Notes

Notes by Frank J. Lanigan, Rex E. Weaver, David Gelber, John A. O\u27Leary, John De Mots, and James E. Bales

An Analysis of the Cost of the Abatement of Ammonia Emissions in Irish Agriculture to 2030

peer-reviewedThis analysis quantifies the potential to abate national ammonia (NH3) emissions up to 2030. This report is an updated marginal abatement cost curve (MACC) analysis where Teagasc has quantified the abatement potential of a range of ammonia mitigation measures, as well as their associated costs/benefits (see Lanigan et al. 2015 for previous analysis). The objective of this analysis is to quantify the extent and costs associated with meeting future ammonia emission targets that were negotiated as part of the amended Clean Air Policy Package. The requirement to reduce ammonia emissions is urgent, both in terms of compliance with the National Emissions Ceilings Directive (NECD), and as a principal loss pathway for agricultural nitrogen (N). Improvement of N efficiency is a key focus for improving farm efficiency and sustainability as well as reducing the ammonia, nitrate and greenhouse gas (GHG) footprint of agriculture. This is particularly relevant in the context of the national strategies on the development of the agri-food sector: Food Wise 2025, Ag-food strategy 2030 and Ag-Climatise (currently under development) and the newly unveiled EU Farm to Fork Strategy, which is a part of the European Green Deal. Under the baseline scenario (S1), agricultural ammonia emissions are projected to increase by 9% (without any mitigation) by 2030 relative to 2005 levels. While these increases are small in comparison to the targeted increase in agricultural output, they will provide a major challenge to meeting emissions targets, particularly as agriculture comprises over 99% of national emissions. The analysis presented in this report seeks to quantify the ammonia mitigation potential under likely uptake pathways. This is not an exhaustive analysis of all mitigation measures, but represents an assessment of best available techniques, based on scientific, peer-reviewed research carried out by Teagasc and associated national and international research partners. Indeed, any future changes in the sector or in the national emission inventory calculations will require further analysis of the applicability of ammonia mitigation techniques, particularly in terms of housing and storage but also in the context of other reactive N1 emissions. It should also be noted that some mitigation measures, particularly those related to nitrogen application to soils, could result in either higher greenhouse gas emissions or higher nitrate leaching. Compared to a future where no mitigation measures are deployed to address emissions, by 2030 the average technical abatement2 potential was estimated to be approximately 15.26 kt NH3 at a net cost of €10.86 million per annum. However, it should be noted that the net cost (€10.86 million) is comprised of 6 measures that are cost negative (-€22.21 million) and 7 measures that are cost positive (€33.07) and that some of the cost negative measures are predicated on efficiency gains driven by best management practice adoption (e.g. liming and clover measures with associate chemical N reductions). Amongst the thirteen mitigation measures selected for this analysis, 80% of the mitigation potential can be achieved by the full implementation of the mitigation pathways for protected urea and low emission slurry spreading (LESS) techniques for bovines. It should be stressed that this is an assessment of the maximum abatement potential and realising this level of abatement in practice will be extremely challenging. Any increase in agricultural activity beyond the baseline scenario will increase absolute emissions. The level of mitigation achievable is based on the draft AgClimatise measures any delay or reduction in the uptake of these measures will reduce the mitigation achieved. It must also be ensured that all mitigation measures should, where possible, be synergistic with reductions in greenhouse gas emissions and N loss to water

Mena deficiency delays tumor progression and decreases metastasis in polyoma middle-T transgenic mouse mammary tumors

Introduction The actin binding protein Mammalian enabled (Mena), has been implicated in the metastatic progression of solid tumors in humans. Mena expression level in primary tumors is correlated with metastasis in breast, cervical, colorectal and pancreatic cancers. Cells expressing high Mena levels are part of the tumor microenvironment for metastasis (TMEM), an anatomical structure that is predictive for risk of breast cancer metastasis. Previously we have shown that forced expression of Mena adenocarcinoma cells enhances invasion and metastasis in xenograft mice. Whether Mena is required for tumor progression is still unknown. Here we report the effects of Mena deficiency on tumor progression, metastasis and on normal mammary gland development. Methods To investigate the role of Mena in tumor progression and metastasis, Mena deficient mice were intercrossed with mice carrying a transgene expressing the polyoma middle T oncoprotein, driven by the mouse mammary tumor virus. The progeny were investigated for the effects of Mena deficiency on tumor progression via staging of primary mammary tumors and by evaluation of morbidity. Stages of metastatic progression were investigated using an in vivo invasion assay, intravital multiphoton microscopy, circulating tumor cell burden, and lung metastases. Mammary gland development was studied in whole mount mammary glands of wild type and Mena deficient mice. Results Mena deficiency decreased morbidity and metastatic dissemination. Loss of Mena increased mammary tumor latency but had no affect on mammary tumor burden or histologic progression to carcinoma. Elimination of Mena also significantly decreased epidermal growth factor (EGF) induced in vivo invasion, in vivo motility, intravasation and metastasis. Non-tumor bearing mice deficient for Mena also showed defects in mammary gland terminal end bud formation and branching. Conclusions Deficiency of Mena decreases metastasis by slowing tumor progression and reducing tumor cell invasion and intravasation. Mena deficiency during development causes defects in invasive processes involved in mammary gland development. These findings suggest that functional intervention targeting Mena in breast cancer patients may provide a valuable treatment option to delay tumor progression and decrease invasion and metastatic spread leading to an improved prognostic outcome.National Cancer Institute (U.S.). Integrative Cancer Biology Program (grant U54 CA112967)Virginia and D.K. Ludwig Fund for Cancer Researc