One of the antimicrobials seen in the study is triclosan, a commonly used antibacterial ingredient in many personal care products. It is among antimicrobials that will be phased out within the next year from hand and bar soaps, according to a ruling Sept. 2 by the U.S. Food and Drug Administration. The findings of the new study reflect relationships in the dust, not that the antimicrobials are the reason for antibacterial genes being present. "We might be tempted to think of the antimicrobial chemicals as being guilty by association," said Erica M. Hartmann, a postdoctoral fellow at the UO's Biology and the Built Environment Center and Institute of Ecology and Evolution who led the study. She joined the faculty at Northwestern University this month. "We don't really know how the genes or the chemicals got there," she said. "They may have arrived by completely different routes and their being found together is a coincidence. However, we know that antimicrobial chemicals can cause an increase in antibiotic resistance in other situations, so I think these results provide a good reason to take a closer look at what's going on in dust." The FDA's ruling, Hartmann noted, does not yet require that antimicrobials be removed from many other products such as paints, baby toys, bedding, and kitchen utensils. "We don't have solid proof that putting antimicrobials in these products makes them any healthier, but we do know that triclosan in the environment can be harmful," she said. The study, published online ahead of print in the journal Environmental Science & Technology, is the first to document the coexistence of the chemicals and genes in indoor dust. In all, the paper reports six significant associations. Levels of triclosan in dust were determined in collaboration with the Biodesign Center for Environmental Security at Arizona State University. Triclosan has been linked with a gene that alters the ribosome—a complex of RNA and protein in cells that is responsible for RNA translation—in a way that makes bacteria antibiotic resistant. The research team identified several antibiotic-resistance genes, the most common of which conferred resistance to tetracycline antibiotics. "While present at low abundances, together these genes cover resistance to a wide spectrum of antibiotics," the researchers wrote. The chemicals and genes came from 44 samples from 31 varied-use spaces, using vacuum-fitted collectors. The building, completed in 1921, has window ventilation as well as infiltration of outdoor air through cracks around doors and windows. DNA processing involved the UO Genomics Core Facility, and data were processed with assistance from the lab of co-author Curtis Huttenhower of Harvard University's School of Public Health. Despite the findings, Hartmann said, people don't need to be readily alarmed. Antibiotic-resistance genes in the environment, for example, are 10 to 100 times less abundant than in the human gut, she said. In infants, the genes occur naturally in the absence of antibiotics during initial microbial colonization. "Antibiotic resistance is common in a lot of different places," she said. "Just because we find it in a certain building doesn't mean that everyone who goes into that building is going to get a MRSA infection. The building is still as safe as it was before the study, but now we have a better idea of how many antibiotic-resistance genes there are, and we have reason to believe that the amount of antibiotic resistance genes may be tied to the amount of antimicrobial chemicals." Triclosan and antibiotic resistance have been found in other places and in the environment, Hartmann said, but finding them in indoor dust brings the threat loser to home. Median concentrations of triclosan found in the dust were much less than those found as the active ingredient in toothpaste, where it helps to reduce plaque and gum disease. The new FDA ban does not include toothpaste. "The World Health Organization has said that we're underestimating community-acquired antibiotic-resistant infections," she said. "We know that hospitals and other healthcare settings are burdened by antibiotic-resistant pathogens. Homes and other buildings also can contain antibiotic resistance genes and and the use of antimicrobial chemicals in these buildings may be a contributing factor." More information: "Antimicrobial chemicals are associated with elevated antibiotic resistance genes in the indoor dust microbiome" Environmental Science & Technology, pubs.acs.org/doi/abs/10.1021/acs.est.6b00262
News Article | April 9, 2015
Bengaluru-based online furniture and home décor company, Urban Ladder has raised $50 million in a new round of funding. Sequoia Capital led the round along with TR Capital and existing investors Steadview Capital, SAIF Partners and Kalaari Capital. The fresh funds will be used for geographical expansion, investment in technology and hiring. Cofounded in July 2012 by Ashish Goel and Rajiv Srivatsa, the company claims to be on a massive growth path with its distinctive designs and exceptional customer service. Ashish said, Over the last 3 years, we have stayed sharply focused on our design thinking, product quality and customer experience. While these will continue to be important themes, geographical expansion will also be a key focus area this year. We will be present in 30 cities by the end of 2015. The online furniture company has already raised $27 million from Kalaari Capital, SAIF Partners and Steadview Capital in the last 3 years. Ratan Tata, Chairman Emeritus, Tata Group made a personal investment in the company in November 2014. Rajiv accepted that the technology will be a key driver in Urban Ladder’s growth. The company is working on several tech innovations to solve complex furniture e-commerce problems. He said, With over 4000 products and 35 categories, at present, Urban Ladder delivers to 12 cities in India which includes Pune, Cochin Ahmedabad, Chandigarh, Surat, and Mangalore apart from the six metros. Also Read: Quick fact file of the Snapdeal-Freecharge acquisition
Excoffier L.,Institute of Ecology and Evolution |
Excoffier L.,Swiss Institute of Bioinformatics |
Dupanloup I.,Institute of Ecology and Evolution |
Dupanloup I.,Swiss Institute of Bioinformatics |
And 6 more authors.
PLoS Genetics | Year: 2013
We introduce a flexible and robust simulation-based framework to infer demographic parameters from the site frequency spectrum (SFS) computed on large genomic datasets. We show that our composite-likelihood approach allows one to study evolutionary models of arbitrary complexity, which cannot be tackled by other current likelihood-based methods. For simple scenarios, our approach compares favorably in terms of accuracy and speed with ∂a∂i, the current reference in the field, while showing better convergence properties for complex models. We first apply our methodology to non-coding genomic SNP data from four human populations. To infer their demographic history, we compare neutral evolutionary models of increasing complexity, including unsampled populations. We further show the versatility of our framework by extending it to the inference of demographic parameters from SNP chips with known ascertainment, such as that recently released by Affymetrix to study human origins. Whereas previous ways of handling ascertained SNPs were either restricted to a single population or only allowed the inference of divergence time between a pair of populations, our framework can correctly infer parameters of more complex models including the divergence of several populations, bottlenecks and migration. We apply this approach to the reconstruction of African demography using two distinct ascertained human SNP panels studied under two evolutionary models. The two SNP panels lead to globally very similar estimates and confidence intervals, and suggest an ancient divergence (>110 Ky) between Yoruba and San populations. Our methodology appears well suited to the study of complex scenarios from large genomic data sets. © 2013 Excoffier et al.
University of Oregon scientists have found that strength in numbers doesn't hold true for microbes in the intestines. A minority population of the right type might hold the key to regulating good health. The discovery, based on research using zebrafish raised completely germ free, is reported in a paper published in the Nov. 11 issue of Cell Host & Microbe. The findings provide a path to study the function of each bacterial species in the gut and to eventually, perhaps, predict and prevent disease, says lead author Annah S. Rolig, a postdoctoral researcher in the UO's Institute of Molecular Biology. In the project, researchers watched for immune response as isolates of species of bacteria, normally associated with healthy zebrafish, were introduced one at a time and in combination into previously germ-free intestines of the fish. In a telling sequence, one bacterial species, Vibrio, drew numerous neutrophils, which indicated a rapid inflammatory response in one fish. Another species, Shewanella, inserted into a separate germ-free fish barely attracted an immune response. In a third germ-free fish, both species were introduced together and assembled with a ratio of 90- percent Vibrio to 10-percent Shewanella. The inflammatory response in the third fish was completely controlled by the low-abundance species. "Until now, we've only been able to capture proportional information, like you'd see displayed in a pie graph, of the makeup of various microbiota, in percentages of their abundance," Rolig said. "Biologists in this field have typically assumed an equal contribution based on that makeup." Low counts of a bacterial species generally have been discounted in importance, but slight shifts in the ratios of abundant microbe populations have been thought to have roles in obesity, diabetes and inflammatory bowel diseases such as Crohn's disease. That thinking is now changing, Rolig said. "The contribution of each bacterium is not equal. There is a per-capita effect that needs to be considered." The keystone - an important participant that functions to regulate a healthy microbiota - may reside in low-abundant bacterial species. The research team found through additional scrutiny that these species secreted molecules - for now unidentified - that allowed them to dampen the immune response to the whole community. "Now we've shown that these minor members can have a major impact. If we can identify these keystone species, and find that in a disease state one species may be missing, we might be able to go in with a specific probiotic to restore healthy functioning," said Rolig, who also is a scientist in the National Institutes of Health-funded Microbial Ecology and Theory of Animals Center for Systems Biology, known as the META Center, at the UO. To develop a model to capture per-capita contributions of microbes in a population, Rolig and her co-authors -- biology graduate student Adam R. Burns, microbiologist Brendan Bohannan of the Institute of Ecology and Evolution and biologist Karen Guillemin, director of the META Center -- turned to UO physicist Raghuveer Parthasarathy. His math-driven model, detailed in the paper, provides formulas that predict collective inflammatory responses of combinations of bacteria. "I'm really proud of this paper because it exemplifies an achievement of one of the major goals of the META Center for Systems Biology, namely to provide a predictive model of how host-microbe systems function," Guillemin said. "This experimental and modeling framework could be readily generalized to more complex systems such as humans, for example to predict disease severity in individuals with inflammatory bowel disease based on the pro-inflammatory capacity of their gut microbes as assayed in cell culture."
Knop E.,Institute of Ecology and Evolution |
Reusser N.,Institute of Ecology and Evolution
Proceedings of the Royal Society B: Biological Sciences | Year: 2012
Invasive alien species might benefit from phenotypic plasticity by being able to (i) maintain fitness in stressful environments ('robust'), (ii) increase fitness in favourable environments ('opportunistic'), or (iii) combine both abilities ('robust and opportunistic'). Here, we applied this framework, for the first time, to an animal, the invasive slug, Arion lusitanicus, and tested (i) whether it has a more adaptive phenotypic plasticity compared with a congeneric native slug, Arion fuscus, and (ii) whether it is robust, opportunistic or both. During one year, we exposed specimens of both species to a range of temperatures along an altitudinal gradient (700-2400 m a.s.l.) and to high and low food levels, and we compared the responsiveness of two fitness traits: survival and egg production. During summer, the invasive species had a more adaptive phenotypic plasticity, and at high temperatures and low food levels, it survived better and produced more eggs than A. fuscus, representing the robust phenotype. During winter, A. lusitanicus displayed a less adaptive phenotype than A. fuscus. We show that the framework developed for plants is also very useful for a better mechanistic understanding of animal invasions. Warmer summers and milder winters might lead to an expansion of this invasive species to higher altitudes and enhance its spread in the lowlands, supporting the concern that global climate change will increase biological invasions. © 2012 The Royal Society.