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This article evaluates the suitability of the ECOSSE model to estimate soil greenhouse gas (GHG) fluxes from short rotation coppice willow ( SRC-Willow), short rotation forestry ( SRF-Scots Pine) and Miscanthus after land-use change from conventional systems (grassland and arable). We simulate heterotrophic respiration ( Rh), nitrous oxide (N2O) and methane ( CH4) fluxes at four paired sites in the UK and compare them to estimates of Rh derived from the ecosystem respiration estimated from eddy covariance ( EC) and Rh estimated from chamber ( IRGA) measurements, as well as direct measurements of N2O and CH4 fluxes. Significant association between modelled and EC-derived Rh was found under Miscanthus, with correlation coefficient ( r) ranging between 0.54 and 0.70. Association between IRGA-derived Rh and modelled outputs was statistically significant at the Aberystwyth site ( r = 0.64), but not significant at the Lincolnshire site ( r = 0.29). At all SRC-Willow sites, significant association was found between modelled and measurement-derived Rh (0.44 ≤ r ≤ 0.77); significant error was found only for the EC-derived Rh at the Lincolnshire site. Significant association and no significant error were also found for SRF-Scots Pine and perennial grass. For the arable fields, the modelled CO2 correlated well just with the IRGA-derived Rh at one site ( r = 0.75). No bias in the model was found at any site, regardless of the measurement type used for the model evaluation. Across all land uses, fluxes of CH4 and N2O were shown to represent a small proportion of the total GHG balance; these fluxes have been modelled adequately on a monthly time-step. This study provides confidence in using ECOSSE for predicting the impacts of future land use on GHG balance, at site level as well as at national level. [ABSTRACT FROM AUTHOR]

Burkholderia pseudomallei is a soil-dwelling organism present throughout the tropics. It is the causative agent of melioidosis, a disease that is believed to kill 89,000 people per year. It is naturally resistant to many antibiotics, requiring at least two weeks of intravenous treatment with ceftazidime, imipenem or meropenem followed by 6 months of orally delivered co-trimoxazole. This places a large treatment burden on the predominantly middle-income nations where the majority of disease occurs. We have established a high-throughput assay for compounds that could be used as a co-therapy to potentiate the effect of ceftazidime, using the related non-pathogenic bacterium Burkholderia thailandensis as a surrogate. Optimization of the assay gave a Z' factor of 0.68. We screened a library of 61,250 compounds and identified 29 compounds with a pIC50 (-log10(IC50)) greater than five. Detailed investigation allowed us to down select to six "best in class" compounds, which included the licensed drug chloroxine. Co-treatment of B. thailandensis with ceftazidime and chloroxine reduced culturable cell numbers by two orders of magnitude over 48 hours, compared to treatment with ceftazidime alone. Hit expansion around chloroxine was performed using commercially available compounds. Minor modifications to the structure abolished activity, suggesting that chloroxine likely acts against a specific target. Finally, an initial study demonstrates the utility of chloroxine to act as a co-therapy to potentiate the effect of ceftazidime against B. pseudomallei. This approach successfully identified potential co-therapies for a recalcitrant Gram-negative bacterial species. Our assay could be used more widely to aid in chemotherapy to treat infections caused by these bacteria. [ABSTRACT FROM AUTHOR]

Highlights: [•] The utility of nasally delivered LL-37 as a post-exposure therapy for tularaemia in mice was examined. [•] Significant reduction in bacterial growth was seen in LVS infected macrophages treated with LL-37. [•] LL-37 stimulated increased neutrophil and pro-inflammatory chemokine and cytokine levels in the lung. [•] 3 doses of LL-37 significantly extended mean time to death of mice infected with F. tularensis LVS. [Copyright &y& Elsevier]

Burkholderia pseudomallei is the causative agent of the tropical disease melioidosis. Its genome encodes an arsenal of virulence factors that allow it, when required, to switch from a soil dwelling bacterium to a deadly intracellular pathogen. With a high intrinsic resistance to antibiotics and the ability to overcome challenges from the host immune system, there is an increasing requirement for new antibiotics and a greater understanding into the molecular mechanisms of B. pseudomallei virulence and dormancy. The peptidoglycan remodeling enzymes, lytic transglycosylases (Ltgs) are potential targets for such new antibiotics. Ltgs cleave the glycosidic bonds within bacterial peptidoglycan allowing for the insertion of peptidoglycan precursors during cell growth and division, and cell membrane spanning structures such as flagella and secretion systems. Using bioinformatic analysis we have identified 8 putative Ltgs in B. pseudomallei K96243. We aimed to investigate one of these Ltgs, LtgG (BPSL3046) through the generation of deletion mutants and biochemical analysis. We have shown that LtgG is a key contributor to cellular morphology, division, motility and virulence in BALB/c mice. We have determined the crystal structure of LtgG and have identified various amino acids likely to be important in peptidoglycan binding and catalytic activity. Recombinant protein assays and complementation studies using LtgG containing a site directed mutation in aspartate 343, confirmed the essentiality of this amino acid in the function of LtgG. [ABSTRACT FROM AUTHOR]