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Blacksburg, VA, United States

Millions of dollars have been spent on insecticides to kill the bugs that have wreaked havoc on everything from hotels in New York City to homes in Los Angeles. But this is the first study to show that overuse of certain insecticides has led to an increased resistance to the compounds, making them much less effective than advertised. "While we all want a powerful tool to fight bed bug infestations, what we are using as a chemical intervention is not working as effectively it was designed and, in turn, people are spending a lot of money on products that aren't working," said Troy Anderson, an assistant professor of entomology in the Virginia Tech College of Agriculture and Life Sciences. Anderson and Alvaro Romero, an assistant professor of entomology at New Mexico State University, published their findings in the Journal of Medical Entomology on Thursday. The two examined the class of insecticides called neonicotinoids, or neonics, which is often paired with pyrethroids in commercial applications to treat bedbugs. "Companies need to be vigilant for hints of declining performance of products that contain neonicotinoids," Romero said. "For example, bedbugs persisting on previously treated surfaces might be an indication of resistance." The researchers conducted their study by comparing bedbugs from homes in Cincinnati and Michigan that had been exposed to neonics with a colony that a researcher has kept isolated since before the insecticide was used. For the last 30 years, the colony has been in an isolated lab run by Harold Harlan with the Armed Forced Pest Management Board. They also examined a pyrethroid-resistant population from New Jersey that had not been exposed to neonics since they were collected in 2008. The bedbugs from Harlan's lab that never have been exposed to neonics died when they were exposed to a very small amount of the insecticide. The New Jersey bedbugs fared slightly better, showing moderate resistance to four different types of neonics. But the bedbugs from Michigan and Cincinnati, which were collected after combinations of insecticides were introduced to the U.S., had much higher levels of resistance to neonics. It only took 0.3 nanograms of a substance called acetamiprid to kill 50 percent of the nonresistant bedbugs from Harlan's lab—but it took more than 10,000 nanograms to kill 50 percent of the Michigan and Cincinnati bedbugs. Just 2.3 nanograms of another substance called imidacloprid was enough to kill 50 percent of Harlan's bedbugs, but it took 1,064 nanograms to kill the Michigan bedbugs and 365 nanograms to kill the Cincinnati bedbugs. Compared with the Harlan control group, the Michigan bedbugs were 462 times more resistant to imidacloprid, 198 times more resistant to dinotefuran, 546 times more resistant to thiamethoxam, and 33,333 times more resistant to acetamiprid. The Cincinnati bedbugs were 163 times more resistant to imidacloprid, 226 times more resistant to thiamethoxam, 358 times more resistant to dinotefuran, and 33,333 times more resistant to acetamiprid. The researchers believe that the detection of neonicotinoid resistance in the New Jersey bedbugs, which were collected before the widespread use of neonics, could be due to pre-existing resistance mechanisms. When exposed to insecticides, bedbugs produce "detoxifying enzymes" to counter them, and the researchers found that the levels of detoxifying enzymes in the New Jersey bedbugs were higher than those of the susceptible Harlan population. "Unfortunately, the insecticides we were hoping would help solve some of our bed bug problems are no longer as effective as they used to be, so we need to reevaluate some of our strategies for fighting them," said Anderson, who is also a researcher at the Fralin Life Science Institute. "If resistance is detected, products with different modes of action need to be considered, along with the use of non-chemical methods," said Romero. More information: "High Levels of Resistance in the Common Bed Bug, Cimex lectularius (Hemiptera: Cimicidae), to Neonicotinoid Insecticides," jme.oxfordjournals.org/lookup/doi/10.1093/jme/tjv253


News Article
Site: http://phys.org/biology-news/

This glue—created when glycoproteins are secreted from a spider's abdomen and interact with the atmosphere—has been studied for the past 12 years by Brent Opell, a professor of biological sciences in the College of Science and a Fralin Life Science Institute affiliate. Material scientists are interested in mimicking this glue—nature's great adhesive—for human products, and rely on biologists to determine factors involved in its creation, as well as its capabilities and limitations. Opell's research team, which included Sarah Stellwagen, a 2015 biological sciences doctoral graduate, and Mary Clouse of Fairfax Station, Virginia, a senior majoring in biological sciences, recently determined that ultraviolet rays, specifically UVB rays, are an important environmental factor in the performance of spider glue. They tested the webs of five local spider species—three that catch prey in broad daylight, and two that hunt at night or in deep forest shade shaded areas. They found that the webs of sun-soaked spiders were far more resistant to UVB rays than the webs of those that hunt in the dark or shade, perhaps indicating an important adaptive trait.The results were published recently in the Journal of Experimental Biology and could inform efforts to develop new adhesives. "Our study adds UVB irradiation to the list of factors known to affect the performance of spider glycoprotein glue, which includes humidity, temperature, and strain rate," Opell said. "It is important to more fully understand these effects as material science moves toward producing environmentally non-toxic and energy conservative adhesives inspired by spider thread glycoprotein." "The work by Opell's research team provides insight on a novel approach used by spiders to withstand UVB light," said Ali Dhinojwala, H.A. Morton Professor in Polymer Science at the University of Akron. "Currently, we add UV stabilizers to prevent degradation of polymers that are exposed to UVB light. Inspired by this study we can learn from the chemistry of spider glue to design new molecules to improve resistance to UVB light." Explore further: Spider web glue spins society toward new biobased adhesives More information: S. D. Stellwagen et al. The impact of UVB radiation on the glycoprotein glue of orb-weaving spider capture thread, Journal of Experimental Biology (2015). DOI: 10.1242/jeb.123067


News Article | June 11, 2016
Site: http://www.techtimes.com/rss/sections/earth.xml

Evolution is part of survival. This rings true for common garter snakes that were found to have evolved to survive on toxic newts. Researchers led by Joel McGlothlin, a Virginia Tech Global Change Center affiliate, have found that several snake species like the common garter snakes are able to prey on poisonous animals such as the rough-skinned newts thanks to a hundred million years of evolution. The snakes' ability to fight toxins produced by the amphibians is due to only one alteration in the gene, which created a domino effect — one genetic change triggers a change in another. Over a period of time, the amino acids acting on three sodium channels present in the snakes' muscles and nerves evolved, allowing some of the snakes to counter the toxicity of the newts. However, the researchers also found that the evolution of resistant muscles can only be possible in species that have the resistant nerves, which evolved about 40 million years before. "Garter snakes and newts are locked in a coevolutionary arms race where as the newts become more toxic, the snakes become more resistant," said McGlothlin, who is also an affiliate of Fralin Life Science Institute and a biological sciences assistant professor at the Virginia Tech College of Science. "However, without the leg-up provided by those resistant nerves, snakes wouldn't have been able to withstand enough toxin to get this whole process started." For their study, the researchers conducted gene sequencing of three sodium channels in 82 species, including 78 snakes, two lizards, one turtle and one bird. Gene mapping revealed when the evolutionary gene started to appear. The researchers noted that the snakes gain more toxin resistance as time passed, with gene changes following a specific order — resistant nerves developing prior to the toxin resistant muscle. "The two nerve channels outside the brain, however, have both evolved resistance to the toxin, and they've done so independently. When we compared the DNA sequences to a closely related lizard, there were changes unique to the snakes that should provide resistance to the toxin," said McGlothlin. They also noted that some species of the birds can prey on toxic newts and still survive. To further understand the pattern, the researchers are planning to study how the birds developed the same resistance. McGlothlin said their study is an important look at the complexity of gene adaptation. The National Science Foundation-funded study will be published in Current Biology on June 20. © 2016 Tech Times, All rights reserved. Do not reproduce without permission.


Cheng Z.,Fralin Life Science Institute | Almeida F.A.,Fralin Life Science Institute
Cell Cycle | Year: 2014

The growing epidemic of type 2 diabetes mellitus (T2DM) and obesity is largely attributed to the current lifestyle of over-consumption and physical inactivity. As the primary platform controlling metabolic and energy homeostasis, mitochondria show aberrant changes in T2DM and obese subjects. While the underlying mechanism is under extensive investigation, epigenetic regulation is now emerging to play an important role in mitochondrial biogenesis, function, and dynamics. In line with lifestyle modifications preventing mitochondrial alterations and metabolic disorders, exercise has been shown to change DNA methylation of the promoter of PGC1α to favor gene expression responsible for mitochondrial biogenesis and function. In this article we discuss the epigenetic mechanism of mitochondrial alteration in T2DM and obesity, and the effects of lifestyle on epigenetic regulation. Future studies designed to further explore and integrate the epigenetic mechanisms with lifestyle modification may lead to interdisciplinary interventions and novel preventive options for mitochondrial alteration and metabolic disorders. © 2014 Landes Bioscience. Source


News Article
Site: http://phys.org/biology-news/

The findings, published in the Proceedings of the National Academy of Sciences today (Monday, March 28) will inform a variety of genetically based mosquito control strategies that focus on creating more males than females. Male mosquitoes do not bite and are harmless to humans, while female mosquitoes bite humans to get the blood they need for egg production. "Thirteen years after the publication of a draft genome of the Anopheles gambiae mosquito, we've finally characterized its Y chromosome," said co-author Zhijian Jake Tu, a professor of biochemistry in the College of Agriculture and Life Sciences and a Fralin Life Science Institute affiliate. "This is one of the last pieces of the puzzle. Having the Y will help us figure out the genetic basis of male biology in future studies." The new information about the Y chromosome will facilitate efforts to reduce female mosquitoes or create sterile males—strategies of interest to research teams across the world. "The Y chromosome had previously not been characterized because it mostly consists of repetitive DNA sequences that stump the algorithms used by computers to assemble the mosquito's entire genetic make-up", said co-author Brantley Hall of Christiansburg, Va., a doctoral student in the genetics, bioinformatics and computational biology program. "We were able to get around this obstacle (at least partially) by using a new long single-molecule sequencing technology, a new bioinformatics algorithm specifically designed to identify Y sequences, and physical mapping of DNA directly to the Y chromosome," said co-author Igor Sharakhov, an associate professor of entomology in the College of Agriculture and Life Sciences and a Fralin Life Science Institute affiliate. "Our study provides a long-awaited foundation for studying mosquito Y chromosome biology and evolution." "Our combined efforts have resulted in the most extensive characterization of Y chromosome to date in additional malaria vectors as well, which will help identify targeted vector control approaches for different species," said co-author Atashi Sharma, a doctoral student in the department of entomology in the College of Agriculture and Life Sciences. The research was in collaboration with Nora Besansky, the Rev. John Cardinal O'Hara C.S.C. professor of biological sciences at the University of Notre Dame. Three graduate students at Virginia Tech were involved in the study, with Brantley Hall and Atashi Sharma being co-first authors on the paper. Xiaofang Jiang, a graduate student in the genetics, bioinformatics, and computational biology and biochemistry, Vladimir Timoshevskiy, a research associate, and Maria Sharakhova, an assistant professor of entomology in the College of Agriculture and Life Sciences, from Virginia Tech also participated in the study. Philippos-Aris Papathanos of the University of Perugia and Changde Cheng of the University of Norte Dame are also co-first authors. Malaria causes as many as 907,000 deaths each year, mostly among children in sub-Saharan Africa. Anopheles mosquitoes, which bite mainly between dusk and dawn, transmit human malaria by spreading Plasmodium parasites that multiply in the human liver and infect red blood cells. Explore further: Mosquito genetics may offer clues to malaria control More information: Radical remodeling of the Y chromosome in a recent radiation of malaria mosquitoes, Proceedings of the National Academy of Sciences, www.pnas.org/cgi/doi/10.1073/pnas.1525164113

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