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Approximately 5% of pigs slaughtered in the UK have been tail-bitten, leading to welfare and production issues. Tail biting is sporadic and not all pigs tail bite. The aim of this study was to identify factors that are common in pigs that perform tail-biting behaviour, and that might be used in a predictive way to identify such animals.

The behaviour of 159 pigs was observed in the post-weaning period. Pigs were weaned at 4 weeks of age. In the week prior to weaning and at 6 weeks of age each pig was individually tested in a tail chew test (tail chew test 1 and 2, respectively). The tail chew test involved recording the pig's behaviour directed towards two ropes, one of which had been soaked in saline solution and the other not. The production performance of the pigs was recorded from birth to 7 weeks of age. Time spent performing tail-biting behaviour correlated positively with time in contact with the rope in tail chew test 2 (r = 0.224, P 1.5% tail biting 8.96 kg, = 1.5% tail biting 15-75 kg, = or = 1.5% tail biting 260 g/day, = 1.5% tail biting 343 g/day, 0.05).

The results suggest that pigs that tail bite have some nutritional deficiency that results in performance of foraging behaviour that is expressed in intensive housing as ear/tail biting.

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Introduction: Cyclooxygenase (COX)-2 influences cardiovascular disease and serum concentration of high-sensitivity C-reactive protein (hsCRP). The study purpose was to determine the influence of single nucleotide polymorphisms (SNPs) of the COX-2 gene on abdominal aortic aneurysm (AAA) development and serum hsCRP concentrations. Patients and Methods: Patients with AAA and disease-free controls were recruited. High-sensitivity C-reactive protein was measured by an enzyme-linked immunosorbent assay (ELISA) test. The distributions of COX-2 SNPs were investigated (rs20417 and rs4648307). The influence of the COX-2 SNPs on the hsCRP serum concentration was assessed.Results: A total of 230 patients with AAA and 279 controls were included. No difference was found in the genotype distribution of the COX-2 SNPs rs20417 (P = .26) and rs4648307 (P = .90). They did not influence the hsCRP concentration (P = .24 and P = .61, respectively). Haplotype analysis of COX-2 SNPs revealed no difference. Conclusion: These COX-2 SNPs do not play any role in AAA development and do not influence serum hsCRP. These results differentiate AAA development from atherosclerotic diseases.