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Short-chain chlorinated paraffins (SCCPs) are a persistent organic pollutant, and limited information is available on their bioaccumulation and trophic transfer, which would be affected by carbon chain length, chlorine content, and hydrophobicity. In this study, relevant data on SCCPs in water, sediments, and organisms collected from Laizhou Bay were analyzed to investigate the specific distribution of SCCPs and their bioaccumulation and trophic transfer. In water and sediments, the average SCCP concentrations (ΣSCCPs) were 362.23 ± 81.03 ng/L and 609.68 ± 90.28 ng/g d.w., respectively. In 28 species of organisms, the ΣSCCPs varied from 70.05 to 47,244.13 ng/g l.w. (average = 648 ± 7360) and the predominant homologs were C13 (average = 34.91%) and Cl5–7 (average = 93.13%), differing from those in water (average = C11 32.75% and average = Cl5–7 88%) and sediments (average = C13 31.60% and average = Cl6–8 87.16%). The logarithm bioaccumulation factors (BAFs) of ΣSCCPs were 1.18–2.74 and were positively correlated with the log Kow. A significant negative linear relationship was observed between biota-sediment accumulation factors (BSAFs) and log Kow. It is suggested that the hydrophobicity may affect the bioaccumulation of SCCPs. SCCPs demonstrated a trophic magnification factor (TMF) ranging from 2.19 to 3.00 (average = 2.51) and exhibited a significant linear correlation with carbon chain length (p < 0.05) and log Kow values (p < 0.05), suggesting that SCCPs have biomagnification potential in Laizhou Bay that is affected by hydrophobicity and carbon chain length. [ABSTRACT FROM AUTHOR]

Background: Intervertebral disc degeneration (IDD) underlies the pathogenesis of degenerative diseases of the spine; however, its exact molecular mechanism is unclear. Purpose: To explore the molecular mechanism of mechanical pressure (MP)-induced IDD and to assess the role and mechanism of Rosuvastatin (RSV) inhibits MP-induced IDD. Methods: SD rat nucleus pulposus cells (NPCs) were cultured in vitro and an apoptosis model of NPCs was constructed using MP. Proliferative activity, reactive oxygen species content, apoptosis, and wound healing were detected in each group of NPCs, respectively. The expression of relevant proteins was detected by qPCR and Western Blot techniques. 18 SD rats were randomly divided into control, pressure and RSV groups. Elisa, qPCR, Western Blot and immunohistochemical staining techniques were used to detect changes in the content of related proteins in the intervertebral discs of each group. HE staining and Modified Saffron-O and Fast Green Stain Kit were used to assess IDD in each group. Results: MP treatment at 1.0 MPa could significantly induce apoptosis of NPCs after 24 h. MP could significantly inhibit the proliferative activity and wound healing ability of NPCs, and increase the intracellular reactive oxygen species content and apoptosis rate; pretreatment with RSV could significantly activate the Nrf2/HO-1 signaling pathway and reverse the cellular damage caused by MP; when inhibit the Nrf2/HO-1 signaling pathway activation, the protective effect of RSV was reversed. In vivo MP could significantly increase the content of inflammatory factors within the IVD and promote the degradation of extracellular matrix, leading to IDD. When the intervention of RSV was employed, it could significantly activate the Nrf2/HO-1 signaling pathway and improve the above results. Conclusion: RSV may inhibit MP-induced NPCs damage and IDD by activating the Nrf2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Three catalyst surfaces are obtained by loading active metal clusters with different Cu doping ratios on ZrO 2 surface: (a) Ni/ZrO 2 , (b) Ni 2 Cu 1 /ZrO 2 , and (c) Ni 1 Cu 2 /ZrO 2. The activation of CH 4 and the formation-removal processes of carbon atoms on the different catalyst surfaces are calculated by the DFT method. The results proved that Cu doping greatly hindered the deep cracking of methane. The energy barriers for the deep cracking of methane on Ni 2 Cu 1 /ZrO 2 and Ni 1 Cu 2 /ZrO 2 catalysts are increased to 1.45 eV and 1.60 eV, respectively, and this value is 1.32 eV for Ni/ZrO 2 surface. Meanwhile, the Cu doping inhibited the occurrence of the initial carbon deposition step. Compared with the Ni/ZrO 2 catalysts, the reaction rate constant k of the initial carbon deposition step is reduced to 1 1 × 10 3 and 1 5 × 10 2 on the Ni 2 Cu 1 /ZrO 2 and Ni 1 Cu 2 /ZrO 2 catalysts, respectively. On the contrary, Cu doping can promote the gasification process of carbon atoms. On the Ni/ZrO 2 surface, the energy barrier for CO generation is 1.31 eV, while on the Ni 2 Cu 1 /ZrO 2 and Ni 1 Cu 2 /ZrO 2 surfaces, this value is reduced to 1.06 eV and 0.89 eV, respectively. The computational results in this paper are of guiding significance for the design and synthesis of efficient and stable DRM reaction catalysts. [Display omitted] • Cu-doping raises the energy barrier for deep cracking of CH 4 by affecting the d -band center of the active metal cluster. • Cu-doping promotes the gasification of surface carbon and lowers the formation of deposited carbon. • The catalyst with high percentage of Cu-doping (Ni 2 Cu 1 /ZrO 2) shows the best coke-resistance. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the molecular mechanism underlying the inhibitory effect of sinomenine (SN) on interleukin-1β (IL-1β)-induced apoptosis in nucleus pulposus cells (NPCs), and to evaluate the potential role of SN in preventing intervertebral disk degeneration (IDD).Methods: The Rat NPCs were cultured in vitro and identified using Hematoxylin-Eosin (HE) staining, toluidine blue staining, and immunofluorescence analysis. NPCs were pretreated with or without SN, then induced with IL-1β to assess cell viability, ROS levels, apoptotic rates, and wound healing ability. Relevant protein expression was detected using Elisa, qPCR and Western Blot techniques. NPCs were pretreated with SN, either alone or in combination with Nrf2-IN-1 or SC, before being induced to undergo apoptosis by IL-1β. Apoptosis was detected using Hoechst staining, while qPCR and Western Blot techniques assessed protein expression. Rat caudal intervertebral discs were induced with IDD, with or without SN injection, and then co-injected with IL-1β. The levels of IDD were evaluated using HE staining and modified saffron-O-fix green cartilage staining. Relevant protein expression was detected using Elisa, qPCR, and Western Blot techniques.Results: IL-1β significantly reduced NPC activity, induced ROS accumulation and apoptosis, decreased cell healing rate, promoted the expression and secretion of inflammatory factors, and inhibited extracellular matrix synthesis. However, pretreatment with SN effectively reversed these effects. Inhibition of the Keap1/Nrf2 signaling pathway or activation of the NF-κB signaling pathway significantly attenuated the cytoprotective effects of SN and increased apoptosis. Acupuncture combined with IL-1β injection markedly induced intervertebral disc degeneration in rat caudal spine, upregulated inflammatory factors expression and secretion, and downregulated extracellular matrix synthesis. SN intervention notably enhanced antioxidant enzyme expression and reversed these outcomes.Conclusion: SN can prevent IL-1β-induced apoptosis of NPCs and ameliorate IDD by activating the Keap1/Nrf2 pathway and inhibiting the NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

The effect of oxygen vacancies on the adsorption and activation of CO2 on the surface of different phases of ZrO2 is investigated by density functional theory (DFT) calculations. The calculations show that the oxygen vacancies contribute greatly to both the adsorption and activation of CO2. The adsorption energy of CO2 on the c-ZrO2, t-ZrO2 and, m-ZrO2 surfaces is enhanced to 5, 4, and 3 folds with the help of oxygen vacancies, respectively. Moreover, the energy barrier of CO2 dissociation on the defective surfaces of c-ZrO2, t-ZrO2, and m-ZrO2 is reduced to 1/2, 1/4, and 1/5 of the perfect surface with the assistance of oxygen vacancies. Furthermore, the activation of CO2 on the ZrO2 surface where oxygen vacancies are present, and changes from an endothermic reaction to an exothermic reaction. This finding demonstrates that the presence of oxygen vacancies promotes the activation of CO2 both kinetically and thermodynamically. These results could provide guidance for the high-efficient utilization of CO2 at an atomic scale. [ABSTRACT FROM AUTHOR]

The adsorption and growth mechanisms of Cn (n = 1–6) on different Cu–Ni surfaces are calculated by density functional theory (DFT). The results demonstrate that Cu doping affects the growth mechanism of the deposited carbon on the catalyst surface. Firstly, the addition of Cu weakens the interaction between Cn and the adsorbed surface, which is proved by the results of density of states (DOS) and partial density of states (PDOS). The weakening of the interaction allows Cn to perform at higher proportions of Cu-doped surfaces with a behavior consistent with that in the gas phase. A comparison of the growth energies of the different pathways of Cn in the gas phase shows that the main pathway for the Cn growth is chain-to-chain (CC). The CC reaction is also the main pathway for the growth of Cn on the surfaces, which is enhanced by the doping of Cu. In addition, analysis of the growth energy revealed that C2–C3 is the rate-determining step in the growth process of Cn. The doping of Cu enhances the growth energy of this step, contributing to the suppression of the growth of the deposited carbon on the adsorbed surface. Moreover, an average carbon binding energy shows that the doping of Cu on the Ni surface could weaken the structural stability of Cn, favoring the elimination of carbon deposited on the catalyst surface. [ABSTRACT FROM AUTHOR]

Methane activation is a key step in the application of natural gas converting into high-value added chemicals via methane steam/dry reforming reactions. Ni element was found to be the most widely used catalyst for these reforming processes. In this work, methane activation on Ni surface from cluster to nanoparticle has been studied through detailed DFT calculations. Ni13, Ni55 and Ni116 show different ability for C–H bond activation of CH 4 molecule. Ni13 is considered as a typical cluster model in the surface reaction, and proved to exhibit unique performance for CH 4 activation due to its size effect. C–H bond activation on Ni13 requires to overcome a relatively low energy barrier of 0.8 eV, indicating it is favored to carry out. With the increase of Ni particle from cluster to nanoparticle, it shows the change of Ni surface structure, which will affect the catalytic performance for CH 4 activation. Ni55 and Ni116 mainly consist of Ni(111), Ni(100) and step/edge surface. Step/edge surface shows a promising ability for C–H bond activation with an energy barrier around 1.0 eV, however, it accounts for the smallest proportion in Ni55 and Ni116 particles, compared to the Ni(111) and Ni(100). It suggests that flat site is dominant on Ni55 and Ni116 nanoparticles, compared to the step/edge site. On the other hand, the CH 4 activation on the Ni(111) and Ni(100) of nanoparticle needs to overcome an energy barrier over 2.0 eV, which is much larger than that on the Ni13 cluster and step/edge surface of Ni nanoparticle. As a result, step/edge site of Ni particle presents the best performance for C–H activation, while flat surface shows weak ability. Thus, to enhance the catalytic ability for CH 4 activation, the particle of Ni should be limited in the cluster-size instead of nano-size. This paper could provide insights into understanding size effect of Ni particle on CH 4 activation, and proposed results would give some guidance for the development of high-efficient Ni reforming catalysts. CH 4 activation on Ni surface from cluster to nanoparticle. [Display omitted] • Ni13 is proved to exhibit unique performance for CH 4 activation due to its size effect. • Flat site is dominant on Ni55 and Ni116 nanoparticles compared to the step/edge site. • Step/edge surface shows a promising ability for C–H bond activation. • Larger amount of charge transfer from catalysts' surface to CH 4 could make the activation of C–H bond more easily. [ABSTRACT FROM AUTHOR]

Evodiamine is a natural alkaloid extracted from Fructus Evodia. This bioactive alkaloid has been reported to have a wide range of biological activities, including anti-injury, antiobesity, vasodilator, and anti-inflammatory effects. In recent years, it has been found that evodiamine has tumor-suppressive effects on a variety of tumors. There is growing evidence that evodiamine can inhibit the rapid proliferation of tumor cells, induce cell cycle arrest at a certain phase, increase the incidence of apoptosis, promote autophagy, inhibit microangiogenesis and migration, and regulate immunotherapy. Evodiamine can inhibit Wnt/β-catenin, mTOR, NF-κB, PI3K/AKT, JAK-STAT, and other signaling pathways in various cancer cells, and it can significantly downregulate the expression of many tumor markers, such as VEGF and COX-2. These facts partially explain the antitumor mechanism of evodiamine. In this article, the antitumor mechanism of evodiamine was reviewed to provide the basis for its clinical application and therapeutic development in the future. [ABSTRACT FROM AUTHOR]

Ankylosing spondylitis (AS) is a progressive systemic disease characterized by chronic inflammation response of the sacroiliac joint and spine. Long non-coding RNAs (lncRNAs) are widely involved in the regulation of various diseases. However, the role of lncRNA maternally expressed gene 3 (MEG3) in the inflammatory response of AS has not been studied. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammatory cytokines interleukin-1β (IL-1β) and interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in tissues and cells. The expression levels of MEG3, microRNA-146a (miR-146a), and inflammatory cytokines were measured by quantitative real-time PCR (qRT-PCR). Correlation between MEG3 or miR-146a and inflammatory cytokines was analyzed by Pearson analysis. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to clarify the interaction between MEG3 and miR-146a. MEG3 was downregulated in AS patients, negatively correlated with the levels of IL-1β, IL-6, and TNF-α, and blocked the inflammatory response of AS. MiR-146a was upregulated in AS patients and could interact with MEG3. The expression of miR-146a was positively correlated with IL-1β, IL-6, and TNF-α levels. Overexpression of miR-146a reversed the inhibitory effect of abnormal MEG3 expression on inflammatory cytokines. LncRNA MEG3 plays an anti-inflammatory role in AS partially through targeting miR-146a, which provides a potential new means for the treatment of AS patients. [ABSTRACT FROM AUTHOR]

The adsorption and growth mechanisms of C n ( n = 1-6) on different Cu-Ni surfaces are calculated by density functional theory (DFT). The results demonstrate that Cu doping affects the growth mechanism of the deposited carbon on the catalyst surface. Firstly, the addition of Cu weakens the interaction between C n and the adsorbed surface, which is proved by the results of density of states (DOS) and partial density of states (PDOS). The weakening of the interaction allows C n to perform at higher proportions of Cu-doped surfaces with a behavior consistent with that in the gas phase. A comparison of the growth energies of the different pathways of C n in the gas phase shows that the main pathway for the C n growth is chain-to-chain (CC). The CC reaction is also the main pathway for the growth of C n on the surfaces, which is enhanced by the doping of Cu. In addition, analysis of the growth energy revealed that C 2 -C 3 is the rate-determining step in the growth process of C n . The doping of Cu enhances the growth energy of this step, contributing to the suppression of the growth of the deposited carbon on the adsorbed surface. Moreover, an average carbon binding energy shows that the doping of Cu on the Ni surface could weaken the structural stability of C n , favoring the elimination of carbon deposited on the catalyst surface.

Background: Mechanical load contributes a lot to the initiation and progression of disc degeneration. Annulus fibrosus (AF) cell biology under mechanical tension remains largely unclear. Objective: The present study was aimed to investigate AF cell senescence under mechanical tension and the potential role of autophagy. Methods: Rat AF cells were cultured and experienced different magnitudes (5% elongation and 20% elongation) of mechanical tension for 12 days. Control AF cells were kept static. Cell proliferation, telomerase activity, cell cycle fraction, and expression of senescence-related molecules (p16 and p53) and matrix macromolecules (aggrecan and collagen I) were analyzed to evaluate cell senescence. In addition, expression of Beclin-1 and LC3, and the ratio of LC3-II to LC3-I were analyzed to investigate cell autophagy. Results: Compared with the control group and 5% tension group, 20% tension group significantly decreased cell proliferation potency and telomerase activity, increased G1/G0 phase fraction, and up-regulated gene/protein expression of p16 and p53, whereas down-regulated gene/protein expression of aggrecan and collagen I. In addition, autophagy-related parameters such as gene/protein expression of Beclin-1 and LC3, and the ratio of LC3-II to LC3-I, were obviously suppressed in the 20% tension group. Conclusion: High mechanical tension promotes AF cell senescence though suppressing cellular autophagy. The present study will help us to better understand AF cell biology under mechanical tension and mechanical load-related disc degeneration., (© 2019 The Author(s).)

Mechanical overload is a risk factor of disc degeneration. It can induce disc degeneration through mediating cell apoptosis. Mechano growth factor (MGF) has been reported to inhibit mechanical overload-induced apoptosis of chondrocytes. The present study is aimed to investigate whether MGF can attenuate mechanical overload-induced nucleus pulposus (NP) cell apoptosis and the possible signaling transduction pathway. Rat NP cells were cultured and subjected to mechanical overload for 7 days. The control NP cells did not experience mechanical load. The exogenous MGF peptide was added into the culture medium to investigate its protective effects. NP cell apoptosis ratio, caspase-3 activity, gene expression of Bcl-2, Bax and caspase-3, protein expression of cleaved caspase-3, cleaved PARP, Bax and Bcl-2 were analyzed to evaluate NP cell apoptosis. In addition, activity of the p38 MAPK pathway was also detected. Compared with the control NP cells, mechanical overload significantly increased NP cell apoptosis and caspase-3 activity, up-regulated gene/protein expression of pro-apoptosis molecules (i.e. Bax, caspase-3, cleaved caspase-3 and cleaved PARP) whereas down-regulated gene/protein expression of anti-apoptosis molecule (i.e. Bcl-2). However, exogenous MGF partly reversed these effects of mechanical overload on NP cell apoptosis. Further results showed that activity of the p38 MAPK pathway of NP cells cultured under mechanical overload was decreased by addition of MGF peptide. In conclusion, MGF is able to attenuate mechanical overload-induced NP cell apoptosis, and the p38 MAPK signaling pathway may be involved in this process. The present study provides that MGF supplementation may be a promising strategy to retard mechanical overload-induced disc degeneration., (© 2019 The Author(s).)