For some time scientists have believed that cholesterol plays a major role in heart disease because people with familial hyperch

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问题     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 (LDL’s), 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.
    Prior to the breakthrough at Kobe University, it was known that LDL’s are secreted from the liver in the form of a precursor, called very low-density lipoproteins (VLDL’s) , which carry triglycerides as well as relatively small amounts of cholesterol. The triglycerides are removed from the VLDL’s by fatty and other tissues. What remains is a remnant particle that must be removed from the blood. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL remnant requires the LDL receptor. Normally, the majority of the VLDL remnants go to the liver where they bind to LDL receptors and are degraded. In the Watanabe rabbit, due to a lack of LDL receptors on liver cells, the VLDL remnants remain in the blood and are eventually converted to LDL’s. The LDL receptors thus have a dual effect in controlling LDL levels. They are necessary to prevent oversynthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood. With this knowledge, scientists are now well on the way toward developing drugs that dramatically lower cholesterol levels in people afflicted with certain forms of familial hypercholesterolemia.
In the passage, the author is primarily concerned with______.

选项 A、presenting a hypothesis and describing compelling evidence in support of it
B、raising a question and describing an important discovery that led to an answer
C、showing that a certain genetically caused disease can be treated effectively with drugs
D、explaining what causes the genetic mutation that leads to heart disease

答案B

解析 主旨大意题。第一段大部分内容都在解释心脏病与胆固醇之间的关系,在最后一句提出问题:科学家们疑惑,引起血液中低密度脂蛋白去除速度降低的基因突变如何使携带胆固醇的蛋白的合成升高?最后一段第四至八句则对这一问题作出了解释。由此可知,本文作者首先提出了一个问题,然后通过一项实验室研究结果对这一问题作出了回答,故答案为[B]项。
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