Mineralogical attenuation for metallic remediation in a passive system for mine water treatment

Passive systems with constructed wetlands have been consistently used to treat mine water from abandoned mines. Long-term and cost-effective remediation is a crucial expectation for these water treatment facilities. To achieve that, a complex chain of physical, chemical, biological, and mineralogical mechanisms for pollutants removal must be designed to simulate natural attenuation processes. This paper aims to present geochemical and mineralogical data obtained in a recently constructed passive system (from an abandoned mine, Jales, Northern Portugal). It shows the role of different solid materials in the retention of metals and arsenic, observed during the start-up period of the treatment plant. The mineralogical study focused on two types of materials: (1) the ochre-precipitates, formed as waste products from the neutralization process, and (2) the fine-grained minerals contained in the soil of the wetlands. The ochre-precipitates demonstrated to be poorly ordered iron-rich material, which gave rise to hematite upon artificial heating. The heating experiments also provided mineralogical evidence for the presence of an associated amorphous arsenic-rich compound. Chemical analysis on the freshly ochre-precipitates revealed high concentrations of arsenic (51,867 ppm) and metals, such as zinc (1,213 ppm) and manganese (821 ppm), indicating strong enrichment factors relative to the water from which they precipitate. Mineralogical data obtained in the soil of the wetlands indicate that chlorite, illite, chlorite–vermiculite and mica–vermiculite mixedlayers, vermiculite, kaolinite and goethite are concentrated in the fine-grained fractions (<20 and <2 μm). The chemical analyses show that high levels of arsenic (up to 3%) and metals are also retained in these fractions, which may be enhanced by the low degree of order of the clay minerals as suggested by an XRD study. The obtained results suggest that, although the treatment plant has been receiving water only since 2006, future performance will be strongly dependent on these identified mineralogical pollutant hosts.Fundação para a Ciência e a Tecnologia (FCT

Low back pain status in elite and semi-elite Australian football codes: a cross-sectional survey of football (soccer), Australian rules, rugby league, rugby union and non-athletic controls

<p>Abstract</p> <p>Background</p> <p>Our understanding of the effects of football code participation on low back pain (LBP) is limited. It is unclear whether LBP is more prevalent in athletic populations or differs between levels of competition. Thus it was the aim of this study to document and compare the prevalence, intensity, quality and frequency of LBP between elite and semi-elite male Australian football code participants and a non-athletic group.</p> <p>Methods</p> <p>A cross-sectional survey of elite and semi-elite male Australian football code participants and a non-athletic group was performed. Participants completed a self-reported questionnaire incorporating the Quadruple Visual Analogue Scale (QVAS) and McGill Pain Questionnaire (short form) (MPQ-SF), along with additional questions adapted from an Australian epidemiological study. Respondents were 271 elite players (mean age 23.3, range 17–39), 360 semi-elite players (mean age 23.8, range 16–46) and 148 non-athletic controls (mean age 23.9, range 18–39).</p> <p>Results</p> <p>Groups were matched for age (p = 0.42) and experienced the same age of first onset LBP (p = 0.40). A significant linear increase in LBP from the non-athletic group, to the semi-elite and elite groups for the QVAS and the MPQ-SF was evident (p < 0.001). Elite subjects were more likely to experience more frequent (daily or weekly OR 1.77, 95% CI 1.29–2.42) and severe LBP (discomforting and greater OR 1.75, 95% CI 1.29–2.38).</p> <p>Conclusion</p> <p>Foolers in Australia have significantly more severe and frequent LBP than a non-athletic group and this escalates with level of competition.</p

Topoisomerase II alpha gene copy loss has adverse prognostic significance in ERBB2-amplified breast cancer: a retrospective study of paraffin-embedded tumor specimens and medical charts

<p>Abstract</p> <p>Background</p> <p>Amplification of the <it>ERBB2 </it>(<it>Her-2/neu</it>) oncogene, which occurs in approximately 25% of breast carcinomas, is a known negative prognostic factor. Available data indicate that a variable number of nearby genes on chromosome 17q may be co-amplified or deleted, forming a continuous amplicon of variable size. In approximately 25% of these patients, the amplicon extends to the gene for <it>topoisomerase II alpha </it>(<it>TOP2A</it>), a target for anthracyclines. We sought to understand the significance of these associated genomic changes for breast cancer prognosis and predicting response to therapy.</p> <p>Methods and patients</p> <p>Archival tissue samples from 63 breast cancer patients with <it>ERBB2 </it>amplification, stages 0–IV, were previously analyzed with FISH probes for genes located near <it>ERBB2</it>. In the present study, the clinical outcome data were determined for all patients presenting at stages I–III for whom adequate clinical follow up was available.</p> <p>Results</p> <p>Four amplicon patterns (Classes) were identified. These were significantly associated with the clinical outcome, specifically, recurrence of breast cancer. The Amplicon class IV with deleted <it>TOP2A </it>had 67% (6/9) cases with recurrence, whereas the other three classes combined had only 12% (3/25) cases (p-value = 0.004) at the time of last follow-up. <it>TOP2A </it>deletion was also significantly associated with time to recurrence (p-value = 0.0002). After adjusting for age in Cox regression analysis, the association between <it>TOP2A </it>deletion and time to recurrence remains strongly significant (p-value = 0.002) whereas the association with survival is marginally significant (p-value = 0.06).</p> <p>Conclusion</p> <p><it>TOP2A </it>deletion is associated with poor prognosis in <it>ERBB2</it>-amplified breast carcinomas. Clarification of the mechanism of this association will require additional study.</p

Epigenetic regulation of centromeric chromatin: old dogs, new tricks?

The assembly of just a single kinetochore at the centromere of each sister chromatid is essential for accurate chromosome segregation during cell division. Surprisingly, despite their vital function, centromeres show considerable plasticity with respect to their chromosomal locations and activity. The establishment and maintenance of centromeric chromatin, and therefore the location of kinetochores, is epigenetically regulated. The histone H3 variant CENP-A is the key determinant of centromere identity and kinetochore assembly. Recent studies have identified many factors that affect CENP-A localization, but their precise roles in this process are unknown. We build on these advances and on new information about the timing of CENP-A assembly during the cell cycle to propose new models for how centromeric chromatin is established and propagated

Synthetic biology to access and expand nature's chemical diversity

Bacterial genomes encode the biosynthetic potential to produce hundreds of thousands of complex molecules with diverse applications, from medicine to agriculture and materials. Accessing these natural products promises to reinvigorate drug discovery pipelines and provide novel routes to synthesize complex chemicals. The pathways leading to the production of these molecules often comprise dozens of genes spanning large areas of the genome and are controlled by complex regulatory networks with some of the most interesting molecules being produced by non-model organisms. In this Review, we discuss how advances in synthetic biology — including novel DNA construction technologies, the use of genetic parts for the precise control of expression and for synthetic regulatory circuits — and multiplexed genome engineering can be used to optimize the design and synthesis of pathways that produce natural products

Behavioural Risk Factors in Mid-Life Associated with Successful Ageing, Disability, Dementia and Frailty in Later Life: A Rapid Systematic Review.

BACKGROUND: Smoking, alcohol consumption, poor diet and low levels of physical activity significantly contribute to the burden of illness in developed countries. Whilst the links between specific and multiple risk behaviours and individual chronic conditions are well documented, the impact of these behaviours in mid-life across a range of later life outcomes has yet to be comprehensively assessed. This review aimed to provide an overview of behavioural risk factors in mid-life that are associated with successful ageing and the primary prevention or delay of disability, dementia, frailty and non-communicable chronic conditions. METHODS: A literature search was conducted to identify cohort studies published in English since 2000 up to Dec 2014. Multivariate analyses and a minimum follow-up of five years were required for inclusion. Two reviewers screened titles, abstracts and papers independently. Studies were assessed for quality. Evidence was synthesised by mid-life behavioural risk for a range of late life outcomes. FINDINGS: This search located 10,338 individual references, of which 164 are included in this review. Follow-up data ranged from five years to 36 years. Outcomes include dementia, frailty, disability and cardiovascular disease. There is consistent evidence of beneficial associations between mid-life physical activity, healthy ageing and disease outcomes. Across all populations studied there is consistent evidence that mid-life smoking has a detrimental effect on health. Evidence specific to alcohol consumption was mixed. Limited, but supportive, evidence was available relating specifically to mid-life diet, leisure and social activities or health inequalities. CONCLUSIONS: There is consistent evidence of associations between mid-life behaviours and a range of late life outcomes. The promotion of physical activity, healthy diet and smoking cessation in all mid-life populations should be encouraged for successful ageing and the prevention of disability and chronic disease.This work was funded by the National Institute for Health and Care Excellence (NICE), invitation to tender reference DDER 42013, and supported by the National Institute for Health Research School for Public Health Research. The scope of the work was defined by NICE and the protocol was agreed with NICE prior to the start of work. The funders had no role in data analysis, preparation of the manuscript or decision to publish.This is the final version of the article. It first appeared from PLOS via http://dx.doi.org/10.1371/journal.pone.014440

Tau Causes Synapse Loss without Disrupting Calcium Homeostasis in the rTg4510 Model of Tauopathy

Neurofibrillary tangles (NFTs) of tau are one of the defining hallmarks of Alzheimer’s disease (AD), and are closely associated with neuronal degeneration. Although it has been suggested that calcium dysregulation is important to AD pathogenesis, few studies have probed the link between calcium homeostasis, synapse loss and pathological changes in tau. Here we test the hypothesis that pathological changes in tau are associated with changes in calcium by utilizing in vivo calcium imaging in adult rTg4510 mice that exhibit severe tau pathology due to over-expression of human mutant P301L tau. We observe prominent dendritic spine loss without disruptions in calcium homeostasis, indicating that tangles do not disrupt this fundamental feature of neuronal health, and that tau likely induces spine loss in a calcium-independent manner