Zeranol, a semi-synthetic oestrogenic growth promoter, was banned in the EU in 1988. The ability of Member States to police the ban on zeranol has been hampered by suggestions from New Zealand and from this laboratory that zeranol may be formed by the in vivo metabolism of naturally occurring Fusarium spp. toxins. The present study demonstrates that zeranol is formed from alpha-zearalenol and zearalenone in vivo and is detected in bovine bile following the oral administration of these compounds. However, it is not detected following administration of beta-zearalenol. These data suggest that hydrogenation of alpha-zearalenol, probably in the rumen, is responsible for the appearance of zeranol. The present study shows that environmental contamination with Fusarium spp. toxins is widespread in Northern Ireland. Fusarium spp. toxins were present in 32% (n = 422) of all bovine bile samples tested for zeranol during 1995. Zeranol itself was confirmed in 6.6% (n = 28) of the samples. However, the mean alpha-zearalenol and beta-zearalenol concentrations in the bile of zeranol-positive animals were 12 and 9 times higher, respectively, than those in the zeranol-negative animals. The alpha-zearalenol concentration always exceeded the zeranol concentration by at least 5:1. This may, in the future, permit differentiation between zeranol abuse and natural contamination.

*Corresponding authors karl.richards@teagasc.ieHighlights  The N 2 O emission factor for CAN was substantially higher than the IPCC default and highly variable between sites and across years. Urea products decreased direct N 2 O emissions from CAN on average by 80%  Switching from CAN to urea products reduces both N 2 O emissions and fertiliser costs. 3 AbstractThe accelerating use of synthetic nitrogen (N) fertilisers, to meet the world's growing food demand, is the primary driver for increased atmospheric concentrations of nitrous oxide (N 2 O). The IPCC default emission factor (EF) for N 2 O from soils is 1% of the N applied, irrespective of its form. However, N 2 O emissions tend to be higher from nitrate-containing fertilisers e.g. calcium ammonium nitrate (CAN) compared to urea, particularly in regions, which have mild, wet climates and high organic matter soils. Urea can be an inefficient N source due to NH 3 volatilisation, but nitrogen stabilisers (urease and nitrification inhibitors) can improve its efficacy. This study evaluated the impact of switching fertiliser formulation from calcium ammonium nitrate (CAN) to urea-based products, as a potential mitigation strategy to reduce N 2 O emissions at six temperate grassland sites on the island of Ireland. The surface applied formulations included CAN, urea and urea with the urease inhibitor N-(nbutyl) thiophosphoric triamide (NBPT) and/or the nitrification inhibitor dicyandiamide (DCD). Results showed that N 2 O emissions were significantly affected by fertiliser formulation, soil type and climatic conditions. The direct N 2 O emission factor (EF) from CAN averaged 1.49% overall sites, but was highly variable, ranging from 0.58% to 3.81.Amending urea with NBPT, to reduce ammonia volatilisation, resulted in an average EF of 0.40% (ranging from 0.21 to 0.69%)-compared to an average EF of 0.25% for urea (ranging from 0.1 to 0.49%), with both fertilisers significantly lower and less variable than CAN.Cumulative N 2 O emissions from urea amended with both NBPT and DCD were not significantly different from background levels. Switching from CAN to stabilised urea formulations was found to be an effective strategy to reduce N 2 O emissions, particularly in wet, temperate grassland. 4Key words nitrous oxide mitigation; emission factor; calcium ammonium nitrate; stabilised urea; nitrification inhibitor Dicyandiamide (DCD); urease inhibitor N-(n-butyl) thiophosphoric triamide (NBPT).5

Gremlin1 has a distinct preference for which bone morphogenetic protein it binds to in kidney epithelial cells. Grem1–BMP-2 complexes are favoured over other BMPs, and this may play an important role in fibrotic kidney disease.

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Mycotoxins are toxic compounds mainly produced by fungi of the genera Aspergillus, Penicillium and Fusarium. They are present, often as mixtures, in many feed and food commodities including cereals, fruits and vegetables. Their ubiquitous presence represents a major challenge to the health and well being of humans and animals. Hundreds of compounds are listed as possible mycotoxins occurring in raw and processed materials destined for human food and animal feed. In this study, mycotoxins of major toxicological relevance to humans and target animal species were investigated in a range of crops of interest (and their derived products). Extensive Literature Searches (ELSs) were undertaken for data collection on: (i) ecology and interaction with host plants of mycotoxin producing fungi, mycotoxin production, recent developments in mitigation actions of mycotoxins in crop chains (maize, small grains, rice, sorghum, grapes, spices and nuts), (ii) analytical methods for native, modified and co-occurring mycotoxins (iii) toxicity, toxicokinetics, toxicodynamics and biomarkers relevant to humans and animals (poultry, suidae (pig, wild boar), bovidae (sheep, goat, cow, buffalo), rodents (rats, mice) and others (horses, dogs), (iv) modelling approaches and key reference values for exposure, hazard and risk modelling. Comprehensive databases were created using EFSA templates and were stored in the MYCHIF platform. A range of approaches were implemented to explore the modelling of external and internal exposure as well as dose-response of mycotoxins in chicken and pigs. In vitro toxicokinetic and in vivo toxicity databases were exploited, both for single compounds and mixtures. However, large data gaps were identified particularly with regards to absence of common statistical and study designs within the literature and constitute an obstacle for the harmonisation of internal exposure and dose-response modelling. Finally, risk characterisation was also performed for humans as well as for two animal species (i.e. pigs and chicken) using available tools for the modelling of internal dose and a component-based approach for selected mycotoxins mixtures.© European Food Safety Authority, 2020 MYCHIF www.efsa.europa.eu/publications 2 EFSA Supporting publication 2020: EN-1757