可汗学院新SAT阅读真题下载(68篇)

可汗学院新SAT阅读真题下载(68篇)

可汗学院新SAT阅读真题下载

到目前为止,新版SAT可汗学院官方不断放出更多真题,已经放出了68篇阅读,具体如下:Level 2 22篇,Level 3 21篇,Level 4 17篇,8篇Diagnostic Quiz,共68篇阅读!

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Level 2 Science篇1

Passage adapted from Nikhil Swaminathan, "Eat (Less) to Live (Longer)," ©2007 by Scientific American.

Scientists have known for more than 70 years that the one surefire way to extend the lives of animals was to cut calories by an average of 30 to 40 percent. The question was: Why? Now a new study begins to unravel the mystery and the mechanism by which reducing food intake protects cells against aging and age-related diseases.

Researchers report in the journal Cell that the phenomenon is likely linked to two enzymes—SIRT3 and SIRT4—in mitochondria (the cell's powerhouse that, among other tasks, converts nutrients to energy). They found that a cascade of reactions triggered by lower caloric intake raises the levels of these enzymes, leading to an increase in the strength and efficiency of the cellular batteries. By invigorating the mitochondria, SIRT3 and SIRT4 extend the life of cells, by preventing flagging mitochondria from developing tiny holes (or pores) in their membranes that allow proteins that trigger apoptosis, or cell death, to seep out into the rest of the cell.

"We didn't expect that the most important part of this pathway was in the mitochondria," says David Sinclair, an assistant professor of pathology at Harvard Medical School and a study co-author. "We think that we've possibly found regulators of aging."

In 2003 Sinclair's lab published a paper in Nature that described the discovery of a gene that switched on in the yeast cell in response to calorie restriction, which Sinclair calls a "master regulator in aging." Since then, his team has been searching for an analogous gene that plays a similar role in the mammalian cell.

The researchers determined from cultures of human embryonic kidney cells that lower caloric intake sends a signal that activates a gene inside cells that codes for the enzyme NAMPT (nicotinamide phosphoribosyltransferase). The two- to four-fold surge in NAMPT in turn triggers the production of a molecule called NAD (nicotinamide adenine dinucleotide), which plays a key role in cellular metabolism and signaling.

The uptick in NAD levels activates the SIRT3 and SIRT4 genes, increasing levels of their corresponding SIRT3 and SIRT4 enzymes, which then flood the interior of the mitochondria. Sinclair says he's not sure exactly how SIRT3 and SIRT4 beef up the mitochondria's energy output, but that events leading to cell death are at the very least delayed when there are vast quantities of the enzymes.

SIRT3 and SIRT4 are part of a family called sirtuins (SIRT1, which helps extend cell life by modulating the number of repair proteins fixing DNA damage both inside and outside the cell's nucleus, is also a member). SIRT is short for sir-2

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