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SAN FRANCISCO, June 20 (Xinhua) -- Google and the British Library announced Monday that the Internet search giant will digitize 250,000 out-of-copyright books from the library's collections, making up to 40 million pages from 1700 to 1870 available to the public online.In a joint statement, the British Library and Google said they will work in partnership over the coming years to deliver the content free through Google Books and the library's website, and full text search, download and reading will be available. Google will cover all digitization costs.The project is going to cover a huge range of printed books, pamphlets and periodicals dated 1700 to 1870, a period of political and technological turmoil, from the Industrial Revolution to the French Revolution, from the introduction of the income tax in Britain and the invention of the telegraph and railway.It will include material in a variety of major European languages and will focus on books that are not yet freely available in digital form online, said the statement.Since December 2004, Google has announced partnership with some 40 high-profile university and public libraries, planning to digitize and make available some 15 million volumes within a decade through Google Books service.The project has triggered controversy as publisher and author associations oppose the plan to put copyrighted titles online in a class action lawsuit.

BEIJING, July 5 (Xinhuanet) -- A black iPhone 4 prototype has appeared for sale on eBay and the highest bidding hit one million U.S. dollars as of Monday, according to media reports.The listing is set to expire on July 11.The seller "jtmaxo" said, "I am a licensed cell phone repairman, this iPhone was bought from a person who really didn't know who he had."The seller later was frustrated to find that it was unable to be activated via iTunes.According to a check through Apple’s database, it is indeed listed as a prototype, and it has the tester code "DF1692" etched in the bottom right corner.Different from the iPhone 4 sold on markets, the handset lacks the + and - on the volume buttons, although the screen is fully functional.The price for the prototype will not remain as high as it is as the seller said that several "non-legitimate" bids have already been deleted.

WASHINGTON, June 23 (Xinhua) -- NASA's next Mars rover has completed the journey from its California birthplace to Florida in preparation for launch this fall, the U.S. space agency said Thursday in a statement.The Mars Science Laboratory (MSL) rover, also known as Curiosity, arrived Wednesday at NASA's Kennedy Space Center aboard an Air Force C-17 transport plane. It was accompanied by the rocket-powered descent stage that will fly the rover during the final moments before landing on Mars.The rover's aeroshell -- the protective covering for the trip to the Red Planet -- and the cruise stage, which will guide it to Mars, arrived at Kennedy last month. The mission is targeted to launch from Cape Canaveral Air Force Station between Nov. 25 and Dec. 18. The car-size rover will land on Mars in August 2012.The rover and other spacecraft components will undergo more testing before mission staff stack them and fuel the onboard propulsion systems. Curiosity should be enclosed in its aeroshell for the final time in September and delivered to Kennedy's Launch Complex 41 in early November for integration with a United Launch Alliance Atlas V rocket.Curiosity is about twice as long and more than five times as heavy as any previous Mars rover. Its 10 science instruments include two for ingesting and analyzing samples of powdered rock delivered by the rover's robotic arm. During a prime mission lasting one Martian year -- nearly two Earth years -- researchers will use the rover's tools to study whether the landing region has had environmental conditions favorable for supporting microbial life and favorable for preserving clues about whether life existed.

LOS ANGELES, July 18 (Xinhua) -- At least 70 genetic mutations may be involved in the formation of colon cancer, far more than scientists previously thought, a new study suggests.The study by researchers at University of Texas (UT) Southwestern Medical Center contradicts previous thinking that only a few mutated genes may play a role in the development of colon cancer."The ways we've been treating patients up to now is to just go after one target when we should be going after three to four different pathways simultaneously," said Dr. Jerry W. Shay, vice chairman and professor of cell biology at UT Southwestern.The new study identified 65 candidate genes and at least five passenger genes whose mutations play significant roles in cancer development. Inactivating the function of any of these tumor- suppressing genes led to a key step in cancer development called anchorage-independent growth, meaning cells piled up on top of each other rather than aligning neatly.According to previous studies, there were 151 candidate genes and that mutations in just eight to 15 of them would lead to cancer. There were 700 other genes classified as passenger genes whose mutations were incidental to cancer growth.Current cancer treatments target just one or two known cancer- driver genes. While patients may get transient tumor burden reduction, almost universally tumor growth returns."Those numbers are dead wrong," Dr. Shay said, suggesting a new approach to colon cancer treatments targeting multiple genes and pathways simultaneously.The next step is further research to classify more accurately which genes drive cancer and which are merely passengers, the researchers said.Study findings were published in the July 2011 Cancer Research (Priority Reports).

WASHINGTON, June 14 (Xinhua) -- Eating a low-carbohydrate, high- protein diet may reduce the risk of cancer and slow the growth of tumors already present, according to a study published Tuesday in Cancer Research, a journal of the American Association for Cancer Research.The study was conducted in mice, but the scientists involved agree that the strong biological findings are definitive enough that an effect in humans can be considered."This shows that something as simple as a change in diet can have an impact on cancer risk," said lead researcher Gerald Krystal, a scientist at the British Columbia Cancer Research Center.Krystal and his colleagues implanted various strains of mice with human tumor cells or with mouse tumor cells and assigned them to one of two diets. The first diet, a typical Western diet, contained about 55 percent carbohydrate, 23 percent protein and 22 percent fat. The second, which is somewhat like a South Beach diet but higher in protein, contained 15 percent carbohydrate, 58 percent protein and 26 percent fat. They found that the tumor cells grew consistently slower on the second diet.As well, mice genetically predisposed to breast cancer were put on these two diets and almost half of them on the Western diet developed breast cancer within their first year of life while none on the low-carbohydrate, high-protein diet did. Interestingly, only one on the Western diet reached a normal life span ( approximately 2 years), with 70 percent of them dying from cancer while only 30 percent of those on the low-carbohydrate diet developed cancer and more than half these mice reached or exceeded their normal life span.Krystal and colleagues also tested the effect of an mTOR inhibitor, which inhibits cell growth, and a COX-2 inhibitor, which reduces inflammation, on tumor development, and found these agents had an additive effect in the mice fed the low-carbohydrate, high-protein diet.When asked to speculate on the biological mechanism, Krystal said that tumor cells, unlike normal cells, need significantly more glucose to grow and thrive. Restricting carbohydrate intake can significantly limit blood glucose and insulin, a hormone that has been shown in many independent studies to promote tumor growth in both humans and mice.Furthermore, a low-carbohydrate, high-protein diet has the potential to both boost the ability of the immune system to kill cancer cells and prevent obesity, which leads to chronic inflammation and cancer.

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