Which type of input is the primary cause of contract changes ？（）

A:Independent estimate B:Organizational policie C:Statement of wor D:Approved changes request

Clever genetic detective work may have found out the reason why a near-starvation diet prolongs the life of many animals.
Ronald Kahn at Harvard Medical School in Boston, US, and his colleagues have been able to extend the lifespan (寿命) of mice by 18 percent by blocking the rodent’s (啮齿动物) increase of fat in specific cells. This suggests that thinness-and not necessarily diet-promotes long life in "calorie (热量单位，卡) restricted" animals.
"It’s very cool work," says aging researcher Cynthia Kenyon of the University of California, San Francisco. "These mice eat all they want, lose weight and live longer. It’s like heaven. "
Calorie restriction dramatically extends the lifespan of organisms as different as worms and rodents. Whether this works in humans is still unknown, partly because few people are willing to submit to such a strict diet.
But many researchers hope they will be able to trigger the same effect with a drug once they understand how less food leads to a longer life. One theory is that eating less reduces the increase of harmful things that can damage cells. But Kahn’s team wondered whether the animals simply benefit by becoming thin.
To find out, they used biology tricks to disrupt the insulin (胰岛素) receptor (受体) gene in lab mice—but only in their fat cells. "Since insulin is needed to help fat cells store fat, these animals were protected against becoming fat," explains Kahn.
This slight genetic change in a single tissue had dramatic effects. By three months of age, Kahn’s modified mice had up to 70 percent less body fat than normal control mice, despite the fact that they ate 55 percent more food per gram of body weight.
In addition, their lifespan increased. The average control mouse lived 753 days, while the thin rodents averaged a lifespan of 887 days. After three years, all the control mice had died, but one-quarter of the modified rodents were still alive.
"That they get these effects by just manipulating the fat cells is controversial, "says Leonard Guarente of the Massachusetts Institute of Technology, who studies calorie restriction and aging.
But Guarente says Kahn has yet to prove that the same effect is responsible for increased lifespan in calorie restricted animals. "It might be the same effect or there might be two routes to long life," he points out, "and that would be very interesting./

According to the passage, we do not know whether humans will benefit from taking in fewer calories partly because （　）.

A:humans, worms and rodents are different B:most people are not willing to be put on a strict diet C:the effect is not known D:genetic changes in tissues can not be performed on humans

Clever genetic detective work may have found out the reason why a near-starvation diet prolongs the life of many animals.
Ronald Kahn at Harvard Medical School in Boston, U.S., and his colleagues have been able to extend the lifespan (寿命) of mice by 18 per cent by blocking the rodent’s (啮齿动物) increase of fat in specific cells. This suggests that thinness--and not necessarily diet--promotes long life in "calorie (热量卡) restricted" animals.
"It’s very cool work," says aging researcher Cynthia Kenyon of the University of California, San Francisco. "These mice eat all they want, lose weight and live longer. It’s like heaven."
Calorie restriction dramatically extends the lifespan of organisms as different as worms and rodents. Whether this works in humans is still unknown partly because few people are willing to submit to such a strict diet.
But many researchers hope they will be able to trigger the same effect with a drug once they understand how less food leads to a longer life. One theory is that eating less reduces the increase of harmful things that can damage cells. But Kahn’s team wondered whether the animals simply benefit by becoming thin.
To find out, they used biology tricks to disrupt the insulin (胰岛素) receptor (受体) gene in lab mice, but only in their fat cells. "Since insulin is needed to help fat cells store fat, these animals were protected against becoming fat," explains Kahn.
This slight genetic change in a single tissue had dramatic effects. By three months of age, Kahn’s modified mice had up to 70 per cent less body fat than normal control mice, despite the fact that they ate 55 per cent more food per gram of body weight.
In addition, their lifespan increased. The average control mouse lived 753 days, while the thin rodents averaged a lifespan of 887 days. After three years, all the control mice had died, but one-quarter of the modified rodents were still alive.
"That they get these effects by just manipulating the fat cells is controversial," says Leonard Guarente of the Massachusetts Institute of Technology, who studies calorie restriction and aging.
But Guarente says Kahn has yet to prove that the same effect is responsible for increased lifespan in calorie-restricted animals. "It might be the same effect or there might be two routes to long life," he points out, "and that would be very interesting./
According to the passage, we do not know whether humans will benefit from taking in fewer calories partly because ______.

A:humans, worms and rodents are different B:most people are not willing to be put on a strict diet C:the effect is not known D:genetic changes in tissues can not be performed on humans

Natural selection describes the biological process in which the differences of individuals within a population influences their abilities to survive and reproduce in an environment. The differences in individuals is a result of their genetic inheritance from their parents. In a population, any characteristic which blocks reproduction success tends to decrease generation by generation. In time, the ill-adapted die out. On the other hand,the individuals who do survive and reproduce will tend to produce offspring which are better adapted to the environment. Natural selection tends to promote adaptations that will increase the organism’s ability to survive in an environment.
Natural selection can serve to stabilize a population if the new traits, called mutations, are eliminated when they appear because they are not as well-adapted to the environment. The opposite effect is obtained when a new trait is introduced which allows individuals to adapt better over time, the species will change as this mutation becomes more widespread in the population. In human beings, increased brain size helped individuals to adapt better, and so brain size increased gradually in the species. Changes in the overall genetic makeup of a population are normal when there are environmental changes, especially sever environmental disruptions. Specialized adaptations to specific environments can lead, over time, to the development of subpopulation of individuals, ones who are better adapted to particular soil conditions food sources and so on. Given
enough time, these subpopulations may develop into separate species, such as zebras and horses, living in distinct environments and not interbreeding.

Individuals in a population differ from one another because（）

A:they have different success generation by generation B:they are ill-adapted and eventually die out C:they have different genetic inheritances D:they want to survive and reproduce successfully

Clever genetic detective work may have found out the reason why a near-starvation diet prolongs the life of many animals.
Ronald Kahn at Harvard Medical School in Boston, US, and his colleagues have been able to extend the lifespan (寿命) of mice by 18 percent by blocking the rodent’s (啮齿动物) increase of fat in specific cells. This suggests that thinness—and not necessarily diet— promotes long life in "calorie (热量单位, 卡) restricted" animals.
"It’s very cool work, "says aging researcher Cynthia Kenyon of the University of California, San Francisco. "These mice eat all they want, lose weight and live longer. It’s like heaven."
Calorie restriction dramatically extends the lifespan of organisms as different as worms and rodents. Whether this works in humans is still unknown, partly because few people are willing to submit to such a strict diet.
But many researchers hope they will be able to trigger the same effect with a drug once they understand how less food leads to a longer life. One theory is that eating less reduces the increase of harmful things that can damage cells. But Kahn’s team wondered whether the animals simply benefit by becoming thin.
To find out, they used biology tricks to disrupt the insulin (胰岛素) receptor (受体) gene in lab mice—but only in their fat cells. "Since insulin is needed to help fat ceils store fat, these animals were protected against becoming fat," explains Kahn.
This slight genetic change in a single tissue had dramatic effects. By three months of age, Kahn’s modified mice had up to 70 percent less body fat than normal control mice, despite the fact that they ate 55 percent more food per gram of body weight.
In addition, their lifespan increased. The average control mouse lived 753 days, while the thin rodents averaged a lifespan of 887 days. After three years, all the control mice had died, but one-quarter of the modified rodents were still alive.
"That they get these effects by just manipulating the fat cells is controversial," says Leonard Guarente of the Massachusetts Institute of Technology, who studies calorie restriction and aging.
But Guarente says Kahn has yet to prove that the same effect is responsible for increased lifespan in calorie-restricted animals. "It might be the same effect or there might be two routes to long life," he points out, "and that would be very interesting./

According to the passage, we do not know whether humans will benefit from taking in fewer calories partly because （　）.

A:humans, worms and rodents are different B:most people are not willing to be put on a strict diet C:the effect is not known D:genetic changes in tissues can not be performed on humans

Eat More, Weigh Less, Live Longer
Clever genetic detective work may have found out the reason why a near-starvation diet prolongs the life of many animals.
Ronald Kahn at Harvard Medical School in Boston, US, and his colleagues have been able to extend the lifespan (寿命) of mice by 18 per cent by blocking the rodent’s (啮齿动物) increase of fat in specific cells. This suggests that thinness—and not necessarily diet—promotes long life in "calorie (热量卡) restricted" animals.
"It’s very coal work," says aging researcher Cynthia Kenyon of the University of California, San Francisco. "These mice eat all they want, lose weight and live longer. It’s like heaven."
Calorie restriction .dramatically extends the lifespan of organisms as different as worms and rodents. Whether this works in humans is still unknown, partly because few people are willing to submit to such a strict diet.
But many researchers hope they will be able to trigger the same effect with a drug once they understand how less .food leads to a longer life. One theory is that eating less reduces the increase of harmful things that can damage cells. But kahn’s team wondered whether the animals simply benefit by becoming thin:
To find out, they used biology tricks to disrupt the insulin (胰岛素) receptor (受体) gene in lab mice—but only in their fat cells. "Since insulin is needed to help fat cells store fat, these animals were protected against becoming fat," explains Kahn.
This slight genetic change in a single tissue had dramatic effects. By three months of age, Kahn’s modified mice had up to 70 per cent less body fat than normal control mice, despite the fact that they ate 55 per cent more food per gram of body weight.
In addition, their lifespan increased. The average control mouse lived 753 days, while the thin rodents averaged a lifespan of 887 days. After three years, all the control mice had died, but one-quarter of the modified rodents were still alive.
"That they get these effects by just manipulating the fat cells is controversial," says Leonard Guarente of the Massachusetts Institute of Technology, who studies calorie restriction and aging..
But Guarente says Kahn has yet to prove that the same effect is responsible for increased lifespan in calorie-restricted animals. "It might be the same effect or there might be two routes to long life," he points out, "and that would be very interesting./

According to the passage, we do not know whether humans will benefit from taking in fewer calories partly because（　）.

A:humans, worms and rodents are different. B:most people are not willing to be put on a strict diet. C:the effect is not known. D:genetic changes in tissues can not be performed on humans.

Eat More, Weigh Less, Live Longer
Clever genetic detective work may have found out the reason why a near-starvation diet prolongs the life of many animals.
Ronald Kahn at Harvard Medical School in Boston, US, and his colleagues have been able to extend the lifespan (寿命) of mice by 18 per cent by blocking the rodent’s (啮齿动物) increase of fat in specific cells. This suggests that thinness—and not necessarily diet—promotes long life in "calorie (热量卡) restricted" animals.
"It’s very coal work," says aging researcher Cynthia Kenyon of the University of California, San Francisco. "These mice eat all they want, lose weight and live longer. It’s like heaven."
Calorie restriction .dramatically extends the lifespan of organisms as different as worms and rodents. Whether this works in humans is still unknown, partly because few people are willing to submit to such a strict diet.
But many researchers hope they will be able to trigger the same effect with a drug once they understand how less .food leads to a longer life. One theory is that eating less reduces the increase of harmful things that can damage cells. But kahn’s team wondered whether the animals simply benefit by becoming thin:
To find out, they used biology tricks to disrupt the insulin (胰岛素) receptor (受体) gene in lab mice—but only in their fat cells. "Since insulin is needed to help fat cells store fat, these animals were protected against becoming fat," explains Kahn.
This slight genetic change in a single tissue had dramatic effects. By three months of age, Kahn’s modified mice had up to 70 per cent less body fat than normal control mice, despite the fact that they ate 55 per cent more food per gram of body weight.
In addition, their lifespan increased. The average control mouse lived 753 days, while the thin rodents averaged a lifespan of 887 days. After three years, all the control mice had died, but one-quarter of the modified rodents were still alive.
"That they get these effects by just manipulating the fat cells is controversial," says Leonard Guarente of the Massachusetts Institute of Technology, who studies calorie restriction and aging..
But Guarente says Kahn has yet to prove that the same effect is responsible for increased lifespan in calorie-restricted animals. "It might be the same effect or there might be two routes to long life," he points out, "and that would be very interesting./

According to the passage, we do not know whether humans will benefit from taking in fewer calories partly because（）

A:humans, worms and rodents are different. B:most people are not willing to be put on a strict diet. C:the effect is not known. D:genetic changes in tissues can not be performed on humans.

Clever genetic detective work may have found out the reason why a near starvation diet prolongs the life of many animals.
Ronald Kahn at Harvard Medical School in Boston, U.S., and his colleagues have been able to extend the lifespan of mice by 18 per cent by blocking the rodent’s increase of fat in specific cells. This suggests that thinness and hot necessarily diet promotes long life in "calorie restricted" animals.
"It’s very cool work." says aging researcher Cynthia Kenyon of the University of California, San Francisco. "These mice eat all they want, lose weight and live longer. It’s like heaven."
Calorie restriction dramatically extends the lifespan of organisms as different as worms and rodents. Whether this works in humans is still unknown, partly because few people are willing to submit to such a strict diet.
But many researchers hope they will be able to trigger the same effect with a drug once they understand how less food leads to a longer life. One theory is that eating less reduces the increase of harmful things that can damage cells. But Kahn’s team wondered whether the animals simply benefit by becoming thin.
To find out they used biology tricks to disrupt the insulin (胰岛素) receptor (受体) gene in lab mice but only in their fat cells. "Since insulin is needed to help fat cells store fat, these animals were protected against becoming fat," explains Kahn.
This slight genetic change in a single tissue had dramatic effects. By three months of age, Kahn’s modified mice had up to 70 percent less body fat than normal control mice, despite the fact that they ate 55 percent more food per gram of body weight.
In addition, their lifespan increased. The average control mouse lived 753 days, while the thin rodents averaged a lifespan of 887 days. After three years, all the control mice had died, but one-quarter of the modified rodents were still alive.
"That they get these effects by just manipulating the fat cells is controversial," says Leonard Guarente of the Massachusetts Institute of Technology, who studies calorie restriction and aging.
But Guarente says Kahn has yet to prove that the same effect is responsible for increased lifespan in calorie restricted animals. "It might be the same effect or there might be two routes to long life," he points out, "and that would be very interesting./
According to the passage, we do not know whether humans will benefit from taking in fewer calories partly because ______.

A:humans, worms and rodents are different. B:most people are not willing to be put on a strict diet. C:the effect is not known. D:genetic changes in tissues can not be performed on humans.

{{B}}第三篇{{/B}}

According to the passage, we do not know whether humans will benefit from taking in fewer calories partly because

A:humans, worms and rodents are different. B:most people are not willing to be put on a strict diet. C:the effect is not known. D:genetic changes in tissues can not be performed on humans.