这
并非是青春之泉带来的结果，而是科学家们已找到了使细胞永保活力之法。
这样做的目的并非使人长生不老，而是找到一种治疗途径，可能在未来治疗或推迟疾病的发作，像渐进性眼疾、肠胃失调及癌症等。
这项研究的重点在于所谓的染色体端粒上，这种起保护作用的覆盖物是位于染色体末端的一小段DNA结构。这些保护罩使我们的染色体免于散开，作用很像鞋带末端的塑料末梢。当染色体端粒保持健康时，细胞就健康。但细胞分裂一次，端粒就短一截。当由于年龄或某种疾病发作使端粒变得极其短时，细胞就失去了分裂性能并最终死亡。
上世纪80年代，三个美国人发现了染色体端粒及构成端粒的 ，称为端粒 ，并于近期因这项研究获得了诺贝尔医学奖。从那时起，越来越多的研究者在探究染色体端粒的工作原理。
实验取得的一项辉煌成就是用端粒 使人类细胞“长生不老”。得克萨斯大学达拉斯西南医学中心 (University of Texas Southwestern Medical Center at Dallas)的科学家及其他研究人员已证明，他们可使某些细胞长久存活，包括胸部、皮肤、视网膜及近来证实的结肠细胞，方式是添加端粒 以保持染色体端粒完好或修复那些长度过短的端粒。研究人员正在研究端粒 如何有助于修复受损细胞及在癌症研究中扮演着如何关键角色。得克萨斯大学达拉斯西南医学中心的谢伊(Jerry Shay)说，研究的目的不应是延长人类的寿命，而是延长人类的健康寿命。是否有某种方式干预并延缓某些问题的发生。谢伊与其同事赖特(Woodring Wright)在上世纪90末首次研究出如何用端粒 使细胞永生。
生物学家称，染色体端粒并非我们衰老的唯一原因。在人类老化过程中，端粒所起的作用至多占10%。但如果细胞能更持久健康，则可能引发严重病变的疾病可能会推迟出现，如从65岁推迟到75岁。
细胞生物学教授谢伊也是西南大学西蒙斯医学癌症中心(Simmons Cancer Center at UT Southwestern)的副主任，他认为，将疾病压缩到生命晚期的一个较小时段可大幅改善人类个体的生活质量，使其独立生活的时间更持久。他说，或许可使人类的身体免于太过衰弱。
谢伊说，端粒 有个限制是仅对可分裂细胞有益，而大多数神经元是不可分裂的，神经元是大脑的主要构成细胞。如果科学家能找出方法让端粒 进入哪怕是很少一部分的可分裂脑细胞，则可对脑细胞带来好处。
谢伊还说，由此也产生一种担忧，即如果端粒 作用于全身细胞，包括癌细胞或前癌细胞，则会有无意产生癌细胞或加快癌细胞发展的可能性。不知什么原因，癌细胞端粒的长度适中且不会缩短，这种完美的分裂过程可使细胞保持其分裂功能。
不过谢伊说，如果将端粒 疗法用于特定细胞的短期治疗，比如说一两周，则可能有成功治疗之效，这能修复染色体端粒，使细胞保持分裂功能。这种治疗方法可用于在试验室培养皿中生长的病人自己的细胞，能帮助细胞受损而端粒配额用完的病变，如贫血、皮肤溃疡及炎症。许多癌症研究专家正在尽力研究如何通过阻断端粒 而治疗癌症。
Shirley S. Wang
这样做的目的并非使人长生不老，而是找到一种治疗途径，可能在未来治疗或推迟疾病的发作，像渐进性眼疾、肠胃失调及癌症等。
这项研究的重点在于所谓的染色体端粒上，这种起保护作用的覆盖物是位于染色体末端的一小段DNA结构。这些保护罩使我们的染色体免于散开，作用很像鞋带末端的塑料末梢。当染色体端粒保持健康时，细胞就健康。但细胞分裂一次，端粒就短一截。当由于年龄或某种疾病发作使端粒变得极其短时，细胞就失去了分裂性能并最终死亡。
上世纪80年代，三个美国人发现了染色体端粒及构成端粒的 ，称为端粒 ，并于近期因这项研究获得了诺贝尔医学奖。从那时起，越来越多的研究者在探究染色体端粒的工作原理。
实验取得的一项辉煌成就是用端粒 使人类细胞“长生不老”。得克萨斯大学达拉斯西南医学中心 (University of Texas Southwestern Medical Center at Dallas)的科学家及其他研究人员已证明，他们可使某些细胞长久存活，包括胸部、皮肤、视网膜及近来证实的结肠细胞，方式是添加端粒 以保持染色体端粒完好或修复那些长度过短的端粒。研究人员正在研究端粒 如何有助于修复受损细胞及在癌症研究中扮演着如何关键角色。得克萨斯大学达拉斯西南医学中心的谢伊(Jerry Shay)说，研究的目的不应是延长人类的寿命，而是延长人类的健康寿命。是否有某种方式干预并延缓某些问题的发生。谢伊与其同事赖特(Woodring Wright)在上世纪90末首次研究出如何用端粒 使细胞永生。
生物学家称，染色体端粒并非我们衰老的唯一原因。在人类老化过程中，端粒所起的作用至多占10%。但如果细胞能更持久健康，则可能引发严重病变的疾病可能会推迟出现，如从65岁推迟到75岁。
细胞生物学教授谢伊也是西南大学西蒙斯医学癌症中心(Simmons Cancer Center at UT Southwestern)的副主任，他认为，将疾病压缩到生命晚期的一个较小时段可大幅改善人类个体的生活质量，使其独立生活的时间更持久。他说，或许可使人类的身体免于太过衰弱。
谢伊说，端粒 有个限制是仅对可分裂细胞有益，而大多数神经元是不可分裂的，神经元是大脑的主要构成细胞。如果科学家能找出方法让端粒 进入哪怕是很少一部分的可分裂脑细胞，则可对脑细胞带来好处。
谢伊还说，由此也产生一种担忧，即如果端粒 作用于全身细胞，包括癌细胞或前癌细胞，则会有无意产生癌细胞或加快癌细胞发展的可能性。不知什么原因，癌细胞端粒的长度适中且不会缩短，这种完美的分裂过程可使细胞保持其分裂功能。
不过谢伊说，如果将端粒 疗法用于特定细胞的短期治疗，比如说一两周，则可能有成功治疗之效，这能修复染色体端粒，使细胞保持分裂功能。这种治疗方法可用于在试验室培养皿中生长的病人自己的细胞，能帮助细胞受损而端粒配额用完的病变，如贫血、皮肤溃疡及炎症。许多癌症研究专家正在尽力研究如何通过阻断端粒 而治疗癌症。
Shirley S. Wang
It's not quite the Fountain of Youth, but scientists have found a way to induce some of our cells to live forever.
The purpose isn't to make people immortal, but rather to create therapies that might one day treat or delay the onset of disease, such as progressive eye disease, gastrointestinal disorders and cancer.
The research is focused on so-called telomeres, small bits of DNA that serve as protective coverings at the end of our chromosomes. These caps keep our chromosomes from unraveling, much like the plastic tips at the ends of shoelaces. When our telomeres are healthy, our cells remain healthy. But each time the cells divide, telomeres get shorter. When they reach a critically short length, as they do with age or the onset of certain diseases, cells lose the ability to divide and eventually die.
Three Americans discovered telomeres and the enzyme that makes them, called telomerase, in the 1980s, work for which they recently won the Nobel Prize in medicine. Since then, a growing number of researchers have been seeking to understand how telomeres work.
One feat researchers have achieved in the lab is using telomerase to 'immortalize' human cells. Scientists from the University of Texas Southwestern Medical Center at Dallas and others have shown they can keep certain cells living forever, including those from the breast, skin, retina and, recently, the colon, by adding telomerase to keep telomeres intact or repair those that are too short. Researchers are studying how telomerase therapies could help repair damaged cells and play an major role in cancer research. 'What our goal should be isn't increasing life span, but healthy life span,' says Jerry Shay who, with his UT Southwestern colleague Woodring Wright, first figured out how to use telomerase to immortalize cells in the late 1990s. 'Is there some way we can intervene and slow down some of the problems?'
Telomeres aren't the only reason we age, likely accounting for 10% or less of the aging process, biologists say. But if cells can be kept healthier longer, diseases that might have caused serious illness at 65 years old could be delayed until, say, 75.
Compressing disease into a smaller window later in life could significantly improve individuals' quality of life, helping them live independently for longer, says Dr. Shay, professor of cell biology and associate director of the Simmons Cancer Center at UT Southwestern. 'Potentially we can keep you from getting too frail,' he says.
A limit to telomerase is that it benefits only cells that divide -- and most neurons, the dominant type of cell in the brain, don't divide. If scientists could figure out a way to get telomerase even to the small portion of brain cells that do divide, there could be some brain benefit, according to Dr. Shay.
A related concern is the possibility of inadvertently creating or accelerating cancer if telomerase were administered throughout the body, including to cancerous or pre-cancerous cells. Somehow, cancer cells have telomeres that are just the right length and don't shorten -- a perfection of the division process that allows cells to keep dividing, Dr. Shay says.
But if a telomerase-based therapy could be given to specific cells temporarily, say for a week or two, it could be a therapeutic 'home run,' repairing telomeres and allowing cells to keep dividing, Dr. Shay says. Such a therapy -- which would occur on a patients' own cells grown in a lab dish -- could help people with conditions where cells have been injured and have used up their allotment of telomeres, such as anemia or skin sores or conditions involving inflammation. Many cancer researchers are trying to figure out how to turn off telomerase and potentially treat cancer.
Shirley S. Wang
The purpose isn't to make people immortal, but rather to create therapies that might one day treat or delay the onset of disease, such as progressive eye disease, gastrointestinal disorders and cancer.
The research is focused on so-called telomeres, small bits of DNA that serve as protective coverings at the end of our chromosomes. These caps keep our chromosomes from unraveling, much like the plastic tips at the ends of shoelaces. When our telomeres are healthy, our cells remain healthy. But each time the cells divide, telomeres get shorter. When they reach a critically short length, as they do with age or the onset of certain diseases, cells lose the ability to divide and eventually die.
Three Americans discovered telomeres and the enzyme that makes them, called telomerase, in the 1980s, work for which they recently won the Nobel Prize in medicine. Since then, a growing number of researchers have been seeking to understand how telomeres work.
One feat researchers have achieved in the lab is using telomerase to 'immortalize' human cells. Scientists from the University of Texas Southwestern Medical Center at Dallas and others have shown they can keep certain cells living forever, including those from the breast, skin, retina and, recently, the colon, by adding telomerase to keep telomeres intact or repair those that are too short. Researchers are studying how telomerase therapies could help repair damaged cells and play an major role in cancer research. 'What our goal should be isn't increasing life span, but healthy life span,' says Jerry Shay who, with his UT Southwestern colleague Woodring Wright, first figured out how to use telomerase to immortalize cells in the late 1990s. 'Is there some way we can intervene and slow down some of the problems?'
Telomeres aren't the only reason we age, likely accounting for 10% or less of the aging process, biologists say. But if cells can be kept healthier longer, diseases that might have caused serious illness at 65 years old could be delayed until, say, 75.
Compressing disease into a smaller window later in life could significantly improve individuals' quality of life, helping them live independently for longer, says Dr. Shay, professor of cell biology and associate director of the Simmons Cancer Center at UT Southwestern. 'Potentially we can keep you from getting too frail,' he says.
A limit to telomerase is that it benefits only cells that divide -- and most neurons, the dominant type of cell in the brain, don't divide. If scientists could figure out a way to get telomerase even to the small portion of brain cells that do divide, there could be some brain benefit, according to Dr. Shay.
A related concern is the possibility of inadvertently creating or accelerating cancer if telomerase were administered throughout the body, including to cancerous or pre-cancerous cells. Somehow, cancer cells have telomeres that are just the right length and don't shorten -- a perfection of the division process that allows cells to keep dividing, Dr. Shay says.
But if a telomerase-based therapy could be given to specific cells temporarily, say for a week or two, it could be a therapeutic 'home run,' repairing telomeres and allowing cells to keep dividing, Dr. Shay says. Such a therapy -- which would occur on a patients' own cells grown in a lab dish -- could help people with conditions where cells have been injured and have used up their allotment of telomeres, such as anemia or skin sores or conditions involving inflammation. Many cancer researchers are trying to figure out how to turn off telomerase and potentially treat cancer.
Shirley S. Wang
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