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Halford, G.S., & Halford, J. M.. (1969). Secondary reinforcement: signal or substitute reward? A preliminary investigation. Aus. J. Psychol, .
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Manning, G. S., & Ratanarat, C. (1970). Fasciolopsis buski (Lankester, 1857) in Thailand. Am J Trop Med Hyg, 19(4), 613–619.
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Nelson, G. S. (1970). Onchocerciasis. Adv Parasitol, 8, 173–224.
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Saayman, G. S. (1971). Behaviour of the adult males in a troop of free-ranging Chacma baboons (Papio ursinus). Folia Primatol (Basel), 15(1), 36–57.
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Sabattini, M. S., Monath, T. P., Mitchell, C. J., Daffner, J. F., Bowen, G. S., Pauli, R., et al. (1985). Arbovirus investigations in Argentina, 1977-1980. I. Historical aspects and description of study sites. Am J Trop Med Hyg, 34(5), 937–944.
Abstract: This is the introductory paper to a series on the ecology of arboviruses in Argentina. Epizootics of equine encephalitis have occurred since at least 1908, principally in the Pampa and Espinal biogeographic zones, with significant economic losses; human cases of encephalitis have been rare or absent. Both western equine and eastern equine encephalitis viruses have been isolated from horses during these epizootics, but the mosquitoes responsible for transmission have not been identified. A number of isolations of Venezuelan equine encephalitis (VEE) virus were reported between 1936 and 1958 in Argentina, but the validity of these findings has been seriously questioned. Nevertheless, serological evidence exists for human infections with a member of the VEE virus complex. Serological surveys conducted in the 1960s indicate a high prevalence of infection of humans and domestic animals with St. Louis encephalitis (SLE), and 2 SLE virus strains have been isolated from rodents. Human disease, however, has rarely been associated with SLE infection. Only 7 isolations of other arboviruses have been described (3 of Maguari, 1 of Aura, 2 of Una, and 1 of an untyped Bunyamwera group virus). In 1977, we began longitudinal field studies in Santa Fe Province, the epicenter of previous equine epizootics, and in 1980 we extended these studies to Chaco and Corrientes provinces. The study sites are described in this paper.
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Honeyman, M. S., & Miller, G. S. (1998). The effect of teaching approaches on achievement and satisfaction of field-dependent and field-independent learners in animal science. J. Anim Sci., 76(6), 1710–1715.
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Van Doorn G.S., Hengeveld G.M., & Weissing F.J. (2003). The Evolution of Social Dominance I: Two-player Models. Behavior, 140(10), 1305–1332.
Abstract: A difference in dominance rank is an often-used cue to resolve conflicts between two animals without escalated fights. At the group level, adherence to a dominance convention efficiently reduces the costs associated with conflicts, but from an individual's point of view, it is difficult to explain why a low ranking individual should accept its subordinate status. This is especially true if, as suggested by several authors, dominance not necessarily reflects differences in fighting ability but rather results from arbitrary historical asymmetries. According to this idea, rank differentiation emerges from behavioural strategies, referred to as winner and loser effects, in which winners of previous conflicts are more likely to win the current conflict, whereas the losers of previous conflicts are less likely to do so. In order to investigate whether dominance, based on such winner and loser effects, can be evolutionarily stable, we analyse a game theoretical model. The model focuses on an extreme case in which there are no differences in fighting ability between individuals at all. The only asymmetries that may arise between individuals are generated by the outcome of previous conflicts. By means of numerical analysis, we find alternative evolutionarily stable strategies, which all utilize these asymmetries for conventional conflict resolution. One class of these strategies is based on winner and loser effects, thus generating evolutionarily stable dominance relations even in the absence of differences in resource holding potential.
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Van Doorn G.S., Hengeveld G.M., & Weissing F.J. (2003). The Evolution of Social Dominance II: Multi-Player Models. Behavior, 140(10), 1333–1358.
Abstract: The social hierarchies observed in natural systems often show a high degree of transitivity. Transitive hierarchies do not only require rank differentiation within pairs of individuals but also a higher level ordering of relations within the group. Several authors have suggested that the formation of linear hierarchies at the group level is an emergent property of individual behavioural rules, referred to as winner and loser effects. Winner and loser effects occur if winners of previous conflicts are more likely to escalate the current conflict, whereas the losers of previous conflicts are less likely to do so. According to this idea, an individual's position in a hierarchy may not necessarily reflect its fighting ability, but may rather result from arbitrary historical asymmetries, in particular the history of victories and defeats. However, if this is the case, it is difficult to explain from an evolutionary perspective why a low ranking individual should accept its subordinate status. Here we present a game theoretical model to investigate whether winner and loser effects giving rise to transitive hierarchies can evolve and under which conditions they are evolutionarily stable. The main version of the model focuses on an extreme case in which there are no intrinsic differences in fighting ability between individuals. The only asymmetries that may arise between individuals are generated by the outcome of previous conflicts. We show that, at evolutionary equilibrium, these asymmetries can be utilized for conventional conflict resolution. Several evolutionarily stable strategies are based on winner and loser effects and these strategies give rise to transitive hierarchies.
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Crosby, M. B., Svenson, J. L., Zhang, J., Nicol, C. J., Gonzalez, F. J., & Gilkeson, G. S. (2005). Peroxisome proliferation-activated receptor (PPAR)gamma is not necessary for synthetic PPARgamma agonist inhibition of inducible nitric-oxide synthase and nitric oxide. J Pharmacol Exp Ther, 312(1), 69–76.
Abstract: Peroxisome proliferation-activated receptor (PPAR)gamma agonists inhibit inducible nitric-oxide synthase (iNOS), tumor necrosis factor-alpha, and interleukin-6. Because of these effects, synthetic PPARgamma agonists, including thiazolidinediones, are being studied for their impact on inflammatory disease. The anti-inflammatory concentrations of synthetic PPARgamma agonists range from 10 to 50 microM, whereas their binding affinity for PPARgamma is in the nanomolar range. The specificity of synthetic PPARgamma agonists for PPARgamma at the concentrations necessary for anti-inflammatory effects is thus in question. We report that PPARgamma is not necessary for the inhibition of iNOS by synthetic PPARgamma agonists. RAW 264.7 macrophages possess little PPARgamma, yet lipopolysaccharide (LPS)/interferon (IFN)gamma-induced iNOS was inhibited by synthetic PPARgamma agonists at 20 microM. Endogenous PPARgamma was inhibited by the transfection of a dominant-negative PPARgamma construct into murine mesangial cells. In the transfected cells, synthetic PPARgamma agonists inhibited iNOS production at 10 microM, similar to nontransfected cells. Using cells from PPARgamma Cre/lox conditional knockout mice, baseline and LPS/IFNgamma-induced nitric oxide levels were higher in macrophages lacking PPARgamma versus controls. However, synthetic PPARgamma agonists inhibited iNOS at 10 microM in the PPARgamma-deficient cells, similar to macrophages from wild-type mice. These results indicate that PPARgamma is not necessary for inhibition of iNOS expression by synthetic PPARgamma agonists at concentrations over 10 microM. Intrinsic PPARgamma function, in the absence of synthetic agonists, however, may play a role in inflammatory modulation.
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Crosby, M. B., Zhang, J., Nowling, T. M., Svenson, J. L., Nicol, C. J., Gonzalez, F. J., et al. (2006). Inflammatory modulation of PPAR gamma expression and activity. Clin Immunol, 118(2-3), 276–283.
Abstract: Nitric oxide (NO) production increases with age in the lupus-prone MRL/lpr mouse, paralleling disease activity. One mechanism for excess NO production in MRL/lpr mice may be a defect in down-regulatory mechanisms of the iNOS pathway. A potential modulator of NO is the nuclear hormone receptor peroxisome proliferation activated receptor gamma (PPARgamma). We demonstrate that renal PPARgamma protein expression was altered as disease progressed in MRL/lpr mice, which paralleled increased iNOS protein expression. Additionally, MRL/lpr-derived primary mesangial cells expressed less PPARgamma than BALB/c mesangial cells and produced more NO in response to LPS and IFNgamma. Furthermore, PPARgamma activity was reduced in mesangial cells following exposure to inflammatory mediators. This activity was restored with the addition of a NOS enzyme inhibitor. These results indicate that the activation of inflammatory pathways may lead to reduced activity and expression of PPARgamma, further exacerbating the disease state.
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