Effluent quality and ammonia emissions from out-wintering pads in England, Wales and Ireland

Out-wintering pads offer a reduced cost system for wintering cattle, minimising damage to pasture, providing animal welfare and production benefits, and generate, potentially, a more manageable effluent and lower ammonia emissions. The objectives of the present study were (i) to contribute to improved understanding of the factors impacting on effluent quality, ammonia emissions and animal welfare via observations on four farm-based out-wintering pads (ComOWPs) in England, Wales and Ireland and more detailed studies undertaken on four experimental OWPs (ExpOWPs) constructed at Rothamsted Research North Wyke, Devon, England and (ii) to corroborate the effluent quality data from both the ComOWPs and the ExpOWPs, with findings in the literature. Woodchip size, feeding management and area allowance were the treatment factors applied on the ExpOWPs. These three factors were randomised across the four ExpOWPs, over four 6–7 week periods. Effluent quality from the ExpOWPs was sampled frequently in a flow proportional way and analysed for total N (TN); total P (TP); total solids (TS); ammonium-N (NH4+-N); nitrate-N (NO3−-N). Beef cattle were periodically weighed for determination of live weight gain (LWG). An approximate nitrogen balance was calculated as a means of understanding its partitioning and fate during and after the ExpOWPs use. Effluent quality from the ComOWPs was sampled frequently, also in a flow-proportional way, and analysed for TN, TP, TS, NH4+-N, NO3−-N, total K and COD. Effluent quality data from the ExpOWPs showed no significant differences (P > 0.05) between treatments, with average concentrations of 1095 mg l−1, and 806 mg l−1, for TN and NH4+-N, respectively. Average effluent concentrations from the ComOWPs were 356 mg l−1 TN and 124 mg l−1 NH4+-N. Ammonia emissions from the ExpOWPs showed no significant differences (P > 0.05) between the treatments, with average mean emission rates of 2.5 g m−2 d−1 NH3-N, respectively. A positive correlation was established between NH3-N emission rate and wind speed. Emission rates from the ComOWPs ranged from 0.7 to 1.6 g m−2 d−1 NH3-N. Average daily LWG on the ExpOWPs was 1.33 kg steer−1 d−1. The effluent from both the ComOWPs and ExpOWPs were more similar with dirty water and of consistently lower strength than beef cattle slurry, as supported by findings in the literature, and therefore, it is suggested to be subject to the regulatory requirements of dirty water rather than slurry.

In vivo selection for metastasis promoting genes in the mouse

Here, we report the identification of a metastasis promoting factor by a forward genetic screen in mice. A retroviral cDNA library was introduced into the nonmetastatic cancer cell line 168FARN, which was then orthotopically transplanted into mouse mammary fat pads, followed by selection for cells that metastasize to the lung. The genes encoding the disulfide isomerase ERp5 and beta-catenin were found to promote breast cancer invasion and metastasis. Disulfide isomerases (thiol isomerases), which catalyze disulfide bond formation, reduction, and isomerization, have not previously been implicated in cancer cell signaling and tumor metastasis. Overexpression of ERp5 promotes both in vitro migration and invasion and in vivo metastasis of breast cancer cells. These effects were shown to involve activation of ErbB2 and phosphoinositicle 3-kinase (PI3K) pathways through dimerization of ErbB2. Activation of ErbB2 and PI3K subsequently stimulates RhoA and beta-catenin, which mediate the migration and invasion of tumor cells. Inhibition of ErbB2 and PI3K reverses the phenotypes induced by ERp5. Finally, ERp5 was shown to be up-regulated in human surgical samples of invasive breast cancers. These data identify a link between disulfide isomerases and tumor development, and provide a mechanism that modulates ErbB2 and PI3K signaling in the promotion of cancer progression.

Pretranslational regulation of the expression of the lipoprotein lipase (EC 3.1, l.34) gene by dietary fatty acids in the rat

Although there have been a number of studies of effects of diet and hormones on lipoprotein lipase (EC 3.1.1.34; LPL) activity and levels of LPL mRNA (Raynolds et al. 1990), there have been no studies which have investigated effects of different dietary fatty acids on LPL gene expression. In the present study male Wistar Albino rats were pair-fed diets containing 50 g fat/kg of different fatty acid composition for 2 weeks. The diets fed were (1) a mixed oil (450 g saturated fatty acids, 420 g monounsaturated fatty acids, 130 g polyunsaturated fatty acids/kg; n 8), (2) maize oil (n 8), or (3) fish oil (n 8). Animals were killed, RNA was extracted from liver and perirenal and epididymal fat pads, and analysed by ‘Northern methodology’. Samples were hybridized to a human cDNA probe for LPL (Gotoda et al. 1989). Two transcripts were identified in epididymai and perirenal adipose tissue which were approximately 3·7 and 1·7 kb in size. The results suggested that (1) fish oil-fed animals had significantly greater production of LPL mRNA in epididymai adipose tissue compared with maize oil-fed animals (P < 0·05), (2) maize oil-fed animals had significantly greater production of LPL mRNA in perirenal fat compared with the other dietary groups (P < 0·05), (3) expression in the liver was not significant. Rats fed on a fish oil diet had significantly reduced plasma triacylglycerol concentrations compared with the mixed-oil group (P < 0·05), but there were no significant differences in plasma cholesterol. The differences in LPL could not be explained directly by the changes in plasma immunoreactive-insulin and glucose-dependent insulinotrophic polypeptide levels in the three groups.

FTO influences adipogenesis by regulating mitotic clonal expansion

The fat mass and obesity-associated (FTO) gene plays a pivotal role in regulating body weight and fat mass; however, the underlying mechanisms are poorly understood. Here we show that primary adipocytes and mouse embryonic fibroblasts (MEFs) derived from FTO overexpression (FTO-4) mice exhibit increased potential for adipogenic differentiation, while MEFs derived from FTO knockout (FTO-KO) mice show reduced adipogenesis. As predicted from these findings, fat pads from FTO-4 mice fed a high-fat diet show more numerous adipocytes. FTO influences adipogenesis by regulating events early in adipogenesis, during the process of mitotic clonal expansion. The effect of FTO on adipogenesis appears to be mediated via enhanced expression of the pro-adipogenic short isoform of RUNX1T1, which enhanced adipocyte proliferation, and is increased in FTO-4 MEFs and reduced in FTO-KO MEFs. Our findings provide novel mechanistic insight into how upregulation of FTO leads to obesity.