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2018SAT阅读题型讲解之篇章结构段落目的题

2018年07月04日14:10 来源:小站整理
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摘要:SAT的阅读题型一直非常的稳定。在宏观上主要考查学生是否了解作者如何谋篇布局(篇章结构题),是否清楚作者的观点及其支撑(文本循证题),在微观上,对细节的把握(事实信息)和对文章叙述的某一点的推断(推断题)。本文分析篇章结构中的段落目的题

SAT阅读篇章结构中的段落目的题关键在于我们在学习SAT的过程中要培养的一种非常重要的能力,即把握全篇结构和各段联系的能力。简言之,就是归纳各段段意。这对我们做好篇章结构的题目和文本循证题有极大的帮助。而SAT的四种文体每一种的结构大体是差不多的。我们今天就以科技文为例来具体分析。

2018SAT阅读题型讲解之篇章结构段落目的题图1

首先,我们可以先想一个问题。假设你是一个刚研究出新成果的科研人员,你想把研究的过程和结果展以文章的形式展示给大家,你会如何写每一段的内容?想必大家心里都有自己的答案,那么最简单直接的写法就四步:

1. 介绍话题(introduction):用人们熟悉的话题引出要讲的科研问题。

2. 实验过程(experiment):描述这个实验是怎么做的。

3. 实验结果(results):展示实验都产生了哪些结果。

4. 实验的意义和局限(significance and limitation): 每个科学研究肯定都是进步的,也肯定不是完美的。

如果要问大家这四个部分哪个最重要,那肯定是实验结果部分,因为这是才是我写文章的目的所在。当然这是科技文类最基本的框架,每篇文章肯定在此基础上添加一些内容,不过从这一年多的科技文来看,几乎都符合这个基本结构,所以大家在第一遍浏览科技文的时候就应该把框架看出来,方便我们后面直接解题。例如:

introduction

Willow trees are well-known sources of salicylic acid, and for thousands of years, humans have extracted the compound from the tree’s bark to alleviate minor pain, fever, and inflammation.

Now, salicylic acid may also offer relief to crop plants by priming their defenses against a microbial menace known as “potato purple top phytoplasma” Outbreaks of the cell-wallless bacterium in the fertile Columbia Basin region of the Pacific Northwest in 2002 and subsequent years inflicted severe yield and quality losses on potato crops. The Agricultural Research Service identified an insect accomplice —the beet leafhopper, which transmits the phytoplasma to plants while feeding.

Application

Carefully timed insecticide applications can deter such feeding. But once infected, a plant cannot be cured. Now, a promising lead has emerged. An ARS-University of Maryland team has found evidence that pretreating tomato plants, a relative of potato, with salicylic acid can prevent phytoplasma infections or at least diminish their severity. Treating crops with salicylic acid to help them fend off bacteria, fungi, and viruses isn’t new, but there are no published studies demonstrating its potential in preventing diseases caused by phytoplasmas.

Quotation

Wei Wu, a visiting scientist, investigated salicylic acid’s effects, together with molecular biologist Yan Zhao and others at ARS’s Molecular Plant Pathology Laboratory in Beltsville, Maryland. “This work reached new frontiers by demonstrating that plants could be beneficially treated even before they become infected and by quantifying gene activity underlying salicylic acid’s preventive role,” according to Robert E. Davis, the lab’s research leader.

Experiment

For the study, published in the July 2012 Annals of Applied Biology, the team applied two salicylic acid treatments to potted tomato seedlings. The first application was via a spray solution 4 weeks after the seedlings were planted. The second was via a root drench 2 days before phytoplasma-infected scions were grafted onto the plants’ stems to induce disease. A control group of plants was not treated.

Results

In addition to visually inspecting the plants for disease symptoms, the team analyzed leaf samples for the phytoplasma’s unique DNA fingerprint, which turned up in 94 percent of samples from untreated plants but in only 47 percent of treated ones. Moreover, symptoms in the treated 45 group were far milder than in untreated plants. In fact, analysis of mildly infected treated plants revealed phytoplasma levels 300 times below those of untreated plants, meaning that the salicylic acid treatment must have suppressed pathogen multiplication. Significantly, the 50 remaining 53 percent of treated plants were symptom- and pathogen-free 40 days after exposure to the infected scions.

Researchers credit salicylic acid with triggering “systemic acquired resistance,” a state of general readiness against microbial or insect attack. Using quantitative polymerase chain reaction procedures, the team also identified three regulatory defense genes whose activity was higher in treated plants than in untreated ones.

Limitation and significance

Why salicylic acid had this effect isn’t known. Other questions remain as well, including how treated plants will fare under field conditions. Nonetheless, such investigations could set the stage for providing growers of potato, tomato, and other susceptible crops some insurance against phytoplasmas in outbreak-prone regions.

通过每段开头蓝色标记的寥寥数字我们已经清楚了整篇文章的结构,出了第二部分多了一个application来讲水杨酸的具体应用外,其他部分都符合我们刚才那个模板。所以这篇文章后面的一道SAT段落目的题就非常简单了。

The main purpose of the sixth paragraph(the underlined paragraph) is to

(答案见文末)

A) describe the steps in an experiment.

B) present the results of an experiment.

C) explain why an experiment was conducted.

D) argue that an experiment should be reproduced.

这道题目比较典型,相对简单。我们再看一道SAT阅读里比较难的题目。

Introduction

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.

Biological basis

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.

Quotation

"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."

The process/history of the revelation(step one)

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.

(step two)

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.

(step three)

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.

Application

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 homologue—a well-studied protein that is known to extend yeast cell longevity. According to Sinclair, all of the mammalian SIRT genes (and their proteins) are possible drug targets for therapies aimed at extending life, as well as staving off age-related illnesses, such as Alzheimer’s disease, cancers and metabolic disorders, like diabetes.

Quotation

"I think SIRT3 is the next most interesting sirtuin from a drug development standpoint," Sinclair says. "It does protect cells, but there's growing evidence that it may mediate the benefits of exercise as well.”

Current situation

Sinclair's lab is now working on developing what he calls a possible "supermouse" with elevated levels of NAMPT to see if it lives longer and is more disease-resistant than normal mice.

Significance and limitation

Matt Kaeberlein, a pathologist at the University of Washington in Seattle, says that Sinclair's team has an interesting hypothesis connecting the mitochondria to longevity, but that it needs to be more directly tested in the context of dietary restriction. "If the NAMPT-overexpressing mice are long-lived and disease resistant, that will provide more support for this idea.”

这篇文章并没有实验过程及结果,因为话题就是结果,所以取而代之的,这篇文章介绍了两种酶的发现过程(酵母细胞---哺乳动物细胞NAD---SIRT酶)。

特别要强调的是第二段是全文的核心,因为第二段用非常学术的角度解释了开篇提出的问题,所以SAT阅读中,我们把这段叫做原理段(basis)。在解释型的科技文中肯定会出现原理段,那么这篇文章是生物领域的,所以我们归纳为biological basis。原理段有两大特点:

1. 用词和语言专业,外行看不太懂。

2. 原理即是原因,是解释how does sth. work。

但有些同学会问,为什么第一篇的例文中没有原理段呢?大家回去再读一些第一篇的最后一段的第一句话就知道原因了。那么,我们来看一下相关题目。

The main purpose of the fifth paragraph (lines 30–37) is to(答案见文末)

A) suggest that caloric reduction has a different effect on yeast cells than mammalian cells.

B) highlight the important role that the kidney plays in the aging process.

C) clarify the intermediate steps between caloric reduction and improve mitochondrial efficiency.

D) identify the negative relationship between NAMPT production and NAD production.

通过上文的分析答案应该很明显。其实,我们在SAT阅读科技文时,要通过段落里面的重点句来判断本段的核心是在讲什么,清晰这些结构后对于做对篇章题甚至是文本循证题都非常有帮助。

以上就是小编为大家带来的《2018SAT阅读题型讲解之篇章结构段落目的题》的全部内容,一场考试一场出境自由行,两者兼而有之,岂不快哉。更多SAT资讯,尽在小站SAT频道。

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