方舟子获自然杂志2012年首届John Maddox科学捍卫奖

[向问天]

这个某人就以笔名为亦明的葛辛为代表吧。
他的论证分析不提，但是是否抄袭，把老方的文章和他人之前写的英文原著对比一看是一目了然的事情，花不了多少时间。
不过你看不看不强求，我也无所谓。你既然都没看过，那我就不和你讨论了。

他不是说他没看过，他是说他看了N个， 不想看N+1个

 

[向问天]

臭豆付也有个臭字
而且农民如果是香的,就太不正常了,太监也会生儿子了.

香农民， 太监的儿子

 

[TIFF]

赫赫，这楼还是搭起来了。等一会儿再来慢慢爬楼看看小篆是怎么涮你们这些PHD的。

 

[ABC28]

你不是保守党内边的么？ 你是说女老板男CEO无间道？成心恶心小麦？

女老板和男CEO就不能共事？不要一看到一男一女就是男盗女娼！

 

[扣 扣]

<<<<<你们这些PHD的。

是P多就是PHD吗～～:blowzy:

听说是～～:blowzy:

 

[mimi_ge]

是P多就是PHD吗～～:blowzy:



听说是～～:blowzy:

屁很多，phd

 

[扣 扣]

屁很多，phd

急～～

 

[臭农民]

屁很多，phd

屁还多

 

[扣 扣]

香农民， 太监的儿子

不是说臭农民吧，他是好人～～:blowzy:

 

[ABC28]

方哥得的大奖=诺贝尔奖

 

[uglyducking]

方哥得的大奖=诺贝尔奖

啊呸！太抬举诺贝尔奖了。

 

[老闹子]

我昨天只是根据自然杂志英文网页的内容简单概括。今天有国内的科学网给出了更完整的翻译说明。

http://news.sciencenet.cn/htmlnews/2012/11/271413.shtm

作者：任春晓 来源：科学网 www.sciencenet.cn 发布时间：2012-11-7 10:43:33

方舟子获《自然》首届约翰·马多克斯奖


以《自然》杂志前主编约翰·马多克斯（John Maddox）命名的约翰·马多克斯奖，近日公布了首届获奖者名单。著名科普专家、“打假斗士”方舟子（本名方是民）和英国伦敦大学国王学院心理医学教授西蒙·威斯利（Simon Wessely）获此殊荣。

该奖是为纪念《自然》前主编约翰· 马多克斯，由《自然》杂志和英国慈善组织“科学智识”（Sense About Science）共同发起。奖项旨在表彰那些在公众利益中，即使面临困难或反对，仍然提倡有力的科学和证据的人士。本年度获奖者奖金为2000英镑。

评审小组称赞方舟子在揭露医学门诊使用未经验证的医学疗法，并引导更多读者意识到寻找真相重要性的过程中，勇敢和坚定地面对一些生命威胁。

西蒙·威斯利则因在慢性疲劳综合症和海湾战争综合症宣传方面所表现出的勇气，以及处理威胁与骚扰的方式而获奖。

评审小组成员之一Colin Blakemore教授评论道：“如果科学家都沉默，那么疯子就赢了。”（科学网 任春晓/编译）

 

[Chiffon]

老方不争气，方粉们难得高兴一回。



但是俺忍不住要再当一回坏人，提醒下方粉上回高兴太早的后果：

上次老方的《吃得少活到老》被人指出抄袭，老方立马自证清白说是田清涞抄的他，让方粉们好一阵欢乐。但是天下没有最牛的只有更牛的，资深方黑深入调查，居然发现老方和老田都是抄的：老方那篇3906字的文章，至少有2535字，约占全文的三分之二，抄自一本名为Biology of Aging: Observations and Principles的英文原著，而且抄的时候还犯了一些低级错误。详细对比和分析都在这里：

http://www.2250s.com/read.php?2-17014-17014

就是不晓得有洁癖的方舟子这回怎么不再自证了。也不知道方粉们是不是要为老方辩护：科普文章抄袭不算抄，论文才算抄(哦对了，社科院的硕士论文抄袭也不能算抄）？把英文原著翻成中文当作自己的论述不算抄？

亦明的中英文对照我拷过来，哪句中文算是抄哪句英文，原英文结构、顺序、用词和中文结构、顺序、用词有什么对应关系？我看不出抄袭来，读者自己判断吧。



大约从人类有了死亡意识时候起，就幻想着能找到一种灵丹妙药，或者常吃某种食物得以长生不老，也有许多人妄图将幻想变成现实，结果当然都失败了。但也有人反过来认为饿着肚子才是长生不老的窍门，比如中国的道教就把“辟谷”视为成仙之道，当然，如果一直那么辟下去，那是非离开人间不可的。这些长生不老术都是没有实际依据的臆想，其主张者根本没有想到，一个主张要站得住脚，必须建立在观察和实验的基础之上。

古希腊哲学家亚里斯多德也曾经思考过寿命的问题，他胜过同时代人之处，在于他是一位敏锐的观察者。他根据其观察，猜想动物的寿命长短与其发育期长短有关，发育得越慢，则寿命越长。例如大象是最长寿的哺乳动物之一，而其怀孕期也最长，相反地，家鼠在一年内就能发育成熟、生儿育女，而其寿命则只有数年。
The experiments of McCay and his colleagues, which we will discuss shortly, grew out of the idea that longevity is inversely proportional to developmental rate. This idea was derived partly from the works of philosophers such as Aristotle ……. (p.313)

这个猜想有一定的道理。一般来说，动物的身体体积越大，则新陈代谢率越低，寿命也倾向于越长；而动物的身体体积越大，也意味着需要用更长的发育时间来实现身体蓝图。因此动物发育期和寿命的关系，可能是由于它们都与身体体积有关。也可能是由于相同的生理因素（例如激素）都参与了发育和衰老的过程。还有一种可能是，动物的发育期越长，则身体这台“机器”制造得也就越精致，也就更能经受得起时间的磨损。

但是亚里斯多德并没有意识到，从其猜想可以得出一个推论：如果想办法延缓发育速度，那就可以延长寿命。

1917年，奥斯本（T. B. Osborne）等三位美国生物学家在用大鼠做营养实验时，发现那些没有喂饱的老鼠，生长迟缓，而其寿命似乎也延长了。受到这个结果的启发，1935年，美国康奈尔大学的麦克凯（C. M. McCay）等人直接验证是否动物寿命真的与发育速度成反比。在大鼠断奶后，他们给其中的一组提供完备的营养物质，但是严格限制其饮食，让它们一直处于饥饿中，而另一组老鼠则任其吃饱。受限制的老鼠发育几乎停止，身体也不再长大，一些老鼠夭折了，但是存活下来的老鼠中，寿命明显增长了。雄鼠所受的影响更显著，寿命平均延长了约50％。
This idea was derived partly from the works of philosophers such as Aristotle and partly from the experimental work of Osborne, Mendel, and Ferry (1917), whose data suggested, but did not prove, that underfed rats live longer. McCay, Crowell, and Maynard (1935) demonstrated that rats that were fed a nutritionally complete but calorie-restricted diet from the time of weaning had significantly increases in the values of mean, median, and maximum life span when compared to animals fed a normal diet conducive to rapid growth (Table 7.1). The animals provided with unlimited calories grew and matured normally. In the restricted group, maturation was greatly slowed, although these animals held their weaning weight and suffered from no other nutritional deficiency, since their diet included adequate amounts of protein, vitamins, and minerals. Growth and development in the restricted animals resumed only after they were given additional calories at about 2 years of age. The restricted animals never attained a normal body size or body weight; they remained about 15% smaller than their normal controls. (p.313)

喂食正常的老鼠中，寿命最长的为965天，而限制喂食的老鼠，有的活到了1800多天（相当于人活到200岁）。
McCay’s oldest control rat died at 965 days, whereas his oldest CR rat lived 1,456 days (150 years in human terms). In the 1960s, CR rats in the laboratory of Morris H. Ross at the Institute For Cancer Research in Philadelphia, survived for more than 1,800 days (180 years in human terms). 【Saul Kent. Aging Research Becomes A Science. LE Magazine December 2001.】

以后许多实验室都做了类似的实验，得到了相当一致的结果。
These observations have since been confirmed and extended by many other investigators. (p.313)

多项实验结果都表明，如果让鼠类的食物包含完备的营养物质，但是把食物中的热量减低25-60％，它们在中年后得慢性病的危险减低了，而寿命也延长了大约30％。例如在1986年对小鼠和大鼠同时做的实验表明，卡路里受限制的小鼠平均活47个月，而控制组活28个月；卡路里受限制的大鼠平均活1300天，而控制组平均活720天。
This finding, that animals on a low calorie, nutrient rich diet far outlived animals allowed to eat as much as they wanted, has been replicated a great number of times. One such study with mice and rats by Weindruch (1986) showed that fully fed mice lived on the average 28 months versus the calorie restricted group who lived 47 months. Rat survivals were shown to be approximately 720 days old for those eating ad lib and 1300 days of life if calories were restricted. In these and other studies, calorie restriction is defined as a reduction in calories of 25-60% from ad lib feeding levels while providing an adequate intake of essential vitamins and nutrients. 【Jean E. Pierog. RECIPE FOR LONGEVITY.】

对其他动物，包括脊椎动物和无脊椎动物所做的类似实验，也得到了类似的结果。
The basic observation has been found to apply to other species, both vertebrate and invertebrate, and is hallmarked by its ease of repeatability. (p.313)

而且限制饮食并不一定非要从小限制起不可。从老鼠的“中年”开始将饮食热量减低约30％，也能显著延长其寿命。

限制饮食热量，是迄今为止我们所知道的唯一能够有效地延长动物生命的环境因素。
In fact, caloric restriction is the only environmental means that has been shown to significantly slow the mortality rate of any mammal. (p.313)

卡路里受限制的老鼠不仅活得长，而且显得更健康。
Are these animals that live longer also healthier, or are they sick and feeble? Is the boon of extended longevity a blessing or a curse? What, in other words, is the effect of caloric restriction on age-related pathologies? Many studies have shown that the dietary history of the rodent has a major effect on the age of onset and the incidence of the various age-related pathologies (see Weindruch and Walford 1988 and Merry and Holehan 1994b for references). (pp.314-315)

麦克凯等人当时已发现这些老鼠得各种癌症的危险性降低了，心血管和肾脏的老化也延缓了。
McCay also discovered that calorie restriction inhibited a large variety of cancers and delayed age related deterioration of the vascular system and the kidneys. 【Jean E. Pierog. RECIPE FOR LONGEVITY.】

后来的研究者还发现其他的延缓衰老的标志，
A large body of data (reviewed by Masoro 1988a, 1992a; Weindruch and Walford 1988; Finch 1990

shows that caloric restriction, in addition to having an effect on the age-related pathologies, delays or eliminates the onset of many normal age-related physiological changes. (p.316)

如慢性炎症减少、
and the incidence of chronic tissue inflammations (for example, chronic glomerulonephritis, myocardial fibrosis) and of endocrine hyperplasias is significantly reduced. (p.315)

免疫力提高、
The early effects of restriction seem to depend on the strain, but a general response to the restriction of calories seems to be a decrease in antibody production coupled with an enhanced cell-mediated immunity. (p.316)

对血糖的耐受性增强、
The ability of calorie-restricted animals to satisfy energy requirements with low levels of
blood glucose implies that they can minimize the age-related effects of glycosylation. (p.322)

晚年记忆力提高等。
prevention of the decline in the mouse’s learning ability, (p.316)

这些老鼠对环境致癌物的抵抗力也增强了，用几种不同的致癌物做试验，发现它们因此患癌症的概率显著低于对照组。
Third, the restricted animals have a greater degree of protection against exogenous carcinogens; these rodents showed significantly fewer tumors after exposure to any of several different carcinogens tested. (p.316)

限制卡路里还显著地减少了体内脂肪细胞的数目，从而防止了晚年肥胖；而如果仅仅限制饮食中的脂肪含量，达不到这个效果。
An example of a normal trait that is eliminated in restricted animals is the normal increase in the number of fat cells found in particular fat depots in the rat. Not only does caloric restriction eliminate the increase in fat cells, but it brings about a significant decrease in the fat depot mass as a result of a reduction in the number of fat cells (Masoro 1992). Restricting the amount of fat without restricting the total energy intake did not have this effect. (p.316)

总之，各种研究都表明限制卡路里对动物的衰老过程有根本性的影响，而不只是某些表面效果。
It seems reasonable to assume that caloric restriction is affecting, either directly or indirectly, some fundamental process(es) involved in the regulation of biological aging. (p.317)

限制卡路里对老鼠健康的负面影响主要是生殖力下降了。这种副作用从自然选择的角度看并不难理解。只有在食物充足、能够保证生下的后代能生存时，才有必要将能量用于生殖。限制卡路里实际上是迫使动物改变了生存策略，将用于生殖的能量改用于生存，从短时间内快速生殖改为降低生殖率并生存更长的时间。
Clearly, caloric restriction works. But why should mammals come equipped with a mechanism that enables them to live long if they stay hungry? What is the evolutionary sense behind this concept? One proposal suggests that caloric restriction is best viewed as a special application of the disposable-soma theory (see chapter 4), which is based on the premise that an organism can devote its excess calories, beyond the amount needed for basic and essential functions, to reproduction and/or somatic maintenance. In this view, caloric restriction evolved as the set of mechanisms by which an organism adjusts its reproductive strategy to the conditions of its environment by shifting from rapid reproduction over a short time period to a reduced rate of reproduction over a longer life span (Holliday 1989; Richardson and Pahlavani 1994). (p.325)

但是限制卡路里是通过什么生理机制有益健康的？在回答这个问题之前，我们必须先确信我们所见到的延缓衰老现象的确是由于限制卡路里引起的，而不是由于其他因素，例如动物体内脂肪减少、某种食物成分减少引起的。
It seems reasonable to assume that caloric restriction is affecting, either directly or indirectly, some fundamental process(es) involved in the regulation of biological aging. But what might these process(es) be? And what specific aspect of dietary manipulation is involved? At a minimum, one could hypothesize that the critical variable is the amount of body fat, or the total amount of food eaten, or the total amount of calories taken, or the decreased intake of specific (toxic?) food components such as fats or carbohydrates or proteins, or perhaps more subtle effects, such as the lack of exercise in well-fed laboratory animals or delayed onset of degenerative disease in the restricted animals. (p.317)

体内脂肪的含量看来并不是重要因素。用遗传工程方法我们可以培养出先天性肥胖的小鼠，它们吃得多，长得快，体内脂肪占的比例高，而其寿命也比其他小鼠短。但是这些先天性肥胖的小鼠在卡路里受限制时，它们也可以获得和卡路里受限制的普通小鼠一样长的寿命，尽管其体内脂肪含量是普通小鼠的3.5倍。延缓衰老的效果看来也不是由于限制了某种营养物引起的。
The amount of body fat is not what is important. The mice in one genetically obese strain eat more, gain weight very rapidly, live a shorter time than other mice, and have a high percentage of fat in their body weight (Table 7.2). Yet when these animals are calorically restricted, they exhibit a median and maximum life span comparable to that of their long-lived, calorically restricted controls, even though they still have about 3.5 times as much body fat as do the controls. The increased longevity appears to be related to food consumption as such in these animals, and not to body composition.

实验表明，仅限制某一种食物成分（蛋白质、脂肪、碳水化合物、维生素或微量元素）的含量，而不限制卡路里总量，并不能延长动物寿命。这个结果也说明我们寿命的缩短并不是由于我们饮食中的某种物质引起的，但是食物的热量却能影响寿命长短。许多人批评限制卡路里表现出来的效果只是在实验室条件下出现的假象，并不一定适用于自然条件下的情形。他们认为，由于老鼠在实验室条件下饮食过度又缺乏锻炼，因此寿命本来就比较短，而限制卡路里不过是起到了类似锻炼的效果。但是研究表明锻炼并不能延长那些任意进食的老鼠的寿命。
Furthermore, the diet restriction does not appear to work if it consists of the elimination of any single deleterious component of the diet. The individual restriction of any single food component (such as protein, fats, carbohydrates, fibers, or minerals) to the same extent as observed in the complete diet restriction regime does not markedly affect longevity (Iwasaki et al. 1988; Masoro et al. 1989). It now appears unlikely that diet restriction experiments extend the life span by reducing the intake of a particular single component of the food. This observation suggests that our life span is not shortened as a result of toxic components in our diet, but it does support the idea that longevity is affected by the daily amount of food (calories) eaten. (p.318)

使限制卡路里发挥作用的具体机制还不清楚。一种可能是老鼠的新陈代谢率降低了，也即食物在体内较慢地转化成了能量。这样，所有的生理过程的速度都缓了下来，“生理时间”调慢，因而动物可以活得长一些。
The mechanisms underlying the effectiveness of caloric restriction are not clear. ……As Masoro (1988a) has pointed out, recent studies have eliminated two hypotheses regarding the mechanism of action of dietary restriction and forced the reconsideration of a third.……The third hypothesis was the idea that dietary restriction increases life span by decreasing the metabolic rate. This idea was particularly attractive, since because it has an obvious theoretical connection to the oxidative-damage theory of aging (see chapter 10). (p.321)

研究表明，限制卡路里对单位体重的代谢率的影响并不大，不过既然它们吃下的食物较少，即使单位代谢率不变，总的能量输出还是减少了。进一步的研究表明限制卡路里改变了动物的代谢模式。这些改变包括体温降低、脂肪合成降低而葡萄糖合成增加、在进食前有较低的代谢率而进食后有较高的代谢率等等。这些改变可能减少了代谢过程中产生的有害副产物的产量。
Recent information suggests that this third hypothesis is too simple to be entirely correct, but it is also not entirely wrong. Dietary restriction does affect metabolism, but not in the simple manner envisioned by this theory. Data from the National Institute on Aging–National Center for Toxicological Research (NIA–NCTR) joint biomarker study have shown that caloric restriction induces a major metabolic reorganization in animals (Duffy et al. 1989; Feuers et al. 1991, 1995).
This reorganization includes a lowering of core body temperature, a shift away from fat synthesis and toward glucose synthesis, a change in motor activity such that it is concentrated about the feeding time, and an alteration in the body’s metabolic rate such that restricted animals have a lower than normal metabolic rate before feeding but a higher-than-normal metabolic rate after feeding. One result of such a metabolic shift would be the lowering of the organism’s steady-state production of harmful metabolic by-products that result in oxidative stress and damage (Sohal and Weindruch 1996). (p.321)

这些老鼠体内的胰岛素调控葡萄糖的效率也增高了，因此血糖含量较低，比较不容易得糖尿病。血液中多余的葡萄糖会与体内蛋白质发生自由基氧化反应，生成化学结构发生了变化的糖基化蛋白，使这些蛋白质的正常功能受到影响。蛋白的糖基化可能是衰老过程中最普遍的一种化学变化。卡路里受限制的老鼠由于血糖含量低，相应地发生蛋白糖基化的可能性也降低了。而且，卡路里受限制的动物组织中，“自由基清除剂”过氧歧化酶活性增强了，在其一生中体内自由基含量都保持在较低水平。自由基对生命分子的破坏作用被许多研究者认为是导致衰老的主要因素。
The ability of calorie-restricted animals to satisfy energy requirements with low levels of blood glucose implies that they can minimize the age-related effects of glycosylation. Maintaining an efficient flow of glucose through glycolysis enables calorie-restricted animals to modulate their NADPH pools better. These latter cofactors are known to play an important role in maintaining some of the enzyme systems responsible for the detoxification of free radicals. Thus the ability to maintain “youthful” regulation of this enzyme may spare the organism the harmful effects of glycosylation and free-radical, or oxidative, damage, two harmful processes that can interact synergistically in contributing to the degeneration characteristic of old age (Kristal and Yu 1992). Caloric restriction has been shown to reduce the age-dependent accumulation of advanced glycosylation end products (AGEs) in both red blood cells and skin collagen (Cefalu et al. 1995). In addition, calorie-restricted animals have, in some but not all tissues, a higher level of superoxide dismutase enzyme activity and a lower level of superoxide and/or hydroxide radicals throughout their life span (Lee and Yu 1990). (p.322)

在分子水平上，限制卡路里还导致了许多其他的变化，包括肝脏组织中的酶活性发生改变，细胞修复DNA的能力增强，DNA与致癌物的结合能力降低等。大脑中神经介质的含量也发生了改变，表明神经内分泌系统也受到影响。
In addition to these changes in energy metabolism, a multitude of other enzyme reactions are affected by diet restriction, including liver enzymes known to be involved in drug metabolism and elimination (Leakey et al. 1989). The complexity of these changes is illustrated by the observation that DNA repair activity increases in diet-restricted rodents (Lipman et al. 1989), while the same treatment simultaneously decreases both normal DNA synthesis and the binding of a chemical carcinogen to DNA in vivo (Chow et al. 1993). The observation that caloric restriction brings about various alterations in brain neurotransmitters suggests neuroendocrine
involvement (Kolta et al. 1989). (p.322)

生物学家通常用放着食物的迷宫测试老鼠的学习能力。试验结果表明，限制饮食的中年老鼠和对照组的中年老鼠的学习能力相当，但是限制饮食的老年老鼠却明显胜过对照组的老年老鼠，而保持着中年时期的学习能力。这个研究表明限制卡路里的老鼠虽然发育缓慢，其成年时期的学习能力却没有恶化，反而能将这种能力维持到老年时期。
One unexpected beneficial outcome of diet restriction is its effect on learning performance in mice (Ingram et al. 1987). Both middle-aged and old mice were tested for their learning abilities in a standard maze test. The control and diet-restricted middle-aged adults had comparable learning levels, as indicated by their number of errors per trial. However, the old diet-restricted animals, exhibiting scores comparable to the middle-aged mice, were clearly superior to the old controls. This study is very important because it indicates that the delayed growth and maturation characteristic of diet-restricted animals have no deleterious effect on adult learning abilities but instead maintain these abilities well into the aging process. (p.323)

限制卡路里对老鼠的健康和寿命的积极作用已被充分证明了。我们更关心的是：它是不是也适用于灵长类和人类？在八十年代末，美国有两个研究小组开始对罗猴做限制卡路里实验。由于罗猴的寿命大约为40年，要知道它们的寿命是否延长了还为时过早。不过，它们在限制卡路里的条件下，出现了与老鼠类似的生理变化。与对照组相比，受限制的罗猴显得更健康，更精瘦，血糖浓度和胰岛素浓度较低，对胰岛素的敏感度增强。
Caloric restriction works wonders for rodents, but what about other mammals? How does caloric restriction affect primates in general and human being in particular? At least two ongoing studies are focusing on the effects of caloric restriction in rhesus monkeys─one located at the National Institute of Aging (Ingram et al. 1990), the other at the University of Wisconsin (Kemnitz et al., 1993). In both studies the treatment is a reduction in caloric intake of about 30 percent. At the end of the first 5 years of the studies, this level of caloric restriction appears to be well tolerated by the animals, and the treatment outcomes identified so far resemble those of the rodent studies (Weindruch 1995b). These results include decreases blood glucose and insulin levels, increased insulin sensitivity, and increased HDL (“good cholesterol”) levels. Interestingly, long-term caloric restriction appears not to affect the animals’ energy metabolism, percent lean body mass, or percent body fat (Lane et al. 1995). (p.323)

我们没法对人类也做类似的实验。战争时期的战俘、饥荒地区的难民被迫忍饥挨饿，饮食热量是受限制了，但是他们也往往营养不良，所以不能说明问题。不过，有一些间接证据表明限制卡路里可能对人体也有积极作用。
No well-controlled, long-term studies deal with the effects of caloric restriction on humans. The severe malnutrition too often practiced on prisoners and refugees in time of war clearly has devastating short- and long-term effects on the health of these people (Mohs 1994a), but such data cannot be used as evidence one way or the other in this question. There is, however, some anecdotal evidence. (p.324)

琉球群岛的居民的饮食有充足的营养，但热量低于普通日本人，他们的寿命也长于普通日本人，其百岁寿星的数目是日本其他地区的2－40倍。
In the past, the caloric intake of much of the population of Okinawa was much lower than the norm in Japan, but the nutrition of the Okinawans was otherwise adequate. Okinawa has a high incidence of centenarians: 2–40 times as many as may be found on any other Japanese island.

世界各地的百岁寿星也极少有肥胖的。
Other anecdotal evidence suggests that very few, if any, centenarians or other long-lived people have been obese. (p.324)

在1991－1993年间，四男四女在一个与外界隔绝的生态系统“生物圈2”住了两年。在此期间，他们的饮食营养齐备，但热量大约为一般饮食的90％。他们的体重明显降低了（男的降低18％，女的降低10％），并出现了与卡路里受限制的老鼠类似的生理变化。“生物圈2”的居民中包括研究衰老的分子生物学、加州大学洛杉矶分校的教授洛伊•瓦尔佛德（Roy Walford）。他成了限制卡路里长寿法的倡导者和实践者，声称他因此至少能活到120岁。
Finally, the seven people who voluntarily entered Biosphere 2 for 2 years and reduced their caloric intake while there are reported to have shown physiological changes similar to those observed in calorically restricted rodents (Walford et al. 2002). (p.324)【注：方舟子此处还照抄了Roy Walford的文章，如这篇：Walford RL, Bechtel R, MacCallum T, Paglia DE, Weber LJ. "Biospheric medicine" as viewed from the two-year first closure of Biosphere 2. Aviat Space Environ Med. 1996 Jul;67(7):609-17.】

正常人一天需要从食物中吸收2000－2500卡路里的热量，其中大约30％来自脂肪，30％来自蛋白质和40％来自碳水化合物。如果把热量供应减低30％，则每天大约只吸收1500卡。这些卡路里将主要来自水果和蔬菜，再加一点淀粉和肉。那些长期严格执行这个饮食计划的人，身体将会变得非常精瘦，总是感到饥饿和寒冷。由于他们体内脂肪已大部分丧失，他们将没有足够的脂肪做为骨骼缓冲物。他们坐下的时候，臀部的骨骼会因为被压着而感到疼痛。由于脚底没有脂肪垫着，走路也会觉得疼。

很少有人能够长期实施限制卡路里饮食，更不要说实施一辈子了。

不过，加州大学河边分校的斯蒂芬•斯宾德勒（Stephen Spindler）实验室在2001年9月发表的一篇论文认为，在短时间内实施限制卡路里饮食，可能就能取得良好的效果。他们用基因芯片技术分析了肝脏中11000个基因在年轻小鼠（7个月大）和年老小鼠（27个月大）的表达情况，发现其中有46个已知基因的表达随着衰老而发生了变化。与炎症、紧张反应有关的基因，表达增强了，而与代谢有关、抑制细胞生长的基因表达则降低了。他们对一批小鼠从小就限制其饮食，热量比正常的减低40％，一直养到27个月老后检测其基因表达情况，发现与年轻的小鼠类似。然后他们对一批34个月老的小鼠（相当于人长到大约80岁）进行卡路里限制一个月，前两周减低卡路里20％，后两周再进一步减低20％。然后处死这些老鼠检测其基因表达情况，发现也与年轻的小鼠类似。这就表明限制卡路里不仅能延缓衰老，甚至能在一定程度上逆转衰老过程，而且即使在老年时期短时间地限制卡路里，就能取得显著的良效。
S.S.: We took a group of animals that had been allowed to eat almost all they wanted their whole life and we intervened when they were quite old-34 months of age. These mice would be the equivalent of people who are probably 80 years old or older-I'm just guessing at the human equivalent age. We took a group of them and said okay gals, the party's over, it's time to diet. We under-fed them first for two weeks by 20%-that is, 20% less than they had been eating previously-and then for two weeks after that we fed them an additional 20% less so that for the second two weeks they were eating 40% less than they had been eating most of their lives. At the end of that time, at 35 months of age, we sacrificed all of the animals. We then compared the gene expression profiles in the livers of these mice to those in four other groups of mice. The old controls were mice that always ate almost all they wanted until being analyzed at 27 months of age. The long-term calorie restriction mice were those mice who had spent their whole lives being under-fed by 40% until the age of 27 months. Finally, the short-term calorie restricted mice were, as I mentioned, switched from fully fed to under-fed for just four weeks, and even at that only two weeks with "full strength" calorie restriction. We also had a young (seven month-old) control group and a young long-term calorie restricted group (also seven months old) so we could look at calorie restriction independently of aging.【注：方舟子此段是抄袭Life Extension Magazine上的系列文章，如2001年12月号上的这两篇：Reversing Aging Rapidly With Short-Term Calorie Restriction; Media Coverage of Anti-Aging Breakthroughs.

人类是否也如此？目前还没有人能够证明。即使能够证明，抑制食欲也不是一种吸引人的方案。瓦尔佛德曾在其新书发布会上，请来宾品尝他根据长寿配方制作的膳食。来宾们都觉得难以入口，有的人认为如果要长期吃这样的食物，还不如短命。但是我们研究限制卡路里实验的目的，当然不是为了使其他动物更长寿。我们研究的目的，是为了发现限制卡路里是如何防止衰老和疾病的，从而帮助我们了解动物衰老的机制。如果我们能在分子水平上对衰老过程有深刻的理解，或许能找到更能让人接受的健康长寿的办法。

 

[老闹子]

。。。
中国人是个很有意思的民族, 方打假怎么也算不上坏事, 可就是有那么多人看方不顺眼, 表说国内了, 就是混CFC的基本都是文化精英了吧:blink::blowzy:, 还不是方黑一大把 说方不干正事, 完全是胡打 为被方打的干正事的人叫屈的不绝于耳

看看为啥获奖吧

awarded the Prize for his bravery and determination in standing up to threats to his life to uncover clinics promoting unproven treatments

除了利益关系，其中也肯定包括一些愚昧的善良人。他们表面上看到方舟子总在揭露别人的短处，便不分青红皂白，就是对方舟子看不顺眼。

这样的愚昧善良人在任何社会和任何民族中都有。之所以在中国人中占比例较大，我相信不是民族特点，而是长期的愚民政策的结果。这些愚昧的善良人，才是让奸诈之徒在中国很有市场的社会基础。

 

[reine02]

亦明的中英文对照我拷过来，哪句中文算是抄哪句英文，原英文结构、顺序、用词和中文结构、顺序、用词有什么对应关系？我看不出抄袭来，读者自己判断吧。

.....

我这里copy & paste一些西方对抄袭和剽窃以及怎么做才不算抄袭/剽窃原则上是怎么掌握的吧：（然后再看亦明的中英文对照是否抄袭/剽窃）

Plagiarism in its simplest terms means cutting and pasting from other studies and papers. It also means taking credit for work that others have done. Plagiarism includes plagiarizing your own work.

You can copy generic phrases

It is perfectly normal to copy phrases from other people’s papers. However, these phrases must be generic.

Let’s look at what you can paste from another paper. Here is an example from the literature review of a very interesting paper entitled International scientific English: Some thoughts on science, language and ownership by Alistair Wood of the University of Brunei Darussalam. In the extract below Wood talks about different styles of scientific writing around the world and how non-native authors may be at a disadvantage with respect to native authors.

I have highlighted phrases in italics that would be perfectly acceptable to paste into your own paper. In fact, these phrases are completely generic.

In fact there is some cross-linguistic contrastive research to suggest that the foreigner is at a disadvantage. Even where the grammar and vocabulary may be perfectly adequate, it seems to be the case that a non-native may tend to transfer the discourse patterns of her native language to English. It has been suggested, for example，that Asian languages such as Chinese, Japanese and Korean have different patterns of argument to English [3]. 。。。

Note how none of the phrases in italics contain unique information. The phrases could be used in many other contexts.

How to quote directly from other papers

If you use any of the parts of Wood’s text that are not in italics without any acknowledgement you are committing plagiarism.

Putting quotation marks (“ … ”) around an unaltered sentence and giving the proper citation for the origin of the work does not technically constitute plagiarism. But it may indicate to supervisors and referees that you have not actually understood what you have written – it is not your own work.

How to quote from another paper by paraphrasing

Rather than quoting directly, you can paraphrase Wood’s sentence using your own words. But you must still reference Wood, otherwise it would appear that these are you own conclusions.

Paraphrasing the work of a third author

Another case is where you want say the same thing as another author (Wood, in S1), regarding a finding that does not belong to Wood but to a third author’s work (Hinds, in S1) which Wood refers to. In this case Wood is discussing the literature, rather than his own personal ideas.

S1. More generally Hinds has put forward a widely discussed position that Japanese has a different expectation as to the degree of involvement of the reader compared to English, with Japanese giving more responsibility to the reader, English to the writer [Ref 5].

You could paraphrase S1 as follows:

S2. Many authors, for example Hinds [Ref 5], have proposed that the level of expected reader involvement in Japanese writing is higher than in English.

S3. It is generally accepted that Japanese writers expect their readers to be more involved than do English writers [Ref 5].


S2 retains the name of the author mentioned by Wood. S3 is stronger and suggests that what Hinds originally proposed has now become generally accepted (an alternative expression is it is well known that). This is commonly the case. In fact, Wood’s article was published in 1997, since then several other papers and books have been published on the topic, which have reinforced what Hinds proposed.