Circulating exosome long non-coding RNAs are associated with atrial structural remodeling by increasing systemic inflammation in atrial fibrillation patients.

Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia with severe clinical sequelae, but its genetic characteristic implicated in pathogenesis has not been completely clarified. Accumulating evidence has indicated that circulating exosomes and their carried cargoes, such as long non-coding RNAs (lncRNAs), involve in the progress of multiple cardiovascular diseases. However, their potential role as clinical biomarkers in AF diagnosis and prognosis remains unknown. Methods: Herein, we conducted the sequence and bioinformatic analysis of circulating exosomes harvested from AF and sinus rhythm patients. Results: A total of 53 differentially expressed lncRNAs were identified, and a total of 6 significantly changed lncRNAs (fold change > 2.0), including NR0046235, NR003045, NONHSAT167247.1, NONHSAT202361.1, NONHSAT205820.1 and NONHSAT200958.1, were verified by qRT-PCR in 215 participants. Moreover, these circulating exosome lncRNA levels were different between paroxysmal and persistent AF patients, which were dramatically associated with abnormal hemodynamics and atrial diameter. Furthermore, we observed that the area under ROC curve (AUC) of six lncRNAs combination for diagnosis of persistent AF was 80.34%. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment pathway analysis indicated these exosome lncRNAs mainly concerning response to chemokine-chemokine receptor interaction, which induced activated inflammation and structural remodeling. In addition, increased plasma levels of CXCR3 ligands, including CXCL4, CXCL9, CXCL10 and CXCL11, were accumulated in AF patient tissues. Conclusion: Our study provides the transcriptome profile revealing pattern of circulating exosome lncRNAs in atrial structural remodeling, which bring valuable insights into improving prognosis and therapeutic targets for AF.

Oxide Ion Conduction in Ca-Doped Yb3Ga5O12 Garnet.

Developing oxide ion conductors with new structural families is important for many energy conversion and storage techniques. Herein, a series of Ca-doped Yb3Ga5O12 garnet-type materials are prepared through a traditional solid-state reaction method, with their oxide ion conduction properties being reported for the first time. The results revealed that Ca substitution for Yb would significantly improve the conductivity of Yb3Ga5O12 from 3.57 × 10-7 S/cm at 900 °C under air to 1.66 × 10-4 S/cm, with an oxide ion transporting number of ∼0.52. The oxygen vacancy defect formation energy (∼0.127 eV) and the local structure around an oxygen vacancy were studied by atomic-level static lattice simulations based on the interatomic potential method. The oxide ion conducting mechanism was studied by the bond-valence-based method, which revealed three-dimensional pathways for oxide ion migration in both the parent and Ca-doped structures. The simulated activation energy of oxide ion migration decreased slightly from ∼0.358 eV in the parent structure to 0.346 eV in the doped one. These discoveries in the Ca-doped Yb3Ga5O12 will stimulate extensive exploitation and fundamental research on garnet-type materials.

Arsenic Exposure Induces Neuro-immune Toxicity in the Cerebral Cortex and the Hippocampus via Neuroglia and NLRP3 Inflammasome Activation in C57BL/6 Mice.

This study aimed to examine the immuntoxic effects of arsenic in the nervous system. Our results showed that arsenic increased corticocerebral and hippocampal weights (p < 0.05). Morris water maze tests revealed that arsenic significantly increased the time spent in latency to platform on the fourth day in 50 mg/L arsenic exposure and the fifth day in 25 and 50 mg/L arsenic exposure, as well as reduced the path length in target quadrant, time spent in target quadrant, and crossing times of the platform (p < 0.05). Hematoxylin-eosin staining showed that the vacuolated degeneration and pyknosis was found in the cerebral cortex and hippocampus of arsenic-treated mice. The mRNA levels of corticocerebral and hippocampal brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) were decreased in the 50 mg/L arsenic-treated group (p < 0.05). In addition, immunofluorescence staining showed that 25 and 50 mg/L arsenic all increased the expression of CD11b and glial fibrillary acidic protein (GFAP) in the cerebral cortex and hippocampus (p < 0.05). Arsenic markedly raised antigen-presenting molecule MHCII and CD40 mRNA levels in the cerebral cortex and hippocampus and upregulated the cell chemokine receptor 5 (CCR5) and CCR7 mRNA levels in the cerebral cortex at the 50 mg/L arsenic group, and increased the CCR7 mRNA levels in the hippocampus at the 25 and 50 mg/L arsenic groups (p < 0.05). Arsenic activated the nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome, and enhanced its upstream promoter NF-κB protein level and downstream regulators IL-18 mRNA levels. Collectively, these results provide new evidences for the neuro-immune toxicity of arsenic.

Sodium Butyrate Ameliorates Fluorosis-Induced Neurotoxicity by Regulating Hippocampal Glycolysis In Vivo.

Fluorosis can induce neurotoxicity. Sodium butyrate (SB), a histone deacetylase inhibitor, has important research potential in correcting glucose metabolism disorders and is widely used in a variety of neurological diseases and metabolic diseases, but it is not yet known whether it plays a role in combating fluoride-induced neurotoxicity. This study aims to evaluate the effect of SB on fluoride neurotoxicity and the possible associated mechanisms. The results of HE staining and Morris water maze showed that, in mice exposed to 100 mg/L fluoride for 3 months, the hippocampal cells arranged in loosely with large cell gaps and diminished in number. One thousand milligram per kilogram per day SB treatment improved fluoride-induced neuronal cell damage and spatial learning memory impairment. Western blot results showed that the abundance of malate dehydrogenase 2 (MDH2) and pyruvate dehydrogenase (PDH) in the hippocampus of fluorosis mice was increased, the abundance of pyruvate kinase M (PKM), lactate dehydrogenase (LDH), hexokinase (HK), phosphatidylinositol 3-kinase (PI3K), phosphorylated Akt (P-AKT), and hypoxia-inducible factor 1α (HIF-1α) was inhibited, and the content of lactate and ATP was decreased. SB treatment reversed the decreased glycolysis in the hippocampus of fluorosis mice. These results suggested that SB could ameliorate fluorosis-induced neurotoxicity, which might be linked with its function in regulating glycolysis as well as inhibition of the PI3K/AKT/HIF-1α pathway. Sodium butyrate ameliorates fluorosis-induced neurotoxicity by regulating hippocampal glycolysis in vivo (created with MedPeer (www.medpeer.cn)).

Arsenic Induces Blood‒Brain Barrier Disruption and Regulates T Lymphocyte Subpopulation Differentiation in the Cerebral Cortex and Hippocampus Associated with the Nrf2 Pathway In Vivo.

Increasing evidence has confirmed that the nervous system shows innate and adaptive immunity, which also participates in nerve damage. This study aimed to explore the neuroimmune imbalance induced by arsenic and its possible mechanism. Mice were exposed to NaAsO2 (0, 5, 10, 25, and 50 mg/L) for 1 month by drinking water. Y-maze and Morris water maze tests revealed that arsenic impaired learning and memory. The optical density of Evans blue showed a marked dose-dependent increase in the brain, and the mRNA and protein levels of the BBB tight junctions (TJs), occludin at 25 and 50 mg/L arsenic, and claudin-5 at 50 mg/L arsenic, were markedly decreased in the cerebral cortex. Arsenic downregulated occludin and claudin-5 mRNA expression at 50 mg/L and protein expression at 25 and 50 mg/L in the hippocampus. Immunohistochemical staining showed that 50 mg/L arsenic increased corticocerebral and hippocampal CD3+ T, CD4+ T, and CD8+ T cells; CD4 and CD8 proteins were increased with 25 and 50 mg/L arsenic. Arsenic decreased the corticocerebral and hippocampal Th1, Th17, and regulatory Treg transcription factors T-bet, Rorγt, and Foxp3 and the cytokine IFN-γ, IL-17, and TGF-ß mRNA levels and increased the Th2 transcription factor GATA3 and cytokine IL-4 mRNA levels. Moreover, arsenic enhanced the expression of nuclear factor E2-related factor (Nrf2) and its downstream enzymes heme oxygenase-1 (HO-1) and glutathione-S-transferase (GST). In conclusion, these results demonstrate that arsenic exposure induces BBB dysfunction and T lymphocyte infiltration and affects CD4+ T lymphocyte differentiation, which may be associated with Nrf2 activation.

Highly effective remediation of high arsenic-bearing wastewater using aluminum-containing waste residue.

Wastewater from non-ferrous metal smelting is known as one of the most dangerous sources of arsenic (As) due to its high acidity and high arsenic content. Herein, we propose a new environmental protection process for the efficient purification and removal of arsenic from wastewater by the formation of an AlAsO4@silicate core-shell structure based on the characteristics of aluminum-containing waste residue (AWR). At room temperature, the investigation with AWR almost achieved 100% As removal efficiency from wastewater, reducing the arsenic concentration from 5500 mg/L to 52 µg/L. With Al/As molar ratio of 3.5, the structural properties of AWR provided good adsorption sites for arsenic adsorption, leading to the formation of arsenate and insoluble aluminum arsenate with As. As-containing AWR silicate shells were produced under alkaline conditions, resulting in an arsenic leaching concentration of 1.32 mg/L in the TCLP test. AWR, as an efficient As removal and fixation agent, shows great potential in the treatment of copper smelting wastewater, and is expected to achieve large-scale industrial As removal.

Arsenic Activates the NLRP3 Inflammasome and Disturbs the Th1/Th2/Th17/Treg Balance in the Hippocampus in Mice.

Arsenic exerts neurotoxicity and immunomodulatory effects. Studies have shown that the nervous system is not considered to be an immune-privileged site. However, the effect of arsenic-induced neuroimmune toxicity has rarely been reported. We aimed to investigate the toxic effects of arsenic on the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and the Th1/Th2/Th17/Treg balance in the brain tissue of mice. Mice were exposed to NaAsO2 (0, 2.5, 5, and 10 mg/kg) for 24 h. Our results showed that 10 mg/kg arsenic exposure significantly decreased brain and hippocampal indices (p < 0.05). The mRNA and protein levels of the blood‒brain barrier (BBB) tight junction protein occludin were decreased in the 5 and 10 mg/kg arsenic-treated groups. Compared with those in the control group, NLRP3 protein levels in 10 mg/kg arsenic-treated mice, caspase-1 protein levels in 2.5, 5, and 10 mg/kg arsenic-treated mice, and IL-1ß protein levels in 5 and 10 mg/kg arsenic-treated mice were increased in the hippocampus (p < 0.05). In addition, arsenic induced a hippocampal inflammatory response by upregulating the mRNA levels of the proinflammatory factors IL-6 and TNF-α and downregulating the mRNA level of the anti-inflammatory factor IL-10. Moreover, arsenic decreased the mRNA levels of the Th1 and Th2 transcription factors T-bet and GATA3 and the cytokines IFN-γ and IL-4 and increased the mRNA levels of the Th17 transcription factor RORγt and the cytokine IL-22 (p < 0.05). Collectively, our study demonstrated that arsenic could induce immune-inflammatory responses by regulating the NLRP3 inflammasome and CD4+ T lymphocyte differentiation. These results provide a novel strategy to block the arsenic-induced impairment of neuroimmune responses.

Environmental Risk Analysis Based on Characterization of Ground Oily Sludge.

Oily sludge is recognized as hazardous waste. To reduce the potential danger and harmful factors of oily sludge, it is very important to analyze its environmental risk. In this paper, the characterization of oily sludge from Shengli Oilfield in China was tested experimentally, including the composition content, particle size, microscopic morphology, heavy metal content, organic composition, inorganic composition, and thermogravimetric analysis, which were used to analyze environmental risks. The results show that the oil content of oily sludge is as high as 10.3%, which will cause serious pollution. It is calculated that China can recover 772.5 million liters of oil and reduce 553.9 million kg of carbon emissions compared with incineration in one year, if the oily sludge can be managed effectively. The content of heavy metals such as Ba, Zn, Cr, As, Ni, Se, Be, and Hg in oily sludge exceeds the standard. It will restrain the self-healing ability of soil, pollute groundwater, and endanger animals and plants. The organic matter of oily sludge is concentrated in C11 to C29. It contains a large amount of benzene series and polycyclic benzene hydrocarbons, which can lead to cancer in the human body. Inorganic substances in oily sludge are mixed with some additives, which can not only reduce the toxicity of heavy metals, but also be used as building materials. The median particle size D50 of oily sludge is 0.91 µm, and it spreads all over the narrow pores. Generally, it needs to be treated under high temperature conditions, which will cause secondary pollution to the environment. The research content of this paper provides a theoretical reference for the management of oily sludge.

Effects of Subchronic Aluminum Exposure on Learning, Memory, and Neurotrophic Factors in Rats.

Aluminum (Al) is a neurotoxin that gradually accumulates in the brain in human life, resulting in oxidative brain injury related to Alzheimer's disease (AD) and other diseases. In this study, the learning and memory of rats exposed to different aluminum concentrations (0.0 g/L, 2.0 g/L, 4.0 g/L, and 8.0 g/L) were studied, and the learning and memory of rats were observed by shuttle box experiment. With hematoxylin and eosin staining, Western blot, immunofluorescence, and RT-PCR, the morphology of nerve cells in the hippocampus of rat brain were observed, and the levels of activator protein-1 (AP-1) gene and protein, nerve growth factor (NGF), neurotrophin-3 (NT3), glial cell line-derived neurotrophic factor (GDNF), and brain-derived neurotrophic factor (BDNF) gene and protein level, etc. The experimental results showed that subchronic aluminum exposure damaged learning and memory in rats. The cognitive function damage in rats was more evident after increasing the aluminum intake dose. The more aluminum intake, the more pronounced the histological changes in the hippocampus will be. The expression level and protein content of neurotrophic factors in the hippocampus of rats showed a negative correlation with aluminum intake. In this experiment, we explored the mechanism of aluminum exposure in learning and memory disorders, and provided some data reference for further elucidation of the damage mechanism of aluminum on the nervous system and subsequent preventive measures.

The synergy between diurnal temperature range and calcium concentration help to predict hospital mortality in patients with acute myocardial infarction.

Epidemiological studies have suggested that cold is an important contributor to acute cardiovascular events and mortality. However, little is known about the Diurnal Temperature Range (DTR) impact on mortality of the patients with myocardial infarction. Calcium ions (Ca2+) play a vital role in the human body, such as cardiac electrophysiology and contraction. To investigate whether DTR on admission moderates the association between serum calcium and in-hospital mortality in patients with acute myocardial infarction (AMI). This retrospective study enrolled consecutive adult patients with AMI at a single center in China (2003-2012). Patients were divided into four groups (Ca-Q1-4) according to serum calcium concentration quartiles. Multivariate logistic regression modeling was used to assess whether DTR moderated the association between serum calcium and in-hospital mortality. The predictive value of serum calcium was evaluated by receiver operating characteristic (ROC) curve and net reclassification improvement (NRI) analyses. The study included 3780 patients. In-hospital mortality was 4.97% (188/3780). DTR moderated the association between serum calcium and in-hospital mortality (P-interaction = 0.020). Patients with low serum calcium in the highest DTR quartile exhibited an increased risk of in-hospital mortality (odds ratio for Ca-Q4 vs. Ca-Q1, 0.03; 95% confidence interval [95% CI], 0.01-0.20). In the highest DTR quartile, adding serum calcium concentration to the risk factor model increased the area under the ROC curve (0.81 vs. 0.76; P < 0.001) and increased NRI by 20.2% (95% CI 7.5-32.9; P = 0.001). Low serum calcium was an independent risk factor for in-hospital mortality in patients with AMI, and this association was moderated by DTR. Careful attention should be paid to patients with low serum calcium who experience a higher DTR on admission.

Removal of arsenic in acidic wastewater using Lead-Zinc smelting slag: From waste solid to As-stabilized mineral.

High-arsenic wastewater has long been considered a major threat to ecological balance and human health because of its strong toxicity and high mobility. Herein, an environmentally friendly process was proposed for As removal and fixation in the form of As-stabilized mineral, using Lead-Zinc smelting (LZS) slag as the in situ Fe donor, neutralizer, and crystal seed. The slag was dissolved in the wastewater and released Fe and Ca ions, while simultaneously increasing the pH value of the solution to help scorodite synthesis. The dissolved Ca2+ ion preferentially reacted with SO42- ion in the form of CaSO4·2H2O precipitate as in situ "seeds" for As precipitation. The dissolved Fe(II) and As(III) ions were oxidized to Fe(III) and As(V) ions by H2O2, and later reacted with each other to generated amorphous ferric arsenate on the surface of CaSO4·2H2O, and then evolved into scorodite crystals with high stability. With a Fe/As molar ratio of 2, a reaction temperature of 90 °C, and a reaction time of 12 h, 98.42% of As was effectively precipitated from the wastewater with an initial As concentration of 7530.00 mg/L. Moreover, the leached As concentration of the As-bearing precipitate in the TCLP test was 3.46 mg/L. The concentration of the residual As and heavy metals ions in the final filtrate was lower than local wastewater discharge standards, successfully realizing the treatment of smelting wastewater. In summary, a prospective process successfully shows a great potential for co-treatment of LZS wastewater and slag, which could advance the large-scale disposal of LZS plants.

Novel iron-supported ZSM-5 molecular sieve remove arsenic from wastewater by heterogeneous nucleation with pH limit breaking.

Molecular sieves have also been used for arsenic adsorption in recent years because of their special structure. In order to solve the problem of arsenic pollution in drinking water and/or industrial wastewater, ZSM-5/Fe adsorbent was prepared by loading iron on ZSM-5 molecular sieve. It is also used as an excellent adsorbent for removing arsenic and other heavy metal ions from industrial wastewater. At room temperature, the concentration of arsenic was reduced from 100 mg/L to 0.006 mg/L after the solution pH was adjusted to the range of weak acid to weak base (4-10) and 0.5 g of ZSM-5/Fe adsorbent was added for reacting 2 h. The adsorption capacity reached 40.00 mg/g, the adsorption efficiency reached 99.99%, reaching the national standard of drinking water. Adsorption thermodynamics, kinetics and isotherms showed that the adsorption mechanism of arsenic is heterogeneous nucleation adsorption (including electrostatic attraction and chemical precipitation). Moreover, ZSM-5/Fe adsorbent can adjust pH spontaneously by using non-skeleton Si-Al phase to achieve effective adsorption from weak acid to weak base. At the same time, ZSM-5/Fe adsorbent showed good reusability and stability in five cycles. This study provides an important idea for the application of ZSM-5 molecular sieve in many fields and the efficient removal of arsenic from drinking water and industrial wastewater.

Arsenic Induces Continuous Inflammation and Regulates Th1/Th2/Th17/Treg Balance in Liver and Kidney In Vivo.

Numerous studies on arsenic-induced hepatonephric toxicity including cancer have been reported. Given that chronic inflammatory response and immune imbalance are associated with oncogenesis, we investigated whether arsenic could influence the hepatic and nephritic expression of inflammatory factors and the differentiation of T cells. Mice were exposed to NaAsO2 (0, 25, and 50 mg/L) for 1 and 3 months. Our data showed the destruction of the structure and inflammatory infiltration in the liver. The arsenic markedly increased the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The myeloperoxidase (MPO) activities increased in the liver at 25 and 50 mg/L arsenic for 3 months as well as in the kidney at both 1 and 3 months. An increased expression of inflammatory indicators (IL-1ß, IL-12, and TNF-α) at 25 and 50 mg/L arsenic for 1 and 3 months in the liver and kidney, as well as IL-1ß in the liver for 3 months and in the kidney at 50 mg/L for 1 and 3 months were demonstrated in our experiments. Besides, a definite tendency toward Th1/Th17 cytokines in the liver while Th2/Th17 cytokines in kidney was also observed by arsenic. Moreover, arsenic enhanced the expression of MAPK/Nrf2/NF-κB signaling molecules. In conclusion, the results of the study suggested that arsenic induces continuous immune-inflammatory responses in the liver and kidney.

Bacteroides fragilis prevents aging-related atrial fibrillation in rats via regulatory T cells-mediated regulation of inflammation.

BACKGROUND: Aging plays a critical role in the genesis of atrial fibrillation (AF) and also changes the gut microbes. Whether the aging-associated gut dysbiosis contributes to the development of aging-related AF and whether the gut microbes can be a target to prevent aging-related AF remains unknown. METHODS AND RESULTS: 16S rRNA gene sequencing was performed to reveal the changes of gut microbes in elderly patients with AF, and the result showed that the intestinal abundance of B. fragilis was significantly decreased in elderly patients with AF. Subsequently, we examined the impact of B. fragilis supplementation on AF promotion, atrial structural remodeling and inflammation response in D-galactose induced aging rats. We found that oral administration of B. fragilis prevented AF inducibility and duration, which was associated with attenuation of atrial senescence, apoptosis and fibrosis. Furthermore, B. fragilis significantly diminished the systemic and atrial inflammation, which is accompanied by an increase in the number of Treg cells in the spleen and blood. More importantly, we found that the circulation level of polysaccharide A (PSA), the metabolite synthesized by B. fragilis, was reduced in elderly patients with AF and could predict the occurrence of AF, and B. fragilis increased the circulation concentration of PSA in D-galactose induced aging rats. CONCLUSIONS: The abundance of B. fragilis was lower in elderly patients with AF. Oral administration of B. fragilis significantly attenuated inflammatory response by increasing Treg cells, thereby preventing atrial structural remodeling and inhibiting AF promotion in D-galactose induced aging rats. This study provides experimental evidence for the effectiveness of targeting gut microbes in the prevention of aging-related AF.

Heme oxygenase-1 (HO-1) assists inorganic arsenic-induced immune tolerance in murine dendritic cells.

Inorganic arsenic, a well-known human carcinogen, poses a major threat to global health. Given the immunosuppressive potentials of inorganic arsenic as well as limited understanding of this metalloid on antigen-presenting dendritic cells (DCs), we systematically screened the immune targets in response to arsenic treatment, as well as its possible molecular mechanism in cultured murine DCs. Our results denoted that arsenite (As) significantly induced immune tolerance by down-regulating the expression of phenotypic molecules, pro-inflammatory factors and T-lymphocyte helper (Th)1/Th17-inducible cytokines in lipopolysaccharides (LPS)-stimulated myeloid-derived dendritic cells (BMDCs). Inconsistent with dampened phosphorylation of immune-related proteins (nuclear factor kappa-B) NF-κB, p38 and JNK, the metalloid drastically induced the expression of Heme oxygenase-1 (HO-1) protein, which enlightened us to continuously explore the possible roles of HO-1 pathway in As-induced immune tolerance in BMDCs. In this respect, immunosuppressive properties of HO-1 pathway in BMDCs were firstly confirmed through pharmacological overexpression of HO-1 by both CoPP and CORM-2. By contrast, limited HO-1 expression by HO-1 inhibitor ZnPP specifically alleviated As-mediated down-regulation of CD80, chemokine factor C-C chemokine receptor 7 (CCR7), tumor necrosis factor (TNF) -α, Interleukin (IL)-23 and IL-6, which reminds us the peculiarity of HO-1 in As-induced immune tolerance in murine DCs. Based on these experimental findings, we postulated the immunosuppressive property of inorganic arsenic might be mediated partially by HO-1 in DCs, thus contributing to the interactions of DCs-polarized differentiation of T-lymphocyte subtype as well as the development of infections and malignant diseases.

[Inorganic arsenic exposure suppresses immunomodulatory effect of renal CD4+ T lymphocytes in mice].

Objective To investigate the effects of inorganic arsenic exposure on the differentiation of renal CD4+T lymphocytes and the possible mechanism. Methods Female C57BL/6 mice were randomly divided into control group, (2.5, 5, 10) mg/kg NaAsO2 exposure groups, 10 mice in each group. As was administered once intragastrically for 24 hours, and control mice were treated with normal saline. Real-time fluorescence quantitative PCR was used to detect T helper type 1 (Th1) cell-specific transcription factor T-box expressed in T cells (T-bet) and IFN-γ, Th2 cell-specific transcription factor GATA-binding protein 3 (GATA3) and interleukin 4 (IL-4), Th17 cell-specific transcription factor retinoic acid related orphan nuclear receptor γt (ROR-γt) and cytokine IL-22, regulatory T cells (Tregs)-specific transcription factor forkhead box P3 (FOXP3) and cytokine transforming growth factor-ß (TGF-ß) mRNA levels. We used commercial kits to detect catalase (CAT) activity and total antioxidant capacity (T-AOC) in serum as well as renal malondialdehyde (MDA) and superoxide dismutase (SOD). Results Compared with the control group, the body mass, renal mass and kidney index of the mice in all arsenic-treated groups have no significant changes. The levels of the master transcription factors T-bet, GATA3, ROR-γt and FOXP3 as well as related cytokines IFN-γ, IL-4, IL-22 and TGF-ß of Th1, Th2, Th17 cells and Tregs decreased in the arsenic-treated groups. Serum CAT activity and T-AOC level in the arsenic-treated mice dropped greatly. In addition, arsenic markedly increased renal MDA level while decreased SOD activity. Conclusion Inorganic arsenic exposure can suppress renal T cell subpopulation function and induce renal oxidative injure.

Desulfurization Performance and Kinetics of Potassium Hydroxide-Impregnated Char Sorbents for SO2 Removal from Simulated Flue Gas.

Potassium hydroxide-impregnated char sorbents (KOH/char) prepared via an ultrasonic-assisted method were used for SO2 removal from flue gas. The desulfurization experiment was analyzed using a fixed-bed reactor under 40-150 °C temperature range, using simulated flue gas. X-ray diffraction (XRD), Fourier-transform infrared spectroscopy, and scanning electron microscopy/energy-dispersive X-ray spectroscopy (SEM/EDS) were used to analyze both the chemical and physical characteristics of the sorbents. The analyzed results exposed that the complete elimination of SO2 from flue gas was achieved when using the char/KOH sorbent with a mass ratio of char to KOH of 11:1. It was noted that temperature had a substantial influence on the desulfurization performance with sulfur capacity maximized at 100 °C. Experimental results also revealed that a small amount of O2 present in the solvent could improve the SO2 removal efficiency of the sorbent. The analyzed XRD patterns showed that K2SO4 was the main desulfurization product, which was consistent with the SEM/EDS analysis. The experimental results were well-described with the Lagergren first-order adsorption kinetics model with the activation energy (E a) of the SO2 adsorption by KOH/char sorbent of 20.25 kJ/mol.

Chronic arsenic exposure induces the time-dependent modulation of inflammation and immunosuppression in spleen.

BACKGROUND: Arsenic exposure has become a matter of worldwide concern, which is associated with immune-related diseases. However, little is known about its effect on inflammatory immune-related homeostasis. The purpose of our study was to understand the potential tuning of above responses exerted by chronic arsenic exposure. METHODS: Kunming mice were treated with 25 and 50 mg/L sodium arsenite for 1, 3 and 12 months via drinking water. At different endpoints of arsenic exposure, all animals and the whole spleen of the mice were weighed. The total arsenic levels of spleen were determined by the HPLC-HG-AFS method. Splenic NF-κB, MAPK and NRF2 protein levels by treatment of 25 mg/L NaAsO2 for 1, 3 and 12 months and 25 mg/L and 50 mg/L NaAsO2 for 12 months were assessed by western blot. Total RNA of spleen was isolated and relative mRNA levels of Foxp3, Il-10, Tnf-α, Il-6, Ifn-γ, Il-1ß and Il-12 were measured by real-time PCR. RESULTS: Our results shown that NF-κB were continuously activated with treatment of 25 mg/L arsenic from 1, 3 to 12 months and 50 mg/L arsenic for 12 months. The transcription factor Foxp3 increased at 1 month but decreased at 3 and 12 months no matter 25 or 50 mg/L arsenic exposure. However, cytokine Il-10 always showed increased trend in mice treated with 25 or 50 mg/L arsenic for 1, 3 and 12 months. The transcriptional profiles of Tnf-α, Il-1ß, Il-6, Ifn-γ and Il-12 revealed transient elevation at 1 and 3 months but shown significant decrease at 12 months on the whole. In addition, the sustained activation of inflammatory MAPK and anti-oxidative Nrf2 signaling pathways were observed in mice exposed to arsenic for 1, 3 and 12 months. CONCLUSION: In summary, our experiment in vivo suggested chronic arsenic exposure induces the time-dependent modulation of the inflammation and immunosuppression in spleen, which may be related to the activation of Tregs induced by MAPK/NF-κB as well as the increased transcription level of Foxp3 and Il-10.

Adverse Effects of Inherent CaO in Coconut Shell-Derived Activated Carbon on Its Performance during Flue Gas Desulfurization.

Activated carbon has been used commercially to remove SO2 from coal combustion flue gas. However, the role of inherent CaO in activated carbon is uncertain. In this study, the adverse effects of inherent CaO in the activated carbon derived from coconut shell (CSAC) on its desulfurization performance were systematically studied at the temperature range of 60-100 °C in a fixed-bed reactor. The solid sorbent samples were analyzed using scanning electron microscopy, X-ray diffraction, X-ray fluorescence, Fourier transform infrared spectroscopy, and Brunauer-Emmett-Teller analysis. The flue gas compositions were analyzed by using an online flue gas analyzer. The experimental results showed that the inherent CaO had a profoundly adverse influence on the desulfurization capacity and efficiency of CSAC at all of the temperatures studied. This adverse influence was clearly identified by a comparison of the desulfurization performance of the raw CSAC to those of the acid-washed CSAC samples. It was found that the removal of the inherent CaO from CSAC using a pretreatment of HCl aqueous solution led to an increase in the desulfurization capacity of 41.7%. The adverse effects were attributed to the conversion of CaO into dihydrate calcium sulfate whiskers which formed solid crystals that blocked the micropores of the CSAC particles.

Tissue- and Region-Specific Accumulation of Arsenic Species, Especially in the Brain of Mice, After Long-term Arsenite Exposure in Drinking Water.

Arsenic is identified as a known carcinogen and ubiquitously exists in nature. It appears that accumulation of inorganic arsenic (iAs) and its methylated metabolites in various tissues is closely correlated with the long-term toxicity and carcinogenicity of this metalloid. In this study, various arsenic species in murine tissues, especially in the cerebral cortex, cerebellum, and hippocampus, were determined after long-term exposure to 25, 50, 100, and 200 mg/L sodium arsenite in drinking water for 1 and 12 months. Our data showed that the amount of total arsenic (TAs) increased in an obvious dose-dependent manner in various tissues, and TAs levels were in the order of urinary bladder > brain > lung > liver > kidney > spleen. Furthermore, iAsIII and DMA could be observed in all tissues and brain regions with DMA being the predominant metabolite. The bladder, brain, and lung orderly contained the higher levels of DMA, while the liver, kidney, and spleen accumulated the higher proportion of iAsIII. MMA was preferentially accumulated in the lung and bladder of mice regardless of arsenic exposure doses or duration. What's more, amazingly higher levels of MMA were observed in the hippocampus, which was distinguished from the cerebral cortex and cerebellum. Together with these results, our study clearly demonstrates that the accumulation of iAs and its methylated metabolites is tissue-specific and even not homogeneous among different brain regions in mice by long-term exposure to arsenite. Our study thus provides crucial information for recognizing arsenical neurotoxicity, and reducing the uncertainty in the risk assessment for this toxic metalloid.