生命時鐘之謎－老化死亡的計畫 Mystery Clock of life - death plan for aging
早 衰症 │ 染 色體 Progeria │ chromosome │ 維 爾納氏症候群 │ DNA │ Werner's syndrome │ DNA 螺 旋脢 │ 過 氧化物 │ 過 氧化物歧化 │ 端 粒 Spiral protease │ peroxide │ superoxide dismutase │ telomere

早衰 症（Premature senility syndrome） Progeria (Premature senility syndrome)
約翰塔凱特今年九歲，臉和雙手卻有老化的跡象，他患了早衰症，患這種病的人，每年老化五至十歲，每年世 界各地這些同病的兒童齊聚一堂，來這裏聚會的病童，大約有二十個，這些同病相憐的兒童，他們的家人彼此關懷勉勵。约翰塔凯特 year old, face and hands and there are signs of aging, he was suffering from progeria, people suffering from this disease, aged five to ten per year, every year around the world, these children with the disease gathered to children gathered here, about 20, which suffered the same fate of the children, their families, care for each other encouragement.

由於基因研 究的進步，早衰症的起因漸漸地顯明了，也使得人何以會老化這個亙古謎團露出曙光。 As advances in genetic research, the causes of progeria gradually manifest, and also makes people why the aging of this age-old mystery may finally heard. 由於基因科學 的發展，使人類可以揭開生命結構之謎。 Since the development of genetic science to human life and structures can reveal the mystery.

老化一直被 視為是自然現象，現在我們知道基因在老化過程上扮演要角。 Aging has been considered a natural phenomenon, and now we know that genes play an important player on the aging process. 自古以來人類就夢想能夠長生不老，大約西元前三百年，秦始皇聽信徐福的話，厚賜鉅金令他出海，尋找長生 不老之靈藥，然而徐福一去不回。 Since ancient times, humans have dreamed of immortality, about the first three centuries AD, the emperor would listen to Xu Fu, Hou Ci giant gold made him out to sea to find the elixir of immortality, but Xu Fu never came back.

在21世紀 前夕基因科學，會圓人類長生不老之夢嗎？ The eve of genetic science in the 21st century will be a round of human immortality dream? 德州大學的研 究發現，能夠延長人類細胞的壽命。 University of Texas study found, could extend the life span of human cells. 基因藍圖在老化死亡過程中的角色，這裏面可以看得到實現長生不老夢的線索。 Genetic blueprint in the role of the aging process of dying, this dream which could see the clues to achieve immortality.

位於熱帶的 沖繩島，在日本的最南端，島民的長壽舉世聞名，島上的百歲人瑞比率，在日本首屈一指，沖繩有許多高齡島民，仍然工作不懈。 In tropical Okinawa, the southernmost tip of Japan, the world-famous longevity islanders, the island centenarian ratio is second to none in Japan, Okinawa has many old islanders, still working hard. 下治初是沖繩 島的一名女性，今年88歲，她紡織宮古上布的技術，已被視為無形的文化資產，把橫紗編入一千多根直紗，精確地交錯形式，她要編織複雜的設計，每個月都有阿 治的小學同班在她家開同學會，暢談歡樂的童年跳豐年舞打開話閘子。 The beginning of the next administration is an Okinawa woman, 88 years old this year, she Miyako on the cloth of textile technology, has been regarded as intangible cultural assets, the horizontal yarn incorporated into more than 1000 root straight yarn, precisely staggered form, she weaving of complex designs every month A government primary school classmate and fellow students in her home will be open, talk about happy childhood hop harvest dance open the conversation. 阿治的同班同 學如今都有88歲了，他們的基因裏究竟有什麼長壽之秘？ A rule now has a 88-year-old classmate, and their genes in what is the secret of longevity?

20年來琉 球大學的鈴木真教授，對沖繩島大約六百位百歲人瑞作過研究，研究他們基因裏的秘密，結果發現這些人瑞的基因，染色體有一個共同的特性。 20 years of Professor Suzuki University of the Ryukyus on Okinawa, about 600 have studied centenarians, the secret of their genes and found that the centenarians of the genes, chromosomes have a common characteristic.

染色體 Chromosome
一個細胞有23對染色體，從父母各遺傳一個，這些染色體按長度編號，把46個染色體，看作46個基因 譜。 1 cells have 23 pairs of chromosomes, one from the parents and the genetic, according to the length of the chromosome number, the 46 chromosomes, as a 46 gene profile. 免疫基因裏的 第6對染色體，有一個共同的特性，能抵抗滋生疾病的微生物，這類基因大致上有18類，我們從父母各得一個。 Immune genes in the chromosome 6, there is a common feature, the breeding of disease resistant micro-organisms, such genes there are 18 general categories, we each get one from their parents. 阿治這一班同 學十分之三，帶有沖繩人瑞的特性。 A rule of this class students to three tenths, with the characteristics of centenarians in Okinawa.

DR-1型這個基因對細菌入侵，迅速地反制；但是DR-9型，並不受歡迎，假如帶有這一型就容易，罹患 風濕症一類的疾病。 DR-1 type of this gene on the bacterial invasion, quickly counter; but the DR-9 type, and unpopular, if it is easy with this type of suffering from rheumatism for a class of diseases. 顯然沖繩島的 百歲人瑞，身上的基因包括DR-1，卻不含DR-9，就是說他們的基因組合有抗病力，長壽的秘訣不僅在免疫基因裏，找長壽基因的行動正在全世界展開。 Obviously Okinawa centenarian, who's genes, including DR-1, but without DR-9, that is their combination of a disease resistance gene, the secret of longevity, not only in immune genes, the action is to find longevity gene Expand the world.

世界上活得最 長的紀錄是122歲，是住在法國亞耳的珍喀爾曼，她於1997年去逝，珍的父親享年90，母親也有93高齡。 The world, live the longest record is 122 years old, is living in France and Asia ears of Jane Kaer Man, she passed away in 1997, Jane's father at the age of 90, mother aged 93. 達文西大學的方斯華夏赫特教授，一直研究法國百歲人瑞的基因，包括珍在內的人瑞，既健康又活躍，19號 染色體、APO-E基因，除了免疫基因以外，他還發現19號染色體內，與腦功能有關有共同特性的基因。 Leonardo da Vinci University, Fang Sihua Professor Xia Hete, has been studying the French centenarian's genes, including Jane, including centenarians, healthy and active, on the 19th chromosome, APO-E gene, in addition to other immune genes, he found within chromosome 19, and brain function of genes related to common characteristics.

人是否容易患 阿茲海默症，跟貝他類澱粉這些有關係，一般認為阿茲海默症是由於一種纖維狀的物質，不易溶解而黏住腦細胞，導致細胞死亡。 Whether the person prone to Alzheimer's disease, beta amyloid with such a relationship is generally believed that Alzheimer's is due to a fibrous material, which sticks easily dissolve brain cells, leading to cell death. E-2型蛋 白質阻止這種物質黏住腦細胞，防止患阿茲海默症，但是E-4型不能。 E-2 proteins to prevent this type of material sticks brain cells, to prevent the risk of Alzheimer's disease, but not E-4 type. 夏赫特教授認為，得父母遺傳E-4型基因，篤定會得阿茲海默症，有兩個第4型基因者，可能會提早開始癡 呆，例如本來是80歲，卻提早在70歲開始，相反地有第2型基因的人，就不會罹患阿茲海默症，即使發病也會在晚年。 Professor Xia Hete that may be the genetic parents of E-4 genotype, certain to get Alzheimer's disease, there are two type 4 gene may result in earlier start of dementia, for example, could have been 80 years old, but early in the 70-year-old Start the contrary have people with type 2 genes, they will not suffer from Alzheimer's disease, even if the disease will be in later years. 珍的的基因組合，屬於2，3型，這種組合使她免於患阿茲海默症。 Jane's combination of genes, are 2,3-type, this combination makes her suffering from Alzheimer's disease.

長壽又有活力 者的基因，還有其他共同的特性，顯然百歲以上的人瑞，有一種基因使他們免於罹患動脈硬化（Arteriosclerosis），或者有酵素基因防止他們患 白內障（Cataract）或癌，這些研究顯示，並沒有長壽的特別基因，長壽者只是有許多使他們免於患病的基因。 Longevity genes and dynamic persons, there are other common features, apparently centenarians, there is a gene to protect them from risk of atherosclerosis (Arteriosclerosis), or a enzyme gene to prevent them suffering from cataracts (Cataract) or cancer These studies show that longevity is not a special gene, longevity is a lot to them from the disease gene. 無論壽命多麼長，人總免不了老化死亡，據說人的壽命極限，大約是120歲，就像珍喀爾曼。 No matter how long life, people always inevitable aging of the death, said to limit people's life expectancy is about 120 years old, just like Jane Kaer Man. 到底是什麼，使人難圓長生不老夢？ In the end what makes a dream come true to live forever? 維爾納氏症候群（Werner's symdrome） 導致過早衰老的病有若干症狀，最近終於發現引起這種疾病的基因，使得這種病的治療有所突破。 Werner's syndrome (Werner's symdrome) lead to premature aging of the disease a number of symptoms, most recently at last discovered the gene causing the disease, making a breakthrough in the treatment of this disease.

維爾 納氏症候群（Werner's symdrome） Werner's syndrome (Werner's symdrome)
導致過早衰老的病有若干症狀，最近終於發現引起這種疾病的基因，使得這種病的治療有所突破。 Lead to premature aging of the disease a number of symptoms, most recently at last discovered the gene causing the disease, making a breakthrough in the treatment of this disease. 。 .

丹尼爾亨利今年43歲，在巴黎近郊地區獨居，他罹患早衰症，叫做維爾納氏症候群。丹尼尔 亨利 43 year old, living alone in the Paris suburbs, he suffered from progeria, called Werner's syndrome. 這種症候群症 狀發生較晚，在30歲左右發作，病人開始以正常老化的兩倍速度衰老。 This syndrome symptoms later in the 30-year-old attack, the patient began to twice the normal rate of senescence of aging. 丹尼爾喜歡騎機車，是運動型的人，他25歲時症狀發生，他是電器技工，發覺手臂大腿失去知覺，他看了好 多家醫院，但是病因仍是個謎，終於在31歲時診斷為早衰症。 Daniel likes to ride motorcycles, is athletic, he age of 25 symptoms, he was electrician, arm and leg found unconscious, he saw a lot of the hospital, but the cause remains a mystery, finally diagnosed at the age of 31 premature disease. 他的雙腿漸漸 失控，好幾次差點摔落屋頂，到後來失業了，他腳部的血管老化，潰爛而壞疽，終於有一部份要切除，同居的女人也離他而去。 Gradually lost control of his legs, several times, almost dropped the roof, unemployment later, his feet of vascular aging, ulceration and gangrene, and finally there is a part should be removed, unmarried women who are away from him.

丹尼爾從未放 棄治療，為了對研究有點幫助，他送血樣給西雅圖和沖繩的研究中心，終於發現導致病變的基因。 Daniel never gave up treatment, in order to study a little help, he sent blood samples to research centers in Seattle and Okinawa, and finally found the genes lead to disease. 美國西雅圖華盛頓大學的喬治馬丁教授，從事維爾納氏症候群的研究，他從世界各地蒐集血樣，想找出基因裏 的共同因素，丹尼爾的血樣也送到馬丁教授那裏。 University of Washington in Seattle, Professor George Martin, in Werner's syndrome research, he collected blood samples from all over the world, trying to find a common factor genes, Daniel, where blood samples are sent to Professor Ma Ding.

DNA 螺旋脢（酵素） DNA helix enzyme (enzyme)

1996年 馬丁教授終於發現了致病的基因，共同因素就是第8對染色體的基因突變，如果從父母遺傳到這種基因，就會防礙某種蛋白質產生，人體在解開DNA雙螺旋時，需 要這種蛋白質酵素，當DNA之間有相似的字母組合時，字母可能會交換位置，DNA就不能適當運作，簡單地的說就是DNA受損。 1996, Professor Ma Ding finally found a disease-causing genes, the common factor is on chromosome 8 gene mutation, if the genetic from the parents of this gene produces a protein will hinder the body in the DNA double helix when solved, need this kind of protein enzymes, when DNA is similar between the combination of letters, the letters may be exchanged positions, DNA can not function properly, simply to say that DNA damage. 這種酵素可 以解開錯誤的連接，以防止DNA受損，不過這種酵素若因為突變失效，損壞的狀況會累積。 This enzyme can unlock the wrong connection, to prevent DNA damage, however, because mutation of this enzyme if the failure to accumulate damaged condition.

丹尼爾的快 速衰老被認為是DNA損壞的快速累積，現在真象大白，就因為損壞累積，粉碎了人類長生不老的夢。 Daniel Fast aging is considered the rapid accumulation of DNA damage, and now the truth to light because of the cumulative damage, crushing the human dream of immortality. 其實即使是健康者的DNA，每天也有損壞。 In fact, even healthy people's DNA, every day of damage.

氧這時候的 狀態叫做過氧化物，過氧化物把電子推入細胞組織裏而損壞細胞，過氧化物進入細胞核，妨礙DNA的功能，因此而導致的DNA損壞每天會在一個細胞的幾千個地 方發生。 This is called when the state of oxygen peroxide, peroxide into the cells in the electronic organization and damaged cells, peroxide into the cell nucleus, impede the function of DNA, the DNA damage caused by every day thousands of cells in a a local place. 不過DNA自 身精巧的結構，防止了損壞後立即致命，方法是產生酵素來修復損壞。 However, the structure of DNA itself compact to prevent the damage immediately after the fatal, is to produce enzymes to repair the damage.

DNA能產生酵素修復損壞，也就是自行療傷，不過並不能完全恢復，損壞狀況會積少成多。 Produce enzymes to repair damaged DNA, which is self-healing, but can not completely restore the damage will add up the situation. 監視酵素的角 色是發掘仍有多少殘存的傷害，當監視酵素判斷不能修復時，就命令破壞性的酵素把該DNA切除掉，這就是自毀，簡單地說就是細胞自殺。 Enzyme's role is to monitor how many still find remnants of injury, when the judge can monitor the repair enzyme, on the order of destructive enzymes to cut out the DNA, which is self-destruction, in short, is the cell suicide. DNA受損的細胞會自殺，以免危害到整個身體。 DNA damaged cells commit suicide, so as not to endanger the whole body.

20多歲的 人腦如果細胞死亡，腦細胞減少，功能退化；80多歲的人腦，心肌裏的細胞若減少，循環全身的血液會不足，就會引起身體老化。 20-year-old human brain, if cell death, brain cell reduction and degradation; 80-year-old human brain, heart cells, if in reduced systemic blood circulation will be insufficient, the body can cause aging. 假如能減少 損壞的DNA，這個導致老化的禍首，是否就能減緩老化過程？ If we can reduce the damage to DNA, the leading culprit of aging, it can slow down the aging process?

琉球大學正 在研究善英的細胞被過氧化物破壞的數量，人愈老損壞部份愈大，在沖繩島像善英這種老人，這種細胞損壞很少。 University of the Ryukyus is of good English peroxide damaged cells are the number of old and damaged some of the more people the greater good English in Okinawa such as the elderly, little damage to the cells. 研究人員認為 這現象有個原因，就是第21對染色體產生的酵素，強力地防止這種損壞。 The researchers reason that this phenomenon is that chromosome 21 produced enzymes, powerful way to prevent such damage.

這種酵素可視 為DNA的防護單位，把過氧化物的額外電子除去，如此一來DNA的損壞減少，防止老化。 This enzyme can be regarded as the protective unit of DNA, the extra electron peroxide removed this way to reduce DNA damage and prevent aging. 這種酵素的力 量因人而異，顯然包括善英在內，沖繩島老人體內的酵素，一定比其他地方老人的酵素更強。 The power of this enzyme varies, obviously including good English, including, Okinawa old body enzymes, some enzymes than other elderly people more. 因此我們日漸 衰老，是由於DNA損壞日漸增加隨著細胞減少老化開始，一旦細胞死去就無法替換嗎？ So we grow older, is due to the increasing DNA damage decreased with the aging of cells start to die once the cells can not replace it?

人體由細胞分 裂產生新細胞，例如細胞分裂可替換血管內損壞脫落的細胞，不論什麼原因，只要細胞分裂困難時，身體就不能產生新細胞，於是導致血管老化。 The body produce new cells by cell division, such as cell division can be replaced within the damaged vessel off the cell, for whatever reason, as long as the cell division problems, the body can not produce new cells, thus leading to vascular aging.

另一個阻撓人 類實現長生不老美夢的關鍵，隱藏在細胞分裂的機制裏。 Another block mankind to achieve eternal youth dream of a key, hidden in the mechanism of cell division. 茂樹是善英的 孫子，高中快畢業了，他要繼承祖父成為人人尊敬的"海霸王"，畢業之後茂樹要追隨祖父，學習海男子的功夫，同時研究現代的養魚科技。 Shigeki is a good England's grandson, graduated from high school soon, he will inherit his grandfather and became a respected "Monarch of the Seas," Shigeki after graduation to follow his grandfather, learning kung fu sea of men, while the fish of modern technology. 像茂樹這種年 輕人，細胞分裂活躍，不過老人的細胞分裂就沒這麼活躍，到後來停止分裂。 Shigeki such as young, active cell division, but not so old active cell division, and later stop dividing.

長久以來科學家一直以為細胞是無限制地分裂，不過海弗利教授在經由持續培殖細胞過程中，發現一種奇怪的 現象，使得細胞分裂有次數的限制。 Scientists have long thought that cells divide without limit, but Professor Hai Fuli continued in the rearing of cells through the process, discovered a strange phenomenon, made a number of restrictions on cell division. 海弗利教授觀察細胞一定有計次或計時機制，細胞複製的次數和物種的長壽大有關係。 Professor Hai Fuli observed cell must have total times or timing mechanism, the number and species of cell replication has much longevity. 以小白鼠為例複製次數為15至20次，人類胚胎細胞的複製次數為50至70次，細胞複製次數最高的是加 拉巴哥大海龜，大約為125倍，最長可以活175年。 Mouse as an example to copy the number to 15 to 20 times the replication of human embryonic cells for the 50 to 70 times the number of cell replication is the highest number of sea turtles off the Galapagos, about 125 times, the longest you can live 175 years. 隱藏在細胞 裏的鐘是什麼？ Hidden in the cell where the clock is what?

如果拿分裂 18次的細胞跟分裂65次的細胞，比較兩者的端粒，後者少了幾千個字母，為什麼細胞每分裂一次，端粒就會更短？ If you take 18 times the cell division with cell division 65 times, compared the telomere, which is less thousands of letters, why each cell divides, the telomeres would be shorter?

一個細胞分裂 為二時，DNA中的一股也要一分為二，為了完成分裂，DNA的雙螺旋有一小部份會解開，其中有酵素會複製這部份，酵素會遍尋未纏繞的DNA複製下來，並且 連接之前酵素所複製的部份，不過酵素要連接DNA並非屢試不爽，所以不能複製的部分就遺漏了，端粒也就短了。 A cell split into two o'clock, DNA of an also 要一分为二, in order to complete the division, DNA's double helix will unlock a small part of which will copy this part of the enzyme, enzyme is not anywhere to be found entangled of DNA replication down, and copied before the connection is part of enzymes, but enzyme to DNA is not a time-tested connection, it can not copy some of the missing, telomeres also shortened. 端粒太短時染 色體就會彼此黏住，使得細胞不正常，所以細胞要未雨綢繆設定停止分裂，每次細胞分裂時端粒就縮短，就像定時炸彈一樣，當細胞停止分裂，身體就開始衰老，端 粒就是一分一秒把生命流失掉的東西。 When the telomere is too short sticks each chromosome will make abnormal cells, so cells stop dividing and to plan ahead to set each cell divides, telomeres to shorten, like a time bomb, like, when the cells stop dividing, the body begins to be old , is a minute of telomere loss of life out of things.

1998年 1月生物投資公司的股票狂飆，不得不停止交易，因為報上說這家公司，發明了長生不老的藥物。 January 1998 Hurricane biological investment company shares, had to stop trading because the newspaper said the company, invented the immortality drug. 這項研究是在 德州大學進行，裘利夏伊教授在這所大學任教，又兼該公司的顧問，夏伊教授多次經由基因操控，成功增長端粒，如此就可以延長人類細胞壽命。 The study was conducted at the University of Texas, Qiu Li Xiayi professor teaching at the university, but also part of the company's consultant, Professor Xia Yi many times through genetic manipulation, the successful growth of the telomere, so you can extend the life of human cells.

能延長細胞壽 命的法師，就是端粒脢（Telomerase），位在第5對染色體內，端粒脢能使時鐘倒轉，把縮短的端粒恢復到原來的長度。 Master can extend cell life, that is, telomerase (Telomerase), located on chromosome 5, the telomerase can turn the clock back, to return to the original shortened telomere length. 總之端粒的要 務是生產精蟲和卵子等生殖細胞，要確保傳給下一代的端粒不會縮短。 In short telomeres should be to produce sperm and eggs and other reproductive cells, to ensure that for the next generation of telomere shortening is not. 除了生殖細 胞，我們的體細胞、端粒脢，平常不做工，若使這種酵素不停地做工，能否使我們長生不老？ In addition to germ cells, our body cells, telomerase, usually does not work, constantly subject the work of this enzyme, can enable us to live forever?

人體有60 兆體細胞，有些細胞內的DNA，被過氧化物嚴重地斷離，正常的情況下這些細胞會死亡，端粒脢會在斷離開的DNA兩頭。 60 trillion human somatic cells, some cells of DNA, has been seriously broken from the peroxide, under normal circumstances these cells die, telomerase from the DNA in the broken ends. 增加端粒可以 讓細胞存活，不過若有不完整的細胞存活，就可能生病，諸如癌症。 Telomeres can increase cell survival, but if not complete cell survival, it may get sick, such as cancer. 即使每個細 胞都變得不朽，它也可能是致命因素。 Even though every cell have become immortal, it can be fatal factor.

為什麼人類 不能長生不老？ Why can not immortal human? 這個答案至今 還在進化的生命裏，生物終究難免一死，生命誕生時並沒有注定要死，生命進化的漫長過程中，有兩種生活方式。 The answer is still the subject of the evolution of life, biological ultimately inevitable death, life is not destined to die during the birth, life long process of evolution, there are two ways of life. 結腸桿菌不像 人類，它的環狀DNA沒有末端，所以不必憂慮端粒會變短，這是結腸桿菌選擇不朽之道，不限制地分裂，複製同樣的DNA給下一代；另一個例子是酵母菌，酵母 菌像人類一樣有線狀DNA，線狀DNA的兩端有端粒，所以使生命有受限的危險，為什麼酵母菌選擇線狀DNA？ Results Enterobacter not human, it's circular DNA does not end, so do not worry telomere becomes shorter, which is immortal Road junction Enterobacter choice, without limiting the split, the same DNA replication to the next generation; Another example is the yeast bacteria, yeasts, like humans, are linear DNA, linear DNA of telomeres at both ends, so there is limited risk to life, why the choice of yeast linear DNA? 酵母菌在有性 生殖之前，重排父母的基因，子代就是由父母不同的基因產生的，這種安排叫作同源的基因重組。 Prior to the sexual reproduction of yeast, the gene rearrangement of parents, offspring are produced by parents of different genes, and this arrangement is called homologous recombination. 一個正常的酵母菌，把父母的DNA用端粒將兩頭連接，沒有端粒的酵母菌就無法做同源基因重組。 A normal yeast, the DNA of parents will be two connections with the telomere, there is no yeast telomere homologous recombination can not be done.

事實上端粒必須在定點上讓父母的DNA接近，然後重新安排部份基因，恢復原先的情況，由重複這種過程把 基因重組傳給後代。 In fact telomeres must be fixed and let the parents of DNA close to, and then re-arranged some of Genes and restore the original situation, repeat this process by the reorganization of the gene to their offspring. 端粒是兩面利刃，一方面由同源重新組合，傳宗接代；一方面又限制我們的壽命。 Telomeres are a double razor, on the one hand by the homologous re-combination, continue the family line; other hand, they restrict our lives. 選擇線狀 DNA的物種，放棄了長生不老，不過他們把新的基因組合，傳給下一代，漸漸進化為更複雜的多細胞物種。 Select linear DNA species, to give up immortality, but they put a new combination of genes, for the next generation, gradually evolved into more complex multicellular species.

原始期的單細 胞動物草履蟲，其DNA裏各有一個大核小核，大核等於我們的體細胞，小核等於生殖細胞。 The original single-cell animals of Paramecium, the DNA in each of a large nuclear small nuclear, large-core is equal to our body cells, germ cells of small nuclear equal. 草履蟲只靠大核生存，努力防止小核受損，這表示大核要負責壽命。 Paramecium rely on large nuclear survival, efforts to prevent small nuclear damage, which means that a large nuclear to be responsible for life.

經由有性生殖生物的DNA，在備受保護的小核內傳給了下一代，有一個叫做端粒的定時炸彈，置入了多細胞 物種體內。 Through sexual reproduction biology of DNA, in much the protection of small nuclear pass to the next generation, there is a time bomb called the telomere, into a multi-cellular species in vivo. 生殖細胞獲得 端粒脢的供應，這是一種延長細胞壽命的酵素，經由有性生殖父母把生殖細胞，在未爆炸前釋出體外生殖細胞傳下之後，父母的體細胞設定死亡時間。 Germ cells of the supply of telomerase, an enzyme to extend the cell life through sexual reproduction parents to germ cells, in vitro did not explode before the release of germ cells passed down, the parents set the time of death the body cells. 不過物種釋出 生殖細胞後，其生命的長短因物種而異，基因使我們可以跟後代，有很長的時間相處，尤其是人類。 After the release of reproductive cells of species, however, the length of their lives vary by species, gene so that we can tell future generations, there is a long time to get along, especially human.

長生不老是人 類夢寐以求的事，當我們破解了老死的基因密碼時，卻發現非得接受美夢難圓的事實，而且由酵母菌和草履蟲來看，我們的祖先刻意選擇死亡之路，這條路留給後代 新的基因組合，繁衍了各樣會死的物種。 Immortality is the dream of human affairs, when we cracked the genetic code die of old age, he discovers that dreams come true have to accept the fact, and by the yeast and paramecium, we deliberately choose the ancestors of a death sentence, this road The new combination of genes for future generations, multiply the kinds of species will die. 我們都用有限的生命，過最充實的人生，而且給下一代新的可能。 We are all with limited life, had the most fulfilling life, but also to the next generation of new possibilities. 時鐘滴答時光流逝，這就是人類的命運，很久以前我們的祖先，放棄了長生不老，選擇為後代創造新的可能， 我們就是這種選擇死亡，但要變化的物種後代，而基因讓我們死後，那生命的時鐘在我們的後裔身上繼續滴答，所以我一面觀看下一代基因，一面傳遞生命的證據， 直到我們的時鐘停止。 Clock tick passage of time, this is the destiny of humanity, our ancestors long ago gave up eternal life, choose to create new possibilities for future generations, we are the death of such a choice, but future generations of species change, and gene so that we died, that the clock of life in our descendants who continue to tick, so I watched the one hand the next generation of gene delivery side of the evidence of life, until we stop the clock.

（原翻者：姜金龍；公視研發部整理 ） (Original translation by: Jiang Jinlong; public order, as the R & D)