GRE阅读练习每日一篇(五十)_GRE阅读

GRE阅读练习每日一篇(五十)

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　　For some time scientists have believed that cholesterol plays a major role in heart disease because people with familial hypercholesterolemia , a genetic defect, have six to eight times the normal level of cholesterol in their blood and they invariably develop heart disease. These people lack cell-surface receptors for low-density lipoproteins , which are the fundamental carriers of blood cholesterol to the body cells that use cholesterol. Without an adequate number of cell-surface receptors to remove LDL s from the blood, the cholesterol-carrying LDL s remain in the blood, increasing blood cholesterol levels. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL s than normal individuals. How, scientists wondered, could a genetic mutation that causes a slowdown in the removal of LDL s from the blood also result in an increase in the synthesis of this cholesterol-carrying protein?

　　Since scientists could not experiment on human body tissue, their knowledge of familial hypercholesterolemia was severely limited. However, a breakthrough came in the laboratories of Yoshio Watanabe of Kobe University in Japan in 1980. Watanabe noticed that a male rabbit in his colony had ten times the normal concentration of cholesterol in its blood. By appropriate breeding, Watanabe obtained a strain of rabbits that had very high cholesterol levels. These rabbits spontaneously developed heart disease. To his surprise, Watanabe further found that the rabbits, like humans with familial hypercholesterolemia, lacked LDL receptors. Thus, scientists could study these Watanabe rabbits to gain a better understanding of familial hypercholesterolemia in humans.