Overlooked mechanism of Pb immobilization on montmorillonite mediated by dissolved organic matter in manure compost.

In this study, three kinds of dissolved organic matter (DOM) derived from fresh chicken manure (FDOM), immature compost (IDOM) and mature compost (MDOM) were employed to compare their effects on Pb adsorption onto montmorillonite (MMT). The potential mechanism was revealed by characterization of mineral structure and calculation of interface force. The results demonstrated that the adsorption capacity (qmax) of Pb onto MMT was decreased by 14.3% and 29.8% in the presence of FDOM and IDOM, respectively, while increased by 44.4% in the presence of MDOM, resulting from the release or co-adsorption of DOM-Pb complexes. Parallel factor (PARAFAC) further indicated that Pb mainly bound to protein-like substances in FDOM and IDOM, and fulvic-like in MDOM. The X-ray diffraction (XRD) analysis proved that MDOM-Pb complex had a stronger ability to enter into the interlayer of MMT. The van der Waals force dominated the adsorption of FDOM-Pb and IDOM-Pb, while ligand exchange was involved in the case of MDOM-Pb. This study provided a comprehensive insight into the geochemical behavior of livestock manure and its compost as well as their interactions with heavy metal and soil mineral.

Effects of biochar underwent different aging processes on soil properties and Cd passivation.

This study aims to determine the efficacy of biochar underwent different aging process including freeze-thaw cycling aging (FB), acidified aging (AB), and microbial aging (MB) on soil physicochemical properties and Cd passivation. The Cd-contaminated soil (3 mg·kg-1) amended with the three kinds of aging biochar (at 4% w:w) were subjected to 56-day incubation. The application of FB and MB in soil increased the soil pH (0.82-1.04, 0.27-9.36), CEC (1.06-2.53 cmol·kg-1, 1.66-2.59 cmol·kg-1), and organic matter content (2.28-4.67 g·kg-1, 3.70-5.48 g·kg-1). FB performed best in stabilizing Cd (17.06-23.65%). On the contrary, AB decreased the soil pH and CEC by 0.82-1.04 and 1.32-2.40 cmol·kg-1 and activated Cd by 11.6-19.24%. In conclusion, the efficacy of biochar on soil remediation and Cd passivation varied with aging method and cycle, and freeze-thaw treatment is an effective approach to improve the performance of biochar.

Remediation of cadmium contaminated soil by composite spent mushroom substrate organic amendment under high nitrogen level.

Cadmium (Cd) contamination in soil poses a serious threat to ecological environment and crop quality, especially under high nitrogen level. Here, the efficiency of composite organic amendment (spent mushroom substrate and its biochar) on remediation of Cd contaminated soil under high nitrogen level has been studied through a 42 days' soil incubation experiment. The results showed: (i) the application of composite organic amendment minimized the repercussions of high nitrogen and significantly reduced the exchangeable Cd proportion by 28.3%-29.5%, especially for Ca(NO3)2 treatment; (ii) the application of composite organic amendment improved the physicochemical properties of soil, such as pH, CEC and organic matter content increased by 0.63-0.99 unit, 39.69%-45.00% and 7.77%-11.47%, and EC decreased by 16.21%-44.47% compared with non-amendment Cd-contaminated soil, respectively; (iii) the application of composite organic amendment significantly increased the soil enzyme activities and microbial biomass, among which urease activity was increased most by 12.06-16.42 mg·g-1·d-1, and the copy number of AOA was decreased by 30.6%- 92.0%, and the copy number of AOB was increased most by about 45 times. In brief, the composite organic amendment can alleviate the adverse effects of Cd and nitrogen on the soil, but its long-term efficacy needs to be verified in further field study.

Insight into interactions of heavy metals with livestock manure compost-derived dissolved organic matter using EEM-PARAFAC and 2D-FTIR-COS analyses.

Dissolved organic matter (DOM), as the most active ingredient in compost, directly determines the speciation and environmental behavior of HMs. Here, the binding properties of DOM derived from chicken-manure compost (CHM), cow-manure compost (COM) and pig-manure compost (PIM) with HMs were explored by analyses of Fluorescence excitation-emission matrix parallel factor (EEM-PARAFAC) and two-dimensional correlation Fourier transform infrared spectroscopy (2D-FTIR-COS). Results showed that the binding characteristics vary with origin of DOM and type of HMs. The fulvic-like component dominated the transformation of HMs speciation, and CHM-DOM had higher affinity with HMs and greater risk causing pollution due to its higher aromaticity, molecular weight and distribution of fluorescent components. Moreover, Cu(II) can efficiently bind to DOM with the stability constants (log kM) ranging from 4.53 to 5.38, followed by Pb(II) (3.34-3.57), whereas Cd(II) can hardly bind to DOM. The amide and polysaccharide were the predominant sites for HMs binding in CHM-DOM, and polysaccharide and phenolic in COM-DOM, while phenolic and amide in PIM-DOM, respectively. Although the proportion of protein-like components and non-fluorescent polysaccharides in DOM were low, their role in HMs binding should not be ignored. In brief, the environmental risk caused by livestock manure compost may originate from interactions between DOM and HMs.

[Overexpression of miR-382-5p Mediated Downregulation of PTEN on Malignant Biological Behavior of Human Glioma U251 Cells].

OBJECTIVE: To investigate the effect of overexpression of miR-382-5p overexpression on malignant biological behavior of human glioma U251 cells. METHODS: U251 cells were transfected with miR-382-5pmimic. Then miR-382-5p and PTEN mRNA levels were detected by reverse transcription-polymerase chain reaction (RT-PCR) after transfection. Used bioinformatics to predicted the presence of base binding sites between miR-382-5p and PTEN, and constructed PTEN pcDNA vector overexpression plasmid was constructed. Luciluciase reporting experiment was used to detect the targeting relationship between miR-382-5p and PTEN. Cells were randomly divided into four groups: control group, mimics group, pc-PTEN group and mimics+pc-PTEN group for follow-up experiments. RT-PCR was carried out to detect the level of PTEN mRNA in each group. Cell proliferation was detected by clone formation method. The mRNA levels of Ki67, Survivin and c-Myc were detected by RT-PCR. Transwell experiment was used to assayed cell invasion ability. The expression levels of E-cadherin, N-cadherin and Vimentin were determined by Western blot. RESULTS: Results showed that miR-382-5p directly targeted PTEN. Compared with the control group, miR-382-5p and c-Myc mRNA levels and E-cadherin protein level were increased (P<0.05),PTEN, Ki67 and Survivin mRNA levels were decreased (P<0.05), cell clonal formation rate and cell invasion number were decreased (P<0.05), N-cadherin and Vimentin protein levels were decreased (P<0.05) in the mimics group; In pc-PTEN group, miR-382-5p mRNA and c-Myc mRNA levels and E-cadherin protein level were decreased (P<0.05),PTEN, Ki67 and Survivin mRNA levels were increased (P<0.05), cell clonal formation rate and cell invasion number were increased (P<0.05), N-cadherin and Vimentin protein levels were increased (P<0.05). Compared with pc-PTEN group, PTEN, Ki67 and Survivin mRNA levels, the cell clone formation rate, the number of invasion cells and the N-cadherin and Vimentin levels of mimics+PC-PTEN group decreased significantly (P<0.05), while the c-Myc mRNA level and E-cadherin protein level increased significantly (P<0.05). CONCLUSION: Overexpression of miR-382-5p mediates the downregulation of PTEN expression, causing the inhibition of the proliferation, invasion, growth and EMT of U251 glioma cells.

p38 Inhibitor Protects Mitochondrial Dysfunction by Induction of DJ-1 Mitochondrial Translocation After Subarachnoid Hemorrhage.

p38 mitogen-activated protein kinase (MAPK) is a major player in mitochondrial dysfunction after subarachnoid hemorrhage (SAH). Moreover, DJ-1, which responds to oxidative stress and translocates to mitochondria, maintains mitochondrial homeostasis. Although a few studies have demonstrated that DJ-1 indirectly regulates p38 activation, the relationship between DJ-1 and p38 in mitochondrial dysfunction after SAH has not been delineated. Using an in vitro SAH model, alterations in p38, p-p38, DJ-1, and autophagic-related protein expression were detected. As expected, p38 inhibitor significantly blocked excessive expression of p38 and p-p38 after SAH, whereas total DJ-1 expression and mitochondrial DJ-1 were up-regulated. Further analysis showed that p38 inhibitor significantly blocked oxyhemoglobin (OxyHb) induced mitochondrial dysfunction, including mitochondrial membrane potential depolarization and reactive oxygen species (ROS) release. In addition, p38 inhibitor restored OxyHb-induced abnormal autophagic flux at the initiation and formation stage by regulating Atg5, beclin-1, the ratio of LC3-II/LC3-I, and p62 expression. This study suggested that overexpression of p38 induced the accumulation of mitochondrial dysfunction partly due to abnormal activation of autophagy, which largely relied on DJ-1 mitochondrial translocation.

Effect of chemokine CC ligand 2 (CCL2) on α­synuclein­induced microglia proliferation and neuronal apoptosis.

The present study aimed to investigate the effect of chemokine CC ligand 2 (CCL2) on α­synuclein­mediated microglia proliferation and neuronal apoptosis. Primary cultured microglia and primary neurons were isolated and cultured in vitro. Microglia were divided into four groups: The cells in the control group were treated with an identical amount of PBS, whereas the cells in the CCL2 group were cultured in medium containing 0.05 ng/µl CCL2; cells in the α­synuclein group were treated with medium containing 0.2 ng/µl α­synuclein; and cells in the CCL2 plus α­synuclein group were cultured in medium containing 0.05 ng/µl CCL2 and 0.2 ng/µl α­synuclein. After incubation for 24 h, the proliferation of glial cells, and the level of α­synuclein in the cells, were measured. The levels of tumor necrosis factor­α (TNF­α), interleukin­1ß (IL­1ß) and nitric oxide (NO) in the culture medium were also measured. Levels of cleaved caspase­3, Akt and phosphorylated (p)­Akt in neurons treated with primary microglia culture medium in each group were subsequently monitored. The proliferation activity and secretion of TNF­α, IL­1ß and NO in the CCL2, α­synuclein and CCL2 plus α­synuclein groups were significantly higher compared with that in the control group (P<0.05), as were the levels of α­synuclein (P<0.01). The levels of neuronal apoptosis and cleaved caspase­3 protein in the CCL2, α­synuclein and CCL2 plus α­synuclein groups were also significantly higher compared with that in the control group (P<0.01). Taken together, these results have demonstrated that CCL2 is able to promote α­synuclein secretion and the apoptosis of neurons induced by α­synuclein, thus inducing proliferation of the microglia and secretion of TNF­α, IL­1ß and NO.

Protein phosphatase 2A regulates the p38 signaling pathway to affect the migration of astrocytes.

The aim of the present study was to investigate the effect and mechanism of protein phosphatase 2A (PP2A) on the migration of astrocytes. The primary astrocytes of neonatal mice were isolated and cultured in vitro, and treated with the PP2A activator D­erythro­sphingosine (DES) (activated group) or inhibitor okadaic acid (inhibitory group). The control group was treated with equal amounts of dimethyl sulfoxide. The activity of PP2A in the cells was detected using a commercial kit and the migration of cells was investigated using a Transwell migration assay. The protein expression of p38, phosphorylated (p)­p38, matrix metalloproteinase (MMP)­2 and MMP­9 was detected by western blotting. Cell migration and the protein expression of p38, p­p38, MMP­2 and MMP­9 was also determined following treatment of astrocytes with the p38 signaling pathway inhibitor SB202190 with or without the PP2A activator DES. The results demonstrated that the activity of PP2A in the PP2A inhibitory group was significantly decreased compared with the control group, while that of the PP2A­activated cells was significantly increased compared with the control. The protein levels of MMP­2 and MMP­9 in the PP2A inhibitory group astrocytes were significantly decreased compared with the control group, while PP2A­activated astrocytes exhibited significantly increased levels of these proteins. By contrast, the p­p38 level in PP2A inhibitory group astrocytes was significantly increased compared with the control group, while astrocytes in the activated group exhibited significantly lower levels compared with the control group. Furthermore, the cell migration ability, and MMP­2 and MMP­9 protein levels, of astrocytes that received combined treatment with SB202190 and the PP2A activator DES were significantly increased compared with the levels in astrocytes treated with SB202190 alone. The results of the current study indicate that PP2A may negatively regulate the p38 signaling pathway to promote astrocyte migration.

Long noncoding RNA ZEB1-AS1 promotes the tumorigenesis of glioma cancer cells by modulating the miR-200c/141-ZEB1 axis.

Long noncoding RNA Zinc Finger E-box-binding homeobox 1 antisense 1 (ZEB1-AS1) reportedly participates in the tumorigenesis of various cancers. However, the clinical significance and biological functions of ZEB1-AS1 in glioma remain virtually unknown. Here, we show that ZEB1-AS1 expression was higher in glioma tissues and cell lines than in corresponding noncancerous samples and primary normal human astrocytes, respectively. The positive correlation of ZEB1-AS1 expression with the poor prognosis and progressive histological stages of glioma patients was clinically proven. In vitro assays revealed that silencing ZEB1-AS1 inhibited glioma cancer-cell growth and motility. Xenograft experiments confirmed that ZEB1-AS1 depletion attenuated tumor growth and metastasis. Dual-luciferase report assay showed that ZEB1-AS1 directly regulated microRNA-200c/141 (miR-200c/141) in glioma cells, which was confirmed by RNA immunoprecipitation assay. Furthermore, the inhibition of miR-200c/141 partially balanced the inhibition effects of cell proliferation and motility induced by ZEB1-AS1 depletion on U87 cells. Additionally, ZEB1-AS1 can regulate ZEB1 through miR-200c/141. Hence, ZEB1-AS1 directly regulated miR-200c/141 in glioma cells and relieved the inhibition of ZEB1 caused by miR-200c/141. Overall, this study revealed a novel regulatory mechanism between ZEB1-AS1 and the miR-200c/141-ZEB1 axis. The interaction between ZEB1-AS1 and miR-200c/141-ZEB1 axis was involved in the progression of glioma cells. Therefore, targeting this interaction was a promising strategy for glioma treatment.

LncRNA PANDAR as a prognostic marker in Chinese cancer.

BACKGROUND: LncRNA promoter of CDKN1A antisense DNA damage activated RNA (PANDAR) is reportedly dysregulated in various cancers. We performed this meta-analysis to clarify the efficacy of PANDAR as a prognostic marker in malignant tumors. METHODS: The PubMed, Medline, OVID, Cochrane Library, and Web of Science databases were searched from inception to July 3, 2017. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated to explore the relationship between PANDAR expression and overall survival (OS). Odds ratios (ORs) were calculated to assess the association between PANDAR expression and pathological parameters. RESULTS: Eight original studies covering 1,132 cancer patients were included. The pooled HR suggested that high PANDAR expression correlated with poor OS (pooled HR=1.60, 95% CI: 1.09-2.33) in cancer patients. PANDAR expression was also related to lymph node metastasis (OR=3.26, 95% CI: 2.09-5.09), advanced tumor stage (OR=3.60, 95% CI: 2.39-5.44) and histological grade (OR=2.75, 95% CI: 1.73-4.38). Begg's funnel plot showed no evidence of obvious asymmetry for overall survival and lymph node metastasis. CONCLUSIONS: Thus high PANDAR expression appears predictive of poor OS, lymph node metastasis, advanced tumor stage and histological grade in multiple cancers. This suggests PANDAR expression could serve as a biomarker of poor prognosis in Chinese cancer patients.

Long non-coding RNA TUG1 as a potential prognostic biomarker in human cancers: a meta-analysis.

LncRNA taurine upregulated gene 1 (TUG1) is reportedly dysregulated in various cancers. We performed this meta-analysis to clarify the usefulness of TUG1 as a prognostic marker in malignant tumors. The PubMed, Medline, OVID, Cochrane Library, and Web of Science databases were searched from inception to Jan 11, 2017. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated to explore the relationship between TUG1 expression and overall survival (OS). Odds ratios (ORs) were calculated to assess the association between TUG1 expression and pathological parameters. Thirteen original studies covering 1,274 cancer patients were included in this meta-analysis. The pooled HR suggested that high TUG1 expression correlated with poor OS (pooled HR=1.41, 95% CI: 1.01-1.98) in cancer types other than non-small cell lung cancer. TUG1 expression was also related to distant metastasis (OR=3.24, 95% CI: 1.18-8.93), large tumor size (OR=4.07, 95% CI: 1.08-15.28) and advanced tumor stage (OR=3.45, 95% CI: 2.19-5.44). Begg's funnel plot and Egger's test showed no evidence of obvious asymmetry for overall survival or tumor stage. Thus high TUG1 expression appears predictive of poor OS, distant metastasis, advanced tumor stage and large tumor size. This suggests TUG1 expression could serve as a biomarker for poor prognosis in cancers.

NAD(P)H quinone oxidoreductase 1 (NQO1) genetic C609T polymorphism is associated with the risk of digestive tract cancer: a meta-analysis based on 21 case-control studies.

The relationships between the NAD(P)H quinone oxidoreductase 1 (NQO1) C609T polymorphism and the risk of digestive tract (DT) cancer are controversial. Therefore, we performed a meta-analysis to assess the relationships. The databases of Medline, Embase, and WanFang (updated to 15 May 2011) were reviewed. Odds ratios and 95% confidence intervals were calculated to assess the strength of the associations. Overall, 21 individual case-control studies in 20 papers with 5340 cases and 5911 controls were included in this meta-analysis. The results of combined analyses indicated that the T allele of NQO1 C609T was significantly associated with increased risk of DT cancer [odds ratio (95% CI): 1.58 (1.22-2.07) for TT vs. CC and 1.13 (1.06-1.22) for T carriers vs. C carriers]. Subgroup analyses for different types of cancers indicated that the T allele was significantly associated with an increased risk of gastric cancer [1.19 (1.13-1.47) for T carriers vs. C carriers], but not with esophageal cancer [1.05 (0.86-1.27) for T carriers vs. C carriers] and colorectal cancer [1.09 (0.98-1.21) for T carriers vs. CC]. Subgroup analyses for ethnicities and countries indicated that the T allele was associated with risk of DT cancer among Europeans [1.52 (1.05-2.19) for TT vs. CC] and Asians [1.52 (1.05-2.19) for TT vs. CC], and German, Indian, and Chinese populations but not among English and Japanese populations. In addition, subgroup analyses also indicated that the T allele was significantly associated with risk of DT cancer in studies with large and small sample sizes and in population-based studies, but not in hospital-based studies. This meta-analysis suggests that NQO1 C609T is significantly associated with risk of DT cancer among both Europeans and Asians, especially gastric cancer. Because of the limited number of cases and controls in the subgroup analyses, more well-designed studies with a large sample of participants are needed to verify our findings.

System review and metaanalysis of the relationships between five metabolic gene polymorphisms and colorectal adenoma risk.

The relationships between some metabolic (including EPHX1, GSTs and NQO1) gene polymorphisms and colorectal adenoma (CRA) risk have been commonly studied, and no conclusions are available up to now. Therefore, we quantitatively studied the relationships by a metaanalysis. The databases of Medline and Embase were retrieved updated to June 15th, 2011. Crude or adjusted odds ratio (crude OR or adjusted OR) and 95% confidence interval (95%CI) were calculated to present the strength of the associations. Overall, nine case-control studies for EPHX1 Tyr113His and His139Arg, five case-control studies for GSTM1, four studies for GSTP1 Ile105Val, two studies for GSTP1 Ala114Val, six studies for GSTT1 and four studies for NQO1 Pro187Ser were included in this metaanalysis. The results of combined analyses indicated that EPHX1 Tyr113His and His139Arg, GSTT1, GSTM1, GSTP1 Ile105Val and Ala114Val were not associated with CRA risk [crude OR (95%CI): 0.98 (0.90-1.07) and P ( z-test) = 0.65 for EPHX1 His carriers vs. Tyr/Tyr; 1.05 (0.97-1.15) and P ( z-test) = 0.21 for EPHX1 Arg carriers vs. His/His; 1.05 (0.92-1.20) and P ( z-test) = 0.47 for GSTT1 Null vs. Present; 1.01 (0.90-1.13) and P ( z-test) = 0.90 for GSTM1 Null vs. Present; 1.04 (0.92-1.17) and P ( z-test) = 0.56 for G carriers vs. AA for GSTP1 Ile105Val; 0.88 (0.70-1.11) and P ( z-test) = 0.28 for T carriers vs. CC for GSTP1 Ala114Val]. In contrast, Ser allele of NQO1 Ser187Pro might be a modest risk factor for CRA development [1.19 (1.06-1.33) and P ( z-test) = 0.003 for Ser carriers vs. Pro/Pro]. To get more precise evidences, adjusted ORs (95%CI) for EPHX1 Tyr113His, His139Arg, GSTP1 Ile105Val and NQO1 Ser187Pro were also calculated based on adjusted ORs (95%CIs) reported in primary studies. The results still indicated that EPHX1 Tyr113His, His139Arg and GSTP1 Ile105Val were not associated with CRA risk except for NQO1 Ser187Pro. When subgroup analyses were performed for population-based case-control studies or studies in HWE for EPHX1 Tyr113His and His139Arg, and NQO1 Ser187Pro polymorphisms, the results were persistent. Although with modest limitations and biases, this metaanalysis suggests that EPHX1 Tyr113His and His139Arg, GSTT1, GSTM1, GSTP1 Ile105Val and Ala114Val polymorphisms may be not risk factors for CRA development, while Ser allele of NQO1 Ser187 Pro may be a modest risk factor for CRA development, and may be used with other genetic markers for screening CRA in the future.