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Spotting Alzheimer’s Disease Early

A tracer molecule designed to bind to amyloid plaques, the neurological hallmark of Alzheimer’s disease, can accurately detect the protein in the living human brain, according to a new study published this week in the Journal of the American Medical Association. Previously, the only definitive way to detect amyloid in the brain, and hence diagnose the disease, was via an autopsy.

“Now we can see this Alzheimer’s lesion in living people, and that’s a big step,” says John Morris, director of the Alzheimer’s Disease Research Center at Washington University. Morris was not involved in the study. “Ultimately, we would like to move diagnosis to the preclinical stage [before symptoms appear] and see if we can devise strategies to prevent the brain damage that produces dementia. But it will be years before we get to that stage.”

An advisory committee for the U.S. Food and Drug Administration will meet on Thursday to decide whether to recommend that the new tracer, developed by Avid Radiopharmaceuticals, be approved to help doctors diagnose the disease or to rule it out. Pharmaceutical giant Eli Lilly acquired the company last December. Avid’s tracer is one of several amyloid binding compounds under development, and the first to complete large-scale clinical trials.

Researchers say the most promising near-term use of the tracer, which is detected via positron emission tomographic (PET) imaging, is in drug development. The ability to detect signs of the disease prior to the development of obvious cognitive problems lets pharmaceutical companies test therapies designed to prevent the development of plaques early on. “It’s enormously important for drug development research,” says Paul Aisen, director of the Alzheimer’s Disease Cooperative Study at the University of California, San Diego. Aisen was not involved in the study. “It allows us to test therapies at the stage of disease where they are most likely to be clinically useful—when people have amyloid deposition but not major cognitive dysfunction.”

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Pharmaceutical companies are currently using the type of amyloid imaging used in the study to gauge the effectiveness of experimental drugs designed to reduce buildup of the protein. (Whether or not drugs that block the buildup of amyloid improve memory loss is still an open question. It’s also not clear whether the plaque buildup is a cause of Alzheimer’s or an effect of it.)

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Blog – Evidence Emerges That Laws of Physics Are Not Fine

One of the more curious debates in science focuses on the laws of physics and why they seem fine-tuned for life.

The problem is that the laws of physics contain various constants that have very specific, mysterious values that nobody can explain. These constants are balanced in such a way that life has evolved at least once, in one small part of the Universe.

But why do the constants have these values? Various scientists have calculated that even the tiniest of changes to these constants would make life impossible. That raises the question of why they are so finely balanced

One explanation is that this is pure accident and that there is no deeper reason for the coincidence. Another idea is that there is some deeper law of nature, which we have yet to discover, that sets the constants as they are. Yet another is that the constants can take more or less any value in an infinite multitude of universes. In ours, they are just right, which is why we have been able to evolve to observe them.

None of these arguments is easy to prove or disprove, although that may change as other evidence accrues, says Don Page, a theoretical physicist at the University of Alberta in Canada.

But there is a fourth line of thought which Page says is easier to attack. This is the idea that the constants have been fine-tuned by some unseen omnipotent being who has set them up in a way that maximises the amount of life that form. So instead of directly creating life, God simply sets the conditions to maximise the chances of it forming.

Today, Page says this idea is potentially falsifiable and says we already have evidence that does the trick.

Here’s the thinking. The cosmological constant is a number that determines the energy density of the vacuum. It acts like a kind of pressure that, depending on its value, acts against gravity to push the universe apart or acts with gravity to pull the universe together towards a final Big Crunch.

Until recently, cosmologists had assumed that the constant was zero, a neat solution. But the recent evidence that the universe is not just expanding but accelerating away from us, suggests that the constant is positive.

But although positive, the cosmological constant is tiny, some 122 orders of magnitude smaller than Planck’s constant, which itself is a small number.

So Page and others have examined the effects of changing this constant. It’s straightforward to show that if the the constant were any larger, matter would not form into galaxies and stars meaning that life could not form, at least not in the form we know it,.

So what value of the cosmological constant best encourages galaxy and star formation, and therefore the evolution of life? Page says that a slightly negative value of the constant would maximise this process. And since life is some small fraction of the amount of matter in galaxies, then this is the value that an omnipotent being would choose.

In fact, he says that any positive value of the constant would tend to decrease the fraction of matter that forms into galaxies, reducing the amount available for life.

Therefore the measured value of the cosmological constant, which is positive, is evidence against the idea that the constants have been fine-tuned for life.

An interesting argument and one that adds to the fine body of work that attempts to prove or disprove the existence of an omnipotent interferer. But not one that is likely to settle the matter one way or the other.

Ref: arxiv.org/abs/1101.2444: Evidence Against Fine Tuning for Life

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Making Electric Vehicles Pay Off

Commercial fleets are a logical place to introduce battery-powered electric vehicles. After all, fleet vehicles operate with relatively predictable driving patterns, return to a central location overnight, and are managed by sophisticated logistics professionals who can weigh the cars’ lower fueling and maintenance costs against their premium purchase price. Last year, managers of large fleets began exploring in earnest what EVs offer, kicking off demonstrations that will come to scale this year.

Companies such as FedEx, PepsiCo (through its Frito-Lay business), and ATT are each deploying tens to hundreds of electric delivery vans from manufacturers such as Navistar, Smith Electric, and Azure Dynamics. And in November General Electric announced an aggressive plan to make EVs account for half of its 30,000-vehicle fleet by 2015 and to lease another 10,000 EVs to other commercial fleets managed by GE Capital.

Motivations vary. Going electric confers an image of corporate responsibility on these early entrants, and for GE it also primes the market for wares such as GE-designed charging stations. But Oliver Hazimeh, director of the automotive practice for the Boston-based management consultancy PRTM and principal author of a November 2010 report on fleet electrification, sees more than a marketing play. Hazimeh says the early adopters anticipate an inevitable shift to electric transportation and are learning through doing: “They’re all looking at the fundamental drivers and saying oil prices are not going to be cheaper and less volatile, emissions regulations are going in one direction, so for the longer term we have to start turning our fleet toward this technology.”

That idea is based on projections that the cost of lithium batteries will plummet over the coming decade. PRTM’s analysis shows EVs offering the lowest overall cost of ownership for fleet vehicles between 2015 and 2018 as lithium battery costs drop below $400 per kilowatt-hour, from an estimated $600 per kilowatt-hour in 2010.

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However, it’s not certain that battery prices will drop that steeply, and major automotive players such as Toyota are betting that they will remain high through 2020 (see “Will Electric Vehicles Finally Succeed?”). This uncertainty, coupled with the batteries’ unproven life expectancy, represents the biggest challenge for fleet operators struggling to make a business case for electric vehicles. “We don’t know exactly how long the batteries will last,” says Hazimeh. “At the end of the day, if I resell the car at auction and have this huge risk provision, it muddies the water quite a bit.”

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New Cancer Marker May Aid Earlier Detection

Compared with their healthy cousins, cancer cells are a chaotic mess, often having extra chromosomes, abnormal shapes, and other odd attributes. Now scientists have discovered a strange feature that appears to be unique to cancer cells: long stretches of repetitive RNA, known as satellites. Preliminary research suggests that the satellites appear early in the development of cancer, a finding that may ultimately aid early detection.

“It’s a very interesting and provocative finding,” says Stuart Orkin, chairman of pediatric oncology at the Dana-Farber Cancer Institute, who was not involved in the research. “It suggests wholesale changes in gene expression in cancer cells that was previously unrecognized. It hints at how chromatin [the mass of DNA and proteins that make up chromosomes] and gene expression in cancer cells are deranged in a global fashion.”

David Ting, Daniel Haber, and collaborators at Massachusetts General Hospital discovered the markers by accident while Ting was studying RNA from tumor cells. The DNA that codes for genes is normally transcribed into RNA, which is then translated into proteins. Ting was puzzled by the appearance of RNA molecules whose sequence didn’t correspond to genes. He found that the sequences corresponded instead to satellites, stretches of repetitive DNA that are transcribed into RNA but never translated into proteins.

“We were surprised to find [the satellites] are expressed in humongous amounts in tumor tissue compared to normal tissue,” says Ting. Follow-up testing in both mouse and human cancer tissue revealed high levels of satellites in different types of tumors, including lung, kidney, ovarian, prostate, and pancreatic cancers.

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“This is a fascinating finding because there is no precedent for a finding a single class of [DNA] that is uniformly overexpressed in different types of cancer,” says Bert Vogelstein, professor of oncology and pathology at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University. “It appears to be true in virtually every cancer they looked at.”

While scientists have known about the existence of satellite repeats in the genome for years—they make up about five percent of the genome—the role they play in healthy cells is still unclear. “For a long time, people have ignored it, thinking it was residual DNA,” says Ting. In fact, most software used to analyze DNA sequences is designed to eliminate these stretches from their analysis, he says.

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