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Hauber, M. E., & Sherman, P. W. (2003). Designing and interpreting experimental tests of self-referent phenotype matching. Anim. Cogn., 6(1), 69–71.
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Komar, N. (2003). West Nile virus: epidemiology and ecology in North America. Adv Virus Res, 61, 185–234.
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Valero, N. (2003). West Nile virus: a new challenge? Invest Clin, 44(3), 175–177.
Abstract: West Nile Virus (WNV), a member of the family Flaviviridae, was first isolated in 1937. Since the original isolation of the WNV outbreaks have occurred with increase in frequency of cases in humans and horses, apparent increase in severe human disease and high avian death rates. In 1999, 2000 and 2002 outbreaks of the WNV encephalitis were reported in horses, birds and humans from New York and Canada. Ornithophilic mosquitoes are the principal vectors of the WNV and birds of several species chiefly migrants appear to be the major introductory or amplifying host. The pattern of outbreaks in the old and new world suggests that viremic migratory birds may also contribute to movement of the virus. If so, Central America, Caribbean Islands and countries of South America including Venezuela, are in potential risk for suffering a severe outbreak for WNV, since several species of birds have populations that pass trough New York and cross the western north Atlantic or Caribbean Sea. It is important the knowledge of the ecology of WNV as well of the efficacy of control efforts in order to minimize the public health impact in these countries, where all population is susceptible to this infection.
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Barker, S. C. (2003). The Australian paralysis tick may be the missing link in the transmission of Hendra virus from bats to horses to humans. Med Hypotheses, 60(4), 481–483.
Abstract: Hendra virus is a new virus of the family Paramyxoviridae. This virus was first detected in Queensland, Australia, in 1994; although, it seems that the virus has infected fruit-eating bats (flying-foxes) for a very long time. At least 2 humans and 15 horses have been killed by this virus since it first emerged as a virus that may infect mammals other than flying-foxes. Hendra virus is thought to have moved from flying-foxes to horses, and then from horses to people. There is a reasonably strong hypothesis for horse-to-human transmission: transmission of virus via nasal discharge, saliva and/or urine. In contrast, there is no strong hypothesis for flying-fox-to-human transmission. I present evidence that the Australian paralysis tick, Ixodes holocyclus, which has apparently only recently become a parasite of flying-foxes, may transmit Hendra virus and perhaps related viruses from flying-foxes to horses and other mammals.
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Branchi, I., Bichler, Z., Berger-Sweeney, J., & Ricceri, L. (2003). Animal models of mental retardation: from gene to cognitive function. Neurosci Biobehav Rev, 27(1-2), 141–153.
Abstract: About 2-3% of all children are affected by mental retardation, and genetic conditions rank among the leading causes of mental retardation. Alterations in the information encoded by genes that regulate critical steps of brain development can disrupt the normal course of development, and have profound consequences on mental processes. Genetically modified mouse models have helped to elucidate the contribution of specific gene alterations and gene-environment interactions to the phenotype of several forms of mental retardation. Mouse models of several neurodevelopmental pathologies, such as Down and Rett syndromes and X-linked forms of mental retardation, have been developed. Because behavior is the ultimate output of brain, behavioral phenotyping of these models provides functional information that may not be detectable using molecular, cellular or histological evaluations. In particular, the study of ontogeny of behavior is recommended in mouse models of disorders having a developmental onset. Identifying the role of specific genes in neuropathologies provides a framework in which to understand key stages of human brain development, and provides a target for potential therapeutic intervention.
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Singer, E. R., Saxby, F., & French, N. P. (2003). A retrospective case-control study of horse falls in the sport of horse trials and three-day eventing. Equine Vet J, 35(2), 139–145.
Abstract: REASONS FOR PERFORMING STUDY: Serious injuries to horses and riders in horse trials (HT) and three-day events (3DE) are usually associated with falls of horses, which invariably involve falls of the riders. Many potential causes for these falls have been discussed. OBJECTIVES: The aim of this case-control study was to investigate the risk factors for horse falls on the cross-country phase of horse trials and three-day events. METHODS: Using retrospective data, significant risk factors identified with unvariable analysis (P value <0.2) were entered into a multivariable logistic regression model. Significant risk factors (P value <0.05) were included in the final model. RESULTS: It was revealed that a number of course, obstacle and rider variables were significantly and independently associated with the risk of falling. Falling was associated with obstacles sited downhill (Odds ratio [OR] 8.41) and with obstacles with ditches in front (OR = 5.77). CONCLUSIONS: The relationship between course variables and the risk of falling was characterised and showed a significantly increased risk with increasing numbers of jumps on the course and for jumping efforts later in the course. In contrast, after allowing for the total number of obstacles on the course, an increase in the total number of jumping efforts appeared to have a protective effect. A later cross-country start time was associated with a decreased risk of a horse fall. Amateur event riders were approximately 20 times more likely to fall than professional riders. POTENTIAL CLINICAL RELEVANCE: This study has identified a number of risk factors associated with horse falls and highlights areas that can be altered to improve safety in cross-country competitions.
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Adolphs, R. (2003). Cognitive neuroscience of human social behaviour. Nat Rev Neurosci, 4(3), 165–178.
Abstract: We are an intensely social species--it has been argued that our social nature defines what makes us human, what makes us conscious or what gave us our large brains. As a new field, the social brain sciences are probing the neural underpinnings of social behaviour and have produced a banquet of data that are both tantalizing and deeply puzzling. We are finding new links between emotion and reason, between action and perception, and between representations of other people and ourselves. No less important are the links that are also being established across disciplines to understand social behaviour, as neuroscientists, social psychologists, anthropologists, ethologists and philosophers forge new collaborations.
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Lee, R. D. (2003). Rethinking the evolutionary theory of aging: transfers, not births, shape senescence in social species. Proc Natl Acad Sci U S A, 100(16), 9637–9642.
Abstract: The classic evolutionary theory of aging explains why mortality rises with age: as individuals grow older, less lifetime fertility remains, so continued survival contributes less to reproductive fitness. However, successful reproduction often involves intergenerational transfers as well as fertility. In the formal theory offered here, age-specific selective pressure on mortality depends on a weighted average of remaining fertility (the classic effect) and remaining intergenerational transfers to be made to others. For species at the optimal quantity-investment tradeoff for offspring, only the transfer effect shapes mortality, explaining postreproductive survival and why juvenile mortality declines with age. It also explains the evolution of lower fertility, longer life, and increased investments in offspring.
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Bloom, P. (2004). Behavior. Can a dog learn a word? Science, 304(5677), 1605–1606.
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Cheung, C., Akiyama, T. E., Ward, J. M., Nicol, C. J., Feigenbaum, L., Vinson, C., et al. (2004). Diminished hepatocellular proliferation in mice humanized for the nuclear receptor peroxisome proliferator-activated receptor alpha. Cancer Res, 64(11), 3849–3854.
Abstract: Lipid-lowering fibrate drugs function as agonists for the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha). Sustained activation of PPARalpha leads to the development of liver tumors in rats and mice. However, humans appear to be resistant to the induction of peroxisome proliferation and the development of liver cancer by fibrate drugs. The molecular basis of this species difference is not known. To examine the mechanism determining species differences in peroxisome proliferator response between mice and humans, a PPARalpha-humanized mouse line was generated in which the human PPARalpha was expressed in liver under control of the tetracycline responsive regulatory system. The PPARalpha-humanized and wild-type mice responded to treatment with the potent PPARalpha ligand Wy-14643 as revealed by induction of genes encoding peroxisomal and mitochondrial fatty acid metabolizing enzymes and resultant decrease of serum triglycerides. However, surprisingly, only the wild-type mice and not the PPARalpha-humanized mice exhibited hepatocellular proliferation as revealed by elevation of cell cycle control genes, increased incorporation of 5-bromo-2'-deoxyuridine into hepatocyte nuclei, and hepatomegaly. These studies establish that following ligand activation, the PPARalpha-mediated pathways controlling lipid metabolism are independent from those controlling the cell proliferation pathways. These findings also suggest that structural differences between human and mouse PPARalpha are responsible for the differential susceptibility to the development of hepatocarcinomas observed after treatment with fibrates. The PPARalpha-humanized mice should serve as models for use in drug development and human risk assessment and to determine the mechanism of hepatocarcinogenesis of peroxisome proliferators.
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