Beyond prejudice: Are negative evaluations the problem and is getting us to like one another more the solution?

publication-status: Acceptedtypes: ArticleThis is a post print version of an article published in Behavioral and Brain Sciences, 2012, 35 (6), pp 438-439 DOI: http://dx.doi.org/10.1017/S0140525X12001252 Copyright © Cambridge University Press 2012For most of the history of prejudice research, negativity has been treated as its emotional and cognitive signature, a conception that continues to dominate work on the topic. By this definition, prejudice occurs when we dislike or derogate members of other groups. Recent research, however, has highlighted the need for a more nuanced and ‘inclusive’ (Eagly 2004) perspective on the role of intergroup emotions and beliefs in sustaining discrimination. On the one hand, several independent lines of research have shown that unequal intergroup relations are often marked by attitudinal complexity, with positive responses such as affection and admiration mingling with negative responses such as contempt and resentment. Simple antipathy is the exception rather than the rule. On the other hand, there is mounting evidence that nurturing bonds of affection between the advantaged and the disadvantaged sometimes entrenches rather than disrupts wider patterns of discrimination. Notably, prejudice reduction interventions may have ironic effects on the political attitudes of the historically disadvantaged, decreasing their perceptions of injustice and willingness to engage in collective action to transform social inequalities. These developments raise a number of important questions. Has the time come to challenge the assumption that negative evaluations are inevitably the cognitive and affective hallmarks of discrimination? Is the orthodox concept of prejudice in danger of side-tracking, if not obstructing, progress towards social justice in a fuller sense? What are the prospects for reconciling a prejudice reduction model of change, designed to get people to like one another more, with a collective action model of change, designed to ignite struggles to achieve intergroup equality

Characterization of the invasive and inflammatory traits of oral Campylobacter rectus in a murine model of fetoplacental growth restriction and in trophoblast cultures

Campylobacter species (C. jejuni, C. fetus) are enteric abortifacient bacteria in humans and ungulates. Campylobacter rectus is a periodontal pathogen associated with human fetal exposure and adverse pregnancy outcomes including preterm delivery. Experiments in pregnant mice have demonstrated that C. rectus can translocate from a distant site of infection to the placenta to induce fetal growth restriction and impair placental development. However, placental tissues from human, small-for-gestational age deliveries have not been reported to harbor C. rectus despite evidence of maternal infection and fetal exposure by fetal IgM response. This investigation examined the temporal relationship between the placental translocation of C. rectus and the effects on fetal growth in mice. BALB/c mice were infected at gestational day E7.5 to examine placental translocation of C. rectus by immunohistology. C. rectus significantly decreased fetoplacental weight at E14.5 and at E16.5. C. rectus was detected in 63% of placentas at E14.5, but not at E16.5. In in vitro trophoblast invasion assays, C. rectus was able to effectively invade human trophoblasts (BeWo) but not murine trophoblasts (SM9-1), and showed a trend for more invasiveness than C. jejuni. C. rectus challenge significantly upregulated both mRNA and protein levels of IL-6 and TNFα in a dose-dependent manner in human trophoblasts, but did not increase cytokine expression in murine cells, suggesting a correlation between invasion and cytokine activation. In conclusion, the trophoblast-invasive trait of C. rectus that appears limited to human trophoblasts may play a role in facilitating bacterial translocation and placental inflammation during early gestation

A potential new tool for the toolbox: assessing gene drives for eradicating invasive rodent populations

Invasive rodents have significant negative impacts on island biodiversity. All but the smallest of rodent eradications currently rely on island-wide rodenticide applications. Although significant advances have been made in mitigating unintended impacts, rodent eradication on inhabited islands remains extremely challenging. Current tools restrict eradication eff orts to fewer than 15% of islands with critically endangered or endangered species threatened by invasive rodents. The Genetic Biocontrol of Invasive Rodents partnership is an interdisciplinary collaboration to develop and evaluate gene drive technology for eradicating invasive rodent populations on islands. Technological approaches currently being investigated include the production of multiple strains of Mus musculus with a modifi ed form of the native t-complex, or a CRISPR gene drive, carrying genes or mechanisms that determine sex. These systems have the potential to skew the sex ratio of off spring to approach 100% single-sex, which could result in population collapse. One goal proposed is to test the ability of constructs to spread and increase in frequency in M. musculus populations in biosecure, captive settings and undertake modelling to inform development and potential deployment of these systems. Structured ecologically-based risk assessments are proposed, along with social and cultural engagement to assess the acceptability of releasing a gene drive system. Work will be guided by an external ethics advisory board. Partners are from three countries with significant regulatory capacity (USA, Australia, New Zealand). Thus, we will seek data sharing agreements so that results from experiments may be used within all three countries and treat regulatory requirements as a minimum. Species-specific, scalable, and socially acceptable new eradication tools could produce substantial biodiversity benefits not possible with current technologies. Gene drive innovation may provide such a tool for invasive species management and be potentially transformative and worthy of exploring in an inclusive, responsible, and ethical manner

Genetic Analysis of Hematological Parameters in Incipient Lines of the Collaborative Cross

Hematological parameters, including red and white blood cell counts and hemoglobin concentration, are widely used clinical indicators of health and disease. These traits are tightly regulated in healthy individuals and are under genetic control. Mutations in key genes that affect hematological parameters have important phenotypic consequences, including multiple variants that affect susceptibility to malarial disease. However, most variation in hematological traits is continuous and is presumably influenced by multiple loci and variants with small phenotypic effects. We used a newly developed mouse resource population, the Collaborative Cross (CC), to identify genetic determinants of hematological parameters. We surveyed the eight founder strains of the CC and performed a mapping study using 131 incipient lines of the CC. Genome scans identified quantitative trait loci for several hematological parameters, including mean red cell volume (Chr 7 and Chr 14), white blood cell count (Chr 18), percent neutrophils/lymphocytes (Chr 11), and monocyte number (Chr 1). We used evolutionary principles and unique bioinformatics resources to reduce the size of candidate intervals and to view functional variation in the context of phylogeny. Many quantitative trait loci regions could be narrowed sufficiently to identify a small number of promising candidate genes. This approach not only expands our knowledge about hematological traits but also demonstrates the unique ability of the CC to elucidate the genetic architecture of complex traits

A Gnotobiotic Mouse Model Demonstrates That Dietary Fiber Protects against Colorectal Tumorigenesis in a Microbiota- and Butyrate-Dependent Manner

It is controversial whether dietary fiber protects against colorectal cancer because of conflicting results from human epidemiologic studies. However, these studies and mouse models of colorectal cancer have not controlled the composition of gut microbiota, which ferment fiber into short-chain fatty acids such as butyrate. Butyrate is noteworthy because it has energetic and epigenetic functions in colonocytes and tumorsuppressive properties in colorectal-cancer cell lines. We utilized gnotobiotic mouse models colonized with wild-type or mutant strains of a butyrate-producing bacterium to demonstrate that fiber does have a potent tumor-suppressive effect but in a microbiota- and butyrate-dependent manner. Furthermore, due to the Warburg effect, butyrate was metabolized less in tumors where it accumulated and functioned as an HDAC inhibitor to stimulate histone acetylation and affect apoptosis and cell proliferation. To support the relevance of this mechanism in human cancer, we demonstrate that butyrate and histone-acetylation levels are elevated in colorectal adenocarcinomas compared to normal colonic tissues

Bioinformatics tools and database resources for systems genetics analysis in mice—a short review and an evaluation of future needs

During a meeting of the SYSGENET working group ‘Bioinformatics’, currently available software tools and databases for systems genetics in mice were reviewed and the needs for future developments discussed. The group evaluated interoperability and performed initial feasibility studies. To aid future compatibility of software and exchange of already developed software modules, a strong recommendation was made by the group to integrate HAPPY and R/qtl analysis toolboxes, GeneNetwork and XGAP database platforms, and TIQS and xQTL processing platforms. R should be used as the principal computer language for QTL data analysis in all platforms and a ‘cloud’ should be used for software dissemination to the community. Furthermore, the working group recommended that all data models and software source code should be made visible in public repositories to allow a coordinated effort on the use of common data structures and file formats

Leveraging a natural murine meiotic drive to suppress invasive populations

Invasive rodents are a major cause of environmental damage and biodiversity loss, particularly on islands. Unlike insects, genetic biocontrol strategies including populationsuppressing gene drives with biased inheritance have not been developed in mice. Here, we demonstrate a gene drive strategy (tCRISPR) that leverages super-Mendelian transmission of the t haplotype to spread inactivating mutations in a haplosufficient female fertility gene (Prl). Using spatially explicit individual-based in silico modeling, we show that tCRISPR can eradicate island populations under a range of realistic field-based parameter values. We also engineer transgenic tCRISPR mice that, crucially, exhibit biased transmission of the modified t haplotype and Prl mutations at levels our modeling predicts would be sufficient for eradication. This is an example of a feasible gene drive system for invasive alien rodent population control.Luke Gierusa, Aysegul Birandc, Mark D. Buntinga, Gelshan I. Godahewa, Sandra G. Piltz Kevin P. Oh, Antoinette J. Piaggio, David W. Threadgill, John Godwin, Owain Edwards, Phillip Cassey, Joshua V. Ross, Thomas A. A. Prowse and Paul Q. Thoma