Explore the vast range of titles available.

The objectives of this study were to determine whether, and to what degree, the aqueous iron concentration in the growing medium affects the growth of, and Fe uptake by, Phragmites australis, and whether the presence of iron in the growing environment affects the uptake of the essential element phosphate. The wetland macrophyte P. australis was grown under laboratory conditions in nutrient solution (0·31 mg L–1 phosphate) containing a range of iron concentrations (0–50 mg L–1 Fe). A threshold of iron concentration (1 mg L–1) was found, above which growth of P. australis was significantly inhibited. No direct causal relationship between iron content in aerial tissues and growth inhibition was found, which strongly suggests that iron toxicity cannot explain these results. Phosphate concentrations in aerial tissues were consistently sufficient for growth and development (2–3 % d. wt) despite significant variation in concentration of phosphate associated with roots. External Fe concentration had a significant effect on the growth of P. australis and on both Fe and phosphate concentrations associated with roots. However, neither direct toxicity nor phosphate deficiency could explain the reduction in growth above 1 mg L–1 external Fe concentration

The physico-chemical properties of iron oxyhydroxide plaques formed on the roots of Phragmites australis under field and laboratory conditions were determined using electron microscopy and energy dispersive spectrometry (EDS) analysis. Plaques were present as an amorphous coating on roots with an uneven distribution. They were shown to be composed of iron in both the field and laboratory, and phosphorus was found to be adsorbed onto the surface of plaques formed in the laboratory. The uptake of copper and manganese in the presence and absence of plaque was investigated under two different pH regimes. Concentrations of Cu were lower in the shoots of P. australis in the presence of plaque (565mg kg−1) than when it was absent (1400mg kg−1), under growth conditions of higher pH (6.0). The adsorption of Cu and Mn onto the plaque surface was not the mechanism by which plaque reduced the uptake of other metals. Alternatively, the plaque may simply act as a physical barrier. Under conditions of lower pH (3.5) the activity of hydrogen ions at the root surface interfered with the movement of metals into the root and masked any potential effect of iron plaque.

Aluminium, a potentially phytotoxic metal, is an important constituent of many mine water discharges but has largely been neglected in the literature. The behaviour of this element in the rhizosphere of the wetland plant Phragmites australis was investigated in the laboratory in the presence and absence of Mn and Fe root plaques. Electron microscopy and chemical extraction techniques were utilized to determine the physico-chemical properties of the plaques and any association of Al. Both Mn and Fe plaques occurred as amorphous coatings on root surfaces with uneven distributions. Al was not adsorbed onto the surface of either plaque type but formed a separate phosphate deposit closely resembling the Fe and Mn plaques. Phosphorus was also found to be adsorbed to the surface of the Fe plaques (but not the Mn plaques). Both mechanisms were found to immobilize P at the root surface but this did not significantly reduce the concentration of P in aerial plant tissues that was sufficient to ensure adequate growth.

The effect of plant growth on surface and porewater concentrations of Fe, Mn, Cu, and S within a natural wetland receiving acidic spoil heap drainage was determined over a period of one year. Comparisons were made between unvegetated sites and those colonized by either Phragmites australis or Eriophorum angustifolium. The presence of vegetation increased surface and porewater concentrations of Fe and Mn in spring and summer largely due to the effects of higher evapotranspiration rates in vegetated areas. Microbiological processes were also thought to be important in controlling iron and sulfur concentrations at depth due to bacterial sulfate reduction and metal sulfide precipitation and iron and manganese concentrations close to the sediment surface due to bacterially mediated oxidation. These processes varied in importance with season due to changes in the dominant chemical and biological processes, although the complexity of the system prevented isolation of the principal mechanism involved.

The contamination and resulting degradation of water courses by effluents from abandoned and active mines is a world-wide problem. Traditional methods of remediating the discharges from mines involve the addition of chemicals and the utilisation of artificial energy sources. Over the last 15-20 years passive treatment systems have been developed that harness natural chemical and biological processes to ameliorate the potentially toxic effects of such discharges. There are many different types of passive system, including compost wetlands, reducing and alkalinity producing systems (RAPS), permeable reactive barriers and inorganic media passive systems. Different waste materials can be utilised as reactive media within each of these systems, dependent upon the type of mine water and treatment technology. In many cases the reactivity of these recycled waste materials is key to the remedial performance of these systems. The materials used may be organic (e.g., composts) or inorganic (e.g., blast furnace slag) and where possible are sourced locally in order to minimise transport costs. The remediation of mine waters in itself can produce large quantities of waste products in the form of iron oxide sludge. Potential uses of this material in the production of pigments and in the treatment of phosphate contaminated waters is also currently under investigation. The exploitation of what are traditionally thought of as waste materials within treatment systems for polluted waters is an expanding technology which provides great scope for recycling.

Aluminium, a potentially phytotoxic metal, is an important constituent of many mine water discharges but has largely been neglected in the literature. The behaviour of this element in the rhizosphere of the wetland plant Phragmites australis was investigated in the laboratory in the presence and absence of Mn and Fe root plaques. Electron microscopy and chemical extraction techniques were utilized to determine the physico-chemical properties of the plaques and any association of Al. Both Mn and Fe plaques occurred as amorphous coatings on root surfaces with uneven distributions. Al was not adsorbed onto the surface of either plaque type but formed a separate phosphate deposit closely resembling the Fe and Mn plaques. Phosphorus was also found to be adsorbed to the surface of the Fe plaques (but not the Mn plaques). Both mechanisms were found to immobilize P at the root surface but this did not significantly reduce the concentration of P in aerial plant tissues that was sufficient to ensure adequate growth.

The occurrence of a range of health outcomes following myocardial infarction (MI) is unknown. Therefore, this study aimed to determine the long-term risk of major health outcomes following MI and generate sociodemographic stratified risk charts in order to inform care recommendations in the post-MI period and underpin shared decision making. This nationwide cohort study includes all individuals aged ≥18 years admitted to one of 229 National Health Service (NHS) Trusts in England between 1 January 2008 and 31 January 2017 (final follow-up 27 March 2017). We analysed 11 non-fatal health outcomes (subsequent MI and first hospitalisation for heart failure, atrial fibrillation, cerebrovascular disease, peripheral arterial disease, severe bleeding, renal failure, diabetes mellitus, dementia, depression, and cancer) and all-cause mortality. Of the 55,619,430 population of England, 34,116,257 individuals contributing to 145,912,852 hospitalisations were included (mean age 41.7 years (standard deviation [SD 26.1]); n = 14,747,198 (44.2%) male). There were 433,361 individuals with MI (mean age 67.4 years [SD 14.4)]; n = 283,742 (65.5%) male). Following MI, all-cause mortality was the most frequent event (adjusted cumulative incidence at 9 years 37.8% (95% confidence interval [CI] [37.6,37.9]), followed by heart failure (29.6%; 95% CI [29.4,29.7]), renal failure (27.2%; 95% CI [27.0,27.4]), atrial fibrillation (22.3%; 95% CI [22.2,22.5]), severe bleeding (19.0%; 95% CI [18.8,19.1]), diabetes (17.0%; 95% CI [16.9,17.1]), cancer (13.5%; 95% CI [13.3,13.6]), cerebrovascular disease (12.5%; 95% CI [12.4,12.7]), depression (8.9%; 95% CI [8.7,9.0]), dementia (7.8%; 95% CI [7.7,7.9]), subsequent MI (7.1%; 95% CI [7.0,7.2]), and peripheral arterial disease (6.5%; 95% CI [6.4,6.6]). Compared with a risk-set matched population of 2,001,310 individuals, first hospitalisation of all non-fatal health outcomes were increased after MI, except for dementia (adjusted hazard ratio [aHR] 1.01; 95% CI [0.99,1.02];p = 0.468) and cancer (aHR 0.56; 95% CI [0.56,0.57];p < 0.001). The study includes data from secondary care only-as such diagnoses made outside of secondary care may have been missed leading to the potential underestimation of the total burden of disease following MI. In this study, up to a third of patients with MI developed heart failure or renal failure, 7% had another MI, and 38% died within 9 years (compared with 35% deaths among matched individuals). The incidence of all health outcomes, except dementia and cancer, was higher than expected during the normal life course without MI following adjustment for age, sex, year, and socioeconomic deprivation. Efforts targeted to prevent or limit the accrual of chronic, multisystem disease states following MI are needed and should be guided by the demographic-specific risk charts derived in this study.

Adverse psychosocial working environments characterized by job strain (the combination of high demands and low control at work) are associated with an increased risk of depressive symptoms among employees, but evidence on clinically diagnosed depression is scarce. We examined job strain as a risk factor for clinical depression. We identified published cohort studies from a systematic literature search in PubMed and PsycNET and obtained 14 cohort studies with unpublished individual-level data from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium. Summary estimates of the association were obtained using random-effects models. Individual-level data analyses were based on a pre-published study protocol. We included six published studies with a total of 27 461 individuals and 914 incident cases of clinical depression. From unpublished datasets we included 120 221 individuals and 982 first episodes of hospital-treated clinical depression. Job strain was associated with an increased risk of clinical depression in both published [relative risk (RR) = 1.77, 95% confidence interval (CI) 1.47-2.13] and unpublished datasets (RR = 1.27, 95% CI 1.04-1.55). Further individual participant analyses showed a similar association across sociodemographic subgroups and after excluding individuals with baseline somatic disease. The association was unchanged when excluding individuals with baseline depressive symptoms (RR = 1.25, 95% CI 0.94-1.65), but attenuated on adjustment for a continuous depressive symptoms score (RR = 1.03, 95% CI 0.81-1.32). Job strain may precipitate clinical depression among employees. Future intervention studies should test whether job strain is a modifiable risk factor for depression.

Staphylococcus aureus is a major cause of healthcare associated mortality, but like many important bacterial pathogens, it is a common constituent of the normal human body flora. Around a third of healthy adults are carriers. Recent evidence suggests that evolution of S. aureus during nasal carriage may be associated with progression to invasive disease. However, a more detailed understanding of within-host evolution under natural conditions is required to appreciate the evolutionary and mechanistic reasons why commensal bacteria such as S. aureus cause disease. Therefore we examined in detail the evolutionary dynamics of normal, asymptomatic carriage. Sequencing a total of 131 genomes across 13 singly colonized hosts using the Illumina platform, we investigated diversity, selection, population dynamics and transmission during the short-term evolution of S. aureus. We characterized the processes by which the raw material for evolution is generated: micro-mutation (point mutation and small insertions/deletions), macro-mutation (large insertions/deletions) and the loss or acquisition of mobile elements (plasmids and bacteriophages). Through an analysis of synonymous, non-synonymous and intergenic mutations we discovered a fitness landscape dominated by purifying selection, with rare examples of adaptive change in genes encoding surface-anchored proteins and an enterotoxin. We found evidence for dramatic, hundred-fold fluctuations in the size of the within-host population over time, which we related to the cycle of colonization and clearance. Using a newly-developed population genetics approach to detect recent transmission among hosts, we revealed evidence for recent transmission between some of our subjects, including a husband and wife both carrying populations of methicillin-resistant S. aureus (MRSA). This investigation begins to paint a picture of the within-host evolution of an important bacterial pathogen during its prevailing natural state, asymptomatic carriage. These results also have wider significance as a benchmark for future systematic studies of evolution during invasive S. aureus disease.

Whole-genome sequencing offers new insights into the evolution of bacterial pathogens and the etiology of bacterial disease. Staphylococcus aureus is a major cause of bacteria-associated mortality and invasive disease and is carried asymptomatically by 27% of adults. Eighty percent of bacteremias match the carried strain. However, the role of evolutionary change in the pathogen during the progression from carriage to disease is incompletely understood. Here we use high-throughput genome sequencing to discover the genetic changes that accompany the transition from nasal carriage to fatal bloodstream infection in an individual colonized with methicillin-sensitive S. aureus. We found a single, cohesive population exhibiting a repertoire of 30 single-nucleotide polymorphisms and four insertion/deletion variants. Mutations accumulated at a steady rate over a 13-mo period, except for a cluster of mutations preceding the transition to disease. Although bloodstream bacteria differed by just eight mutations from the original nasally carried bacteria, half of those mutations caused truncation of proteins, including a premature stop codon in an AraC-family transcriptional regulator that has been implicated in pathogenicity. Comparison with evolution in two asymptomatic carriers supported the conclusion that clusters of protein-truncating mutations are highly unusual. Our results demonstrate that bacterial diversity in vivo is limited but nonetheless detectable by whole-genome sequencing, enabling the study of evolutionary dynamics within the host. Regulatory or structural changes that occur during carriage may be functionally important for pathogenesis; therefore identifying those changes is a crucial step in understanding the biological causes of invasive bacterial disease.