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Though there is a burgeoning interest in applied Buddhist ethics, Buddhist animal research ethics remains an underdeveloped area. In this paper I will explore how some central Buddhist ethical considerations can usefully engage our use of other animals (henceforth, animals) in science. As the scientific use of animals is broad, I will narrow my focus to laboratory science. I will show that, though a Buddhist abolitionism would not be unmotivated, it is possible to reject it. While doing so, it will be important to resist emphasizing elements of Buddhist thought that merely provide reasons to adopt the dominant ethical framework governing laboratory animal research ethics, known as the 3Rs. Though I will suggest how a Buddhist animal research ethics can sometimes permit the use of animals in harmful research, it will also require ethical constraints that resonate with some of the more progressive elements in 'Western' bioethics. [ABSTRACT FROM AUTHOR]

Chronic infections may have negative impacts on wildlife populations, yet their effects are difficult to detect in the absence of long-term population monitoring. Brucella abortus, the bacteria responsible for bovine brucellosis, causes chronic infections and abortions in wild and domestic ungulates, but its impact on population dynamics is not well understood., We report infection patterns and fitness correlates of bovine brucellosis in African buffalo based on (1) 7 years of cross-sectional disease surveys and (2) a 4-year longitudinal study in Kruger National Park ( KNP), South Africa. We then used a matrix population model to translate these observed patterns into predicted population-level effects., Annual brucellosis seroprevalence ranged from 8·7% (95% CI = 1·8-15·6) to 47·6% (95% CI = 35·1-60·1) increased with age until adulthood (>6) and varied by location within KNP. Animals were on average in worse condition after testing positive for brucellosis ( F = −5·074, P < 0·0001), and infection was associated with a 2·0 (95% CI = 1·1-3·7) fold increase in mortality (χ2 = 2·039, P = 0·036). Buffalo in low body condition were associated with lower reproductive success ( F = 2·683, P = 0·034), but there was no association between brucellosis and pregnancy or being observed with a calf., For the range of body condition scores observed in the population, the model-predicted growth rate was λ = 1·11 (95% CI = 1·02-1·21) in herds without brucellosis and λ = 1·00 (95% CI = 0·85-1·16) when brucellosis seroprevalence was 30%., Our results suggest that brucellosis infection can potentially result in reduced population growth rates, but because these effects varied with demographic and environmental conditions, they may remain unseen without intensive, longitudinal monitoring. [ABSTRACT FROM AUTHOR]

Host extinction can alter disease transmission dynamics, influence parasite extinction and ultimately change the nature of host-parasite systems. While theory predicts that single-host parasites are among the parasite species most susceptible to extinction following declines in their hosts, documented parasite extinctions are rare., Using a comparative approach, we investigate how the richness of single-host and multi-host parasites is influenced by extinction risk among ungulate and carnivore hosts. Host-parasite associations for free-living carnivores (order Carnivora) and terrestrial ungulates (orders Perissodactyla + Cetartiodactyla minus cetaceans) were merged with host trait data and IUCN Red List status to explore the distribution of single-host and multi-host parasites among threatened and non-threatened hosts., We find that threatened ungulates harbour a higher proportion of single-host parasites compared to non-threatened ungulates, which is explained by decreases in the richness of multi-host parasites. However, among carnivores threat status is not a significant predictor of the proportion of single-host parasites, or the richness of single-host or multi-host parasites., The loss of multi-host parasites from threatened ungulates may be explained by decreased cross-species contact as hosts decline and habitats become fragmented. Among carnivores, threat status may not be important in predicting patterns of parasite specificity because host decline results in equal losses of both single-host parasites and multi-host parasites through reduction in average population density and frequency of cross-species contact., Our results contrast with current models of parasite coextinction and highlight the need for updated theories that are applicable across host groups and account for both inter- and intraspecific contact. [ABSTRACT FROM AUTHOR]

Smoking increases the risk of developing lung cancer. Genetic loci have been identified which could form the basis of a lung cancer susceptibility test; but little is known whether such a test would interest or motivate those trying to quit smoking. To address this, we investigated the attitudes of people trying to quit smoking towards genetic susceptibility testing for lung cancer. Participant's attitudes to topics associated with lung cancer susceptibility testing were assessed; were they interested in genetic testing? What impact would a hypothetical high- or low- risk result have on smoking cessation? 680 self-completion questionnaires were given to individuals attending National Health Service stop smoking clinics in three different areas of the United Kingdom between 2011 and 2012. 139 questionnaires were returned, giving a 20 % response rate. Participants expressed an interest in a genetic susceptibility test for lung cancer and almost all reported that a high-risk result would increase their motivation to stop smoking. However, many participants had a neutral attitude towards a low-risk result. Most participants agreed their smoking habit could lead to lung cancer. Lung cancer susceptibility testing may be a useful incentive to help people quit smoking. This study suggests the need for genetic services to work with smoking cessation teams if routine testing becomes available in the future. [ABSTRACT FROM AUTHOR]

Previous analyses of empirical food webs (the networks of who eats whom in a community) have revealed that parasites exert a strong influence over observed food web structure and alter many network properties such as connectance and degree distributions. It remains unclear, however, whether these community-level effects are fully explained by differences in the ways that parasites and free-living species interact within a food web., To rigorously quantify the interrelationship between food web structure, the types of species in a web and the distinct types of feeding links between them, we introduce a shared methodology to quantify the structural roles of both species and feeding links. Roles are quantified based on the frequencies with which a species (or link) appears in different food web motifs - the building blocks of networks., We hypothesized that different types of species (e.g. top predators, basal resources, parasites) and different types of links between species (e.g. classic predation, parasitism, concomitant predation on parasites along with their hosts) will show characteristic differences in their food web roles., We found that parasites do indeed have unique structural roles in food webs. Moreover, we demonstrate that different types of feeding links (e.g. parasitism, predation or concomitant predation) are distributed differently in a food web context. More than any other interaction type, concomitant predation appears to constrain the roles of parasites. In contrast, concomitant predation links themselves have more variable roles than any other type of interaction., Together, our results provide a novel perspective on how both species and feeding link composition shape the structure of an ecological community and vice versa. [ABSTRACT FROM AUTHOR]

Animals' social and movement behaviours can impact the transmission dynamics of infectious diseases, especially for pathogens transmitted through close contact between hosts or through contact with infectious stages in the environment., Estimating pathogen transmission rates and R0 from natural systems can be challenging. Because host behavioural traits that underlie the transmission process vary predictably with body size, one of the best-studied traits among animals, body size might therefore also predict variation in parasite transmission dynamics., Here, we examine how two host behaviours, social group living and the intensity of habitat use, scale allometrically using comparative data from wild primate, carnivore and ungulate species. We use these empirical relationships to parameterize classical compartment models for infectious micro- and macroparasitic diseases, and examine how the risk of pathogen invasion changes as a function of host behaviour and body size. We then test model predictions using comparative data on parasite prevalence and richness from wild mammals., We report a general pattern suggesting that smaller-bodied mammal species utilizing home ranges more intensively experience greater risk for invasion by environmentally transmitted macroparasites. Conversely, larger-bodied hosts exhibiting a high degree of social group living could be more readily invaded by directly transmitted microparasites. These trends were supported through comparison of micro- and macroparasite species richness across a large number of carnivore, primate and ungulate species, but empirical data on carnivore macroparasite prevalence showed mixed results., Collectively, our study demonstrates that combining host behavioural traits with dynamical models of infectious disease scaled against host body size can generate testable predictions for variation in parasite risk across species; a similar approach might be useful in future work focused on predicting parasite distributions in local host communities. [ABSTRACT FROM AUTHOR]

For all parasites, transmission is composed of two processes: host contact with parasites ('exposure') and risk of infection given such contact ('susceptibility'). Classic models, such as mass action (density-dependent) transmission, lump these processes together., However, separating these processes could enhance predictions for disease dynamics, especially for free-living parasites. Here, we outline three transmission models that partition exposure and susceptibility., Using data from a study of Schistosoma mansoni (trematode) infections in Biomphalaria glabrata snails, we competed these three models against four alternative models, including the mass action model (which lumps exposure and susceptibility)., The models that separately accounted for exposure and susceptibility best predicted prevalence across the density gradients of hosts and parasites, outperforming all other models based on Akaike information criterion. When embedded into a dynamic epidemiological model, the exposure-explicit models all predicted lower equilibrium densities of infected snails and human-infectious cercariae., Thus, population-level epidemiological models that utilize the classic mass action transmission model might overestimate human risk of schistosomiasis. More generally, the presented approach for disentangling exposure and susceptibility can distinguish between behavioural and immunological resistance, identify mechanisms of 'disease dilution' and provide a more complete dissection of drivers of parasite transmission. [ABSTRACT FROM AUTHOR]

How bacteria coordinate cell growth with division is not well understood. Bacterial cell elongation is controlled by actin-MreB while cell division is governed by tubulin-FtsZ. A ring-like structure containing FtsZ (the Z ring) at mid-cell attracts other cell division proteins to form the divisome, an essential protein assembly required for septum synthesis and cell separation. The Z ring exists at mid-cell during a major part of the cell cycle without contracting. Here, we show that MreB and FtsZ of Escherichia coli interact directly and that this interaction is required for Z ring contraction. We further show that the MreB-FtsZ interaction is required for transfer of cell-wall biosynthetic enzymes from the lateral to the mature divisome, allowing cells to synthesise the septum. Our observations show that bacterial cell division is coupled to cell elongation via a direct and essential interaction between FtsZ and MreB. [ABSTRACT FROM AUTHOR]

This paper integrates some Buddhist moral values, attitudes and self-cultivation techniques into a discussion of the ethics of cognitive enhancement technologies – in particular, pharmaceutical enhancements. Many Buddhists utilize meditation techniques that are both integral to their practice and are believed to enhance the cognitive and affective states of experienced practitioners. Additionally, Mahāyāna Buddhism's teaching on skillful means permits a liberal use of methods or techniques in Buddhist practice that yield insight into our selfnature or aid in alleviating or eliminating du kha (i.e. dissatisfaction). These features of many, if not most, Buddhist traditions will inform much of the Buddhist assessment of pharmaceutical enhancements offered in this paper. Some Buddhist concerns about the effects and context of the use of pharmaceutical enhancements will be canvassed in the discussion. Also, the author will consider Buddhist views of the possible harms that may befall human and nonhuman research subjects, interference with a recipient's karma, the artificiality of pharmaceutical enhancements, and the possible motivations or intentions of healthy individuals pursuing pharmacological enhancement. Perhaps surprisingly, none of these concerns will adequately ground a reflective Buddhist opposition to the further development and continued use of pharmaceutical enhancements, either in principle or in practice. The author argues that Buddhists, from at least certain traditions – particularly Mahāyāna Buddhist traditions – should advocate the development or use of pharmaceutical enhancements if a consequence of their use is further insight into our self-nature or the reduction or alleviation of du kha. [ABSTRACT FROM AUTHOR]

In moral psychology, it has long been argued that empathy is a necessary capacity of both properly developing moral agents and developed moral agency ( Blair, 2008 ; Hume et al., 1978 ). This view stands in tension with the belief that some individuals diagnosed with autism—which is typically characterized as a deficiency in social reciprocity (including empathy)—are moral agents. In this paper we propose to explore this tension and perhaps trouble how we commonly see those with autism. To make this task manageable, we will consider whether high functioning individuals diagnosed with an autism spectrum disorder are capable of empathetic responses. If they are, then they possess a capacity that, on the view above, is required for moral agency. If they are not so capable, and yet sometimes engage in moral behaviour, this casts some doubt on the claim that empathy is required for moral agency. This second possibility will necessitate an exploration of the capacity of some individuals with autism to engage in moral behaviour, giving us further grounds to re-see these individuals as moral agents. [ABSTRACT FROM AUTHOR]

Using empirically derived relationships between temperature and development rate, a stochastic simulation model was used to predict the seasonal pattern of abundance of the sheep blowfly Lucilia sericata. Sensitivity analysis suggests that, at the levels of mortality observed on sheep farms in Britain. L. sericata abundance may not be strongly influenced by the number of oviposition sites available. Hence, control techniques aimed at reducing the number of sites in the field may have little impact on the blowfly population and the resulting incidence of sheep strike. The model shows that variations in adult mortality have a much greater effect on the blowfly population than variations in pre-adult mortality, both in terms of the number of flies present in each generation and the probability of extinction of the population. With levels of pre-adult mortality of 50% per generation, adult mortality levels in excess of 30% per day would be needed to prevent the growth of a population of L. sericata. In contrast, at the lowest level of adult mortality examined, pre-adult mortality levels of 90% per generation were unable to prevent the population from increasing. The simulations suggest that unless consistently high levels of larval mortality can be maintained by a control programme, suppression of a L. sericata population is unlikely to be achieved. In contrast, relatively small increases in adult mortality may have a significant impact on L. sericata abundance, and attempts to suppress L. sericata populations by targeting the adult population may be an effective future approach. [ABSTRACT FROM AUTHOR]