2009年8月25日 星期二
2009年8月20日 星期四
《娱乐周刊》超薄显示屏
当《娱乐周刊》(Entertainment Weekly)的部分读者下月打开杂志时，将看到美国电视剧中的角色从嵌入页面的超薄显示屏上对他们说话。
由美国哥伦比亚广播公司(CBS)和软饮料制造商百事可乐(Pepsi)携手进行的这项市场营销实验，让人想起了《哈利波特》(Harry Potter)系列电影中的魔幻报纸。这种广告的播放方式非常类似于音乐贺卡，读者只要翻到屏幕所在页面，视频就会自动开始播放。
两家公司没有披露这种全动态视频广告的成本，但了解该技术的高管表示，成本将远高于传统的印刷广告。这项技术是由一家名为Americhip的美国公司开发的。
营销商不惜花大钱进行此类宣传，显示出在越来越多的人正为了回避广告而使用数字录像机(DVR)等新技术之际，营销商正在采取更激进的方式，以期接触消费者。
“这代表着未来——以新颖且出人意料的方式吸引消费者，”CBS营销总裁乔治•施魏茨尔(George Schweitzer)说。 “如何检验一种饮料？你让消费者去品尝。”
《哈利波特》系列电影中的《预言家日报》(Daily Prophet)就具有动态图片。《娱乐周刊》上的广告将呈现CBS周一晚间挡的几部电视剧中的角色，并将通过视频宣传一款面向男性的百事健怡可乐。
上述视频将在一个与手机屏幕一般大的显示屏上播放。纽约与洛杉矶地区的订户所收到的《娱乐周刊》（时代华纳(Time Warner)旗下杂志）将嵌有该显示屏。
一名了解这项技术的杂志业高管估计，在10万份杂志上投放一则视频广告的成本将达到一两百万美元，分摊到每份杂志的成本将达数美元。相比之下，在《娱乐周刊》上投放一则全页彩色广告，每份每页的成本仅在9美分左右。
此次宣传的费用由CBS和百事共同承担。两家公司此举的目的是，通过广告引起人们对其产品的充分“热议”，使昂贵的高科技广告变得物有所值。
译者/章晴
2009年8月19日 星期三
法國科學家稱發現翼龍的"跑道"
法國科學家稱發現翼龍的"跑道"
理論上翼龍在地面的時候是很笨拙的
法國古生物學家馬贊在英國皇家學會的期刊上發表文章說，他在法國西南部發現了1億5千萬年前翼龍用來起飛降落的"跑道"。
馬贊說，他率領的一支國際研究小組在法國西南部的克雷薩克地區發現了一個已經至少有1億5千萬年的長條形平地。
他認為，從這個平地上的跡象觀察，翼龍降落的時候是足部先落地，接著再步履蹣跚地換成四肢著地。
直到目前，科學家也還沒有研究出來翼龍是如何起飛的。
鳥和翼龍
翼龍的翼展一般大約1米長，但是從發現的最大翼龍化石來估算，翼展可能可以高達10米，但是足部卻平均只有5公分長。
科學家認為，翼龍和現代鳥類的飛行方式頗為接近。
生物學上自成一目的翼龍生存在三疊紀晚期到白堊紀，也就是距今大約2億2千萬年到6千5百多萬年前。
俗稱"翼手龍"的翼龍最早是1784年在意大利發現的，在德國、巴西、法國、英國和中國都曾經有翼龍化石出土。
也有科學家認為翼龍是恐龍演化成為鳥類的證據。
2009年8月17日 星期一
Can A Tiny Fish Save Your Ears?
WSJ
2009年 08月 17日 07:14
Can A Tiny Fish Save Your Ears?
For many people, loss of hearing is irreversible.
For scientists trying to figure out what can be done about that, one answer may lie -- or swim, actually -- in freshwater aquariums.
About one of every 10 Americans suffers from hearing impairment, according to a survey conducted by the Better Hearing Institute, a nonprofit advocacy group. By far the most common cause of hearing loss is damage to the so-called hair cells in the inner ear as a result of excessive noise, certain illnesses and drugs, and simple aging. The problem is that once hair cells die, humans (like other mammals) aren't able to grow new ones.
In recent years, a research team at the University of Washington in Seattle has been working on finding a way to resolve that problem in experiments involving the zebrafish, a common aquarium denizen. The zebrafish, like many aquatic creatures, has clusters of hair cells running along the outside of its body that help sense vibrations in the water, working in a similar way to hair cells in the human inner ear. But unlike humans, zebrafish are able to regenerate their damaged hair cells. Researchers hope their work can unlock secrets to protect human hair cells from becoming damaged and to stimulate the cells to regenerate.
Hair cells, which took their name because under the microscope they look like cells with little hairs growing out of them, are an essential link in hearing. The filament hairs, or cilia, bend with vibrations caused by sound waves entering the ear. That induces the hair cell to create an electrical signal that is passed on to the auditory nerve and sent to the brain. Devices such as hearing aids, which amplify sounds, and cochlear implants, which stimulate the auditory nerve directly, help people hear, but neither restores hearing to normal.
Until the mid-1980s, researchers thought warm-blooded vertebrates, including humans, weren't able to regenerate hair cells. Then, researchers around the country began observing that hair cells grew back in birds whose hearing was damaged either by noise or drugs. They also determined that hair-cell regeneration can result in improved hearing; in experiments, song birds that had grown new hair cells were able to resume singing their original songs with perfect pitch again.
But there is no indication that mammals can regenerate hair cells. And why some animals, even within the same species, are more vulnerable to hair-cell death, while others are more resistant to it, is a mystery. 'I literally walked around for years wondering about this variability,' says Ed Rubel, a professor of hearing sciences who leads part of the University of Washington research effort.
There are two main approaches to efforts aimed at inducing hair cells to regenerate. Some research groups are attempting to get stem cells -- undifferentiated cells that can develop into various specialized cells -- to turn into hair cells, either by transplanting them from other parts of the body, or by stimulating stem cells naturally occurring in the inner ear to transform themselves. Albert Edge, an associate professor at Harvard Medical School and a researcher at the Massachusetts Eye and Ear Infirmary, says his team has been able to turn mouse stem cells into hair cells in a laboratory dish, though it isn't clear whether those cells are functional or not.
Other researchers, like those at the University of Washington, are focused on understanding the molecules and genetics involved with hair-cell regeneration, and how to mimic this process in animals that don't spontaneously regenerate hair cells. Scientists say aspects of such research, likely will be the first to have applications in humans. One encouraging angle: Dr. Rubel, in collaboration with another University of Washington scientist, David Raible, has identified chemicals that seem to protect hair cells from damage. In this experiment, zebrafish are exposed to a dye that highlights living hair cells. Then, one or two of the zebrafish -- the young ones used in the lab measure just 1/8 of an inch long -- are placed in each of 96 shallow holes contained on a plate. Different chemicals are administered to each fish group that might confer protection to the hair cells.
Finally, another chemical known to kill the fish hair cells is added. Under a microscope, researchers then examine the fish to look for cases where the dye is still evident, signaling that the cells are still alive and suggesting that the protective chemical appears to have done its job.
Those chemicals found to confer protection on fish hair cells are currently also being tested on mice and rats. The idea is that, once a drug is discovered that effectively protects hair cells from dying and is safe for humans, the medicine could be used to help protect the hearing of patients receiving drugs known for killing hair cells, like chemotherapeutic agents.
Dr. Rubel's and Dr. Raible's teams also are studying the genetics of zebrafish to identify markers that confer hair-cell protection.
Last year, their labs jointly identified several genetic mutations and drug-like compounds that seemed to protect hair cells from death, publishing their findings in the journal PLoS Genetics. In a separate study, published in 2007 in Hearing Research, they identified several drugs that also appear to be protective and were already approved for other purposes by the Food and Drug Administration. No tests have been performed on humans, however.
The teams also are working on a separate group of studies to understand the genes and other molecules that allow the regeneration of hair cells in zebrafish, birds and mice.
Surrounding cells known as support cells can both turn into hair cells or generate new hair cells. Dr. Rubel's lab is investigating both processes. 'If we understand the template of genes that are expressed by the cells we would want to divide, then we could tap into that template' to mimic regeneration efforts in mammals, he says.
One finding identified a developmental protein that appears to be turned on in animals able to regenerate hair cells. In one study, a team member found a type of protein increased in a chick (which can regenerate hair cells) after its cells were damaged. But in running the same experiment in a mouse (which can't regenerate hair cells), the protein didn't increase, suggesting the protein could be involved in regeneration.
Scientists involved in the experiments say there could be therapeutic trials to prevent hearing loss using drugs within a decade. However, finding a cure for hearing loss using hair-cell regeneration is likely to be at least 20 years away, they say.
'Hearing aids are Band-aids on a problem that already exists,' says Nancy Freeman, director of the regenerative and development program in hearing loss at the National Institute on Deafness and Other Communication Disorders.
'The hope with this type of [regeneration] approach is that at the end of the day you'd end up with something that natively restores function.'
一條小魚可以拯救你的聽力？
對致力於研究這一問題的科學家來說﹐避免聽力喪失的一個辦法可以在淡水水族館里找到。
非 營利組織改善聽力協會(Better Hearing Institute)的一項調查表明﹐大約每10個美國人中就有一人患有聽力障礙。到目前為止﹐聽力喪失最常見的原因就是內耳中所謂的“毛細胞”受到損害 或者僅僅是因為上了年紀。過量的噪音以及某些疾病和藥物會損害毛細胞。問題的症結在於毛細胞一旦死亡﹐人類（像其他哺乳動物一樣）不能再生出新的毛細胞。
近 年來﹐華盛頓大學西雅圖分校的一個研究團隊一直在對一種水族館里常見的觀賞魚類──斑馬魚進行研究﹐試圖解決人類聽力喪失的問題。和許多其他水生生物一樣 ﹐斑馬魚在身體表面長有毛細胞。這些毛細胞的作用是探測水中的振動﹐其原理與人類內耳中的毛細胞相似。但是﹐與人類不同的是﹐斑馬魚的毛細胞在受損後還可 以再生。研究人員希望他們的工作可以揭開謎底﹐保護人類的毛細胞免受損傷、並推動毛細胞的再生。
內耳中的這種細胞是人類聽覺不可或缺的一 環。之所以稱為“毛細胞”﹐是因為它們在顯微鏡下看上去就像是在細胞外長出了絨毛。這些細細的絨毛﹐或者說纖毛﹐會因為聲波進入耳朵以後產生的振動而擺 動。這種運動會讓毛細胞產生出一種能夠經由聽覺神經傳給大腦的電信號。像助聽器和人工耳蝸等設備都有助聽效果﹐但都無法讓人們的聽力恢復到正常水平。助聽 器能夠增加聲音的強度﹐而人工耳蝸則會直接刺激聽覺神經。
上世紀80年代中期以前﹐研 究人員認為毛細胞無法在包括人類在內的溫血脊椎動物的體內再生。後來﹐美國的研究人員開始注意到﹐鳥類的聽力在因噪音或藥物受損後﹐它們的毛細胞會重新再 生出來。研究者們還認定﹐毛細胞再生可以提高聽力。實驗發現﹐新長出毛細胞的鳴禽可以重新以完美的音調唱出它們從前的歌曲。
但是﹐沒有跡 象表明哺乳動物的毛細胞可以再生。此外﹐即便在同一物種中﹐為什麼某些動物的毛細胞更容易死亡﹐而某些動物的毛細胞卻生命力更頑強﹐這仍舊是一個謎。“這 些年來﹐我真的甚至在走路的時候都在思索為什麼會有這個不同﹐”聽力科學教授埃德•魯貝爾(Ed Rubel)說。魯貝爾負責領導華盛頓大學科研項目的一部分工作。
促 進毛細胞再生主要有兩種辦法。有些研究組織正在試圖將幹細胞──一種未特化的細胞﹐它可以特化出其它類型細胞──培育成為毛細胞。方法是將它們從身體的其 它部位移植﹐或者促使內耳里自然生長的幹細胞發生轉變﹐特化為毛細胞。阿爾伯特•埃奇(Albert Edge)是哈佛大學醫學院(Harvard Medical School)的副教授﹐也是麻省醫院眼耳科(Massachusetts Eye and Ear Infirmary)的研究人員。埃奇表示﹐他的團隊已經能夠在實驗室中將老鼠的幹細胞分化成毛細胞﹐但是現在還不清楚這些細胞是否能夠正常工作。
而 華盛頓大學等組織的其他研究人員則將注意力集中在同毛細胞再生有關的分子和遺傳學原理﹐以及如何在毛細胞無法再生的動物身上重復這一過程上面。科學家說﹐ 這類研究的某些成果有可能最先應用在人類身上。一條令人鼓舞的消息是﹐魯貝爾已經和華盛頓大學另一名科學家大衛•雷布爾(David Raible)一起合作識別出了能夠保護毛細胞不受損害的化學物質。在他們的實驗中﹐斑馬魚身上活的毛細胞被染色。然後﹐研究人員在一個盤子上的96個淺 孔中放上一至兩條斑馬魚──實驗室使用的小斑馬魚僅有1/8英寸長。可能會對毛細胞起到保護作用的不同的化學物質被施用於每一個淺孔中。
最後﹐他們再向淺孔中加入一種能夠殺死魚類毛細胞的化學物質。在顯微鏡下﹐研究人員仔細觀察﹐尋找染液顏色依然鮮亮的斑馬魚﹐因為這標志著它們的毛細胞還活著﹐意味著起保護作用的化學物質看上去完成了它的任務。
研究人員目前還在老鼠身上試驗那些對魚類毛細胞有保護作用的化學物質。科學家們認為﹐一旦一種藥物被發現可以有效保護毛細胞﹐而且使用起來對人類是安全的﹐這種藥物就可以用來幫助保護病人們的聽力──他們接受的藥物治療﹐如化療藥物﹐能將毛細胞殺死。
魯貝爾和雷布爾的團隊也在研究斑馬魚的遺傳基因﹐以識別對毛細胞有保護作用的基因標記。
去 年﹐他們的實驗室合作識別出了幾個似乎可以保護毛細胞的突變基因和類藥性混合物。他們的科研成果發表在《科學公共圖書館──遺傳學》(PLoS Genetics)雜志上。在2007年發表在《聽力研究》(Hearing Research)上的另一項研究中﹐他們確認了幾種對毛細胞有保護作用且已被美國食品和藥物管理局批准用作其他用途的藥物。不過﹐目前為止還沒有對人體 進行過試驗。
他們的團隊同時還在進行另一組研究﹐試圖瞭解導致斑馬魚、鳥類和老鼠的毛細胞再生的基因和其他分子。
毛細胞週圍的細胞被稱為“支持細胞”﹐它們可以轉化成毛細胞或者產生新的毛細胞。魯貝爾的實驗室正在研究這兩個進程。“如果我們理解了這種細胞的基因模板﹐那麼我們就可以利用這個模板在哺乳動物身上模擬毛細胞再生﹐”他說。
有 一項研究發現了一種似乎可以讓動物毛細胞再生的發育蛋白。在研究中﹐一名團隊成員發現了小雞的毛細胞受損後體內一種蛋白質的含量（小雞的毛細胞可以再生） 有所上升。但是﹐在對老鼠進行的同樣的實驗中（老鼠的毛細胞不能再生）﹐該蛋白質的含量沒有上升﹐這意味著該蛋白質可能與毛細胞再生有關。
參與這些實驗的科學家們說﹐使用藥物防止聽力喪失的臨床實驗有可能會在十年內實現。但是﹐找到利用毛細胞再生治療聽力喪失的辦法可能還需要至少20年的時間。
“ 助聽器是解決問題的一個權宜之計﹐”美國耳聾和其他溝通障礙研究所(National Institute on Deafness and Other Communication Disorders)聽力喪失再生和發展項目的負責人南希•弗里曼(Nancy Freeman)表示。
“利用這種（促進毛細胞再生的）方法﹐我們希望有朝一日可以找到一種方法讓聽力能夠自然地得到恢復。”
Shirley S. Wang
2009年 08月 17日 07:14
Can A Tiny Fish Save Your Ears?
For many people, loss of hearing is irreversible.
For scientists trying to figure out what can be done about that, one answer may lie -- or swim, actually -- in freshwater aquariums.
About one of every 10 Americans suffers from hearing impairment, according to a survey conducted by the Better Hearing Institute, a nonprofit advocacy group. By far the most common cause of hearing loss is damage to the so-called hair cells in the inner ear as a result of excessive noise, certain illnesses and drugs, and simple aging. The problem is that once hair cells die, humans (like other mammals) aren't able to grow new ones.
In recent years, a research team at the University of Washington in Seattle has been working on finding a way to resolve that problem in experiments involving the zebrafish, a common aquarium denizen. The zebrafish, like many aquatic creatures, has clusters of hair cells running along the outside of its body that help sense vibrations in the water, working in a similar way to hair cells in the human inner ear. But unlike humans, zebrafish are able to regenerate their damaged hair cells. Researchers hope their work can unlock secrets to protect human hair cells from becoming damaged and to stimulate the cells to regenerate.
Hair cells, which took their name because under the microscope they look like cells with little hairs growing out of them, are an essential link in hearing. The filament hairs, or cilia, bend with vibrations caused by sound waves entering the ear. That induces the hair cell to create an electrical signal that is passed on to the auditory nerve and sent to the brain. Devices such as hearing aids, which amplify sounds, and cochlear implants, which stimulate the auditory nerve directly, help people hear, but neither restores hearing to normal.
Until the mid-1980s, researchers thought warm-blooded vertebrates, including humans, weren't able to regenerate hair cells. Then, researchers around the country began observing that hair cells grew back in birds whose hearing was damaged either by noise or drugs. They also determined that hair-cell regeneration can result in improved hearing; in experiments, song birds that had grown new hair cells were able to resume singing their original songs with perfect pitch again.
But there is no indication that mammals can regenerate hair cells. And why some animals, even within the same species, are more vulnerable to hair-cell death, while others are more resistant to it, is a mystery. 'I literally walked around for years wondering about this variability,' says Ed Rubel, a professor of hearing sciences who leads part of the University of Washington research effort.
There are two main approaches to efforts aimed at inducing hair cells to regenerate. Some research groups are attempting to get stem cells -- undifferentiated cells that can develop into various specialized cells -- to turn into hair cells, either by transplanting them from other parts of the body, or by stimulating stem cells naturally occurring in the inner ear to transform themselves. Albert Edge, an associate professor at Harvard Medical School and a researcher at the Massachusetts Eye and Ear Infirmary, says his team has been able to turn mouse stem cells into hair cells in a laboratory dish, though it isn't clear whether those cells are functional or not.
Other researchers, like those at the University of Washington, are focused on understanding the molecules and genetics involved with hair-cell regeneration, and how to mimic this process in animals that don't spontaneously regenerate hair cells. Scientists say aspects of such research, likely will be the first to have applications in humans. One encouraging angle: Dr. Rubel, in collaboration with another University of Washington scientist, David Raible, has identified chemicals that seem to protect hair cells from damage. In this experiment, zebrafish are exposed to a dye that highlights living hair cells. Then, one or two of the zebrafish -- the young ones used in the lab measure just 1/8 of an inch long -- are placed in each of 96 shallow holes contained on a plate. Different chemicals are administered to each fish group that might confer protection to the hair cells.
Finally, another chemical known to kill the fish hair cells is added. Under a microscope, researchers then examine the fish to look for cases where the dye is still evident, signaling that the cells are still alive and suggesting that the protective chemical appears to have done its job.
Those chemicals found to confer protection on fish hair cells are currently also being tested on mice and rats. The idea is that, once a drug is discovered that effectively protects hair cells from dying and is safe for humans, the medicine could be used to help protect the hearing of patients receiving drugs known for killing hair cells, like chemotherapeutic agents.
Dr. Rubel's and Dr. Raible's teams also are studying the genetics of zebrafish to identify markers that confer hair-cell protection.
Last year, their labs jointly identified several genetic mutations and drug-like compounds that seemed to protect hair cells from death, publishing their findings in the journal PLoS Genetics. In a separate study, published in 2007 in Hearing Research, they identified several drugs that also appear to be protective and were already approved for other purposes by the Food and Drug Administration. No tests have been performed on humans, however.
The teams also are working on a separate group of studies to understand the genes and other molecules that allow the regeneration of hair cells in zebrafish, birds and mice.
Surrounding cells known as support cells can both turn into hair cells or generate new hair cells. Dr. Rubel's lab is investigating both processes. 'If we understand the template of genes that are expressed by the cells we would want to divide, then we could tap into that template' to mimic regeneration efforts in mammals, he says.
One finding identified a developmental protein that appears to be turned on in animals able to regenerate hair cells. In one study, a team member found a type of protein increased in a chick (which can regenerate hair cells) after its cells were damaged. But in running the same experiment in a mouse (which can't regenerate hair cells), the protein didn't increase, suggesting the protein could be involved in regeneration.
Scientists involved in the experiments say there could be therapeutic trials to prevent hearing loss using drugs within a decade. However, finding a cure for hearing loss using hair-cell regeneration is likely to be at least 20 years away, they say.
'Hearing aids are Band-aids on a problem that already exists,' says Nancy Freeman, director of the regenerative and development program in hearing loss at the National Institute on Deafness and Other Communication Disorders.
'The hope with this type of [regeneration] approach is that at the end of the day you'd end up with something that natively restores function.'
一條小魚可以拯救你的聽力？
對
許多人來講﹐聽力的喪失是一件無法挽回的事。對致力於研究這一問題的科學家來說﹐避免聽力喪失的一個辦法可以在淡水水族館里找到。
Photo Researchers
在放大2.1萬倍的照片中可以清楚的看到耳蝸內的“毛細胞”
近 年來﹐華盛頓大學西雅圖分校的一個研究團隊一直在對一種水族館里常見的觀賞魚類──斑馬魚進行研究﹐試圖解決人類聽力喪失的問題。和許多其他水生生物一樣 ﹐斑馬魚在身體表面長有毛細胞。這些毛細胞的作用是探測水中的振動﹐其原理與人類內耳中的毛細胞相似。但是﹐與人類不同的是﹐斑馬魚的毛細胞在受損後還可 以再生。研究人員希望他們的工作可以揭開謎底﹐保護人類的毛細胞免受損傷、並推動毛細胞的再生。
內耳中的這種細胞是人類聽覺不可或缺的一 環。之所以稱為“毛細胞”﹐是因為它們在顯微鏡下看上去就像是在細胞外長出了絨毛。這些細細的絨毛﹐或者說纖毛﹐會因為聲波進入耳朵以後產生的振動而擺 動。這種運動會讓毛細胞產生出一種能夠經由聽覺神經傳給大腦的電信號。像助聽器和人工耳蝸等設備都有助聽效果﹐但都無法讓人們的聽力恢復到正常水平。助聽 器能夠增加聲音的強度﹐而人工耳蝸則會直接刺激聽覺神經。
上世紀80年代中期以前﹐研 究人員認為毛細胞無法在包括人類在內的溫血脊椎動物的體內再生。後來﹐美國的研究人員開始注意到﹐鳥類的聽力在因噪音或藥物受損後﹐它們的毛細胞會重新再 生出來。研究者們還認定﹐毛細胞再生可以提高聽力。實驗發現﹐新長出毛細胞的鳴禽可以重新以完美的音調唱出它們從前的歌曲。
但是﹐沒有跡 象表明哺乳動物的毛細胞可以再生。此外﹐即便在同一物種中﹐為什麼某些動物的毛細胞更容易死亡﹐而某些動物的毛細胞卻生命力更頑強﹐這仍舊是一個謎。“這 些年來﹐我真的甚至在走路的時候都在思索為什麼會有這個不同﹐”聽力科學教授埃德•魯貝爾(Ed Rubel)說。魯貝爾負責領導華盛頓大學科研項目的一部分工作。
Photo Researchers
斑馬魚體內的毛細胞能發揮與人類耳蝸內毛細胞類似的作用
而 華盛頓大學等組織的其他研究人員則將注意力集中在同毛細胞再生有關的分子和遺傳學原理﹐以及如何在毛細胞無法再生的動物身上重復這一過程上面。科學家說﹐ 這類研究的某些成果有可能最先應用在人類身上。一條令人鼓舞的消息是﹐魯貝爾已經和華盛頓大學另一名科學家大衛•雷布爾(David Raible)一起合作識別出了能夠保護毛細胞不受損害的化學物質。在他們的實驗中﹐斑馬魚身上活的毛細胞被染色。然後﹐研究人員在一個盤子上的96個淺 孔中放上一至兩條斑馬魚──實驗室使用的小斑馬魚僅有1/8英寸長。可能會對毛細胞起到保護作用的不同的化學物質被施用於每一個淺孔中。
最後﹐他們再向淺孔中加入一種能夠殺死魚類毛細胞的化學物質。在顯微鏡下﹐研究人員仔細觀察﹐尋找染液顏色依然鮮亮的斑馬魚﹐因為這標志著它們的毛細胞還活著﹐意味著起保護作用的化學物質看上去完成了它的任務。
研究人員目前還在老鼠身上試驗那些對魚類毛細胞有保護作用的化學物質。科學家們認為﹐一旦一種藥物被發現可以有效保護毛細胞﹐而且使用起來對人類是安全的﹐這種藥物就可以用來幫助保護病人們的聽力──他們接受的藥物治療﹐如化療藥物﹐能將毛細胞殺死。
魯貝爾和雷布爾的團隊也在研究斑馬魚的遺傳基因﹐以識別對毛細胞有保護作用的基因標記。
去 年﹐他們的實驗室合作識別出了幾個似乎可以保護毛細胞的突變基因和類藥性混合物。他們的科研成果發表在《科學公共圖書館──遺傳學》(PLoS Genetics)雜志上。在2007年發表在《聽力研究》(Hearing Research)上的另一項研究中﹐他們確認了幾種對毛細胞有保護作用且已被美國食品和藥物管理局批准用作其他用途的藥物。不過﹐目前為止還沒有對人體 進行過試驗。
他們的團隊同時還在進行另一組研究﹐試圖瞭解導致斑馬魚、鳥類和老鼠的毛細胞再生的基因和其他分子。
毛細胞週圍的細胞被稱為“支持細胞”﹐它們可以轉化成毛細胞或者產生新的毛細胞。魯貝爾的實驗室正在研究這兩個進程。“如果我們理解了這種細胞的基因模板﹐那麼我們就可以利用這個模板在哺乳動物身上模擬毛細胞再生﹐”他說。
有 一項研究發現了一種似乎可以讓動物毛細胞再生的發育蛋白。在研究中﹐一名團隊成員發現了小雞的毛細胞受損後體內一種蛋白質的含量（小雞的毛細胞可以再生） 有所上升。但是﹐在對老鼠進行的同樣的實驗中（老鼠的毛細胞不能再生）﹐該蛋白質的含量沒有上升﹐這意味著該蛋白質可能與毛細胞再生有關。
參與這些實驗的科學家們說﹐使用藥物防止聽力喪失的臨床實驗有可能會在十年內實現。但是﹐找到利用毛細胞再生治療聽力喪失的辦法可能還需要至少20年的時間。
“ 助聽器是解決問題的一個權宜之計﹐”美國耳聾和其他溝通障礙研究所(National Institute on Deafness and Other Communication Disorders)聽力喪失再生和發展項目的負責人南希•弗里曼(Nancy Freeman)表示。
“利用這種（促進毛細胞再生的）方法﹐我們希望有朝一日可以找到一種方法讓聽力能夠自然地得到恢復。”
Shirley S. Wang
2009年8月10日 星期一
C³ AP 三次元光子晶體
微軟將與網通國家型計畫(NCP)合作，將在臺灣新竹建立亞洲第一個雲端運算通訊應用平台展示中心(C³ AP；Computing and Communications on the Cloud：Application and Platform)，微軟並將與國科會資助研究經費，讓國內各大專院校能夠進行雲端運算相關的研究開發。...
三次元光子晶體 日簡化製程
〔編 譯鄭曉蘭／綜合報導〕日本京都大學研究團隊以創新手法，成功研發被視為下一代高速計算重要元件材料—「三次元光子晶體」的簡易製程。該項技術若能進一步加 以實用，將可大幅縮減該材料的製作時間及成本，並應用在光電驅動的「量子電腦」研發，或光纖訊號的高速處理。相關研究成果已於十日發表於英國科學雜誌「自 然材料（Nature Materials）」。
三次元光子晶體是一種能將光粒封存於內部的半導體結晶，外部接受光線照射時，微小的立體規則矽反射板結構，能讓晶體內的光電重複交互作用，進而產生比以往半導體雷射效率更高的光能。這種材料被視為能夠自由運用光能的新一代元件材料。
30天縮短成5天
日本「產經新聞」十日報導指出，製造三次元光子晶體最大的難題之一，在於「曠日廢時」。製造三次元光子晶體必須使用特殊半導體製造機器，以顯微鏡進行細膩的組合作業，像是製作一個邊長一公分（厚二微米等於百萬分之二米）的八層構造結晶，即須耗時約一個月。
不過，京都大學工學研究科電子工學教授野田進領導的研究團隊，已研發出全新製程，能將上述同樣晶體的製作時間大幅縮短為四至五天。野田表示，簡化製程可望促進超小型光晶片的研發，相關技術將運用於量子電腦研發、光纖訊號高速處理，或人工衛星、飛機的技術提升等領域。
2009年8月8日 星期六
Staving Off a Spiral Toward Oblivion
Staving Off a Spiral Toward Oblivion
Mariners' Museum, Newport News, Va.
The largest sailing ship, the Thomas W. Lawson, in 1902. By that time, it was clear that steamships were the future of sea transportation.
DRIVEN by the pressure to innovate, companies facing major technological change have wholeheartedly embraced management gurus’ advice on how to develop creative, breakthrough products. As a result, corporate America is flush with incubators, skunk works and innovation silos.
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The New York Times
Mechanical typesetter machines in the old composing room of The New York Times.
But has the pendulum swung too far? New technologies are obviously important, but even in today’s fast-paced environment, they can take a long time to substitute for the old. In the meantime, incremental innovation based on old technologies can help a company survive.
When Sony announced its Mavica electronic camera in 1981, headlines trumpeted that “Film Is Dead.” But it took 28 more years for Kodachrome, the film immortalized by Paul Simon, to finally die this past June.
E-book software by companies like Electronic Book Technologies was released in the early 1990s. Yet despite the recent buzz over the Kindle and other electronic reading devices, e-books are still less than 5 percent of overall book sales.
The reality is that most technologies eventually die. But unlike the ancient Greeks, who believed their destiny was controlled by the Fates, today’s managers need not assume that an old technology’s fate is predetermined. Companies can proactively manage the innovation endgame. Continuing improvements to extend the life of technology, particularly given the attractive margins on the old, can be a wise business decision — and not necessarily a reflection of narrow-mindedness.
The key is to extend the profitable life of the old just long enough to have a fighting chance in the new. But how?
Customers move at different speeds, so investments should be focused on market segments that most value the old. Criticisms of Kodak’s digital strategy abound, but one overlooked strength has been its ability to maintain its market position in segments like motion pictures, which, though small, are moving to digital more slowly.
History provides another illustration. Mechanical machines that used molten lead had dominated the typesetter industry for more than 60 years when photography-based machines were introduced in 1949. Along with many new entrants, the leading old-technology companies, Mergenthaler Linotype and Intertype, invested heavily in the new technology.
But the mechanical technology “was well known by the people who were using it,” Carl Schlesinger, a former typesetter operator for The New York Times and author of two books on the history of printing, said in a recent interview. The new technology required customers, particularly unionized newspapers, to make huge investments in retraining.
So throughout the 1950s and ’60s, Mergenthaler Linotype and Intertype continued to develop highly innovative mechanical machines, Herb Klepper, a lead engineer for Mergenthaler at the time, said in a recent interview. The speed of the old machines more than doubled, and newspapers kept using them. By 1978, when The Times retired its old mechanical machines, Mergenthaler Linotype was an established leader in the new technology, and Intertype, while not a leader, had survived to move on to yet the next generation of technology, digital typesetters.
Now, of course, newspapers are struggling to extend the life of print so they can develop new capability and business models for the Web and other forms of electronic distribution.
One mechanism for extending the life of the old is to borrow from the new. Daniel C. Snow, a Harvard Business School professor, says that the useful life of the carburetor was extended significantly by incorporating technology from electronic fuel-injection. Interestingly, he finds that only companies that were also developing electronic fuel-injection technology benefited.
The old can also create a bridge to the new through hybrid products that combine elements of each. Research on electric vehicles has been under way for many years, but a direct leap from gasoline-powered vehicles to electric vehicles has proved challenging.
“Hybrids were an easy way for carmakers to start this transition,” says Felix Kramer, founder of CalCars, a nonprofit organization. Because the required shift in behavior is minimal, many drivers have been willing to make the change. Later, as these drivers become accustomed to the electric-vehicle features of hybrids — the quiet ride, for example — they will presumably become more willing to acquire a purely electric vehicle.
“Once they started down that road, it pointed to the future of plug-in hybrids,” says Mr. Kramer, whose organization promotes the plug-in vehicles. While hybrids like the Toyota Prius use electricity as a supplement, plug-in hybrids go the next step and rely primarily on electricity, with gasoline as the secondary energy source.
“Because of plug-in hybrids, the supply chain and all the technologies will improve, so we gradually get batteries that are cheaper with longer range, and eventually we get all-electric vehicles,” he explains.
OF course, managers still need to know when to move on. When steamships began to compete with sailing ships for freight traffic, the sailing-ship producers responded with what the technology historian S. C. Gilfillan described in his 1935 book, “Inventing the Ship,” as a “noble flowering of the sailing ship.”
But the producers went too far. By 1902, with the building of the Thomas W. Lawson, the largest sailing ship ever, with seven masts and 25 sails, sailing technology had reached a point of diminishing returns, and the competition with steamships had already been lost.
Ultimately, it’s all about balance. The future of a company depends on success in the new. But the old needn’t be framed as simply as a “cash cow” or as a source of inertia holding back the company’s creative juices. Selective, intelligent innovation in the old may just hold the key to the future.
Microsoft’s SharePoint
Microsoft’s SharePoint Thrives in the Recession
By Ashlee VanceHang around at Microsoft’s Redmond, Wash., headquarters for five or ten minutes and someone dressed in khaki pants and a blue shirt is bound to tell you about the wonders of SharePoint — one of the company’s most successful and increasingly controversial lines of software.
Think of SharePoint as the jack-of-all-trades in the business software realm. Companies use it to create Web sites and then manage content for those sites. It can help workers collaborate on projects and documents. And it has a variety of corporate search and business intelligence tools too.
Microsoft wraps all of this software up into a package and sells the bundle at a reasonable price. In fact, the total cost of the bundle often comes in below what specialist companies would charge for a single application in, say, the business intelligence or corporate search fields.
It can’t do everything. Executives at Microsoft will readily admit that the bits and pieces of SharePoint lack the more sophisticated features found in products from specialist software makers.
“We don’t claim we do everything,” said Chris Capossela, a senior vice president at Microsoft. “If we do 50 percent of the functions that these other companies do, but they’re the ones customers really want, that’s fine. The magic is that end users actually like to use the software.”
This strategy seems to have worked even during the recession.
While Microsoft’s Windows sales fell for the first time in history this year, its SharePoint sales have gone up. Microsoft declines to break out the exact sales figures for the software but said that SharePoint broke the $1 billion revenue mark last year and continued to rise past that total this year, making it the hottest selling server-side product ever for the company.
Companies like Ferrari, Starbucks and Viacom have used SharePoint to create their public-facing Web sites and for various other tasks. All told, more than 17,000 customers use SharePoint.
In many ways, SharePoint mimics the strategy Microsoft took with Office by linking together numerous applications into a single unit. This approach appeals to customers looking to save money and also represents a real threat to a variety of business software makers.
Many of these specialists like Cognos, a business intelligence software maker, and Documentum, a content management software maker, have been gobbled up by larger players looking to create their own suites. I.B.M., for example, bought Cognos, while EMC bought Documentum. Other companies like Autonomy, a maker of top-of-the-line corporate search software, remain independent.
Crucially, Microsoft has found a way to create ties between SharePoint and its more traditional products like Office and Exchange. Companies can tweak Office documents through SharePoint and receive information like whether a worker is online or not through tools in Exchange. These links have Microsoft carrying along its old-line software as it builds a more Internet-focused software line.
“SharePoint is saving Microsoft’s Office business even as it paves the way for a new era of Microsoft lock-in,” said Matt Asay, an executive at Alfresco, which makes an open-source content management system. “It is simultaneously the most interesting and dangerous Microsoft technology, and has largely caught its competitors napping.”
Along these lines, Steve Ballmer, Microsoft’s chief executive, has talked about SharePoint as the company’s next big operating system.
Microsoft has managed to undercut even the panoply of open-source companies playing in the business software market by giving away a free basic license to SharePoint if they already have Windows Server. “It’s a brilliant strategy that mimics open source in its viral, free distribution, but transcends open source in its ability to lock customers into a complete, not-free-at-all Microsoft stack - one for which they’ll pay more and more the deeper they get into SharePoint,” Mr. Asay said.
A number of smaller software companies have been eager to piggyback on SharePoint’s success. Based in San Diego, Sharepoint360 provides consulting services and software development help around the product. The company started after employees at a construction company built some Sharepoint applications and decided to market the software to other construction firms.
The start-up has helped construction companies create systems for managing projects, allowing various people to check-in on the progress of a building and keep track of documents tied to the site. It has also expanded beyond the construction area doing work for NASA, Nestle and Toshiba, according to Paul West, a co-founder of SharePoint360.
The company offers to host SharePoint applications for customers. Microsoft too wants to host more software for companies as it moves toward the cloud computing model.
Mr. West recognizes that Microsoft may begin stepping on its partners’ toes. “It may certainly come to pass that they pull the switch,” he said. “That would have implications for us.”
In the meantime, however, Microsoft subsidizes training courses and consulting work for companies like Sharepoint360.
Next year, Microsoft plans to release a new version of the software packed full of more advanced features, including stronger ties to the corporate search technology it acquired in the $1.2 billion purchase of Fast Search and Transfer, a Norwegian start-up.
Best Buy uses the Fast technology today to provide on-the-fly pricing information to customers performing product searches on its Web site.
By making these more sophisticated tools available to customers, Microsoft thinks it can keep pushing niche software makers out of the way and give business people, rather than just the tech folks, a way to work with business applications.
“We believe customers can turn off some of these point solutions,” said Kirk Koenigsbauer, a general manager in Microsoft’s business software group. “With SharePoint, we can deliver a very, very approachable application to end users.”
2009年8月5日 星期三
Mobile Internet Hot Spots: Hot or Not?
Mobile Internet Hot Spots: Hot or Not?
By Saul HansellWill your next cellphone be without a microphone, keyboard or screen?
It may well, argued Daniel R. Hesse, the chief executive of Sprint Nextel, when I spoke to him after the embattled wireless carrier announced its second-quarter earnings last week. He said that an increasing number of customers were going to use mobile hot spots — tiny devices that connect any nearby gadget equipped with Wi-Fi to the Internet using a cellular data network. (In May, David Pogue reviewed one of the first of these hot spots, Novatel’s MiFi 2200, calling the concept a “jaw-dropper.”)
As devices like digital cameras and portable game machines seek to communicate with the world over the Internet, Mr. Hesse argues, this sort of hot spot is better than trying to put a cellphone connection on each gadget or accepting the one-device limit of a wireless data card for a laptop.
“If it’s your iTouch or MP3 player or your netbook or your PC or whatever it might be, even your BlackBerry phone, it can use Wi-Fi to connect to the mobile hot spot to connect to our 3G network,” Mr. Hesse said. “You won’t need a separate bill for each and every device.”
Mr. Hesse said that there were already 425 million computers and other gadgets with Wi-Fi connections.
The one bill you do have won’t be small, however. Sprint charges $99, after rebate, for the Novatel device and $59.99 a month for up to 5 gigabytes of usage. Verizon Wireless offers the same device with a range of price plans.
Mr. Hesse said the hot spot, MiFi, is selling well, but he expected the concept to take off as Sprint introduces its faster 4G network in conjunction with its Clearwire affiliate.
He imagines that people will put the hot spots “in the coffee-cup holder of the car.” He added, “As you go down the road, everybody is connected.”
This isn’t entirely fanciful. J. Wilson, who reviewed the Verizon version of the device on Amazon.com, is already taking it on the road:
It’s surprising how easy it is to connect when traveling in an RV (I’m retired, so I find myself in many geographical locations, when connecting …) and this gadget has provided me with Wi-Fi connection in the Grand Canyon’s RV Trailer Village, in the mountains above Boulder, Co, and at the border of Glacier Nat’l Park (at the portal of West Glacier, East of Whitefish).
And on my commuter bus ride to New Jersey, my laptop is picking up hot spots called MiFi, implying that people are already throwing these gadgets in their purses or briefcases so they can surf on the road.
This sort of mobile hot spot clearly has some uses. It’s great for groups of business travelers. And even some families that travel with more than one laptop might well lust after one. I’m not convinced this is a mainstream product, though. It’s expensive and adds yet another gadget in your life to recharge. I wonder whether you would rather simply carry a cellphone that can connect — by way of Wi-Fi or Bluetooth — to your camera, game machine and so on. But I do think more and more people will want some version of what David Pogue called the “personal Wi-Fi bubble.”
Still, Sprint, which is still losing customers rapidly, needs every weapon it can muster to generate excitement.
What do you think? Would you pay for a portable Internet hot spot so that any gadget you own can go online?
2009年8月4日 星期二
The Internet takes over Europe
Internet | 04.08.2009
The Internet takes over Europe
The study found that those aged under 24 years are Europe's biggest Internet users. 66 percent of this age group surf the web every day compared with only 43 percent of the rest of the EU population.
The study found that this young group - dubbed the "new digital generation" - does not want to pay for the services offered on the Internet. Almost 75 percent have used file sharing services – for example, music sharing services -many of which are illegal.
These users wrongly believe many of the services and content available on the Internet to be free, or provided as part of flat-rate Internet connection fees. One third of young people say they don't want to pay for Internet services including video or music content.
Germany leads the field when it comes to downloading computer games, said Martin Selmayr, spokesman for the EU's Commissioner for Telecommunications. However, "when it comes to reading magazines or newspapers online, Germany is only in 19th position (of the 27 member states)," he added.
Are surfers' social skills suffering?
Highly popular are social networking platforms like MySpace, Facebook and the German language StudiVZ. There's increasing criticism, however, that such platforms can cause social skills to deteriorate.
Sites like MySpace and Facebook do not “provide rounded communication, so they will not build a rounded community,” said the head of the Roman Catholic Church in England and Wales, Archbishop Vincent Nichols in an interview with the Sunday Telegraph. He said he was concerned that the number of social contacts was taking precedence over quality.
One result is "Facebook Fatigue", as people start to cancel their memberships. Microsoft chairman, Bill Gates recently cancelled his Facebook presence, after "more than 10,000 people wanted to be (his) friends." He just couldn't keep up, Gates said.
Once on the Internet, always on the Internet
Other studies have found that some young people abuse such platforms by placing sexually explicit or other embarrassing or harmful images on the Internet.
“If a relationship breaks down or someone finds a mobile phone (with pictures on it) then the image could und up on a website, a social networking site like Facebook, or even end in the wrong hands, as has happened, and end up on a paedophile network,” said Helen Penn of the London-based Child Exploitation and Online Protection Centre (CEOP).
The Internet has also become a dumping ground for consumer complaints, reports the MSNBC website. Instead of being forced to wait for long periods of time on consumer complaint phone lines, it's easier to write one's complaint on Twitter or Facebook.
Stay anonymous, data experts warn
There have been numerous data scandals in recent months in the digital world. Coupled with the fact that browsers like Google can dig up information on just about anyone, even years later, if it's been published on the Internet, privacy specialists say consumers should place as little data in circulation as possible and seek to retain their anonymity. “Employers have discovered social networking sites provide a source of information about applications and employees,” warns German data protection expert Thilo Weichert. “Internet users should carefully consider what they release, especially when it comes to photographs,” he warns.
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Editor: Susan Houlton
Finally, the Spleen Gets Some Respect
Finally, the Spleen Gets Some Respect
As a confirmed crab apple who has often been compared to the splenetic Lucy Van Pelt character from Peanuts, I am gratified to learn that should my real spleen ever decide to vent in earnest, the outburst may just help save my life.
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Scientists have discovered that the spleen, long consigned to the B-list of abdominal organs and known as much for its metaphoric as its physiological value, plays a more important role in the body’s defense system than anyone suspected.
Reporting in the current issue of the journal Science, researchers from Massachusetts General Hospital and Harvard Medical School describe studies showing that the spleen is a reservoir for huge numbers of immune cells called monocytes, and that in the event of a serious trauma to the body like a heart attack, gashing wound or microbial invasion, the spleen will disgorge those monocyte multitudes into the bloodstream to tackle the crisis.
“The parallel in military terms is a standing army,” said Matthias Nahrendorf, an author of the report. “You don’t want to have to recruit an entire fighting force from the ground up every time you need it.”
That researchers are only now discovering a major feature of a rather large organ they have been studying for at least 2,000 years demonstrates yet again that there is nothing so foreign as the place we call home.
“Often, if you come across something in the body that seems like a big deal, you think, ‘Why didn’t anybody check this before?’ ” Dr. Nahrendorf said. “But the more you learn, the more you realize that we’re just scratching on the surface of life. We don’t know the whole story about anything.”
Dr. Nahrendorf, with Filip K. Swirski, Mikael J. Pittet and a dozen other colleagues, performed the initial studies using mice, but the scientists suspect the results will apply to humans as well.
Ulrich H. von Andrian, an immunologist at Harvard Medical School who was not involved with the research, agreed that the findings were a surprise. “If one had to guess the source of these cells, one would have thought it likely that they were mobilized from the bone marrow rather than from the spleen,” he said. “The discovery adds another layer of complexity not previously associated with that organ.”
The latest work also sounds a cautionary note against underestimating a body part or dismissing it as vestigial, expendable or past its prime. In an accompanying essay, Ting Jia and Eric G. Pamer of Memorial Sloan-Kettering Cancer Center admit that “the spleen lacks the gravitas of neighboring organs” like the liver or the stomach “because we can survive without it.”
Spleens can rupture during contact sports, say, or in a motorcycle accident, at which point surgeons have no choice.
“It’s such a vascularized organ, and the risk of big-time hemorrhaging is so great, that if the spleen ruptures, it’s a surgical emergency,” said James N. George, a hematologist with the University of Oklahoma Health Sciences Center. “You have to remove it.”
The new findings in no way counter the necessity of excising a ruptured spleen, the researchers said, but they do suggest that the loss of the organ is more than a mere “inconvenience,” as it has often been depicted, and could help explain previous reports showing an enhanced risk of early death among people who have undergone splenectomies.
In one study that appeared in The Lancet in 1977, for example, researchers compared a group of 740 American veterans of World War II who had had their spleens removed as a result of battle injuries with a similar size sample of veterans who had suffered other war injuries but had kept their spleens. The splenectomized men, the researchers found, were twice as likely to die of cardiovascular disease as were the veterans in the control group. All of which means that despleening should be diligently guarded against, particularly among our little sports warriors, perhaps through the wearing of appropriate protective gear.
Researchers cite other cases in which organs were presumed to be so dispensable that they could be removed “prophylactically” — often with unfortunate outcomes. In recent years, for example, many older women undergoing hysterectomies have been advised to have their healthy ovaries removed at the same time, the rationale being: if you are past your childbearing years, why hang on to reproductive organs that might turn cancerous and kill you? Yet follow-up surveys have shown that women who underwent elective ovariectomy had a heightened risk of dying during a given study period, were more susceptible to heart disease and lung cancer and were twice as likely to develop Parkinson’s disease compared with women who had kept their ovaries. “Evolution has an edge on us,” Dr. Nahrendorf said. “I would be very careful about saying, ‘You don’t need this organ, get rid of it.’ ”
Another reason to esteem the spleen — a purplish, fist-size, five-ounce organ in the upper left quadrant of the abdominal cavity, just behind the stomach and under the diaphragm — is its illustrious medical and poetic history. Galen considered the spleen to be a source of one of the four bodily humors, specifically the black bile associated with irritable, melancholic cranks. In his poem, “Spleen,” Charles Baudelaire describes a young narrator so weary and despondent, unresponsive even to beautiful women and jesting men, that it is as if the “green waters of Lethe” fills his veins.
More recently, researchers determined that the spleen is like an elaborate wetlands, a Mississippi bayou for filtering and freshening the blood. In other organs, blood flows through an interconnected mesh of increasingly narrow arteries, veins and capillaries. The spleen, by contrast, has a so-called noncapillary circulatory system: as the blood flows in, it is dumped into puddle-like sinusoids, and to get back out it must squeeze between cells. That dumping and squeezing help filter out blood-borne parasites, aging blood cells too brittle for compression and the little oxidized pellets, the BB’s, with which red blood cells are often pocked. The spleen has often been called a graveyard for red blood cells, but it is more of a recycling center, for the iron and other components are plucked out of the cells and used to stock new hemoglobin cages.
Filtration, cannibalization, and now — serious monocyte cultivation. In the new study, the researchers began by looking at monocytes, the largest of the body’s white blood cells. “It was recognized that these cells are the major repair workers after a heart attack,” Dr. Nahrendorf said. “They remove dead muscle cells, they start rebuilding stable scar tissue, they stimulate the generation of new blood vessels.”
The cells make haste to cut and paste. “Within 24 hours after a myocardial infarction,” Dr. Nahrendorf said, “there are millions of monocytes” congregating around the broken heart. All of which would seem sensible, desirable, an excellent display of emergency preparedness, except that Dr. Nahrendorf and his principal colleagues were puzzled by one big unknown: Where did the rapid response team come from? The numbers circulating in the blood were simply too low. The researchers searched one organ after another, until they checked the spleen and found the monocytic mother lode. “The numbers there were huge, 10 times higher than what was in the bloodstream,” Dr. Nahrendorf said.
By the researchers’ reckoning, monocytes, like all blood cells, are born in the bone marrow and at some point migrate to the spleen, lured by cues yet to be identified. They sit and wait, a sessile bunch, but when aroused by such chemical signatures of damage as angiotensin, the cells surge forth without hesitation, a reaction the researchers hope someday to understand well enough to recapitulate at will. Hail to the chief, hail to the queen and hail to the monocytes residing in my spleen.
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