered the structure of gut microbiota, especially Veillonella, Romboutsia, Monoglobus, Parabacteroides, norank_f_Coriobacteriales_Incertae_Sedis. These bacteria have been linked to the production of SCFAs and the metabolism of BAs. Untargeted metabolomics suggested that DSS may play a role via BAs metabolism. Subsequently, targeted metabolomics and RT-qPCR further confirmed the key role of DSS in increasing SCFAs levels and regulating BAs metabolism. CONCLUSIONS: DSS can alleviate CCl4-induced HF and protect the gut barrier. DSS may exert its beneficial effects on HF by affecting the gut microbiota and its metabolites (SCFAs, BAs).

Synthesis of Low-Cost and High-Performance Dual-Atom Doped Carbon-Based Materials with a Simple Green Route as Anodes for Sodium-Ion Batteries.

Sodium-ion batteries (SIBs) are promising alternatives to replace lithium-ion batteries as future energy storage batteries because of their abundant sodium resources, low cost, and high charging efficiency. In order to match the high energy capacity and density, designing an atomically doped carbonous material as the anode is presently one of the important strategies to commercialize SIBs. In this work, we report the preparation of high-performance dual-atom-doped carbon (C) materials using low-cost corn starch and thiourea (CH4N2S) as the precursors. The electronegativity and radii of the doped atoms and C are different, which can vary the embedding properties of sodium ions (Na+) into/on C. As sulfur (S) can effectively expand the layer spacing, it provides more channels for embedding and de-embedding Na+. The synergistic effect of N and S co-doping can remarkably boost the performance of SIBs. The capacity is preserved at 400 mAh g -1 after 200 cycles at 500 mA g-1; more notably, the initial Coulombic efficiency is 81%. Even at a high rate of high current of 10 A g-1, the cell capacity can still reach 170 mAh g-1. More importantly, after 3000 cycles at 1 A g-1, the capacity decay is less than 0.003% per cycle, which demonstrates its excellent electrochemical performance. These results indicate that high-performance carbon materials can be prepared using low-cost corn starch and thiourea.

Soil moisture determines the recovery time of ecosystems from drought.

Recovery time, the time it takes for ecosystems to return to normal states after experiencing droughts, is critical for assessing the response of ecosystems to droughts; however, the spatial dominant factors determining recovery time are poorly understood. We identify the global patterns of terrestrial ecosystem recovery time based on remote sensed vegetation indices, analyse the affecting factors of recovery time using random forest regression model, and determine the spatial distribution of the dominant factors of recovery time based on partial correlation. The results show that the global average recovery time is approximately 3.3 months, and that the longest recovery time occurs in mid-latitude drylands. Analysis of affecting factors of recovery time suggests that the most important environmental factor affecting recovery time is soil moisture during the recovery period, followed by temperature and vapour pressure deficit (VPD). Recovery time shortens with increasing soil moisture and prolongs with increasing VPD; however, the response of recovery time to temperature is nonmonotonic, with colder or hotter temperatures leading to longer recovery time. Soil moisture dominates the drought recovery time over 58.4% of the assessed land area, mostly in the mid-latitudes. The concern is that soil moisture is projected to decline in more than 65% regions in the future, which will lengthen the drought recovery time and exacerbate drought impacts on terrestrial ecosystems, especially in southwestern United States, the Mediterranean region and southern Africa. Our research provides methodological insights for quantifying recovery time and spatially identifies dominant factors of recovery time, improving our understanding of ecosystem response to drought.

Aging Impairs Adaptive Unfolded Protein Response and Drives Beta Cell Dedifferentiation in Humans.

CONTEXT: Diabetes is an age-related disease; however, the mechanism underlying senescent beta cell failure is still unknown. OBJECTIVE: The present study was designed to investigate whether and how the differentiated state was altered in senescent human beta cells by excluding the effects of impaired glucose tolerance. METHODS: We calculated the percentage of hormone-negative/chromogranin A-positive endocrine cells and evaluated the expressions of forkhead box O1 (FoxO1) and Urocortin 3 (UCN3) in islets from 31 nondiabetic individuals, divided into young (<40 years), middle-aged (40-60 years) and elderly (>60 years) groups. We also assessed adaptive unfolded protein response markers glucose-regulated protein 94 (GRP94), and spliced X-box binding protein 1 (XBP1s) in senescent beta cells and their possible contributions to maintaining beta cell identity and differentiation state. RESULTS: We found an almost 2-fold increase in the proportion of dedifferentiated cells in elderly and middle-aged groups compared with the young group (3.1 ± 1.0% and 3.0 ± 0.9% vs 1.7 ± 0.5%, P < .001). This was accompanied by inactivation of FoxO1 and loss of UCN3 expression in senescent human beta cells. In addition, we demonstrated that the expression levels of adaptive unfolded protein response (UPR) components GRP94 and XBP1s declined with age. In vitro data showed knockdown GRP94 in Min6-triggered cells to dedifferentiate and acquire progenitor features, while restored GRP94 levels in H2O2-induced senescent Min6 cells rescued beta cell identity. CONCLUSION: Our finding highlights that the failure to establish proper adaptive UPR in senescent human beta cells shifts their differentiated states, possibly representing a crucial step in the pathogenesis of age-related beta cell failure.

Resveratrol reduces inflammatory response and detrimental effects in chronic cerebral hypoperfusion by down-regulating stimulator of interferon genes/TANK-binding kinase 1/interferon regulatory factor 3 signaling.

Inflammatory responses induced by chronic cerebral hypoperfusion (CCH) play a critical role in the progression of vascular dementia. Stimulator of interferon genes (STING) signaling function as a key mediator of inflammation and immunological responses in the central nervous system (CNS), and resveratrol (RES) exerts potent anti-inflammatory effects. However, the role of STING signaling and the relationship between RES and STING signaling in persistent hypoperfusion-induced cerebral inflammation remain unclear. In this study, Sprague-Dawley rats were subjected to either Sham or bilateral common carotid artery occlusion (2VO) surgery and received RES or vehicle daily by intraperitoneal injection for 4 or 8 weeks. Morris's water maze was used for the analysis of cognitive function. The neuroinflammatory responses in white matter and hippocampus of the rat brain were assessed by Western blot, Immunofluorescence staining, and qRT-PCR analyses. Myelin integrity, neutrophil infiltration, and microglia proliferation were assessed by Immunohistochemistry and histologic analysis. We demonstrated that after CCH, neurons, microglia, and astrocyte under endoplasmic reticulum (ER) stress upregulated the expression of STING, TANK-binding kinase 1 (TBK1), and the transcription factor interferon regulatory factor 3 (IRF3), as well as translocation of IRF3 into the nucleus. These were accompanied by infiltration of neutrophils, activation of microglia, and overproduction of proinflammatory mediators. Improvements in cognitive deficits were related to reduced hippocampal neuronal cell death and increased myelin integrity in RES-treated rats. The neuroprotective effects of RES were associated with suppression of the expression of tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecule 1 (ICAM-1), VCAM-1, interferon-ß (IFN-ß), and IL-1ß, likely through mitigation of the STING/TBK1/IRF3 pathway. These inhibitory effects exerted by RES also inhibited the levels of myeloperoxidase, reduced excess expression of reactive astrocytes, and activated microglia. In conclusion, the STING/TBK1/IRF3 axis may be critical for proinflammatory responses in cerebral tissue with persistent hypoperfusion, and RES exerts its anti-inflammatory effects by suppressing STING/TBK1/IRF3 signaling.

Formononetin attenuates Aß25-35-induced adhesion molecules in HBMECs via Nrf2 activation.

Brain vascular inflammation plays a crucial role in the pathogenesis of Alzheimer's disease (AD). As a central pathogenic factor in AD, the extracellular buildup of amyloid-ß (Aß) induces brain microvascular endothelial cells activation, impairs endothelial structure and function. Formononetin (FMN) has been reported to protect against Alzheimer's disease (AD) and attenuates vascular inflammation in atherosclerosis. However, its involvement in regulating vascular inflammation of AD has not been investigated. In the study, we found that FMN significantly attenuates Aß25-35-induced expression of adhesion molecules, including intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the human brain microvascular endothelial cells (HBMECs), suggesting that FMN inhibits Aß25-35-induced brain endothelial cells inflammatory response. Moreover, we observed that FMN attenuates Aß25-35-induced translocation of NFκB (p65) into the nucleus of HBMECs, and found that FMN treatment induces Nrf2 expression and attenuates Nrf2-Keap1 association in a dose-dependent manner in HBMECs. Furthermore, we demonstrated that Nrf2 silencing significantly attenuates FMN-reduced NFκB (p65) activation and nuclear translocation. Lastly, our results showed that FMN treatment attenuates Aß25-35-induced adhesion of THP-1 cell to endothelial cell monolayer. Collectively, these findings suggest that FMN attenuates Aß25-35-induced activation in human brain microvascular endothelial cells, which at least in part was mediated through Nrf2 pathways.

Requirement of RORα for maintenance and antitumor immunity of liver-resident natural killer cells/ILC1s.

BACKGROUD AND AIMS: Liver type 1 innate lymphoid cells (ILC1s), also known as liver-resident natural killer (LrNK) cells, comprise a high proportion of total hepatic ILCs. However, factors regulating their maintenance and function remain unclear. APPROACH AND RESULTS: In this study, we found high expression of retinoid-related orphan nuclear receptor alpha (RORα) in LrNK cells/ILC1s. Mice with conditional ablation of retinoid-related orphan nuclear receptor alpha (Rorα) in LrNK cells/ILC1s and conventional natural killer (cNK) cells had decreased LrNK cells/ILC1s but normal numbers of cNK cells. RORα-deficient LrNK cells/ILC1s displayed increased apoptosis and significantly altered transcriptional profile. Using a murine model of colorectal cancer liver metastasis, we found that RORα conditional deficiency resulted in more aggressive liver tumor progression and impaired effector molecule expression in LrNK cells/ILC1s. Consequently, treatment with the RORα agonist efficiently limited liver metastases and promoted effector molecule expression of LrNK cells/ILC1s. CONCLUSIONS: This study reveals a role of RORα in LrNK cell/ILC1 maintenance and function, providing insights into the harnessing of LrNK cell/ILC1 activity in the treatment of liver cancer.

On-Site, On-Demand 3D-Printed Nasopharyngeal Swabs to Improve the Access of Coronavirus Disease-19 Testing.

Diagnostic testing that facilitates containment, surveillance, and treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), or future respiratory viruses, depends on a sample collection device that efficiently collects nasopharyngeal tissue and that can be manufactured on site when an outbreak or public health emergency is declared by a government. Here two novel stereolithography-based three-dimensional (3D)-printed nasopharyngeal swabs are reported which are made using a biocompatible and sterilizable photoresist. Such swabs are readily manufactured on-site and on-demand to ensure availability, if supply chain shortages emerge. Additionally, the 3D-printed swabs easily adapt to current workflow and testing procedures in hospital clinical laboratories to allow for effortless scaling up of test kits. Finally, the 3D-printed nasopharyngeal swabs demonstrate concordant SARS-CoV-2 testing results between the 3D-printed swabs and the COPAN commercial swabs, and enable detection of SARS-CoV-2 in clinical samples obtained from autopsies.

METTL3-mediated m6A RNA methylation promotes the anti-tumour immunity of natural killer cells.

Natural killer (NK) cells exert critical roles in anti-tumor immunity but how their functions are regulated by epitranscriptional modification (e.g., N6-methyladenosine (m6A) methylation) is unclear. Here we report decreased expression of the m6A "writer" METTL3 in tumor-infiltrating NK cells, and a positive correlation between protein expression levels of METTL3 and effector molecules in NK cells. Deletion of Mettl3 in NK cells alters the homeostasis of NK cells and inhibits NK cell infiltration and function in the tumor microenvironment, leading to accelerated tumor development and shortened survival in mice. The gene encoding SHP-2 is m6A modified, and its protein expression is decreased in METTL3-deficient NK cells. Reduced SHP-2 activity renders NK cells hyporesponsive to IL-15, which is associated with suppressed activation of the AKT and MAPK signaling pathway in METTL3-deficient NK cells. These findings show that m6A methylation safeguards the homeostasis and tumor immunosurveillance function of NK cells.

Shikonin Attenuates Chronic Cerebral Hypoperfusion-Induced Cognitive Impairment by Inhibiting Apoptosis via PTEN/Akt/CREB/BDNF Signaling.

Shikonin (SK) exerts neuroprotective effects; however, to date, its protective effect against chronic cerebral hypoperfusion- (CCH-) induced vascular dementia (VaD) has not been investigated. Therefore, the current study investigated whether SK could mitigate the cognitive deficits caused by CCH. The effects of SK treatment on the PTEN/Akt/CREB/BDNF signaling pathway and apoptosis in hippocampal neurons were examined in a rat model of VaD established via bilateral common carotid artery occlusion (BCCAO). Fifty-two rats were randomly divided into 4 groups: sham, vehicle, SK-L (10 mg/kg SK per day), and SK-H (25 mg/kg SK per day). SK was regularly administered by gavage for 2 weeks. The results of the water maze test revealed that the escape latency in the vehicle group was significantly longer than that in the sham group, and rats in the vehicle group spent a smaller proportion of time in the target quadrant than those in the sham group. SK treatment reduced the escape latencies and increased the proportion of time spent in the target quadrant. Nissl staining showed morphological damage in the CA1 areas of the hippocampus in the vehicle group. SK treatment alleviated the injuries to hippocampal neurons. Western blot analysis showed higher p-PTEN and lower p-Akt, p-CREB, and BDNF expression in the vehicle group than in the sham group. SK administration reversed the upregulation of p-PTEN and the downregulation of p-Akt, p-CREB, and BDNF. The number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling- (TUNEL-) positive cells in the hippocampal CA1 region of the vehicle group was significantly increased. Treatment with SK decreased the number of positive cells. Furthermore, as marker proteins of apoptosis, bcl-2 expression was decreased and bax expression was increased; thus, the ratio of bcl-2/bax was decreased in the vehicle group. SK treatment upregulated the expression of bcl-2 and downregulated the expression of bax, thereby elevating the bcl-2/bax ratio. Moreover, the aforementioned effects of SK were dose-dependent. The effect of 25 mg/kg per day was more obvious than that of 10 mg/kg per day. In conclusion, SK inhibited hippocampal neuronal apoptosis to protect against CCH-induced injury by regulating the PTEN/Akt/CREB/BDNF signaling pathway, consequently improving cognitive impairment.

Efficient removal of emerging contaminant sulfamethoxazole in water by ozone coupled with calcium peroxide: Mechanism and toxicity assessment.

Sulfamethoxazole (SMX) is a widely distributed emerging contaminant, which will bring serious harm to ecology and human health. Herein, evaluation of ozone (O3) coupled with calcium peroxide (CaO2) for SMX elimination was carried out. The results showed that CaO2 could promote SMX elimination in O3 system. The removal efficiency was improved from 65.6% to 73.9% when the CaO2 dosage was 0.06 g L-1. O3 dosage of 0.55 g h-1 was beneficial to SMX degradation. With decrease of initial SMX concentration, the removal of SMX firstly enhanced and then declined. Compared with alkaline, acidic and neutral conditions were favorable for SMX degradation. ROS including ·OH, ·O2- and 1O2 play critical role for SMX degradation. Synergetic effect could be established between O3 and CaO2, which encouraged formation of ·OH and accelerated SXM decomposition. The total organic carbon (TOC) and chemical oxygen demand (COD) were all declined after O3/CaO2 treatment. According to results of liquid chromatography-mass spectrometry (LC-MS) and references, four major pathways were proposed. The O3/CaO2 technology was also suitable for practical wastewater treatment. QSAR calculation and seed germination experiment showed that toxicity of the treatment solution was alleviated after O3/CaO2 treatment.