Access to bedding and outdoor runs for growing-finishing pigs: is it possible to improve welfare without increasing environmental impacts?

Providing bedding or access to an outdoor run are husbandry aspects intended to improve pig welfare, which is currently financially supported through animal welfare schemes in several European countries. However, they may significantly affect the environment through changes in feed efficiency and manure management. Therefore, the aim of this paper was to compare farms differing in animal welfare relevant husbandry aspects regarding (1) the welfare of growing-finishing pigs and (2) environmental impact categories such as global warming (GW), acidification (AC), and freshwater (FE) and marine eutrophication (ME), by employing an attributional Life Cycle Assessment. We collected data on 50 farms with growing-finishing pigs in seven European countries. Ten animal-based welfare indicators were aggregated into three pig welfare indices using principal component analysis. Cluster analysis of farms based on husbandry aspects resulted in three clusters: NOBED (31 farms without bedding or outdoor run), BED (11 farms with bedding only) and BEDOUT (eight farms with bedding and outdoor run). Pigs on farms with bedding (BED and BEDOUT) manipulated enrichment more often (P < 0.001), pen fixtures less frequently (P = 0.003) and showed fewer oral stereotypies (P < 0.001) than pigs on NOBED farms. There were fewer pigs with a short(er) tail on farms with than without bedding (P < 0.001). Acidification of BEDOUT and BED farms was significantly higher (compared to NOBED farms P = 0.002) due to higher ammonia emissions related to farmyard manure. Also, BEDOUT farms had higher ME than NOBED farms (P = 0.035). There were no significant differences regarding GW and FE between husbandry clusters, due to the large variability within clusters regarding feed composition and conversion. Therefore, both husbandry aspects associated with improved animal welfare have a significant influence on some environmental impacts, such as acidification and marine eutrophication. Nevertheless, the large variation within clusters suggests that trade-offs may be minimised through e.g. AC and ME.

Stem and endothelial progenitor cells in erection biology.

Erectile dysfunction (ED) is defined as the consistent inability to obtain or maintain an erection for satisfactory sexual relations. The past 20 years of basic science research on erection physiology has been devoted to investigating the pathogenesis of ED and has led to the conclusion that ED is predominately a disease of vascular origin with dramatic changes occurring in the endothelium. Research has also led to an understanding of the biochemical factors and intracellular mechanisms responsible for corporal smooth muscle contraction and relaxation and the influence of endothelium-derived relaxing factors. The development of methods to deliver both stem and endothelial cells to the penis has kindled a keen interest in treating ED with gene- and cell-based therapies. In this paper, erection physiology and stem cell biology is reviewed, and the potential application of novel cell-based therapies for the treatment of ED is discussed.

High affinity binding of heparin by necrotic tumour cells neutralises anticoagulant activity--implications for cancer related thromboembolism and heparin therapy.

We have observed a striking neutralisation of the anticoagulant activity of unfractionated heparin in the presence of a pancreatic carcinoma cell line (MIA PaCa-2) due to binding of around 9 microg of heparin per 10(7) cells (apparent Kd, 30 nM). The loss of anticoagulant activity was less marked in the presence of low molecular weight forms of heparin. Binding to the cell blocked acceleration of the thrombin:antithrombin interaction by heparin. Neutralisation of heparin activity was also shown to occur in the presence of a number of other tumour cell lines. FACS analysis demonstrated that live cells did not bind heparin and high affinity binding only occurred to dead MIA PaCa-2 cells. Heparin binding proteins accumulating in cell medium were identified as histone and ribosomal proteins that will become exposed during necrosis. The release of these proteins from cells within the necrotic core of a tumour or from cells killed during chemotherapy may abrogate the heparan sulphate/antithrombin system and possibly contribute to the idiopathic thromboembolism often associated with cancer (Trousseau's syndrome). The findings also suggest a reason for the reported advantage of LMWH over UFH in treating venous thromboembolism in cancer patients and in improving patient survival.