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[原始] 805--之后的-悦毒(原始狗庄50-98)

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楼主
发表于 2010-8-10 12:29:40 | 只看该作者 回帖奖励 |倒序浏览 |阅读模式
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我只是吧狗庄中51-98 (也就是8月5日 golden 停下来后到现在的阅读)copy过来.
原始狗庄参看这里:http://forum.chasedream.com/GMAT_Math/thread-472388-1-1.html
很粗,没啥细分,大家将就看了.  我就弄到golden 回来吧。
祝8月的都能700+

更新说明:
8.11上午10---狗庄89-98

8.10晚上10---增狗庄84-88

8.10中午1---增狗庄51-84

ps:刚才看到golden同学回归了。。撒花欢迎。请大家移步到:
http://forum.chasedream.com/GMAT_Math/thread-472647-1-1.html

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沙发
发表于 2010-8-10 12:30:51 | 只看该作者
感谢楼主,向你学习。我也来和大家分享一下我的成果,对临考的机友可能会有用。灰色经济
眼球微动
金星氢元素逃逸
地质时间
火山熔岩
八哥学说话
新:肥胖症

1. 《灰色经济》的英语原版出处:The Economist 18 June 2004
If so, then depending on your local lawsyou may have been participating in what economists call the"informal" or "grey" economy. In essence, the grey economyconsists of legal activities whose participants fail to pay tax or comply withregulations. The informal (or "underground" or "parallel"economy) is often taken to mean something broader, including illegal activitiessuch as prostitution and drug dealing as well, although there is no agreedstrict definition.
The grey economy is often thought of assomething found at the margins of poor countries, such as a hawker stand inThailand or a roadside vendor in Ghana. But that is misleading. Although itrepresents a greater share of total output in poor countries, it exists in richand poor places alike. Recent research suggests that the grey economy isgrowing. Moreover, a new study suggests that it may be slowing the overalleconomic growth of developing countries.
By its very nature, the informaleconomy's size in any country is hard to observe. In a paper published a coupleof years ago ("Size and Measurement of the Informal Economy in 110Countries Around the World," World Bank Working Paper, July 2002),Friedrich Schneider, of the Johannes Kepler University of Linz, exhaustivelyexamined the ways of estimating it. There are two basic approaches. The firstis direct: you could ask people whether they dodge taxes, or look at theresults of spot tax-audits. However, people are unlikely to confess to breakingthe law, and tax inspectors do not usually check on a random sample of thepopulation. So the second method, indirect detective-work, is better. Forexample, you might compare data on cash transactions or electricity consumptionwith official output figures. If the use of cash or electricity is growing muchfaster than the measured economy, this might indicate that the informal shareof total activity is rising.
Using such techniques, Mr Schneiderestimated that the informal economy in developing countries in 2000 wasequivalent to 41% of their official GDP. In Zimbabwe, the figure was 60%. InBrazil and Turkey, around half of non-farm workers are in the informal sector.In OECD countries the share of the informal economy was lower, but far fromnegligible, at 18%.
There is little mystery about why theinformal economy exists. There are a lot of advantages to operating in theshadows. For a start, there are no income taxes to pay. Avoidingsocial-security charges, which often drive a chunky wedge between take-home payand employers' wage bills, can both cut labour costs and thicken wage packets.People can also save a fair bit by ignoring safety, environmental and healthrules, not to mention intellectual property rights.
Indeed, in cross-country comparisons,the more expensive and more complicated are taxes and regulations, the biggeris the informal economy as a share of GDP. That explains why, among richcountries, Spain, Greece, Italy and Belgium have some of the largest grey economiesand why America, Canada and Switzerland have much smaller ones. In recentyears, the growth in the grey market in some poor countries may owe a lot tothe International Monetary Fund's austerity programmes, which increase taxesand thus encourage many entrepreneurs to opt out.
A booming grey economy sounds like goodnews, if only because many of the officially jobless are in fact earning aliving. So if the poorest are winning, who loses? The entire economy does,according to a new study by Diana Farrell of the McKinsey Global Institute. Theprice for having a large grey economy can be much lower productivity. Greyfirms tend to be small and want to stay that way lest they come to theattention of the authorities. However, their small scale limits their abilityto make the most of new technology and business practices.


2. 《微眼动》的英语原版出处:Windows on the Mind; August 2007; Scientific American Magazine
And yet only recently have researcherscome to appreciate the profound importance of such “fixational” eye movements.For five decades, a debate has raged about whether the largest of theseinvoluntary movements, the so-called microsaccades, serve any purpose at all.Some scientists have opined that microsaccades might even impair eyesight byblurring it. But recent work has made the strongest case yet that theseminuscule ocular meanderings separate vision from blindness when a person looksout at a stationary world.
Indeed, animal nervous systems haveevolved to detect changes in the environment, because spotting differencespromotes survival. Motion in the visual field may indicate that a predator isapproaching or that prey is escaping. Such changes prompt visual neurons torespond with electrochemical impulses. Unchanging objects do not generally posea threat, so animal brains – and visual systems – did not evolve to noticethem. Frogs are an extreme case. A fly sitting still on the wall is invisibleto a frog, as are all static objects. But once the fly is aloft, the frog willimmediately detect it and capture it with its tongue.
Frogs cannot see unmoving objectsbecause, as Helmholtz hypothesized, an unchanging stimulus leads to neuraladaptation, in which visual neurons adjust their output such that theygradually stop responding. Neural adaptation saves energy but also limitssensory perception. Human visual system does much better than a frog’s atdetecting unmoving objects, because human eyes create their own motion.Fixational eye movements shift the entire visual scene across the retina,prodding visual neurons into action and counteracting neural adaptation. Theythus prevent stationary objects from fading away.
The results of these experiments,published in 2000 and 2002, showed that microsaccades increased the rate ofneural impulses generated by both LGN and visual cortex neurons by usheringstationary stimuli, such as the bar of light, in and out of a neuron’sreceptive field, the region of visual space that activates it. This findingbolstered the case that microsaccades have an important role in preventingvisual fading and maintaining a visible image. And assuming such a role formicrosaccades, our neuronal studies of microsaccades also began to crack thevisual system’s code for visibility. In our monkey studies we found thatmicrosaccades were more closely associated with rapid bursts of spikes thansingle spikes from brain neurons, suggesting that bursts of spikes are a signalin the brain that something is visible.
In our experiments, we asked volunteersto perform a version of Troxler’s fading task. Our subjects were to fixate on asmall spot while pressing or releasing a button to indicate whether they couldsee a static peripheral target. The target would vanish and then reappear aseach subject naturally fixated more – and then less – at specific times duringthe course of the experiment. During the task, we measured each person’sfixational eye movements with a high-precision video system.
Aswe had predicted, the subjects’ microsaccades became sparser, smaller andslower just before the target vanished, indicating that a lack of microsaccades– leads to adaptation and fading. Also consistent with our hypothesis, microsaccadesbecame more numerous, larger and faster right before the peripheral targetreappeared. These results, published in 2006, demonstrated for the first timethat microsaccades engender visibility when subjects try to fix their gaze onan image and that bigger and faster microsaccades work best for this purpose.And because the eyes are fixating – resting between the larger, voluntarysaccades – the vast majority of the time, microsaccades are critical for mostvisual perception.

《金星氢元素逃逸》 英语原版出处:Global Climate Change on Venus; New Light on the Solar System; Special Editions; by Mark A. Bullock and David H. Grinspoon
THE STUNNING DIFFERENCES between theclimates of Earth and Venus today are intimately linked to the history of wateron these two worlds. Liquid water is the intermediary in reactions of carbondioxide and surface rocks that can form minerals. In addition, water mixed intothe underlying mantle is probably responsible for the low-viscosity layer, orasthenosphere, on which Earth’s lithospheric plates slide. The formation of carbonateminerals and their subsequent descent on tectonic plates prevent carbon dioxidefrom building up. Models of planet formation predict that the two worlds shouldhave been endowed with roughly equal amounts of water, delivered by the impactof icy bodies from the outer solar system. But, when the Pioneer Venus missionwent into orbit in 1978, it measured the ratio of deuterium to ordinaryhydrogen within the water of Venus’s clouds. The ratio was an astonishing 150times the terrestrial value. The most likely explanation is that Venus once hadfar more water and lost it. When water vapor drifted into the upper atmosphere,solar ultraviolet radiation decomposed it into oxygen and either hydrogen or deuterium.Because hydrogen, being lighter, escapes to space more easily, the relativeamount of deuterium increased. Why did this process occur on Venus but not onEarth? In 1969 Andrew P. Ingersoll of the California Institute of Technologyshowed that if the solar energy available to a planet were strong enough, anywater at the surface would rapidly evaporate. The added water vapor wouldfurther heat the atmosphere and set up what he called the runaway greenhouse effect.The process would transport the bulk of the planet’s water into the upperatmosphere, where it would ultimately be decomposed and lost. Later James F.Kasting of Pennsylvania State University and his co-workers developed a moredetailed model of this effect. They estimated that the critical solar flux requiredto initiate a runaway greenhouse was about 40 percent larger than the presentflux on Earth. This value corresponds roughly to the solar flux expected at theorbit of Venus shortly after it was formed, when the sun was 30 percent fainter.An Earth ocean’s worth of water could have fled Venus in the first 30 millionyears of its existence. A shortcoming of this model is that if Venus had athick carbon dioxide atmosphere early on, as it does now, it would haveretained much of its water. The amount of water that is lost depends on howmuch of it can rise high enough to be decomposed—which is less for a planetwith a thick atmosphere. Furthermore, any clouds that developed during theprocess would have reflected sunlight back into space and shut off the runawaygreenhouse. So Kasting’s group also considered a solar flux slightly below thecritical value. In this scenario, Venus had hot oceans and a humidstratosphere. The seas kept levels of carbon dioxide low by dissolving the gasand promoting carbonate formation. With lubrication from water in theasthenosphere, plate tectonics might have operated. In short, Venus possessed climate-stabilizingmechanisms similar to those on Earth today. But the atmosphere’s lower densitycould not prevent water from diffusing to high altitudes. Over 600 millionyears, an ocean’s worth of water vanished. Any plate tectonics shut down,leaving volcanism and heat conduction as the interior’s ways to cool.Thereafter carbon dioxide accumulated in the air.
This picture, termed the moistgreenhouse, illustrates the intricate interaction of solar, climate andgeologic change. Atmospheric and surface processes can preserve the status quo,or they can conspire in their own destruction. If the theory is right, Venusonce had oceans—perhaps even life, although it may be impossible to know.

《八哥学说话》英语原版出处:Social influences on vocal development 作者:Charles T. Snowdon,Martine Hausberger
The vocal talent of starlings havebeen known since antiquity, when Pliny considered their ability to mimic humanspeech noteworthy. Ornithologist know that this species possesses a rich repertoireof call and songs, composed of whistles, clicks, snarls, and screeches. Inaddition, starlings are well know for their ability to mimic the sounds ofother animals or even mechanical noises. Descriptions of starling song in thepast reflect the difficulty of describing all the variety of sounds included.Witherby mentioned a “lively rambling medlody of throaty warbling, chiring,clicking and gurgling notes interspersed with musical whistles and pervaded bya peculiar creaking quality.”
This complexity explains why detailedstudies of starling song have delayed long after the arrival of the soundspectrograph. As mentioned by West & King, “the problem with starlings isthat they vocalized too much, too often and in too great numbers, sometimes inchoruses numbering in the thousands. Even the seemingly elementary step ofcreating an accurate catalogue of the vocal repertoire of wild starlings is anintimidating task because of the variety of their sounds.”

Chaiken have compared the sons ofyoung males raised in different social conditions: either with a wild-caughtadult song tutor, individually housed but tape-tutored by a tape-recording orraised in total isolation. All birds had been taken from the nest at an earlyage (8-10 days) and were hand raised. Untutored birds produced mostly anabnormal song, where even the basic organization of song was missing. Incontrast, both tape- and live-tutored birds develped songs with a normal basicorganization, but with some syntactical abnormalities for the tape-tutoredbirds. Tape-tutored birds had repertoires half as large as those oflive-tutored birds. Large differences occurred between both groups of birds intheir …

《火山熔岩》(The Origin of the Land Under the Sea; February 2009; Scientific American Magazine; by Peter B. Kelemen; 6 Page(s)
Knowledge of the intense heat and pressure inthe mantle led researchers to hypothesize in the late 1960s that ocean crustoriginates as tiny amounts of liquid rock known as meltalmost as though the solid rocks were “sweating.” Even a minuscule releaseof pressure (because of material rising from its original position) causes meltto form in microscopic pores deep within the mantle rock. Explaining how therock sweat gets to the surface was more difficult. Melt is less dense than themantle rocks in which it forms, so it will constantly try to migrate upward,toward regions oflower pressure. But what laboratory experiments revealedabout the chemical composition of melt did not seem to match up with thecomposition of rock samples collected from the mid-ocean ridges, where eruptedmelt hardens. Using specialized equipment to heat and squeeze crystalsfrom mantle rocks in the laboratory, investigators learned that the chemical compositionof melt in the mantle varies depending on the depth at which it forms; the compositionis controlled by an exchange of atoms between the melt and the minerals that makeup the solid rock it passes through. The experiments revealed that as meltrises, it dissolves one kind of mineral, orthopyroxene, and precipitates, or leaves behind, another mineral, olivine. Researcherscould thus infer that the higher in the mantle melt formed, the moreorthopyroxene it would dissolve, and the more olivine it would leave behind.(melt上升时, 溶解Ort产生Oli, 所以melthigher 溶解的Ort越多,产生的/留在身后的Oli也越多) Comparing these experimental findingswith lava samples from the mid-ocean ridges revealed that almost all of them have the composition of melts thatformed at depths greater than 45kilometers. This conclusion spurred a lively debate about how meltis able to rise through tens of kilometers of overlying rock while preservingthe composition appropriate for a greater depth. If melt rose slowly in smallpores in the rock, as researchers suspected, it would be logical to assume thatall melts would reflect the composition of the fashallowest part of the mantle,at 10 kilometers or less. Yet the composition of most mid-ocean ridge lavasamples suggests their source melt migrated through the uppermost 45 kilometers of the mantle withoutdissolving any orthopyroxene from the surrounding rock. But how?(疑大概为狗狗第一段的背景内容)


In the early 1970s scientists proposed ananswer: the melt must make the last leg of its upward journey along enormous cracks. Open cracks wouldallow the melt to rise so rapidly that it would not have time to interact withthe surrounding rock, nor would melt in the core of the crack ever touch thesides. Although open cracks are not a natural feature of the upper mantle the pressure is simply too greatsome investigators suggested that the buoyant force of migrating meltmight sometimes be enough to fracture the solid rock above, like an icebreaker shipforcing its way through polar pack ice. Adolphe Nicolas of the University ofMontpellier in France and his colleagues discovered tantalizing evidence forsuch cracks while examining unusual rock formations called ophiolites. Typically,when oceanic crust gets old and cold, it becomes so dense that it sinks backinto the mantle along deep trenches known as subduction zones, such as thosethat encircle the Pacific Ocean. Ophiolites, on the other hand, are thick sectionsof old seafloor and adjacent, underlying mantle that are thrust up ontocontinents when two of the planet’s tectonic plates collide. A famous example,located in the Sultanate of Oman, was exposed during the ongoing collision ofthe Arabian and Eurasian plates. In this and other ophiolites, Nicolas’s teamfound unusual, light-colored veins called dikes, which they interpreted ascracks in which melt had crystallized before reaching the seafloor. The problemwith this interpretation was that the dikes are filled with rock thatcrystallized from a melt that formed in the uppermost reaches of the mantle,not below 45 kilometers, where most mid-ocean ridge lavas originate. Inaddition, the icebreaker scenario may not work well for the melting regionunder mid-ocean ridges: below about 10 kilometers, the hot mantle tends to flowlike caramel left too long in the sun, rather than cracking easily.


To explain the ongoing mystery, I beganworking on an alternative hypothesis for lava transport in the melting region. In my dissertation in the late 1980s, I developeda chemical theory proposing that as rising melt dissolves orthopyroxene crystals,it precipitates a smaller amount of olivine, so that the net result is a greatervolume of melt. Our calculations revealedhow this dissolution process gradually enlarges the open spaces at the edges ofsolid crystals, creating larger pores and carving a more favorable pathwaythrough which melt can flow. As the pores grow, they connect to form elongate channels.In turn, similar feedbacks drive the coalescence of several small tributariesto form larger channels. Indeed, our numerical models suggested that more than90 percent of the melt is concentrated into less than 10 percent of theavailable area. That means millions of microscopic threads of flowing melt may eventuallyfeed into only a few dozen, high porosity channels 100 meters or more wide. Evenin the widest channels, many crystals of the original mantle rock remainintact, congesting the channels and inhibiting movement of the fluid. That iswhy melt flows slowly, at only a few centimeters a year. Over time, however, somuch melt passes through the channels that all the soluble orthopyroxenecrystals dissolve away, leaving only crystals of olivine and other mineralsthat the melt is unable to dissolve. As a result, the composition of the meltwithin such channels can no longer adjust to decreasing pressure and insteadrecords the depth at which it last “saw” an orthopyroxene crystal. One of themost important implications of this process, called focused porous flow, is that only the melt at the edges of channelsdissolves orthopyroxene from the surrounding rock; melt within the inner part of the conduit can rise unadulterated.

《研究地质时间》Scientific American Jan 1990
The Yugoslav astronomer MilutinMilankovitch refined and formalized the hypothesis in the 1920’s and 1930’s.The astronomical pacemaker he advocated has three components, two that changethe intensity of the seasons and a third that affects the interaaction betweenthe two driving factors. The first is the tilt of the earth’s spin axis.Currently about 23.5 degrees from the vertical, it fluctuates from 21.5 degreesto 24.5 degrees and back every 41,000 years. The greater the tilt is, the moreintense seasons in both hemispheres become: summers get hotter and wintercolder.
The second, weaker factor controllingseasonality is the shape of the earth’s orbit. Over a period of 100,000 years,the orbit stretches into a more eccentric ellipse and then grows more nearlycircular again. As the orbital eccentricty increases, the difference in theearth’s distance from the sun at the orbit’s nearest and farthest points grows,intensifying the seasons in one hemisphere and moderating them in the other.(At present the earth reaches its farthest point during the Southern Hemispherewinter; as a result, southern winters are a little colder – than their northerncounterparts.)
A third astronomical fluctuation governsthe interplay between the tilt and eccentricity effects. It is the precession,or wobble, of the earth’s spin axis, which traces out a complete circle on thebackground of stars about every 23,000 years. The precession deterimineswhether summer in a given hemisphere falls at near or a far point in the orbit– in other words, whether tilt seasonality is enhanced or weakened by distancesesonablity. When these two controllers of seasonality reinforce each other inone hemisphere, they oppose each other in the opposite hemisphere.
Milankovitch calculated that these threefactors work together to vary the amount of sunshine reaching the high northernlatitudes in summer over a range of some 20 percent – enough, he argued, toallow the great ice sheets that advanced across the northern continents to growduring intervals of cool summers and mild winters. For many years, however, thelack of an independent record of ice-age timing made the hypothesis untestable.
In the early 1950’s Cesare Emilianiproduced the first complete record of the waxings and waning of pastglaciations. It came from a seemingly odd place, the sea floor. Single-cellmarine organisms called foraminifera house themselves in shells made of calciumcarbonate. When the foraminifera die, sink to the bottom and contribute to thesea-floor sediments, the carbonate of their shells preserves certaincharacteristics of the seawater they inhabited. In particular, the ratio of aheavy isotope of oxygen (oxygen 18) to odinary oxygen (oxygen 16) in the carbonatepreserves the ratio of the two oxygen in the water molecules.
It is now understood that the ratio ofoxygen isotopes in seawater closely tracks the proportion of the world’s waterthat is locked up in glaciers and ice sheets. A kind of meteorological distillationaccounts for the link. Water molecules containing the heavier isotope tend tocondense and fall as precipitation a tiny bit more readily than moleculescontaining the lighter isotope. Hence, as water vapor evaporated from warmoceans moves away from the source, its oxygen 18 preferentially returns to theoceans in precipitation. What ultimately falls as snow on ice sheets andmountain glaciers is relatively depleted of oxygen 18. As the oxygen 18-poorice builds up,  the oceans becomerelatively enriched in the isotope. The larger the ice sheets grow, the higherthe proportion of oxygen 18 becomes in seawater – and hence in the sediments.
Analyzing cores drilled from seafloorsediments, Emiliani found that the isotopic ratio rose and fell in rough accordwith the cycles Milankovitch had predicted. A chronology for the combinedrecord showed in 1976 that the record contains the very same periodicities asthe orbital process.
……
Others have found that during the last iceage the earth’s mountain glaciers also expanded. The evidence – from the heapsof debris plowed up by the glaciers, knows as moraines – is as clear in thetropics and the southern temperate latuitudes. On all the mountains studied sofar, regardless of geograhic setting or precipitation rate, the snow linedescended by about one kilometer, correpsonding to a drop in temperature ofabout five degrees Celsius.
Where organic material was trapped in themoraines, radiocarbon dating shows that the glaciers advanced and retreated onthe same schedule. They fluctuated near their maxium extent between about19,500 and 14,000 years ago, about the same time as the glaciation of northernice sheets began to shrink, the mountain glaciers underwent a dramatic retreatthat sharply reduced their size by about 12,500 years ago.
How could changes in summer sunshine at thelatitude of Iceland have caused glaciers to grow and retreat in New Zealand andthe southern Andes? If orbital cycles do indeed drive glacial cycles by actingdirectly on northern ice sheets, the response to seasonality changes in thehigh northern latitudes must be strong enough to override the effects of thevery different changes in the Southern Hemisphere. One possiblity is that thenorthern ice sheets themselves translate Northern Hemisphere seasonality intoclimatic change around the world.
……


狗狗里的所谓《肥胖症》的那篇,其实是讲food intolerance,把第一狗主dec0412找到的原文贴上来,未删节因为狗狗不够详细。
New scientist 1989 July 15
Title: Another man’s poison
Author: Linda Gamlin
It must be rare for a small paperback bookaimed at popular market to introduce a radical new idea into medical thought.Yet most of the Britisch doctors now studying and treating food intolerancetrace their interest back to the publication of Not All In The Mind by RichardMackarness, in 1976. Doectors in the US had first recognised food intolerancemore than 50 years earlier, but it was Mackarness, a psychiatrist and physicianat Basingstoke District Hospital, who was responsible for introducing theconcept to Britain.
In Not all In The Mind, Mackarness tells thefollowing tale about one of his former colleagues in the psychiatricdepartment. During a lecture by Mackarness on food intolerance – also know as“masked food allergy” – the psychiatrist began to wonder if his severe andunexplained fatigue might be due to some such cause. According to Mackarness,fatigue could be a symptom of food intolerance, and the sufferer might cravethe particular food causing the problem. The only food for which thepsychiatrist had any craving was bacon, and although sceptical, he decided totry cutting out bacon, and other forms of pork, for a while. The result tookhim completely by surprise. Initially he felt a great deal worse, but within aweek his fatigue had completely disaapeared and his former energy returned.When he told his colleagues about his “cure”, they reacted, not surprisingly,with total disbelief. Convinced that the improvement in his health must be dueto some other cause, they arranged for the hospital cook to adulterate thesteak pie she was preparing for lunch with some finely chopped bacon. Thesubject of the experiment tucked into the pie unsuspectingly, under thewatchful eyes of his colleagues. To their collective astonishment, halfwaythrough the meal he pushed his plate aside, laid his head down on the table andfell soundly asleep. In Mackarness’s words: “The doctors who were in on theexperiment were impressed and some of them even admitted that there might besomething to masked food allergy after all.”
A decade later, the idea of food intolerancehas much wider acceptance among doctors, but the orthodox medical view is stillone of scepticism, despite several impressive double-blind controlled studies.Much of the medical establishment’s reluctance to accept food intolerance stemsfrom the lack of any obvious mechanism: how on earth can bacon make a personfall asleep? How, for that matter, can common foods such as wheat, milk or eggscause migraine, headaches, joint pains, diarrhoea, hyperactivity, fatigue,asthma, eczema or a constant runny noise? Moreover, why should a differentcluster of symptoms appear in every patient? Those doctors who study foodintolerance, and who are convinced that it is a real phenomenon, realise thatthey must demonstrate the underlying mechanisms responsible for such complexreactions if they are to convince their colleagues.
The study of food intolerance is historicallylinked with that of food allergy, and until relatively recently most attemptsto find a mechanism centred on the immune system. The cause of classical ortrue allergies, including those to food, is the production of IgE antibodies tothe offending molecule, or antigen. IgE binds to mast cells, and if ismolecules then become cross-linked by binding to their particular antigen (afood protein, for example), this causes the mast cell to release variousmediators, or chemical messenger. These mediators include histamine, serotoninand prostaglandins, and they have a dramatic effect on the body. In smallquantities, they cause intense local inflammation. In larger amounts, theyenter the circulatio, making the capillaries dilate and become more permeable,so that there is a sudden drop in blood pressure. This reaction, known asanaphylactic shock, can be fatal.
In individuals with true food allergy,laboratory tests show high levels of total IgE, as well as IgE to specificfoods. But this is not the case in food intolernace: in fact, the involvementof IgE is the crucial distinction between the two. Although some experimentshave shown slight increases in IgE for the culprit foods in patients withmigraine, it seems unlikely that IgE is the predominant cause of most foodintolerance.
Where IgE may be important, however, is thewall of the gut. The drug sodium crooglycate is known to prevent mast cellsfrom releasing their medidators (degranulating). Once food-intolerant patientshave identified the foods that trigger their symptoms and elminated them fromthe diet, they remain sensitive to those foods for a period of several months.Eating the food will provoke the symptoms, but if the patient takes sodiumcromoglycate shortly before consuming the food, there is no response. JonathanBrostoff, of the Middlesex Hospital in London, has tested sodium cromoglycateon his food-intolerant patients, and believes that a reaction with IgE and mastcells in the gut wall may underlie some food intolerance. When the patient eatsthe offending food, it could combine with IgE antibody in the gut walls andthus set off localised inflammation. The amount of IgE present is presumablyfairly small, so that the acute reactions typical of true food allergy do notoccur. But the inflammation could be sufficient to make the gut wall morepermeable, allowing more indigested food molecules to get through. Onceabsorbed, those molecules might cause symptoms in a variety of ways.
Several studies substantiate this idea byshowing that patients with food intolerance generally have more leaky guts thanhealthy individuals, although it is certainly not true of all patients. Indeed,those with symptoms affecting the gut alone often show fewer intact foodmolecules in the blood than normal people. In these cases, the molecules couldbe locked in immune complexes with antibodies in the gut wall, causing onlylocalised inflammation.
Where intact food molecules do enter theblood, they usually form circulating immune complexes (CICs) with antibodies.Such complexes are not an unhealthy sign: everyone has some afer a meal,because even healthy individuals absorb a few incompletely digested molecules.The formation of immune complexes is a necessary prelude to the removal ofthese molecules from the bloodstream by phagocytic cells: such cells engulfCICs and destroy them. But food-intolerant individuals tend to have larger CICsthan other people, and more of them. Furthermore, the antibodies involved arenot exactly the same as in normal individuals. Although researchers disagreeabout the details, it seems that in the food-molecule CICs of normalindividuals, IgG and IgA predominate, whereas in food-intolerant individualsthere is less IgA, more IgG and some IgE.
These difference could be important, becausethey make the CICs more likely to promote inflammation. IgE is present, andcould trigger mast cells, whereas IgA, which is largely non-inflammatory, isunder-represented.
But it is by no means certain that these abnormalCICs actually do any damage in the patient with food intolerance. To do harm,they would have to form deposits in the blood vessels, causing inflammation ofthe blood-vessel wall. This sort of reaction is a feature of more seriousdiseases, such as the autoimmune disorder, systemic lupus erythematosus(SLE). Patientswith SLE form antibodies to their own proteins and have so many immunecomplexes in their blood that the phagocytic cells are unable to cope. Depositsform whereever there is turbulent flow through tiny blood vessels, such as inthe kidney, the joints, the skin and around the lungs. Rashes, joint pains andfever are among the symptoms.
Some doctors see a parallel with foodintolerance, and have suggested that a similar reaction, but in a very muchmilder form, could be occurring, except that the antibodies are binding to foodmolecules rather than to the body’s own molecules. This might  account for the joint pains seen insome patients, and , perhaps, for migraine, since this involves blood vesselsin the brain. But at present there is no concrete evidence to support thisidea.
IgE and CICs are not the only means by whichthe immune system could generate some of the symptoms of food intolerance.Another possible mechanism is via lymphokines or cytokines, hormone-likepeptides that form a communications link between different cells of the immuncesystem. Doctors first noticed their adverse effects when one type oflymphokine, interferon, came into use as a drug for hepatitis B. The side effectsof interferon are legion and range from headache, lethargy and dizziness, toabdominal discomfort, bowel disturbance, nausea and joint pain. Doctorsspeculate that the release of lymphokines may cause much of the malaise ofinfluenza and other infections, rather than the toxins that the pathogen itselfproduces. Lymphokines might also be responsible for the mysterious ailmentcalled postviral syndrome or mylagic encephalitis. In the case of fooditolernace, an abnormal immune response to food molecules could lead to therelease of lymphokines and thus to the unpleasant symptoms. Although there islittle direct evidence for this, several research groups around the world arenow investigating the idea.
While the immune system undoubtedly plays apart in some cases of food intolerance – and perhaps in most cases – fewdoctors involved in this field now believe that it is the whole story. Somesymptoms are difficult to reconcile with immunological causes, particularly thephenomenon of addictive eating: about half of all food-intolerant patientscrave the food or foods that cause their symptoms. In many cases this cravingis for wheat or milk and may go unnoticed because these foods tend to appear inevery meal. But a few patients have rather odd cravings: some need eggs atevery meal, and one patient, seen by Ronald Finn of the Royal LiverpoolHospital, ate raw potato daily.
A possible explanation for this bizzarefeature of food intolernace has recently emerged. The incomplete digestion offood proteins produces certain peptides that can mimic the body’sown peptidehormones. Laboratory investigations show that some of these peptides can bindto the brain’s receptros for endogenous opioids, or endorphins, and they aretherefore knows as exorphins. Partial digests of wheat, maize and milk containthese exorphins, and other foods may also produce them, although a moreextensive search among foodstuffs has et to take place. It is not et certainthat exorphins do actually reach the right receptors in the body, but one pieceof circumstantial evidence suggests that they do. Researchers have shown thatpartially digested wheat increases the transit time of food in the gut, andnaloxone, a drug that binds to opioid receptors, can block the effect.
So it seems that while a fix of wheat and milkis unlikey to get you high – the amounts of exorphin involved are much toosmall – these foods might induce a sense of wellbing in susceptibleindividuals. But the conclusive proof that they act as opioids in the brai andproduce addctive eating, or any other symptoms, is still lacking. A shortage offunds for research into food intolerance ( an unpromising area forpharmaceuticals companies, as treatment does not generally involve drugs) meansthat progress in investigating these noval ideas is bound to be slow.
If food can yield opiods and otherhormone-like peptides, why do they affect some people but not others? No oneknows the answer to this, but the greater permeability of the gut in those withfood intolerance may be one factor – more peptides get though the gut wall andinto the bloodstream. Another possibility is that enzyme deficiencies arepartially to blame. If certain digestive enzymes are in short supply in the gutor operate inefficiently, this might lead too more peptides being available forabsorption. Deficient enzymes could also allow the peptides to survive longerin the bloodstream.
Although the role of inadequate enzymes in theexorphin story remains spectulative, there is little doubt that enzymedeficiencies are relevant to food intolerance as a whole. No one has yet lookedin detail at digestive enzymes in the gut, but there is a growing body ofevidence concerning enzymes that detoxify compounds absorbed into thebloodstream.
Research into theenzyme capabilities of patients with food intolerance has so far identified atleast three types of enzyme deficiency. The first concerns phenolsulphotransferase(PST) which is responsible for the first step in thedegradation of phenols. People with food-induced migraine tend to be deficientin one type of PST, called PST-P. No one knows how phenols might causemigraine, but they could have act as happens, molecules that are too small tobe antigens on their own,  but whichcan act as antigens when combine with proteins.
板凳
发表于 2010-8-10 12:31:17 | 只看该作者
LZ你人不是一点点好!!!!!!!!!! LZ一定考700+!!
地板
发表于 2010-8-10 12:31:29 | 只看该作者
感谢lz~~~~~~~~~~~~
辛苦lz了~~
5#
发表于 2010-8-10 12:31:39 | 只看该作者
谢谢LZ
6#
 楼主| 发表于 2010-8-10 12:35:19 | 只看该作者
大家都加油啊。。
我就剩2天了。。。。
7#
发表于 2010-8-10 12:41:59 | 只看该作者
楼主辛苦!!我也还剩两天。。狂看寂静中
8#
发表于 2010-8-10 12:42:46 | 只看该作者
感谢lz啊~~~~~!~救命了可是
9#
发表于 2010-8-10 12:57:25 | 只看该作者
感谢LZ!!!!!!813小朋友和大家一起奋斗!
10#
发表于 2010-8-10 13:12:25 | 只看该作者
感谢大家的分享,加油加油!
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