Transformation of A1/A2 Astrocytes Participates in Brain Ischemic Tolerance Induced by Cerebral Ischemic Preconditioning via Inhibiting NDRG2.

Cerebral ischemic preconditioning (CIP) has been shown to improve brain ischemic tolerance against subsequent lethal ischemia. Reactive astrocytes play important roles in cerebral ischemia-reperfusion. Recent studies have shown that reactive astrocytes can be polarized into neurotoxic A1 phenotype (C3d) and neuroprotective A2 phenotype (S100A10). However, their role in CIP remains unclear. Here, we focused on the role of N-myc downstream-regulated gene 2 (NDRG2) in regulating the transformation of A1/A2 astrocytes and promoting to brain ischemic tolerance induced by CIP. A Sprague Dawley rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) was used. Rats were divided into the following six groups: (1) sham group; (2) CIP group: left middle cerebral artery was blocked for 10 min; (3) MCAO/R group: left middle cerebral artery was blocked for 90 min; (4) CIP + MCAO/R group: CIP was performed 72 h before MCAO/R; (5) AAV-NDRG2 + CIP + MCAO/R group: adeno-associated virus (AAV) carrying NDRG2 was administered 14 days before CIP + MCAO/R; (6) AAV-Ctrl + CIP + MCAO/R group: empty control group. The rats were subjected to neurological evaluation 24 h after the above treatments, and then were sacrificed for 2, 3, 5-triphenyltetraolium chloride staining, thionin staining, immunofluorescence and western blot analysis. In CIP + MCAO/R group, the neurological deficit scores decreased, infarct volume reduced, and neuronal density increased compared with MCAO/R group. Notably, CIP significantly increased S100A10 expression and the number of S100A10+/GFAP+ cells, and also increased NDRG2 expression. MCAO/R significantly decreased S100A10 expression and the number of S100A10+/GFAP+ cells yet increased C3d expression and the number of C3d+/GFAP+ cells and NDRG2 expression, and these trends were reversed by CIP + MCAO/R. Furthermore, over-expression of NDRG2 before CIP + MCAO/R, the C3d expression and the number of C3d+/GFAP+ cells increased, while S100A10 expression and the number of S100A10+/GFAP+ cells decreased. Meanwhile, over-expression of NDRG2 blocked the CIP-induced brain ischemic tolerance. Taken together, these results suggest that CIP exerts neuroprotective effects against ischemic injury by suppressing A1 astrocyte polarization and promoting A2 astrocyte polarization via inhibiting NDRG2 expression.

Mechanical strength changes of combustible municipal solid waste components during their early pyrolysis stage and mechanism analysis.

Implementation of municipal solid waste (MSW) source segregation leads to a more convenient recycle of combustible MSW components. Textiles, plastics and papers are commonly available combustible components in MSW. Their shredding is conducive to resources recovery. But these components usually have high tensile strengths and are difficult to shred. To understand their mechanical strength changes in their early pyrolysis stage will help to address this problem. In this study, a universal electronic testing machine was used to determine the breaking strengths of the materials including cotton towel, polyethylene glycol terephthalate (PET), ivory board (IB), kraft paper (KP) and wool scarf in the temperature range of 30-250°C under N2 atmosphere, and the mechanisms of their strength changes were explored. The reaction force field molecular dynamics (ReaxFF-MD) simulation was used to explain the decomposition behaviours of different sugar groups of hemicellulose in cotton and paper and the change of van der Waals energy of wool during their early pyrolysis stages. The results showed that breaking strengths of all the combustible MSW components reduced as the temperature increased. The breaking strength of PET was found to have the highest descent rate with increasing temperature, then the descent rates of wool and cotton came as the second and third, respectively. Compared with cotton, the breaking strengths of KP and IB decreased more slowly. As the temperature increased, the breaking strength of cotton reduced mainly due to the decomposition of the glucuronic acid in hemicellulose, and the reduction was characterized by CO2 release. The breaking strength reduction of PET was caused by its molecular chain being relaxed. The breaking strength reduction of wool was firstly caused by the decrease in the van der Waals energy between its molecules, and then caused by molecular chain breaking. In addition, in order to understand the influence of material size on the breaking strength change during thermal treatment, the breaking strengths of cotton yarn bundles were correlated with their yarn number and temperature. This study lays the foundation for understanding changes in mechanical strengths of combustible MSW components during their early pyrolysis stage.

Effects of monolaurin on intestinal barrier, blood biochemical profile, immunity and antioxidant function in porcine epidemic diarrhoea virus-infected piglets.

The effects of monolaurin (ML) on the health of piglets infected with porcine epidemic diarrhoea virus (PEDV) have not been fully understood. This study aimed to investigate its role in blood biochemical profile, intestinal barrier function, antioxidant function and the expression of antiviral genes in piglets infected with PEDV. Thirty-two piglets were randomly divided into four groups: control group, ML group, PEDV group and ML + PEDV group. Piglets were orally administrated with ML at a dose of 100 mg/kg·BW for 7 d before PEDV infection. Results showed that PEDV infection significantly decreased D-xylose content and increased intestinal fatty acid-binding protein content, indicating that PEDV infection destroyed intestinal barrier and absorption function. While it could be repaired by ML administration. Moreover, ML administration significantly decreased plasma blood urea nitrogen and total protein content upon PEDV infection. These results suggested ML may increase protein utilisation efficiency. ML administration significantly decreased the number of large unstained cells and Hb and increased the number of leucocytes and eosinophils in the blood of PEDV-infected piglets, indicating ML could improve the immune defense function of the body. In the presence of PEDV infection, ML administration significantly increased superoxide dismutase and catalase activities in blood and colon, respectively, indicating ML could improve antioxidant capacity. Besides, ML administration reversed the expression of ISG15, IFIT3 and IL-29 throughout the small intestine and Mx1 in jejunum and ileum, indicating the body was in recovery from PEDV infection. This study suggests that ML could be used as a kind of feed additive to promote swine health upon PEDV infection.

STAT4-Mediated Klotho Up-Regulation Contributes to the Brain Ischemic Tolerance by Cerebral Ischemic Preconditioning via Inhibiting Neuronal Pyroptosis.

Our previous study has proved that the Klotho up-regulation participated in cerebral ischemic preconditioning (CIP)-induced brain ischemic tolerance. However, the exact neuroprotective mechanism of Klotho in CIP remains unclear. We explored the hypothesis that STAT4-mediated Klotho up-regulation contributes to the CIP-induced brain ischemic tolerance via inhibiting neuronal pyroptosis. Firstly, the expressions of pyroptosis-associated proteins (i.e., NLRP3, GSDMD, pro-caspase-1, and cleaved caspase-1) in hippocampal CA1 region were determined during the process of brain ischemic tolerance. We found the expression of pyroptosis-associated proteins was significantly up-regulated in the ischemic insult (II) group, and showed no significant changes in the CIP group. The expression level of each pyroptosis-associated proteins was lower in the CIP + II group than that in the II group. Inhibition of Klotho expression increased the expression of pyroptosis-associated proteins in the CIP + II group and blocked the CIP-induced brain ischemic tolerance. Injection of Klotho protein decreased the expression of pyroptosis-associated proteins in the II group, and protected neurons from ischemic injury. Secondly, the transcription factor STAT4 of Klotho was identified by bioinformatic analysis. Double luciferase reporter gene assay and chromatin immunoprecipitation assay showed STAT4 can bind to the site between nt - 881 and - 868 on the Klotho promoter region and positively regulates Klotho expression. Moreover, we found CIP significantly enhanced the expression of STAT4. Knockdown STAT4 suppressed Klotho up-regulation after CIP and blocked the CIP-induced brain ischemic tolerance. Collectively, it can be concluded that STAT4-mediated the up-regulation of Klotho contributed to the brain ischemic tolerance induced by CIP via inhibiting pyroptosis.

The Role of Astrocytic Mitochondria in the Pathogenesis of Brain Ischemia.

The morbidity rate of ischemic stroke is increasing annually with the growing aging population in China. Astrocytes are ubiquitous glial cells in the brain and play a crucial role in supporting neuronal function and metabolism. Increasing evidence shows that the impairment or loss of astrocytes contributes to neuronal dysfunction during cerebral ischemic injury. The mitochondrion is increasingly recognized as a key player in regulating astrocyte function. Changes in astrocytic mitochondrial function appear to be closely linked to the homeostasis imbalance defects in glutamate metabolism, Ca2+ regulation, fatty acid metabolism, reactive oxygen species, inflammation, and copper regulation. Here, we discuss the role of astrocytic mitochondria in the pathogenesis of brain ischemic injury and their potential as a therapeutic target.

Adsorption of pyrolysis oil model compound (phenol) with plasma-modified hydro-chars and mechanism exploration.

Phenol is one of the important ingredients of pyrolysis oil, contributing to the high biotoxicity of pyrolysis oil. To promote the degradation and conversion of phenol during anaerobic digestion, cheap hydro-chars with high phenol adsorption capacity were produced. The phenol adsorption capabilities of the plain hydro-char, plasma modified hydro-char at 25 °C (HC-NH3-P-25) and 500 °C (HC-NH3-P-500) were evaluated, and their adsorption kinetics and thermodynamics were explored. Experimental results indicate that the phenol adsorption capability of HC-NH3-P-500 was the highest. The phenol adsorption kinetics of all samples followed the pseudo-second-order equation and interparticle diffusion model, indicating that the adsorption rate of phenol was controlled by interparticle diffusion and chemistry adsorption simultaneously. By DFT calculations, π-π stacking and hydrogen bond are the main interactions for phenol adsorption. It was observed that an enriched graphite N content decreased the average vertical distance between hydro-chars and phenol in π-π stacking complex, from 3.5120 to 3.4532 Å, causing an increase in the negative adsorption energy between phenol and hydro-char from 13.9330 to 23.4181 kJ/mol. For hydrogen bond complex, the average vertical distance decreased from 3.4885 to 3.3386 Å due to the increase in graphite N content; causing the corresponding negative adsorption energy increased from 19.0233 to 19.9517 kJ/mol. Additionally, the presence of graphite N in the hydro-char created a positive diffusion region and enhanced the electron density between hydro-char and phenol. Analyses suggest that enriched graphite N contributed to the adsorption complex stability, resulting in an improved phenol adsorption capacity.

Ecological risk assessment of heavy metals in bottom ashes generated by small-scale thermal treatment furnaces for domestic waste in villages and towns of China.

Small-scale Solid Waste Thermal Treatment (SSWTT) is prevalent in remote Chinese locations. However, the ecological threats associated with heavy metals in resultant bottom ash remain undefined. This research study scrutinized such ash from eight differing sites, assessing heavy metal content, chemical form, and leaching toxicity. Most bottom ash samples met soil contamination standards for development land (GB36600-2018). However, levels of As, Cd, Cr, Cu, Ni, Pb, and Zn in some samples exceeded agricultural land standards GB15618-2018) by 1591%, 64,478%, 1880%, 3886%, 963%, 1110%, and 2011% respectively. Additionally, the As and Cd contents surpassed the construction land control limit value by 383% and 13% respectively. The mean values of the combined oxidizable and residual fraction (F3 + F4) for each heavy metal in all samples exceeded 65%, with Cr, Cu, Ni, and Pb reaching over 95%. All sample leaching concentrations, obtained via the HJ/T 299 procedure, were less than limits set by the identification standards for hazardous wastes (GB5085.3-2007). However, only the leaching concentrations of three samples via the leaching procedure HJ/T 300 met the "Solid Waste Landfill Pollution Control Standard" (GB 16889-2008). The results indicate that the location and type of SSWTT equipment play a crucial role in determining an appropriate solution for bottom ash management.

MSW pyrolysis volatiles' reforming by incineration fly ash for both pyrolysis products upgrading and fly ash stabilization.

The effective disposal of municipal solid wastes (MSW) and its incineration-derived fly ash (IFA), which contains large amounts of heavy metals (HMs) and chlorine (Cl), is an urgent task. In this study, IFA was used to reform MSW pyrolysis volatiles within 500-800 °C. The changes of reformed pyrolysis products, the migration characteristics of HMs and Cl between IFA and pyrolysis products were investigated. The results indicated that the O- and Cl-containing compounds in pyrolysis oil tended to decrease, light hydrocarbons and its calorific value increased accordingly after reforming; more CH4 and H2 gases were produced concurrently. The increase in reforming temperature enhanced these trends. The IFA absorbed Cl from volatiles during reforming, which reduced HCl in the gas product. The toxicity equivalent (TEQ) of PCDD/Fs in IFA decreased dramatically from 0.47 µg/kg to 0.0055 µg/kg after reforming at 500 °C, and it decreased with increasing reforming temperature. Some of the HMs' concentrations in the used IFAs increased, but their leaching capacity all decreased significantly at 800 °C except for Cr. The used IFA at 800 °C (IFA-800) corresponded to the lowest HMs leaching concentrations and could meet the landfill requirements; while the used IFA at 500 °C (IFA-500) corresponded to the maximum carbon deposition of 14.63 wt%, providing the energy source for its melting. Therefore 800 °C was recommended for harmless disposal of IFA, and 500 °C was better for a further melting of IFA., The contamination of pyrolysis liquid caused by inorganic Cl-containing compounds at 500 and 800 °C with much lower levels than the original. This study showed the hazardous properties of IFA can be dampened after interacting with MSW pyrolysis volatiles within the tested temperature range, and provided a good chance for the simultaneous disposal of IFA and recovery of high-quality MSW pyrolysis products.

Promotion of methane production and degradation of pyrolysis oil during its co-anaerobic digestion process via addition of N-doping hydro-chars.

Pyrolysis of wastes usually produces toxic pyrolysis oil (PO), which has complex ingredients, including benzene series and long-chain macromolecule organic pollutants. Co-anaerobic digestion (co-AD) can be an economic and high-efficiency method for PO degradation and recovery of methane simultaneously, but complete degradation of PO has not been achieved yet. Addition of a hydro-char in the process is beneficial to PO degradation and methane production. In this study, to further enhance the effectiveness of the hydro-char, nitrogen (N) was doped into the hydro-char by plasma modification in a NH3 atmosphere; and the effectiveness of the N-doped hydro-chars for promoting PO degradation and methane production during the co-AD process were evaluated. The experimental results indicated that all the hydro-chars can reduce the biotoxicity of the PO, improve its degradation during the co-AD process, and increase the methane yield. Compared with the plain hydro-char (HC), the hydro-chars modified at ambient temperature (HC-NH3-P-25) and at 500 °C (HC-NH3-P-500) can help achieving complete PO degradation and increasing the methane yield more effectively. The anaerobic digestor containing the HC-NH3-P-500 had the highest apparent methane yield (169.03 mLCH4/mLPO) and highest COD removal rate (79.5%). The nitrogen content, specific surface area, and electron transfer capability are found to be the key factors affecting PO degradation and methane yield; and the HC-NH3-P-500 had the highest N-doping, most specific surface area and electron transfer capability, explaining its best performance. The microbial communities of the digestate with the addition of the hydro-chars were founded to be richer with Clostridia and Methanosarcina, which could enhance the electron transfer between different microorganisms and contribute to the PO degradation.

Klotho Upregulation via PPARγ Contributes to the Induction of Brain Ischemic Tolerance by Cerebral Ischemic Preconditioning in Rats.

Cerebral ischemic preconditioning (CIP)-induced brain ischemic tolerance protects neurons from subsequent lethal ischemic insult. However, the specific mechanisms underlying CIP remain unclear. In the present study, we explored the hypothesis that peroxisome proliferator-activated receptor gamma (PPARγ) participates in the upregulation of Klotho during the induction of brain ischemic tolerance by CIP. First we investigated the expression of Klotho during the brain ischemic tolerance induced by CIP. Lethal ischemia significantly decreased Klotho expression from 6 h to 7 days, while CIP significantly increased Klotho expression from 12 h to 7 days in the hippocampal CA1 region. Inhibition of Klotho expression by its shRNA blocked the neuroprotection induced by CIP. These results indicate that Klotho participates in brain ischemic tolerance by CIP. Furthermore, we tested the role of PPARγ in regulating Klotho expression after CIP. CIP caused PPARγ protein translocation to the nucleus in neurons in the CA1 region of the hippocampus. Pretreatment with GW9962, a PPARγ inhibitor, significantly attenuated the upregulation of Klotho protein and blocked the brain ischemic tolerance induced by CIP. Taken together, it can be concluded that Klotho upregulation via PPARγ contributes to the induction of brain ischemic tolerance by CIP.

The Regulation of Autophagy by p38 MAPK-PPARγ Signaling During the Brain Ischemic Tolerance Induced by Cerebral Ischemic Preconditioning.

Several studies indicated that autophagy activation participates in brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP). However, the mechanism of autophagy activation during the process still remains unclear. The present study aimed to evaluate the role of p38 MAPK-peroxisome proliferator-activated receptor γ (PPARγ) signaling cascade in autophagy during the CIP-induced BIT. The results shown that, initially, autophagy activation was observed after CIP in the model of global cerebral ischemia in rats, as was indicated by the upregulation of Beclin 1 expression, an increase in LC3-II/LC3-I ratio, the enhanced LC3 immunofluorescence, and a rise in the number of autophagosomes in the neurons of the hippocampal CA1 area. Besides, the inhibitor of autophagy 3-methyladenine obliterated the neuroprotection induced by CIP. Furthermore, the upregulation of p-p38 MAPK and PPARγ expressions was earlier than autophagy activation after CIP. In addition, pretreatment with SB203580 (the inhibitor of p38 MAPK) reversed CIP-induced PPARγ upregulation, autophagy activation, and neuroprotection. Pretreatment with GW9662 (the inhibitor of PPARγ) reversed autophagy activation and neuroprotection, while it had no effect on p-p38 MAPK upregulation induced by CIP. These data suggested that the p38 MAPK-PPARγ signaling pathway participates in autophagy activation during the induction of BIT by CIP.

LncRNA BIRF Promotes Brain Ischemic Tolerance Induced By Cerebral Ischemic Preconditioning Through Upregulating GLT-1 via Sponging miR-330-5p.

Long noncoding RNAs (lncRNAs) play an important regulatory role in various diseases. However, the role of lncRNAs in brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIPC) is still unknown. The lncRNA profile of rat cortical astrocytes pretreated with ischemic preconditioning was analyzed by high-throughput sequencing. The results of Cell-Counting Kit-8 (CCK-8) assay showed that a novel lncRNA, NONRATT009133.2, which we referred to as brain ischemia-related factor (BIRF), was highly correlated with BIT. Through bioinformatics analysis, we predicted that BIRF, miR-330-5p, and GLT-1 (also named Slc1a2) might constitute a ceRNA regulatory network in the induction of BIT. We found that BIRF was upregulated by CIPC, which promoted GLT-1 expression and BIT induction. BIRF could directly bind to miR-330-5p. Furthermore, miR-330-5p directly targeted GLT-1, and miR-330-5p inhibited both GLT-1 expression and BIT induction in vitro and in vivo. Moreover, BIRF acts as a molecular sponge to competitively bind to miR-330-5p with GLT-1 mRNA, while the miR-330-5p inhibitor reversed all the effects of BIRF siRNA on GLT-1 expression and neuronal vitality. Taken together, our results demonstrate the important roles of the BIRF/miR-330-5p/GLT-1 axis in the induction of BIT by CIPC. BIRF may be a potentially effective therapeutic strategy against stroke injury.

Mechanism of Fuel Gas Denitration on the KOH-Activated Biochar Surface.

Previous experimental studies have found that biochar after KOH activation can significantly improve the efficiency of NO removal, but its mechanism is still unclear. To investigate the reaction mechanism of this denitration reaction, in this study, the aromatic benzene ring structure was used to simulate the surface of biochar, and the reaction process was calculated by density functional theory (DFT). The reaction process on the pristine biochar was simulated for comparison. The results indicated that there were two potential mechanisms for NO removal and had the identical rate-determining step, with an activation energy of 161.5 kJ/mol. Second, the influence by K coadsorbates on the NO reduction mechanism was studied. The adsorption by K atoms does not alter the last reaction step, but it was found to reduce the activation energy of this rate-determining step (to 129.3 kJ/mol). A third type of reaction mechanism was theoretically studied for the situation with both K and OH coadsorbates on the biochar surface. The reaction mechanism changed with an increase in the overall reaction rate by increasing the pre-exponential factor. In summary, the rate-determining activation energy for the heterogeneous NO reduction was found to decrease in the following order: 161.5 kJ/mol (pristine biochar) → 129.3 kJ/mol (activation by K adsorbates) → 125.8 kJ/mol (activation by both K and OH adsorbates); the pre-exponential factor was found to change in the following order: 6.23 × 1014 s-1 (pristine biochar) → 4.86 × 1014 s-1 (activation by K adsorbates) → 8.89 × 1014 s-1 (activation by K and OH adsorbates). Hence, the role by K adsorbates is primarily to reduce the rate-determining activation energy, while the OH group adsorbate increases the number of active sites on the surface of biochar.

The p38 MAPK/NF-κB pathway mediates GLT-1 up-regulation during cerebral ischemic preconditioning-induced brain ischemic tolerance in rats.

Our previous finding suggests that p38 MAPK contributes to the GLT-1 upregulation during induction of brain ischemic tolerance by cerebral ischemic preconditioning (CIP), however, the underlying mechanism is still unclear. Here, we investigated the molecular mechanisms underlying the CIP-induced GLT-1 upregulation by using Western blotting, Co-immunoprecipitation (Co-IP), electrophoretic mobility shift assay (EMSA) and thionin staining in rat hippocampus CA1 subset. We found that application of BAY11-7082 (an inhibitor of NF-κB), or dihydrokainate (an inhibitor of GLT-1), or SB203580 (an inhibitor of p38 MAPK) could attenuate the CIP-induced neuronal protection in hippocampus CA1 region of rats. Moreover, CIP caused rapid activation of NF-κB, as evidenced by nuclear translocation of NF-κB p50 protein, which led to active p50/p65 dimer formation and increased DNA binding activity. GLT-1 was also increased after CIP. Pretreatment with BAY11-7082 blocked the CIP-induced GLT-1 upregulation. The above results suggest that NF-κB participates in GLT-1 up-regulation during the induction of brain ischemic tolerance by CIP. We also found that pretreatment with SB203580 caused significant reduction of NF-κB p50 protein in nucleus, NF-κB p50/p65 dimer nuclear translocation and DNA binding activity of NF-κB. Together, we conclude that p38 MAPK/NF-κB pathway participates in the mediation of GLT-1 up-regulation during the induction of brain ischemic tolerance induced by CIP.

Gastric-cancer-derived mesenchymal stem cells: a promising target for resveratrol in the suppression of gastric cancer metastasis.

The tumor microenvironment (TM) is an essential factor of tumor progression. Mesenchymal stem cells (MSCs) are important components of the TM and play critical roles in cancer metastasis. Resveratrol (RES) is a potential antitumor drug that has attracted extensive attention. However, it remains unclear whether RES can exert its antitumor activity by targeting MSCs located in the TM. In this study, we demonstrated that the conditioned medium of gastric-cancer-derived MSCs (GC-MSCs) promoted gastric cancer (GC) metastasis and facilitated the progression of epithelialmesenchymal transition (EMT) of GC cells. However, after pretreatment with RES, the prometastatic effect of GC-MSCs on GC cells was reversed. Furthermore, RES reduced GC-MSC (IL-6, IL-8, MCP-1, VEGF) gene expression and protein secretion, and counteracted the activation of the GC-MSC-induced Wnt/ß-catenin signaling of GC cells, with less ß-catenin nuclear transport and declined expression of ß-catenin, CD44, and CyclinD3 in GC cells. Re-expression of ß-catenin impaired the inhibitory effect of RES on GC cells. In conclusion, RES restricted the mobility increase of GC cells and reversed the progress of EMT induced by GC-MSCs by inactivating the Wnt/ß-catenin signaling. GC-MSCs are promising target for RES in the inhibition of GC metastasis.

Therapeutic Advances of Stem Cell-Derived Extracellular Vesicles in Regenerative Medicine.

Extracellular vesicles (EVs), which are the main paracrine components of stem cells, mimic the regenerative capacity of these cells. Stem cell-derived EVs (SC-EVs) have been used for the treatment of various forms of tissue injury in preclinical trials through maintenance of their stemness, induction of regenerative phenotypes, apoptosis inhibition, and immune regulation. The efficiency of SC-EVs may be enhanced by selecting the appropriate EV-producing cells and cell phenotypes, optimizing cell culture conditions for the production of optimal EVs, and further engineering the EVs produced to transport therapeutic and targeting molecules.

Preparation of activated sewage sludge char for low temperature De-NOx and its CO emission inhibition.

Sewage sludge (SS) char can be potentially applied to De-NOx processes but it should be active enough and the relevant CO emissions should be controlled. In this paper activated SS chars have been prepared by using a simple KOH impregnation-carbonisation method and the activated chars are applied to remove NOx from flue gases within temperature range of 100-250 °C, acting as both reductants and catalysts. Special attention is paid to inhibiting CO emission in the process. Four reductive agents are adopted to check the catalytic effect of the activated SS chars. The results show that the activated SS chars (i.e. SC-KOHs) present a higher adsorption-reduction ability with much lower CO emission than that of non-activated SS chars (i.e. SC-Raws). SC-KOH produced at 800 °C (SC-KOH-800) shows obvious chemical adsorption behaviors, its adsorption capacity for NO is higher than 8.06 mg.L-1, superior to the coal-based activated carbon. Hydrazine hydrate is found to enhance De-NOx performance with SC-KOHs acting as catalysts, especially at higher temperatures. However, the De-NOx efficiency decreased when ammonia, urea and urea involved reductants were used. The physicochemical structure of the SS chars was characterized to show that the SC-KOHs are more porous with higher BET areas and pore volumes. Simultaneously, the SC-KOHs are crystallized to much lower extent, less graphitised, but have richer O-containing functional groups and zeolite structure on the surface when compared to the SC-Raws, which contributed to their high activities. Moreover, SC-KOH-800 can be recommended as the suitable adsorbent/catalyst for De-NOx within 100-250 °C.

Human umbilical cord mesenchymal stem cell exosomes alleviate sepsis-associated acute kidney injury via regulating microRNA-146b expression.

Human umbilical cord mesenchymal stem cell-derived exosomes (HucMSC-Ex) are a promising tool for the repair of acute kidney injury (AKI) caused by cisplatin and ischemia/reperfusion. However, the roles of hucMSC-Ex in sepsis-associated AKI repair and its mechanism are largely unknown. Hence, we constructed a sepsis model through cecal ligation and puncture (CLP), testing the benefits of hucMSC-Ex in the sepsis in terms of survival rate, serum renal markers levels, morphological changes and apoptosis. Immunohistochemistry staining and immunofluorescence assay were used to investigate the role of NF-κB activity in the repair of sepsis-associated AKI with hucMSC-Ex. HK-2 cells were transfected with microRNA-146b (miR-146b) mimics and inhibitors, respectively, and the regulatory effect of miR-146b on NF-κB activity was studied. We found that hucMSC-Ex treatment significantly decreased the serum creatinine (Cr) and blood urea nitrogen (BUN) levels, ameliorated the morphological damage and inhibited renal tubular cells apoptosis. More importantly, the survival rate at 72 h was 28% in CLP group and 45% in hucMSC-Ex group, respectively. Treatment with hucMSC-Ex improved survival in mice with sepsis. These effects of hucMSC-Ex were mediated by the inhibition of NF-κB activity and the lessening of pro-inflammatory response. Furthermore, hucMSC-Ex significantly increased miR-146b expression in kidney tissues. Conversely, interleukin (IL)-1 receptor-associated kinase (IRAK1) level, which is the target gene of miR-146b, clearly decreased in hucMSC-Ex group. In brief, this study showed that treatment with hucMSC-Ex decreased IRAK1 expression through the up-regulation of miR-146b level, led to the inhibition of NF-κB activity, and eventually alleviated sepsis-associated AKI and improved survival in mice with sepsis. HucMSC-Ex may be a novel therapeutic agent for the reduction of sepsis-associated AKI.

Chlorine removal from MSWI fly ash by thermal treatment: Effects of iron/aluminum additives.

The high content of alkali chlorides in municipal solid waste incineration (MSWI) fly ash limit its resource reuse due to the potential environmental risks. In this paper, with superheated steam as the gasifying agent and inducer, chlorides in fly ash were removed by thermal treatment within a moderate temperature range. Thermal treatment experiments were performed under different conditions: temperature (500-800°C), steam addition (mass ratio of steam to fly ash = 0.25-1) and residence time (0.5-3 hr). Iron and aluminum powders were added to fly ash to improve the chlorine removal efficiency. Water-soluble chlorides included NaCl and KCl, and insoluble chlorides mainly included Ca(OH)Cl. The heating process with the addition of water steam was more efficient than that without steam in terms of the removal performance of water-soluble chlorides. The removal efficiency of soluble chlorides reached 75.25% for a mass ratio of 1:1 after 1-hr thermal treatment at 700°C. When the residence time was increased above 1 hr, the total dechlorination efficiency was not increased dramatically. Moreover, adding iron and aluminum powder into the fly ash improved the removal of water-insoluble chlorides, and the total dechlorination efficiency was increased by 11.41%-16.64%.

Peroxidase-like Activity of Metal-Organic Framework [Cu(PDA)(DMF)] and Its Application for Colorimetric Detection of Dopamine.

A metal-organic framework (MOF) [Cu(PDA)(DMF)] was synthesized under mild mixed solvothermal conditions. It is constructed by 1,10-phenanthroline-2,9-dicarboxylic acid (H2PDA) and Cu2+ ions. The complex exhibits high peroxidase-like activity and can catalytically oxidize the colorless substrate 3,3',5,5'-tetramethylbenzidine to a blue product in the presence of H2O2. However, the peroxidase-like activity of [Cu(PDA)(DMF)] can be potently inhibited in the presence of dopamine. Based on this phenomenon, the colorimetric detection of dopamine was demonstrated with good selectivity and high sensitivity. [Cu(PDA)(DMF)] showed good stability and robust catalytic activity, which has been employed in the detection of dopamine in human urine and pharmaceutical samples.