Selective Adsorption of Gadolinium by Nitrogen-Doped Carboxymethylated Cellulose Nanocrystalline Carbon Aerogels Functionalized in the Ammonia-Urea System.

In this paper, an ammonia-urea system was developed to induce the shedding of carboxymethylcellulose carbon aerogels to form defects, and the specific surface area of the aerogels was significantly increased after carbonization, and the three-dimensional disordered pore structure of cellulose was preserved. The material showed the selective adsorption of gadolinium ions using the carboxylate active sites provided by carboxymethylation and the microporous or mesoporous structures formed after carbon burning. The successful synthesis of the material was demonstrated by relevant characterization, and the results of static adsorption experiments showed that the material was more consistent with the quasi second-order kinetic model at pH = 5.0. The maximum adsorption capacity was 99.65 mg g-1. The material showed a high adsorption capacity for gadolinium ions in the presence of competing ions and maintained 84.07% of the adsorption performance after five adsorption cycles. The simple use of urea ensured that the cellulose maintained its pore structure, and the specific surface area was greatly increased after carbonization, which provided a feasible direction for the industrial adsorption and recycling of rare-earth elements for reuse.

A Self-Cleaning TiO2 Bacterial Cellulose Super-Hydrophilic Underwater Super-Oleophobic Composite Membrane for Efficient Oil-Water Separation.

Due to the increasingly serious problem of offshore oil spills, research related to oil-water separation has attracted more and more attention. Here, we prepared a super-hydrophilic/underwater super-oleophobic membrane (hereinafter referred to as BTA) using poly-dopamine (PDA) to adhesive TiO2 nanoparticles on the surface of bacterial cellulose, coated with sodium alienate by vacuum-assisted filtration technique. This demonstrates its excellent underwater super-oleophobic property. Its contact angle is about 153°. Remarkably, BTA has 99% separation efficiency. More importantly, BTA still showed excellent anti-pollution property under ultraviolet light after 20 cycles. BTA has the advantages of low cost, environmentally friendliness and good anti-fouling performance. We believe it can play an important role in dealing with problems related to oily wastewater.

Dencichine prevents ovariectomy-induced bone loss and inhibits osteoclastogenesis by inhibiting RANKL-associated NF-κB and MAPK signaling pathways.

AIMS: To investigate the effect of dencichine on osteoclastogenesis in vivo and in vitro. METHODS: RANKL-induced osteoclastogenesis were treated with different concentrations of dencichine. Pit forming assays were applied to evaluate the degree of bone resorption. Osteoclastogenic markers were detected by real-time quantitative PCR (RT-qPCR) and Western blot. Micro CT was conducted to investigate the effects of dencichine on osteoclastogenesis in ovariectomized (OVX) mice. RESULTS: Dencichine suppressed osteoclastogenesis through the inhibition of phosphorylation of p65, p50 (NF-κB pathway), p38, ERK and JNK (MAPKs pathway) in vitro. Furthermore, dencichine inhibited the function of osteoclasts in a dose-dependent manner. In addition, the expression levels of the nuclear factor of activated T cells 1 (NFATc1) and osteoclastogenesis markers were decreased by dencichine, including MMP-9, Cathepsin K (CTSK), Tartrate-Resistant Acid Phosphatase (TRAP), C-FOS, dendritic cell specific transmembrane protein (DC-STAMP). In vivo data proved that dencichine alleviated ovariectomy-induced bone loss and osteoclastogenesis in mice. CONCLUSION: Our results demonstrate that dencichine alleviates OVX-induced bone loss in mice and inhibits RANKL-mediated osteoclastogenesis via inhibition of NF-κB and MAPK pathways in vitro, suggesting that dencichine might serve as a promising candidate for treatment of bone loss diseases, including PMOP and rheumatoid arthritis.

Study of the mechanism underlying hsa-miR338-3p downregulation to promote fibrosis of the synovial tissue in osteoarthritis patients.

Osteoarthritis (OA) is a degenerative joint disease characterized by the degradation of joint cartilage, the formation of osteophyma at joint margins, and synovial changes. Whereas lesions of the joint cartilage were the key point of the research and treatment of osteoarthritis before, a recent study showed that the synovium plays a crucial role in the pathological progress of OA. The inflammatory environment in the joints of OA patients always results in the overactivation of fibroblast-like synoviocytes (FLSs), which produce a multitude of inflammatory factors and media, not only leading to the degradation and injury of the cartilage tissue and promoting the development of osteoarthritis but also resulting in synovial fibrosis and joint stiffness. Therefore, the synovium has attracted increasing attention in the research of OA, and the study of the mechanism of activation of FLSs and the fibrosis of joint synovium may shed new light on OA treatment. By using high-throughput screening, we have identified that hsa-miR338-3p is significantly downregulated in the synovial tissue and joint effusion from OA patients. A functional study showed that overexpression of hsa-miR338-3p in the FLSs inhibited the TGF-ß1-induced overactivation of the TGF-ß/Smad fibrosis regulation pathway by suppressing TRAP-1 expression and thus reducing the TGF-ß1-induced activation of the FLSs and the expression of vimentin and collagen I, two fibrosis markers. Meanwhile, a mechanism study also showed that the upregulation of hsa-miR338-3p reduced Smad2/3 phosphorylation by suppressing TRAP-1 and thus inhibited the TGF-ß/Smad pathway and TIMP1, a downstream protein. The present study, for the first time, illustrates the role of hsa-miR338-3p in synovial fibrosis in OA patients and the related mechanism, which is of importance to the treatment of OA and its complications by targeting the FLSs and synovial tissue. Hsa-miR338-3p not only has the potential to be a target for the gene therapy of OA but also has the potential to be a new marker for the diagnosis of clinical progression in OA patients.

[Efficacy of Hebi Formula Combined Methotrexate on Early Rheumatoid Arthritis Patients with Dis- harmony of Gan and Pi Syndrome and Its Effects on Serum MMP-3 and RANK/RANKL/OPG Expressions].

Objective To observe the efficacy of Hebi Formula (HF) combined Methotrexate (MTX) on early rheumatoid arthritis (RA) patients with disharmony of Gan and Pi syndrome (DGPS) and its effects on matrix metalloproteinase-3 (MMP-3) activator of nuclear factor-KB/receptor activator of nu- clear factor-KB/osteoprotegerin (RANK/RANKL/OPG). Methods Totally 72 early RA patients with DGPS were assigned to the treatment group and the control group according to random digit table, 36 in each group. Patients in the control group took MTX, while those in the treatment group additionally took HF. MTX dose was increased from 7. 5 mg to 12. 5 mg gradually, once per week, and the course of treatment was 24 weeks. Efficacy for Chinese medicine (CM) syndromes, ACR20 improvement rate, laboratory re- lated indices [ rheumatoid factor ( RF ) , erythrocyte sedimentation rate ( ESR ) , C-reactive protein (CRP) , anti-cyclic citrullinated peptide antibody (CCP)], serum levels of MMP-3, OPG, RANKL, and adverse reactions were observed. Results The standard arriving rate of ACR20 was 82. 86% (2935) in the treatment group, higher than that in the control group [51. 52% (173) ;P <0. 05). The effective rate of CM syndrome was 85. 7% (30f35) in the treatment group, higher than that in the control group [63. 6% (21/33) ;P <0. 05). Compared with before treatment in the same group, levels of RF,ESR,CRP,MMP-3, and RANKL decreased, the OPG level increased in the two groups after treatment (P <0. 05, P <0. 01). Compared with the control group, levels of RF, ESR, CRP, and RANKL all decreased with statistical difference (P <0. 01 , P <0. 05). Liver dysfunction occurred in 1 case of the treatment group. Leucopenia occurred in 1 case and liver dysfunction occurred in 2 cases of the control group. Conclusion HF com- bined MTX could improve symptoms of early RA patients with DGPS, and regulate bone destruction in- duced by RANK/RANKL/OPG systems.

[In vitro anti-tumor effect of human dendritic cells vaccine induced by astragalus polysacharin: an experimental study].

OBJECTIVE: To explore the in vitro anti-tumor effect and mechanism of dendritic cell (DC) tumor vaccine induced by astragalus polysacharin (APS). METHODS: Peripheral blood mononuclear cells (PBMCs) isolated from human peripheral blood. DCs obtained from human peripheral blood were cultivated and added with culture solution for in vitro inducing them to immature DCs. On the 5th day of culture, 100 microg/mL (as the final concentration) APS was added to cells in the APS group. DCs were induced to mature in the cytokine groups by adding 20 ng/mL rhTNF-alpha (as the final concentration). Changes of morphology and phenotype of DCs were observed. Mature DCs were sensitized with tumor antigen SGC-7901 and co-cultured with allogeneic T cells. The proliferative function of T lymphocytes was detected by MTT assay. Levels of IL-12 and IFN-gamma in co-cultured supernatant were detected by ELISA. Cytotoxic lymphocytes (CTL) activated by DC were co-cultured with tumor cell SGC-7901. The specific killing capacity of CTL to target cells was detected by LDH release assay. RESULTS: The morphological observation and phenotypic identification of APS induced DCs were in accordance with the characteristics of mature DCs. APS induced mature DCs could stimulate the proliferation of allogeneic T lymphocytes. The proliferation index of T cells increased with increased ratio of stimulator cells to effector cells (P < 0.05). Levels of IL-12 and IFN-gamma in co-culture supernatant significantly increased in a time-dependent manner (P < 0.05). CTL cells activated by sensitization of DCs could significantly kill tumor cells, and the killing effect increased along with increased effector-to-target ratio. CONCLUSION: APS could in vitro induce DCs to mature, promote its antigen-presenting capacity, effectively activate CTLs, and enhance anti-tumor function of the organism.

Porous carboxymethyl cellulose nanocrystalline imprinted composite aerogels for selective adsorption of gadolinium.

Gadolinium is widely applied in medical and high-tech materials because of special magnetic properties. Recovery of gadolinium from waste rare earth products has both economic and environmental value. In this experiment, honeycomb porous composite aerogels were constructed using sericin and sodium alginate mixed with functionally modified carboxymethylated cellulose nanocrystals for the adsorption and separation of gadolinium ions. There were large numbers of carboxyl groups as well as hydroxyl groups on the surface of sodium alginate and filamentous protein, which provided more sites for the adsorption of gadolinium ions. Besides, a stable honeycomb structure appeared on the surface of composite aerogels when the mixture of filamentous protein and sodium alginate was 1:1, which increased the specific surface area of materials to 140.65 m2 g-1. Additionally, the imprinted composite aerogels Ic-CNC/SSA were prepared by virtue of the imprinting technology, enhancing the adsorption selectivity of composite aerogels for gadolinium. The adsorption experiments revealed that the maximum adsorption capacity of Ic-CNC/SSA reached 93.41 mg g-1 at pH 7.0, indicating good selective adsorption of gadolinium ions. In summary, such composite aerogels provide great potential and reference value for the selective adsorption of gadolinium ions in industry.

Analysis of the Potential Angiogenic Mechanisms of BuShenHuoXue Decoction against Osteonecrosis of the Femoral Head Based on Network Pharmacology and Experimental Validation.

OBJECTIVE: Osteonecrosis of the femoral head (ONFH) is a common orthopedic disease with a high disability rate. The clinical effect of BuShenHuoXue decoction (BSHX) for ONFH is satisfactory. We aimed to elucidate the potential angiogenic mechanisms of BSHX in a rat femoral osteonecrosis model and bone marrow mesenchymal stem cells (BMSCs). METHODS: With in vivo experiments, we established the steroid-induced osteonecrosis of the femoral head (SONFH) model using Sprague-Dawley (SD) rats (8-week-old). The rats were randomly divided into five group of 12 rats each and given the corresponding interventions: control, model (gavaged with 0.9% saline), BSHX low-, medium- and high-dose groups (0.132 3, 0.264 6, and 0.529 2 g/mL BSHX solution by gavage). After 12 weeks, haematoxylin and eosin (H&E) staining was preformed to evaluate rat osteonecrosis. the expression of angiogenic factors (CD31, VEGFA, KDR, VWF) in rat femoral head was detected by immunohistochemistry, qPCR and western blotting. In cell experiment, BMSCs were isolated and cultured in the femoral bone marrow cavity of 4-week-old SD rats. BMSCs were randomly divided into eight groups and intervened with different doses of BSHX-containing serum and glucocorticoids: control group (CG); BSHX low-, medium-, and high-dose groups (CG + 0.661 5, 1.323, and 2.646 g/kg BSHX gavage rat serum); dexamethasone (Dex) group; and Dex + BSHX low-, medium-, and high-dose groups (Dex + 0.661 5, 1.323, and 2.646 g/kg BSHX gavaged rat serum), the effects of BSHX-containing serum on the angiogenic capacity of BMSCs were examined by qPCR and Western blotting. A co-culture system of rat aortic endothelial cells (RAOECs) and BMSCs was then established. Migration and angiogenesis of RAOECs were observed using angiogenesis and transwell assay. Identification of potential targets of BSHX against ONFH was obtained using network pharmacology. RESULTS: BSHX upregulated the expression of CD31, VEGFA, KDR, and VWF in rat femoral head samples and BMSCs (p < 0.05, vs. control group or model group). Different concentrations of BSHX-containing serum significantly ameliorated the inhibition of CD31, VEGFA, KDR and VWF expression by high concentrations of Dex. BSHX-containing serum-induced BMSCs promoted the migration and angiogenesis of RAOECs, reversed to some extent the adverse effect of Dex on microangiogenesis in RAOECs, and increased the number of microangiogenic vessels. Furthermore, we identified VEGFA, COL1A1, COL3A1, and SPP1 as important targets of BSHX against ONFH. CONCLUSION: BSHX upregulated the expression of angiogenic factors in the femoral head tissue of ONFH model rats and promoted the angiogenic capacity of rat RAOECs and BMSCs. This study provides an important basis for the use of BSHX for ONFH prevention and treatment.

Preparation of imprinted bacterial cellulose aerogel with intelligent modulation of thermal response stimulation for selective adsorption of Gd(III) from wastewater.

Research on recycling of used rare earth elements has been of great interest. Adsorption is one of the advantageous methods to recover gadolinium with high value. In the process of adsorption and separation of gadolinium from materials, the selectivity of materials for gadolinium can be significantly improved by using ion imprinting technique. However, gadolinium elution process is a traditional pickling process, which may affect the construction of imprinting sites. In this study, bacterial cellulose with three-dimensional spatial structure was used as the base material of aerogel material, and functional materials containing a large number of carboxyl groups were introduced by chemical grafting method. In combination with ion imprinting technology and N-polyacrylamide as intelligent temperature control valve, intelligent imprinting aerogel (PNBC-IIPS) with specific selectivity to gadolinium was prepared. The properties of aerogel materials were analyzed by SEM, FT-IR, and BET characterization. The experimental analysis shows that the desorption of gadolinium can be achieved by controlling the temperature change. The adsorption experiments show that PNBC-IIPS can selectively adsorb gadolinium ions from aqueous solution. The maximum adsorption capacity reached 95.51 mg g-1. Compared with unimprinted aerogel, the maximum adsorption capacity of gadolinium ion is significantly increased, which proves that the introduced ion imprinting technique plays a key role in the adsorption process. Cyclic experiments show that the adsorption capacity of PNBC-IIPS can still maintain 88% of the original adsorption capacity after 5 times of adsorption and desorption. In conclusion, PNBC-IIPS is a green adsorbent for selective recovery of gadolinium ions.

Regulation of inflammatory response in human chondrocytes by lentiviral mediated RNA interference against S100A10.

OBJECTIVE: The aim of the present study was to evaluate the effects of S100A10 silencing on the inflammatory response in human chondrocytes (HCs).The inflammation induced by lipopolysaccharide (LPS) was investigated in HCs in which the S100A10 was blocked with a lentiviral shRNA vector. METHODS: A lentiviral shRNA vector targeting S100A10 was constructed and packaged to effectively block S100A10 expression in HCs. HCs were infected with the lentivirus. S100A10 expression levels in HCs were detected by western blot analysis. Enzyme-linked immunosorbent assay (ELISA) was employed to evaluate the change of cytokine secretion levels. The effects of S100A10 silencing on the activation of mitogen-activated protein kinases (MAPKs) and NF-κB signaling pathway were also determined by western blot analysis. In addition, fluo-3-AM was used to demonstrate the change in calcium mobilization. RESULTS: Lentivirus effectively infected the HCs and inhibited the expression of S100A10. HCs with downregulated S100A10 showed significantly decreased production of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-10. S100A10 silencing markedly suppressed the activation of MAPKs induced by LPS. Furthermore, the calcium concentration increase in HCs stimulated by LPS was also inhibited by S100A10 knockdown. CONCLUSION: Our investigation demonstrated that S100A10 might be considered as a potential target for anti-inflammatory treatment.

Spatiotemporal Variation and Influencing Factors of TSP and Anions in Coastal Atmosphere of Zhanjiang City, China.

Water-soluble anions and suspended fine particles have negative impacts on ecosystems and human health, which is a current research hotspot. In this study, coastal suburb, coastal urban area, coastal tourist area, and coastal industrial area were explored to study the spatiotemporal variation and influencing factors of water-soluble anions and total suspended particles (TSP) in Zhanjiang atmosphere. In addition, on-site monitoring, laboratory testing, and analysis were used to identify the difference of each pollutant component at the sampling stations. The results showed that the average concentrations of Cl-, NO3-, SO42-, PO43-, and TSP were 29.8 µg/m3, 19.6 µg/m3, 45.6 µg/m3, 13.5 µg/m3, and 0.28 mg/m3, respectively. The concentration of Cl-, NO3-, PO43-, and atmospheric TSP were the highest in coastal urban area, while the concentration of SO42- was the highest in coastal industrial area. Moreover, there were significantly seasonal differences in the concentration of various pollutants (p < 0.05). Cl- and SO42- were high in summer, and NO3- and TSP were high in winter. Cl-, SO42-, PO43-, and TSP had significant correlations with meteorological elements (temperature, relative humidity, atmospheric pressure, and wind speed). Besides, the results showed the areas with the most serious air pollution were coastal urban area and coastal industrial area. Moreover, the exhaust emissions from vehicles, urban enterprise emissions, and seawater evaporation were responsible for the serious air pollution in coastal urban area. It provided baseline information for the coastal atmospheric environment quality in Zhanjiang coastal city, which was critical to the mitigation strategies for the emission sources of air pollutants in the future.

Effect of astragaloside IV and salvianolic acid B on antioxidant stress and vascular endothelial protection in the treatment of atherosclerosis based on metabonomics.

Vascular endothelial cells and oxidation reduction system play an important role in the pathogenesis of atherosclerosis (AS). If these conditions are disordered, it will inevitably lead to plaque formation and even rupture. Astragaloside IV (AsIV) and salvianolic acid B (Sal B) are the main active ingredients of Astragalus membranaceus and Salvia miltiorrhiza, respectively, and found to ameliorate vascular endothelial dysfunction and protect against oxidative stress in recent studies. However, it is still unknown if the combination of AsIV and Sal B (AsIV + Sal B) can inhibit the development of plaque through amplifying the protective effect of vascular endothelial cells and anti-oxidative stress effect. To clarify the role of AsIV + Sal B in AS, we observed the efficacy of each group (Control, Model, AsIV, Sal B, and AsIV + Sal B) by biomolecular assays, such as observing the pathological morphology of the aorta by oil red O staining, evaluating the level of oxidative stress and endothelial cells in the serum by the Elisa test, and analyzing the changes of all small molecule metabolites in liver tissue by UPLC-QTOF-MS. Results showed that AsIV, Sal B and AsIV + Sal B decreased the deposition of lipid in the arterial wall, so as to exert the effect of anti-oxidant stress and vascular endothelial protection, where the inhibitory effect of AsIV + Sal B was the most obvious. Metabonomics analysis showed that Sal B regulated the metabolic pathways of arginine and proline. AsIV regulated glycerol metabolism and saturated fatty acid biosynthesis metabolism. AsIV + Sal B is mainly related to the regulation of the citrate cycle (TCA cycle), alanine, aspartic acid, and glutamate metabolism, cysteine, and methionine metabolism. Succinic acid and methionine are synergistic metabolites that exert an enhancing effect when AsIV and Sal B were used in combination. In conclusion, we demonstrated that AsIV acompanied with Sal B can be successfully used for anti-oxidative stress and vascular endothelial protection of AS, and succinic acid and methionine are the synergistic metabolites.

[Paeonol attenuates oxygen-glucose deprivation injury and inhibits NMDA receptor activation of cultured rat hippocampal neurons].

The purpose of this study is to determine if paeonol can protect hippocampal neurons against injury due to oxygen-glucose deprivation (OGD) injury. The rat neurons were cultured in an OGD environment and the model of OGD injury was established. Paeonol and MK-801, a positive control drug, were added before deprivation. Neuron viability was measured by the reduction of MTT; glutamate was analyzed by amino acid analyzer; binding activity of NMDA receptor was evaluated by liquid scintillation counting and the expression of NMDA receptor NR1 subunit mRNA was semiquantitatively determined by RT-PCR. Compared with OGD injury group, paeonol treatment obviously increased cell survival rate and reduced the binding activity of NMDA receptors and the release of glutamate; and down-regulating the expression of NR1 subunit. These results suggest that paeonol may exhibit its protective effect against OGD injury by the action on NMDA receptor of rats.

Protective effects of paeonol on cultured rat hippocampal neurons against oxygen-glucose deprivation-induced injury.

Mounting evidence has suggested that paeonol possesses plenty of pharmacologic actions. Our research is to determine if paeonol can protect cultured rat hippocampal neurons from oxygen-glucose deprivation(OGD)-induced injury and elucidate the underlying mechanism. We cultivated the rat hippocampal neurons as the object of study and then established the model of oxygen-glucose deprivation. Neuronal viability was measured by the reduction of 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), while intracellular Ca(2+) concentration was observed by fluorospectrophotometer. The binding force of N-methyl-D-aspartate (NMDA) receptor was evaluated by liquid scintillation counting. Compared with oxygen-glucose deprivation group, paeonol treatment obviously increased cell survival rate and reduced the activity of the binding force of NMDA receptors, reversing the overload of intracellular Ca(2+). These results demonstrate that paeonol protected rat neurons from oxygen-glucose deprivation-induced injury, resulting in alleviating the morphological damage and increasing neuron viability and suggest that paeonol may exhibit its protective effect against oxygen-glucose deprivation-induced injury by targeting on NMDA receptors.

Pregnancy alters glucose-6-phosphate dehydrogenase trafficking, cell metabolism, and oxidant release of maternal neutrophils.

Pregnancy is associated with changes in host susceptibility to infections and inflammatory disease. We hypothesize that metabolic enzyme trafficking affects maternal neutrophil activation. Specifically, immunofluorescence microscopy has shown that glucose-6-phosphate dehydrogenase (G-6-PDase), the rate-controlling step of the hexose monophosphate shunt (HMS), is located near the cell periphery in control neutrophils but is found near the microtubule-organizing centers in cells from pregnant women. Cytochemical studies confirmed that the distribution of the G-6-PDase antigen is coincident with functional G-6-PDase activity. Metabolic oscillations within activated pregnancy neutrophils are higher in amplitude, though lower in frequency, than activated control neutrophils, suggesting limited HMS activity. Analysis of radioisotope-labeled carbon flux from glucose to CO(2) indicates that the HMS is intact in leukocytes from pregnant women, but its level is not enhanced by cell stimulation. Using extracellular fluorescent markers, activated pregnancy neutrophils were found to release reactive oxygen metabolites (ROMs) at a lower rate than activated control neutrophils. However, basal levels of ROM production in polarized pregnancy neutrophils were greater than in control neutrophils. Microtubule-disrupting agents reversed the observed changes in G-6-PDase trafficking, metabolic oscillations, and ROM production by maternal neutrophils. G-6-PDase trafficking appears to be one mechanism regulating ROM production by maternal neutrophils.

2,5-Deoxyfructosazine, a D-glucosamine derivative, inhibits T-cell interleukin-2 production better than D-glucosamine.

D-Glucosamine has been widely reported to have immunosuppressive actions on neutrophils, lymphocytes, and other cells of the immune system. However, under conditions used in biological experiments (e.g., neutral pH, and phosphate buffers), we have found that D-glucosamine self-reacts to form 2,5-deoxyfructosazine [2-(D-arabino-tetrahydroxybutyl)-5-(D-erythro-2,3,4-trihydroxybutyl)pyrazine] (1) and 2,5-fructosazine [2,5-bis(D-arabino-tetrahydroxybutyl)pyrazine] (2). When tested for bioactivity at nontoxic concentrations, these D-glucosamine derivatives were more effective inhibitors of IL-2 release from PHA-activated T cells than d-glucosamine. Hence, fructosazines constitute a novel class of immunomodulators.

Treatment of tannery wastewater by electrocoagulation.

Treatment of tannery wastewater by electrocoagulation with low cell current (< or = 1A) and soluble electrodes (mild steel electrodes and aluminum electrodes) was studied. Compared with aluminum electrodes, mild steel electrodes were more effective for the removal of sulfide, with a removal efficiency of over 90%. But during the treatment process, black color precipitate typical to iron(II) sulfides was produced. While aluminum electrodes were effective to eliminate the colority of the effluent, the removal efficiency of sulfide was lower than 12%. The mechanisms of the removal of chemical oxygen demand, ammonia, total organic carbon, sulfide and colority with the two soluble electrodes (mild steel and aluminum electrodes) were discussed in detail. In order to exert the predominance of diffenent types of electrodes, the tannery wastewater was treated using mild steel electrodes first followed by the filter and finally by the aluminum electrodes, the elimination rates of chemical oxygen demand, ammonia, total organic carbon, sulfide and colority were 68.0%, 43.1%, 55.1%, 96.7% and 84.3%, respectively, with the initial concentrations 2413.1 mg/L, 223.4 mg/L, 1000.4 mg/L, 112.3 mg/L and 256 dilution times, respectively. The absorbance spectra and energy consumption during electrocoagulation process were also discussed.

Spatiotemporal expression of FOXA1 correlates with reactive gliosis after spinal cord injury.

Forkhead box A1 (FOXA1) is a member of the FOX family of transcription factors and involved in various mammalian processes. However, the expression and function of FOXA1 in central nervous system (CNS) are still with limited acquaintance. In present study, we performed an acute spinal cord injury (SCI) model in adult rats and investigated the dynamic changes of FOXA1 expression in spinal cord. We found that FOXA1 protein levels were significantly increased after SCI and we observed that the expression of FOXA1 is enhanced in the white matter. Meanwhile, double immunofluorescence staining showed that increased levels of FOXA1 were striking in astrocytes and microglia. We also examined the expression of proliferating cell nuclear antigen (PCNA), whose changes were correlated with the expression profiles of FOXA1. In vitro, FOXA1 depletion by siRNA inhibited astrocyte proliferation and migration. Meanwhile, FOXA1 knockdown also reduce cell cycle related proteins. Which indicated that FOXA1 might modulate cell cycle progression and play a crucial role in cell proliferation. Furthermore, FOXA1 knockdown also inhibited LPS-induced synthesis/secretion of IL-1ß and TNF-α in primary microglia. These results indicated that FOXA1 might play an important role in pathophysiology after SCI.