Religious but not ethical: The effects of extrinsic religiosity, ethnocentrism and self-righteousness on consumers' ethical judgements

The current research investigates how religiosity can influence unethicality in a consumption context. In particular, considering the link between extrinsic religious orientations and unethicality, this research clarifies why and when extrinsic religiosity leads to unethical decisions. Across two studies, findings show that ethnocentrism is both a mediator (Study 1) and a moderator (Studies 1 and 2) of the effects of extrinsic religiosity on consumers’ ethical judgments. This is because extrinsic religiosity leads to ethnocentrism, and in-group loyalty manifested through ethnocentrism increases support for unethical consumer actions, thus establishing ethnocentrism as a mediator. At the same time, different levels of ethnocentrism can also influence how extrinsic religiosity leads to supporting unethical consumption via self-righteousness, thus establishing ethnocentrism as a moderator. The findings from this research have significant implications for diverse stakeholders who have an interest in religiosity and consumer behavior

Communication: Bubbles, Crystals, and Laser-Induced Nucleation

Short intense laser pulses of visible and infrared light can dramatically accelerate crystal nucleation from transparent solutions; previous studies invoke mechanisms that are only applicable for nucleation of ordered phases or high dielectric phases. However, we show that similar laser pulses induce CO2bubblenucleation in carbonated water. Additionally, in water that is cosupersaturated with argon and glycine, argon bubbles escaping from the water can induce crystal nucleation without a laser. Our findings suggest a possible link between laser-induced nucleation of bubbles and crystals

Mendelian randomization study of adiposity-related traits and risk of breast, ovarian, prostate, lung and colorectal cancer

Background: Adiposity traits have been associated with risk of many cancers in observational studies, but whether these associations are causal is unclear. Mendelian randomization (MR) uses genetic predictors of risk factors as instrumental variables to eliminate reverse causation and reduce confounding bias. We performed MR analyses to assess the possible causal relationship of birthweight, childhood and adult body mass index (BMI), and waist-hip ratio (WHR) on the risks of breast, ovarian, prostate, colorectal and lung cancers. Methods: We tested the association between genetic risk scores and each trait using summary statistics from published genome-wide association studies (GWAS) and from 51 537 cancer cases and 61 600 controls in the Genetic Associations and Mechanisms in Oncology (GAME-ON) Consortium. Results: We found an inverse association between the genetic score for childhood BMI and risk of breast cancer [odds ratio (OR)=0.71 per standard deviation (s.d.) increase in childhood BMI; 95% confidence interval (CI): 0.60, 0.80; P=6.5×10-5). We also found the genetic score for adult BMI to be inversely associated with breast cancer risk (OR=0.66 per s.d. increase in BMI; 95% CI: 0.57, 0.77; P=2.5×10-7), and positively associated with ovarian cancer (OR=1.35; 95% CI: 1.05, 1.72; P=0.017), lung cancer (OR=1.27; 95% CI: 1.09, 1.49; P=2.9×10-3) and colorectal cancer (OR=1.39; 95% CI: 1.06, 1.82, P=0.016). The inverse association between genetically predicted adult BMI and breast cancer risk remained even after adjusting for directional pleiotropy via MR-Egger regression. Conclusions: Findings from this study provide additional understandings of the complex relationship between adiposity and cancer risks. Our results for breast and lung cancer are particularly interesting, given previous reports of effect heterogeneity by menopausal status and smoking status.</p

Connectivity: insights from the U.S. Long Term Ecological Research Network

Ecosystems across the United States are changing in complex and surprising ways. Ongoing demand for critical ecosystem services requires an understanding of the populations and communities in these ecosystems in the future. This paper represents a synthesis effort of the U.S. National Science Foundation-funded Long-Term Ecological Research (LTER) network addressing the core research area of “populations and communities.” The objective of this effort was to show the importance of long-term data collection and experiments for addressing the hardest questions in scientific ecology that have significant implications for environmental policy and management. Each LTER site developed at least one compelling case study about what their site could look like in 50–100 yr as human and environmental drivers influencing specific ecosystems change. As the case studies were prepared, five themes emerged, and the studies were grouped into papers in this LTER Futures Special Feature addressing state change, connectivity, resilience, time lags, and cascading effects. This paper addresses the “connectivity” theme and has examples from the Phoenix (urban), Niwot Ridge (alpine tundra), McMurdo Dry Valleys (polar desert), Plum Island (coastal), Santa Barbara Coastal (coastal), and Jornada (arid grassland and shrubland) sites. Connectivity has multiple dimensions, ranging from multi-scalar interactions in space to complex interactions over time that govern the transport of materials and the distribution and movement of organisms. The case studies presented here range widely, showing how land-use legacies interact with climate to alter the structure and function of arid ecosystems and flows of resources and organisms in Antarctic polar desert, alpine, urban, and coastal marine ecosystems. Long-term ecological research demonstrates that connectivity can, in some circumstances, sustain valuable ecosystem functions, such as the persistence of foundation species and their associated biodiversity or, it can be an agent of state change, as when it increases wind and water erosion. Increased connectivity due to warming can also lead to species range expansions or contractions and the introduction of undesirable species. Continued long-term studies are essential for addressing the complexities of connectivity. The diversity of ecosystems within the LTER network is a strong platform for these studies

Association between Adult Height and Risk of Colorectal, Lung, and Prostate Cancer:Results from Meta-analyses of Prospective Studies and Mendelian Randomization Analyses

Background: Observational studies examining associations between adult height and risk of colorectal, prostate, and lung cancers have generated mixed results. We conducted meta-analyses using data from prospective cohort studies and further carried out Mendelian randomization analyses, using height-associated genetic variants identified in a genome-wide association study (GWAS), to evaluate the association of adult height with these cancers. Methods and Findings: A systematic review of prospective studies was conducted using the PubMed, Embase, and Web of Science databases. Using meta-analyses, results obtained from 62 studies were summarized for the association of a 10-cm increase in height with cancer risk. Mendelian randomization analyses were conducted using summary statistics obtained for 423 genetic variants identified from a recent GWAS of adult height and from a cancer genetics consortium study of multiple cancers that included 47,800 cases and 81,353 controls. For a 10-cm increase in height, the summary relative risks derived from the meta-analyses of prospective studies were 1.12 (95% CI 1.10, 1.15), 1.07 (95% CI 1.05, 1.10), and 1.06 (95% CI 1.02, 1.11) for colorectal, prostate, and lung cancers, respectively. Mendelian randomization analyses showed increased risks of colorectal (odds ratio [OR] = 1.58, 95% CI 1.14, 2.18) and lung cancer (OR = 1.10, 95% CI 1.00, 1.22) associated with each 10-cm increase in genetically predicted height. No association was observed for prostate cancer (OR = 1.03, 95% CI 0.92, 1.15). Our meta-analysis was limited to published studies. The sample size for the Mendelian randomization analysis of colorectal cancer was relatively small, thus affecting the precision of the point estimate. Conclusions: Our study provides evidence for a potential causal association of adult height with the risk of colorectal and lung cancers and suggests that certain genetic factors and biological pathways affecting adult height may also affect the risk of these cancers.</p

Association between Adult Height and Risk of Colorectal, Lung, and Prostate Cancer: Results from Meta-analyses of Prospective Studies and Mendelian Randomization Analyses.

BACKGROUND: Observational studies examining associations between adult height and risk of colorectal, prostate, and lung cancers have generated mixed results. We conducted meta-analyses using data from prospective cohort studies and further carried out Mendelian randomization analyses, using height-associated genetic variants identified in a genome-wide association study (GWAS), to evaluate the association of adult height with these cancers. METHODS AND FINDINGS: A systematic review of prospective studies was conducted using the PubMed, Embase, and Web of Science databases. Using meta-analyses, results obtained from 62 studies were summarized for the association of a 10-cm increase in height with cancer risk. Mendelian randomization analyses were conducted using summary statistics obtained for 423 genetic variants identified from a recent GWAS of adult height and from a cancer genetics consortium study of multiple cancers that included 47,800 cases and 81,353 controls. For a 10-cm increase in height, the summary relative risks derived from the meta-analyses of prospective studies were 1.12 (95% CI 1.10, 1.15), 1.07 (95% CI 1.05, 1.10), and 1.06 (95% CI 1.02, 1.11) for colorectal, prostate, and lung cancers, respectively. Mendelian randomization analyses showed increased risks of colorectal (odds ratio [OR] = 1.58, 95% CI 1.14, 2.18) and lung cancer (OR = 1.10, 95% CI 1.00, 1.22) associated with each 10-cm increase in genetically predicted height. No association was observed for prostate cancer (OR = 1.03, 95% CI 0.92, 1.15). Our meta-analysis was limited to published studies. The sample size for the Mendelian randomization analysis of colorectal cancer was relatively small, thus affecting the precision of the point estimate. CONCLUSIONS: Our study provides evidence for a potential causal association of adult height with the risk of colorectal and lung cancers and suggests that certain genetic factors and biological pathways affecting adult height may also affect the risk of these cancers.US NIH (Grant ID: R37CA070867), Ingram Professorship, Anne Potter Wilson , National Institutes of Health (Grant IDs: R25CA160056-03, U19CA148065, U19CA148107, U19CA148127, U19CA148537, Cancer Research UK, Prostate Cancer UK, The Institute of Cancer Research, Royal Marsden Biomedical Research Centre, National Institute of Health Research (Grant ID: C5047/A17528)This is the final version of the article. It first appeared from the Public Library of Science via http://dx.doi.org/10.1371/journal.pmed.100211