2011 German Escherichia coli outbreak: Alignment-free whole-genome phylogeny by feature frequency profiles

Accuracy of SNP-based whole-genome phylogeny reconstruction relies heavily on quality of sequence alignment which is particularly hindered by poorly assembled genomes. Alignment-free methods might provide additional insights. Here, we constructed a whole-genome phylogeny of 9 E.coli isolates from the 2011 German outbreak against existing E. coli genomes using the alignment-free feature frequency profile method. In addition, we looked for gene elements that distinguish the outbreak group from the other E. coli strains and possibly accounted for the emergence of the outbreak isolates using the distinguishing feature analysis

THE VALIDITY OF USING VIRTUAL REALITY HEAD-MOUNTED DISPLAY FOR AGILITY TRAINING

Virtual reality (VR) provides a fully controlled environment with the potential of making sports training easier. However, to date very few studies concerned creating a locomotion training environment enabling multi-directional movements for mimicking realistic locomotion. This study aims to investigate the validity of using low-cost VR head-mounted display (HMD) for agility training in a virtual environment (VE) for ‘real-walking’ locomotion. Three male college participants (age: 24.00±1.00years, height: 1.68±0.09m, weight: 65.63±4.65kg) participated in this study. They were asked to complete two agility ladder training tasks: the forward and backward icky shuffle, in the real environment (RE) and VE. The correlations of the segment trajectories in the RE and VE were calculated, respectively. Moreover, the correlations of the segment trajectories between the two environments were also calculated. The z-test results show that no significant difference has been obtained in the consistency of the movements between the two environments. Also, high correlations in the segment trajectories were obtained between the virtual and real training environment. The results indicate that it is feasible to use VR HMD for agility training

2011 German Escherichia coli O104:H4 outbreak: whole-genome phylogeny without alignment

<p>Abstract</p> <p>Background</p> <p>A large-scale <it>Escherichia coli </it>O104:H4 outbreak occurred in Germany from May to July 2011, causing numerous cases of hemolytic-uremic syndrome (HUS) and deaths. Genomes of ten outbreak isolates and a historical O104:H4 strain isolated in 2001 were sequenced using different new generation sequencing platforms. Phylogenetic analyses were performed using various approaches which either are not genome-wide or may be subject to errors due to poor sequence alignment. Also, detailed pathogenicity analyses on the 2001 strain were not available.</p> <p>Findings</p> <p>We reconstructed the phylogeny of <it>E. coli </it>using the genome-wide and alignment-free feature frequency profile method and revealed the 2001 strain to be the closest relative to the 2011 outbreak strain among all available <it>E. coli </it>strains at present and confirmed findings from previous alignment-based phylogenetic studies that the HUS-causing O104:H4 strains are more closely related to typical enteroaggregative <it>E. coli </it>(EAEC) than to enterohemorrhagic <it>E. coli</it>. Detailed re-examination of pathogenicity-related virulence factors and secreted proteins showed that the 2001 strain possesses virulence factors shared between typical EAEC and the 2011 outbreak strain.</p> <p>Conclusions</p> <p>Our study represents the first attempt to elucidate the whole-genome phylogeny of the 2011 German outbreak using an alignment-free method, and suggested a direct line of ancestry leading from a putative EAEC-like ancestor through the 2001 strain to the 2011 outbreak strain.</p

2011 German Escherichia coli outbreak: Prophage analysis of close-assembled TY2482 against 55989 using PHAST

Using the Hiseq data of the German E. coli outbreak isolate TY2482, preliminary prophage analyses have been performed by some researchers previously. With the closed assembly of the same isolate being available, another round of analysis might help in resolving questions that remain unclear due to the incompleteness of the dataset

Immunoprotection against influenza H5N1 virus by oral administration of enteric-coated recombinant Lactococcus lactis mini-capsules

AbstractEdible vaccines that can be made widely available and easily administered could bring great benefit to the worldwide battle against pandemic viral infections. They can be used not only for the vaccination of humans and domesticated animals, but also for wild herds and live stock which are otherwise difficult to vaccinate. In this study, we report the development of an edible mini-capsule form of live, non-persisting, recombinant Lactococcus lactis (L. lactis) vaccine against the highly virulent influenza H5N1 strain. Recombinant L. lactis-based H5N1 HA antigen expression constructs were made and shown to be able to induce higher levels of HA-specific serum IgG and fecal IgA antibody production after oral administration. The vectors were then formulated into a mini-capsule dosage form and fed to mouse. Four doses of oral administration rendered complete protection of the mouse against lethal challenges of H5N1 virus

Methylation of the oxytocin receptor gene mediates the effect of adversity on negative schemas and depression

Building upon various lines of research, we posited that methylation of the oxytocin receptor gene (OXTR) would mediate the effect of adult adversity on increased commitment to negative schemas and in turn the development of depression. We tested our model using structural equation modeling and longitudinal data from a sample of 100 middle-aged, African American women. The results provided strong support for the model. Analysis of the 12 CpG sites available for the promoter region of the OXTR gene identified four factors. One of these factors was related to the study variables, whereas the others were not. This factor mediated the effect of adult adversity on schemas relating to pessimism and distrust, and these schemas, in turn, mediated the impact of OXTR methylation on depression. All indirect effects were statistically significant, and they remained significant after controlling for childhood trauma, age, romantic relationship status, individual differences in cell types, and average level of genome-wide methylation. These finding suggest that epigenetic regulation of the oxytocin system may be a mechanism whereby the negative cognitions central to depression become biologically embedded

The effect of neighborhood disadvantage, social ties, and genetic variation on the antisocial behavior of African American women: A multilevel analysis

Social disorganization theory posits that individuals who live in disadvantaged neighborhoods are more likely to engage in antisocial behavior than are those who live in advantaged neighborhoods and that neighborhood disadvantage asserts this effect through its disruptive impact on social ties. Past research on this framework has been limited in two respects. First, most studies have concentrated on adolescent males. In contrast, the present study focused on a sample of adult African American females. Second, past research has largely ignored individual-level factors that might explain why people who grow up in disadvantaged neighborhoods often do not engage in antisocial behavior. We investigated the extent to which genetic variation contributes to heterogeneity of response to neighborhood conditions. We found that the impact of neighborhood disadvantage on antisocial behavior was mediated by neighborhood social ties. Further, the analysis indicated that the effects of neighborhood disadvantage and social ties on antisocial behavior were moderated by genetic polymorphisms. Examination of these moderating effects provided support for the differential susceptibility model of Gene × Environment. The effect of Gene × Neighborhood Disadvantage on antisocial behavior was mediated by the effect of Gene × Neighborhood Social Ties, providing support for an expanded view of social disorganization theory

Methylation of MTHFR Moderates the Effect of Smoking on Genomewide Methylation Among Middle Age African Americans

Differential methylation at MTHFR (mMTHFR) has been examined previously as a moderator of changes in methylation among nascent smokers, but the effects of mMTHFR on genomewide patterns of methylation among established smokers in middle age are unknown. In the current investigation we examined a sample of 180 African American middle-aged smokers and non-smokers to test for patterns indicative of three different potential mechanisms of impact on epigenetic remodeling in response to long-term smoking. We found that mMTHFR moderated the association between smoking and changes in methylation for more than 25% of the 909 loci previously identified as being associated with smoking at a genomewide level of significance in middle-aged African Americans. Observed patterns of effect indicated amplification of both hyper and hypo methylating responses to smoking among those with lower mMTHFR. Moderating effects were robust to controls for sex, age, diet, and cell-type variation. Implications for potential mechanisms conferring effects are discussed. Of particular potential practical importance was a strong effect of mMTHFR on hypomethylation at GPR15 in response to smoking, indicative of the differential impact of MTHFR activity on changes in a specific cell population linked to inflammatory disease in smokers

Stress, relationship satisfaction, and health among African American women: Genetic moderation of effects

We examined whether romantic relationship satisfaction would serve as a link between early and later stressors which in turn would influence the Thyroid Function Index (TFI), an indicator of physiological stress response. Using the framework of genetic susceptibility theory combined with hypotheses derived from the vulnerability-stress-adaptation and stress-generation models, we tested whether the hypothesized mediational model would be conditioned by 5-HTTLPR genotype, with greater effects and stronger evidence of mediation among carriers of the “s” allele. In a sample of African American women in romantic relationships (n = 270), we found that 5-HTTLPR moderated each stage of the hypothesized mediational model in a “for better or for worse” manner. That is genetic polymorphisms function to exacerbate not only the detrimental impact of negative environments (i.e. “for worse effects”) but also the beneficial impact of positive environments (i.e. “for better effects”). The effect of early stress on relationship satisfaction was greater among carriers of the “short” allele than among those who did not carry the short allele, and was significantly different in both the “for better” and “for worse” direction. Likewise, the effect of relationship satisfaction on later stressors was moderated in a “for better” or “for worse” manner. Finally, impact on physiological stress, indexed using TFI level, indicated that the impact of later stressors on TFI level was greater in the presence of the short allele, and also followed a “for better” or “for worse” pattern. As expected, the proposed mediational model provided a better fit for “s” allele carriers

Economic hardship and biological weathering: The epigenetics of aging in a U.S. sample of black women

Background—Past research has linked low socio-economic status (SES) to inflammation, metabolic dysregulation, and various chronic and age-related diseases such as type 2 diabetes, coronary heart disease, stroke, and dementia. These studies suggest that the challenges and adversities associated with low SES may result in premature aging and increased risk of morbidity and mortality. Objective—Building upon this research, the present study investigates additional avenues whereby low income might accelerate biological aging. Methods—Structural equation modeling and longitudinal data from a sample of 100 Black, middle-aged women residing in the United States was used to investigate the effect of income on a recently developed epigenetic measure of biological aging. This measure can be used as a “biological clock” to assess, at any point during adulthood, the extent to which an individual is experiencing accelerated or decelerated biological aging. Results—Low income displayed a robust association with accelerated aging that was unaffected after controlling for other SES-related factors such as education, marital status, and childhood adversity. Further, our analyses indicated that the association between income and biological aging was not explained by health-related behaviors such as diet, exercise, smoking, alcohol consumption, or having health insurance. Rather, in large measure, it was financial pressure (difficulty paying bills, buying necessities, or meeting daily expenses) that accounted for the association between low income and accelerated aging. Conclusions—These findings support the view that chronic financial pressures associated with low income exerts a weathering effect that results in premature aging