Rodents mediate the relationship between seed rain, seed bank, and plant community with increased grazing disturbance.

Seed rain and the soil seed bank represent the dispersal of seeds in space and time, respectively, and can be important sources of recruitment of new individuals during plant community regeneration. However, the temporal dynamics of seed rain and the mechanisms by which the seed rain and soil seed bank may play a role in plant community regeneration with increased grazing disturbance remain unclear. Seed rain, soil seed bank, aboveground vegetation, and rodent density were sampled along a grazing gradient in an alpine marsh on the eastern Tibetan Plateau. We described the temporal dynamics of seed dispersal using Bayesian generalized mixed models, and nonmetric multidimensional scaling and the structural equation model were used to examine the effects of grazing disturbance on the relative role of seed rain and soil seed bank on aboveground plant community regeneration. The temporal dynamics of seed rain changed from a unimodal to a bimodal pattern with increased grazing disturbance. Both species diversity and seed density of the seed rain and seed bank increased significantly with increased grazing disturbance. Increased grazing disturbance indirectly increased the similarity of composition between seed rain, seed bank, and aboveground plant community by directly increasing species diversity and abundance of aboveground plant community. However, increased grazing disturbance also indirectly decreased the similarity of seed rain, soil seed bank, and aboveground plant community by directly increasing rodent density. The similarity between seed rain and aboveground plant community was greater than that of the soil seed bank and aboveground plant community with increased grazing disturbance. Grazing disturbance spreads the risk of seed germination and seedling establishment by changing the temporal dynamics of seed dispersal. Plants (positive) and rodents (negative) mediated the role of seed rain and soil seed bank in plant community regeneration. The role of seed rain in plant community regeneration is higher than the seed bank in disturbed alpine marshes. Our findings increase our understanding of the regeneration process of the plant community, and they provide valuable information for the conservation and restoration of alpine marsh ecosystems.

Warming reduced flowering synchrony and extended community flowering season in an alpine meadow on the Tibetan Plateau.

The timing of phenological events is highly sensitive to climate change, and may influence ecosystem structure and function. Although changes in flowering phenology among species under climate change have been reported widely, how species-specific shifts will affect phenological synchrony and community-level phenology patterns remains unclear. We conducted a manipulative experiment of warming and precipitation addition and reduction to explore how climate change affected flowering phenology at the species and community levels in an alpine meadow on the eastern Tibetan Plateau. We found that warming advanced the first and last flowering times differently and with no consistent shifts in flowering duration among species, resulting in the entire flowering period of species emerging earlier in the growing season. Early-flowering species were more sensitive to warming than mid- and late-flowering species, thereby reducing flowering synchrony among species and extending the community-level flowering season. However, precipitation and its interactions with warming had no significant effects on flowering phenology. Our results suggest that temperature regulates flowering phenology from the species to community levels in this alpine meadow community, yet how species shifted their flowering timing and duration in response to warming varied. This species-level divergence may reshape flowering phenology in this alpine plant community. Decreasing flowering synchrony among species and the extension of community-level flowering seasons under warming may alter future trophic interactions, with cascading consequences to community and ecosystem function.

Nano-Calcium Carbonate Affect the Respiratory and Function Through Inducing Oxidative Stress: A Cross-sectional Study Among Occupational Exposure of Workers and a Further Research for Underlying Mechanisms.

OBJECTIVE: The aim of the study is to investigate whether nano-calcium carbonate (nano-CaCO 3 ) occupational exposure could induce adverse health effects in workers. METHODS: A cross-sectional study was conducted in a nano-CaCO 3 manufacturing plant in China. Then, we have studied the dynamic distribution of nano-CaCO 3 in nude mice and examined the oxidative damage biomarkers of subchronic administrated nano-CaCO 3 on Sprague-Dawley rats. RESULTS: The forced vital capacity (%) and the ratio of FEV1 to FVC is the rate of one second of workers were significantly decreased than unexposed individuals. Dynamic imaging in mice of fluorescence labeled nano-CaCO 3 showed relatively high uptake and slow washout in lung. Similar to population data, the decline in serum glutathione level and elevation in serum MDA were observed in nano-CaCO 3 -infected Sprague-Dawley rats. CONCLUSIONS: We found that nano-CaCO 3 exposure may result in the poor pulmonary function in workers and lead to the changes of oxidative stress indexes.

Deregulation of the cell cycle and related microRNA expression induced by vinyl chloride monomer in the hepatocytes of rats.

Vinyl chloride (VC) is a confirmed human carcinogen associated with hepatocellular carcinoma and angiosarcoma. However, the role of microRNAs (miRNAs) in liver cell cycle changes under VC exposure remains unclear, which prevents research on the mechanism of VC-induced carcinogenesis. In this study, male rats were injected intraperitoneally with VC (0, 5, 25, and 125 mg/kg body weight) for 6, 8, and 12 weeks. Cell cycle analysis of liver cells, miRNA-222, miRNA-199a, miRNA-195, and miRNA-125b expression in the liver and serum, and target protein expression were performed at different time points. The results showed a higher percentage of hepatocytes in the G1/G0 and S phases at the end of 6 and 12 weeks of VC exposure, respectively. MiRNA-222 expression decreased initially and then increased, whereas miRNA-199a, miRNA-195, and miRNA-125b expression increased initially and then decreased, which corresponded with changes in cell cycle distribution and related target proteins expression (p27, cyclinA, cyclinD1, and CDK6). The corresponding expression levels of miRNAs in serum did not change. Dynamic changes in miR-222, miR-199a, miR-195, and miR-125b induced by VC can lead to cell cycle deregulation by affecting cell cycle-related proteins, and these miRNAs can serve as early biomarkers for malignant transformation caused by VC.

Transformation and Cytotoxicity of Surface-Modified Silver Nanoparticles Undergoing Long-Term Aging.

Silver nanoparticles (AgNPs) are constituents of many consumer products, but the future of their production depends on ensuring safety. The stability of AgNPs in various physiological solutions and aging in storage may affect the accuracy of predicted nanoparticle toxicity. The goal of this study was to simulate the transformation of AgNPs in different media representatives to the life cycle in the environment and to identify their toxicity to Hepa1c1c7 cells in a long-term aging process. AgNPs coated with citrate, polyethylene glycol (PEG), polyvinylpyrrolidone (PVP), and branched polyethyleneimine (BPEI) were studied. Our results show that the exposure media had a significant impact on the transformation of AgNPs. Citrate-coated AgNPs showed significant aggregation in phosphate-buffered saline. The aging of AgNPs in optimal storage showed that the charge-stabilized particles (citrate) were more unstable, with significant aggregation and shape changes, than sterically stabilized particles (PEG AgNPs, PVP AgNPs). The BPEI AgNPs showed the highest dissolution of AgNPs, which induced significantly increased toxicity to Hepa1c1c7 cells. Overall, our findings showed that storage and media of AgNPs influenced the transformation of AgNPs and that the resulting changes in the AgNPs' physicochemical properties influenced their toxicity. Our study contributes to the understanding of AgNPs' transformations under realistic exposure scenarios and increasing the predictability of risk assessments.

A novel tumor suppressor ZBTB1 regulates tamoxifen resistance and aerobic glycolysis through suppressing HER2 expression in breast cancer.

Transcriptional repressor zinc finger and BTB domain containing 1 (ZBTB1) is required for DNA repair. Because DNA repair defects often underlie genome instability and tumorigenesis, we determined to study the role of ZBTB1 in cancer. In this study, we found that ZBTB1 is down-regulated in breast cancer and this down-regulation is associated with poor outcome of breast cancer patients. ZBTB1 suppresses breast cancer cell proliferation and tumor growth. The majority of breast cancers are estrogen receptor (ER) positive and selective estrogen receptor modulators such as tamoxifen have been widely used in the treatment of these patients. Unfortunately, many patients develop resistance to endocrine therapy. Tamoxifen-resistant cancer cells often exhibit higher HER2 expression and an increase of glycolysis. Our data revealed that ZBTB1 plays a critical role in tamoxifen resistance in vitro and in vivo To see if ZBTB1 regulates HER2 expression, we tested the recruitments of ZBTB1 on HER2 regulatory sequences. We observed that over-expressed ZBTB1 occupies the estrogen receptor α (ERα)-binding site of the HER2 intron in tamoxifen-resistant cells, suppressing tamoxifen-induced transcription. In an effort to identify potential microRNAs (miRNAs) regulating ZBTB1, we found that miR-23b-3p directly targets ZBTB1. MiR-23b-3p regulates HER2 expression and tamoxifen resistance via targeting ZBTB1. Finally, we found that miR-23b-3p/ZBTB1 regulates aerobic glycolysis in tamoxifen-resistant cells. Together, our data demonstrate that ZBTB1 is a tumor suppressor in breast cancer cells and that targeting the miR-23b-3p/ZBTB1 may serve as a potential therapeutic approach for the treatment of tamoxifen resistant breast cancer.

Norcantharidin regulates ERα signaling and tamoxifen resistance via targeting miR-873/CDK3 in breast cancer cells.

MiR-873/CDK3 has been shown to play a critical role in ERα signaling and tamoxifen resistance. Thus, targeting this pathway may be a potential therapeutic approach for the treatment of ER positive breast cancer especially tamoxifen resistant subtype. Here we report that Norcantharidin (NCTD), currently used clinically as an ani-cancer drug in China, regulates miR-873/CDK3 axis in breast cancer cells. NCTD decreases the transcriptional activity of ERα but not ERß through the modulation of miR-873/CDK3 axis. We also found that NCTD inhibits cell proliferation and tumor growth and miR-873/CDK3 axis mediates cell proliferation suppression of NCTD. More important, we found that NCTD sensitizes resistant cells to tamoxifen. NCTD inhibits tamoxifen induced the transcriptional activity as well ERα downstream gene expressions in tamoxifen resistant breast cancer cells. In addition, we found that NCTD restores tamoxifen induced recruitments of ERα co-repressors N-CoR and SMRT. Knockdown of miR-873 and overexpression of CDK3 diminish the effect of NCTD on tamoxifen resistance. Our data shows that NCTD regulates ERα signaling and tamoxifen resistance by targeting miR-873/CDK3 axis in breast cancer cells. This study may provide an alternative therapy strategy for tamoxifen resistant breast cancer.

Bioaccumulation and effects of sediment-associated gold- and graphene oxide nanoparticles on Tubifex tubifex.

With the development of nanotechnology, gold (Au) and graphene oxide (GO) nanoparticles have been widely used in various fields, resulting in an increased release of these particles into the environment. The released nanoparticles may eventually accumulate in sediment, causing possible ecotoxicological effects to benthic invertebrates. However, the impact of Au-NPs and GO-NPs on the cosmopolitan oligochaete, Tubifex tubifex, in sediment exposure is not known. Mortality, behavioral impact (GO-NP and Au-NP) and uptake (only Au-NP) of sediment-associated Au-NPs (4.9±0.14nm) and GO-NPs (116±0.05nm) to T. tubifex were assessed in a number of 5-day exposure experiments. The results showed that the applied Au-NP concentrations (10 and 60µg Au/g dry weight sediment) had no adverse effect on T. tubifex survival, while Au bioaccumulation increased with exposure concentration. In the case of GO-NPs, no mortality of T. tubifex was observed at a concentration range of 20 and 180µg GO/g dry weight sediment, whereas burrowing activity was significantly reduced at 20 and 180µg GO/g dry weight sediment. Our results suggest that Au-NPs at 60µg Au/g or GO-NPs at 20 and 180µg GO/g were detected by T. tubifex as toxicants during short-term exposures.

Quinoline-degrading strain Pseudomonas aeruginosa KDQ4 isolated from coking activated sludge is capable of the simultaneous removal of phenol in a dual substrate system.

Quinoline is a refractory organic compound in the treatment of coking wastewater. The isolation of high efficiency quinoline-degrading bacteria from activated sludge and the evaluation of their degradation characteristics in the presence of phenol or in the actual coking wastewater are important for the improvement of effluent quality. The novel bacterial strain Pseudomonas aeruginosa KDQ4 was isolated from a quinoline enrichment culture obtained from the activated sludge of a coking wastewater treatment plant. The optimum temperature and initial pH for quinoline degradation were 33-38°C and 8-9, respectively. KDQ4 completely degraded 400 mg/L of quinoline within 24 h and 800 mg/L of phenol within 30 h. In the dual-substrate system, the removal efficiencies of quinoline and phenol at the same initial concentration (200 mg/L) by KDQ4 were 89% and 100% within 24 h, respectively, indicating that KDQ4 could simultaneously and quickly degrade quinoline and phenol in a coexistence system. Moreover, KDQ4 was able to adapt to actual coking wastewater containing high quinoline and phenol concentrations and rapidly remove them. KDQ4 also exhibited heterotrophic nitrification and aerobic denitrification potential under aerobic conditions. These results suggested a potential bioaugmentation role for KDQ4 in the removal of nitrogen-heterocyclic compounds and phenolics from coking wastewater.

[Study of teratogenicity of 2, 2-dinitroethene-1, 1-diamine in sprague dawley rats].

OBJECTIVE: To detect the toxicity and teratogenicity of 2, 2-dinitroethene-1, 1-diamine (FOX-7) in rats. METHODS: 125 adult SD rats were randomly divided into five groups, which are negative control (0 mg/kg) , positive control (280 mg/kg aspirin) , and three dose groups (5, 15, and 45 mg/kg) . They were administrated by gavage once a day from the 5th days to 19th days after pregnancy. The weight changes and toxicity of pregnant rats are recorded within the study, and the skeleton and internal organs malformations are detected by the recommended methods. RESULTS: After 5 or 6 days being poisoned, the pregnant rats appear significantly toxicity symptoms, such as exciting, irritability, and so on. The net weight raise in high dose group is less than the negative group, while the numbers of dead foetus in median and high dose groups are both more than that of negative group. Comparing with the negative group, the body weight and body lenghth of foetus rats in median and high dose groups, and the tail lenghth in high dose group are lower significantly. There are no external malformations in negative group and three dose groups. However, the foetus of high dose group appear significant skeleton and internal organs malformation prevalences that are significant more than negative group, including lateral cerebral ventricles enlarged, which accounts for 9.17%, occipital bone lost, which accounts for 2.59%. CONCLUSION: FOX-7 can induced maternal reproductive toxicity, foetus toxicity and teratogenicity hazards to rats.

[Study of embryo toxicity and the teratogenicity of 2, 4-dinitroanisole in rats].

OBJECTIVE: To detect the embryo toxicity and the teratogenicity of DNAN in rats and provide basic data to occupational protection. METHODS: 120 adult female SD rats and 60 male rats are mating for 1: 1, and the pregnant rats were randomly divided into five groups by the pregnant time. The negative control group are gavaged with 4% starch, and the three experiment groups are gavaged with DNAN suspension with the dose of 5 mg/kg, 15 mg/kg and 45 mg/kg respectively, while the positive control give aspirin of 280 mg/kg. All rats of the five groups are administrated gavage from gestation day 5 (GD5) to GD19 continuously. The rats are dislocated in GD20, and the toxicity of embryo and toetus are detected. RESULTS: The net weight growth in all three dose group are less than that of negative group, while the dead foetus in high dose group is more than negative group. Moreover, the body weight, body lenghth, tail lenghth and the anal genital distance of foetus rats in high dose group are all less than that of negative group. The foetus external malformations of three dose groups appear no significant compared with negative group.However, the prevalences of skeleton malformation in high dose group and the internal organs malformation in the median and high dose group appear significant higher than that of negative group. There are significantly maternal reproductive toxicity, embryo toxicity and toetus toxicity in positive group. CONCLUSION: DNAN can induced maternal reproductive toxicity, embryo toxicity and the teratogenicity to rats.