Tag Archives: University of California

There is a 50 per cent chance that time will end within the next 3.7 billion years, according to a new model of the universe. A team of physicists led by Raphael Bousso at the University of California, Berkeley rebel against this idea. They say an infinitely expanding universe is contrary to the laws of physics do not work in an infinite cosmos. For these laws to make any sense, the universe must come to an end

There Their argument is simple yet surprisingly powerful: If the universe lasts forever, then any event that can happen, will happen, no matter how unlikely. In fact, this event will happen an infinite number of times, which leads to the key obstacle: When there are an infinite number of instances of every possible observation, it becomes impossible to determine the probabilities of any of these events occurring. And when that happens, the laws of physics simply don’t apply. They just break down. “This is known as the “measure problem” of eternal inflation,” say Bousso and buddies. In short, the laws of physics abhor an eternal universe.

There The only way out of this logic trap is to introduce some kind of catastrophe x factor that brings an end to the universe. Then all the probabilities make sense again and the laws of physics regain their power. “Time is unlikely to end in our lifetime, but there is a 50% chance that time will end within the next 3.7 billion years,” Bousso says.

There The imminent end of time is unnerving but the argument depends crucially on an important assumption about the laws of physics: that we ought to be able to understand why they work, not just observe that they do work. And that’s a philosophical point of view rather than a physical argument. Buosso raises some interesting questions, says the MIT Technology Review, “but nothing to lose any sleep over. At least, not for another 3.7 billion years.”


In a kind of evolutionary bridge-burning, once a gene has morphed into its current state, the road back gets blocked, new research suggests. So there’s no easy way to turn back.

“Evolutionary biologists have long been fascinated by whether evolution can go backwards,” said study researcher Joe Thornton of the University of Oregon’s Center for Ecology and Evolutionary Biology and the Howard Hughes Medical Institute. “But the issue has remained unresolved, because we seldom know exactly what features our ancestors had, or the mechanisms by which they evolved into their modern forms.”

Thornton’s team solved this problem by looking at evolution at the molecular level, where they could figure out the steps taken between the ancestral form of a protein and its successor.

Their results, detailed in the Sept. 24 issue of the journal Nature, reveal that over long time scales certain genetic blockades arise that make it nearly impossible to transform a modern protein into its ancestral state, even if ancient environmental pressures were to exist.

“This is the best demonstration of the molecular foundations of evolutionary irreversibility that I have ever read,” said Michael Rose, a professor of ecology and evolutionary biology at the University of California, Irvine, who was not involved in the current study.

Turning back the genetic clock

The team looked at the so-called glucocorticoid receptor, a protein that binds with the hormone cortisol and regulates stress responses, immunity and other bodily processes in humans.

They knew that during a relatively short stint more than 400 million years ago, that receptor gained its current abilities from its ancestral state, which was sensitive to another hormone.

So Thornton’s team created both forms of the protein. “We resurrected the first protein to have the modern function and from just before that the last protein to have the ancestral function,” Thornton said.

They found seven key mutations that together gave the ancient protein its updated function. To figure out if they could coax the modern protein into its former function, the researchers reversed those seven key mutations.

“We expected to get the ancestral function back out of it,” Thornton said during a telephone interview. “But instead we got a dead protein. It didn’t work at all. It was completely non-functional.”

Burning bridges

Here’s what they suggest is behind the phenomenon: As the ancient protein evolved, five other mutations made subtle changes in the protein’s structure that were incompatible with the primordial form.

“Suppose you’re redecorating your bedroom — first you move the bed, then you put the dresser where the bed used to be,” Thornton said. “If you decide you want to move the bed back, you can’t do it unless you get that dresser out of the way first.”

He added, “The restrictive mutations in the GR (glucocorticoid receptor) prevented evolutionary reversal in the same way.”

This same restrictive process might not occur over shorter time scales, as Rose has found in his research.

“What this new Nature publication shows is that on a much longer time-scale (more than a million generations), it is harder to get evolution to reverse itself,” Rose told LiveScience. “This is how evolutionists explain things like the failure to reverse-evolve gills in whales or dolphins. Too many generations have elapsed since the ancestors of the Cetaceans had functional gills as adults.”

Thornton hopes to study the reversibility of evolution in other proteins. “I expect that this will be a fairly general observation that other proteins and other traits will often be irreversible,” he said.



Though most of us spend a lifetime pursuing happiness, new research is showing that that goal may be largely out of our control. Two new studies this month add to a growing body of evidence that factors like genes and age may impact our general well-being more than our best day-to-day attempts at joy.

In one study, researchers at the University of Edinburgh suggest that genes account for about 50% of the variation in people’s levels of happiness — the underlying determinant being genetically determined personality traits, like “being sociable, active, stable, hardworking and conscientious,” says co-author Timothy Bates. What’s more, says Bates, these happiness traits generally come as a package, so that if you have one you’re likely to have them all.

Bates and his Edinburgh colleagues drew their conclusions after looking at survey data of 973 pairs of adult twins. They found that, on average, a pair of identical twins shared more personality traits than a pair of non-identical twins. And when asked how happy they were, the identical twin pairs responded much more similarly than other twins, suggesting that both happiness and personality have a strong genetic component. The study, published in Psychological Science, went one step further: it suggested that personality and happiness do not merely coexist, but that in fact innate personality traits cause happiness. Twins who had similar scores in key traits — extroversion, calmness and conscientiousness, for example — had similar happiness scores; once those traits were accounted for, however, the similarity in twins’ happiness scores disappeared.

Another larger study, released in January ahead of its publication in Social Science & Medicine this month, shows that whatever people’s individual happiness levels, we all tend to fall into a larger, cross-cultural and global pattern of joy. According to survey data representing 2 million people in more than 70 countries, happiness typically follows a U-shaped curve: among people in their mid-40s and younger, happiness trends downward with age, then climbs back up among older people. (That shift doesn’t necessarily hold for the very old with severe health problems.) Across the world, people in their 40s generally claim to be less happy than those who are younger or older, and the global happiness nadir appears to hit somewhere around 44.

What happens at 44? Lots of things, but none that can be pinned down as the root cause of unhappiness. It’s not anxiety from the kids, for starters. Even among the childless, those in midlife reported lower life satisfaction than the young or old, says study co-author Andrew Oswald, an economics professor at the University of Warwick in Britain. Other things that didn’t alter the happiness curve: income, marital status or education. “You can adjust for 100 things and it doesn’t go away,” Oswald says. He and co-author David Blanchflower, an economist at Dartmouth College in New Hampshire, also adjusted their results for cohort effects: their data spanned more than 30 years, making them confident that whatever makes people miserable about being middle-aged, it isn’t related, say, to being born in the year 1960 and growing up with that generation’s particular set of experiences.

At first glance, the new studies may appear at odds with some previous ones, largely because in happiness research, a lot depends on how you ask the question. Oswald and Blanchflower looked at responses to a sweeping, general question: “Taken all together, how would you say things are these days — would you say that you are very happy, pretty happy or not too happy?” (The wording changes slightly depending on where the survey was conducted, but the question is essentially the same.) In a 2001 study, Susan Charles at University of California, Irvine, measured something slightly different: changes in positive affect, or positive emotions, versus negative affect over more than 25 years. Charles found that positive affect stayed roughly stable through young adulthood and midlife, falling off a little in older age; negative affect, meanwhile, fell consistently with age.

Charles thinks that feelings like angst, disgust and anger may fade because as we get older we learn to care less about what others think of us, or perhaps because we become more adept at avoiding situations we don’t like. (The Edinburgh researchers, too, found that older study participants scored lower than younger ones on scales of neuroticism — worry and nervousness — and higher on scales of agreeableness.) Oswald chalks up the midlife dip in happiness shown in his study to people “letting go of impossible aspirations” — first, there’s the pain of fading youth and the realization that we may never accomplish all that we had dreamed, then the contentment we gain later in life through acceptance and self-awareness. “When you’re young you can’t do that,” Oswald says.

An oft-cited finding from other happiness research suggests, however, that neither very good events nor very bad events seem to change people’s happiness much in the long term. Most people, it seems, revert back to some kind of baseline happiness level within a couple years of even the most devastating events, like the death of a spouse or loss of limbs. Perhaps that kind of stability is due to heredity — those happiness-inducing personality traits that identical twins have been shown to share.

Still, lack of control doesn’t necessarily mean lack of joy. “The research also shows that most people consider themselves happy most of the time,” says University of Edinburgh’s Bates. “We’re wired to be optimistic. Most people think they’re happier than most [other] people.” And even if you aren’t part of that lucky majority, Bates says, there’s always that other 50% of overall life satisfaction that, according to his research, is not genetically predetermined. To feel happier, he recommends mimicking the personality traits of those who are: Be social, even if it’s only with a few people; set achievable goals and work toward them; and concentrate on putting setbacks and worries in perspective. Don’t worry, as the saying goes. Be happy.


What does a Y-chromosome sound like? Now you can answer that question for yourself, using a novel molecule-to-melody conversion scheme that could open up new frontiers in biomedical research as well as computer-generated music. 
Rie Takahashi and Jeffrey Miller of the University of California at Los Angeles describe the system in the open-access journal
Genome Biology. They set up a system is to translate amino acids – the building blocks for human protein sequences – into musical chords. 
isn’t the first time someone has tried to represent protein sequences musically, but Takahashi – an accomplished musician as well as a microbiologist – worked with Miller to come up with a more artful way to represent the standard 20 amino acids with the standard 13-note scale. 
“The challenge was to find a way to be completely faithful to the science … but also make the music more dimensional and add rhythm,” Miller told me.
Takahashi added some extra twists: For example, similar amino acids are represented by the same chord – say, G-major for tyrosine and phenylalanine – but the arrangement is different. Also, more frequently encountered amino acids get longer notes than the less common ones.
With the aid of a colleague at UCLA, Frank Pettit, the researchers devised a
Web-based program that can take the three-base code for each amino acid in a sequence, triplet by triplet, and turn it into a playable MIDI file. 
Miller said the resulting music is completely determined by the protein sequence rather than tunefulness. “There are no fudge factors at all,” he said.
The examples on the researchers’
Gene2Music Web site range from horse hemoglobin to human thymidylate synthase A. “In principle, one could take the entire human genome and have it translated into 30,000 different protein sequences,” Miller said. 
Just for fun, I took a sequence from 
one of the markers on the human Y-chromosome and fed it through the converter. You can hear the MIDI result here – and it doesn’t sound all that bad, if I say so myself. But you’ll notice that there’s a section where the same note sounds over and over. And that hints at the scientific application of the system. 
The repeated notes are caused by repeating triplets in the protein code. In most cases, those repeats are harmless. But triplet repeats can also be associated with
genetic neurodegenerative disorders such as Huntington’s disease. Takahashi said one expert on Huntington’s is already interested in using the musical system with his patients. 
“It’s a great way of explaining to the patient why the protein is dysfunctional,” Takahashi said. “You can hear that through the repeated glutamines, over and over like a broken record.”
The system could also be used to compare protein sequences by playing them together. A sharp-eared researcher should be able to hear the difference between a normal and abnormal protein. “What you’ll hear is basically a dissonance or a difference in the chords,” Takahashi said.
Miller said the technique might eventually be used to help vision-impaired researchers hear rather than see genetic code. “Admittedly, that’s a future direction,” he said. 
The researchers’ main goal is to use Gene2Music as a way to bring the joy of science to a generation raised on iPods and MP3 players.
“Music is a universal language and a bridge, and a way of making things interesting,” Miller said. “For example, when I was a kid, ‘Peter and the Wolf’ was the way that young people got interested in classical music, because it had a different instrument for each character and it had a story. So that was a goal, to find ways to use music as a teaching tool.”
I can imagine a day when
getting your genome done will be as easy as getting your colors done – and when having a theme song based on your personal genetic code will be a musical status symbol. 
Takahashi is already looking into tweaking some of the raw molecular melodies into polished musical compositions. “Ideally, I would like to complete a set of variations of different proteins, and ultimately make a CD of that,” she said.