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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。
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.
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.
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.
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.
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.
The main purpose of the sixth paragraph(the underlined paragraph) is to
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.
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."
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.
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 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.
"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.”
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.”
2. 原理即是原因，是解释how does sth. work。
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.