5 resultados para Fauna - Autotoxaemia - Experimental studies

em Brock University, Canada


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Catalase dismutes H20 2 to O2 and H20. In successive twoelectron reactions H20 2 induces both oxidation and reduction at the heme group. In the first step the protoheme prosthetic group of beef liver catalase forms compound I, in which the heme has been oxidized from Fe3+ to Fe4+=0 and a porphyrin radical has been created. Compound II is formed by the oneelectron reduction of comp I. It retains Fe4+=0 but lacks the porphyrin radical and is catalytically inert. Molecular structures are available for Escherichia coli Hydroperoxidase II, Micrococcus Iysodeiktus, Penicillium vitale and beef liver enzymes, which contain different hemes and heme pockets. In the present work, the pockets and substrate access channels of protoheme (beef liver & Micrococcus) and heme d (HPII of E. coli and Penicillium) catalases have been analysed using Quanta™ and CharmMTM molecular modeling packages on the Silicon Graphics Iris Indigo 2 computer. Experimental studies have been carried out with two catalases, HPII (and its mutants) and beef liver. Fluoride and formate' are inhibitors of both enzymes, and their binding is modulated by the heme and by distal residues N201 & H128. Both HPII and beef liver enzymes form compound I with H202 or peracetate. The reduction of beef liver enzyme compound I to II and the decay of compound II are accelerated by fluoride. The decay of compound II is also accelerated by formate, and this reagent acts as a 2-electron donor towards compound I of both enzymes. It is concluded that heme d enzymes (Penicillium and HPII of E. coli) are formed by autocatalytic transformation of protoheme in a modified pocket which contains a characteristic serine residue as well as a partially occluded heme channel. They are less active than protoheme enzymes but also do not form the inactive compound II species. Binding of peroxide as well as fluoride and formate is prevented by mutation of H128 and modulated by mutation of N201.

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Inter and intrachromosomal viability interactions have been detected in a few experimental studies. Computer simulations and analytical models have led to postulation of nonadditivity of gene action. This study reports evidence of strong nonadditive interactions between the arms of the metacentric second chromosome of Drosophila melanogaster. Mean viability for 40 homozygous lines of the second chromosomes was 0.720+0.265 • Mean viability for 40 half homozygous second chromosomes was 0.928!O.)10 • Significant heterogeneity among and within lines was found in both groups of chromosomes, as well as a highly significant viability difference between the two groups. Comparison of observed viabilities with the expected values, according to the theories of additive and multi - plicative gene action. was made for both groups. Highly significant departures from the expected values were found for over 90% of the lines in both groups of chromosomes, for both additive and multiplicative models of gene action.

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Experimental research has shown that playing violent video games produces higher levels of aggressive cognition, aggressive affect, physiological arousal, and aggressive behavior (in the short-term) than non-violent video games (see Anderson, Gentile & Buckley, 2007). However, there are two major limitations with these studies. First, the majority of experimental studies that have compared the effects of violent versus non-violent video games on aggression have failed to equate these games in terms of competitiveness, difficulty, and pace of action. Thus, although the common finding is that violent video games produce higher levels of aggression than nonviolent video games, other unmatched factors beyond the actual violent content may be responsible for the elevated levels of aggression. Second, previous experimental studies have tended to use a measure of aggression that may also measure competitiveness, leading to questions about whether violent video games are related to aggression or competitiveness. The present thesis addressed these two issues by fIrst equating a violent and non-violent video game on competitiveness, difficulty and pace of action in Experiment I , and then comparing the effect of each game on aggressive behavior using an unambiguous measure of aggressive behavior (i.e., the Hot Sauce Paradigm). We found that video game violence was not sufficient to elevate aggressive behavior compared to a non-violent video game. Practical implications and directions for future research are discussed.

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Recent research in the marketing literature has indicated that, while consumers’ interests in ethical products are growing, demand for such products still remains weak. Previous research has indicated that anticipated guilt can have a positive effect on ethical consumption. Thus, the objective of the current study is to investigate the moderating role of consumers’ socially responsible consumption behaviour (SRCB) on the relationship between anticipated guilt and ethical consumption. Specifically, the current study hypothesizes that, when viewing a guilt ad, high (vs. low) SRCB individuals will generate higher, ethical purchase intentions, willingness to pay an ethical premium, and attitudes toward an ethical brand. The findings from the two experimental studies indicate that, when viewing a guilt ad for an ethical product, high SRCB individuals are willing to pay a higher ethical premium and generate more favourable brand attitudes than low SRCB individuals. However, when viewing a non-guilt ad, high SRCB individuals did not differ from low SRCB individuals in their willingness to pay an ethical premium or brand attitudes. Further, consumers’ socially conscious self-identity was explored as a mediator of these effects. By understanding the moderating role that SRCB plays in the relationship between anticipated guilt and ethical consumption, this paper intends to assist marketers in understanding for which consumers a guilt appeal is an appropriate strategy in marketing ethical products.

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A brand-harm crisis not only affects the scandalized brand, but may also influence competing brands. Thus, marketers of competing brands need to develop response strategies for reducing negative spillover effects. This research takes a competitor’s perspective and introduces two types of response strategies used to convey a sense of denial: sensegiving and sensehiding. It also investigates how the effects of response strategies are contingent upon brand relatedness and individual thinking styles. The results from three experimental studies show that using a sensegiving strategy reduces negative spillover effects more than using a sensehiding strategy. Additionally, the studies suggest that the observed difference in the effects of response strategy tends to be greater when the level of brand relatedness is high than when it is low. However, individual thinking styles (holistic vs. analytic) seem to have little impact on consumers’ responses to the two denial strategies. This research contributes to the brand-harm crisis literature and provides novel insights into a competitor’s response to potential negative spillover effects.