The Name Game: The Importance of Resourcefulness, Ruses, and Recall in Stock Ticker Symbols

Previous research reported that a portfolio of stocks with clever ticker symbols outperformed the overall market by a significant margin during the years 1984 to 2005. This paper reports the performance of those stocks during the subsequent years 2006 to 2018, and also investigates the 2006-2008 performance of a new set of clever-ticker stocks. Both clever-ticker portfolios beat the market by a substantial margin, supporting the resiliency of the clever-ticker phenomenon

Trans Fatty Acids Induce Vascular Inflammation and Reduce Vascular Nitric Oxide Production in Endothelial Cells

Intake of trans fatty acids (TFA), which are consumed by eating foods made from partially hydrogenated vegetable oils, is associated with a higher risk of cardiovascular disease. This relation can be explained by many factors including TFA's negative effect on endothelial function and reduced nitric oxide (NO) bioavailability. In this study we investigated the effects of three different TFA (2 common isomers of C18 found in partially hydrogenated vegetable oil and a C18 isomer found from ruminant-derived—dairy products and meat) on endothelial NF-κB activation and nitric oxide (NO) production. Human endothelial cells were treated with increasing concentrations of Elaidic (trans-C18:1 (9 trans)), Linoelaidic (trans-C18:2 (9 trans, 12 trans)), and Transvaccenic (trans-C18:1 (11 trans)) for 3 h. Both Elaidic and Linoelaidic acids were associated with increasing NF-κB activation as measured by IL-6 levels and phosphorylation of IκBα, and impairment of endothelial insulin signaling and NO production, whereas Transvaccenic acid was not associated with these responses. We also measured superoxide production, which has been hypothesized to be necessary in fatty acid-dependent activation of NF-κB. Both Elaidic acid and Linoelaidic acid are associated with increased superoxide production, whereas Transvaccenic acid (which did not induce inflammatory responses) did not increase superoxide production. We observed differential activation of endothelial superoxide production, NF-κB activation, and reduction in NO production by different C18 isomers suggesting that the location and number of trans double bonds effect endothelial NF-κB activation

Identification of novel risk loci, causal insights, and heritable risk for Parkinson's disease: a meta-analysis of genome-wide association studies

Background Genome-wide association studies (GWAS) in Parkinson's disease have increased the scope of biological knowledge about the disease over the past decade. We aimed to use the largest aggregate of GWAS data to identify novel risk loci and gain further insight into the causes of Parkinson's disease. Methods We did a meta-analysis of 17 datasets from Parkinson's disease GWAS available from European ancestry samples to nominate novel loci for disease risk. These datasets incorporated all available data. We then used these data to estimate heritable risk and develop predictive models of this heritability. We also used large gene expression and methylation resources to examine possible functional consequences as well as tissue, cell type, and biological pathway enrichments for the identified risk factors. Additionally, we examined shared genetic risk between Parkinson's disease and other phenotypes of interest via genetic correlations followed by Mendelian randomisation. Findings Between Oct 1, 2017, and Aug 9, 2018, we analysed 7·8 million single nucleotide polymorphisms in 37 688 cases, 18 618 UK Biobank proxy-cases (ie, individuals who do not have Parkinson's disease but have a first degree relative that does), and 1·4 million controls. We identified 90 independent genome-wide significant risk signals across 78 genomic regions, including 38 novel independent risk signals in 37 loci. These 90 variants explained 16–36% of the heritable risk of Parkinson's disease depending on prevalence. Integrating methylation and expression data within a Mendelian randomisation framework identified putatively associated genes at 70 risk signals underlying GWAS loci for follow-up functional studies. Tissue-specific expression enrichment analyses suggested Parkinson's disease loci were heavily brain-enriched, with specific neuronal cell types being implicated from single cell data. We found significant genetic correlations with brain volumes (false discovery rate-adjusted p=0·0035 for intracranial volume, p=0·024 for putamen volume), smoking status (p=0·024), and educational attainment (p=0·038). Mendelian randomisation between cognitive performance and Parkinson's disease risk showed a robust association (p=8·00 × 10−7). Interpretation These data provide the most comprehensive survey of genetic risk within Parkinson's disease to date, to the best of our knowledge, by revealing many additional Parkinson's disease risk loci, providing a biological context for these risk factors, and showing that a considerable genetic component of this disease remains unidentified. These associations derived from European ancestry datasets will need to be followed-up with more diverse data. Funding The National Institute on Aging at the National Institutes of Health (USA), The Michael J Fox Foundation, and The Parkinson's Foundation (see appendix for full list of funding sources)

Genetic Variation in Antimicrobial Activity of Honey Bee (Apis mellifera) Seminal Fluid

Honey bees can host a remarkably large number of different parasites and pathogens, and some are known drivers of recent declines in wild and managed bee populations. Here, we studied the interactions between the fungal pathogen Nosema apis and seminal fluid of the Western honey bee (Apis mellifera). Honey bee seminal fluid contains multiple antimicrobial molecules that kill N. apis spores and we therefore hypothesized that antimicrobial activities of seminal fluid are genetically driven by interactions between honey bee genotype and different N. apis strains/ecotypes, with the virulence of a strain depending on the genotype of their honey bee hosts. Among the antimicrobials, chitinases have been found in honey bee seminal fluid and have the predicted N. apis killing capabilities. We measured chitinase activity in the seminal fluid of eight different colonies. Our results indicate that multiple chitinases are present in seminal fluid, with activity significantly differing between genotypes. We therefore pooled equal numbers of N. apis spores from eight different colonies and exposed subsamples to seminal fluid samples from each of the colonies. We infected males from each colony with seminal fluid exposed spore samples and quantified N. apis infections after 6 days. We found that host colony had a stronger effect compared to seminal fluid treatment, and significantly affected host mortality, infection intensity and parasite prevalence. We also found a significant effect of treatment, as well as a treatment x colony interaction when our data were analyzed ignoring cage as a blocking factor. Our findings provide evidence that N. apis-honey bee interactions are driven by genotypic effects, which could be used in the future for breeding purposes of disease resistant or tolerant honey bee stock.ISSN:2296-701

Synergistic effects of pathogen and pesticide exposure on honey bee (Apis mellifera) survival and immunity

Declines in native insect pollinator populations and substantial losses in managed honey bees have been reported on a global scale and become a widespread concern because of the importance of these insects for human food production and ecosystem stability. Several potential factors have been studied as possible causes of declining pollinator health, such as parasites and pathogens, exposure to agricultural pesticides, habitat loss and/or climate change. More recently, a combination of these factors rather than a single cause have been blamed for observed pollinator losses, but field studies of such interactions are challenging, especially in the presence of confounding environmental stressors. We therefore examined the impact of single and combined stressors on the honey bee (Apis mellifera) in a generally healthy Australian population. We exposed workers during their larval development and drones until they reached sexual maturity to the neonicotinoid pesticide Thiamethoxam, at concentrations more than 20 times lower than we initially measured in the field, the microsporidian gut pathogen Nosema apis or both stressors at the same time. We found that simultaneous exposure significantly reduced bee health. We observed a substantial increase in mortality and a reduction of immunocompetence in workers exposed to both the pathogen and the pesticide. We conclude that the exposure of generally healthy bees to multiple environmental stressors results in synergistic effects where the effects are expected to negatively impact performance and could be sufficient to trigger colony collapse. We found that the vast majority of males did not survive to sexual maturity after exposure to very low levels of Thiamethoxam. This would not only reduce the reproductive success of individual colonies, but can also impact gene flow and genetic diversity at the population level, which are both known as key components of honey bee health

Cumulative Effects of Spontaneous Mutations for Fitness in Caenorhabditis: Role of Genotype, Environment and Stress

It is often assumed that the mutation rate is an evolutionarily optimized property of a taxon. The relevant mutation rate is for mutations that affect fitness, U, but the strength of selection on the mutation rate depends on the average effect of a mutation. Determination of U is complicated by the possibility that mutational effects depend on the particular environmental context in which the organism exists. It has been suggested that the effects of deleterious mutations are typically magnified in stressful environments, but most studies confound genotype with environment, so it is unclear to what extent environmental specificity of mutations is specific to a particular starting genotype. We report a study designed to separate effects of species, genotype, and environment on the degradation of fitness resulting from new mutations. Mutations accumulated for >200 generations at 20° in two strains of two species of nematodes that differ in thermal sensitivity. Caenorhabditis briggsae and C. elegans have similar demography at 20°, but C. elegans suffers markedly reduced fitness at 25°. We find little evidence that mutational properties differ depending on environmental conditions and mutational correlations between environments are close to those expected if effects were identical in both environments

Mutational Bias for Body Size in Rhabditid Nematodes

Mutational bias is a potentially important agent of evolution, but it is difficult to disentangle the effects of mutation from those of natural selection. Mutation-accumulation experiments, in which mutations are allowed to accumulate at very small population size, thus minimizing the efficiency of natural selection, are the best way to separate the effects of mutation from those of selection. Body size varies greatly among species of nematode in the family rhabditidae; mutational biases are both a potential cause and a consequence of that variation. We report data on the cumulative effects of mutations that affect body size in three species of rhabditid nematode that vary fivefold in adult size. Results are very consistent with previous studies of mutations underlying fitness in the same strains: two strains of Caenorhabditis briggsae decline in body size about twice as fast as two strains of C. elegans, with a concomitant higher point estimate of the genomic mutation rate; the confamilial Oscheius myriophila is intermediate. There is an overall mutational bias, such that mutations reduce size on average, but the bias appears consistent between species. The genetic correlation between mutations that affect size and those underlying fitness is large and positive, on average