Enteropathogen survival in soil from different land-uses is predominantly regulated by microbial community composition

peer-reviewedMicrobial enteropathogens can enter the environment via landspreading of animal slurries and manures. Biotic interactions with the soil microbial community can contribute to their subsequent decay. This study aimed to determine the relative impact of biotic, specifically microbial community structure, and physico-chemical properties associated with soils derived from 12 contrasting land-uses on enteropathogen survival. Phenotypic profiles of microbial communities (via phospholipid fatty acid (PLFA) profiling), and total biomass (by fumigation-extraction), in the soils were determined, as well as a range of physicochemical properties. The persistence of Salmonella Dublin, Listeria monocytogenes, and Escherichia coli was measured over 110 days within soil microcosms. Physicochemical and biotic data were used in stepwise regression analysis to determine the predominant factor related to pathogen-specific death rates. Phenotypic structure, associated with a diverse range of constituent PLFAs, was identified as the most significant factor in pathogen decay for S. Dublin, L. monocytogenes, non-toxigenic E. coli O157 but not for environmentally-persistent E. coli. This demonstrates the importance of entire community-scale interactions in pathogen suppression, and that such interactions are context-specific

Overlapping Climate Policies

Major carbon-pricing systems in Europe and North America involve multiple jurisdictions (countries or states). Individual jurisdictions often pursue additional Initiatives – such as unilateral carbon price oors, legislation to phase out coal, aviation taxes or support programs for renewable energy – that overlap with the wider carbon-pricing system. We develop a general framework to study how the climate benefit of such overlapping policies depends on their design, location and timing. Some policies leverage additional climate benefits elsewhere in the system while others backfire by raising aggregate emissions. Our model encompasses almost every type of carbon-pricing system used in practice

Early increase in blood pressure and diastolic left ventricular malfunction in patients with glomerulonephritis

Early increase in blood pressure and diastolic left ventricular malfunction in patients with glomerulonephritis. In patients with diabetic nephropathy blood pressure increases progressively before the conventional threshold of normal blood pressure (140/90mm Hg) is transgressed. In patients with glomerulonephritis, no information on this point is available. To clarify this issue we sequentially examined 20 untreated patients with biopsy-proven primary chronic glomerulonephritis (GN) who had casual blood pressure below 140/90mm Hg and normal GFR by inulin clearance. Patients were compared with normotensive healthy controls who were matched for BMI, gender and age. We measured ambulatory 24-hour blood pressure (SpaceLab system), echocardiography (ASE criteria, Acuson 128 XP 10), CIn and CPAH, urinary Na excretion, PRA and insulin concentration. In patients with GN, the median 24 hour (P < 0.0005), daytime (P < 0.001) and nocturnal sleeping time (P < 0.0001) MAP values were significantly higher than in matched controls (daytime, mean 97mm Hg, 85 to 106 GN vs. 89 controls range 82 to 102; nocturnal sleeping time, mean 80.3mm Hg, 71 to 89.5 GN vs. 73 controls, range 63 to 84). Echocardiographic examination showed significantly greater posterior wall thickness (P < 0.01) and ventricular septal thickness (P < 0.003). In addition the early diastolic to late diastolic (E/A) ratio of mitral valve peak inflow velocity was significantly (P < 0.0008) lower in patients. The data point to left ventricular wall thickening accompanied by LV diastolic malfunction. The study documents elevated ambulatory blood pressure in patients with primary chronic glomerulonephritis despite normal body weight and normal GFR. This is associated with evidence of target organ damage in the heart. The findings suggest that in patients with glomerulonephritis blood pressure increases initially within the normotensive range. This observation in conjunction with evidence of early target organ changes provides an argument for early antihypertensive intervention, but controlled trials to test efficacy and safety of this proposal are necessary

A practical approach to estimate resting energy expenditure in frail elderly people

Objectives: Some prediction equations of resting energy expenditure (REE) are available and can be used in clinical wards to determine energy requirements of patients. The aim of the present study was to assess the accuracy of those equations in sick elderly patients, using the Bland &amp; Altman methods with our database of 187 REE measurements.Design: The 3 equations tested were Harris &amp; Benedict equation of 1919, WHO/FAO/UNU equation of 1985 and Fredrix et al. equation of 1990. In addition, three models developed from the present data were tested.Results: The present study shows that the Fredrix et al equation gave an accurate prediction of REE without significant bias along the whole range of REE. It also shows that under-weight sick elderly patients (BMI ≤ 21 kg/m2) had a greater weight-adjusted REE than their normal weight counterparts.Conclusion: A simple formula using a factor multiplying body weight, i.e. 22 kcal/kg/d in under-weight and 19 kcal/kg/d in normal weight sick elderly was accurate to predicting REE and bias was not influenced by the level of REE. This model included half of the group in the range of ±10% of the difference between predicted REE and measured REE, but the confidence interval of the bias was ±400 kcal/d. Conversely, the Harris &amp; Benedict and WHO formulae did accurately predict REE

Discovery of spatial periodicities in a coronal loop using automated edge-tracking algorithms

A new method for automated coronal loop tracking, in both spatial and temporal domains, is presented. Applying this technique to TRACE data, obtained using the 171 Å filter on 1998 July 14, we detect a coronal loop undergoing a 270 s kink-mode oscillation, as previously found by Aschwanden et al. However, we also detect flare-induced, and previously unnoticed, spatial periodicities on a scale of 3500 km, which occur along the coronal loop edge. Furthermore, we establish a reduction in oscillatory power for these spatial periodicities of 45% over a 222 s interval. We relate the reduction in detected oscillatory power to the physical damping of these loop-top oscillations

Is skeletal muscle mitochondrial dysfunction a cause or an indirect consequence of insulin resistance in humans?

The precise cause of insulin resistance and type 2 diabetes is unknown. However, there is a strong association between insulin resistance and lipid accumulation — and, in particular, lipotoxic fatty acid metabolites — in insulin-target tissues. Such accumulation is known to cause insulin resistance, particularly in skeletal muscle, by reducing insulin-stimulated glucose uptake. Reduced fat-oxidation capacity appears to cause such lipid accumulation and, over the past few years, many studies have concluded that decreased mitochondrial oxidative phosphorylation could be the initiating cause of lipid deposition and the development of insulin resistance. The aim of this review is to summarize the latest findings regarding the link between skeletal muscle mitochondrial dysfunction and insulin resistance in humans. At present, there are too few studies to definitively conclude that, in this context, mitochondria are functionally impaired (dysfunction in the respiratory chain). Indeed, insulin resistance could also be related to a decrease in the number of mitochondria or to a combination of this and mitochondrial dysfunction. Finally, we also consider whether or not these aberrations could be the cause of the development of the disease or whether mitochondrial dysfunction may simply be the consequence of an insulin-resistant state

Mitochondrial effects of dexamethasone imply both membrane and cytosolic-initiated pathways in HepG2 cells

Glucocorticoid treatment is often linked to increased whole-body energy expenditure and hypermetabolism. Glucocorticoids affect mitochondrial energy production, notably in the liver, where they lead to mitochondrial uncoupling reducing the efficacy of oxidative phosphorylation. However, the signaling pathways involved in these phenomena are poorly understood. Here we treated HepG2 cells with dexamethasone for different times and, by using different combinations of inhibitors, we showed that dexamethasone treatment leads to recruitment of two main signaling pathways. The first one involves a G-protein coupled membrane glucocorticoid binding site and rapidly decreases complexes I and II activities while complex III activity is upregulated in a p38MAPK dependent mechanism. The second one implies the classical cytosolic glucocorticoid receptor and triggers long-term transcriptional increases of respiration rates and of complex IV activity and quantity. We concluded that mitochondria are the target of multiple dexamethasone-induced regulatory pathways that are set up gradually after the beginning of hormone exposure and that durably influence mitochondrial oxidative phosphorylation