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Archive - Nov 15, 2013

Wind Turbines Killed 600,000 Bats in U.S. Last Year by Conservative Estimates

More than 600,000 bats were killed by wind energy turbines in 2012, a serious blow to creatures who pollinate crops and help control flying insects, according to a new study from the University of Colorado (CU) Denver, described in a November 15, 2013 press release from the University. "The development and expansion of wind energy facilities is a key threat to bat populations in North America," said study author Mark Hayes, Ph.D., research associate in integrated biology at CU Denver. "Dead bats are being found underneath wind turbines across North America. The estimate of bat fatalities is probably conservative." The study, which analyzed data on the number of dead bats found at wind turbine sites, will be published next week in the journal BioScience. Dr. Hayes said areas near the Appalachian Mountains like Buffalo, Tennessee, and Mountaineer, West Virginia had the highest bat fatality rates. Little information is available on bat deaths at wind turbine facilities in the Rocky Mountain West or the Sierra Nevadas. The bats are killed when they fly into the towering turbines which spin at up to 179 mph with blades that can stretch 130 feet. Earlier estimates of bat deaths ranged from 33,000 to 880,000. Dr. Hayes said his estimates are likely conservative for two reasons. First, when a range of fatality estimates were reported at a wind facility, he chose the minimum estimate. Secondly, the number of deaths was estimated for just migratory periods, not the entire year, likely leaving out many other fatalities. "The number could be as high as 900,000 dead," he said. There are 45 known bat species in the contiguous U.S., many of which have important economic impacts. Not only do they control flying insects like mosquitoes, they also pollinate commercial crops, flowers, and various cacti.

New Mutations in P. vivax Malaria Parasite May Increase Human Susceptibility

Researchers at Case Western Reserve University and Cleveland Clinic Lerner Research Institute have discovered recent genetic mutations in a parasite that causes over 100 million cases of malaria annually—changes that may render tens of millions of Africans who had been considered resistant, susceptible to infection. Dr. Peter A. Zimmerman, professor of international health, biology, and genetics at the Case Western Reserve School of Medicine, and Dr. David Serre, a scientific staff member of the Genomic Medicine Institute at Lerner and assistant professor of genomics at Case Western Reserve, report their findings at the American Society of Tropical Medicine and Hygiene annual meeting today, Friday, November 15, 2013. They and fellow researchers describe the changes in the Plasmodium vivax genome in papers scheduled to be published in the journal PLoS Neglected Tropical Disease on November 21 and December 5, 2013. To learn the functions of the mutations, and whether the parasite is evolving around a natural defense, Drs. Zimmerman and Serre have received a $3.5 million grant from the National Institute of Allergy and Infectious Disease at the National Institutes of Health. They will begin their field study in early 2014. "We've found a duplication of a gene known to enable the parasite to infect red blood cells and two possible additional components to a more complex red cell invasion mechanism," Dr. Zimmerman said. Researchers have long thought that P. vivax infects a person one way: a protein on the parasite, called the Duffy binding protein, latches onto a Duffy receptor on the surface of the person's red blood cell and works itself through the membrane. People who lack the receptor are called Duffy-negative and are resistant to infection.

Ash Fungus Might Have Mechanism to Define Territory and Combat Viruses

The fungus which causes Chalara dieback of ash trees has the potential to defend itself against virus attacks, research by British scientists has shown. Plant pathologists Dr. Joan Webber, from Forest Research, the research agency of the Forestry Commission, and Professor Clive Brasier found that the defense mechanisms which the Chalara fraxinea (C. fraxinea) fungus uses to defend its territory could make it more resistant to virus-based control methods. Their research findings will be published in the December 2013 issue of Fungal Ecology and are available online now. Professor Brasier and Dr. Webber studied C. fraxinea’s genetic recognition system, called a vegetative compatibility (vc) system, in samples of the fungus from three different UK sites. Their results suggest that for most of these UK samples the fungal colonies are likely to be vegetatively incompatible with each other. This has implications for studying the biology of the fungus and for controlling its spread. Vegetative compatibility (vc) systems are a fungal equivalent of the tissue rejection systems in humans, enabling the fungus to distinguish between self and non-self. Fungal colonies of the same vc-type can fuse to form a single individual, but those of a different vc-type cannot. Vc systems are central to the ecology and survival of a fungus, enabling it to define its territory, to resist viral attack and to promote outbreeding. Initial results show that the vc system of C. fraxinea generates a reaction between incompatible colonies which makes their filaments (the mycelium) collapse, creating a zone between the two colonies where growth is inhibited.