Leading academic journals are distorting the scientific process and represent a “tyranny” that must be broken, according to a Nobel prize winner who has declared a boycott on the publications.
Randy Schekman, a US biologist who won the Nobel prize in physiology or medicine this year and receives his prize in Stockholm on Tuesday, said his lab would no longer send research papers to the top-tier journals, Nature, Cell and Science.
Schekman said pressure to publish in “luxury” journals encouraged researchers to cut corners and pursue trendy fields of science instead of doing more important work. The problem was exacerbated, he said, by editors who were not active scientists but professionals who favoured studies that were likely to make a splash.
The prestige of appearing in the major journals has led the Chinese Academy of Sciences to pay successful authors the equivalent of $30,000 (£18,000). Some researchers made half of their income through such “bribes”, Schekman said in an interview.
Writing in the Guardian, Schekman raises serious concerns over the journals’ practices and calls on others in the scientific community to take action.
“I have published in the big brands, including papers that won me a Nobel prize. But no longer,” he writes. “Just as Wall Street needs to break the hold of bonus culture, so science must break the tyranny of the luxury journals.”
Schekman is the editor of eLife, an online journal set up by the Wellcome Trust. Articles submitted to the journal – a competitor to Nature, Cell and Science – are discussed by reviewers who are working scientists and accepted if all agree. The papers are free for anyone to read.
Schekman criticises Nature, Cell and Science for artificially restricting the number of papers they accept, a policy he says stokes demand “like fashion designers who create limited-edition handbags.” He also attacks a widespread metric called an “impact factor”, used by many top-tier journals in their marketing.
A journal’s impact factor is a measure of how often its papers are cited, and is used as a proxy for quality. But Schekman said it was “toxic influence” on science that “introduced a distortion”. He writes: “A paper can become highly cited because it is good science – or because it is eye-catching, provocative, or wrong.”
Daniel Sirkis, a postdoc in Schekman’s lab, said many scientists wasted a lot of time trying to get their work into Cell, Science and Nature. “It’s true I could have a harder time getting my foot in the door of certain elite institutions without papers in these journals during my postdoc, but I don’t think I’d want to do science at a place that had this as one of their most important criteria for hiring anyway,” he told the Guardian.
Sebastian Springer, a biochemist at Jacobs University in Bremen, who worked with Schekman at the University of California, Berkeley, said he agreed there were major problems in scientific publishing, but no better model yet existed. “The system is not meritocratic. You don’t necessarily see the best papers published in those journals. The editors are not professional scientists, they are journalists which isn’t necessarily the greatest problem, but they emphasise novelty over solid work,” he said.
Springer said it was not enough for individual scientists to take a stand. Scientists are hired and awarded grants and fellowships on the basis of which journals they publish in. “The hiring committees all around the world need to acknowledge this issue,” he said.
Philip Campbell, editor-in-chief at Nature, said the journal had worked with the scientific community for more than 140 years and the support it had from authors and reviewers was validation that it served their needs.
“We select research for publication in Nature on the basis of scientific significance. That in turn may lead to citation impact and media coverage, but Nature editors aren’t driven by those considerations, and couldn’t predict them even if they wished to do so,” he said.
“The research community tends towards an over-reliance in assessing research by the journal in which it appears, or the impact factor of that journal. In a survey Nature Publishing Group conducted this year of over 20,000 scientists, the three most important factors in choosing a journal to submit to were: the reputation of the journal; the relevance of the journal content to their discipline; and the journal’s impact factor. My colleagues and I have expressed concerns about over-reliance on impact factors many times over the years, both in the pages of Nature and elsewhere.”
Monica Bradford, executive editor at Science, said: “We have a large circulation and printing additional papers has a real economic cost … Our editorial staff is dedicated to ensuring a thorough and professional peer review upon which they determine which papers to select for inclusion in our journal. There is nothing artificial about the acceptance rate. It reflects the scope and mission of our journal.”
Emilie Marcus, editor of Cell, said: “Since its launch nearly 40 years ago, Cell has focused on providing strong editorial vision, best-in-class author service with informed and responsive professional editors, rapid and rigorous peer-review from leading academic researchers, and sophisticated production quality. Cell’s raison d’etre is to serve science and scientists and if we fail to offer value for both our authors and readers, the journal will not flourish; for us doing so is a founding principle, not a luxury.”
• This article was amended on 10 December 2013 to include a response from Cell editor Emilie Marcus, which arrived after the initial publication deadline.
The Nobel Assembly at Karolinska Institutet has today decided to award
for their discoveries of machinery regulating vesicle traffic,
a major transport system in our cells
The 2013 Nobel Prize honours three scientists who have solved the mystery of how the cell organizes its transport system. Each cell is a factory that produces and exports molecules. For instance, insulin is manufactured and released into the blood and chemical signals called neurotransmitters are sent from one nerve cell to another. These molecules are transported around the cell in small packages called vesicles. The three Nobel Laureates have discovered the molecular principles that govern how this cargo is delivered to the right place at the right time in the cell.
Randy Schekman discovered a set of genes that were required for vesicle traffic. James Rothman unravelled protein machinery that allows vesicles to fuse with their targets to permit transfer of cargo. Thomas Südhof revealed how signals instruct vesicles to release their cargo with precision.
Through their discoveries, Rothman, Schekman and Südhof have revealed the exquisitely precise control system for the transport and delivery of cellular cargo. Disturbances in this system have deleterious effects and contribute to conditions such as neurological diseases, diabetes, and immunological disorders.
How cargo is transported in the cell
In a large and busy port, systems are required to ensure that the correct cargo is shipped to the correct destination at the right time. The cell, with its different compartments called organelles, faces a similar problem: cells produce molecules such as hormones, neurotransmitters, cytokines and enzymes that have to be delivered to other places inside the cell, or exported out of the cell, at exactly the right moment. Timing and location are everything. Miniature bubble-like vesicles, surrounded by membranes, shuttle the cargo between organelles or fuse with the outer membrane of the cell and release their cargo to the outside. This is of major importance, as it triggers nerve activation in the case of transmitter substances, or controls metabolism in the case of hormones. How do these vesicles know where and when to deliver their cargo?
Traffic congestion reveals genetic controllers
Randy Schekman was fascinated by how the cell organizes its transport system and in the 1970s decided to study its genetic basis by using yeast as a model system. In a genetic screen, he identified yeast cells with defective transport machinery, giving rise to a situation resembling a poorly planned public transport system. Vesicles piled up in certain parts of the cell. He found that the cause of this congestion was genetic and went on to identify the mutated genes. Schekman identified three classes of genes that control different facets of the cell´s transport system, thereby providing new insights into the tightly regulated machinery that mediates vesicle transport in the cell.
Docking with precision
James Rothman was also intrigued by the nature of the cell´s transport system. When studying vesicle transport in mammalian cells in the 1980s and 1990s, Rothman discovered that a protein complex enables vesicles to dock and fuse with their target membranes. In the fusion process, proteins on the vesicles and target membranes bind to each other like the two sides of a zipper. The fact that there are many such proteins and that they bind only in specific combinations ensures that cargo is delivered to a precise location. The same principle operates inside the cell and when a vesicle binds to the cell´s outer membrane to release its contents.
It turned out that some of the genes Schekman had discovered in yeast coded for proteins corresponding to those Rothman identified in mammals, revealing an ancient evolutionary origin of the transport system. Collectively, they mapped critical components of the cell´s transport machinery.
Timing is everything
Thomas Südhof was interested in how nerve cells communicate with one another in the brain. The signalling molecules, neurotransmitters, are released from vesicles that fuse with the outer membrane of nerve cells by using the machinery discovered by Rothman and Schekman. But these vesicles are only allowed to release their contents when the nerve cell signals to its neighbours. How is this release controlled in such a precise manner? Calcium ions were known to be involved in this process and in the 1990s, Südhof searched for calcium sensitive proteins in nerve cells. He identified molecular machinery that responds to an influx of calcium ions and directs neighbour proteins rapidly to bind vesicles to the outer membrane of the nerve cell. The zipper opens up and signal substances are released. Südhof´s discovery explained how temporal precision is achieved and how vesicles´ contents can be released on command.
Vesicle transport gives insight into disease processes
The three Nobel Laureates have discovered a fundamental process in cell physiology. These discoveries have had a major impact on our understanding of how cargo is delivered with timing and precision within and outside the cell. Vesicle transport and fusion operate, with the same general principles, in organisms as different as yeast and man. The system is critical for a variety of physiological processes in which vesicle fusion must be controlled, ranging from signalling in the brain to release of hormones and immune cytokines. Defective vesicle transport occurs in a variety of diseases including a number of neurological and immunological disorders, as well as in diabetes. Without this wonderfully precise organization, the cell would lapse into chaos.
James E. Rothman was born 1950 in Haverhill, Massachusetts, USA. He received his PhD from Harvard Medical School in 1976, was a postdoctoral fellow at Massachusetts Institute of Technology, and moved in 1978 to Stanford University in California, where he started his research on the vesicles of the cell. Rothman has also worked at Princeton University, Memorial Sloan-Kettering Cancer Institute and Columbia University. In 2008, he joined the faculty of Yale University in New Haven, Connecticut, USA, where he is currently Professor and Chairman in the Department of Cell Biology.
Randy W. Schekman was born 1948 in St Paul, Minnesota, USA, studied at the University of California in Los Angeles and at Stanford University, where he obtained his PhD in 1974 under the supervision of Arthur Kornberg (Nobel Prize 1959) and in the same department that Rothman joined a few years later. In 1976, Schekman joined the faculty of the University of California at Berkeley, where he is currently Professor in the Department of Molecular and Cell biology. Schekman is also an investigator of Howard Hughes Medical Institute.
Thomas C. Südhof was born in 1955 in Göttingen, Germany. He studied at the Georg-August-Universität in Göttingen, where he received an MD in 1982 and a Doctorate in neurochemistry the same year. In 1983, he moved to the University of Texas Southwestern Medical Center in Dallas, Texas, USA, as a postdoctoral fellow with Michael Brown and Joseph Goldstein (who shared the 1985 Nobel Prize in Physiology or Medicine). Südhof became an investigator of Howard Hughes Medical Institute in 1991 and was appointed Professor of Molecular and Cellular Physiology at Stanford University in 2008.
|Novick P, Schekman R: Secretion and cell-surface growth are blocked in a temperature-sensitive mutant of Saccharomyces cerevisiae. Proc Natl Acad Sci USA 1979; 76:1858-1862.|
|Balch WE, Dunphy WG, Braell WA, Rothman JE: Reconstitution of the transport of protein between successive compartments of the Golgi measured by the coupled incorporation of N-acetylglucosamine. Cell 1984; 39:405-416.|
|Kaiser CA, Schekman R: Distinct sets of SEC genes govern transport vesicle formation and fusion early in the secretory pathway. Cell 1990; 61:723-733.|
|Perin MS, Fried VA, Mignery GA, Jahn R, Südhof TC: Phospholipid binding by a synaptic vesicle protein homologous to the regulatory region of protein kinase C. Nature 1990; 345:260-263.|
|Sollner T, Whiteheart W, Brunner M, Erdjument-Bromage H, Geromanos S, Tempst P, Rothman JE: SNAP receptor implicated in vesicle targeting and fusion. Nature 1993;
|Hata Y, Slaughter CA, Südhof TC: Synaptic vesicle fusion complex contains unc-18 homologue bound to syntaxin. Nature 1993; 366:347-351.|
A retooling of Japan’s drug authorization framework, on its way to becoming law, could produce the world’s fastest approval process specifically designed for regenerative medicine. “I don’t know of any other countries that have broken out with a separate and novel system” for cellular therapies, says University College London regenerative medicine expert Chris Mason, who recently met with Japanese policymakers to discuss the law.
Japan has recently been trying to shake its ‘drug lag’, a term used to describe its historically slow review process that sometimes translates into therapies reaching the market well after they have received the green light elsewhere. But the country is now ready to speed the translation of regenerative medicine to the bedside.
The move comes in response to the potential offered by its homegrown induced pluripotent stem (iPS) cell technology, which netted Shinya Yamanaka, of the University of Kyoto, last year’s Nobel Prize in Medicine or Physiology. The government already flooded the field with more than 20 billion yen ($206 million) in a supplementary budget announced earlier this year, and it’s expected to allocate another 90 billion yen into the sector over the coming decade.
Under the Pharmaceutical Affairs Law as it currently stands, regenerative therapies, like small-molecule drugs, must undergo three phases of costly and cumbersome clinical trials to get approval by Japan’s Pharmaceutical and Medical Devices Agency.
The proposed amendments to the pharmaceutical law will create a new, separate approval channel for regenerative medicine. Rather than using phased clinical trials, companies will have to demonstrate efficacy in pilot studies of as few as ten patients in one study, if the change is dramatic enough, or a few hundred when improvement is more marginal. According to Toshio Miyata, deputy director of the Evaluation and Licensing Division at the Pharmaceutical and Food Safety Bureau in Tokyo, if efficacy can be “surmised,” the treatment will be approved for marketing. At that stage, the treatment could be approved for commercial use and, crucially for such expensive treatments, for national insurance coverage.
With the bar for regenerative therapies dramatically lowered by requiring only limited safety and efficacy data—and essentially doing away with the need for high-powered phase 3 trials—the amendments’ architects say it will be possible to get a stem cell treatment to the market in just three years, rather than the typical six or more. The law should also give local producers of regenerative medicine an edge even over those selling stem cell therapies in South Korea, where an accelerated system has helped companies get more stem cell treatments on the market than any other country (see Nat. Med. 18, 329, 2012). “It’s bold,” says Yoshihide Esaki, director of Bio-Industry Division, a bureau of the Ministry of Economy, Trade and Industry based in Tokyo, which promoted legislation calling for the update.
Following approval, there will be a post-market surveillance period of five to seven years, after which the treatment will be evaluated again for safety and efficacy. Every patient must be entered in a registry during that period, says Miyata. If the therapies prove inefficacious or unsafe, approval can be withdrawn.
Doug Sipp worries whether post-market surveillance will turn up relevant data. Sipp, who studies regulatory issues related to stem cells at the RIKEN Center for Developmental Biology in Kobe, Japan, says that making people who receive the therapies during this period cough up even the 30% co-pay generally required under Japan’s national insurance plan “will essentially be asking patients to pay for the privilege of serving as the subjects of medical experiments.” And since the patients are paying, the studies cannot be randomized or blinded. Paying patients are also more likely to experience placebo effects, Sipp warns.
“There’s also the opportunity costs to patients,” who might be able to find better therapies elsewhere, adds Mason. “We have to make sure these therapies are safe and effective. Otherwise these regulatory routes are going to be closed.”
Despite these concerns, passage of the pre-vetted law is almost a given. Esaki says there’s a 50% chance the Japanese parliament will pass the law during the current session, ending in June. If so, it would go into effect next April. If not, scientists might have to wait until November 2014 or as late as April 2015.
Murray suffered a stroke at his suburban Boston home on Thanksgiving and died at Brigham and Women’s Hospital on Monday, hospital spokesman Tom Langford said.
Since the first kidney transplants on identical twins, hundreds of thousands of transplants on a variety of organs have been performed worldwide. Murray shared the Nobel Prize in Physiology or Medicine in 1990 with Dr. E. Donnall Thomas, who won for his work in bone marrow transplants.
“Kidney transplants seem so routine now,” Murray told The New York Times after he won the Nobel. “But the first one was like Lindbergh’s flight across the ocean.”
Murray’s breakthroughs did not come without criticism, from ethicists and religious leaders. Some people “felt that we were playing God and that we shouldn’t be doing all of these, quote, experiments on human beings,” he told The Associated Press in a 2004 interview in which he also spoke out in favor of stem cell research.
In the early 1950s, there had never been a successful human organ transplant. Murray and his associates at Boston’s Peter Bent Brigham Hospital, now Brigham and Women’s Hospital, developed new surgical techniques, gaining knowledge by successfully transplanting kidneys in dogs. In December 1954, they found the right human patients, 23-year-old Richard Herrick, who had end-stage kidney failure, and his identical twin, Ronald Herrick.
Because of their identical genetic background, they did not face the biggest problem with transplant patients, the immune system’s rejection of foreign tissue.
After the operation, Richard had a functioning kidney transplanted from Ronald. Richard lived another eight years, marrying a nurse he met at the hospital and having two children.
Murray performed more transplants on identical twins over the next few years and tried kidney transplants on other relatives, including fraternal twins, learning more about how to suppress the immune system’s rejection of foreign tissue. One patient who received a kidney transplant from a fraternal twin in 1959, plus radiation and a bone marrow transplant to suppress his immune response, lived for 29 more years.
But it was the development of drugs to suppress the body’s immune response, a less radical approach than radiation, that made real breakthroughs in transplants possible. In 1962, Murray and his team successfully completed the first organ transplant from an unrelated donor. The 23-year-old patient, Mel Doucette, received a kidney from a man who had died.
Murray continued a long career in plastic surgery, his original specialty, and transplants. He was guided by his own deep religious convictions.
“Work is a prayer,” he told the Harvard University Gazette in 2001. “And I start off every morning dedicating it to our Creator.”
Murray told the Journal of the American Medical Association in 2004 that he continued to get letters from patients he helped years earlier and from relatives of those who died during the early efforts.
“They often say … that they are happy to have played some small part in the eventual success of organ transplants,” he said, praising the courage of his patients and their families.
Murray was honored at the 2004 Transplant Games, for athletes who have received organ transplants, along with Ronald Herrick, the man who had donated a kidney to his twin brother a half-century earlier.
Murray continued to support and mentor others at Brigham and Women’s Hospital after his retirement, hospital president Dr. Elizabeth Nabel said. An exhibit in the hospital’s library housing his Nobel Prize, she said, is framed by his own words: “Service to society is the rent we pay for living on this planet.”
Murray’s interest in transplants developed during his time in the Army during World War II when he was assigned to Valley Forge General Hospital in Pennsylvania while awaiting overseas duty. The hospital performed reconstructive surgery on troops who had been injured in battle.
The burn patients, who often were treated with skin grafts from other people, intrigued Murray.
“The slow rejection of the foreign skin grafts fascinated me,” Murray wrote in autobiography for the Nobel Prize ceremony. “How could the host distinguish another person’s skin from his own?”
The hospital’s chief of plastic surgery had performed skin grafts on civilians and noticed that the closer the donor and recipient were related, the slower the tissue was rejected. A skin graft between identical twins had taken permanently.
Murray said that was “the impetus” of his study of organ transplantation.
Murray was ever the optimist and kept on his desk a quotation, “Difficulties are opportunities,” his son Rick Murray said.
“It reflects the unwavering optimism of a great man who was generous, curious, and always humble,” Rick Murray said in a statement released by the hospital.
Source: Yahoo News
Recent winners of the Nobel Prize in physiology or medicine, and their research, according to the Nobel Foundation:
— 2012: Briton John Gurdon and Japan’s Shinya Yamanaka for their discovery that mature cells can be reprogrammed into immature cells that can be turned into all tissues of the body, a finding that revolutionized understanding of how cells and organisms develop.
— 2011: American Bruce Beutler and French researcher Jules Hoffmann for their discoveries concerning the activation of innate immunity, sharing it with Canadian-born Ralph Steinman for his discovery of the dendritic cell and its role in adaptive immunity.
— 2010: British researcher Robert Edwards for the development of in vitro fertilization.
— 2009: Americans Elizabeth Blackburn, Carol Greider and Jack Szostak for their discovery of how chromosomes are protected by telomeres and the enzyme telomerase, research that has implications for cancer and aging research.
— 2008: Harald zur Hausen and Francoise Barre-Sinoussi and Luc Montagnier for discoveries of human papilloma viruses causing cervical cancer and the discovery of human immunodeficiency virus.
— 2007: Mario R. Capecchi and Oliver Smithies of the United States and Martin J. Evans of the United Kingdom, for their discoveries leading to a powerful technique for manipulating mouse genes.
— 2006: Andrew Z. Fire and Craig C. Mello, of the United States, for their work in controlling the flow of genetic information.
— 2005: Barry J. Marshall and Robin Warren, of Australia, for their work in how the bacterium Helicobacter pylori plays a role in gastritis and peptic ulcer disease.
— 2004: Richard Axel and Linda B. Buck, both of the United States, for their work in studying odorant receptors and the organization of the olfactory system in human beings.
— 2003: Paul C. Lauterbur, United States, and Sir Peter Mansfield, Britain, for discoveries in magnetic resonance imaging, a technique that reveals the brain and inner organs in breathtaking detail.
— 2002: Sydney Brenner and John E. Sulston, Britain, and H. Robert Horvitz, United States, for discoveries concerning how genes regulate organ development and a process of programmed cell death.
— 2001: Leland H. Hartwell, United States, R. Timothy Hunt and Sir Paul M. Nurse, Britain, for the discovery of key regulators of the process that lets cells divide, which is expected to lead to new cancer treatments.
— 2000: Arvid Carlsson, Sweden, Paul Greengard and Eric R. Kandel, United States, for research on how brain cells transmit signals to each other, thus increasing understanding on how the brain functions and how neurological and psychiatric disorders may be treated better.
— 1999: Guenter Blobel, United States, for protein research that shed new light on diseases, including cystic fibrosis and early development of kidney stones.
— 1998: Robert F. Furchgott, Louis J. Ignarro and Ferid Murad, United States, for the discovery of properties of nitric oxide, a common air pollutant but also a lifesaver because of its capacity to dilate blood vessels.
* The 2012 prize was awarded “for the discovery that mature cells can be reprogrammed to become pluripotent”. The two scientists discovered that mature, specialized cells can be reprogrammed to become immature cells capable of developing into all tissues of the body. Their findings revolutionized understanding of how cells and organisms develop.
* Nobel Prizes in Physiology or Medicine have been awarded 102 times since 1901. In all but 38 cases they were given to more than one recipient.
* Of the 199 individuals awarded the Nobel Prize in Physiology or Medicine, only ten are women. Of these eight, Barabara McClintock is the only one who has received an unshared Nobel Prize.
* Famous Winners: Robert Koch, the German physician and bacteriologist, won in 1905 for his work on tuberculosis. Frederick Banting, the Canadian physiologist who with his assistant Charles Best discovered insulin, the principal remedy for diabetes, won the prize in 1923.
* The oldest living recipient is Rita Levi-Montalcini, the first Nobel laureate to reach her hundredth birthday, who won the prize in 1986 with Stanley Cohen for their discoveries of growth factors. She celebrated her 103rd birthday last April.
STOCKHOLM – Scientists from Britain and Japan shared a Nobel Prize on Monday for the discovery that adult cells can be transformed back into embryo-like stem cells that may one day regrow tissue in damaged brains, hearts or other organs.
John Gurdon, 79, of the Gurdon Institute in Cambridge, Britain and Shinya Yamanaka, 50, of Kyoto University in Japan, discovered ways to create tissue that would act like embryonic cells, without the need to harvest embryos.
They share the $1.2 million Nobel Prize for Medicine, for work Gurdon began 50 years ago and Yamanaka capped with a 2006 experiment that transformed the field of “regenerative medicine” – the field of curing disease by regrowing healthy tissue.
All of the body’s tissue starts as stem cells, before developing into skin, blood, nerves, muscle and bone. The big hope for stem cells is that they can be used to replace damaged tissue in everything from spinal cord injuries to Parkinson’s disease.
Scientists once thought it was impossible to turn adult tissue back into stem cells, which meant that new stem cells could only be created by harvesting embryos – a practice that raised ethical qualms in some countries and also means that implanted cells might be rejected by the body.
In 1958, Gurdon was the first scientist to clone an animal, producing a healthy tadpole from the egg of a frog with DNA from another tadpole’s intestinal cell. That showed developed cells still carry the information needed to make every cell in the body, decades before other scientists made headlines around the world by cloning the first mammal, Dolly the sheep.
More than 40 years later, Yamanaka produced mouse stem cells from adult mouse skin cells, by inserting a few genes. His breakthrough effectively showed that the development that takes place in adult tissue could be reversed, turning adult cells back into cells that behave like embryos. The new stem cells are known as “induced pluripotency stem cells”, or iPS cells.
“The eventual aim is to provide replacement cells of all kinds,” Gurdon’s Institute explains on its website.
“We would like to be able to find a way of obtaining spare heart or brain cells from skin or blood cells. The important point is that the replacement cells need to be from the same individual, to avoid problems of rejection and hence of the need for immunosuppression.”
The science is still in its early stages, and among important concerns is the fear that iPS cells could grow out of control and develop into tumors.
Nevertheless, in the six years since Yamanaka published his findings the discoveries have already produced dramatic advances in medical research, with none of the political and ethical issues raised by embryo harvesting.
“NOT A ONE-WAY STREET”
Thomas Perlmann, Nobel Committee member and professor of Molecular Development Biology at the Karolinska Institute said: “Thanks to these two scientists, we know now that development is not strictly a one-way street.”
“There is lot of promise and excitement, and difficult disorders such as neurodegenerative disorders, like perhaps Alzheimer’s and, more likely, Parkinson’s disease, are very interesting targets.”
The techniques are already being used to grow specialized cells in laboratories to study disease, the chairman of the awards committee, Urban Lendahl, told Reuters.
“You can’t take out a large part of the heart or the brain or so to study this, but now you can take a cell from for example the skin of the patient, reprogram it, return it to a pluripotent state, and then grow it in a laboratory,” he said.
“The second thing is for further ahead. If you can grow different cell types from a cell from a human, you might – in theory for now but in future hopefully – be able to return cells where cells have been lost.”
Yamanaka’s paper has already been cited more than 4,000 times in other scientists’ work. He has compared research to running marathons, and ran one in just over four hours in March to raise money for his lab.
In a news conference in Japan, he thanked his team of young researchers: “My joy is very great. But I feel a grave sense of responsibility as well.”
Gurdon has spoken of an unlikely career for a young man who loved science but was steered away from it at school. He still keeps a discouraging school report on his office wall.
“I believe he has ideas about becoming a scientist… This is quite ridiculous,” his teacher wrote. “It would be a sheer waste of time, both on his part and of those who have to teach him.” The young John “will not listen, but will insist on doing his work in his own way.”
Source: Yahoo News