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Investigations on the relationship of toxicities between species play an important role in the understanding of toxic mechanisms to environmental organisms. In this paper, the toxicity data of 949 chemicals to fish and 1470 chemicals to V. fischeri were used to investigate the modes of action (MOAs) between species. The results show that although there is a positive interspecies correlation, the relationship is poor. Analysis on the excess toxicity calculated from toxic ratios (TR) shows that many chemicals have close toxicities and share the same MOAs between the two species. Linear relationships between the toxicities and octanol/water partition coefficient (log KOW) for baseline and less inert compounds indicate that the internal critical concentrations (CBRs) approach a constant both to fish and V. fischeri for neutral hydrophobic compounds. These compounds share the same toxic mechanisms and bio-uptake processes between species. On the other hand, some hydrophilic compounds exhibit different toxic effects with greatly different log TR values between V. fischeri and fish species. These hydrophilic compounds were identified as reactive MOAs to V. fischeri, but not to fish. The interspecies correlation is improved by adding a hydrophobic descriptor into the correlation equation. This indicates that the differences in the toxic ratios between fish and V. fischeri for these hydrophilic compounds can be partly attributed to the differences of bioconcentration between the two species, rather than the differences of reactivity with the target macromolecules. These hydrophilic compounds may more easily pass through the cell membrane of V. fischeri than the gill and skin of fish, react with the target macromolecules and exhibit excess toxicity. The compounds with log KOW > 7 exhibiting very low toxicity (log TR < -1) to both species indicate that the bioconcentration potential of a chemical plays a very important role in the identification of excess toxicity and MOAs.

Sphingosine-1-phosphate (S1P) plays an important role in regulating many biological processes. Sphingosine-1-phosphate phosphatase 1 (SGPP1) can dephosphorylate S1P into sphingosine and tip the balance of sphingosine-S1P. Increased levels of sphingosine leads to a decrease in the ability of cell invasion as well as an increase in the ability of cell apoptosis. However, little is known regarding the effects of SGPP1 in gastric cancer. The present study examined the function of SGPP1 on gastric cancer cell lines as well as its clinical relevance in gastric cancer progression. Using immunohistochemistry and RT-qPCR techniques, the clinical significance of SGPP1 expression was analyzed in 288 paraffin-embedded gastric tissue specimens and 219 fresh gastric tissues, respectively. Transgenes encoding ribozymes to specifically target human SGPP1 (pEF-SGPP1) was constructed. Human gastric cancer cell lines (AGS and HGC27) were transfected with pEF-SGPP1 transgene and examined by functional analysis. SGPP1 was downregulated in gastric cancer tissues, compared with adjacent normal gastric tissues (p=0.034). SGPP1 mRNA levels in gastric cancer tissues were significantly decreased when compared with their adjacent non-cancerous tissues (p<0.001). Weakly expressed SGPP1 was positively correlated with the lymph node metastasis (p=0.005) and distant metastasis (p=0.031). Kaplan-Meier survival curves revealed that patients with SGPP1 positive expression had a significant increase in overall survival (OS) (p=0.034) and progression-free survival (PFS) (p=0.041). Multivariate analysis indicated the expression of SGPP1 was an independent prognostic factor in gastric cancer patients (p=0.041). In vitro experiments showed that knockdown of SGPP1 resulted in an increase in the invasion (2-fold) and migration (5-fold) of AGS and HGC27. The two gastric cancer cells transfected with pEF-SGPP1 exhibited a slower rate of growth with less adhesion. Thus, our findings provided evidence that SGPP1 may serve as a prognostic biomarker for patients with advanced gastric cancers.

Macrophage migration inhibitory factor (MIF) is pleiotropic cytokine that has multiple effects in many inflammatory and immune diseases. This study reveals a potential role of MIF in acute kidney injury (AKI) in patients and in kidney ischemic reperfusion injury (IRI) mouse model in MIF wild‐type (WT) and MIF knockout (KO) mice. Clinically, plasma and urinary MIF levels were largely elevated at the onset of AKI, declined to normal levels when AKI was resolved and correlated tightly with serum creatinine independent of disease causes. Experimentally, MIF levels in plasma and urine were rapidly elevated after IRI‐AKI and associated with the elevation of serum creatinine and the severity of tubular necrosis, which were suppressed in MIF KO mice. It was possible that MIF may mediate AKI via CD74/TLR4‐NF‐κB signalling as mice lacking MIF were protected from AKI by largely suppressing CD74/TLR‐4‐NF‐κB associated renal inflammation, including the expression of MCP‐1, TNF‐α, IL‐1β, IL‐6, iNOS, CXCL15(IL‐8 in human) and infiltration of macrophages, neutrophil, and T cells. In conclusion, our study suggests that MIF may be pathogenic in AKI and levels of plasma and urinary MIF may correlate with the progression and regression of AKI.

We have recently noticed an accidental error in part of a figure which appeared in the above‑mentioned article. In Fig. 3A, the image for the HGC27‑pEF, 15 h panel was mistakenly replicated as the HGC27‑KD, 0 h panel in the same figure, and the AGS‑pEF, 15 h and AGS KD, 0 h panels were mistakenly switched with each other. We have reviewed the original files and the individual figures for the submitted composite figure, and realized that the error occurred when we produced the composite figure by marrying the individual images to the final figure. The same image was accidentally pasted twice without us being fully aware of the error. We have identified all the original images, and the corrected version of Fig. 3 is shown below. We regret that this error occurred, and thank the Editor for affording us the opportunity to publish this Corrigendum. [the original article was published in the Oncology Reports 34: 1977-1987, 2015; DOI: 10.3892/or.2015.4162].

We have recently noticed an accidental error in part of a figure which appeared in the above‑mentioned article. In Fig. 3A, the image for the HGC27‑pEF, 15 h panel was mistakenly replicated as the HGC27‑KD, 0 h panel in the same figure, and the AGS‑pEF, 15 h and AGS KD, 0 h panels were mistakenly switched with each other. We have reviewed the original files and the individual figures for the submitted composite figure, and realized that the error occurred when we produced the composite figure by marrying the individual images to the final figure. The same image was accidentally pasted twice without us being fully aware of the error. We have identified all the original images, and the corrected version of Fig. 3 is shown below. We regret that this error occurred, and thank the Editor for affording us the opportunity to publish this Corrigendum. [the original article was published in the Oncology Reports 34: 1977-1987, 2015; DOI: 10.3892/or.2015.4162].We have recently noticed an accidental error in part of a figure which appeared in the above‑mentioned article. In Fig. 3A, the image for the HGC27‑pEF, 15 h panel was mistakenly replicated as the HGC27‑KD, 0 h panel in the same figure, and the AGS‑pEF, 15 h and AGS KD, 0 h panels were mistakenly switched with each other. We have reviewed the original files and the individual figures for the submitted composite figure, and realized that the error occurred when we produced the composite figure by marrying the individual images to the final figure. The same image was accidentally pasted twice without us being fully aware of the error. We have identified all the original images, and the corrected version of Fig. 3 is shown below. We regret that this error occurred, and thank the Editor for affording us the opportunity to publish this Corrigendum. [the original article was published in the Oncology Reports 34: 1977-1987, 2015; DOI: 10.3892/or.2015.4162].

Background Gait deficits are important clinical symptoms of Parkinson’s disease (PD). However, existing behavioral tests for the detection of motor impairments in rodents with systemic dopamine depletion only measure akinesia and dyskinesia, and data focusing on gait are scarce. We evaluated gait changes in the methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced C57BL/6 murine model of PD by using a computer-assisted CatWalk system. Correlations of gait parameters with tyrosine hydroxylase (TH) protein levels in the substantia nigra (SN) were also investigated. Results The gait readouts, including the walking duration, variation of walking speed, step cycle, duty cycle, stance, initial dual stance, terminal dual stance, three- and four-point supports, and the base of support between hind limbs was noted to increase significantly one week after MPTP injection. In contrast, values of the stride length, cadence, swing speed, and diagonal dual support decreased substantially following MPTP treatment (p < 0.05). All of these changes lasted for three weeks after the last MPTP administration. Except for the stance in the fore limbs and the swing speed in the hind limbs, the gait variability in the PD mice showed a closer correlation with the protein levels of TH in the SN than the walking distances in the conventional open field test. Coordination parameters of the regularity index and step pattern were not affected in mice treated with MPTP. Conclusion Data of the study suggest that the computer-assisted CatWalk system can provide reliable and objective criteria to stratify gait changes arising from MPTP-induced bilateral lesions in C57/BL6 mice. The extent of gait changes was noted to correlate with the expression of the biomarker for dopaminergic neurons. This novel analytical method may hold promise in the study of disease progression and new drug screening in a murine PD model.

Aim： Severe painful sensory neuropathy often occurs during paclitaxel chemotherapy. Since paclitaxel can activate mast cell and basophils, whereas quercetin, a polyphenolic flavonoid contained in various plants, which can specifically inhibit histamine release as a mast cell stabilizer. In this study we explore whether quercetin could ameliorate paclitaxel-induced neuropathic pain and elucidated the underlying mechanisms. Methods： Quercetin inhibition on histamine release was validated in vitro by detecting histamine release from rat basophilic leukemia （RBL-2H3） cells stimulated with paclitaxel （10 μmol/L）. In the in vivo experiments, rats and mice received quercetin （20, 40 mg·kg^-1·d^-1） for 40 and 12 d, respectively. Meanwhile, the animals were injected with paclitaxel （2 mg/kg, ip） four times on d 1, 3, 5 and 7. Heat hyperalgesia and mechanical allodynia were evaluated at the different time points. The animals were euthanized and spinal cords and dorsal root ganglions were harvested for analyzing PKCε and TRPV1 expression levels. The plasma histamine levels were assessed in rats on d 31. Results： Pretreatment with quercetin （3, 10, 30 μmol/L） dose-dependently inhibited excessive histamine release from paclitaxel- stimulated RBL-2H3 cells in vitro, and quercetin administration significantly suppressed the high plasma histamine levels in paclitaxel- treated rats. Quercetin administration dose-dependently raised the thresholds for heat hyperalgesia and mechanical allodynia in paclitaxel-treated rats and mice. Furthermore, quercetin administration dose-dependently suppressed the increased expression levels of PKCc and TRPVl in the spinal cords and DRGs of paclitaxel-treated rats and mice. Moreover, quercetin administration may inhibited the translocation of PKCε from the cytoplasm to the membrane in the spinal cord and DRG of paclitaxel-treated rats. Conclusion： Our results reveal the underlying mechanisms of paclitaxel-induced peripheral neuropathy and demonstrate the therapeutic potential of quercetin for treating this side effect.

Desulfurization performance with low binary basicity refining slag in 72 grade tire cord steel was calculated using FactSage and it is found that sulfur content in steel decreases with the increase of basicity of slag, MgO content in slag and slag/steel ratio while sulfur partition ratio between slag and steel increases gradually with the increase of basicity of slag as well as MgO content. Experiments were carried out and the results are of great agreements with theoretical calculation. Then industrial application tests were performed in a domestic plant and good results were achieved. Sulfur content in steel decreases gradually during refining process, as a result, sulfur content in the billets is controlled in the range of 0.007 1%-0.008 1%. Sulfur content in steel refined with slag basicity of 1.21 is lower than that of 1.02, while the plasticity of oxide compound inclusions is a little better controlled in low basicity heats. Using refining slag with basicity of 1.0-1.2 and MgO content of 5%-10% and reducing the slag takeover of LD are favorable for improving the desulfurization performance and the plasticity of inclusions during the industrial production.

Iron-based waterworks sludge was activated using 0.5-3 mol/L H2SO4 acid to obtain the acid-activated iron-based waterworks sludge (AAIBWS). The sludge treated with 1 mol/L H2SO4 acid was best for phosphorus adsorption and used to carry out batch phosphorus adsorption experiments. The influencing factors including solution pH, contact time and reaction temperature were investigated. The results indicated that the acid environment was favourable for P adsorption. The phosphorus adsorption increased with the rising reaction time and temperature. The pseudo-second-order equation was best to describe the adsorption process among the three kinetic models. The Langmuir isotherm provided a better fit of the data than the Freundlich model. Thermodynamic parameters showed that the phosphorus adsorption on AAIBWS-1 had a spontaneous and endothermic nature.

The urban expansion process in China from the 1970s to 2013 was retrieved based on remote sensing and GIS technology. With the latest zoning method used as reference, annual expansion area per city, urban expansion type, and fractal dimension index were employed to analyze the Chinese urban expansion characteristics and its spatial difference from the aspects of urban expansion process, influence of urban expansion on land use, and urban spatial morphological evolutions. Results indicate that 1） under the powerful guidance of policies, urban expansion in China went through six different stages, and cities in the eastern region entered the rapid expansion period the earliest, followed by cities in the central, northeastern and western regions; 2） cultivated lands and rural settlements and industrial traffic lands were the important land sources for urban expansion in China; the influence of urban expansion on land use in the eastern region was the strongest, followed by the central, northeastern and western regions; 3） urban spatial morphology tended to be complex and was directly related to the adopted spatial expansion mode. Infilling expansion became the main urban expansion mode in the western region first, then in the central and northeastern regions, and finally in the eastern region. This study establishes the foundation for an in-depth recognition of urban expansion in China and optimization of future urban planning.