Electron acceptors determine the BTEX degradation capacity of anaerobic microbiota via regulating the microbial community.

Anaerobic degradation is the major pathway for microbial degradation of benzene, toluene, ethylbenzene, and xylenes (BTEX) under electron acceptor lacking conditions. However, how exogenous electron acceptors modulate BTEX degradation through shaping the microbial community structure remains poorly understood. Here, we investigated the effect of various exogenous electron acceptors on BTEX degradation as well as methane production in anaerobic microbiota, which were enriched from the same contaminated soil. It was found that the BTEX degradation capacities of the anaerobic microbiota gradually increased along with the increasing redox potentials of the exogenous electron acceptors supplemented (WE: Without exogenous electron acceptors < SS: Sulfate supplement < FS: Ferric iron supplement < NS: Nitrate supplement), while the complexity of the co-occurring networks (e.g., avgK and links) of the microbiota gradually decreased, showing that microbiota supplemented with higher redox potential electron acceptors were less dependent on the formation of complex microbial interactions to perform BTEX degradation. Microbiota NS showed the highest degrading capacity and the broadest substrate-spectrum for BTEX, and it could metabolize BTEX through multiple modules which not only contained fewer species but also different key microbial taxa (eg. Petrimonas, Achromobacter and Comamonas). Microbiota WE and FS, with the highest methanogenic capacities, shared common core species such as Sedimentibacter, Acetobacterium, Methanobacterium and Smithella/Syntrophus, which cooperated with Geobacter (microbiota WE) or Desulfoprunum (microbiota FS) to perform BTEX degradation and methane production. This study demonstrates that electron acceptors may alter microbial function by reshaping microbial community structure and regulating microbial interactions and provides guidelines for electron acceptor selection for bioremediation of aromatic pollutant-contaminated anaerobic sites.

Sporoderm-Removed Ganoderma lucidum Spore Powder May Suppress the Proliferation, Migration, and Invasion of Esophageal Squamous Cell Carcinoma Cells Through PI3K/AKT/mTOR and Erk Pathway.

Tumor metastasis is a key factor of therapeutic failure in tumor patients, but the underlying molecular mechanism remains to be explored and novel effective curative strategies are urgently required. Emerging evidence suggests that sporoderm-removed Ganoderma lucidum spore powder can suppress tumor growth and metastasis. However, the molecular mechanisms of action remain elusive. In the present study, we investigated the effects and mechanisms of sporoderm-removed Ganoderma lucidum spore powder against esophageal squamous cell carcinomas (ESCC). The expression of MCP-1 in esophageal squamous cell carcinoma cells was detected by Western blotting. The MTS assay was used to assess the esophageal squamous cell carcinoma cells viability. The clone formation assay was used to evaluate to the proliferation ability of KYSE140 and KYSE510 cells. Apoptosis and the cell cycle were analyzed by flow cytometry. Wound healing and Transwell assays were used to analyze the migration of KYSE140 and KYSE510 cells. Invasion was also analyzed by the Transwell assay. The expressions of PI3K, AKT/p-AKT, Erk/p-Erk, JNK1, and mTOR were detected by Western blotting. We found that the MCP-1 protein was highly expressed in KYSE140 and KYSE510. In addition, sporoderm-removed Ganoderma lucidum spore powder treatment was found to inhibit esophageal squamous cell carcinoma cell proliferation, to block the cell cycle, to induce cell apoptosis and to inhibit cell migration and invasion. Finally, we found that sporoderm-removed Ganoderma lucidum spore powder decreased the expression of PI3K/AKT/mTOR and Erk signaling pathways. Taken together, these findings demonstrate that sporoderm-removed Ganoderma lucidum spore powder suppresses esophageal squamous cell carcinomas by involving MCP-1, regulated by PI3K/AKT/mTOR and Erk signal pathways.

A Synergistic Consortium Involved in rac-Dichlorprop Degradation as Revealed by DNA Stable Isotope Probing and Metagenomic Analysis.

rac-Dichlorprop, a commonly used phenoxyalkanoic acid herbicide, is frequently detected in environments and poses threats to environmental safety and human health. Microbial consortia are thought to play key roles in rac-dichlorprop degradation. However, the compositions of the microbial consortia involved in rac-dichlorprop degradation remain largely unknown. In this study, DNA stable isotope probing (SIP) and metagenomic analysis were integrated to reveal the key microbial consortium responsible for rac-dichlorprop degradation in a rac-dichlorprop-degrading enrichment. OTU340 (Sphingobium sp.) and OTU348 (Sphingopyxis sp.) were significantly enriched in the rac-[13C]dichlorprop-labeled heavy DNA fractions. A rac-dichlorprop degrader, Sphingobium sp. strain L3, was isolated from the enrichment by a traditional enrichment method but with additional supplementation of the antibiotic ciprofloxacin, which was instructed by metagenomic analysis of the associations between rac-dichlorprop degraders and antibiotic resistance genes. As revealed by functional profiling of the metagenomes of the heavy DNA, the genes rdpA and sdpA, involved in the initial degradation of the (R)- and (S)-enantiomers of dichlorprop, respectively, were mostly taxonomically assigned to Sphingobium species, indicating that Sphingopyxis species might harbor novel dichlorprop-degrading genes. In addition, taxonomically diverse bacterial genera such as Dyella, Sphingomonas, Pseudomonas, and Achromobacter were presumed to synergistically cooperate with the key degraders Sphingobium/Sphingopyxis for enhanced degradation of rac-dichlorprop. IMPORTANCE Understanding of the key microbial consortium involved in the degradation of the phenoxyalkanoic acid herbicide rac-dichlorprop is pivotal for design of synergistic consortia used for enhanced bioremediation of herbicide-contaminated sites. However, the composition of the microbial consortium and the interactions between community members during the biodegradation of rac-dichlorprop are unclear. In this study, DNA-SIP and metagenomic analysis were integrated to reveal that the metabolite 2,4-dichlorophenol degraders Dyella, Sphingomonas, Pseudomonas, and Achromobacter synergistically cooperated with the key degraders Sphingobium/Sphingopyxis for enhanced degradation of rac-dichlorprop. Our study provides new insights into the synergistic degradation of rac-dichlorprop at the community level and implies the existence of novel degrading genes for rac-dichlorprop in nature.

Paying for volume: British Columbia's experiment with funding hospitals based on activity.

INTRODUCTION: For decades, Canadian hospitals have been funded using global budgets, a lump sum for providing care irrespective of the volume or mix of patients. In 2010, British Columbia (BC) introduced a controversial, but limited, form of activity-based funding (ABF) for hospitals. This study uses a quasi-experimental design to evaluate the impact of the introduction of ABF funding in the province. METHODS: Our analysis used the population of patient-level acute hospitalization and day surgery discharge summaries from BC's acute hospitals from April 1, 2008 to March 31, 2013. Our outcome measures focused on both the intended and unintended impacts of ABF including the volume of cases, the efficiency of care, and the quality of care delivered. Our analysis used interrupted time series analysis. RESULTS: There was an increase in the volume of inpatient surgical activity associated with the implementation of ABF. The volume of medical cases dropped, and medical patients' lengths of stays increased. There were no changes in measures of quality. CONCLUSIONS: Hospitals' measurable responses to ABF policies on a number of key performance measures were mixed. Though BC's experiment with ABF was not associated with increases in hospital volumes for all types of care, the experience provides key lessons that small magnitude and short-term reforms are unlikely to change hospitals' behaviors quickly.

Childlessness, psychological well-being, and life satisfaction among the elderly in China.

This paper examines the effects of childlessness on the well-being of persons aged 65 and above in China. It is based on an application of ordered-logit regression in the analysis of the data from the 2002 wave of the Chinese Longitudinal Healthy Longevity Survey (CLHLS) conducted in 22 provinces of China (N = 13,447). It compares parents with the childless elderly, focusing on three dimensions of psychological well-being, namely feelings of anxiety, loneliness, and uselessness, and on life satisfaction. The findings include the following. First, with control of social demographic variables of age, gender and education, childlessness is significantly associated with life satisfaction, feeling of anxiety and loneliness, but not feeling of uselessness. The childless elderly are less satisfied with their lives and feel more anxious and lonely than do parents, but they do not necessarily feel significantly more useless. Second, when controlled with social-demographic variables and additional socioeconomic variables of residence, living arrangement, availability of pension and medical services, childlessness is no longer significantly related to anxiety and loneliness, and it is related at only a marginally-significant level to life satisfaction. Third, individual education, place of residence, living arrangements, economic security and access to medical services are consistently related to life satisfaction and psychological well-being among the elderly. We conclude that providing social investments in education in early life and economic security and medical insurance in later life for both the childless and parents are crucial for improving individual psychological well-being and life satisfaction for the elderly.