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Governments ban drug, eliminate toxic corpses to save a vulture population

The overuse of drugs in large-scale agriculture poses a variety of risks to human health. But one that played out in India and the surrounding countries was remarkably indirect: an overabundance of rotting cow carcasses. Thanks to repeated government interventions, the root of that problem—plunging populations of vultures—may finally be on the mend.

The problem started with an anti-inflammatory drug, diclofenac, that was being mass-produced after the patents on it had expired. It found widespread use in veterinary settings in India, Bangladesh, Nepal, and Pakistan. From there, it made its way to the vultures. These birds normally scavenge a large number of cow carcasses that would otherwise end up rotting in the open. Unfortunately, as the drug ended up building up in the vultures, it caused fatal kidney toxicity. Populations of some species plunged to one percent of their historic levels—and the bodies of dead cattle began festering in the countryside.

A perspective in today's issue of Science tracks the efforts involved in saving the vultures. Several of the countries first banned diclofenac in 2006, but that turned out to be only a partial solution. Doses of the drug intended for humans were repurposed for the agricultural market, so further interventions were needed before the contamination problem ended up dropping significantly. Since then, the four nations involved (which are not always on the best terms) have agreed to cooperate to prevent further threats to the vultures.

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A drug that activates only your father’s version of a gene may treat neural disorder

Anyone who's passed basic biology knows that we get one copy of a gene from our mother, a second from our father. But few people realize that not all of these genes end up being treated equally. Imprinted genes are expressed from only the maternal or paternal allele, rather than both. And, when this process goes wrong, it can actually lead to diseases. Now, researchers have identified a possible way to treat imprinting errors.

In the brain, Ube3a is an imprinted gene; only the maternal allele is expressed, even if it is mutated and the paternal allele is normal. This is the case in Angelman syndrome, a severe neurodevelopmental disorder caused by mutation or deletion of the maternal allele of Ube3a. Ube3a is imprinted only in the brain, though; in other tissues, the paternal allele is expressed along with the maternal one. 

This led Benjamin Philpot and his colleagues at UNC Chapel Hill to wonder: wouldn’t it be great if we could get the normal, paternal version of Ube3a to work in the brain—to unsilence it? Maybe this could help kids with Angelman syndrome.

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