Tuesday, March 31, 2015
Monday, March 30, 2015
Sunday, March 29, 2015
Bee pesticide study furore is called a 'scandal' - environment - 27 March 2015 - New Scientist#.VRe24_lQOM5
Do neonicotinoid pesticides kill bumblebees? We still don't know, but the latest research is alarming – and casts doubt on the integrity of science.
The study, by Helen Thompson of the government's Food and Environment Research Agency, found "no clear consistent relationships" between pesticide residues and measures of the health of bee colonies, such as the number of new queens. "The absence of these effects is reassuring but not definitive," she said.
But Dave Goulson of the University of Sussex in Brighton has reanalysed the data and says that in fact the results "strongly suggest that wild bumblebee colonies in farmland can be expected to be adversely affected by exposure to neonicotinoids".
"This is a scandal," said Matt Shardlow of the charity Buglife, which has campaigned on the issue. "The scientific process appears to have been deliberately manipulated to agree with the environment secretary's views."
Thompson now works for agribusiness Syngenta, which manufactures some pesticides. She was not willing to speak on the record to New Scientist about Goulson's conclusions, but is understood to have submitted a new study on the issue for publication.
Saturday, March 28, 2015
In an age when commercial competition is only a click away, the new mandate is to make products and services that generate compulsive behavior: in essence, to get users hooked on a squirt of dopamine to the brain’s reward center to ensure that they’ll come back.”
It starts with a trigger, a prod that propels users into a four-step loop. Think of the e-mail notification you get when a friend tags you in a photo on Facebook. The trigger prompts you to take an action—say, to log in to Facebook. That leads to a reward: viewing the photo and reading the comments left by others. In the fourth step, you inject a personal stake by making an investment: say, leaving your own comment in the thread. This pattern, Eyal says, kicks off a cycle that lodges behaviors in the basal ganglia, the part of the brain where automatic behaviors are stored and where, according to neuroscientists, they last a lifetime.
The hook’s final stage, investment, closes the loop by “loading the next trigger,” Eyal says, an idea inspired in part by work on game psychology by Jesse Schell, a Disney Imagineer turned Carnegie Mellon professor. Take Twitter. When you make an investment by posting a tweet, a follower’s reply to your contribution triggers an e-mail notification to your in-box, inciting you to take yet another spin through the cycle.
Enzyme Families--Shared Evolutionary History or Shared Design? A Study of the GABA-Aminotransferase FamilyMariclair A. Reeves, Ann K. Gauger, Douglas D. Axe
AbstractThe functional diversity of enzyme families is thought to have been caused by repeated recruitment events--gene duplications followed by conversions to new functions. However, mathematical models show this can only work if beneficial new functions are achievable by just one or two base changes in the duplicate genes. Having found no convincing demonstration that this is feasible, we previously chose a highly similar pair of E. coli enzymes from the GABA-aminotransferase-like (GAT) family, 2-amino-3-ketobutyrate CoA ligase (Kbl2) and 8-amino-7-oxononanoate synthase (BioF2), and attempted to convert the first to perform the function of the second by site-directed mutagenesis. In the end we were unable to achieve functional conversion by that rational approach. Here we take a complementary approach based on random mutagenesis. Focusing first on single mutations, we prepared mutated libraries of nine genes from the GAT family and tested for BioF2 function in vivo. None of the singly mutated genes had this function. Focusing next on double mutations, we prepared and tested 70% of the 6.5 million possible mutation pairs for Kbl2 and for BIKB, an enzyme described as having both Kbl2 and BioF2 activities in vitro. Again, no BioF2 activity was detected in vivo. Based on these results, we conclude that conversion to BioF2 function would require at least two changes in the starting gene and probably more, since most double mutations do not work for two promising starting genes. The most favorable recruitment scenario would therefore require three genetic changes after the duplication event: two to achieve low-level BioF2 activity and one to boost that activity by overexpression. But even this best case would require about 10^15 years in a natural population, making it unrealistic. Considering this along with the whole body of evidence on enzyme conversions, we think structural similarities among enzymes with distinct functions are better interpreted as supporting shared design principles than shared evolutionary histories.
Physiology is rocking the foundations of evolutionary biology
Denis Noble Department of Physiology, Anatomy & Genetics, Oxford, UK
The ‘Modern Synthesis’ (Neo-Darwinism) is amid-20th century gene-centric view of evolution, based on randommutations accumulating to produce gradual change through natural selection. Any role of physiological function in influencing genetic inheritance was excluded. The organism became a mere carrier of the real objects of selection, its genes. We now know that genetic change is far from random and often not gradual. Molecular genetics and genome sequencing have deconstructed this unnecessarily restrictive view of evolution in a way that reintroduces physiological function and interactions with the environment as factors influencing the speed and nature of inherited change. Acquired characteristics can be inherited, and in a few but growing number of cases that inheritance has nowbeen shown to be robust formany generations. The 21st century can look forward to a new synthesis that will reintegrate physiology with evolutionary biology.