关于晨读青春英语美文
中国的网络文学，自上个世纪90年代末开始到现在已经有10余年的发展历史，作为与网络有千丝万缕联系的青春文学在近几年的发展也越来越引起公众的关注，逐步走上了产业化的道路。下面是学习啦小编带来的关于晨读青春英语美文，欢迎阅读!
关于晨读青春英语美文篇一
对青春和音乐的激情
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."
画家罗丹的名字是奥古斯特•罗丹(1840 - 1917) 的中文音译，法国著名雕塑家，作品有《青铜时代》、《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.
他的画家父亲罗中立，一位多才多艺的艺术家，四川美术学院院长，在艺术界对他的儿子寄予厚望。
"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.
“坦率地说，我的生活一直很顺利，但这并不意味着我的艺术之路一直很容易，” 32岁的罗丹说，他的画在思南公馆展出。
With his father also a famous artist, comparisons are inevitable, but Luo says they are unfair.
由于他的父亲也是一个著名艺术家，比较是不可避免的，但罗丹说这是不公平的。
"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."
“我总是要面对同样的问题，我是否感觉到父亲的阴影，”他说。“不，我没有。我们有不同的背景。把我们放在一块是毫无意义的。”
Luo Dan also plays the piano, violin and likes to sing.
罗丹也会弹钢琴，拉小提琴，喜欢唱歌。
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.
音乐是他作品中的一个常规主题，尤其是叛逆的摇滚乐。他作品中人物歌唱并陶醉在音乐中。从他们的面部表情，观众可以感受到他们的热情，听到他们所听到的音乐。
Luo is quick to say that his paintings do not have a social message.
罗丹很快就说他的画没有社会信息。
"I am not reflecting on history and society," he says. "I only care about the existing world, the lifestyles of my peers."
“我没有反思历史和社会，”他说。“我只关心现有的世界，我同代人的生活方式。”
His works have evolved toward themes of tradition colliding with modernity, wildness clashing with stillness.
他的作品从传统与现代碰撞、野性与沉静冲突的主题演变而来。
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.
罗丹出生在重庆，2000年毕业于四川美术学院附属中学。他在德国卡塞尔艺术学院学习。2004年，他毕业于四川美术学院油画系，曾在英国威尔士大学卡地夫学院深造。
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."
问及这些年他的父亲是否给予他艺术指导，罗丹说，“我试图对他隐藏我的绘画，因为我感到有点尴尬。我想保留自己艺术的纯洁和特殊之处。”
关于晨读青春英语美文篇二
Ageing
衰老
Forever young?
青春永驻?
A way to counteract part of the process of growing old
一个减缓衰老进程的途径
BIOLOGISTS have made a lot of progress in understanding ageing.
在对人类衰老过程的探索中生物学家们取得了长足的进步。
They have not, however, been able to do much about slowing it down.
可是如何减缓衰老他们还没有太多的办法。
Particular versions of certain genes have been shown to prolong life,
与延长寿命相关的特定基因已经找到，
but that is no help to those who do not have them.
但这还帮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.
本周《自然》杂志发表了明尼苏达州梅奥诊所的Dr.Darren Baker的一项实验报告，描述了其所采取的方法使得衰老进程得到改善，结果非常好。
Dr Baker has shown—in mice, at least—that ageing body cells not only suffer themselves,
至少在实验小白鼠体内是这样，
but also have adverse effects on otherwise healthy cells around them.
Dr.Barker称体细胞不仅自己逐渐衰老,还将不利的影响传达到周围健康的细胞。
More significantly, he has shown that if such ageing cells are selectively destroyed, these adverse effects go away.
更神奇的是，如果这些衰老的细胞被人为破坏掉，它们对健康细胞的负面影响也会随之消失。
The story starts with an observation, made a few years ago, that senescent cells often produce a molecule called P16INK4A.
故事还得从几年前的一项实验开始讲起，他们观察到衰老的细胞通常会产生一种叫P16INK4A的分子。
Most body cells have an upper limit on the number of times they can divide—and thus multiply in number.
大部分体细胞分裂次数会有一个上限-数量的翻倍，
P16INK4A is part of the control mechanism that brings cell division to a halt when this limit is reached.
当这个上限接近时，P16INK4A作为控制机制的一部分会使细胞的分裂停止。
The Hayflick limit, as the upper bound is known, is believed to be an anticancer mechanism.
海弗利克极限，即我们所知的上限现在认为可作为一种抗癌机制，
It provides a backstop that prevents a runaway cell line from reproducing indefinitely, and thus becoming a tumour.
它可以拦截、阻断细胞链的无限期、失常的增生，正是这种失常的增生形成了肿瘤。
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.
这种极限随物种不同而不同，人类大致的分裂次数上限是60次，极限的大小与相应动物的预期生命期限有关。
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.
细胞的海弗利克极限累加就是动物的寿命长度，很多的生物学家推测它们控制着生命期限最长值。Dr.Barker的实验证明了推测是正确的。
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 通过基因工程处理的一组小白鼠非常特别，
They had a condition called progeria, meaning that they aged much more rapidly than normal mice.
它们的症状也称早老症，意味着它们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,
他在这些小白鼠的DNA中加入了可杀死能产生P16INK4A分子的细胞的特别基因，具体做法是在实验小白鼠P16INK4A旁边的基因插入另一段动物基因，
because of this proximity, controlled by the same genetic switch.
因为在它旁边，第二段基因也受相同的遗传开关控制。
This second gene, activated whenever the gene for P16INK4A was active, produced a protein that was harmless in itself,
这第二段基因编码产生的蛋白质对自身无害，但在特殊的药物作用下，它就会变的很致命，只要P16INK4A分子有活性它就能被激活。
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.
给实验小白鼠服用这种药后，就会杀死那些接近海弗利克极限的细胞，其它细胞则完好无损。 Dr Baker 培养这些小白鼠,给它们服用药物后，观察它们。
The results were spectacular.
结果是出人意料的。
Mice given the drug every three days from birth suffered far less age-related body-wasting than those which were not.
小白鼠出生后每3天给一次药,服药小白鼠比没服药小白鼠的与衰老相关的机体耗损要少的多。
They lost less fatty tissue. Their muscles remained plump.
它们耗损的脂肪组织更少，肌肉丰满,
And they did not suffer cataracts of the eye.
并且都没患上白内障。
They did, though, continue to experience age-related problems in tissues that do not produce P16INK4A as they get old.
接下来，他们还对那些老化的但并没有出现P16INK4A分子的器官也进行了衰老相关问题的实验，
In particular, their hearts and blood vessels aged normally.
特别是它们的心脏和血管，老化的进程很正常，
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脏衰竭，所以它们的预期寿命不会再延长了。
The drug, Dr Baker found, produced some benefit even if it was administered to a mouse only later in life.
Dr Baker发现，这种药物即使是饲喂给生命快到尽头的的小白鼠也会有一定的疗效，
Though it could not clear cataracts that had already formed, it partly reversed muscle-wasting and fatty-tissue loss.
尽管对已经形成的白内障没法再变回清澈，但能使肌肉及脂肪组织的耗损部分得以缓解，
Such mice were thus healthier than their untreated confrères.
这些小白鼠因此比没有服药的更健康。
Analysis of tissue from mice killed during the course of the experiment showed that the drug was having its intended effect.
对那些在实验中死亡小白鼠的组织进行分析发现，药物达到了预期的效果。
Cells producing P16INK4A were killed and cleared away as they appeared.
细胞一旦产生了P16INK4A分子就立即被杀死了。
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,
因此这一结果证实了早先未被验证的推测，即，达到海弗利克极限的细胞不仅自身的不再正常运作。
they also have malign effects on their otherwise healthy neighbours.
还会还会把负面的影响带给周围正常的细胞。
Regardless of the biochemical details, the most intriguing thing Dr Baker's result provides:
先不管其中生化方面的细节，Dr.Baker的实验结论最引人入胜的是：
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.
人类有了延缓衰老进程的新方法-与其抗衡，不如顺应自然法则。
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.
延长预期寿命现有的办法，一是通过消除细胞的海弗利克极限，这可能会出现各种不利的后果。
But these chemicals are a by-product of the metabolic activity that powers the body.
二是抑制体内氧化物水平。氧化物被认为是引起细胞损伤的元凶，和细胞衰老划等号的一个词，但这些化学物质本身就是给身体提供能量的代谢活动所产生的副产品。
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40亿年前的自然选择都没有摒弃这体内的代谢副产品，那就意味着抑制它们可能比不抑制它们所带来的后果更严重。
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，真正的消除掉衰老细胞可能是延长机体细胞正常运作的一个符合逻辑的作法,也不会再有不利结果了。
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.
世上没有生命可以长生不老，随着机体内越来越多的细胞到了自己的海弗利克极限，最终，机体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.
但是未来的我们可能会比现在更健康、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.
毫无疑问，在可预见的未来某天，Dr. Baker在小白鼠身上采用的基因技术就能应用在人类身上。
But if some other means of clearing cells rich in P16INK4A from the body could be found, it might have the desired effect.
但如果还能找到其它方法消除体内富含P16INK4A分子的细胞，那可能才是我们期望的效果。
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.
伴随着衰老而产生的机体组织耗损、衰弱都将成为过去，年老只意味着真正意义上的成熟!
关于晨读青春英语美文篇三
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.
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