Insight into the role of SO2 on selenium conversion during adsorption by CaO: Theoretical calculation and experimental study.

SO2 can noticeably impact the control of high toxic selenium emissions from flue gas by CaO. Surprisingly, our experiments showed that under certain conditions, SO2 can promote selenium capture by CaO, rather than hinder it. To elucidate the underlying mechanism, a combination of theoretical calculations and experiments was conducted. Thermodynamic equilibrium analysis revealed that gaseous SO2 and solid Ca-S reaction products can promote SeO2 converting to SeO/Se0. The Ca-S products facilitated greater SeO2 conversion compared to SO2. Experimental results demonstrated that selenium adsorption capacity of incompletely sulfurized CaO (CaO with pre-adsorbed SO2) was higher than that of completely sulfurized CaO (Ca-S products), highlighting the importance of adsorption sites of CaO. Density functional theory calculations showed that the pre-adsorbed SO2 hardly affected selenium adsorption energy on the SO2/CaO surface, while completely sulfurized CaO had low selenium adsorption energy, explaining the experimental phenomenon and proving necessary of CaO. Additionally, SeO/Se0 had higher adsorption energy on CaO than SeO2. Overall, the promotion of SO2 on selenium adsorption was primarily affected by two factors: 1) sulfur facilitating SeO2 conversion to SeO/Se0 which can be adsorbed more easily by CaO; 2) sufficient adsorption sites on CaO surface existing for SeO/Se0 adsorption, despite co-adsorption with sulfur.

Transformation of Cr under sintering of Ca-rich solid waste with kaolin: Analysis of multi-element coupled interactions.

The high toxicity of Cr-Ca compounds generated during the heat treatment of solid waste will heavily threat the environment. In this work, a kind of Ca-rich river sludge which is bound with Ca and heavy metals was combusted with kaolin under 900 °C for 3 h in a muffle to study the transformation of Cr. The effects of kaolin on Cr transformation were investigated through sequential extraction, the risk assessment of heavy metals, and constant pH leaching test, also combined with crystal phase analysis of Ca-Al-Si minerals. The experimental results showed that the formation of Ca10(SiO4)3(SO4)3Cl2 was inhibited by the addition of 10% (mass fraction) kaolin and the released Cl promoted the evaporation of target elements in priority while 30% kaolin addition further inhibited the solidification of Cr. Furthermore, the effect of NaCl and CaCO3 on the Cr solidification by kaolin were also explored by leaching procedure or XRD analysis of calcination products of their mixtures. It should be noticed that the addition of kaolin in Cr2O3-CaCO3 mixture will directly react with CaCrO4 and fixed the generated Cr2O3 into internal layered structure, preventing its re-oxidization by the free CaO. This work aims to help illustrate the Cr transformation with existence of Ca during sintering of Ca-rich solid wastes and reduce the Cr contamination in future.

Respiratory Variations in Peak Peripheral Artery Velocities and Waveforms for Rapid Assessment of Fluid Responsiveness in Traumatic Shock Patients.

BACKGROUND This study aimed to assess the correlation between the variability of the end-inspiratory and end-expiratory blood flow waveform and fluid responsiveness (FR) in traumatic shock patients who underwent mechanical ventilation by evaluating peripheral arterial blood flow parameters. MATERIAL AND METHODS A cohort of 60 patients with traumatic shock requiring mechanical ventilation-controlled breathing received ultrasound examinations to assess the velocity of carotid artery (CA), femoral artery (FA) and brachial artery (BA). A rehydration test was performed in which of 250 mL of 0.9% saline was administered within 30 min between the first and second measurement of cardiac output by echocardiography. Then, all patients were divided into 2 groups, a responsive group (FR+) and a non-responsive group (FR-). The velocity of end-inspiratory and end-expiratory peripheral arterial blood flow of all patients was ultrasonically measured, and the variability were measured between end-inspiratory and end-expiratory. RESULTS The changes in the end-inspiratory and end-expiratory carotid artery blood flow velocity waveforms of the FR+ groups were significantly different from those of the FR- group (P<0.001). A statistically significant difference in ΔVmax (CA), ΔVmax (BA), and ΔVmax (FA) between these 2 groups was found (all P<0.001). The ROC curve showed that DVmax (CA) and ΔVmax (BA) were more sensitive values to predict FR compared to ΔVmax (FA). The sensitivity of ΔVmax (CA), ΔVmax (FA), and ΔVmax (BA) was 70.0%, 86.7%, and 93.3%, respectively. CONCLUSIONS The study showed that periodic velocity waveform changes in the end-inspiratory and end-expiratory peripheral arterial blood flow can be used for quick assessment of fluid responsiveness.

Green production of a novel sorbent from kaolin for capturing gaseous PbCl2 in a furnace.

The pollution of semi-volatile heavy metals is one of the key environmental risks for municipal solid waste incineration, and in-situ adsorption of metals within the furnace by mineral sorbents such as kaolin has been demonstrated as a promising emission control method. To lessen the consumption of sorbent, a novel material of amorphous silicate was produced from kaolin through pressurised hydrothermal treatment. Its performance of gaseous PbCl2 capture was tested in a fixed bed furnace and compared with unmodified kaolin and metakaolin. With increasing temperature, the adsorption rates for all sorbents declined due to higher saturated vapour pressure, while the partitions of residual form lead increased which indicated higher stability of heavy metals in the sorbent because of melting effect. The new sorbent with a larger surface area and reformed structure presented 26% more adsorption efficiency than raw kaolin at 900 °C, and increasing the modification pressure improved these properties. Additionally, the production of this high-temperature sorbent was relatively inexpensive, required little thermal energy and no chemicals to produce and no waste effluent was generated, thus being much cleaner than other modification methods.

Tomentosin Inhibits Lipopolysaccharide-Induced Acute Lung Injury and Inflammatory Response by Suppression of the NF-κB Pathway in a Mouse Model of Sepsis.

Acute lung injury (ALI) is a severe inflammatory disorder that causes respiratory failure. Cases of ALI are reported with increasing mortality rates each year. In this study, we investigated the anti-inflammatory role of tomentosin and its fundamental mechanisms against lipopolysaccharide (LPS)-induced ALI via the suppression of Toll-like receptor (TLR4)/nuclear factor-kappa beta (NF-κB) pathway in a mouse model of sepsis. ALI was induced to BALB/c mice through the administration of 10 µg of LPS concomitantly with tomentosin (20 and 25 mg/kg) treatment. Dexamethasone was used as a standard drug. Inflammatory cells were measured using a hemocytometer; myeloperoxidase (MPO) enzyme activity and pro-inflammatory cytokines were determined using commercial kits. The lung tissues of animals were examined histologically. The expression level of TLR4/NF-κB signaling molecules were analyzed by Western blotting. Tomentosin treatment decreased lung edema and reduced the levels of macrophages, lymphocytes, and neutrophils in the bronchoalveolar lavage fluid. Tomentosin also suppressed the status of pro-inflammatory markers and reduced the activation of iNOS, MPO, COX-2, and PGE2 in the lung. Tomentosin appreciably down-regulated the NF-κB/TLR4 signaling pathway in sepsis mice. Histological study also showed the protective effects of tomentosin. These findings show that tomentosin protects the LPS-induced ALI via suppression of TLR4/NF-κB signaling pathway in sepsis mice. Tomentosin could be a promising therapeutic agent to treat sepsis.

Resveratrol loaded oxidized mesoporous carbon nanoparticles: A promising tool to treat triple negative breast cancer.

Currently, breast cancer has become the most commonly diagnosed malignancy among females and triple negative breast cancer (TNBC) is a highly aggressive and metastatic subtype. The natural polyphenolic compound, resveratrol (3, 4', 5-trihydroxy-trans-stilbene, RES), has drawn great attention for its potential against TNBC. However, due to the poor aqueous solubility, the bioactivity of RES against TNBC is extremely hampered. In this study, oxidized mesoporous carbon nanoparticles (oMCNs) with size below 200 nm and excellent water dispersibility were synthesized using mild oxidation method and RES was successfully encapsulated into the pores of oMCNs with high drug loading efficiency (24.8% w/w). oMCNs exhibited good biocompatibility and excellent cellular uptake efficiency. Compared to pure RES, oMCNs-RES greatly improved the saturated solubility and in vitro release property. In vitro cytoxicity assay and apoptosis analysis showed that oMCNs-RES induced enhanced cytotoxic effect and pro-apoptosis effect mediated via the PARP and Caspase-3 protein cleavage in TNBC cell line, respectively. These results demonstrate oMCNs have the potential to deliver hydrophobic drugs and oMCNs-RES are promising in treating TNBC.

Low Dose of Paclitaxel Combined with XAV939 Attenuates Metastasis, Angiogenesis and Growth in Breast Cancer by Suppressing Wnt Signaling.

Triple-negative breast cancer (TNBC) accounts for 15% of overall breast cancer. A lack of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2 receptor) makes TNBC more aggressive and metastatic. Wnt signaling is one of the important pathways in the cellular process; in TNBC it is aberrantly regulated, which leads to the progression and metastasis. In this study, we designed a therapeutic strategy using a combination of a low dose of paclitaxel and a Wnt signaling inhibitor (XAV939), and examined the effect of the paclitaxel-combined XAV939 treatment on diverse breast cancer lines including TNBC cell lines (MDA-MB-231, MDA-MB-468, and BT549) and ER+ve cell lines (MCF-7 and T-47D). The combination treatment of paclitaxel (20 nM) and XAV939 (10 µM) exerted a comparable therapeutic effect on MDA-MB-231, MDA-MB-468, BT549, MCF-7, and T-47D cell lines, relative to paclitaxel with a high dose (200 nM). The paclitaxel-combined XAV939 treatment induced apoptosis by suppressing Bcl-2 and by increasing the cleavage of caspases-3 and PARP. In addition, the in vivo results of the paclitaxel-combined XAV939 treatment in a mice model with the MDA-MB-231 xenograft further confirmed its therapeutic effect. Furthermore, the paclitaxel-combined XAV939 treatment reduced the expression of ß-catenin, a key molecule in the Wnt pathway, which led to suppression of the expression of epithelial-mesenchymal transition (EMT) markers and angiogenic proteins both at mRNA and protein levels. The expression level of E-cadherin was raised, which potentially indicates the inhibition of EMT. Importantly, the breast tumor induced by pristane was significantly reduced by the paclitaxel-combined XAV939 treatment. Overall, the paclitaxel-combined XAV939 regimen was found to induce apoptosis and to inhibit Wnt signaling, resulting in the suppression of EMT and angiogenesis. For the first time, we report that our combination approach using a low dose of paclitaxel and XAV939 could be conducive to treating TNBC and an external carcinogen-induced breast cancer.

5-hydroxymethylfurfural-embedded poly (vinyl alcohol)/sodium alginate hybrid hydrogels accelerate wound healing.

Treating large acute or chronic wounds remains a challenging task because of a lack of effective methods to accelerate wound healing. Though growth factor-based wound products are found to be effective, they are costly and are potentially associated with increased cancer mortality. Effective, safe, and affordable strategies to tackle large or chronic wounds need to further be designed and developed. Here, we designed a new antioxidant-embedded hydrogel system for speeding up the wound healing process. We prepared multifunctional poly (vinyl alcohol)/sodium alginate (PVA/SA) hydrogels with the incorporation of 5-hydroxymethylfurfural (5-HMF) and silver nanoparticles (Ag-NPs), and investigated their physiochemical and biological properties in vitro and in vivo. PVA, SA, 5-HMF, and Ag-NPs were employed for good mechanical properties, good biocompatibility, anti-inflammation, and anti-bacterial activity, respectively. 5-HMF is commonly found in many food products (e.g. honey, coffee, and black garlic) and is known as an antioxidant. In our in vitro study, 5-HMF was found to effectively facilitate the proliferation and migration of human skin fibroblasts (HSF), and collagen production. Besides, 5-HMF-embedded PVA/SA hybrid hydrogels supported controlled release and good cell compatibility, and more importantly accelerated wound healing in vivo through ameliorated inflammation, enhanced angiogenesis/vascularization, increased collagen production, and promoted re-epithelialization.

miR-29b-3p promotes progression of MDA-MB-231 triple-negative breast cancer cells through downregulating TRAF3.

BACKGROUND: Breast cancer is the second common malignant cancer among females worldwide. Accumulating studies have indicated that deregulation of miRNA expression in breast cancer will contribute to tumorigenesis and form different cancer subtypes. However, the reported studies on miR-29b-3p-regulated breast cancer are limited so far. Herein, we investigated the role and mechanism of miR-29b-3p in the triple negative breast cancer cell line MDA-MB-231. METHODS: The relative miR-29b-3p expression in different breast cancer cell lines were determined by qRT-PCR. CCK8 and colony formation assay were used to determine the influence of miR-29b-3p on cell proliferation. Migration assay and invasion assay were performed for cell migration and invasion respectively. To study the cell integrity immunofluorescence was performed. TUNEL assay, flow cytometry assay, hoechst staining and western blot were conducted to determine the influence of miR-29b-3p inhibitor on cell apoptosis. TRAF3 was found to be the target gene of miR-29b-3p using bioinformatics predictions. Dual-luciferase assay was performed to determine the relative luciferase activity in NC, miR-29b-3p mimic, miR-29b-3p inhibitor with TRAF3 3'-UTR wt or TRAF3 3'-UTR mt reporter plasmids. The proteins expression of NF-κB signaling pathway in MDA-MB-231 after transfection with NC, miR-29b-3p mimic, miR-29b-3p inhibitor were determined by western blot. RESULTS: The miR-29b-3p expression was significantly increased in MDA-MB-231 compare with MCF-10A. miR-29b-3p inhibitor reduced the cell viability of MDA-MB-231 and inhibited cell migration and invasion. Cell cytoskeleton integrity destroyed after miR-29b-3p inhibitor treatment. Furthermore, we identified the mechanism and found miR-29b-3p targets the TRAF3 and activates NF-κB signaling pathway. CONCLUSIONS: From the above studies, our results indicated that miR-29b-3p acts as a promoter for the development of MDA-MB-231.

miR-29b-3p promotes progression of MDA-mB-231 triple-negative breast cancer cells through downregulating TRAF3

BACKGROUND: Breast cancer is the second common malignant cancer among females worldwide. Accumulating studies have indicated that deregulation of miRNA expression in breast cancer will contribute to tumorigenesis and form different cancer subtypes. However, the reported studies on miR-29b-3p-regulated breast cancer are limited so far. Herein, we investigated the role and mechanism of miR-29b-3p in the triple negative breast cancer cell line MDA-MB-231. METHODS: The relative miR-29b-3p expression in different breast cancer cell lines were determined by qRT-PCR. CCK8 and colony formation assay were used to determine the influence of miR-29b-3p on cell proliferation. Migration assay and invasion assay were performed for cell migration and invasion respectively. To study the cell integrity immunofluorescence was performed. TUNEL assay, flow cytometry assay, hoechst staining and western blot were conducted to determine the influence of miR-29b-3p inhibitor on cell apoptosis. TRAF3 was found to be the target gene of miR-29b-3p using bioinformatics predictions. Dual-luciferase assay was performed to determine the relative luciferase activity in NC, miR-29b-3p mimic, miR-29b-3p inhibitor with TRAF3 3'-UTR wt or TRAF3 3'-UTR mt reporter plasmids. The proteins expression of NF-κB signaling pathway in MDA-MB-231 after transfection with NC, miR-29b-3p mimic, miR-29b-3p inhibitor were determined by western blot. RESULTS: The miR-29b-3p expression was significantly increased in MDA-MB-231 compare with MCF-10A. miR-29b-3p inhibitor reduced the cell viability of MDA-MB-231 and inhibited cell migration and invasion. Cell cytoskeleton integrity destroyed after miR-29b-3p inhibitor treatment. Furthermore, we identified the mechanism and found miR-29b-3p targets the TRAF3 and activates NF-κB signaling pathway. CONCLUSIONS: From the above studies, our results indicated that miR-29b-3p acts as a promoter for the development of MDA-MB-231.

NF-κB inhibition attenuates LPS-induced TLR4 activation in monocyte cells.

Toll-like receptor (TLR) family are receptors for extracellular or intracellular signaling, such as lipopolysaccharide (LPS), or 12-O-tetradecanoylphorbol-13-acetate. TLR induces the differentiation of human myeloid monocytic­leukemia cells (THP-1) to macrophages. However, the relationship between extracellular or intracellular signaling and the TLR protein level remain to be determined. Using RT-PCR and western blot analysis, the aim of the present study was to determine whether TLR4, a major TLR family member, could be moderately upregulated by high concentration of LPS and whether it promoted the maturation of THP1 cells. The results showed that, upregulated TLR4 at the protein level and mRNA level enriched the TLR4 modulation style. In addition, TLR4 expression was blocked by nuclear factor (NF)-κB inhibitor, and LPS stimulated NF-κB binding in the TLR4 gene promoter. Therefore, the increased expression of TLR4 in the responsiveness of LPS-treated THP1 cells occurred in response to the upregulation of their respective receptors, as well as a tight binding of NF-κB in the TLR4 gene promoter.