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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]

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]

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.