Effect of Application of Farmyard Manure to Ley on Forage Yield and Quality of Grass Silage

A two-year field trial was performed on ley near Uppsala, Sweden, with the following treatments (3 plots/treatment): A, no manure or fertiliser; B, manure applied in Oct.; C, manure applied in Oct. followed by rolling plots in May; D, manure applied in May; E, mineral fertiliser only. Apart from cattle manure, plots allocated to treatments B, C and D received the same amount of mineral nutrients as treatment E. The objective of this experiment was to get an indication of how different times of manure application (before or after the growth period) affected forage yields and the quality of the resulting silage. Annual forage yields (2 cuts/year) did not differ significantly in either year among treatments that received manure. Only the unfertilised control treatment (A) had a significantly lower yield. No differences were found between treatments that received only mineral fertilisers (E) or mineral fertilisers and manure (B, C and D). The 1998 ensiling experiment resulted in a very low overall silage quality, indicated by excessive formation of ammonia and very high counts of Clostridium spores (\u3e 106 cfu/g silage). In 1999, the best silage, with the lowest counts of Clostridium spores (\u3c 50 cfu/g), was produced from plots, which received manure in Oct. and were rolled in May (C). The same treatment without rolling in May (B) resulted in silage with a significantly higher pH, more butyric acid, and more Clostridium spores (\u3e 105 cfu/g). Other silage from manured plots, particularly that made from unchopped forage, also had high counts of Clostridium spores

Caspase-8 inhibition represses initial human monocyte activation in septic shock model

In septic patients, the onset of septic shock occurs due to the over-activation of monocytes. We tested the therapeutic potential of directly targeting innate immune cell activation to limit the cytokine storm and downstream phases. We initially investigated whether caspase-8 could be an appropriate target given it has recently been shown to be involved in microglial activation. We found that LPS caused a mild increase in caspase-8 activity and that the caspase-8 inhibitor IETD-fmk partially decreased monocyte activation. Furthermore, caspase-8 inhibition induced necroptotic cell death of activated monocytes. Despite inducing necroptosis, caspase-8 inhibition reduced LPS-induced expression and release of IL-1β and IL-10. Thus, blocking monocyte activation has positive effects on both the pro and anti-inflammatory phases of septic shock. We also found that in primary mouse monocytes, caspase-8 inhibition did not reduce LPS-induced activation or induce necroptosis. On the other hand, broad caspase inhibitors, which have already been shown to improve survival in mouse models of sepsis, achieved both. Thus, given that monocyte activation can be regulated in humans via the inhibition of a single caspase, we propose that the therapeutic use of caspase-8 inhibitors could represent a more selective alternative that blocks both phases of septic shock at the source.Unión Europea, Ministerio de Economía y Competitividad SAF2012-39029Unión Europea, Ministerio de Economía y Competitividad SAF2015-64171REspaña,Junta de Andalucía P10-CTS-649

Toward catchment hydro-biogeochemical theories

Headwater catchments are the fundamental units that connect the land to the ocean. Hydrological flow and biogeochemical processes are intricately coupled, yet their respective sciences have progressed without much integration. Reaction kinetic theories that prescribe rate dependence on environmental variables (e.g., temperature and water content) have advanced substantially, mostly in well-mixed reactors, columns, and warming experiments without considering the characteristics of hydrological flow at the catchment scale. These theories have shown significant divergence from observations in natural systems. On the other hand, hydrological theories, including transit time theory, have progressed substantially yet have not been incorporated into understanding reactions at the catchment scale. Here we advocate for the development of integrated hydro-biogeochemical theories across gradients of climate, vegetation, and geology conditions. The lack of such theories presents barriers for understanding mechanisms and forecasting the future of the Critical Zone under human- and climate-induced perturbations. Although integration has started and co-located measurements are well under way, tremendous challenges remain. In particular, even in this era of "big data," we are still limited by data and will need to (1) intensify measurements beyond river channels and characterize the vertical connectivity and broadly the shallow and deep subsurface; (2) expand to older water dating beyond the time scales reflected in stable water isotopes; (3) combine the use of reactive solutes, nonreactive tracers, and isotopes; and (4) augment measurements in environments that are undergoing rapid changes. To develop integrated theories, it is essential to (1) engage models at all stages to develop model-informed data collection strategies and to maximize data usage; (2) adopt a "simple but not simplistic," or fit-for-purpose approach to include essential processes in process-based models; (3) blend the use of process-based and data-driven models in the framework of "theory-guided data science." Within the framework of hypothesis testing, model-data fusion can advance integrated theories that mechanistically link catchments' internal structures and external drivers to their functioning. It can not only advance the field of hydro-biogeochemistry, but also enable hind- and fore-casting and serve the society at large. Broadly, future education will need to cultivate thinkers at the intersections of traditional disciplines with hollistic approaches for understanding interacting processes in complex earth systems.This article is categorized under:Science of Water > Method

Genetic Control of the Variable Innate Immune Response to Asymptomatic Bacteriuria

The severity of urinary tract infection (UTI) reflects the quality and magnitude of the host response. While strong local and systemic innate immune activation occurs in patients with acute pyelonephritis, the response to asymptomatic bacteriuria (ABU) is low. The immune response repertoire in ABU has not been characterized, due to the inherent problem to distinguish bacterial differences from host-determined variation. In this study, we investigated the host response to ABU and genetic variants affecting innate immune signaling and UTI susceptibility. Patients were subjected to therapeutic urinary tract inoculation with E. coli 83972 to ensure that they were exposed to the same E. coli strain. The innate immune response repertoire was characterized in urine samples, collected from each patient before and after inoculation with bacteria or PBS, if during the placebo arm of the study. Long-term E. coli 83972 ABU was established in 23 participants, who were followed for up to twelve months and the innate immune response was quantified in 233 urine samples. Neutrophil numbers increased in all but two patients and in an extended urine cytokine/chemokine analysis (31 proteins), the chemoattractants IL-8 and GRO-α, RANTES, Eotaxin-1 and MCP-1, the T cell chemoattractant and antibacterial peptide IP-10, inflammatory regulators IL-1-α and sIL-1RA and the T lymphocyte/dendritic cell product sIL-2Rα were detected and variably increased, compared to sterile samples. IL-6, which is associated with symptomatic UTI, remained low and numerous specific immune mediators were not detected. The patients were also genotyped for UTI-associated IRF3 and TLR4 promoter polymorphisms. Patients with ABU associated TLR4 polymorphisms had low neutrophil numbers, IL-6, IP-10, MCP-1 and sIL-2Rα concentrations. Patients with the ABU-associated IRF3 genotype had lower neutrophils, IL-6 and MCP-1 responses than the remaining group. The results suggest that the host-specific, low immune response to ABU mainly includes innate immune mediators and that host genetics directly influence the magnitude of this response