2007年12月28日星期五
Microsoft's Piracy Fight Gains Momentum in China
Pirates at work Despite the progress being made, pirated software is still readily available on the streets of Shanghai. Fuzhou Road in the former British concession near the Bund, an area famous for bookstores and art boutiques, is also locally renowned as a place to buy pirate PCs and software. The small alleyways running off Fuzhou Road host dozens of pirate PC shops, which usually have no signs. Locals ask passersby if they want to buy "cheap" PCs or software before leading potential customers to the store. Once a computer is assembled, the customer is given a list of pirated software options, ranging from Microsoft Office to Adobe Systems' Photoshop. If a software program is not there, it can be ordered. The government decree requiring PC makers to pre-install an operating system sought to address the problem of Chinese consumers buying computers without software and then opting to buy less expensive counterfeit software. Beijing went one step further, calling on any Chinese companies wanting to do business with the government to run properly licensed software. "The whole situation is heading in the right direction," said Hao Jing, spokeswoman at Founder Technology Group, China's second-largest PC maker. "Pre-installing genuine copyrighted operating systems has become an industry standard." Earlier this year, the Chinese police and the U.S. Federal Bureau of Investigation seized $500 million worth of pirated software, including counterfeit Microsoft and Symantec products, from a Chinese piracy syndicate. "We've seen in the last two years significant emphasis on legitimate intellectual property use in China," said Cori Hartje, director of Microsoft's genuine software initiative. Microsoft said it needs to do more in educating consumers to the benefits of getting genuine software like access to software updates and better security. Improved technology also serves to deter piracy. Windows Vista, the latest version of its operating system, has been more effective in preventing piracy. Microsoft has said piracy rates for Vista are half the level of its predecessor Windows XP. In Vista's first major update due out next year, Microsoft said it plans to close two primary methods used by software pirates to illegally copy Windows Vista.
2007年12月27日星期四
Japan's DoCoMo May Tap Google on Phones
2007年12月21日星期五
U.S. Wavers Again on ITER
By Dennis Normile
with reporting by Daniel Clery and Adrian Cho.
ScienceNOW Daily News
21 December 2007
"I don't think there would be a big impact on the overall ITER plan" if the U.S. contribution is delayed, says Hiroki Matsuo, director for fusion energy at Japan's Ministry of Education, Culture, Sports, Science, and Technology. He says that the project is at the stage at which partners are making components, and rescheduling could accommodate a late part or two. It would be a more serious matter if the United States withdraws from ITER or fails to provide the funding it has promised, says Norbert Holtkamp, principal deputy director-general of the ITER organization. Even then, however, Holtkamp says a 9%26#37; hole in the budget "will do harm, but it's not going to kill" ITER. The European Union, as host, has agreed to provide 49%26#37; of the budget, with the other partners--Japan, China, India, Russia, South Korea, and the United States--divvying up the rest.
This is just the latest U.S. flip-flop on ITER, which is intended to demonstrate the feasibility of harnessing the fusion reaction that powers the sun to produce electricity without the emission of greenhouse gases. In 1985, the United States and the then-Soviet Union announced the project, which soon became a global effort. Midway through the design phase, however, Congress cut all funding, and the United States dropped out (ScienceNOW, 7 May 1998). In 2003, the United States got back into the game for the implementation phase (ScienceNOW, 31 January 2003).
As much as money, what the other ITER partners now want from the United States is clarity. "ITER is waiting for a statement from the U.S. on how they will deal with this," Holtkamp says. So, it turns out, are officials from the U.S. Department of Energy (DOE), the agency responsible for providing the U.S. share. "The Department of Energy is reviewing the budget situation and its implications, as well as assessing options for the U.S. government to continue to meet its commitment to this important international research program," says a department spokesperson, calling the 2008 number a "disappointing" level of funding.
In addition to zeroing out the budget line for ITER, Congress expressly forbade DOE to shuffle money from other programs to satisfy its promise to the ITER partners. But John Marburger, science adviser to President George W. Bush, believes that the prohibition will not stand and that DOE will be forced to dip into other programs. "I can't see DOE not living up to its obligations," Marburger told Science earlier this week. "The department will have to use its money to stay in the project, so [the language] really just amounts to another earmark."
Ironically, Congress did provide DOE with $93.5 million to operate the three smaller U.S. fusion experiments--$6 million more than it requested. Ordinarily, the extra money would come as a great relief to fusion researchers, who in recent years have worried that DOE will sacrifice the domestic fusion program to fund ITER. But U.S. researchers don't want to sacrifice ITER to maintain the domestic program, either, says Stewart Prager, a physicist at the University of Wisconsin, Madison, and chair of DOE's Fusion Energy Sciences Advisory Committee: "This goes catastrophically the other way."
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2007年12月20日星期四
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2007年12月15日星期六
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2007年12月13日星期四
Ape See, Ape Do
By Mitch Leslie
ScienceNOW Daily News
13 December 2007
Whether we're watching a movie or having coffee with an old friend, often we rapidly and unconsciously mirror the facial expressions of people we are looking at. Smiles, laughs, and grimaces of disgust are contagious. Why we're such copycats isn't clear. Youngsters might be learning the right moves for communication. Facial mimicry may also aid interpretation: To understand an expression, the brain recreates it. Some researchers think that emulating an expression might elicit the same feelings in the viewer, creating empathy.
To determine whether the ability extends to apes, behavioral biologist Marina Davila Ross and colleagues at the University of Veterinary Medicine Hannover in Germany videotaped pairs of young orangutans at play. They analyzed instances in which one of the playmates produced a neutral expression or a so-called open-mouth face (see video), which might be equivalent to the human smile. As the team reports this week in Biology Letters, if an orangutan showed the open-mouth face, its partner was likely to follow suit in less than half a second. When the researchers broke down the interactions by age, they found that mimicry was more common among juveniles and adolescents and when the two playmates were more than 2 years apart in age.
"The study showed for the first time that involuntary mimicry is present in animals, at least for facial displays," says lead author Davila Ross, who's now at the University of Portsmouth in the U.K. However, orangutans didn't always emulate their playmates, and the researchers now want to determine what other factors influence the behavior.
"It's important to demonstrate that facial expression and mimicry have an evolutionary context," says behavioral neuroscientist Stephanie Preston of the University of Michigan, Ann Arbor. That knowledge might help researchers work out how the behavior originated and what role it plays in social situations, she says.
SAP, Nakisa Tackle Workforce Management
2007年12月12日星期三
EMC Tries Again With Invista
2007年12月10日星期一
IBM Blasts Taiwan's Asustek Over Patents
IBM Acquires Arsenal Digital
O RLY? Thank Photoshop For Internet's Goofy Memes
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2007年12月6日星期四
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Fox's Faith-Based Acquisition
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2007年12月5日星期三
Facebook Apologizes For Beacon Blunders
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2007年12月4日星期二
Antibody Therapy Shows Promise for Diabetes
By Jennifer Couzin
ScienceNOW Daily News
3 December 2007
Type 1 diabetes occurs when the immune system attacks and destroys insulin-producing cells in the pancreas. For years, T cells were considered enemy number one, because they commit the actual attacks. But more recently, scientists have eyed another potential culprit: B cells, which may be setting the T cells off by presenting them with antigens, proteins that stimulate the immune system. The drug rituximab, made by Genentech, is an antibody that depletes B cells and has been shown to combat rheumatoid arthritis, another autoimmune disease. With that in mind, an international network of researchers successfully lobbied for a clinical trial of the drug in type 1 diabetes, even though mouse studies were lacking. That trial, begun last year, has enrolled 82 people--the youngest being 8 years old--and will take another year or so to finish.
The absence of mouse studies was "a concern in our scientific community," says immunologist Li Wen of Yale University. With that in mind, she, along with Yale immunologist Mark Shlomchik and their colleagues, genetically engineered a mouse model to test the drug. Wen's animals are predisposed to diabetes and have the human version of CD20, the molecule rituximab targets, on the surface of their B cells. Because mice have an immune response to rituximab, Wen and her colleagues designed a rituximab-like antibody that wouldn't cause this problem.
The researchers tested the drug in mice of various ages, including 4- and 9-week-old animals that didn't have diabetes and older mice within 6 days of diagnosis. In the animals that were still healthy, about 70%26#37; of those receiving the antibody therapy were diabetic by 35 weeks of age, compared to nearly 100%26#37; of those that received a placebo. This translates to a 10- or 15-week delay in developing diabetes--the equivalent of 10 or 15 years in humans, says Wen. In the 14 mice with established diabetes, five stopped needing insulin for more than 2 months, some for up to 5 months, the researchers report in the 3 December issue of the Journal of Clinical Investigation.
As the animals regained their B cells, Wen and her colleagues found that those cells were better behaved than their B-cell predecessors that were wiped out by the drug. For example, the new B cells were less likely to produce autoantibodies that often precede type 1 diabetes, suggesting that the drug had somehow recalibrated the immune system.
Mark Pescovitz, a transplant immunologist at Indiana University, Indianapolis, and head of the rituximab clinical trial, is heartened by the results. "[I'm] even more confident that our study will succeed," he says. Still, Pescovitz worries that the new mouse findings will cause physicians to jump the gun. "I would hope that [doctors] aren't going to run out there with their next diabetic and throw rituximab at them, but there's nothing to stop them," he says. The drug is not without side effects such as infections and rashes, and although Pescovitz is impressed with the mouse work, he notes that many drugs that work in mice fare less well in people.
Waste Energy, Fight Disease
By Steve Mitchell
ScienceNOW Daily News
4 December 2007
Cells produce a molecule called ATP in their mitochondria that provides energy for the body. The weight loss drug 2,4-dinitrophenol (DNP) blocks this process, causing mitochondria to produce heat instead of ATP and forcing cells to metabolize stores of carbohydrates and fat for energy. Although popular in the 1930s, DNP use was discontinued in 1938 after several people died from overheating. More recent research in mice indicates that uncoupling proteins, which reside in the mitochondria and work like DNP, may offer an alternative strategy for weight reduction. Now, a team led by endocrinologist Clay Semenkovich of the Washington University School of Medicine in St. Louis, Missouri, has found that uncoupling protein 1 (UCP1) may also help ward off other conditions.
UCP1 is normally found in body fat, but the researchers genetically engineered mice to express low levels in their skeletal muscles. The mice had higher rates of metabolism but appeared healthy otherwise, and their core body temperature was only 0.5?C higher than that of normal animals. The UCP1 mice lived longer on average, dying at 30 months compared to the 27-month life span of normal animals. Although cancer of the lymphatic system was the most common cause of death in the normal animals, killing 12 of 53, only four of the 51 UCP1 mice died from the disease.
That wasn't the only benefit. Mice that normally develop hardening of the arteries were protected from the condition after being bred to express UCP1 in their skeletal muscles. When UCP1 expression was triggered in the skeletal muscles of mice that were already obese, weight and blood pressure decreased, whereas weight increased in the normal obese animals, the researchers report in the December issue of Cell Metabolism.
Semenkovich's team speculates that the beneficial effects of UCP1 may be due to increased metabolism. Such activity can trigger molecular pathways that result in less of the chronic inflammation that has been associated with age-related diseases. Physiologist Kevin Conley of the University of Washington Medical Center in Seattle thinks something else is going on. The inefficient muscles may spur the genesis of more mitochondria, he says, which could lead to "a rebuilding of the cell that reverses cellular damage that occurs with age and age-related diseases."
Regardless of the mechanism, Semenkovich says the approach may be applicable to humans. "If we can figure out a way to target therapies to do this in skeletal muscles of people, it might be a way to treat age-related diseases," he says. Biologist Patrick Schrauwen of Maastricht University in the Netherlands agrees, but he adds that little is known about uncoupling proteins in humans and more investigation will be necessary before attempting to manipulate them to prevent disease.
2007年11月27日星期二
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2007年11月25日星期日
Researchers Turn Skin Cells Into Stem Cells
By Gretchen Vogel
ScienceNOW Daily News
20 November 2007
The work builds on a study published last year by Shinya Yamanaka of Kyoto University in Japan, which showed that mouse tail cells could be transformed into ES-like cells by inserting four genes (ScienceNOW, 3 July 2006). Those genes are normally switched off after embryonic cells differentiate into the various cell types. In June this year, Yamanaka and another group reported that the cells were truly pluripotent, meaning that they had the potential to grow into any tissue in the body (ScienceNOW, 6 June).
Now the race to repeat the feat in human cells has ended in a tie: Two groups report today that they have reprogrammed human skin cells into so-called induced pluripotent cells (iPSs). In a paper published online in Cell, Yamanaka and his colleagues show that their mouse technique works with human cells as well. And in a paper published online in Science, James Thomson of the University of Wisconsin, Madison, and his colleagues report success in reprogramming human cells, again by inserting just four genes, two of which are different from those Yamanaka uses.
In the new work, Yamanaka and his colleagues used a retrovirus to ferry into adult cells the same four genes they had previously used to reprogram mouse cells: OCT3/4, SOX2, KLF4, and c-MYC. They reprogrammed cells taken from the facial skin of a 36-year-old woman and from connective tissue from a 69-year-old man. Roughly one iPS cell line was produced for every 5000 cells the researchers treated using the technique, an efficiency that enabled them to produce several cell lines from each experiment.
Thomson's team started from scratch, identifying its own list of 14 candidate reprogramming genes. Like Yamanaka's group, the team used a systematic process of elimination to identify four factors: OCT3 and SOX2, as Yamanaka used, and two different genes, NANOG and LIN28. The group reprogrammed cells from fetal skin and from the foreskin of a newborn boy. The researchers were able to transform about one in 10,000 cells, less than Yamanaka's technique achieved, Thomson says, but still enough to create several cell lines from a single experiment.
Although promising, both techniques share a downside. The retroviruses used to insert the genes could cause tumors in tissues grown from the cells. The crucial next step, everyone agrees, is to find a way to reprogram cells by switching on the genes rather than inserting new copies. The field is moving quickly toward that goal, says stem cell researcher Douglas Melton of Harvard University. "It is not hard to imagine a time when you could add small molecules that would tickle the same networks as these genes" and produce reprogrammed cells without genetic alterations, he says.
Once the kinks are worked out, "the whole field is going to completely change," says stem cell researcher Jose Cibelli of Michigan State University in East Lansing. "People working on ethics will have to find something new to worry about."
For a more in-depth news story on this topic, see this week's issue of Science, available online 22 November.
Lyme Disease's Unusual Suspects
By Martin Enserink
ScienceNOW Daily News
21 November 2007
Lyme disease can cause anything from rash to arthritic and psychiatric diseases. Borrelia burgdorferi sensu stricto, the bacterium that causes Lyme disease in the United States, is transmitted to humans by blacklegged ticks. Researchers have assumed that the vast majority of ticks become infected when, as larvae, they take their first blood meal from a white-footed mouse. Indeed, lab studies have shown that as many as 90%26#37; of ticks feeding on an infected mouse pick up the bug, an "extremely high number," says disease ecologist Dustin Brisson of the University of Pennsylvania.
But other species that transmit B. burgdorferi to ticks less efficiently might also spread the disease if they are more numerous or if they are bitten by a large number of ticks. And some studies had suggested this to be the case. For instance, a field trial published in 2004 showed that vaccinating mice against Lyme disease and then releasing them led to only a small decrease in the number of infected ticks.
To get a fuller picture, Brisson and his colleagues pulled together data from their own studies in the Hudson Valley in New York state and from other papers. The team looked at an outer surface protein of B. burgdorferi found in ticks--which can give clues about the vertebrate host--as well as the probabilities that different host species transmit the microbe during a tick bite, the number of larvae feeding on the animals, and population densities. Then they calculated the importance of each of the host species.
White-footed mice account for only a quarter of the total number of infected ticks, the team found. Short-tailed shrews and masked shrews were responsible for another quarter each, and chipmunks for as much as 13%26#37;. That means that mice aren't the "dominant" host at all, says Brisson, and vaccination strategies aimed at mice alone are unlikely to bring Lyme disease under control. Brisson speculates that mice have received a lot of attention in part because they're conspicuous, easy to catch, and ideal lab subjects.
"It's a nice paper," says Durland Fish of Yale University School of Medicine, a co-author of the 2004 vaccination study. However, he believes there are even more culprits. In particular, the team barely looked at birds, he notes, even though one study has shown that robins, which often live close to humans, are very good at transmitting B. burgdorferi to ticks in the lab. "The situation is probably even more complex than we think," Fish says.
Odd Little Stars
By Phil Berardelli
ScienceNOW Daily News
21 November 2007
White dwarfs earn their moniker by being quite small, astronomically speaking. They start out as normal stars, but over billions of years, they expand into red giants before exhausting their energy and collapsing into objects not much bigger than Earth. Until this year, all known white dwarfs followed this pattern, and they all boasted atmospheres consisting of either hydrogen or helium, which can be easily identified by the spectral lines of their respective light.
Not so the nine discovered by an international team and reported in tomorrow's issue of Nature. Plucked from millions of stars and galaxies analyzed over the past 7 years by the Sloan Digital Sky Survey, this bunch burns considerably cooler than normal and contains atmospheres made entirely of carbon, with no traces of hydrogen or helium. Astronomers don't have a clue why. Usually, a star produces excess carbon when it is about to shut down the nuclear-fusion cycle that keeps it burning. No fusion means gravitational collapse followed by a supernova explosion that splashes the star all over its galaxy.
So why are these white dwarfs still around? One possibility, notes astronomer and lead author Patrick Dufour of the University of Arizona, Tucson, is that the stars simply might not have grown massive enough--about 10 times heavier than the sun--to explode but are so close to the limit that they might be harboring abnormally high amounts of carbon. The unique chemical signature of the stars may provide clues to what's going on. "It tells us that nature has found a way that we didn't know to make white dwarf stars without the usual hydrogen or helium surface layers," Dufour says.
A whole new class of carbon-dominated white dwarf stars is a "major discovery," says astronomer Pierre Bergeron of the University of Montreal in Canada. It's something that occurs only once in a decade or so, he says, and the underlying process governing these white dwarfs "will launch an entirely new field of research." Astronomer Klaus Werner of the Institute for Astronomy and Astrophysics in T?bingen, Germany, agrees. "There is currently no explanation how such stars can be formed," he says. "It's a real challenge to stellar-evolution theory."