Posts Tagged ‘Fb’

Charles Darwin performed the world’s first terraforming experiment [Mad Science]

Thursday, September 2nd, 2010

(reprinted from: io9)

Charles Darwin performed the world's first terraforming experimentNearly two centuries ago, famed scientists Charles Darwin and Joseph Hooker transformed the barren volcanic island of Ascension into a lush artificial ecosystem, unwittingly inventing terraforming. Now, Darwin's incredible achievement could help us transform Mars into a livable environment.

Darwin and Hooker, with the assistance of the Royal Navy, managed to create a functional ecosystem in decades, rather than the million of years it would have taken for such a system to develop naturally. Although much of Ascension remains arid, they were able to plant enough trees to capture rainwater without it all evaporating away, creating a self-sustaining ecosystem that made life a whole lot easier for its inhabitants.

Dr. Dave Wilkinson, an ecologist at Liverpool John Moores University, explains why he found the Ascension ecosystem so strange when he first visited in 2003, and why it's important:

"I remember thinking, this is really weird. There were all kinds of plants that don't belong together in nature, growing side by side. I only later found out about Darwin, Hooker and everything that had happened. What it tells us is that we can build a fully functioning ecosystem through a series of chance accidents or trial and error."

Wilkinson believes these principles could be adapted to colonization efforts on Mars, although he notes scientists have yet to seriously consider the lessons Darwin's work on Ascension could teach us. For more on this remarkable story, check out the full article at BBC News

[BBC News; thanks to Mathmos for the tip!]

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The Sun is changing the rate of radioactive decay, and breaking the rules of chemistry [Mad Science]

Monday, August 23rd, 2010

(reprinted from: io9)

The Sun is changing the rate of radioactive decay, and breaking the rules of chemistryThe Sun is changing the supposedly constant rates of decay of radioactive elements, and we have absolutely no idea why. But an entirely unknown particle could be behind it. Plus, this discovery could help us predict deadly solar flares.

It's one of the most basic concepts in all of chemistry: Radioactive elements decay at a constant rate. If that weren't the case, carbon-14 dating wouldn't tell us anything reliable about the age of archaeological materials, and every chemotherapy treatment would be a gamble. It's such a fundamental assumption that scientists don't even bother testing it anymore. That's why researchers had to stumble upon this discovery in the most unlikely of ways.

A team at Purdue University needed to generate a string of random numbers, a surprisingly tricky task that is complicated by the fact that whatever method you use to generate the numbers will have some influence on them. Physics professor Ephraim Fischbach decided to use the decay of radioactive isotopes as a source of randomness. Although the overall decay is a known constant, the individual atoms would decay in unpredictable ways, providing a random pattern.

That's when they discovered something strange. The data produced gave random numbers for the individual atoms, yes, but the overall decay wasn't constant, flying in the face of the accepted rules of chemistry. Intrigued, they checked out long range observations of silicon-32 and radium-226 decay, both of which showed a slight but definite variation over time. Intriguingly, the decay seemed to vary with the seasons, with the rate a little faster in the winter and a little slower in the summer.

At first, the researchers tried to rationalize the seasonal fluctuations as the result of instrument error, perhaps caused by changing heat and humidity. But that idea fell apart when nuclear engineer Jere Jenkins noticed the decay rate of the short-lived isotope manganese-54 dropped slightly during a solar flare. In fact, the decrease began a good 36 hours before the flare occurred.

That suggests two things: one that's theoretically puzzling, and another that's hugely exciting from a practical perspective. If decay rates really are affected by solar flares before the flares even occur, that could provide the first truly reliable early warning system for flares. Considering severe solar flares can wreak havoc on electrical grids and even kill astronauts who aren't properly protected, that would be a huge benefit for humanity.

But practical pluses aside, why is this happening? The seasonal fluctuations suggested the Sun could be involved somehow, and the solar flare connection confirmed it. The scientists speculated that solar neutrinos, the nearly massless particles created as byproducts of the sun's fusing of hydrogen atoms into helium, might be causing these variations. The fact that these neutrinos pass straight through the Earth with ease fit well with the fact that the decay rates were changing even at night, when the entire planet was between the radioactive isotopes and the Sun.

Once the researchers conclusively ruled out environmental influences, that left the Sun as the only possible cause of the decay variations. They also found that the amount of change varied in time with the Earth's orbit - the effect was greater when the orbit brought the Earth closer to the Sun and thus into contact with more neutrinos.

That's where renowned Stanford physics professor Peter Sturrock entered the picture. Confronted with this mystery, he advised the researchers to test how the decay fluctuations correlated with the Sun's own rotation. They found the decay rates recurred every 33 days, which didn't quite fit with the Sun's known surface rotation length of 28 days. But the neutrinos wouldn't be coming from the surface - they would be coming from deep inside the core. Unlikely as it might seem, the sun's core must be rotating a little slower than its surface, apparently once every 33 days.

All of this relies on some unlikely assumptions and the occasional bold intuitive leap, but the model they propose seems to hang together. And yet one mystery remains - how are the neutrinos managing to interact with the radioactive particles in this way? It doesn't fit with the known behavior of neutrinos, and it opens up the very real possibility that some previously unknown subatomic particle is actually behind this bizarre effect.

As Peter Sturrock explains:

"It's an effect that no one yet understands. Theorists are starting to say, 'What's going on?' But that's what the evidence points to. It's a challenge for the physicists and a challenge for the solar people too. [If it's not neutrinos,] it would have to be something we don't know about, an unknown particle that is also emitted by the sun and has this effect, and that would be even more remarkable."

If these new discoveries hold up, then we've discovered that the sun changes rates radioactive decay, that we can predict solar flares before they happen, that the sun's core rotates slower than its surface, and maybe even that an entirely unknown particle exists and is affecting our world in a tangible way. Not a bad set of results for what was supposed to be a simple search for some random numbers.

[Symmetry Breaking]

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Is evolution pushing our DNA towards diabetes? [Evolution]

Tuesday, August 17th, 2010

(reprinted from: io9)

Is evolution pushing our DNA towards diabetes?Eighty DNA variants associated with type-1 diabetes have undergone positive selection, increasing in prevalence over recent generations. Here's the crazy part - 58 of those variantsincrease the risk of the deadly disease. Why is evolution seemingly out to get us?

The answer, of course, is that evolution can't be out to get us - by definition, positive selection of genes and traits works to maximize our species's chance of survival. So something about those particular DNA combinations that increase the risk of type-1 diabetes must also be conferring some positive benefit that outweighs the dangers of diabetes.

Of course, it would have to be a pretty big benefit. Type-1 diabetes, also known as juvenile diabetes, primarily affects children by causing a potentially lethal shortage of insulin in their bodies. The fact that it affects people who haven't yet reached reproductive age is crucial - natural selection should pretty much always select against diseases that can kill people before they get a chance to pass on their genes. (On the other hand, there wouldn't be nearly as much evolutionary pressure on the more common type-2 diabetes, which mostly affects post-reproductive adults.)

Lead researcher Atul Butte, a biologist at Stanford medical school, explains the conundrum:

"At first we were completely shocked because, without insulin treatment, type-1 diabetes will kill you as a child. Everything we've been taught about evolution would indicate that we should be evolving away from developing it. But instead, we've been evolving toward it. Why would we have a genetic variant that predisposes us to a deadly condition?"

The best answer is that the genetic variants that increase the diabetes risk are also decreasing the risk of certain viral or bacterial infection. That would have made particular sense in a past where infectious diseases ran rampant, and the risks of dying young from these mostly untreatable illnesses far outstripped the dangers of diabetes. It's not yet clear whether the same mutated genes that increase the diabetes risk also provide this protection, or if it's neighboring genes whose allocation from generation to generation is intertwined with the diabetes gene.

Maybe the best example of this genetic phenomenon is seen with the disease sickle cell anemia. A particular recessive gene causes the painful, potentially deadly disease if both parents pass it along to their offspring. It's the sort of trait that natural selection would have weeded out if not for the fact that people with only a single copy of the gene have increased protection against malaria. As such, the sickle cell gene is a net positive, because more people are protected from malaria than become sickle cell patients. (Although that evolutionary balance might shift if we ever managed to wipe out malaria.)

The diabetes question is more complex than the sickle-cell anemia case because it's not limited to the mutation of a single gene. Complex diseases like diabetes are tied to a number of DNA variants, or locations where the nucleotide combinations vary between different people. These variants are known as single nucleotide polymorphisms, or SNPs for short. You can calculate a person's susceptibility to a particular disease by figuring out the net effect of his or her variants, which will likely be a mix of beneficial, malicious, and neutral.

Genome studies have revealed several hundred variants that can play a role in diabetes, so it's supremely complicated to figure out the precise interplay of all these different strands of DNA. Still, the raw numbers are striking - of the 80 DNA variants that have increased in prevalence, only 22 increase protection while 58 cause greater risk of developing the disorder.

There are some possible candidates for the diseases these variants are protecting against. For instance, the gene IFIH1 has been found to increase diabetes risk while also protecting against enterovirus infection, which can cause severe, possibly lethal, abdominal pains. Another disease the researchers found had a majority of increasing risk factors, rheumatoid arthritis, has had its less protective gene variants linked to a sharp decrease in tuberculosis risk.

Still, the picture is far from complete, and Butte and his team are going to keep testing more and more SNPs until they can figure out why natural selection keeps favoring a greater risk of diabetes over the alternative. Until then, Butte says it's a mystery with only the sketchiest answers available:

"It's possible that, in areas of the world where associated triggers for some of these complex conditions are lacking, carriers would experience only the protective effect against some types of infectious disease. Even though we've been finding more and more genetic contributions to disease risk, that's not really an appealing answer. There have got to be some other reasons why we have these conditions."

[PLoS ONE]

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String theory and black holes show a possible path to practical superconductors [Mad Physics]

Friday, August 6th, 2010

(reprinted from: io9)

String theory and black holes show a possible path to practical superconductorsA leading candidate for room temperature superconductors is the copper compound cuprate, but no one knew how cuprates facilitated superconductivity...until some brave souls looked inside a black hole and broke out the string theory to explain how they work.

Superconductors that can transmit massive amounts of electricity with zero resistance at room temperature are pretty much the holy grail of applied physics (with good reason), but we're still a long way away from actually building one. Indeed, even figuring out the theoretical underpinnings of a room temperature superconductor has proven tremendously difficult, although a team of MIT physicists may have found an unlikely - and brilliant - way to learn more about how they would work. But first, a little backstory.

Currently, there are two types of superconductors. One group is the low temperature superconductors, which can only work at temperatures near absolute zero and thus require gigantically impractical amounts of coolants. The other set is the high temperature superconductors, which still have to be kept more than a hundred degrees Celsius below zero. They require slightly less impractical but still pretty damn impractical amounts of coolants (that's a technical term). Researchers focus on the second set to see if they can boost the working temperature another hundred or so degrees.

Cuprates are compounds that include copper anions, or copper atoms with more electrons than protons and, as a result, a negative charge. The physicists Georg Bednorz and Karl Müller discovered a cuprate compound, specifically lanthanum barium copper oxide, was a superconductor at the relatively high temperature of 135 degrees Celsius above absolute zero. They won a Nobel Prize for their efforts, and a bunch of other cuprate compounds have since been discovered that also have superconductivity properties.

String theory and black holes show a possible path to practical superconductors

Although we know a lot about what cuprates do, physicists have struggled to explain how they do it. Cuprates are what's called a "many-body system", which basically means they're made up of huge groups of electrons that interact with each other in ways that are difficult to model mathematically. Quantum mechanics can usually help with many-body systems, but cuprates behave so differently than other such systems that little headway has been made in understanding their workings. That's kind of a problem, because physicists are fairly sure it's precisely that peculiar behavior that gives cuprates their superconductivity, and understanding it might allow us to move towards superconductors at much higher temperatures.

Part of the problem is that cuprates don't follow Fermi's laws, a subset of quantum mechanics that describe the actions of most - but apparently not all - microscopic objects at temperatures near absolute zero. In regular Fermi liquids, electrical resistivity is proportional to the temperature squared, while in materials like cuprates - known as strange metals - the resistivity is proportional to just the temperature. That exponential reduction in resistance is the key to superconductivity. But physicists have absolutely no idea how to explain that fact on a theoretical level.

Here's where the MIT physicists and their offbeat ideas enter the picture. They figured out there was another system that shared the same properties as these superconducting strange metals, and best of all this system could be explained using gravitational mechanics and relativity instead of quantum mechanics. That system is a black hole. At low energy levels, the black hole model is a good match for the traits and behaviors that cuprates exhibit. Most importantly, electrical resistance in a black hole is directly proportional to temperature, not the temperature squared, which is the crucial match for superconducting cuprates.

None of these revelations would be particularly useful if it wasn't possible to correlate the features of the black hole model with those of the strange metals, and that's a tricky task because black holes are described by relativistic features while the cuprates are governed by quantum mechanics. String theory solves that problem, providing a bridge between quantum and gravitational mechanics called gauge/gravity duality.

The physicists simply used general relativity to figure out various key values of the black hole model, then used the duality to translate them to the quantum world of the strange metals. At that point, it was just a matter of connecting the right values, such as the fact that the strength of the electromagnetic field in the black hole corresponds to electron density in the cuprates.

These connections represent a theoretical breakthrough in the study of high temperature superconductors, and will hopefully illuminate a path towards the really high temperature superconductors that would work at room temperature. If nothing else, this represents the first time the gauge/gravity duality has been used to describe anything that existed after the very, very beginning of the universe, and the physicists hope to apply the duality to other modern forms of matter.

[Science]

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Meet your true ancestor: The segmented worm [Evolution]

Tuesday, July 27th, 2010

(reprinted from: io9)

Meet your true ancestor: The segmented wormSegmentation, the replication of anatomical structures throughout the body, is found in many animal species. It's also a huge reason why all those species succeeded, and it comes from a single common ancestor 600 million years ago.

Specifically, segmentation refers to instances where identical anatomical units are repeated on the axis running from the top to a bottom of an animal. (So the fact that we have eyes, ears, arms, and legs that are all identical doesn't count as segmentation.) Obviously segmented species include centipedes and millipedes, in which a single structure is repeated dozens, even hundreds, of times over, but they're hardly the only examples. Anything from earthworms to humans can possess segmented features.

Three of the most basic groups of animals - arthropods (insects, arachnids, and crustaceans), vertebrates (most animals that we're familiar with), and annelid worms (sea and earthworms, basically) - all heavily make use of segmentation throughout their individual species, and yet they're very distantly related groups. Recent evidence indicates that the genes controlling segmentation are essentially the same in anthropod and worm species, indicating that there was indeed a single common ancestor, probably a worm-like creature, some 600 million years ago that proved phenomenally successful because of its ability to segment.

So why does segmentation provide such a huge evolutionary advantage, and why has it helped bring about such fantastic animal diversity? The answer might be quite simple: segmentation creates ready-made spare parts, producing duplicated anatomical units that can be repurposed as needed. If a species is under heavy pressure to fit into a changing environmental niche, it may need to develop new structures that can deal with the altered conditions. In that instance, it would be much easier to modify an existing organ than build a whole new one. Segmentation would give species a better shot at quickly adapting to new environments, which would create more pronounced changes in the species and, thus, greater diversity.

In that case, segmentation is the ultimate example of what Stephen Jay Gould dubbed an exaptation, in which a trait becomes extremely useful for reasons unrelated to its initial development. If nothing else, there's a certain evolutionary irony in that the exact duplication of body parts is responsible for why animal species all look so wildly different.

via Science

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The amazing electrons that let nothing stand in their way (with a little help from antimony) [Mad Science]

Monday, July 19th, 2010

(reprinted from: io9)

The amazing electrons that let nothing stand in their way (with a little help from antimony)Even the most minuscule, atom-sized surface imperfections can pose colossal obstacles for the speedy flow of electrons. But certain substances create a remarkable condition where the electrons are able to completely ignore these pitfalls and move ultra-fast.

On most surfaces, tiny imperfections are like gigantic cliffs to electrons, which can become temporarily trapped and jam up the proper flow of the particles. For circuits that process information using electron flow, that's a major problem that needs to be carefully guarded against, which limits their maximum potential performance.

However, recent theories hold that certain compounds that contain the element antimony (or other elements with very similar chemical properties, but antimony works best) would provide electrons an essentially smooth surface. Although these nano-sized cliffs and crevasses would still exist, antimony helps create a special form of electron wave that allows the electrons to effortlessly flow around any possible imperfection.

Princeton physicist Ali Yazdani, who discovered this remarkable property, explains the potential applications of this discovery:

"Material imperfections just cannot trap these surface electrons. This demonstration suggests that surface conduction in these compounds may be useful for high-current transmission even in the presence of atomic scale irregularities — an electronic feature sought to efficiently interconnect nanoscale devices."

Antimony has a long history of practical use, but its strange properties with regards to surface conduction had been ignored until now. Admittedly, it's only recently become possible to even study how electrons flow at just the surface, requiring the development of incredibly precise techniques able to visualize surface electrons. Antimony is one of the so-called "topological" materials, which are able to give surface electrons these unique, free-flowing properties.

[Nature]

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Antidepressants in the water are making shrimp suicidal [Mad Science]

Monday, July 12th, 2010

(reprinted from: io9)

Antidepressants in the water are making shrimp suicidalImproving human mental health is having some serious unintended consequences for our friends in the ocean. Exposure to antidepressants makes shrimp five times more likely to place themselves in life-threatening situations, and the broader effects could damage the entire ecosystem.

Exposure to the antidepressant fluoxetine causes shrimp to radically alter their behavior. While normal shrimp are more likely to avoid swimming towards light because it's often associated with prey like birds or fishermen, those exposed to fluoxetine become five times more likely to swim towards light than away from it. That change in behavior places them in harm's way, and if enough shrimp are exposed to the antidepressant the entire population could be at risk.

Alex Ford, a marine biologist at the UK's University of Portsmouth, explains how that can reverberate throughout the oceanic ecosystem and why this is a serious concern:

Crustaceans are crucial to the food chain and if shrimps' natural behaviour is being changed because of antidepressant levels in the sea this could seriously upset the natural balance of the ecosystem. Much of what humans consume you can detect in the water in some concentration. We're a nation of coffee drinkers and there is a huge amount of caffeine found in waste water, for example. It's no surprise that what we get from the pharmacy will also be contaminating the country's waterways.

Ford exposed some shrimp to the same amount of fluoxetine that humans excrete into the waste water that gets carried out to sea. He found that even this seemingly small amount was enough to trigger this major behavioral change in the shrimp. He had been motivated to investigate this question by a parasite that is known to cause such changes by altering serotonin levels in shrimp. He wanted to find out whether the same deleterious result could be obtained using human antidepressants; the answer, sadly, is yes.

He explains how small individual amounts of antidepressants adds up to a big problem:

Effluent [outflowing waste water] is concentrated in river estuaries and coastal areas, which is where shrimps and other marine life live — this means that the shrimps are taking on the excreted drugs of whole towns.

Prescriptions for antidepressants have skyrocketed in recent years, but this is one of the very first attempts to figure out what ecological impact all that pharmaceutical sewage could have. The most worrying part of it all is that this might just be the tip of an ecosystem-altering iceberg - there are lots of other drugs other than fluoxetine that affect serotonin levels, and Ford hasn't even tested any of those yet to see what they do to shrimp and other marine organisms.

[Aquatic Toxicology]

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A new facility is being built to harvest rare atoms [Mad Science]

Wednesday, July 7th, 2010

(reprinted from: io9)

A new facility is being built to harvest rare atomsFind out how a particle accelerator will be used to make rare isotopes used for nuclear medicine.

Technetium 99m sounds like something in a bad fifties science fiction film that would be injected into someone to give them psychic powers, or twelve hours, or both. This goes double when it's combined with the ominous phrase ‘nuclear medicine.' Together they call to mind a hapless tourist being held down by a hulking orderly named Nurse Mugsy while a guy with salt and pepper hair and a lab coat brandishes a glowing syringe and talks about how the only way humans will survive the coming nuclear winter is by spiking the water supply with technetium 99m. It may or may not be raining, depending on the sensibilities of the director.

A new facility is being built to harvest rare atoms

The realities of nuclear medicine aren't that much brighter. Technetium 99m and nuclear medicine are not fun things to experience. The isotope is radioactive, and throws off x-rays from inside a person's body. X-rays go through flesh like it's not even there, so the technetium 99m inside a person is measurable from outside of the person's body. In medicine it is often added to a chemical that will attach itself to tumors or growths inside a person. That chemical attaches itself to the tumor, and technetium 99m's x-rays allow doctors to see how big a tumor is without having to cut that person open. Being a human x-ray projector is much, much better.

Seriously, though, technetium is both massively useful and massively used. The problem is, x-rays are not thrown off because an element is planning to stick around. They are tossed out as an unstable atom becomes more stable, and the isotope technetium 99m doesn't have a long shelf life. This means that the has to be a way of getting it. Nuclear reactors are able to produce it, but they are not the safest things around.

A new facility is being built to harvest rare atoms

Canada, perhaps encouraged by the fact that the Large Hadron Collider did not turn out to be a doomsday device, has come up with a plan to build a particle accelerator in order to make and harvest technetium 99m. The accelerator will hurl a stream of electrons at a metal target. Once at the target, the electrons will either swerve off course, or stop dead in their tracks in the comical fashion of Wyle E Coyote, after he has been fired at a wall in a Warner Brothers cartoon.

A new facility is being built to harvest rare atoms

Either way, the electrons will produce high-energy photons through bremsstrahlung.

‘Bremsstrahlung' comes to us courtesy of the Germans, who are fresh off their win with schadenfreude and looking for other compound words to popularize. It means ‘braking energy.' When the electrons swerve off course or stop at the target, they lose momentum, thus losing energy. Any hippie will tell us that, like, energy goes on forever, man, and can never really be lost, and of course hippies are never wrong. To conserve energy, some photons are produced to make up for the energy lost by the electrons. The electrons whizzing by also mess with the electromagnetic fields at the target, producing even more photons.

These photons form another beam which hits another target, this one made of heavy elements. These elements break down, producing rare isotopes. Those isotopes, including technetium 99m are harvested and used in nuclear medicine. Possibly also by a nurse named Mugsy. People will call their kids anything these days.

Sources: About.com, NDT, Physics World, and TRIUMF.

Top image of facility for rare isotope beams at at Michigan State.

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We round up Inception’s early reviews. Does it live up to the hype? [Early Reviews]

Tuesday, July 6th, 2010

(reprinted from: io9)

We round up Inception's early reviews. Does it live up to the hype?Will the director of The Dark Knight rescue us from Hollywood's summer of meh? Early reviews of Christopher Nolan's Inception are out, and they promise a complex, thrilling movie. Will it live up to the hype? Some spoilers ahead.

So basically we'll round up what the reviewers said, in a spoiler-free fashion, and then at the bottom, we'll summarize the spoilery bits. So if you are one of those people who is frantically trying to avoid Inception spoilers, you'll have a chance to jump off before we careen into spoiler-land.

UGO basically says it's one of the best movies of the year, an action film for intellectuals that sets a standard for all other Hollywood movies. You may have to watch Transformers 2 afterwards, just to balance it out.

Variety calls it "commandingly clever," and adds, "Even when its ambition occasionally outstrips its execution, Inception tosses off more ideas and fires on more cylinders than most blockbusters would have the nerve to attempt."

Thompson on Hollywood calls it a strong Best Picture Oscar candidate, and calls it a "taut suspense thriller" as well as a moving love story. It's full of Kubrick homages and actually recalls the best of Kubrick's work.

Empire Magazine's Nev Pierce is one of a few reviewers to compare it to a James Bond movie, and says it's like Charlie Kaufman's take on 007.

Awards Daily says it's easily one of the best pictures of the year, and maybe even of the decade.

AICN says it represents Nolan visually peaking, and "cinema doesn't get much purer than Inception."

InContention says, "Every single moment of Inception is more gripping than the last," and it may solidify Nolan's place among the modern masters of cinema.

We round up Inception's early reviews. Does it live up to the hype?

JoBlo gives it 10 out of 10 and says you'll be discussing and debating about the film for ages after watching it, until you feel compelled to see it again.

FilmSchoolRejects calls it the best big-budget film of the year so far, and adds: "Inception is what The Wachowskis wish the rest of The Matrix films after the first could have been."

Cinematical says "Inception is nothing short of a stunning, spectacular, visionary achievement."

HitFix says it's an exhilarating experience, but not really an action film.

Chud says, "Inception is a masterpiece." It barely even feels like a movie, it's so immersive, and at times it feels like a miracle.

Box Office Magazine gushes, "A bold, inventive, audacious entertainment, Inception charts a new course for motion pictures and sets the bar very, very high."

The Hollywood Reporter says that it's one of the most original movies of the year, and praises all the performances — but says that two and a half hours of tense situations and mind-bending complexity may leave you exhausted. And you'll have to see it three times to understand everything.

The one dissenting opinion comes from Coming Soon, which says Inception is an exceptional film. "So how is it that Inception comes together as such a bore?" Coming Soon blames a too-exposition-heavy screenplay and and flat, lifeless characters, and says it's like a less-exciting mix of Solaris and On Her Majesty's Secret Service.

We round up Inception's early reviews. Does it live up to the hype?

So now that you're in a lather of excitement about this film (unless you choose to believe Coming Soon over all the other reviewers), are you ready for some pretty heavy-duty spoilers? Last chance to jump off, otherwise!

So as you've no doubt heard, Dom Cobb (Leonardo DiCaprio) specializes in extraction, pulling secrets out of people's dreams. His point man is Arthur (Joseph Gordon-Levitt).

Cobb is a broken man, and his dead wife Mal (Marion Cotillard) tends to show up in dreams and haunt him, screwing up his work. This happens at the start of the film, when Cobb is leading an extraction mission inside the dreams of a wealthy businessman, Saito (Ken Watanabe). Saito is aware they're all inside his subconscious. We wind up with Mal holding a gun on Arthur, who gets killed in the dream and wakes up in reality — where he, Saito and Cobb are attached intravenously to a machine.

Back in the real world, Cobb and his team try to scatter to the four winds, but Saito catches up with them. And it turns out the screwed up mission inside Saito's head was just Saito's way of auditioning Cobb for a different assignment — going inside the dreams of Saito's future rival Robert Fischer Jr. (Cillian Murphy) and planting an idea, instead of stealing one. (That's the "Inception" of the film's title.)

Because he was accused of killing his wife, Cobb unable to go back to the United States, and he longs to go home and rejoin his two toddlers. Saito offers him a chance to get his life back, if he can just pull off this difficult mission of planting an idea in Fischer's mind. Fischer is soon to be heir to his family's company, and Saito wants Cobb to trick him into dissolving the company for "emotional" reasons.

To this end, Cobb hires an actual architect named Ariadne (Ellen Page) to design every street, room and building in the fake dream, so it looks real enough to deceive the dreamer. In the process, he teaches her about his work, and she finds she can't resist the dream world. Among other things, we learn the rules of the dream world, including the fact that time moves ten times as fast in a dream as in real life, and the dangers of layering dreams within dreams. If you die in a dream, you wake up, but if you get lost in a deep-layer dream, your mind may never emerge intact. At one point, it's raining in a dream, and we're told that's because the dreamer didn't go to the bathroom before falling asleep. Also, another dreamer's "projections" may be adversarial and even dangerous. Even though we learn the rules in detail, the film later breaks some of them or renders them irrelevant, in some surprising but logical twists.

Cobb also recruits other members of his dream team: Eames (Tom Hardy), a "forger" who can shapeshift in the dream world, and Yusuf (Dileep Rao) a chemist who supplies the powerful sedative that puts Fischer and Cobb's gang into the dream state.

Eventually, our heroes plunge inside Fischer's mind, and get lost in the maze of chambers and antechambers. Many of the dreams resemble action movies, natch. There's a huge snow-bound set piece filmed in Calgary, Canada. Towards the end, there are no less than four different lines of action intercutting at once. The stakes keep getting higher, and yet more personal at the same time. Oh, and there's no trick or twist ending — most of the answers are given to us in the very first scene. As the film goes along, the ghost of Cobb's wife becomes more and more dangerous, because of his repressed subconscious. We realize as the film goes along that Cobb is keeping his emotions under wraps because he's trying to guard his secrets, which eventually spill out.

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Cancer caused by DNA repair gone haywire [Medical Science]

Thursday, July 1st, 2010

(reprinted from: io9)

Cancer caused by DNA repair gone haywireWe don't know how to cure it, but now we've got a better idea what causes cancer. The disease starts when cells mess up their attempts to repair damage to their DNA.

There's a certain tragic irony to this, as these terrible diseases seem to begin with cells trying to fix the far more minor problem of damage to DNA strands. According to James Haber, Wade Hicks, and Minlee Kim of Brandeis University, cells that are showing the very earliest signs of cancer start to have errors in the DNA replication process. To fix this, the cells use a number or methods to repair the damage, one of which is known as gene conversion.

Gene conversion repairs the break in the DNA strand by using an almost identical sequence from elsewhere in the cell's DNA, providing a template from which the original strand can be reconstructed. Although this was once thought to be a mostly error-free process, the new study actually suggests it leads to a far greater number - about 1,400 times the usual amount - of DNA mutations than would otherwise be expected. Once these mutations affect the various genes that provide the cell's ability to control its own growth, the cell quickly becomes cancerous.

Coauthor James Haber says this theory explains why cells turn cancerous so quickly:

"It has been hard to imagine how cells could accumulate so many mutations in the few generations that they undergo cell division on the way to becoming cancerous. We think that the elevated rate of mutation at sites where DNA has been broken may be an important source of these gene changes."

Wade Hicks builds on this by noting that the mutations are themselves unique, and this could help test the validity of their ideas:

"During repair, mutation rates increase, and the types of mutation during repair are different from normal mutagenesis. It would be interesting to do an in depth analysis of the types of mutations in cancer cells and compare to those we observed in a repair event to see if they match up."

Their examination of gene conversion revealed that the copying of DNA during repair was often interrupted, which presented major complications. Most strikingly, the copying mechanisms would often choose the wrong template when they restarted, choosing an unhelpful sequence that provided little useful information for the strand in need of repair, which naturally created errors and mutations in the repair process. Gene conversion also fails to use another cellular repair system known as "mismatch repair", which is the only way the cell can notice and fix mutations that crop up. As such, gene conversion leaves all mutations in place, hastening their takeover of the cell's DNA.

The researchers say they will next focus on how often these template switches occur and what proteins are involved in the process. The hope is that this will better explain the runaway mutagenesis that leads to cancer and perhaps offer some clue as to how to prevent it from happening in the first place.

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