喀什治妇科病哪家比较正规(喀什阳痿早泄手术去哪做好) (今日更新中)

WASHINGTON, Aug. 18 (Xinhua) -- Using integrated radar observations from a consortium of international satellites, NASA-funded researchers have created the first complete map of the speed and direction of ice flow in Antarctica, the U.S. National Aeronautics and Space Administration (NASA) announced Thursday.The map, which shows glaciers flowing thousands of miles from the continent's deep interior to its coast, will be critical for tracking future sea-level increases from climate change."This is like seeing a map of all the oceans' currents for the first time. It's a game changer for glaciology," said Eric Rignot of NASA's Jet Propulsion Laboratory and the University of California (UC), Irvine. Rignot is lead author of a paper about the ice flow published online Thursday in Science Express. "We are seeing amazing flows from the heart of the continent that had never been described before."Rignot and UC Irvine scientists used billions of data points captured by European, Japanese and Canadian satellites to weed out cloud cover, solar glare and land features masking the glaciers. With the aid of NASA technology, the team painstakingly pieced together the shape and velocity of glacial formations, including the previously uncharted East Antarctica, which comprises 77 percent of the continent.Like viewing a completed jigsaw puzzle, the scientists were surprised when they stood back and took in the full picture. They discovered a new ridge splitting the 5.4-million-square-mile landmass from east to west.The team also found unnamed formations moving up to 800 feet annually across immense plains sloping toward the Antarctic Ocean and in a different manner than past models of ice migration."The map points out something fundamentally new: that ice moves by slipping along the ground it rests on," said Thomas Wagner, NASA's cryospheric program scientist in Washington. "That's critical knowledge for predicting future sea level rise. It means that if we lose ice at the coasts from the warming ocean, we open the tap to massive amounts of ice in the interior."

WASHINGTON, June 16 (Xinhua) -- Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage. New research by a team of scientists at the University of Rochester has unveiled an important new mechanism that allows cells to recognize when they are under stress and prime the DNA repair machinery to respond to the threat of damage.Their findings will be published Friday in journal Science. Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage.The scientists, led by biologists Vera Gorbunova and Andrei Seluanov, focused on the most dangerous type of DNA damage -- double strand breaks. Unrepaired, this type of damage can lead to premature aging and cancer. They studied how oxidative stress affects efficiency of DNA repair. Oxidative stress occurs when the body is unable to neutralize the highly-reactive molecules, which are typically produced during routine cellular activities.The research team found that human cells undergoing oxidative stress synthesized more of a protein called SIRT6. By increasing SIRT6 levels, cells were able to stimulate their ability to repair double strand breaks. When the cells were treated with a drug that inactivated SIRT6, DNA repair came to a halt, thus confirming the role of SIRT6 in DNA repair. Gorbunova notes that the SIRT6 protein is structurally related to another protein, SIR2, which has been shown to extend lifespan in multiple model organisms."SIRT6 also affects DNA repair when there is no oxidative stress," explains Gorbunova. "It's just that the effect is magnified when the cells are challenged with even small amounts of oxidative stress."SIRT6 allows the cells to be economical with their resources, priming the repair enzymes only when there is damage that needs to be repaired. Thus SIRT6 may be a master regulator that coordinates stress and DNA repair activities, according to Gorbunova.

WASHINGTON, June 16 (Xinhua) -- Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage. New research by a team of scientists at the University of Rochester has unveiled an important new mechanism that allows cells to recognize when they are under stress and prime the DNA repair machinery to respond to the threat of damage.Their findings will be published Friday in journal Science. Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage.The scientists, led by biologists Vera Gorbunova and Andrei Seluanov, focused on the most dangerous type of DNA damage -- double strand breaks. Unrepaired, this type of damage can lead to premature aging and cancer. They studied how oxidative stress affects efficiency of DNA repair. Oxidative stress occurs when the body is unable to neutralize the highly-reactive molecules, which are typically produced during routine cellular activities.The research team found that human cells undergoing oxidative stress synthesized more of a protein called SIRT6. By increasing SIRT6 levels, cells were able to stimulate their ability to repair double strand breaks. When the cells were treated with a drug that inactivated SIRT6, DNA repair came to a halt, thus confirming the role of SIRT6 in DNA repair. Gorbunova notes that the SIRT6 protein is structurally related to another protein, SIR2, which has been shown to extend lifespan in multiple model organisms."SIRT6 also affects DNA repair when there is no oxidative stress," explains Gorbunova. "It's just that the effect is magnified when the cells are challenged with even small amounts of oxidative stress."SIRT6 allows the cells to be economical with their resources, priming the repair enzymes only when there is damage that needs to be repaired. Thus SIRT6 may be a master regulator that coordinates stress and DNA repair activities, according to Gorbunova.

LOS ANGELES, July 28 (Xinhua) -- Mainly due to rampant obesity, Americans' life expectancy is one-and-a-half-year shorter than that of Western Europeans on the average, according to a new study published on Thursday.But 40 years ago, Americans could expect to live slightly longer than Europeans, said the study jointly conducted by researchers from University of Southern California (USC), the Harvard School of Public Health and the RAND Corp., a non-profit think tank.In addition to Western Europeans, Americans also die younger than the residents of most other developed nations, according to the study appearing in the July issue of Social Science & Medicine.The life-expectancy disparity, which begins around the age of 50, stems from higher levels of middle-age obesity and obesity-related chronic diseases, such as hypertension and diabetes, said the study.In the first half of the last century, average life expectancy increased by saving more babies, said author Dana Goldman, director of the Schaeffer Center for Health Policy and Economics at the USC."But now it is reduction in mortality among the elderly, rather than the young, that propels increases in life expectancy," he said. "The question is whether 'being American' is an independent mortality risk factor."If 50-year-old U.S. adults could be as healthy as Europeans, it could save Medicare and Medicaid 632 billion dollars by 2050, the study said.Though the transition to better health initially raises expenditures, the researchers estimate that by 2050 healthcare savings from health improvements among the middle age could total more than 1.1 trillion dollars."The international life expectancy gap appears much easier to explain than gaps within countries: there is no American-specific effect on longevity beyond differences in disease at age 50," said Darius Lakdawalla, an associate professor in the USC School of Policy, Planning and Development.

来源：资阳报