这个像是学术论文的要求。即使从这个要求来看，中文的行文，没有直接引用（照抄原文）可以确定，但没有在有间接引用的每句后引用知识来源(加标注)。一篇科普文章如何在行文中对知识来源进行引用，这个解释中没有例子。两篇科普文章如果介绍同一个第三方原创的事情，它们之间的一致性到什么程度算抄袭？
最好的例子其实就是那个所谓被抄袭的英文书。那个英文的原文，在字里行间有没有根据你这个规定来引用它介绍的东西呢(加标注)？我没有看原书，但是高度怀疑没有。这就是说，那个英文的范文本身恐怕并没有遵守你贴的规定，这个规定不适用于此类书籍或文章。
从你给出的亦明的中英文对照来看，老方抄袭的英文书（虽然给出的只有其中部分）还是非常严格遵守西方论文标准的（不是什么我的标准），用了别人的结论，就给人家credit. 都加了标注的（我用红色highlight了）。
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 。。。
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
A large body of data (reviewed
by Masoro 1988a, 1992a; Weindruch and Walford 1988; Finch 1990 shows 。。。
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).
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).
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 (I
wasaki et al. 1988; Masoro et al. 1989). It now appears 。。。
The mechanisms underlying the effectiveness of caloric restriction are not clear. ……As
Masoro (1988a) has pointed out, recent 。。。
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).
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).
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).
One unexpected beneficial outcome of diet restriction is its effect on learning performance in mice (
Ingram et al. 1987). Both 。。。
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).
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反正闲着也是闲着。
