Hudson’s team is focusing on the state of matter that exists at temperatures just above the temperature at which materials start to superconduct. This state, known as the pseudogap, is poorly understood, but physicists have long believed that characterizing the pseudogap is important to understanding superconductivity.
In their latest work, published online on July 6 in Nature Physics, they suggest that the pseudogap is not a precursor to superconductivity, as has been theorized, but a competing state. If that is true, it could completely change the way physicists look at superconductivity, said Hudson.
“Now, if you want to explain high-temperature superconductivity and you believe the pseudogap is a precursor, you need to explain both. If it turns out that it is a competing state, you can instead focus more on superconductivity,” he said.
Until recently that would also have been the opinion of most scientists. Genes, it was thought, were highly resilient. Even if people did wreck their own DNA through bad diet, smoking and getting fat, that damage was unlikely to be passed to future generations.
Now, however, those assumptions are being re-examined. At the heart of this revolution is a simple but controversial idea: that DNA can be modified or imprinted with the experiences of your parents and grandparents.
According to this new science, known as epigenetics, your ancestors’ diet, smoking habits, exposure to pollutants and levels of obesity could be affecting you today. In turn, your lifestyle could affect your children and grandchildren.
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If we drink heavily, take drugs, get fat or wait too long to reproduce, then epigenetics might start tying up some of the wrong genes and loosening the bonds on others. Sometimes those changes will affect sperm and egg cells.
This mystery bug has not been seen in the UK before and has made the Natural History Museum’s Wildlife Garden its home. The tiny bug is baffling insect experts at the Museum who are still trying to identify the mystery newcomer. The almond-shaped bug is red and black and about the size of a grain of rice
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Experts checked the new bug with those in the Museum’s national insect collection of more than 28 million specimens. Amazingly, there is no exact match.
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The bug closely resembles the fairly rare species Arocatus roeselii, which is usually found in central Europe. However, the roeselii bugs are brighter red than this new bug and they are usually associated with alder trees rather than plane trees.
However, the National Museum in Prague discovered an exact match to the mystery bug in their collections – an insect that was found in Nice and is classified as Arocatus roeselii. ‘There are two possible explanations,’ explains Barclay. ‘That the bug is roeselii and by switching to feed on the plane trees it could suddenly become more abundant, successful and invasive. The other possibility is that the insect in our grounds may not be roeselii at all.’
The Museum is working with international colleagues to analyse the bug’s body shape, form and DNA to see whether it is a newly discovered species or if it is in fact Arocatus roeselii.
The water became as acidic as lemon juice, creating a toxic brew of heavy metal poisons including arsenic, lead, and zinc. No fish live there, and no plants line the shores. There aren’t even any insects buzzing about. The Berkeley Pit had become one of the deadliest places on earth, too toxic even for microorganisms. Or so it was thought.
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the researchers identified it as Euglena mutabilis, a protozoan which has the remarkable ability of being able to survive in the toxic waters of the Berkeley Pit by altering its local environment to something more hospitable. Through photosynthesis, it increases the oxygen level in the water, which causes dissolved metals to oxidize and precipitate out. In addition, it pulls iron out of the water and sequesters it inside of itself. This makes it a classic example of an extremophile.
I post often on examples of scientific inquiry in action. I think it is an important way to see how science works while searching for answers. The process is not a simple one, but after a solution is found it can often be presented as obvious. But while trying to find answers it is quite difficult.
But the success of Prozac hasn’t simply transformed the treatment of depression: it has also transformed the science of depression. For decades, researchers struggled to identify the underlying cause of depression, and patients were forced to endure a series of ineffective treatments. But then came Prozac. Like many other antidepressants, Prozac increases the brain’s supply of serotonin, a neurotransmitter. The drug’s effectiveness inspired an elegant theory, known as the chemical hypothesis: Sadness is simply a lack of chemical happiness. The little blue pills cheer us up because they give the brain what it has been missing.
There’s only one problem with this theory of depression: it’s almost certainly wrong, or at the very least woefully incomplete. Experiments have since shown that lowering people’s serotonin levels does not make them depressed, nor does it does not make them depressed, nor does it worsen their symptoms if they are already depressed.
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In this sense, Prozac is simply a bottled version of other activities that have a similar effect, such as physical exercise.
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It is jarring to think of depression in terms of atrophied brain cells, rather than an altered emotional state. It is called “depression,” after all. Yet these scientists argue that the name conceals the fundamental nature of the illness, in which the building blocks of the brain – neurons – start to crumble. This leads, over time, to the shrinking of certain brain structures, like the hippocampus, which the brain needs to function normally.
A few weeks ago we posted about Tracking Down Tomato Troubles as another example of the challenges of scientific inquiry. Too often, in the rare instances that science is even discussed in the news, the presentation provides the illusion of simple obvious answers. Instead it is often a very confusing path until the answers are finally found (posts on scientific investigations in action). At which time it often seems obvious what was going on. But to get to the solutions we need dedicated and talented scientists to search for answers.
Federal investigators retraced their steps Monday as suspicions mount that fresh unprocessed tomatoes aren’t necessarily causing the salmonella outbreak that has sickened hundreds across the USA.
Three weeks after the Food and Drug Administration warned consumers to avoid certain types of tomatoes linked to the salmonella outbreak, people are still falling ill, says Robert Tauxe with the Centers for Disease Control and Prevention. The latest numbers as of Monday afternoon were 851 cases, some of whom fell ill as recently as June 20, says Tauxe, deputy director of the CDC’s division of foodborne diseases.
The CDC launched a new round of interviews over the weekend. “We’re broadening the investigation to be sure it encompasses food items that are commonly consumed with tomatoes,” Tauxe says. If another food is found to be the culprit after tomatoes were recalled nationwide and the produce industry sustained losses of hundreds of millions of dollars, food safety experts say the public’s trust in the government’s ability to track foodborne illnesses will be shattered.
“It’s going to fundamentally rewrite how we do outbreak investigations in this country,” says Michael Osterholm of the Center for Infectious Disease Research and Policy at the University of Minnesota. “We can’t let this investigation, however it might turn out, end with just the answer of ‘What caused it?’ We need to take a very in-depth look at foodborne disease investigation as we do it today.”
I am inclined to believe the FDA is not enough focused on food safety. Perhaps we are not funding it enough, but we sure are spending tons of money on something so I can’t believe more money needs to be spent. Maybe just fewer bills passed (that the politicians don’t even bother to read) with favors to special interests instead of funding to support science and food safety. Or perhaps we are funding enough (though I am skeptical of this contention) and we just are not allowing food safety to get in the way of what special interests want (so we fund plenty for FDA to have managed this much better, to have systems in place that would provide better evidence but they are either prevented from doing so or failed to do so). I am inclined to believe special interests have more sway in agencies like (NASA, EPA, FDA…) than the public good and scientific openness – which is very sad. And, it seems to me, politicians have overwhelmingly chosen not to support more science in places like FDA, CDC, NIH… while increasing federal spending in other areas dramatically.
For the new study, researchers first collected DNA samples collected in 1991 and again between 2002 and 2006 from 600 participants already enrolled in the AGES Reykjavik Study. The AGES study is renowned for its value to genetics research because of the historic isolation and reduced number of genetic “variables” among Iceland’s population, making certain patterns of genetic information easier to identify.
Among the 600, the research team measured the total amount of DNA methylation in each of 111 samples and compared total methylation from DNA collected in 2002 to 2005 to that person’s DNA collected in 1991.
They discovered that in almost one-third of the subjects, methylation changed over that 11-year span, with some gaining DNA methylation and others losing it.
“The key thing this part of the study told us is that levels changed over time, proof of principle that an individual’s epigenetic profile does change with age,” said M. Daniele Fallin, Ph.D., an associate professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health.
Still a puzzle, though, was why or how, Fallin said, “so we wondered whether the tendency to those changes was also inherited, right along with our DNA sequences. That would explain why certain families are more susceptible to certain diseases.”
Foldit is a revolutionary new computer game enabling you to contribute to important scientific research. This is another awesome combination of technology, distributed problem solving, science education…
Essentially the game works by allowing the person to make some decisions then the computer runs through some processes to determine the result of those decisions. It seems the human insight of what might work provides an advantage to computers trying to calculate solutions on their own. Then the results are compared to the other individuals working on the same protein folding problem and the efforts are ranked.
This level of interaction is very cool. SETI@home, Rosetta@home and the like are useful tools to tap the computing resources of millions on the internet. But the use of human expertise really makes fold.it special. And you can’t help but learn by playing. In addition, if you are successful you can gain some scientific credit for your participation in new discoveries.
Proteins are the workhorses in every cell of every living thing. Your body is made up of trillions of cells, of all different kinds: muscle cells, brain cells, blood cells, and more. Inside those cells, proteins are allowing your body to do what it does: break down food to power your muscles, send signals through your brain that control the body, and transport nutrients through your blood. Proteins come in thousands of different varieties, but they all have a lot in common. For instance, they’re made of the same stuff: every protein consists of a long chain of joined-together amino acids.
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structure specifies the function of the protein. For example, a protein that breaks down glucose so the cell can use the energy stored in the sugar will have a shape that recognizes the glucose and binds to it (like a lock and key) and chemically reactive amino acids that will react with the glucose and break it down to release the energy.
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Proteins are involved in almost all of the processes going on inside your body: they break down food to power your muscles, send signals through your brain that control the body, and transport nutrients through your blood. Many proteins act as enzymes, meaning they catalyze (speed up) chemical reactions that wouldn’t take place otherwise. But other proteins power muscle contractions, or act as chemical messages inside the body, or hundreds of other things.
David Acheson is the nation’s top food detective, but so far he has met his match in the wily tomato.
With the salmonella scare that has plagued tomatoes, Acheson has faced perhaps his biggest test—at least as far as outbreaks of illness go—since he assumed the newly created “food safety czar” post at the U.S. Food and Drug Administration about a year ago.
That position was born amid a growing concern that the FDA couldn’t get a grip on food safety, as tales of food-borne illnesses multiplied. Now comes salmonella-laden tomatoes that have sickened at least 277 people nationwide, hospitalizing 43.
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The FDA concluded that the tainted tomatoes most likely came from Mexico or a certain part of Florida. The agency managed to narrow down the possible origins of the tainted tomatoes largely by a process of elimination. Based on the timing of their growing seasons and tomato harvests, many states or countries could not be the source of the tomatoes that caused illnesses, so they were deemed safe sources.
Restaurants and food retailers say they are now sourcing tomatoes from places deemed safe by the FDA. The outbreak has been a particularly tough one to crack because it has been so widespread. Illness has shown up in people who frequented a variety of restaurants, and who bought tomatoes at myriad grocery stores.
A major evolutionary innovation has unfurled right in front of researchers’ eyes. It’s the first time evolution has been caught in the act of making such a rare and complex new trait. And because the species in question is a bacterium, scientists have been able to replay history to show how this evolutionary novelty grew from the accumulation of unpredictable, chance events.
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sometime around the 31,500th generation, something dramatic happened in just one of the populations – the bacteria suddenly acquired the ability to metabolise citrate, a second nutrient in their culture medium that E. coli normally cannot use. Indeed, the inability to use citrate is one of the traits by which bacteriologists distinguish E. coli from other species.
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The replays showed that even when he looked at trillions of cells, only the original population re-evolved Cit+ – and only when he started the replay from generation 20,000 or greater. Something, he concluded, must have happened around generation 20,000 that laid the groundwork for Cit+ to later evolve.
Lenski and his colleagues are now working to identify just what that earlier change was, and how it made the Cit+ mutation possible more than 10,000 generations later.
