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Bloom, P. (2004). Behavior. Can a dog learn a word? Science, 304(5677), 1605–1606.
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Houpt, K. A., Perry, P. J., Hintz, H. F., & Houpt, T. R. (1988). Effect of meal frequency on fluid balance and behavior of ponies. Physiol. Behav., 42(5), 401–407.
Abstract: Twelve ponies were fed their total daily ration either as one large meal or divided into six small meals. Pre- and post-feeding behavior was recorded six times a day. Blood samples were taken for 30 min before and two hr after the meal. Plasma protein increased from 7.0 to a peak of 7.3 g/dl with small meals and from 7.3 to 8.1 g/dl with large meals, and returned to pre-feeding levels by 90 min post-feeding. Hematocrit rose from 33.3 to 34.1% with small meals and from 33.0 to 36.0% with large meals. These rapid and short-lived increases indicate a decrease in plasma volume. Plasma osmolality rose with feeding from 283 to 285 mosmoles/kg with small meals and from 281 to 288 mosmoles/kg with large meals. Water availability had no significant effect on blood changes. Digestibility and rate of passage were measured with chromic oxide, but there were no differences. Vocalizing (neighing) and walking occurred more often before than after feeding, while eating bedding and engaging in other oral behaviors were more frequent after feeding.
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Nicol, C. J., Brown, S. N., Glen, E., Pope, S. J., Short, F. J., Warriss, P. D., et al. (2006). Effects of stocking density, flock size and management on the welfare of laying hens in single-tier aviaries. Br Poult Sci, 47(2), 135–146.
Abstract: Management practices, stocking rate and flock size may affect laying hen welfare but there have been few replicated studies in commercial non-cage systems that investigate this. This study used a broad range of physical and physiological indicators to assess the welfare of hens in 36 commercial flocks. Six laying period treatments were examined with each treatment replicated 6 times. It was not possible to randomly allocate treatments to houses, so treatment and house were largely confounded. Three stocking rates were compared: 7 birds/m(2) (n = 2450), 9 birds/m(2) (n = 3150) and 12 birds/m(2) in either small (n = 2450) or large (n = 4200) flocks. In addition, at 12 birds/m(2), in both small and large flocks, birds were subjected to either standard (SM) or modified (MM) management. MM flocks had nipple drinkers and no nest-box lights. Bone strength, fracture incidence, heterophil:lymphocyte (H:L) ratio, live weight, organ weights, serum creatine, serum osmolality, muscle pH and faecal corticosterone were measured on samples of birds at the end of the rearing period and at the end of lay. During the laying period, mortality, production and integument condition were recorded at regular intervals. Birds housed at 9 birds/m(2) had higher mortality than birds housed at 12 birds/m(2) by the end of lay, but not higher than birds housed at 7 birds/m(2). Birds housed at 7 and 9 birds/m(2) had lower percent liver weight, and worse plumage condition than most of the 12 bird/m(2) treatments. Modified management tended to improve plumage condition. There were no clear effects of flock size on the welfare indicators recorded. At the end of the rearing period fracture incidence was almost negligible and H:L ratio was within a normal range. By the end of lay fracture incidence was 60% and H:L ratio was high, with no treatment effect for either measure. This, together with information on faecal corticosterone, feather loss and mortality, suggests that the welfare of birds in all treatments was relatively poor by the end of lay.
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Haslam, S. M., Brown, S. N., Wilkins, L. J., Kestin, S. C., Warriss, P. D., & Nicol, C. J. (2006). Preliminary study to examine the utility of using foot burn or hock burn to assess aspects of housing conditions for broiler chicken. Br Poult Sci, 47(1), 13–18.
Abstract: 1. Eleven broiler chicken farms, representing 4 production system types, were visited during the last 5 d of the flock cycle: bird and flock details were recorded. Litter friability was assessed at 9 sites within the house, atmospheric ammonia was measured at three sites and bird cleanliness was assessed on a numerical rating scale. 2. For these flocks, hock burn, foot burn and breast burn were measured at the processing plant by standardised assessors. 3. Significant correlations were identified between the percentage of birds with foot burn and average litter score, average house ammonia concentrations and feather score. 4. No correlation was found between the percentage of birds with hock burn or breast burn and average litter scores, average ammonia concentrations or feather score. 5. No correlation was found between stocking density and foot burn, hock burn or breast burn.6. If confirmed, these findings may have implications for the draft EU Broiler Directive, for which it is proposed that permitted stocking density on farm may be determined by the incidence and severity of contact dermatitis measured on plant.
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Wells, P. G., Bhuller, Y., Chen, C. S., Jeng, W., Kasapinovic, S., Kennedy, J. C., et al. (2005). Molecular and biochemical mechanisms in teratogenesis involving reactive oxygen species. Toxicol Appl Pharmacol, 207(2 Suppl), 354–366.
Abstract: Developmental pathologies may result from endogenous or xenobiotic-enhanced formation of reactive oxygen species (ROS), which oxidatively damage cellular macromolecules and/or alter signal transduction. This minireview focuses upon several model drugs (phenytoin, thalidomide, methamphetamine), environmental chemicals (benzo[a]pyrene) and gamma irradiation to examine this hypothesis in vivo and in embryo culture using mouse, rat and rabbit models. Embryonic prostaglandin H synthases (PHSs) and lipoxygenases bioactivate xenobiotics to free radical intermediates that initiate ROS formation, resulting in oxidation of proteins, lipids and DNA. Oxidative DNA damage and embryopathies are reduced in PHS knockout mice, and in mice treated with PHS inhibitors, antioxidative enzymes, antioxidants and free radical trapping agents. Thalidomide causes embryonic DNA oxidation in susceptible (rabbit) but not resistant (mouse) species. Embryopathies are increased in mutant mice deficient in the antioxidative enzyme glucose-6-phosphate dehydrogenase (G6PD), or by glutathione (GSH) depletion, or inhibition of GSH peroxidase or GSH reductase. Inducible nitric oxide synthase knockout mice are partially protected. Inhibition of Ras or NF-kB pathways reduces embryopathies, implicating ROS-mediated signal transduction. Atm and p53 knockout mice deficient in DNA damage response/repair are more susceptible to xenobiotic or radiation embryopathies, suggesting a teratological role for DNA damage, consistent with enhanced susceptibility to methamphetamine in ogg1 knockout mice with deficient repair of oxidative DNA damage. Even endogenous embryonic oxidative stress carries a risk, since untreated G6PD- or ATM-deficient mice have increased embryopathies. Thus, embryonic processes regulating the balance of ROS formation, oxidative DNA damage and repair, and ROS-mediated signal transduction may be important determinants of teratological risk.
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Wilkins, L. J., Brown, S. N., Zimmerman, P. H., Leeb, C., & Nicol, C. J. (2004). Investigation of palpation as a method for determining the prevalence of keel and furculum damage in laying hens. Vet. Rec., 155(18), 547–549.
Abstract: Old breaks of the keel and furculum were identified by palpation in 500 end-of-lay hens from 10 flocks housed in free-range and barn systems, and the results were compared with the results obtained by a full dissection and inspection. The method was considered to be sufficiently precise to be used as a diagnostic tool although people using it would need to be trained. The results obtained by dissection indicated that 50 to 78 per cent of the birds in the flocks had breaks of the furculum and keel, but no other breaks of bones were detected.
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Nicol, C. J., Davidson, H. P. D., Harris, P. A., Waters, A. J., & Wilson, A. D. (2002). Study of crib-biting and gastric inflammation and ulceration in young horses. Vet. Rec., 151(22), 658–662.
Abstract: Nineteen young horses that had recently started to perform the stereotypy of crib-biting were compared with 16 non-stereotypic horses for 14 weeks. After initial observations of their behaviour and an endoscopic examination of the condition of their stomachs, the horses were randomly allocated to a control or an antacid diet At the start of the trial, the stomachs of the crib-biting foals were significantly more ulcerated and inflamed than the stomachs of the normal foals. In addition, the faecal pH of the crib-biting foals (6.05) was significantly lower than that of the normal foals (6.58). The antacid diet resulted in a significant improvement in the condition of the horses' stomachs. The crib-biting behaviour declined in most of the foals, regardless of their diet, but tended to decline to a greater extent in the foals on the antacid diet.
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McGreevy, P. D., Webster, A. J., & Nicol, C. J. (2001). Study of the behaviour, digestive efficiency and gut transit times of crib-biting horses. Vet. Rec., 148(19), 592–596.
Abstract: The spontaneous behaviour and the apparent digestibility of dry matter and fibre and transit times of digesta were compared in four normal horses and four crib-biters. A technique was developed for measuring total gut transit times (TGTT) by using single-stool analysis of the passage of radio-opaque polyethylene markers. Longer TGTT were recorded in the crib-biters than in the normal horses but the orocaecal transit times did not differ. The crib-biters rested less than the normal horses.
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McGreevy, P. D., & Nicol, C. J. (1998). Prevention of crib-biting: a review. Equine Vet J Suppl, (27), 35–38.
Abstract: Crib-biting is a common oral stereotype. Because of perceived deleterious effects on the health and appearance of subjects the prevention of crib-biting is regularly attempted. The resourcefulness of horses in satisfying their motivation to perform this behaviour often frustrates owners' efforts at prevention. This paper reviews the efficacy and observable consequences of attempting to prevent crib-biting by a variety of methods. These include attempts to prevent the grasping of objects, to interfere with air-engulfing and to introduce punishment for grasping and neck-flexion. Other approaches include the use of surgery, acupuncture, pharmaceuticals, operant feeding and environmental enrichment. A remedy that is effective for every crib-biter remains elusive. We conclude that, rather than concentrating on remedial prevention, further research should be directed at establishing why horses crib-bite and how the emergence of crib-biting can be avoided.
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McGreevy, P. D., & Nicol, C. J. (1998). The effect of short-term prevention on the subsequent rate of crib-biting in thoroughbred horses. Equine Vet J Suppl, (27), 30–34.
Abstract: The results of an experimental study of the motivational consequences of short-term prevention of crib-biting are reported here. Eight test horses wore a cribbing collar for 24 h. This was effective in preventing crib-biting in 6 subjects. Using analysis of co-variance that accounted for baseline differences in crib-biting rate, test horses showed significantly more crib-biting than control horses on the first day after prevention (P < 0.05). There was also a highly significant increase in the crib-biting rate of test horses on the first day after prevention in comparison with their baseline rate (P < 0.01). This defines the increase as a post inhibitory rebound. An increase in the novelty of the cribbing bar and an increase in feeding motivation during the period of prevention are rejected as explanations of the rebound in this study. Instead, it is suggested that the rebound reflected a rise in internal motivation to crib-bite during the period of prevention. Behaviours that exhibit this pattern of motivation are generally considered functional; and it has been argued that their prevention may compromise welfare.
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