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Poultry litter is used as soil amendment or organic fertilizer. While poultry litter is enriched with organic matter suitable for land, the presence of pathogens such as Salmonella in poultry litter is a concern. To investigate the effect of gaseous ozone on pathogen reductions in poultry litter, this study conducted a series of experiments that involved understanding of Salmonella Typhimurium and Escherichia coli O157:H7 inactivation at various doses of Ozone (O3) in wet and dry poultry litter conditions. Previously, ozone treatment has been shown to disinfect the surface of foods and plant materials including fruits, juices, and wastewater, however, additional research are needed to better understand the impacts of ozone on treatment of soil amendments. Sanitizing methods capable of eliminating pathogens of soil amendments are crucial to mitigate disease outbreaks related with litter/manure-based fertilizers. In this study, a bench scale continuous ozone treatment system was designed to produce O3 gas, with a range O3 concentrations (7.15–132.46 mg·L−1), monitor ozone concentrations continuously, and control the ozone exposure time (15 to 90 mins) to understand the effectiveness of O3 in eliminating S. Typhimurium and E. coli O157:H7 in poultry litter. Results showed that 7.15 mg·L-1 did not reduce the counts of S. Typhimurium until exposure to O3 for 90 min. The O3 concentrations of 43.26 ~ 132.46 mg·L-1 exposure reduced the bacterial counts. Furthermore, the moisture content of poultry litter was found to be an influencing factor for pathogen reduction. The pathogen reduction rates were reduced when the moisture content was increased. At higher moisture content, high concentrations of O3 (132.46 mg·L-1) were needed for pathogen reductions. The moisture content of 30% or lower was found to be more effective for controlling pathogen levels in poultry litter. Our study demonstrates that gaseous O3 treatment could be used as an additional decontamination technique to ensure the certain degree of microbiological safety of poultry litter based soil amendment.

Summary The amyloid-like aggregation propensity present in most globular proteins is generally considered to be a secondary side effect resulting from the requirements of protein stability. Here, we demonstrate, however, that mutations in the globular and amyloid state are thermodynamically correlated rather than simply associated. In addition, we show that the standard genetic code couples this structural correlation into a tight evolutionary relationship. We illustrate the extent of this evolutionary entanglement of amyloid propensity and globular protein stability. Suppressing a 600-Ma-conserved amyloidogenic segment in the p53 core domain fold is structurally feasible but requires 7-bp substitutions to concomitantly introduce two aggregation-suppressing and three stabilizing amino acid mutations. We speculate that, rather than being a corollary of protein evolution, it is equally plausible that positive selection for amyloid structure could have been a driver for the emergence of globular protein structure., Graphical Abstract, Highlights • Mutations in the globular and amyloid state are thermodynamically correlated • The genetic code tightens this relationship between the amyloid and native state • Strongly amyloidogenic sequences in globular proteins are deeply conserved • Positive selection of amyloid propensity will favor globular protein stability, Langenberg et al. show that amyloid propensity favors protein stability. This results from the energetic correlation of mutation in the native and amyloid state. The genetic code tightens this relationship so that stable amyloidogenic sequences are deeply conserved. Positive selection of amyloidogenic sequences could therefore have favored the evolution of globular structure.

Recently a number of aggregation disease polypeptides have been shown to spread from cell to cell thereby displaying prionoid behaviour. Studying aggregate internalisation however is often hampered by the complex kinetics of the aggregation process resulting in the concomitant uptake of aggregates of different sizes by competing mechanisms, which makes it difficult to isolate pathway-specific responses to aggregates. We designed synthetic aggregating peptides bearing different aggregation propensities with the aim of producing modes of uptake that are sufficiently distinct to differentially analyse the cellular response to internalization. We found that small acidic aggregates (≤500 nm diameter) were taken up by non-specific endocytosis as part of the fluid phase and travelled through the endosomal compartment to lysosomes. By contrast, basic bigger aggregates (>1 μm) were taken up through a mechanism dependent of cytoskeletal reorganization and membrane remodelling with the morphological hallmarks of phagocytosis. Importantly, the properties of these aggregates not only determined the mechanism of internalization but also the involvement of the proteostatic machinery (the assembly of interconnected networks that control the biogenesis, folding, trafficking and degradation of proteins) in the process: while the internalization of small acidic aggregates is HSF1 independent, the uptake of larger basic aggregates was HSF1 dependent requiring Hsp70. Our results show that the biophysical properties of aggregates determine both their mechanism of internalisation and proteostatic response. It remains to be seen whether these differences in cellular response contribute to the particular role of specific aggregated proteins in disease. ispartof: Journal of Biological Chemistry vol:290 issue:1 pages:242-58 ispartof: location:United States status: published

Patients with atrioventricular (AV) block can develop left ventricular (LV) dysfunction with long-term right ventricular pacing (RVP). We investigated the role of RVP-induced LV dyssynchrony in this adverse remodeling.Nineteen patients with normal LV function undergoing pacemaker implantation for AV block were included. Right ventricular pacing leads were positioned at the apex. Two-dimensional and tissue Doppler echocardiography was performed before and immediately after implantation and at the end of follow-up. The maximal delay between peak velocities of opposing basal LV walls was measured using tissue Doppler echocardiography, as an index of LV dyssynchrony. With the initiation of RVP, LV dyssynchrony increased in some patients and decreased in others, as compared with intrinsic rhythm. The RVP-induced change in dyssynchrony inversely correlated with baseline dyssynchrony (r = -0.686, P = .010). After 28 ± 3.6 months, LV end-systolic volume (ESV) increased, and ejection fraction decreased (from 34 ± 12 to 40 ± 20 mL, P = .010 and from 65% ± 6% to 56% ± 11%, P.001, respectively). The change in LV ESV was greater in patients with 60% or greater cumulative RVP (9.9 vs 0.08 mL, P = .027). Within this frequently paced group, the RVP-induced change in dyssynchrony correlated with the increase in LV ESV (r = 0.727, P = .026). Patients who had a 15% or greater increase in LV ESV had greater RVP-induced change in dyssynchrony (28.4 vs -7.8 milliseconds, P = .037).Some patients with AV block experience an increase in LV dyssynchrony with RVP. Increased LV dyssynchrony predicts adverse LV remodeling during long-term follow-up.