The Influences of Rainfall Intensity and Timing on the Assemblage of Dung Beetles and the Rate of Dung Removal in an Alpine Meadow.

Changes in precipitation patterns, including rainfall intensity and rainfall timing, have been extensively demonstrated to impact biological processes and associated ecosystem functions. However, less attention has been paid to the effects of rainfall intensity and rainfall timing on the assembly of detritivore communities and the decomposition rate of detritus such as animal dung. In a grazed alpine meadow on the eastern Qinghai-Tibet Plateau, we conducted a manipulative experiment involving two levels of rainfall intensity (heavy rainfall, 1000 mL/5 min; light rainfall, 100 mL/5 min) and five levels of rainfall timing (0, 2, 4, 24, and 48 h after yak dung deposition). The aim was to determine the effects of rainfall intensity, timing, and their interaction on the assemblage of dung beetles and dung removal rate during the early stage (i.e., 96 h after yak dung deposition) of dung decomposition. Light rainfall significantly increased species richness in the treatment of 48 h after dung pats were deposited. Heavy rainfall significantly decreased beetle abundance in both the 0 h and 48 h treatments while light rainfall had no effect on beetle abundance. Dung mass loss was significant lower in the 2 h treatment compared to other treatments regardless of rainfall intensity. The structural equation model further revealed that the species richness of dung beetles and dung mass loss were significantly affected by rainfall timing but not by rainfall intensity. However, no significant relationships were observed between any variables examined. These findings suggest that changes in precipitation patterns can influence both the structure of dung beetles and the rate of dung decomposition but may also decouple their relationship under a certain circumstance. Therefore, it is crucial to pay greater attention to fully understand local variability between the biological processes and ecosystem functions within a global climate change scenario.

Biodegradability of polyethylene mulch film by Bacillus paramycoides.

Discarded polyethylene (PE) mulch film has led to persistent agricultural pollution. Biodegradation of plastic waste is considered as a promising solution that can potentially overcome environmental and economic problems. In this study, a novel bacterium (Bacillus paramycoides) was isolated from a waste mulch recycling plant and showed an extraordinary ability to customize polyethylene film. It was observed by scanning electron microscopy that a large number of pits and wrinkle cracks existed on the polyethylene, indicating that the strain used PE film as the sole carbon source. Meanwhile, the loss of weight of the film was tested continuously, and approximately 12% of the initial weight of the film was found to be lost within 45 days after coincubation with TW-2. The surface hydrophobicity of the polyethylene film decreased while the surface tension increased from 9.755 to 31.013. Fourier transform infrared (FTIR) analysis indicated that absorption peaks near 1740 cm-1 and 2760 cm-1 were attributed to the stretching vibrations of aldehyde and carboxyl groups, respectively, suggesting that hydrophilic groups were produced. This was also confirmed by XPS spectroscopy analysis. X-ray diffraction (XRD) analysis also showed that the relative crystallinity decreased from 33% to 11.51%. In addition, GPC analysis showed that the molecular weight decreased, while the proportion of low molecular weight fragments increased. These results strongly indicated that the PE film was able to be degraded to some extent by the strain. Finally, a new biodegradable mechanism for polyethylene was proposed.

Effect of an Acinetobacter pittobacter on low-density polyethylene.

Low-density polyethylene (LDPE) is a major cause of persistent and long-term environmental pollution. In this study, we report the successful isolation of an efficient LDPE degrading bacterial strain from the wastewater sediment of an agricultural land film recycling plant and identified and designated it as Acinetobacter sp. LW-1, respectively. The surface analyses including scanning electron microscopy (SEM) and atomic force microscopy (AFM) of LW-1-treated samples revealed the existence of appreciable pits and cavities on the facet of PE film, while the formation of carbonyl group was also verified by XPS and FTIR. Moreover, water contact angle assay substantiated the chemical transformation of the LDPE film from hydrophobic to hydrophilic transition after treatment with LW-1. In addition, co-incubation of LDPE film and Acinetobacter sp. LW-1 at 35 °C for 90 days significantly decreased the weight of LDPE film with an optimal weight loss of 15 ± 0.85%. This work enriches the LDPE degradation bacterial library and shows the tremendous potential of Acinetobacter sp. LW-1 to be used in the degradation of LDPE waste.

Corrigendum to "Determination of Serum Lost Goodwill Target Proteome in Patients with Severe Traumatic Brain Injury".

[This corrects the article DOI: 10.1155/2015/183821.].

Shikonin inhibits TNF-α production through suppressing PKC-NF-κB-dependent decrease of IL-10 in rheumatoid arthritis-like cell model.

Shikonin, a major effective component in the Chinese herbal medicine Lithospermum erythrorhizon Sieb., exhibits an anti-inflammatory property towards rheumatoid arthritis (RA), but the potential mechanism is unclear. Our aim was to investigate the mechanism of shikonin on the lipopolysaccharide (LPS)-induced fibroblast-like synoviocyte (LiFLS) inflammation model. Fibroblast-like synoviocytes (FLSs) were treated with 200 µg/ml of LPS for 24 h to establish the RA-like model, LiFLS. FLSs were pretreated with shikonin (0.1-1 µM) for 30 min in the treatment groups. Quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assays were used to detect mRNA and protein levels of interleukin (IL)-10 and tumor necrosis factor (TNF)-α. Signal proteins involved in IL-10 production were analyzed by Western blotting. Shikonin significantly reversed the inhibitory effects of LPS on IL-10 expression in FLSs by inactivating the PKC-NF-κB pathway. In addition, shikonin inhibited LPS-induced TNF-α expression in FLSs, and this effect was markedly diminished by IL-10-neutralizing antibody. The IL-10-mediated suppression of TNF-α transcription was demonstrated by no response to the protein synthesis inhibitor cyclohexamide and no mRNA decay. Shikonin inhibits LPS-induced TNF-α production in FLSs through suppressing the PKC-NF-κB-dependent decrease in IL-10, and this study also highlights the potential application of shikonin in the treatment of RA.

Determination of Serum Lost Goodwill Target Proteome in Patients with Severe Traumatic Brain Injury.

This study investigates the biokinetics of LGT proteome, a potential biomarker of severe TBI, in serum of severe TBI patients. The LGT proteome presents in the serum of severe TBI patients. The abundance diversity of LGT proteome is closely associated with pathologic condition of TBI patients. Serum LGT proteome may be used as a promising marker for evaluating severity of severe TBI.

Edaravone protects osteoblastic cells from dexamethasone through inhibiting oxidative stress and mPTP opening.

Existing evidences have emphasized an important role of oxidative stress in dexamethasone (Dex)-induced osteoblastic cell damages. Here, we investigated the possible anti-Dex activity of edaravone in osteoblastic cells, and studied the underlying mechanisms. We showed that edaravone dose-dependently attenuated Dex-induced death and apoptosis of established human or murine osteoblastic cells. Further, Dex-mediated damages to primary murine osteoblasts were also alleviated by edaravone. In osteoblastic cells/osteoblasts, Dex induced significant oxidative stresses, tested by increased levels of reactive oxygen species and lipid peroxidation, which were remarkably inhibited by edaravone. Meanwhile, edaravone repressed Dex-induced mitochondrial permeability transition pore (mPTP) opening, or mitochondrial membrane potential reduction, in osteoblastic cells/osteoblasts. Significantly, edaravone-induced osteoblast-protective activity against Dex was alleviated with mPTP inhibition through cyclosporin A or cyclophilin-D siRNA. Together, we demonstrate that edaravone protects osteoblasts from Dex-induced damages probably through inhibiting oxidative stresses and following mPTP opening.

Perinatal exposure to Di-(2-ethylhexyl)-Phthalate leads to cognitive dysfunction and phospho-tau level increase in aged rats.

Di-(2-ethylhexyl)-Phthalate (DEHP) can affect glucose and insulin homeostasis in periphery and lead to insulin resistance, especially exposure of DEHP during critical developmental period. Given the potential relationship between insulin resistance and pathogenesis of Alzheimer's disease (AD) in elderly life, we investigated the relationship between perinatal DEHP exposure and AD pathogenesis. Our results suggested that perinatal exposure to DEHP can affect the expression of insulin and insulin-Akt- GSK-3ß signal pathway in hippocampus. Furthermore, impaired cognitive ability and increased level of phospho-Tau was observed in DEHP-exposed rat offspring (1.25 ± 0.11 vs. 0.47 ± 0.07, P < 0.05). The present study demonstrates that perinatal exposure to DEHP may be a potential risk factor for AD pathogenesis associated with insulin resistance and insulin metabolism disorder in the hippocampus.