關於晨讀青春英語美文

　　中國的網路文學，自上個世紀90年代末開始到現在已經有10餘年的發展歷史，作為與網路有千絲萬縷聯絡的青春文學在近幾年的發展也越來越引起公眾的關注，逐步走上了產業化的道路。下面是小編帶來的，歡迎閱讀!

　　篇一

　　對青春和音樂的激情

　　PAINTER Luo Dan's name is the Chinese transliteration of Auguste Rodin ***1840-1917***, the French sculptor famous for works such as "The Age of Bronze," "The Thinker" and "The Kiss."

　　畫家羅丹的名字是奧古斯特•羅丹***1840 - 1917*** 的中文音譯，法國著名雕塑家，作品有《青銅時代》、《思想者》和《吻》。

　　His painter father, Luo Zhongli, an accomplished artist and president of the Sichuan Academy of Fine Arts, had high hopes for his son in the art world.

　　他的畫家父親羅中立，一位多才多藝的藝術家，四川美術學院院長，在藝術界對他的兒子寄予厚望。

　　"Frankly, my life has been quite smooth but that doesn't mean my path in art has been easy," says 32-year-old Luo, whose paintings are on exhibit at Sinan Mansions.

　　“坦率地說，我的生活一直很順利，但這並不意味著我的藝術之路一直很容易，” 32歲的羅丹說，他的畫在思南公館展出。

　　With his father also a famous artist, comparisons are inevitable, but Luo says they are unfair.

　　由於他的父親也是一個著名藝術家，比較是不可避免的，但羅丹說這是不公平的。

　　"I always face the same question, whether or not I feel the shadow of my father," he says. "No, I don't. We have different backgrounds. It would be meaningless to put us together."

　　“我總是要面對同樣的問題，我是否感覺到父親的陰影，”他說。“不，我沒有。我們有不同的背景。把我們放在一塊是毫無意義的。”

　　Luo Dan also plays the piano, violin and likes to sing.

　　羅丹也會彈鋼琴，拉小提琴，喜歡唱歌。

　　Music is a regular theme in his work, especially the rebelliousness of rock 'n' roll. His subjects sing and revel in music. From their facial expressions, viewers can almost feel their passion and hear the music that they hear.

　　音樂是他作品中的一個常規主題，尤其是叛逆的搖滾樂。他作品中人物歌唱並陶醉在音樂中。從他們的面部表情，觀眾可以感受到他們的熱情，聽到他們所聽到的音樂。

　　Luo is quick to say that his paintings do not have a social message.

　　羅丹很快就說他的畫沒有社會資訊。

　　"I am not reflecting on history and society," he says. "I only care about the existing world, the lifestyles of my peers."

　　“我沒有反思歷史和社會，”他說。“我只關心現有的世界，我同代人的生活方式。”

　　His works have evolved toward themes of tradition colliding with modernity, wildness clashing with stillness.

　　他的作品從傳統與現代碰撞、野性與沉靜衝突的主題演變而來。

　　Born in Chongqing, Luo graduated from the Middle School attached to the Sichuan Fine Arts Institute in 2000. He studied at Kunsthochschule Kassel in Germany. In 2004, he graduated from the Oil Painting Department of the Sichuan Fine Arts Institute and studied at the University of Wales Institute in Cardiff, the UK.

　　羅丹出生在重慶，2000年畢業於四川美術學院附屬中學。他在德國卡塞爾藝術學院學習。2004年，他畢業於四川美術學院油畫系，曾在英國威爾士大學卡地夫學院深造。

　　Asked whether his father gave him artistic advice over the years, Luo says, "I tried to hide my paintings from him since I felt a bit awkward. I want to retain the purity and distinctiveness of my own art."

　　問及這些年他的父親是否給予他藝術指導，羅丹說，“我試圖對他隱藏我的繪畫，因為我感到有點尷尬。我想保留自己藝術的純潔和特殊之處。”

　　篇二

　　Ageing

　　衰老

　　Forever young?

　　青春永駐?

　　A way to counteract part of the process of growing old

　　一個減緩衰老程序的途徑

　　BIOLOGISTS have made a lot of progress in understanding ageing.

　　在對人類衰老過程的探索中生物學家們取得了長足的進步。

　　They have not, however, been able to do much about slowing it down.

　　可是如何減緩衰老他們還沒有太多的辦法。

　　Particular versions of certain genes have been shown to prolong life,

　　與延長壽命相關的特定基因已經找到，

　　but that is no help to those who do not have them.

　　但這還幫不了那些此段基因缺失的人。

　　A piece of work reported in this week's Nature by Darren Baker of the Mayo Clinic, in Minnesota, though, describes an extraordinaryresult that points to a way the process might be ameliorated.

　　本週《自然》雜誌發表了明尼蘇達州梅奧診所的Dr.Darren Baker的一項實驗報告，描述了其所採取的方法使得衰老程序得到改善，結果非常好。

　　Dr Baker has shown—in mice, at least—that ageing body cells not only suffer themselves,

　　至少在實驗小白鼠體內是這樣，

　　but also have adverse effects on otherwise healthy cells around them.

　　Dr.Barker稱體細胞不僅自己逐漸衰老,還將不利的影響傳達到周圍健康的細胞。

　　More significantly, he has shown that if such ageing cells are selectively destroyed, these adverse effects go away.

　　更神奇的是，如果這些衰老的細胞被人為破壞掉，它們對健康細胞的負面影響也會隨之消失。

　　The story starts with an observation, made a few years ago, that senescent cells often produce a molecule called P16INK4A.

　　故事還得從幾年前的一項實驗開始講起，他們觀察到衰老的細胞通常會產生一種叫P16INK4A的分子。

　　Most body cells have an upper limit on the number of times they can divide—and thus multiply in number.

　　大部分體細胞分裂次數會有一個上限-數量的翻倍，

　　P16INK4A is part of the control mechanism that brings cell division to a halt when this limit is reached.

　　當這個上限接近時，P16INK4A作為控制機制的一部分會使細胞的分裂停止。

　　The Hayflick limit, as the upper bound is known, is believed to be an anticancer mechanism.

　　海弗利克極限，即我們所知的上限現在認為可作為一種抗癌機制，

　　It provides a backstop that prevents a runaway cell line from reproducing indefinitely, and thus becoming a tumour.

　　它可以攔截、阻斷細胞鏈的無限期、失常的增生，正是這種失常的增生形成了腫瘤。

　　The limit varies from species to species—in humans, it is about 60 divisions—and its size is correlated with the lifespan of the animal concerned.

　　這種極限隨物種不同而不同，人類大致的分裂次數上限是60次，極限的大小與相應動物的預期生命期限有關。

　　Hayflick-limited cells thus accumulate as an animal ages, and many biologists believe they are one of the things which control maximum lifespan. Dr Baker's experiment suggests this is correct.

　　細胞的海弗利克極限累加就是動物的壽命長度，很多的生物學家推測它們控制著生命期限最長值。Dr.Barker的實驗證明了推測是正確的。

　　Age shall not weary them

　　老而未衰的器官

　　Dr Baker genetically engineered a group of mice that were already quite unusual.

　　Dr. Baker 通過基因工程處理的一組小白鼠非常特別，

　　They had a condition called progeria, meaning that they aged much more rapidly than normal mice.

　　它們的症狀也稱早老症，意味著它們比一般的小白鼠衰老的更快。

　　The extra tweak he added to the DNA of these mice was a way of killing cells that produce P16INK4A. He did this by inserting into the animals' DNA, near the gene for P16INK4A, a second gene that was,

　　他在這些小白鼠的DNA中加入了可殺死能產生P16INK4A分子的細胞的特別基因，具體做法是在實驗小白鼠P16INK4A旁邊的基因插入另一段動物基因，

　　because of this proximity, controlled by the same genetic switch.

　　因為在它旁邊，第二段基因也受相同的遺傳開關控制。

　　This second gene, activated whenever the gene for P16INK4A was active, produced a protein that was harmless in itself,

　　這第二段基因編碼產生的蛋白質對自身無害，但在特殊的藥物作用下，它就會變的很致命，只要P16INK4A分子有活性它就能被啟用。

　　but which could be made deadly by the presence of a particular drug. Giving a mouse this drug, then, would kill cells which had reached their Hayflick limits while leaving other cells untouched. Dr Baker raised his mice, administered the drug, and watched.

　　給實驗小白鼠服用這種藥後，就會殺死那些接近海弗利克極限的細胞，其它細胞則完好無損。 Dr Baker 培養這些小白鼠,給它們服用藥物後，觀察它們。

　　The results were spectacular.

　　結果是出人意料的。

　　Mice given the drug every three days from birth suffered far less age-related body-wasting than those which were not.

　　小白鼠出生後每3天給一次藥,服藥小白鼠比沒服藥小白鼠的與衰老相關的機體耗損要少的多。

　　They lost less fatty tissue. Their muscles remained plump.

　　它們耗損的脂肪組織更少，肌肉豐滿,

　　And they did not suffer cataracts of the eye.

　　並且都沒患上白內障。

　　They did, though, continue to experience age-related problems in tissues that do not produce P16INK4A as they get old.

　　接下來，他們還對那些老化的但並沒有出現P16INK4A分子的器官也進行了衰老相關問題的實驗，

　　In particular, their hearts and blood vessels aged normally.

　　特別是它們的心臟和血管，老化的程序很正常，

　　For that reason, since heart failure is the main cause of death in such mice, their lifespans were not extended.

　　小白鼠的主要是死因心臟衰竭，所以它們的預期壽命不會再延長了。

　　The drug, Dr Baker found, produced some benefit even if it was administered to a mouse only later in life.

　　Dr Baker發現，這種藥物即使是飼餵給生命快到盡頭的的小白鼠也會有一定的療效，

　　Though it could not clear cataracts that had already formed, it partly reversed muscle-wasting and fatty-tissue loss.

　　儘管對已經形成的白內障沒法再變回清澈，但能使肌肉及脂肪組織的耗損部分得以緩解，

　　Such mice were thus healthier than their untreated confrères.

　　這些小白鼠因此比沒有服藥的更健康。

　　Analysis of tissue from mice killed during the course of the experiment showed that the drug was having its intended effect.

　　對那些在實驗中死亡小白鼠的組織進行分析發現，藥物達到了預期的效果。

　　Cells producing P16INK4A were killed and cleared away as they appeared.

　　細胞一旦產生了P16INK4A分子就立即被殺死了。

　　Dr Baker's results therefore support the previously untested hypothesis that not only do cells which are at the Hayflick limit stop working well themselves,

　　因此這一結果證實了早先未被驗證的推測，即，達到海弗利克極限的細胞不僅自身的不再正常運作。

　　they also have malign effects on their otherwise healthy neighbours.

　　還會還會把負面的影響帶給周圍正常的細胞。

　　Regardless of the biochemical details, the most intriguing thing Dr Baker's result provides:

　　先不管其中生化方面的細節，Dr.Baker的實驗結論最引人入勝的是：

　　is a new way of thinking about how to slow the process of ageing—and one that works with the grain of nature, rather than against it.

　　人類有了延緩衰老程序的新方法-與其抗衡，不如順應自然法則。

　　Existing lines of inquiry into prolonging lifespan are based either on removing the Hayflick limit, which would have all sorts of untoward consequences, or suppressing production of the oxidative chemicals that are believed to cause much of the cellular damage which is bracketed together and labelled as senescence.

　　延長預期壽命現有的辦法，一是通過消除細胞的海弗利克極限，這可能會出現各種不利的後果。

　　But these chemicals are a by-product of the metabolic activity that powers the body.

　　二是抑制體內氧化物水平。氧化物被認為是引起細胞損傷的元凶，和細胞衰老劃等號的一個詞，但這些化學物質本身就是給身體提供能量的代謝活動所產生的副產品。

　　If 4 billion years of natural selection have not dealt with them it suggests that suppressing them may have worse consequences than not suppressing them.

　　如果40億年前的自然選擇都沒有摒棄這體內的代謝副產品，那就意味著抑制它們可能比不抑制它們所帶來的後果更嚴重。

　　By contrast, actually eliminating senescent cells may be a logical extension of the process of shutting them down, and thus may not have adverse consequences.

　　相反的，真正的消除掉衰老細胞可能是延長機體細胞正常運作的一個符合邏輯的作法,也不會再有不利結果了。

　　It is not an elixir of life, for eventually the body will run out of cells, as more and more of them reach their Hayflick limits.

　　世上沒有生命可以長生不老，隨著機體內越來越多的細胞到了自己的海弗利克極限，最終，機體也就到了消亡的那一天。

　　But it could be a way of providing a healthier and more robust old age than people currently enjoy.

　　但是未來的我們可能會比現在更健康、更有活力的老去。

　　Genetically engineering people in the way that Dr Baker engineered his mice is obviously out of the question for the foreseeable future.

　　毫無疑問，在可預見的未來某天，Dr. Baker在小白鼠身上採用的基因技術就能應用在人類身上。

　　But if some other means of clearing cells rich in P16INK4A from the body could be found, it might have the desired effect.

　　但如果還能找到其它方法消除體內富含P16INK4A分子的細胞，那可能才是我們期望的效果。

　　The wasting and weakening of the tissues that accompanies senescence would be a thing of the past, and old age could then truly become ripe.

　　伴隨著衰老而產生的機體組織耗損、衰弱都將成為過去，年老只意味著真正意義上的成熟!

　　篇三

　　Choose Optimism

　　If you expect something to turn out badly, it probably will. Pessimism is seldom disappointed. But the same principle also works in reverse. If you expect good things to happen, they usually do! There seems to be a natural cause-and-effect relationship between optimism and success. Optimism and pessimism are both powerful forces, and each of us must choose which we want to shape our outlook and our expectations. There's enough good and bad in everyone's life ample sorrow and happiness, sufficient joy and pain to find a rational basis for either optimism or pessimism. We can choose to laugh or cry, bless or curse. From which perspective do we want to view life? Will we look up in hope or down in despair?

　　It's all about our decision. I believe in upward look. I choose to highlight the positive and slip right over the negative. I am an optimist by choice as much as by nature. Sure, I know that sorrow exists. But when all is said and done, the good in life far outweighs the bad. An optimistic attitude is not a luxury; it's a necessity. The way you look at life will determine how you feel, how you perform, and how well you will get along with other people. Conversely, negative thoughts, attitudes, and expectations feed on themselves; they become a self-fulfilling prophecy. Pessimism creates a dismal place where no one wants to live. Optimism doesn't need to be naive. You can be an optimist and still recognize that problems exist and that some of them are not dealt with easily. But what a difference optimism makes in the attitude of the problem solver! Optimism diverts our attention away from negativism and channels it into positive, constructive thinking. When you're an optimist, you're more concerned with problem-solving than with useless carping about issues.