Monkeys Born From Eggs With DNA Transplant
Malcolm Ritter, Associated Press
http://dsc.discovery.com/news/2009/08/26/monkey-dna-transfer.html
Born From DNA-Altered Egg | Discovery News Video
Aug. 26, 2009 -- An experimental procedure that someday may enable women to avoid passing certain genetic diseases on to their children has gained an early success, with the birth of four healthy monkeys, scientists report.
The technique still faces safety questions and perhaps ethical hurdles, but an expert called the work exciting.
The experiment, which involved transferring DNA between eggs from rhesus macaques, was described Wednesday on the Web site of the journal Nature by researchers from the Oregon Health and Science University.
Someday, the technique may be used against diseases caused by inherited defects in the "power plants" of cells, called mitochondria. These conditions are uncommon and unfamiliar to most people, such as Leber hereditary optic neuropathy. Roughly one person in every 4,000 or 5,000 either has one of these mitochondrial diseases or is at risk for one.
Symptoms of these potentially fatal illnesses include muscle weakness, dementia, movement disorders, blindness, hearing loss, and problems of the heart, muscle and kidney.
An egg contains the vast majority of its DNA in the nucleus, but mitochondria contain DNA elsewhere in the egg. So if a woman has a disease caused by defects in the mitochondrial DNA, the new technique might someday make it possible for her to pass on her normal DNA from the nucleus but not the flawed DNA from the mitochondria.
To allow for that, doctors may transplant nucleus DNA from the eggs of such women into donor eggs that have healthy mitochondria. The donor eggs would have had their own nucleus DNA removed. After test-tube fertilization, this egg would in theory produce a baby without mitochondrial defects. (Fathers do not pass along their mitochondria.)
Researcher Shoukhrat Mitalipov said more safety studies must be done in monkeys. He noted that the technique would face regulatory hurdles for human studies because it would change the DNA inherited by future generations, an idea that has long provoked ethical concerns.
Douglas Wallace of the University of California, Irvine, an authority on mitochondria who wasn't involved in the federally funded experiment, said the results were exciting and the technique is "potentially very interesting."
But "there are safety issues that are going to need to be addressed before one could think about it in humans," Wallace said.
Friday, August 28, 2009
Kidney dialysis machine 'small enough to be worn as a belt'
Scientists have developed a kidney dialysis machine small enough to be worn as a belt which can allow patients to receive the treatment as they walk around.
By Kate Devlin, Medical Correspondent
Published: 8:00AM BST 21 Aug 2009
The breakthrough could potentially free thousands of patients from attending hospital every other day.
More than 25,000 people in Britain need to have regular dialysis, usually around three times a week, because their kidneys do not function properly.
Described as “small and light enough to be wearable”, the battery-powered machine weighs around 10lb.
Researchers hope that the device will give patients the freedom to have their treatment whenever and wherever they choose.
Dr Victor Gura, from the David Geffen School of Medicine at UCLA, one of the team behind the new machine, said: “Our vision of a technological breakthrough has materialized in the form of a Wearable Artificial Kidney, which provides continuous dialysis 24 hours a day, seven days a week.”
While hospital patients have to receive a fairly intensive form of dialysis, because of the limited time available, the researchers hope that this machine can offer a gentler form, more akin to that provided naturally by the kidneys themselves.
The researchers are carrying out preliminary tests on the machine, including in patients who need dialysis.
“However, the long-term effect of this technology on the well-being of dialysis patients must be demonstrated in much-needed clinical trials,” Dr Gura said.
“Although successful, this is but one additional step on a long road still ahead of us to bring about a much-needed change in the lives of this population.”
Timothy Statham, chief executive of the National Kidney Federation (NKF) said that few patients would want round the clock dialysis but many would appreciate the extra freedom the device could offer.
He added that many of the estimated two per cent of patients who had been able to have more regular dialysis, thorough machines in their own homes, had seen “remarkable results”.
The findings are published in the Clinical Journal of the American Society of Nephrology.
By Kate Devlin, Medical Correspondent
Published: 8:00AM BST 21 Aug 2009
The breakthrough could potentially free thousands of patients from attending hospital every other day.
More than 25,000 people in Britain need to have regular dialysis, usually around three times a week, because their kidneys do not function properly.
Described as “small and light enough to be wearable”, the battery-powered machine weighs around 10lb.
Researchers hope that the device will give patients the freedom to have their treatment whenever and wherever they choose.
Dr Victor Gura, from the David Geffen School of Medicine at UCLA, one of the team behind the new machine, said: “Our vision of a technological breakthrough has materialized in the form of a Wearable Artificial Kidney, which provides continuous dialysis 24 hours a day, seven days a week.”
While hospital patients have to receive a fairly intensive form of dialysis, because of the limited time available, the researchers hope that this machine can offer a gentler form, more akin to that provided naturally by the kidneys themselves.
The researchers are carrying out preliminary tests on the machine, including in patients who need dialysis.
“However, the long-term effect of this technology on the well-being of dialysis patients must be demonstrated in much-needed clinical trials,” Dr Gura said.
“Although successful, this is but one additional step on a long road still ahead of us to bring about a much-needed change in the lives of this population.”
Timothy Statham, chief executive of the National Kidney Federation (NKF) said that few patients would want round the clock dialysis but many would appreciate the extra freedom the device could offer.
He added that many of the estimated two per cent of patients who had been able to have more regular dialysis, thorough machines in their own homes, had seen “remarkable results”.
The findings are published in the Clinical Journal of the American Society of Nephrology.
Wednesday, August 19, 2009
DNA Evidence Can Be Fabricated, Scientists Show
http://www.nytimes.com/2009/08/18/science/18dna.html?_r=3&pagewanted=print
August 18, 2009
DNA Evidence Can Be Fabricated, Scientists Show
By ANDREW POLLACK
Scientists in Israel have demonstrated that it is possible to fabricate DNA evidence, undermining the credibility of what has been considered the gold standard of proof in criminal cases.
The scientists fabricated blood and saliva samples containing DNA from a person other than the donor of the blood and saliva. They also showed that if they had access to a DNA profile in a database, they could construct a sample of DNA to match that profile without obtaining any tissue from that person.
“You can just engineer a crime scene,” said Dan Frumkin, lead author of the paper, which has been published online by the journal Forensic Science International: Genetics. “Any biology undergraduate could perform this.”
Dr. Frumkin is a founder of Nucleix, a company based in Tel Aviv that has developed a test to distinguish real DNA samples from fake ones that it hopes to sell to forensics laboratories.
The planting of fabricated DNA evidence at a crime scene is only one implication of the findings. A potential invasion of personal privacy is another.
Using some of the same techniques, it may be possible to scavenge anyone’s DNA from a discarded drinking cup or cigarette butt and turn it into a saliva sample that could be submitted to a genetic testing company that measures ancestry or the risk of getting various diseases. Celebrities might have to fear “genetic paparazzi,” said Gail H. Javitt of the Genetics and Public Policy Center at Johns Hopkins University.
Tania Simoncelli, science adviser to the American Civil Liberties Union, said the findings were worrisome.
“DNA is a lot easier to plant at a crime scene than fingerprints,” she said. “We’re creating a criminal justice system that is increasingly relying on this technology.”
John M. Butler, leader of the human identity testing project at the National Institute of Standards and Technology, said he was “impressed at how well they were able to fabricate the fake DNA profiles.” However, he added, “I think your average criminal wouldn’t be able to do something like that.”
The scientists fabricated DNA samples two ways. One required a real, if tiny, DNA sample, perhaps from a strand of hair or drinking cup. They amplified the tiny sample into a large quantity of DNA using a standard technique called whole genome amplification.
Of course, a drinking cup or piece of hair might itself be left at a crime scene to frame someone, but blood or saliva may be more believable.
The authors of the paper took blood from a woman and centrifuged it to remove the white cells, which contain DNA. To the remaining red cells they added DNA that had been amplified from a man’s hair.
Since red cells do not contain DNA, all of the genetic material in the blood sample was from the man. The authors sent it to a leading American forensics laboratory, which analyzed it as if it were a normal sample of a man’s blood.
The other technique relied on DNA profiles, stored in law enforcement databases as a series of numbers and letters corresponding to variations at 13 spots in a person’s genome.
From a pooled sample of many people’s DNA, the scientists cloned tiny DNA snippets representing the common variants at each spot, creating a library of such snippets. To prepare a DNA sample matching any profile, they just mixed the proper snippets together. They said that a library of 425 different DNA snippets would be enough to cover every conceivable profile.
Nucleix’s test to tell if a sample has been fabricated relies on the fact that amplified DNA — which would be used in either deception — is not methylated, meaning it lacks certain molecules that are attached to the DNA at specific points, usually to inactivate genes.
Copyright 2009 The New York Times Company
August 18, 2009
DNA Evidence Can Be Fabricated, Scientists Show
By ANDREW POLLACK
Scientists in Israel have demonstrated that it is possible to fabricate DNA evidence, undermining the credibility of what has been considered the gold standard of proof in criminal cases.
The scientists fabricated blood and saliva samples containing DNA from a person other than the donor of the blood and saliva. They also showed that if they had access to a DNA profile in a database, they could construct a sample of DNA to match that profile without obtaining any tissue from that person.
“You can just engineer a crime scene,” said Dan Frumkin, lead author of the paper, which has been published online by the journal Forensic Science International: Genetics. “Any biology undergraduate could perform this.”
Dr. Frumkin is a founder of Nucleix, a company based in Tel Aviv that has developed a test to distinguish real DNA samples from fake ones that it hopes to sell to forensics laboratories.
The planting of fabricated DNA evidence at a crime scene is only one implication of the findings. A potential invasion of personal privacy is another.
Using some of the same techniques, it may be possible to scavenge anyone’s DNA from a discarded drinking cup or cigarette butt and turn it into a saliva sample that could be submitted to a genetic testing company that measures ancestry or the risk of getting various diseases. Celebrities might have to fear “genetic paparazzi,” said Gail H. Javitt of the Genetics and Public Policy Center at Johns Hopkins University.
Tania Simoncelli, science adviser to the American Civil Liberties Union, said the findings were worrisome.
“DNA is a lot easier to plant at a crime scene than fingerprints,” she said. “We’re creating a criminal justice system that is increasingly relying on this technology.”
John M. Butler, leader of the human identity testing project at the National Institute of Standards and Technology, said he was “impressed at how well they were able to fabricate the fake DNA profiles.” However, he added, “I think your average criminal wouldn’t be able to do something like that.”
The scientists fabricated DNA samples two ways. One required a real, if tiny, DNA sample, perhaps from a strand of hair or drinking cup. They amplified the tiny sample into a large quantity of DNA using a standard technique called whole genome amplification.
Of course, a drinking cup or piece of hair might itself be left at a crime scene to frame someone, but blood or saliva may be more believable.
The authors of the paper took blood from a woman and centrifuged it to remove the white cells, which contain DNA. To the remaining red cells they added DNA that had been amplified from a man’s hair.
Since red cells do not contain DNA, all of the genetic material in the blood sample was from the man. The authors sent it to a leading American forensics laboratory, which analyzed it as if it were a normal sample of a man’s blood.
The other technique relied on DNA profiles, stored in law enforcement databases as a series of numbers and letters corresponding to variations at 13 spots in a person’s genome.
From a pooled sample of many people’s DNA, the scientists cloned tiny DNA snippets representing the common variants at each spot, creating a library of such snippets. To prepare a DNA sample matching any profile, they just mixed the proper snippets together. They said that a library of 425 different DNA snippets would be enough to cover every conceivable profile.
Nucleix’s test to tell if a sample has been fabricated relies on the fact that amplified DNA — which would be used in either deception — is not methylated, meaning it lacks certain molecules that are attached to the DNA at specific points, usually to inactivate genes.
Copyright 2009 The New York Times Company
X-ray machines 'could be helping to spread infection'
X-ray machines could be helping to spread infection in intensive care units, a new study has found.
http://www.telegraph.co.uk/health/healthnews/5978059/X-ray-machines-could-be-helping-to-spread-infection.html
By Kate Devlin, Medical Correspondent
Published: 7:00AM BST 06 Aug 2009
Researchers found that one in three x-ray machines that they tested carried bacteria which could cause infections Photo: GETTY
Researchers found that one in three of the machines that they tested carried bacteria which could cause infections.
They warn that better cleaning of the equipment could reduce the chance of spreading potentially dangerous infections within hospitals.
X-ray photographs
Official figures show that there were more than 20 million x-rays taken in British hospitals over the last year.
The scans are used to diagnose and help treat a wide range of illnesses and conditions.
But researchers in Israel warn that the machines themselves could be helping to increase the number of hospital-acquired infections.
They found that 130 of the 406 machines that they tested contained forms of bacteria called drug resistant gram-negative bacteria.
Last year the Health Protection Agency warned that there was an urgent need for new antibiotics to deal with gram-negative bacteria, a group which includes E.coli, which had become resistant to medication.
The findings of the study are published in CHEST, the journal of the American College of Chest Physicians.
http://www.telegraph.co.uk/health/healthnews/5978059/X-ray-machines-could-be-helping-to-spread-infection.html
By Kate Devlin, Medical Correspondent
Published: 7:00AM BST 06 Aug 2009
Researchers found that one in three x-ray machines that they tested carried bacteria which could cause infections Photo: GETTY
Researchers found that one in three of the machines that they tested carried bacteria which could cause infections.
They warn that better cleaning of the equipment could reduce the chance of spreading potentially dangerous infections within hospitals.
X-ray photographs
Official figures show that there were more than 20 million x-rays taken in British hospitals over the last year.
The scans are used to diagnose and help treat a wide range of illnesses and conditions.
But researchers in Israel warn that the machines themselves could be helping to increase the number of hospital-acquired infections.
They found that 130 of the 406 machines that they tested contained forms of bacteria called drug resistant gram-negative bacteria.
Last year the Health Protection Agency warned that there was an urgent need for new antibiotics to deal with gram-negative bacteria, a group which includes E.coli, which had become resistant to medication.
The findings of the study are published in CHEST, the journal of the American College of Chest Physicians.
Saturday, August 15, 2009
Gene Therapy Creates a New Fovea, Blind from birth and can now read
Friday, August 14, 2009
Gene Therapy Creates a New Fovea
Treatment leads to an unexpected improvement in vision for one patient.
By Emily Singer
Twelve months after receiving an experimental gene therapy for a rare, inherited form of blindness, a patient discovered that she could read an illuminated clock in the family car for the first time in her life. The unexpected findings suggest that the brain can adapt to new sensory capacity, even in people who have been blind since birth.
The patient, who remains anonymous, suffers from a disease called Leber congenital amaurosis, in which an abnormal protein in sufferers' photoreceptors severely impairs their sensitivity to light. "It's like wearing several pairs of sunglasses in a dark room," says Artur Cideciyan, a researcher at the University of Pennsylvania in Philadelphia, who oversaw the trial.
At the start of the study, physicians injected a gene encoding a functional copy of the protein into a small part of one eye--about eight-to-nine millimeters in diameter--of three patients, all in their twenties and blind since birth. In preliminary results published last year, Cideciyan and colleagues found that all three patients showed substantial improvements in their ability to detect light three months after treatment.
The researchers have now published new results of the study in the journal Human Gene Therapy, showing that these improvements remained stable after one year. And in a letter to the New England Journal of Medicine, they describe surprising gains in one patient's vision. "It was unexpected because the major improvement of vision had occurred within weeks after the treatment," says Cideciyan.
Probing further, the researchers found that the patient appeared to be using the treated part of her eye like a second fovea--the part of the retina that is most densely populated with photoreceptors and is typically used for detailed vision, such as reading. The patient could detect dimmer light using the treated region than she could with her natural fovea. "We realized she was slowly adapting to her newfound vision by subconsciously focusing her attention to the treated area as opposed to the untreated central fovea," says Cideciyan. "It suggests that there is a plasticity, an ability to adapt in the adult visual brain."
"It's very encouraging," says Kang Zhang, an ophthalmologist and director of the Institute for Genomic Medicine at the University of California, San Diego, who was not involved in the study. "The formation of almost another vision center has implications as we go forward for patients with congenital blindness. They might not be able to use their normal fovea, but they might be able to develop a new center of vision."
Researchers now plan to study other patients in the trial to determine if they have experienced similar improvements. They also hope to figure out how to accelerate these gains, perhaps by using visual training targeted to the area treated with gene therapy.
The scientists also say that the fact that patients' visual improvements held for a year after injection is promising. "It means that for congenital or childhood blindness," says Zhang, "there is the potential to at least stabilize, if not improve, visual function."
Copyright Technology Review 2009.
Gene Therapy Creates a New Fovea
Treatment leads to an unexpected improvement in vision for one patient.
By Emily Singer
Twelve months after receiving an experimental gene therapy for a rare, inherited form of blindness, a patient discovered that she could read an illuminated clock in the family car for the first time in her life. The unexpected findings suggest that the brain can adapt to new sensory capacity, even in people who have been blind since birth.
The patient, who remains anonymous, suffers from a disease called Leber congenital amaurosis, in which an abnormal protein in sufferers' photoreceptors severely impairs their sensitivity to light. "It's like wearing several pairs of sunglasses in a dark room," says Artur Cideciyan, a researcher at the University of Pennsylvania in Philadelphia, who oversaw the trial.
At the start of the study, physicians injected a gene encoding a functional copy of the protein into a small part of one eye--about eight-to-nine millimeters in diameter--of three patients, all in their twenties and blind since birth. In preliminary results published last year, Cideciyan and colleagues found that all three patients showed substantial improvements in their ability to detect light three months after treatment.
The researchers have now published new results of the study in the journal Human Gene Therapy, showing that these improvements remained stable after one year. And in a letter to the New England Journal of Medicine, they describe surprising gains in one patient's vision. "It was unexpected because the major improvement of vision had occurred within weeks after the treatment," says Cideciyan.
Probing further, the researchers found that the patient appeared to be using the treated part of her eye like a second fovea--the part of the retina that is most densely populated with photoreceptors and is typically used for detailed vision, such as reading. The patient could detect dimmer light using the treated region than she could with her natural fovea. "We realized she was slowly adapting to her newfound vision by subconsciously focusing her attention to the treated area as opposed to the untreated central fovea," says Cideciyan. "It suggests that there is a plasticity, an ability to adapt in the adult visual brain."
"It's very encouraging," says Kang Zhang, an ophthalmologist and director of the Institute for Genomic Medicine at the University of California, San Diego, who was not involved in the study. "The formation of almost another vision center has implications as we go forward for patients with congenital blindness. They might not be able to use their normal fovea, but they might be able to develop a new center of vision."
Researchers now plan to study other patients in the trial to determine if they have experienced similar improvements. They also hope to figure out how to accelerate these gains, perhaps by using visual training targeted to the area treated with gene therapy.
The scientists also say that the fact that patients' visual improvements held for a year after injection is promising. "It means that for congenital or childhood blindness," says Zhang, "there is the potential to at least stabilize, if not improve, visual function."
Copyright Technology Review 2009.
Thursday, July 30, 2009
Strange! Humans Glow in Visible Light
http://www.livescience.com/health/090722-body-glow.html
Strange! Humans Glow in Visible Light
By Charles Q. Choi, Special to LiveScience
posted: 22 July 2009 09:10 am ET
The human body literally glows, emitting a visible light in extremely small quantities at levels that rise and fall with the day, scientists now reveal.
Past research has shown that the body emits visible light, 1,000 times less intense than the levels to which our naked eyes are sensitive. In fact, virtually all living creatures emit very weak light, which is thought to be a byproduct of biochemical reactions involving free radicals.
(This visible light differs from the infrared radiation — an invisible form of light — that comes from body heat.)
To learn more about this faint visible light, scientists in Japan employed extraordinarily sensitive cameras capable of detecting single photons. Five healthy male volunteers in their 20s were placed bare-chested in front of the cameras in complete darkness in light-tight rooms for 20 minutes every three hours from 10 a.m. to 10 p.m. for three days.
The researchers found the body glow rose and fell over the day, with its lowest point at 10 a.m. and its peak at 4 p.m., dropping gradually after that. These findings suggest there is light emission linked to our body clocks, most likely due to how our metabolic rhythms fluctuate over the course of the day.
Faces glowed more than the rest of the body. This might be because faces are more tanned than the rest of the body, since they get more exposure to sunlight — the pigment behind skin color, melanin, has fluorescent components that could enhance the body's miniscule light production.
Since this faint light is linked with the body's metabolism, this finding suggests cameras that can spot the weak emissions could help spot medical conditions, said researcher Hitoshi Okamura, a circadian biologist at Kyoto University in Japan.
"If you can see the glimmer from the body's surface, you could see the whole body condition," said researcher Masaki Kobayashi, a biomedical photonics specialist at the Tohoku Institute of Technology in Sendai, Japan.
The scientists detailed their findings online July 16 in the journal PLoS ONE.
Blue Dye May Reduce Spine Injuries
http://www.cnn.com/2009/HEALTH/07/28/spinal.injury.blue.dye/index.html
(CNN) -- The same blue food dye found in M&Ms and Gatorade could be used to reduce damage caused by spine injuries, offering a better chance of recovery, according to new research.
Rats injected with BBG not only regained their mobility but temporarily turned blue.
Researchers at the University of Rochester Medical Center found that when they injected the compound Brilliant Blue G (BBG) into rats suffering spinal cord injuries, the rodents were able to walk again, albeit with a limp.
The only side effect was that the treated mice temporarily turned blue.
The results of the study, published in the "Proceedings of the National Academy of Sciences," build on research conducted by the same center five years ago.
In August 2004, scientists revealed how Adenosine triphosphate, which is known as ATP and described as the "energy currency of life," surges to the spinal cord soon after injury occurs.
Researchers found that the sudden influx of ATP killed off healthy cells, making the initial injury far worse. But when they injected oxidized ATP into the injury, it was found to block the effect of ATP, allowing the injured rats to recover and walk again.
"While we achieved great results when oxidized ATP was injected directly into the spinal cord, this method would not be practical for use with spinal cord-injured patients," said lead researcher Maiken Nedergaard, professor of Neurosurgery and director of the Center for Translational Neuromedicine at the University of Rochester Medical Center.
"First, no one wants to put a needle into a spinal cord that has just been severely injured, so we knew we needed to find another way to quickly deliver an agent that would stop ATP from killing healthy motor neurons. Second, the compound we initially used, oxidized ATP, cannot be injected into the bloodstream because of its dangerous side effects."
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Back in 2004, Nedergaard's team discovered that the spinal cord was rich in a molecule called P2X7, which is also known as "the death receptor" for its ability to allow ATP to latch onto motor neurons and send the signals which eventually kill them.
Nedergaard knew that BBG could thwart the function of P2X7, and its similarity to a blue food dye approved by the Food and Drug Administration (FDA) in 1982 gave her the confidence to test it intravenously.
It worked. The rats given BBG immediately after their injury could walk again with a limp. Those that didn't receive a dose never regained their mobility.
Nedergaard told CNN that there is currently no standard treatment for patients with spinal injury when they reach the hospital emergency room.
"Right now we only treat 15 percent of the patients we receive with steroids and many hospitals question if that even works for that 15 percent; it's a very moderate benefit to only a subset of patients. So right now 85 percent of patients are untreated," she said.
Nedergaard said the research team isn't claiming that BBG can cure spinal injuries, instead that it offers a potential improvement in patients' condition.
"Even a moderate improvement in functional performance of the patient is a big, big event for these patients," she said. "They can control their bladder. If they can just take small steps instead of sitting in a wheelchair all the time, it's a tremendous benefit for these patients," she added.
The dose must be administered immediately after the injury, before additional tissue dies as a result of the initial injury.
Researchers are currently pulling together an application to be lodged with the FDA to stage the first clinical trials of BBG on human patients.
"Our hope is that this work will lead to a practical, safe agent that can be given to patients shortly after injury, for the purpose of decreasing the secondary damage that we have to otherwise expect," said Steven Goldman, Chair of the University of Rochester Department of Neurology.
Wednesday, July 8, 2009
Scientists Reprogram Clearly Defined Adult Cells Into Pluripotent Stem Cells -- Directly And Without Viruses
Web address:
http://www.sciencedaily.com/releases/2009/07/
090707131824.htm
Scientists Reprogram Clearly Defined Adult Cells Into Pluripotent Stem Cells -- Directly And Without Viruses
These are unipotent germline stem cells (fluorescent green) in the sperm duct of a mouse testis. (Credit: Image: MPI Münster / Kinarm Ko)
ScienceDaily (July 8, 2009) — Kinarm Ko and Hans Schöler's team at the Max Planck Institute for Molecular Biomedicine in Münster have succeeded for the first time in culturing a clearly defined cell type from the testis of adult mice and converting these cells into pluripotent stem cells without introduced genes, viruses or reprogramming proteins. These stem cells have the capacity to generate all types of body tissue. The culture conditions alone were the crucial factor behind the success of the reprogramming process.
The testis is a sensitive organ and an astonishing one at that. Even at the age of 70, 80 or 85, men have cells that constantly produce new sperm. Therefore, they can conceive embryos and become fathers at almost any age - assuming they can find a sufficiently young female partner. Based on this, researchers have long assumed that cells from the testis have a similar potential as in embryonic stem cells: that is, a pluripotency that enables them to form over 200 of the body's cell types.
In fact, a number of researchers have recently stumbled on the multiple talents in the male gonads of humans and mice. It all began with the work of Takashi Shinohara's team in 2004. The Japanese scientists discovered that, like embryonic stem cells, certain cells in the testis of newborn mice are able to develop into different kinds of tissue. In 2006, scientists working with Gerd Hasenfuß and Wolfgang Engel in Göttigen reported that such adaptable cells can also be found in adult male mice. Additionally, Thomas Skutella and his colleagues at the University of Tübingen recently made headlines when they cultured comparable cells from human testis tissue.
A bewildering variety of cells
"At first glance, it would appear that it has long been established that pluripotent cells exist in the testis of adult humans and mice," says Schöler. "However, it is often unclear as to exactly which cells are being referred to in the literature and what these cells can actually do." (See *Background Information)
This is not only due to the fact that the testis contains a multitude of different cells. Scientists who dismantle tissue in the laboratory must carefully separate and analyse the cells to establish which cell type they have under the microscope. The question of potency is a controversial one among stem cell researchers, as binding benchmarks have yet to be defined. What some scientists would define as "pluripotent" is just about deemed "multi-potent", that is, as having a limited capacity for differentiation, by others.
Greater certainty can be provided by carrying out the relevant tests. These include, among other things, a test to establish whether, after injection into early embryos, the cells are able to contribute to the development of the new organism and gamete formation, and to pass on their genes to further generations. However, not every team carries out all of these tests and important questions are left unanswered, even in articles published in renowned journals.
Stable original cell line
With their work, Ko and his colleagues wanted to establish clarity from the outset. To this end, they started by culturing a precisely defined type of cell, so-called germline stem cells (GSCs), from the testis of adult mice. In their natural environment, these cells can only do one thing: constantly generate new sperm. Moreover, their own reproduction is an extremely rare occurrence. Only two or three of them will be found among the 10,000 cells in the testis tissue of a mouse. However, they can be isolated individually and reproduced as cell lines with stable characteristics. Under the usual cell culturing conditions, they retain their unipotency for weeks and years. Consequently, all they can do is reproduce or form sperm.
What nobody had guessed until now, however, was that a simple trick is enough to incite these cells to reprogramme. If the cells are distributed on new petri dishes, some of them revert to an embryonic state once they are given sufficient space and time. "Each time we filled around 8000 cells into the individual wells of the cell culture plates, some of the cells reprogrammed themselves after two weeks," reports Ko. And when the switch in these germline-derived pluripotent stem cells (gPS) has been reversed, they start to reproduce rapidly.
The researchers have proven that the "reignition" of the cells has actually taken place with the aid of numerous tests. Not only can the reprogrammed cells be used to generate heart, nerve or endothelial cells, as is the case with embryonic stem cells, the scientists can also use them to produce mice with mixed genotypes, known as chimeras, from the new gPs, and thus demonstrate that cells obtained from the testis can pass their genes on to the next generation.
Whether this process can also be applied to humans remains an open question. There is much to suggest, however, that gPS cells exceed all previously artificially reprogrammed cells in terms of the simplicity of their production and their safety.
Journal reference:
Ko et al. Induction of Pluripotency in Adult Unipotent Germline Stem Cells. Cell Stem Cell, 2009; 5 (1): 87 DOI: 10.1016/j.stem.2009.05.025
Adapted from materials provided by Max-Planck-Gesellschaft.
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Max-Planck-Gesellschaft (2009, July 8). Scientists Reprogram Clearly Defined Adult Cells Into Pluripotent Stem Cells -- Directly And Without Viruses. ScienceDaily. Retrieved July 8, 2009, from http://www.sciencedaily.com /releases/2009/07/090707131824.htm
http://www.sciencedaily.com/releases/2009/07/
090707131824.htm
Scientists Reprogram Clearly Defined Adult Cells Into Pluripotent Stem Cells -- Directly And Without Viruses
These are unipotent germline stem cells (fluorescent green) in the sperm duct of a mouse testis. (Credit: Image: MPI Münster / Kinarm Ko)
ScienceDaily (July 8, 2009) — Kinarm Ko and Hans Schöler's team at the Max Planck Institute for Molecular Biomedicine in Münster have succeeded for the first time in culturing a clearly defined cell type from the testis of adult mice and converting these cells into pluripotent stem cells without introduced genes, viruses or reprogramming proteins. These stem cells have the capacity to generate all types of body tissue. The culture conditions alone were the crucial factor behind the success of the reprogramming process.
The testis is a sensitive organ and an astonishing one at that. Even at the age of 70, 80 or 85, men have cells that constantly produce new sperm. Therefore, they can conceive embryos and become fathers at almost any age - assuming they can find a sufficiently young female partner. Based on this, researchers have long assumed that cells from the testis have a similar potential as in embryonic stem cells: that is, a pluripotency that enables them to form over 200 of the body's cell types.
In fact, a number of researchers have recently stumbled on the multiple talents in the male gonads of humans and mice. It all began with the work of Takashi Shinohara's team in 2004. The Japanese scientists discovered that, like embryonic stem cells, certain cells in the testis of newborn mice are able to develop into different kinds of tissue. In 2006, scientists working with Gerd Hasenfuß and Wolfgang Engel in Göttigen reported that such adaptable cells can also be found in adult male mice. Additionally, Thomas Skutella and his colleagues at the University of Tübingen recently made headlines when they cultured comparable cells from human testis tissue.
A bewildering variety of cells
"At first glance, it would appear that it has long been established that pluripotent cells exist in the testis of adult humans and mice," says Schöler. "However, it is often unclear as to exactly which cells are being referred to in the literature and what these cells can actually do." (See *Background Information)
This is not only due to the fact that the testis contains a multitude of different cells. Scientists who dismantle tissue in the laboratory must carefully separate and analyse the cells to establish which cell type they have under the microscope. The question of potency is a controversial one among stem cell researchers, as binding benchmarks have yet to be defined. What some scientists would define as "pluripotent" is just about deemed "multi-potent", that is, as having a limited capacity for differentiation, by others.
Greater certainty can be provided by carrying out the relevant tests. These include, among other things, a test to establish whether, after injection into early embryos, the cells are able to contribute to the development of the new organism and gamete formation, and to pass on their genes to further generations. However, not every team carries out all of these tests and important questions are left unanswered, even in articles published in renowned journals.
Stable original cell line
With their work, Ko and his colleagues wanted to establish clarity from the outset. To this end, they started by culturing a precisely defined type of cell, so-called germline stem cells (GSCs), from the testis of adult mice. In their natural environment, these cells can only do one thing: constantly generate new sperm. Moreover, their own reproduction is an extremely rare occurrence. Only two or three of them will be found among the 10,000 cells in the testis tissue of a mouse. However, they can be isolated individually and reproduced as cell lines with stable characteristics. Under the usual cell culturing conditions, they retain their unipotency for weeks and years. Consequently, all they can do is reproduce or form sperm.
What nobody had guessed until now, however, was that a simple trick is enough to incite these cells to reprogramme. If the cells are distributed on new petri dishes, some of them revert to an embryonic state once they are given sufficient space and time. "Each time we filled around 8000 cells into the individual wells of the cell culture plates, some of the cells reprogrammed themselves after two weeks," reports Ko. And when the switch in these germline-derived pluripotent stem cells (gPS) has been reversed, they start to reproduce rapidly.
The researchers have proven that the "reignition" of the cells has actually taken place with the aid of numerous tests. Not only can the reprogrammed cells be used to generate heart, nerve or endothelial cells, as is the case with embryonic stem cells, the scientists can also use them to produce mice with mixed genotypes, known as chimeras, from the new gPs, and thus demonstrate that cells obtained from the testis can pass their genes on to the next generation.
Whether this process can also be applied to humans remains an open question. There is much to suggest, however, that gPS cells exceed all previously artificially reprogrammed cells in terms of the simplicity of their production and their safety.
Journal reference:
Ko et al. Induction of Pluripotency in Adult Unipotent Germline Stem Cells. Cell Stem Cell, 2009; 5 (1): 87 DOI: 10.1016/j.stem.2009.05.025
Adapted from materials provided by Max-Planck-Gesellschaft.
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Max-Planck-Gesellschaft (2009, July 8). Scientists Reprogram Clearly Defined Adult Cells Into Pluripotent Stem Cells -- Directly And Without Viruses. ScienceDaily. Retrieved July 8, 2009, from http://www.sciencedaily.com /releases/2009/07/090707131824.htm
Monday, June 29, 2009
Bone marrow transplant suppresses AIDS in patient
Bone marrow transplant suppresses AIDS in patient
Wed Nov 12, 2008 9:06pm EST
BERLIN (Reuters) - A bone marrow transplant using stem cells from a donor with natural genetic resistance to the AIDS virus has left an HIV patient free of infection for nearly two years, German researchers.
The patient, an American living in Berlin, was infected with the human immunodeficiency virus that causes AIDS and also had leukemia. The best treatment for the leukemia was a bone marrow transplant, which takes the stem cells from a healthy donor's immune system to replace the patient's cancer-ridden cells.
Dr. Gero Hutter and Thomas Schneider of the Clinic for Gastroenterology, Infections and Rheumatology of the Berlin Charite hospital said on Wednesday the team sought a bone marrow donor who had a genetic mutation known to help the body resist AIDS infection.
The mutation affects a receptor, a cellular doorway, called CCR5 that the AIDS virus uses to get into the cells it infects.
When they found a donor with the mutation, they used that bone marrow to treat the patient. Not only did the leukemia disappear, but so did the HIV.
"As of today, more than 20 months after the successful transplant, no HIV can be detected in the patient," the clinic said in a statement.
"We performed all tests, not only with blood but also with other reservoirs," Schneider told a news conference.
"But we cannot exclude the possibility that it's still there."
The researchers stressed that this would never become a standard treatment for HIV. Bone marrow stem cell transplants are rigorous and dangerous and require the patient to first have his or her own bone marrow completely destroyed.
Patients risk death from even the most minor infections because they have no immune system until the stem cells can grow and replace their own.
HIV has no cure and is always fatal. Cocktails of drugs can keep the virus suppressed, sometimes to undetectable levels. But research shows the virus never disappears -- it lurks in so-called reservoirs throughout the body.
Hutter's team said they have been unable to find any trace of the virus in their 42-year-old patient, who remains unnamed, but that does not mean it is not there.
"The virus is tricky. It can always return," Hutter said.
The CCR5 mutation is found in about 3 percent of Europeans, the researchers said. They said the study suggests that gene therapy, a highly experimental technology, might someday be used to help treat patients with HIV.
(Reporting by Oliver Denzer; Writing by Maggie Fox in Washington; Editing by Vicki Allen)
© Thomson Reuters 2008. All rights reserved. Users may download and print extracts of content from this website for their own personal and non-commercial use only. Republication or redistribution of Thomson Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Thomson Reuters. Thomson Reuters and its logo are registered trademarks or trademarks of the Thomson Reuters group of companies around the world.
Thomson Reuters journalists are subject to an Editorial Handbook which requires fair presentation and disclosure of relevant interests.
Wed Nov 12, 2008 9:06pm EST
BERLIN (Reuters) - A bone marrow transplant using stem cells from a donor with natural genetic resistance to the AIDS virus has left an HIV patient free of infection for nearly two years, German researchers.
The patient, an American living in Berlin, was infected with the human immunodeficiency virus that causes AIDS and also had leukemia. The best treatment for the leukemia was a bone marrow transplant, which takes the stem cells from a healthy donor's immune system to replace the patient's cancer-ridden cells.
Dr. Gero Hutter and Thomas Schneider of the Clinic for Gastroenterology, Infections and Rheumatology of the Berlin Charite hospital said on Wednesday the team sought a bone marrow donor who had a genetic mutation known to help the body resist AIDS infection.
The mutation affects a receptor, a cellular doorway, called CCR5 that the AIDS virus uses to get into the cells it infects.
When they found a donor with the mutation, they used that bone marrow to treat the patient. Not only did the leukemia disappear, but so did the HIV.
"As of today, more than 20 months after the successful transplant, no HIV can be detected in the patient," the clinic said in a statement.
"We performed all tests, not only with blood but also with other reservoirs," Schneider told a news conference.
"But we cannot exclude the possibility that it's still there."
The researchers stressed that this would never become a standard treatment for HIV. Bone marrow stem cell transplants are rigorous and dangerous and require the patient to first have his or her own bone marrow completely destroyed.
Patients risk death from even the most minor infections because they have no immune system until the stem cells can grow and replace their own.
HIV has no cure and is always fatal. Cocktails of drugs can keep the virus suppressed, sometimes to undetectable levels. But research shows the virus never disappears -- it lurks in so-called reservoirs throughout the body.
Hutter's team said they have been unable to find any trace of the virus in their 42-year-old patient, who remains unnamed, but that does not mean it is not there.
"The virus is tricky. It can always return," Hutter said.
The CCR5 mutation is found in about 3 percent of Europeans, the researchers said. They said the study suggests that gene therapy, a highly experimental technology, might someday be used to help treat patients with HIV.
(Reporting by Oliver Denzer; Writing by Maggie Fox in Washington; Editing by Vicki Allen)
© Thomson Reuters 2008. All rights reserved. Users may download and print extracts of content from this website for their own personal and non-commercial use only. Republication or redistribution of Thomson Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Thomson Reuters. Thomson Reuters and its logo are registered trademarks or trademarks of the Thomson Reuters group of companies around the world.
Thomson Reuters journalists are subject to an Editorial Handbook which requires fair presentation and disclosure of relevant interests.
Thursday, June 11, 2009
Tuesday, June 9, 2009
Growing Organs in the Lab
http://singularityhub.com/2009/06/08/growing-organs-in-the-lab/
Growing Organs in the Lab
Written on June 8, 2009 – 3:19 pm | by Drew Halley |
Why transplant an organ when you can grow yourself a new one?
This research isn’t something that might happen in the distant future. It’s being used today to grow fresh
organs, open up new ways to study disease and the immune system, and reduce the need for organ
transplants. Organ-farming laboratories are popping up across the planet, and showing impressive results.
Here we look at the state of the union of a rapidly advancing field called tissue engineering: what’s been
accomplished so far, and what’s right around the corner.
Patients who undergo organ transplants require loads of toxic drugs to suppress their immune systems;
otherwise their body might reject the organ. But tissue engineering could make organ transplants a thing of
the past. By using a patient’s cells to grow new types of tissue in the lab, researchers are finding new ways
to custom-engineer you new body parts by using your own cells.
At the cutting edge of organ engineering is Tengion, a clinical-stage biotech company based outside of
Philadelphia. Their most successful research to date led to the creation of the Neo-Bladder. Tengion takes
some of your cells and grows them in culture for five to seven weeks around a biodegradable scaffold.
When the organ is ready, it can be transplanted without the need to suppress the patient’s immune system
(because the organ was grown from the patient’s own cells, it carries no risk of rejection). Once the organ is
in, the scaffold degrades and the bladder adapts to its new (old) home.
The Tengion Neo-Bladder is in Phase II testing, meaning that they have already implanted the organ into
individuals and studied how the body adapts to it. After 5 years, the company was able to show that the
homegrown organs are safe and effective, capable of treating the bladder effects of spina bifida (a neural
tube defect that effects bladder function, among other things). After another round of Phase II trials, Tengion
will move on to Phase III testing; after that, the Neo-Bladder should be approved and be made commercially
available.
Atala wants to grow you an
organ
Tengion’s Neo-bladder is nearing the completion of its clinical trials, but they weren’t the first to grow one.
If anyone on Earth deserves the job title “Organ Farmer,” it’s Dr. Anthony Atala. He and his research team
at Wake Forest University Medical Center pioneered the world’s first lab-grown bladder, and they remain at
the forefront of the organ-growing field (Atala is also the chairman of Tengion’s scientific advisory board).
Wake Forest is the world’s largest regenerative medicine research center, and their current research is
growing 22 different types of tissue: heart valves, muscle cells, arteries, and even fingers.
So how many different types of human organs have been grown and transplanted? The lab-grown bladders
are among the only transplants of an entire organ, but a wide variety of partial organ transplants have taken
place. Skin cells are regularly grown in culture and grafted onto patients’ bodies. A graft was grown from a
patient’s trachea cells and transplanted to replace part of her airway that had degraded due to disease.
Cartilage has been grown and transplanted into a patient’s knee.
A number of technologies are under development but have yet to be transplanted into human bodies.
Recently, Dr. Nicholas Kotov and his lab at the University of Michigan have engineered artificial bone
marrow, a task that was previously doomed to failure. Kotov and his colleagues realized that in the body,
stem cell differentiation relies on chemical signals in three dimensions (whereas in a petri dish, it takes place
in two dimensions). This insight led to a new methodology that more closely replicated the natural
environment of stem cell differentiation in bone marrow tissue. The resultant homegrown marrow grew and
divided normally, even releasing antibodies in fight off an introduced influenza strain. It can be used to
study the role of bone marrow in fighting disease within the body, as well as creating a “bioreactor”:
harnessing the artificial marrow within a device to grow cells and tissues.
Tengion is pretty busy these days as well. Their new website lists a variety of new applications on the
horizon, including a Neo-Kidney augment, artery replacements (including in the heart), and variations on
their bladder technique to replace cancerous organs. Their company pipeline gives a general idea of the
relative stages of each project.
A number of initiatives are under way to create an artificial pancreas, which would revolutionize the way
we treat diabetes. By providing diabetics with a healthy pancreas, doctors could restore their natural control
of blood glucose by giving them an endogenous source of insulin. Anyone with experience of diabetes
knows the difficulty of manually monitoring and controlling your sugar levels, not to mention regularly
injecting insulin. A lab-grown pancreas replacement would be an incredible benefit to the 23.6 million
individuals in America alone who suffer from diabetes.
The Minnesota rat heart
As we previously reported, researchers at the University of Minnesota grew an entire rat heart in a
laboratory last year. Their next goal is to grow a pig heart, a significant milestone towards growing a human
heart due to their similar structure. Researchers hope to combine the scaffold of a pig heart with human
cardiac tissue to grow a hybrid heart suitable for transplant.
Another exciting frontier is the field of printable tissue and organs, which is just what it sounds like. Inkjet
cartidges are cleaned out and loaded with a mixture of live human cells and “smart gel.” Then, layer by
layer, the cells are printed atop one another until a 3D organ is constructed. Just as a normal printer can
deposit different colored ink, organ printing allows scientists to specify where to place different cell types.
Organ printing has already created beating cardiac cells, and could soon produce organs that are viable for
transplant. But unlike other 3D printers, I wouldn’t want this one in my living room.
The hottest areas in tissue growth are the types hardest to make: nerve, liver, kidney, heart and pancreas
cells. But these are precisely where Alata and Tengion are heading, pushing the industry into fresh territory.
Coupled with new regenerative treatments like Cook biotech’s foams and stem-cell organ patching, tissue
engineering will be keeping our organs young and healthy in the years to come.
Merely a decade ago, tissue engineering was still a new field that struggled to find funding and support.
Today, thousands of scientists worldwide are coordinating efforts to reach new breakthroughs, and the
demonstrated potential of these methods has helped bring in investors. That should keep the organ growing
field moving forward in the future months and years, and we’ll be covering new advances as they emerge.
Growing Organs in the Lab
Written on June 8, 2009 – 3:19 pm | by Drew Halley |
Why transplant an organ when you can grow yourself a new one?
This research isn’t something that might happen in the distant future. It’s being used today to grow fresh
organs, open up new ways to study disease and the immune system, and reduce the need for organ
transplants. Organ-farming laboratories are popping up across the planet, and showing impressive results.
Here we look at the state of the union of a rapidly advancing field called tissue engineering: what’s been
accomplished so far, and what’s right around the corner.
Patients who undergo organ transplants require loads of toxic drugs to suppress their immune systems;
otherwise their body might reject the organ. But tissue engineering could make organ transplants a thing of
the past. By using a patient’s cells to grow new types of tissue in the lab, researchers are finding new ways
to custom-engineer you new body parts by using your own cells.
At the cutting edge of organ engineering is Tengion, a clinical-stage biotech company based outside of
Philadelphia. Their most successful research to date led to the creation of the Neo-Bladder. Tengion takes
some of your cells and grows them in culture for five to seven weeks around a biodegradable scaffold.
When the organ is ready, it can be transplanted without the need to suppress the patient’s immune system
(because the organ was grown from the patient’s own cells, it carries no risk of rejection). Once the organ is
in, the scaffold degrades and the bladder adapts to its new (old) home.
The Tengion Neo-Bladder is in Phase II testing, meaning that they have already implanted the organ into
individuals and studied how the body adapts to it. After 5 years, the company was able to show that the
homegrown organs are safe and effective, capable of treating the bladder effects of spina bifida (a neural
tube defect that effects bladder function, among other things). After another round of Phase II trials, Tengion
will move on to Phase III testing; after that, the Neo-Bladder should be approved and be made commercially
available.
Atala wants to grow you an
organ
Tengion’s Neo-bladder is nearing the completion of its clinical trials, but they weren’t the first to grow one.
If anyone on Earth deserves the job title “Organ Farmer,” it’s Dr. Anthony Atala. He and his research team
at Wake Forest University Medical Center pioneered the world’s first lab-grown bladder, and they remain at
the forefront of the organ-growing field (Atala is also the chairman of Tengion’s scientific advisory board).
Wake Forest is the world’s largest regenerative medicine research center, and their current research is
growing 22 different types of tissue: heart valves, muscle cells, arteries, and even fingers.
So how many different types of human organs have been grown and transplanted? The lab-grown bladders
are among the only transplants of an entire organ, but a wide variety of partial organ transplants have taken
place. Skin cells are regularly grown in culture and grafted onto patients’ bodies. A graft was grown from a
patient’s trachea cells and transplanted to replace part of her airway that had degraded due to disease.
Cartilage has been grown and transplanted into a patient’s knee.
A number of technologies are under development but have yet to be transplanted into human bodies.
Recently, Dr. Nicholas Kotov and his lab at the University of Michigan have engineered artificial bone
marrow, a task that was previously doomed to failure. Kotov and his colleagues realized that in the body,
stem cell differentiation relies on chemical signals in three dimensions (whereas in a petri dish, it takes place
in two dimensions). This insight led to a new methodology that more closely replicated the natural
environment of stem cell differentiation in bone marrow tissue. The resultant homegrown marrow grew and
divided normally, even releasing antibodies in fight off an introduced influenza strain. It can be used to
study the role of bone marrow in fighting disease within the body, as well as creating a “bioreactor”:
harnessing the artificial marrow within a device to grow cells and tissues.
Tengion is pretty busy these days as well. Their new website lists a variety of new applications on the
horizon, including a Neo-Kidney augment, artery replacements (including in the heart), and variations on
their bladder technique to replace cancerous organs. Their company pipeline gives a general idea of the
relative stages of each project.
A number of initiatives are under way to create an artificial pancreas, which would revolutionize the way
we treat diabetes. By providing diabetics with a healthy pancreas, doctors could restore their natural control
of blood glucose by giving them an endogenous source of insulin. Anyone with experience of diabetes
knows the difficulty of manually monitoring and controlling your sugar levels, not to mention regularly
injecting insulin. A lab-grown pancreas replacement would be an incredible benefit to the 23.6 million
individuals in America alone who suffer from diabetes.
The Minnesota rat heart
As we previously reported, researchers at the University of Minnesota grew an entire rat heart in a
laboratory last year. Their next goal is to grow a pig heart, a significant milestone towards growing a human
heart due to their similar structure. Researchers hope to combine the scaffold of a pig heart with human
cardiac tissue to grow a hybrid heart suitable for transplant.
Another exciting frontier is the field of printable tissue and organs, which is just what it sounds like. Inkjet
cartidges are cleaned out and loaded with a mixture of live human cells and “smart gel.” Then, layer by
layer, the cells are printed atop one another until a 3D organ is constructed. Just as a normal printer can
deposit different colored ink, organ printing allows scientists to specify where to place different cell types.
Organ printing has already created beating cardiac cells, and could soon produce organs that are viable for
transplant. But unlike other 3D printers, I wouldn’t want this one in my living room.
The hottest areas in tissue growth are the types hardest to make: nerve, liver, kidney, heart and pancreas
cells. But these are precisely where Alata and Tengion are heading, pushing the industry into fresh territory.
Coupled with new regenerative treatments like Cook biotech’s foams and stem-cell organ patching, tissue
engineering will be keeping our organs young and healthy in the years to come.
Merely a decade ago, tissue engineering was still a new field that struggled to find funding and support.
Today, thousands of scientists worldwide are coordinating efforts to reach new breakthroughs, and the
demonstrated potential of these methods has helped bring in investors. That should keep the organ growing
field moving forward in the future months and years, and we’ll be covering new advances as they emerge.
Wednesday, May 6, 2009
Protein Controls Blood Vessel Formation, Offers New Drug Target
ScienceDaily (Dec. 5, 2007) — After an injury, the body grows new blood vessels to repair damaged tissue. But sometimes too much growth causes problems, as when new blood vessels in the eyes leak, causing diabetic retinopathy and blindness if not treated.
A protein called CIB1 discovered by researchers at the University of North Carolina at Chapel Hill School of Medicine appears to play a major role in controlling new blood vessel growth, offering a target for drug treatments to help the body repair itself after injury and control unwanted blood vessel growth.
"In the future, this knowledge may help our ability to control blood vessel growth in disease situations such as wound healing, retinal diseases and diabetes," said Leslie Parise, Ph.D., senior study author and professor and chair of biochemistry and biophysics in the UNC School of Medicine.
The results will appear in an upcoming print issue of the journal Circulation Research and were published online Nov. 1, 2007. The research was funded by the National Institutes of Health.
Parise's lab first discovered the protein, called CIB1 in 1997. It was originally found in blood platelets. CIB1 keeps blood platelets from sticking together, acting as a natural anti-coagulant to prevent clots that might lead to heart attacks or strokes. But further research showed CIB1 appears in almost every cell type in the body, Parise said. For example, male mice bred without both copies of the CIB1 gene are infertile.
In the current study, Parise and her colleagues found CIB1 in the endothelial cells that line all blood vessels. These cells jump-start new blood vessel growth via a process called angiogenesis. During angiogenesis, biological signals prompt endothelial cells to release enzymes and other chemicals that allow them to move away from existing blood vessels and form new ones.
While angiogenesis plays a critical role in embryo growth, CIB1 appears to only affect blood vessel growth after injury (sometimes called pathological or adaptive angiogenesis). Mice born without copies of the CIB1 gene survive and are reasonably healthy unless injured, Parise said.
"CIB1 appears to be an attractive drug target to control blood vessel growth since it does not play an essential role during fetal development but instead plays an important role in pathological forms of blood vessel growth," said first author and medical student at UNC Mohamed Zayed, Ph.D.
In experiments in mice missing CIB1 genes, the researchers found that CIB1 is critical for angiogenesis in the retina, as well as angiogenesis in hind legs. In both cases, the new blood vessel growth was prompted by ischemia, or restricted blood flow. However, clinicians treating retinal disease need to restrict blood vessel growth in the eyes, while patients with restricted blood flow in their limbs need to grow need blood vessels. Therefore, CIB1 could be a target for both pro- and anti-angiogenic drug therapies.
Parise notes that the lab is still determining the exact role CIB1 plays in angiogenesis. "We think it's involved in the chemical pathways that control blood vessel growth, such as signal transduction events," she said. It is also likely that CIB1 is one of many genes that contribute to angiogenesis during ischemia, inflammation and perhaps even tumor growth.
Study co-authors with Parise and Zayad include Weiping Yuan, Tina M. Leisner, Dan Chalothorn, Andrew W. McFadden, Michael D. Schaller, M. Elizabeth Hartnett and James E. Faber, all of UNC-Chapel Hill.
A protein called CIB1 discovered by researchers at the University of North Carolina at Chapel Hill School of Medicine appears to play a major role in controlling new blood vessel growth, offering a target for drug treatments to help the body repair itself after injury and control unwanted blood vessel growth.
"In the future, this knowledge may help our ability to control blood vessel growth in disease situations such as wound healing, retinal diseases and diabetes," said Leslie Parise, Ph.D., senior study author and professor and chair of biochemistry and biophysics in the UNC School of Medicine.
The results will appear in an upcoming print issue of the journal Circulation Research and were published online Nov. 1, 2007. The research was funded by the National Institutes of Health.
Parise's lab first discovered the protein, called CIB1 in 1997. It was originally found in blood platelets. CIB1 keeps blood platelets from sticking together, acting as a natural anti-coagulant to prevent clots that might lead to heart attacks or strokes. But further research showed CIB1 appears in almost every cell type in the body, Parise said. For example, male mice bred without both copies of the CIB1 gene are infertile.
In the current study, Parise and her colleagues found CIB1 in the endothelial cells that line all blood vessels. These cells jump-start new blood vessel growth via a process called angiogenesis. During angiogenesis, biological signals prompt endothelial cells to release enzymes and other chemicals that allow them to move away from existing blood vessels and form new ones.
While angiogenesis plays a critical role in embryo growth, CIB1 appears to only affect blood vessel growth after injury (sometimes called pathological or adaptive angiogenesis). Mice born without copies of the CIB1 gene survive and are reasonably healthy unless injured, Parise said.
"CIB1 appears to be an attractive drug target to control blood vessel growth since it does not play an essential role during fetal development but instead plays an important role in pathological forms of blood vessel growth," said first author and medical student at UNC Mohamed Zayed, Ph.D.
In experiments in mice missing CIB1 genes, the researchers found that CIB1 is critical for angiogenesis in the retina, as well as angiogenesis in hind legs. In both cases, the new blood vessel growth was prompted by ischemia, or restricted blood flow. However, clinicians treating retinal disease need to restrict blood vessel growth in the eyes, while patients with restricted blood flow in their limbs need to grow need blood vessels. Therefore, CIB1 could be a target for both pro- and anti-angiogenic drug therapies.
Parise notes that the lab is still determining the exact role CIB1 plays in angiogenesis. "We think it's involved in the chemical pathways that control blood vessel growth, such as signal transduction events," she said. It is also likely that CIB1 is one of many genes that contribute to angiogenesis during ischemia, inflammation and perhaps even tumor growth.
Study co-authors with Parise and Zayad include Weiping Yuan, Tina M. Leisner, Dan Chalothorn, Andrew W. McFadden, Michael D. Schaller, M. Elizabeth Hartnett and James E. Faber, all of UNC-Chapel Hill.
Fat Protein Cuts Blood Vessel Inflammation, May Help Heart, Scientists Find
ScienceDaily (June 4, 2007) — A natural substance secreted by fat cells can protect blood vessels from the damaging effects of inflammation, one of the factors that contribute to heart disease. Researchers at Jefferson Medical College have shown for the first time in an animal model that the substance – a protein called adiponectin – helps prevent immune system white blood cells from binding to the inside of blood vessel walls. Harnessing adiponectin’s properties, the scientists suggest, may someday help protect against the blood vessel damage so prevalent in patients with obesity and diabetes.
Reporting June 1, 2007 in the Journal of Clinical Investigation, researchers led by Barry Goldstein, M.D., Ph.D., professor of medicine and director of the Division of Endocrinology, Diabetes and Metabolic Diseases and Rosario Scalia, M.D., Ph.D., associate professor of molecular physiology and biophysics, both of Jefferson Medical College of Thomas Jefferson University in Philadelphia, discovered that mice lacking adiponectin had an increase in so-called “adhesion” molecules and high levels of white blood cells sticking to the inside of blood vessel walls, which are signs of inflammation. When they gave the animals the “active” piece of the normal adiponectin molecule for 10 days, inflammation in the blood vessels was greatly reduced.
“This is translational work,” says Dr. Scalia. “We’ve used a mouse model to prove conceptually what we see in a test tube system in isolated cells is relevant to an intact physiological system. It’s a necessary step before going to humans. These results suggest that perhaps restoring this protein could be important to preventing atherosclerosis and vascular disease.”
They used a technique, intravital microscopy, which permits researchers to illuminate blood vessels using fluorescent signals, enabling them to “see” reductions in white cells on the vessel wall and subsequent lessening in inflammation.
The scientists also looked at the effects of adiponectin on inflammation in normal mice. They gave mice a substance, TNF-alpha, which caused the release of inflammatory substances called cytokines. Injecting the mice with the active adiponectin-fragment reversed the effects of the cytokines and the resulting inflammation.
Inflammation is common in cardiovascular disease. Adiponectin has been shown in cells in culture to block some “adhesion molecules” and receptors that are necessary for white blood cells to interact with the vessel wall, explains Dr. Scalia. “This is the first study to show in animals that this is one of the key mechanisms involved in this protein’s anti-inflammatory effect on the vascular system,” he notes. “That suggests thinking about either activating the receptors of the target of this protein or administering the fragment.”
Adiponectin is the most abundant protein found in the bloodstream that originates from fat tissue, and circulates as large complexes. Low levels of adiponectin are associated with obesity, diabetes and heart disease. The fragment, called the globular domain, can function as an active, anti-inflammatory part, notes Dr. Goldstein. “The findings demonstrate clearly that the fragment has the active portions,” he says. “Since the globular domain is relatively easy to produce, it could eventually lead to clinical trials taking advantage of its effects in the vasculature in inflammation.”
“What’s novel about the work is that it’s in animals, and involves a specialized technique in Dr. Scalia’s laboratory in which you can visualize the interaction between the white blood cell and blood vessel wall,” says Dr. Goldstein.
Studying normal mice, Dr. Goldstein notes, is an important aspect of the work. While using genetically altered mice is crucial, animals completely lacking adiponectin don’t exactly mimic the human condition. Most obese individuals, for example, at least have low levels of adiponectin. Part of the work demonstrated that adiponectin also protected against vascular inflammation in normal mice, a result that helps to relate the findings to humans with increased risk of vascular disease.
Next, Dr. Scalia says, they would like to better understand how adiponectin prevents the increase in white blood cell-blood vessel “anchoring” molecules in disease conditions.
The group is also testing the effects of adiponectin in conditions mimicking diabetes by exposing cells in the laboratory and blood vessels in animals to high glucose levels. “High glucose also causes dramatic inflammatory changes in the blood vessel lining,” Dr. Goldstein says. “We’re working to determine whether adiponectin can also reverse these changes. This process is occurring in every patient with high blood sugars and we are hoping that adiponectin can reverse the adverse effects of glucose and protect the vessel wall from damage.”
Reporting June 1, 2007 in the Journal of Clinical Investigation, researchers led by Barry Goldstein, M.D., Ph.D., professor of medicine and director of the Division of Endocrinology, Diabetes and Metabolic Diseases and Rosario Scalia, M.D., Ph.D., associate professor of molecular physiology and biophysics, both of Jefferson Medical College of Thomas Jefferson University in Philadelphia, discovered that mice lacking adiponectin had an increase in so-called “adhesion” molecules and high levels of white blood cells sticking to the inside of blood vessel walls, which are signs of inflammation. When they gave the animals the “active” piece of the normal adiponectin molecule for 10 days, inflammation in the blood vessels was greatly reduced.
“This is translational work,” says Dr. Scalia. “We’ve used a mouse model to prove conceptually what we see in a test tube system in isolated cells is relevant to an intact physiological system. It’s a necessary step before going to humans. These results suggest that perhaps restoring this protein could be important to preventing atherosclerosis and vascular disease.”
They used a technique, intravital microscopy, which permits researchers to illuminate blood vessels using fluorescent signals, enabling them to “see” reductions in white cells on the vessel wall and subsequent lessening in inflammation.
The scientists also looked at the effects of adiponectin on inflammation in normal mice. They gave mice a substance, TNF-alpha, which caused the release of inflammatory substances called cytokines. Injecting the mice with the active adiponectin-fragment reversed the effects of the cytokines and the resulting inflammation.
Inflammation is common in cardiovascular disease. Adiponectin has been shown in cells in culture to block some “adhesion molecules” and receptors that are necessary for white blood cells to interact with the vessel wall, explains Dr. Scalia. “This is the first study to show in animals that this is one of the key mechanisms involved in this protein’s anti-inflammatory effect on the vascular system,” he notes. “That suggests thinking about either activating the receptors of the target of this protein or administering the fragment.”
Adiponectin is the most abundant protein found in the bloodstream that originates from fat tissue, and circulates as large complexes. Low levels of adiponectin are associated with obesity, diabetes and heart disease. The fragment, called the globular domain, can function as an active, anti-inflammatory part, notes Dr. Goldstein. “The findings demonstrate clearly that the fragment has the active portions,” he says. “Since the globular domain is relatively easy to produce, it could eventually lead to clinical trials taking advantage of its effects in the vasculature in inflammation.”
“What’s novel about the work is that it’s in animals, and involves a specialized technique in Dr. Scalia’s laboratory in which you can visualize the interaction between the white blood cell and blood vessel wall,” says Dr. Goldstein.
Studying normal mice, Dr. Goldstein notes, is an important aspect of the work. While using genetically altered mice is crucial, animals completely lacking adiponectin don’t exactly mimic the human condition. Most obese individuals, for example, at least have low levels of adiponectin. Part of the work demonstrated that adiponectin also protected against vascular inflammation in normal mice, a result that helps to relate the findings to humans with increased risk of vascular disease.
Next, Dr. Scalia says, they would like to better understand how adiponectin prevents the increase in white blood cell-blood vessel “anchoring” molecules in disease conditions.
The group is also testing the effects of adiponectin in conditions mimicking diabetes by exposing cells in the laboratory and blood vessels in animals to high glucose levels. “High glucose also causes dramatic inflammatory changes in the blood vessel lining,” Dr. Goldstein says. “We’re working to determine whether adiponectin can also reverse these changes. This process is occurring in every patient with high blood sugars and we are hoping that adiponectin can reverse the adverse effects of glucose and protect the vessel wall from damage.”
White Blood Cells Can Sprout 'Legs' And Move Like Millipedes
http://www.sciencedaily.com/releases/2009/05/090504094424.htm
ScienceDaily (May 4, 2009) — How do white blood cells – immune system ‘soldiers’ – get to the site of infection or injury? To do so, they must crawl swiftly along the lining of the blood vessel – gripping it tightly to avoid being swept away in the blood flow – all the while searching for temporary ‘road signs’ made of special adhesion molecules that let them know where to cross the blood vessel barrier so they can get to the damaged tissue.
In research recently published in the journal Immunity, Prof. Ronen Alon and his research student Ziv Shulman of the Weizmann Institute’s Immunology Department show how white blood cells advance along the length of the endothelial cells lining the blood vessels. Current opinion maintains that immune cells advance like inchworms, but Alon’s new findings show that the rapid movement of the white blood cells is more like that of millipedes.
Rather than sticking front and back, folding and extending to push itself forward, the cell creates numerous tiny ‘legs’ no more than a micron in length – adhesion points, rich in adhesion molecules (named LFA-1) that bind to partner adhesion molecules present on the surface of the blood vessels. Tens of these legs attach and detach in sequence within seconds – allowing them to move rapidly while keeping a good grip on the vessels’ sides.
Next, the scientists turned to the Institute’s Electron Microscopy Unit. Images produced by scanning and transmission electron microscopes, taken by Drs. Eugenia Klein and Vera Shinder, showed that upon attaching to the blood vessel wall, the white blood cell legs ‘dig’ themselves into the endothelium, pressing down on its surface. The fact that these legs – which had been thought to appear only when the cells leave the blood vessels – are used in crawling the vessel lining suggests that they may serve as probes to sense exit signals.
The researchers found that the shear force created by the blood flow was necessary for the legs to embed themselves. Without the thrust of the rushing blood, the white blood cells couldn’t sense the exit signals or get to the site of the injury. These results explain Alon’s previous findings that the blood’s shear force is essential for the white blood cells to exit the blood vessel wall. The present study suggests that shear forces cause their adhesion molecules to enter highly active states. The scientists believe that the tiny legs are trifunctional: Used for gripping, moving and sensing distress signals from the damaged tissue.
In future studies, the scientists plan to check whether it is possible to regulate aggressive immune reactions (such as in autoimmune diseases) by interrupting the ‘digging’ of immune cell legs into the endothelium. They also plan to investigate whether cancerous blood cells metastasize through the blood stream using similar mechanisms in order to exit the blood vessels and enter different tissues.
Prof. Ronen Alon’s research is supported by the De Benedetti Foundation-Cherasco 1547. Prof. Alon is the incumbent of the Linda Jacobs Chair in Immune and Stem Cell Research.
ScienceDaily (May 4, 2009) — How do white blood cells – immune system ‘soldiers’ – get to the site of infection or injury? To do so, they must crawl swiftly along the lining of the blood vessel – gripping it tightly to avoid being swept away in the blood flow – all the while searching for temporary ‘road signs’ made of special adhesion molecules that let them know where to cross the blood vessel barrier so they can get to the damaged tissue.
In research recently published in the journal Immunity, Prof. Ronen Alon and his research student Ziv Shulman of the Weizmann Institute’s Immunology Department show how white blood cells advance along the length of the endothelial cells lining the blood vessels. Current opinion maintains that immune cells advance like inchworms, but Alon’s new findings show that the rapid movement of the white blood cells is more like that of millipedes.
Rather than sticking front and back, folding and extending to push itself forward, the cell creates numerous tiny ‘legs’ no more than a micron in length – adhesion points, rich in adhesion molecules (named LFA-1) that bind to partner adhesion molecules present on the surface of the blood vessels. Tens of these legs attach and detach in sequence within seconds – allowing them to move rapidly while keeping a good grip on the vessels’ sides.
Next, the scientists turned to the Institute’s Electron Microscopy Unit. Images produced by scanning and transmission electron microscopes, taken by Drs. Eugenia Klein and Vera Shinder, showed that upon attaching to the blood vessel wall, the white blood cell legs ‘dig’ themselves into the endothelium, pressing down on its surface. The fact that these legs – which had been thought to appear only when the cells leave the blood vessels – are used in crawling the vessel lining suggests that they may serve as probes to sense exit signals.
The researchers found that the shear force created by the blood flow was necessary for the legs to embed themselves. Without the thrust of the rushing blood, the white blood cells couldn’t sense the exit signals or get to the site of the injury. These results explain Alon’s previous findings that the blood’s shear force is essential for the white blood cells to exit the blood vessel wall. The present study suggests that shear forces cause their adhesion molecules to enter highly active states. The scientists believe that the tiny legs are trifunctional: Used for gripping, moving and sensing distress signals from the damaged tissue.
In future studies, the scientists plan to check whether it is possible to regulate aggressive immune reactions (such as in autoimmune diseases) by interrupting the ‘digging’ of immune cell legs into the endothelium. They also plan to investigate whether cancerous blood cells metastasize through the blood stream using similar mechanisms in order to exit the blood vessels and enter different tissues.
Prof. Ronen Alon’s research is supported by the De Benedetti Foundation-Cherasco 1547. Prof. Alon is the incumbent of the Linda Jacobs Chair in Immune and Stem Cell Research.
Tuesday, May 5, 2009
Anger is in the genes
Being able to keep your cool or lose your temper is down to genes, according to a new study.
By Chris Irvine
Last Updated: 1:09AM BST 04 May 2009
Isolation of a gene called DARPP-32 helps explain why some people fly into a rage at the slightest provocation, while
others can remain calm.
More than 800 people were asked to fill in a questionnaire designed to study how they handle anger.
The German researchers also administered a DNA test to determine which of three versions of the DARPP-32 gene
people were carrying.
The gene affects levels of dopamine, a brain chemical linked to anger and aggression.
Those who had the "TT" or "TC" versions of the gene portrayed significantly more anger than those with the "CC" version.
The study, from the University of Bonn, also found that those who display more anger have less grey matter in the
amygdala, a part of the brain that helps keep our emotions balanced.
Martin Reuter, one of the researchers, who is a TC, said: "In other words, they are not able to control their feelings as well
as those without the mutation.
"I am not an angry person but I can get angry if it is important."
TT and TC versions are much more common in Western populations, with the researchers suggesting that demonstrations
of anger can help people get ahead in life.
"High degrees of anger are of course of low social desirability but a certain amount of dominance-related behaviour helps
to assert position in a social hierarchy," the researchers added.
Reporting in the journal Behavioural Brain Research, they added that genetics only account for around half of our
disposition towards anger, while DARPP-32 is one of several genes involved.
Earlier this year it was reported that showing anger rather than repressing emotions is the key to a successful professional
and personal life. The study by the Harvard Study of Adult Development found those who keep a check on their
frustrations are at least three times more likely to admit they have disappointing personal lives and have hit a glass ceiling
in their career.
© Copyright of Telegraph Media Group Limited 2009
By Chris Irvine
Last Updated: 1:09AM BST 04 May 2009
Isolation of a gene called DARPP-32 helps explain why some people fly into a rage at the slightest provocation, while
others can remain calm.
More than 800 people were asked to fill in a questionnaire designed to study how they handle anger.
The German researchers also administered a DNA test to determine which of three versions of the DARPP-32 gene
people were carrying.
The gene affects levels of dopamine, a brain chemical linked to anger and aggression.
Those who had the "TT" or "TC" versions of the gene portrayed significantly more anger than those with the "CC" version.
The study, from the University of Bonn, also found that those who display more anger have less grey matter in the
amygdala, a part of the brain that helps keep our emotions balanced.
Martin Reuter, one of the researchers, who is a TC, said: "In other words, they are not able to control their feelings as well
as those without the mutation.
"I am not an angry person but I can get angry if it is important."
TT and TC versions are much more common in Western populations, with the researchers suggesting that demonstrations
of anger can help people get ahead in life.
"High degrees of anger are of course of low social desirability but a certain amount of dominance-related behaviour helps
to assert position in a social hierarchy," the researchers added.
Reporting in the journal Behavioural Brain Research, they added that genetics only account for around half of our
disposition towards anger, while DARPP-32 is one of several genes involved.
Earlier this year it was reported that showing anger rather than repressing emotions is the key to a successful professional
and personal life. The study by the Harvard Study of Adult Development found those who keep a check on their
frustrations are at least three times more likely to admit they have disappointing personal lives and have hit a glass ceiling
in their career.
© Copyright of Telegraph Media Group Limited 2009
Japanese scientist claims breakthrough with organ grown in sheep
May 5, 2009
http://www.timesonline.co.uk/tol/news/world/asia/article6222361.ece#cid=OTC-RSS&attr=797093
Leo Lewis in Tochigi
Huddled at the back of her shed, bleating under a magnificent winter coat and tearing cheerfully at a bale of hay, she is possibly the answer to Japan’s chronic national shortage of organ donors: a sheep with a revolutionary secret.
Guided by one of the animal’s lab-coated creators, the visitor’s hand is led to the creature’s underbelly and towards a spot in the middle under eight inches of greasy wool. Lurking there is a spare pancreas.
If the science that put it there can be pushed further forward, Japan may be spared an ethical and practical crisis that has split medical and political opinion.
As the sheep-based chimera organ technology stands at the moment, says the man who is pioneering it, the only viable destination for the pancreas underneath his sheep would be a diabetic chimpanzee.
The organ growing on the sheep was generated from monkey stem cells but the man behind the science, Yutaka Hanazono, believes that the technology could be developed eventually to make sheep into walking organ banks for human livers, hearts, pancreases and skin.
It could happen within a decade, he guesses, perhaps two.
“We have made some very big advances here. There has historically been work on the potential of sheep as producers of human blood, but we are only slowly coming closer to the point where we can harvest sheep for human organs,” Professor Hanazono told The Times.
“We have shown that in vivo (in a living animal) creation of organs is more efficient than making them in vitro (in a test tube) but now we really need to hurry.”
The reason for Professor Hanazono’s sense of urgency — and for the entire organ harvest project being undertaken at the Jichi Medical University — lies many miles away in Tokyo and with a historical peculiarity of the Japanese legal system.
Japan defines death as the point when the heart permanently stops. The concept of brain death — the phase at which organs can most effectively be harvested from donors — does exist, but organs cannot be extracted at that point.
The long-term effect of the legal definition has been striking: organ donation in Japan is virtually nonexistent, forcing many people to travel abroad in search of transplants. In the United States, the rate of organ donors per million people is about 27; in Japan it is under 0.8.
The effect, say paediatricians, has been especially severe for children. The same law that discounts brain death as suitable circumstances for organ donation broadly prevents children under 15 from allowing their organs to be harvested.
To make matters worse, international restrictions on transplant tourism are becoming ever tougher, making Japan’s position even more untenable. To avert disaster, say doctors, Japan either needs the science of synthetic organ generation to advance faster than seems possible, or it needs a complete rethink on the Japanese definition of death.
In response to the impending crisis, and with Professor Hanazono’s sheep still very much at the experimental stage, a series of revisions to the transplant law have been proposed, but the debate has been divisive.
Taro Nakayama, the MP behind the most liberal revision — a change that would allow organs to be harvested from the brain-dead — is a former paediatrician. “Organ tourism is finished and Japan has to change its ways very quickly,” he said.
Source: Times archive
http://www.timesonline.co.uk/tol/news/world/asia/article6222361.ece#cid=OTC-RSS&attr=797093
Leo Lewis in Tochigi
Huddled at the back of her shed, bleating under a magnificent winter coat and tearing cheerfully at a bale of hay, she is possibly the answer to Japan’s chronic national shortage of organ donors: a sheep with a revolutionary secret.
Guided by one of the animal’s lab-coated creators, the visitor’s hand is led to the creature’s underbelly and towards a spot in the middle under eight inches of greasy wool. Lurking there is a spare pancreas.
If the science that put it there can be pushed further forward, Japan may be spared an ethical and practical crisis that has split medical and political opinion.
As the sheep-based chimera organ technology stands at the moment, says the man who is pioneering it, the only viable destination for the pancreas underneath his sheep would be a diabetic chimpanzee.
The organ growing on the sheep was generated from monkey stem cells but the man behind the science, Yutaka Hanazono, believes that the technology could be developed eventually to make sheep into walking organ banks for human livers, hearts, pancreases and skin.
It could happen within a decade, he guesses, perhaps two.
“We have made some very big advances here. There has historically been work on the potential of sheep as producers of human blood, but we are only slowly coming closer to the point where we can harvest sheep for human organs,” Professor Hanazono told The Times.
“We have shown that in vivo (in a living animal) creation of organs is more efficient than making them in vitro (in a test tube) but now we really need to hurry.”
The reason for Professor Hanazono’s sense of urgency — and for the entire organ harvest project being undertaken at the Jichi Medical University — lies many miles away in Tokyo and with a historical peculiarity of the Japanese legal system.
Japan defines death as the point when the heart permanently stops. The concept of brain death — the phase at which organs can most effectively be harvested from donors — does exist, but organs cannot be extracted at that point.
The long-term effect of the legal definition has been striking: organ donation in Japan is virtually nonexistent, forcing many people to travel abroad in search of transplants. In the United States, the rate of organ donors per million people is about 27; in Japan it is under 0.8.
The effect, say paediatricians, has been especially severe for children. The same law that discounts brain death as suitable circumstances for organ donation broadly prevents children under 15 from allowing their organs to be harvested.
To make matters worse, international restrictions on transplant tourism are becoming ever tougher, making Japan’s position even more untenable. To avert disaster, say doctors, Japan either needs the science of synthetic organ generation to advance faster than seems possible, or it needs a complete rethink on the Japanese definition of death.
In response to the impending crisis, and with Professor Hanazono’s sheep still very much at the experimental stage, a series of revisions to the transplant law have been proposed, but the debate has been divisive.
Taro Nakayama, the MP behind the most liberal revision — a change that would allow organs to be harvested from the brain-dead — is a former paediatrician. “Organ tourism is finished and Japan has to change its ways very quickly,” he said.
Source: Times archive
Pig organs ‘available to patients in a decade’
November 7, 2008
http://www.timesonline.co.uk/tol/news/uk/science/article5102153.ece
Lewis Smith, Science Reporter
Organs from pigs could be widely available for transplanting into patients in a decade, Lord Winston said yesterday.
The first organs suitable for transplanting, most likely kidneys, are expected to be ready within three years and, if tests are successful, their use could be widespread by 2018.
A herd of as few as 50 pigs is expected to be kept as breeding stock to provide organs “to order” and to slash waiting times for thousands of people needing transplants.
Professor Winston, of Imperial College, London, and his collaborator, Carol Readhead, of the California Institute of Technology, Pasadena, are leading research into transplanting animal organs into people.
They are attempting to breed pigs that have been genetically modified so that porcine organs are accepted by the human body instead of being immediately rejected.
Human immune systems are quick to react to “foreign bodies” but the scientists are confident that they are close to modifying the genetic make-up of pigs to “humanise” their organs and make animal-to-human transplants possible.
The humanisation process of the organs is expected to be achieved by breeding genes into the pigs, probably by injecting them directly into the parent boar’s testicles, that provoke a greatly reduced response in the patient’s immune system.
Patients who received pig organs would have to take immune suppressant drugs for the rest of their lives, but no more than those who received organ transplants from other people.
Dr Readhead said it was comparatively easy to bring about such genetic modification in mice, but the process is much harder in pigs and other large animals.
A “mini-pig” weighing about 100kg has been selected for the research because, while a quarter of the size of most of those grown for the meat industry, they are big enough to have organs of a similar size to adult human beings.
Pigs are regarded as ideal for animal-to-human transplants, xenotransplantation, and other research because of the similarity in the physiological make-up and because they get many of the same diseases, such as diabetes.
Dr Readhead said: “Our interest was to try to make transgenic pigs for biomedical research to understand human diseases better and eventually to try to make their organs suitable for xenotransplantation.”
Professor Winston said that “organs that might be transplantable” could be ready “within two to three years” and on the basis that research went smoothly they would be fully licensed and tested in as little as ten years. He expected the first “proof of principle” pigs to be bred next year.
Two months ago he hit out at the “red tape” blocking the project’s progress in Britain. Under UK and EU rules, his team has been banned from mating and producing offspring from the transgenic pigs. Research in developing transgenic pigs is now likely to move to the US where the regulatory system is more relaxed.
The new strain of pig, which once established would retain its genetic modifications from generation to generation, is expected to take £3 million to develop over the next five years.
He said that transplants were one of several potential benefits from the research. Others include enabling drugs which today have to be tested on people during late development phases to be tested on animals, avoiding reactions such as that suffered during trials at Northwick Park Hospital in 2006 when six volunteers almost died. Dr Readhead said kidneys are likely to be the first pig organs that researchers attempt to transplant into a sick human. “The kidney is a really good candidate,” she said. “There’s a huge shortage and it would make a big difference.”
http://www.timesonline.co.uk/tol/news/uk/science/article5102153.ece
Lewis Smith, Science Reporter
Organs from pigs could be widely available for transplanting into patients in a decade, Lord Winston said yesterday.
The first organs suitable for transplanting, most likely kidneys, are expected to be ready within three years and, if tests are successful, their use could be widespread by 2018.
A herd of as few as 50 pigs is expected to be kept as breeding stock to provide organs “to order” and to slash waiting times for thousands of people needing transplants.
Professor Winston, of Imperial College, London, and his collaborator, Carol Readhead, of the California Institute of Technology, Pasadena, are leading research into transplanting animal organs into people.
They are attempting to breed pigs that have been genetically modified so that porcine organs are accepted by the human body instead of being immediately rejected.
Human immune systems are quick to react to “foreign bodies” but the scientists are confident that they are close to modifying the genetic make-up of pigs to “humanise” their organs and make animal-to-human transplants possible.
The humanisation process of the organs is expected to be achieved by breeding genes into the pigs, probably by injecting them directly into the parent boar’s testicles, that provoke a greatly reduced response in the patient’s immune system.
Patients who received pig organs would have to take immune suppressant drugs for the rest of their lives, but no more than those who received organ transplants from other people.
Dr Readhead said it was comparatively easy to bring about such genetic modification in mice, but the process is much harder in pigs and other large animals.
A “mini-pig” weighing about 100kg has been selected for the research because, while a quarter of the size of most of those grown for the meat industry, they are big enough to have organs of a similar size to adult human beings.
Pigs are regarded as ideal for animal-to-human transplants, xenotransplantation, and other research because of the similarity in the physiological make-up and because they get many of the same diseases, such as diabetes.
Dr Readhead said: “Our interest was to try to make transgenic pigs for biomedical research to understand human diseases better and eventually to try to make their organs suitable for xenotransplantation.”
Professor Winston said that “organs that might be transplantable” could be ready “within two to three years” and on the basis that research went smoothly they would be fully licensed and tested in as little as ten years. He expected the first “proof of principle” pigs to be bred next year.
Two months ago he hit out at the “red tape” blocking the project’s progress in Britain. Under UK and EU rules, his team has been banned from mating and producing offspring from the transgenic pigs. Research in developing transgenic pigs is now likely to move to the US where the regulatory system is more relaxed.
The new strain of pig, which once established would retain its genetic modifications from generation to generation, is expected to take £3 million to develop over the next five years.
He said that transplants were one of several potential benefits from the research. Others include enabling drugs which today have to be tested on people during late development phases to be tested on animals, avoiding reactions such as that suffered during trials at Northwick Park Hospital in 2006 when six volunteers almost died. Dr Readhead said kidneys are likely to be the first pig organs that researchers attempt to transplant into a sick human. “The kidney is a really good candidate,” she said. “There’s a huge shortage and it would make a big difference.”
Thursday, April 30, 2009
Study Links Anesthesia To Learning Disabilities
http://www.npr.org/templates/story/story.php?storyId=102306350
by Joseph Shapiro
Morning Edition, March 25, 2009 · Children who have had multiple surgeries under general anesthesia by the age of 4 may be at a higher risk of developing learning disabilities, according to a new study by scientists at the Mayo Clinic in Rochester, Minn.
Dr. Robert Wilder, a Mayo Clinic anesthesiologist, says his study was motivated by recent research on baby rats and other young animals. Those studies, conducted in the last several years, show that exposure to anesthesia at a very young age can kill off brain cells. But results in rodents don't necessarily translate to humans.
"The initial reaction of the pediatric anesthesia community was, 'This must be wrong, we've been giving anesthetics to kids for years and we don't see a big problem,''' Wilder says. He, too, was skeptical.
The Mayo Clinic sits in Olmsted County. Both the research clinic and the county have kept precise records on the health care and hospitalization of its residents. Wilder sorted through the records of more than 5,000 children. About 600 of them had one or more surgeries with a general anesthesia, a class of drugs that enters the blood stream, reaches the brain and leaves a patient in a state of unconsciousness. Local anesthesia (like what's used by dentists when filling a cavity) and regional anesthesia (like an epidural that's common during childbirth) numb just a part of the body, but don't cause the patient to lose consciousness.
The surgeries ranged from those for serious problems, like open heart surgery, to more routine ones, like putting in ear tubes or removing adenoids and tonsils. Most of the kids in the study — about 80 percent — had surgeries for the small and common problems.
Wilder found that children who had undergone a single operation with a general anesthetic by the time they turned 4 were no more likely than other children to develop a learning disability.
But kids who had had two surgeries were one and a half times more at risk. And for children who had undergone three operations, the risk went up to two and a half times. Of the kids in Wilder's study who had had three or more operations, 50 percent of them later developed a learning disability.
Wilder speculates that anesthesia could cause learning problems in young children because it travels to the brain at a time when the brain is developing rapidly.
"If you're exposed to these drugs at just the right time in your life," he says, "you have a lot more cell death than you otherwise would — and some of that is in the hippocampus, which is part of the brain that is involved in learning new things and it, therefore, does not work as well throughout the rest of your life."
That makes sense to Amanda Rathbun, who lives outside Salt Lake City.
"I always thought that things like this ran in families, like if your dad has brown eyes, then you're more likely to have brown eyes. But there's not a history of this in our family," she says.
Rathbun has three very smart kids. Her 11-year-old daughter has no learning disabilities. But another daughter, who's 8, and her son, who's 13, have both been diagnosed with attention deficit disorder. Both kids had several surgeries soon after birth.
In addition, the son has struggled to write legibly. Fine motor skills are a problem for him, and Rathbun wonders if he could have gotten more attention for that sooner.
"If general anesthesia early in life can really cause these sorts of problems," she says, "I think it would be good to know that, because maybe we could start more early intervention services for these kids and maybe prevent some of these later problems."
The new research is published in the current issue of Anesthesiology, the journal of the American Society of Anesthesiologists. The co-authors write that more studies are needed to be certain it's the anesthesia that's causing the problem. It might be the illness that requires the surgery — although the researchers took the sickest children out of the study.
Wilder says parents shouldn't avoid surgery when kids younger than 4 need it.
"My advice is that if their child needs a surgical or diagnostic procedure that requires an anesthetic, then they should go ahead and have that surgical or diagnostic procedure with the anesthetic," he says.
Dr. Piyush Patel, who wrote an accompanying editorial in the same journal, agrees. He adds that parents can, however, ask their doctor if it's better to postpone a surgery until a child is older.
"Based on these data, the parents of children have to be comfortable that the surgery is absolutely needed and they have to balance the risk of waiting for the surgery to be done versus the complication that may arise," says Patel, a professor of anesthesiology at the University of California, San Diego. "This is a decision that is best made by the surgeon and the anesthesiologist."
Wilder's study, and others, have created a sense of urgency to answer questions about the effects of anesthesia on the brain development of infants and young children. Earlier this month, the federal Food and Drug Administration announced a collaboration with Mayo and other clinics to support further research.
by Joseph Shapiro
Morning Edition, March 25, 2009 · Children who have had multiple surgeries under general anesthesia by the age of 4 may be at a higher risk of developing learning disabilities, according to a new study by scientists at the Mayo Clinic in Rochester, Minn.
Dr. Robert Wilder, a Mayo Clinic anesthesiologist, says his study was motivated by recent research on baby rats and other young animals. Those studies, conducted in the last several years, show that exposure to anesthesia at a very young age can kill off brain cells. But results in rodents don't necessarily translate to humans.
"The initial reaction of the pediatric anesthesia community was, 'This must be wrong, we've been giving anesthetics to kids for years and we don't see a big problem,''' Wilder says. He, too, was skeptical.
The Mayo Clinic sits in Olmsted County. Both the research clinic and the county have kept precise records on the health care and hospitalization of its residents. Wilder sorted through the records of more than 5,000 children. About 600 of them had one or more surgeries with a general anesthesia, a class of drugs that enters the blood stream, reaches the brain and leaves a patient in a state of unconsciousness. Local anesthesia (like what's used by dentists when filling a cavity) and regional anesthesia (like an epidural that's common during childbirth) numb just a part of the body, but don't cause the patient to lose consciousness.
The surgeries ranged from those for serious problems, like open heart surgery, to more routine ones, like putting in ear tubes or removing adenoids and tonsils. Most of the kids in the study — about 80 percent — had surgeries for the small and common problems.
Wilder found that children who had undergone a single operation with a general anesthetic by the time they turned 4 were no more likely than other children to develop a learning disability.
But kids who had had two surgeries were one and a half times more at risk. And for children who had undergone three operations, the risk went up to two and a half times. Of the kids in Wilder's study who had had three or more operations, 50 percent of them later developed a learning disability.
Wilder speculates that anesthesia could cause learning problems in young children because it travels to the brain at a time when the brain is developing rapidly.
"If you're exposed to these drugs at just the right time in your life," he says, "you have a lot more cell death than you otherwise would — and some of that is in the hippocampus, which is part of the brain that is involved in learning new things and it, therefore, does not work as well throughout the rest of your life."
That makes sense to Amanda Rathbun, who lives outside Salt Lake City.
"I always thought that things like this ran in families, like if your dad has brown eyes, then you're more likely to have brown eyes. But there's not a history of this in our family," she says.
Rathbun has three very smart kids. Her 11-year-old daughter has no learning disabilities. But another daughter, who's 8, and her son, who's 13, have both been diagnosed with attention deficit disorder. Both kids had several surgeries soon after birth.
In addition, the son has struggled to write legibly. Fine motor skills are a problem for him, and Rathbun wonders if he could have gotten more attention for that sooner.
"If general anesthesia early in life can really cause these sorts of problems," she says, "I think it would be good to know that, because maybe we could start more early intervention services for these kids and maybe prevent some of these later problems."
The new research is published in the current issue of Anesthesiology, the journal of the American Society of Anesthesiologists. The co-authors write that more studies are needed to be certain it's the anesthesia that's causing the problem. It might be the illness that requires the surgery — although the researchers took the sickest children out of the study.
Wilder says parents shouldn't avoid surgery when kids younger than 4 need it.
"My advice is that if their child needs a surgical or diagnostic procedure that requires an anesthetic, then they should go ahead and have that surgical or diagnostic procedure with the anesthetic," he says.
Dr. Piyush Patel, who wrote an accompanying editorial in the same journal, agrees. He adds that parents can, however, ask their doctor if it's better to postpone a surgery until a child is older.
"Based on these data, the parents of children have to be comfortable that the surgery is absolutely needed and they have to balance the risk of waiting for the surgery to be done versus the complication that may arise," says Patel, a professor of anesthesiology at the University of California, San Diego. "This is a decision that is best made by the surgeon and the anesthesiologist."
Wilder's study, and others, have created a sense of urgency to answer questions about the effects of anesthesia on the brain development of infants and young children. Earlier this month, the federal Food and Drug Administration announced a collaboration with Mayo and other clinics to support further research.
Wednesday, April 29, 2009
Key Gene Linked to High Blood Pressure Discovered
Tuesday , December 30, 2008
A gene that affects how the kidneys process salt may help determine a person's risk of high blood pressure, a discovery that could lead to better ways to treat the condition, researchers said on Monday.
People with a common variant of the gene STK39 tend to have higher blood pressure levels and are more likely to develop full-blown high blood pressure, also called hypertension, University of Maryland School of Medicine researchers found.
They identified the gene's role in high blood pressure susceptibility by analyzing the genes of 542 people in the insular Old Order Amish community in Lancaster County, Pennsylvania.
The researchers confirmed the findings by looking at the genes of another group of Amish people as well as four other groups of white people in the United States and Europe.
About 20 percent of the people studied had either one or two copies of this particular variant, the researchers said.
The gene produces a protein involved in regulating the way the kidneys process salt in the body — a key factor in determining blood pressure, the researchers said.
Yen-Pei Christy Chang, who led the study appearing in the journal Proceedings of the National Academy of Sciences, said the findings could lead to the development of new high blood pressure drugs targeting the activity of STK39.
"What we hope is that by understanding STK39 we can use that information for personalized medicine, so we can actually predict which hypertensive patients should be on what class of medication and know that they will respond well and have minimal risk for side effects," Chang said in a telephone interview.
People with high blood pressure are more likely to develop heart attacks, heart failure, strokes and kidney disease.
While STK39 may play a pivotal role in some people, Chang said numerous other genes also may be involved. Many factors are involved in high blood pressure such as being overweight, lack of exercise, smoking and too much salt in the diet.
Several different types of medications are used to treat high blood pressure, including diuretics, beta blockers, ACE inhibitors, calcium channel blockers and others. Their effectiveness varies depending on the person, and doctors have a hard time knowing which is best for a particular patient.
Chang said the researchers want to determine how people with different versions of this gene respond to the various drugs and to lifestyle interventions such as cutting the amount of salt in the diet.
The Lancaster Amish are seen as ideal for genetic research because they are a genetically homogenous people whose ancestry can be traced to a small group who arrived from Europe in the 1700s. In addition to genetic similarity, they also maintain similar lifestyles in their close-knit rural communities.
© Associated Press. All rights reserved.
This material may not be published, broadcast, rewritten, or redistributed.
Copyright 2009 FOX News Network, LLC. All rights reserved.
All market data delayed 20 minutes.
A gene that affects how the kidneys process salt may help determine a person's risk of high blood pressure, a discovery that could lead to better ways to treat the condition, researchers said on Monday.
People with a common variant of the gene STK39 tend to have higher blood pressure levels and are more likely to develop full-blown high blood pressure, also called hypertension, University of Maryland School of Medicine researchers found.
They identified the gene's role in high blood pressure susceptibility by analyzing the genes of 542 people in the insular Old Order Amish community in Lancaster County, Pennsylvania.
The researchers confirmed the findings by looking at the genes of another group of Amish people as well as four other groups of white people in the United States and Europe.
About 20 percent of the people studied had either one or two copies of this particular variant, the researchers said.
The gene produces a protein involved in regulating the way the kidneys process salt in the body — a key factor in determining blood pressure, the researchers said.
Yen-Pei Christy Chang, who led the study appearing in the journal Proceedings of the National Academy of Sciences, said the findings could lead to the development of new high blood pressure drugs targeting the activity of STK39.
"What we hope is that by understanding STK39 we can use that information for personalized medicine, so we can actually predict which hypertensive patients should be on what class of medication and know that they will respond well and have minimal risk for side effects," Chang said in a telephone interview.
People with high blood pressure are more likely to develop heart attacks, heart failure, strokes and kidney disease.
While STK39 may play a pivotal role in some people, Chang said numerous other genes also may be involved. Many factors are involved in high blood pressure such as being overweight, lack of exercise, smoking and too much salt in the diet.
Several different types of medications are used to treat high blood pressure, including diuretics, beta blockers, ACE inhibitors, calcium channel blockers and others. Their effectiveness varies depending on the person, and doctors have a hard time knowing which is best for a particular patient.
Chang said the researchers want to determine how people with different versions of this gene respond to the various drugs and to lifestyle interventions such as cutting the amount of salt in the diet.
The Lancaster Amish are seen as ideal for genetic research because they are a genetically homogenous people whose ancestry can be traced to a small group who arrived from Europe in the 1700s. In addition to genetic similarity, they also maintain similar lifestyles in their close-knit rural communities.
© Associated Press. All rights reserved.
This material may not be published, broadcast, rewritten, or redistributed.
Copyright 2009 FOX News Network, LLC. All rights reserved.
All market data delayed 20 minutes.
Professor Hiromitsu Nakauchi uses induced pluripotent stem to grow kidneys in genetically modified mouse
NEWS.com.auMarch 10, 2009 06:37am
Professor Hiromitsu Nakauchi uses induced pluripotent stem
to grow kidneys in genetically modified mouse
Breaking News
SCIENTISTS have successfully used implanted cells to create kidneys inside a mouse whose
parents were genetically engineered so their offspring would not be born with the organs.
The team, headed by Professor Hiromitsu Nakauchi of Tokyo University's Institute of Medical
Science, extracted a fertilised egg obtained through the normal mating of the genetically modified
parents.
The embryo was then implanted with induced pluripotent stem, or iPS, cells from a mouse with
kidneys and then transplanted into the womb of a surrogate mother.
The baby mouse was born with kidneys and it is believed its bladder inflated and it produced urine as
normal, MCT news agency reported
Implanted iPS cells are thought to have compensated for the kidneys the mouse should have been
born without.
The team now plans to use the research to create internal organs of monkeys inside pigs.
"If we become able in the future to create human kidneys inside pigs, we'll be able to solve the
problem of a lack of organs for transplant surgery," Prof Nakauchi told MCT.
Professor Hiromitsu Nakauchi uses induced pluripotent stem
to grow kidneys in genetically modified mouse
Breaking News
SCIENTISTS have successfully used implanted cells to create kidneys inside a mouse whose
parents were genetically engineered so their offspring would not be born with the organs.
The team, headed by Professor Hiromitsu Nakauchi of Tokyo University's Institute of Medical
Science, extracted a fertilised egg obtained through the normal mating of the genetically modified
parents.
The embryo was then implanted with induced pluripotent stem, or iPS, cells from a mouse with
kidneys and then transplanted into the womb of a surrogate mother.
The baby mouse was born with kidneys and it is believed its bladder inflated and it produced urine as
normal, MCT news agency reported
Implanted iPS cells are thought to have compensated for the kidneys the mouse should have been
born without.
The team now plans to use the research to create internal organs of monkeys inside pigs.
"If we become able in the future to create human kidneys inside pigs, we'll be able to solve the
problem of a lack of organs for transplant surgery," Prof Nakauchi told MCT.
Human kidneys grown in mice raise transplant hopes
December 23, 2002
Human kidneys grown in mice raise transplant hopes
By Steve Connor Science Editor
Scientists grown entire kidneys in laboratory mice using human stem cells in a development that raises the prospect of growing full-sized human organs in pigs – a breakthrough that would alleviate the worldwide shortage of kidneys for transplant operations.
Scientists grown entire kidneys in laboratory mice using human stem cells in a development that raises the prospect of growing full-sized human organs in pigs – a breakthrough that would alleviate the worldwide shortage of kidneys for transplant operations.
An Israeli team led by Professor Yair Reisner of the Weizmann Institute of Science in Rehovot grew miniature human kidneys inside the body cavities of mice in which human kidney stem cells had been transplanted. The kidneys were fully functional and produced urine.
The scientists were also able to produce pig kidneys with the same technique although in both cases the kidneys were the size of the normal mouse organ. The scientists hope now to attempt to grow human kidneys inside pigs to produce organs of a comparable size to those for human transplants.
Alternatively, they might be able to grow functioning pig kidneys inside human patients using pig foetal tissue, although this would require more careful ethical consideration because of the possibility of transferring pig viruses to people.
The study, published in the journal Nature Medicine, pinpointed the ideal time during embryonic development in which the stem cells had the best chance of forming well-functioning kidneys with minimal risk of immune rejection.
Their findings suggest that tissue seven to eight weeks old in humans and four-week-old pig tissue offers the best opportunity for transplantation. If taken earlier, the tissue could include non-kidney structures such as bone, cartilage and muscle. If taken later, then the risk of rejection by the immune system is substantial.
The work is part of a series of studies on growing entire organs using stem cells. In 1998, Marc Hammerman of Washington University in St Louis announced he had managed to grow miniature rat kidneys inside the body cavities of mice.
Professor Reisner's team also studied how the human immune system might respond to a kidney grown from human stem cells inside an animal. The scientists injected human lymphocytes – the "killer cells" of the immune system – into mice that lacked an immune system of their own.
"The findings were encouraging: as long as the kidney precursors were transplanted within the right time range, the lymphocytes did not attack the new pig or human kidneys – despite the fact that lymphocytes and kidney precursors originated from different donors," a spokesman for the Weizmann Institute said.
This suggests that such organs may not be rejected so readily if they were ever used in transplant medicine.
The team said the research was in a pre-clinical study stage, but that if all went well, a treatment could follow within a few years.
In SeptemberAmerican researchers said they had managed to grow teeth in rats, which suggested the existence of dental stem cells, and there was no reason why the technique used in rodents would not work in humans.
The shortage of kidneys for transplants is getting worse each year, according to the UK Transplant Authority. There are about 1,600 kidney transplants each year, with more than 5,000 people on the waiting list at any one time.
Human kidneys grown in mice raise transplant hopes
By Steve Connor Science Editor
Scientists grown entire kidneys in laboratory mice using human stem cells in a development that raises the prospect of growing full-sized human organs in pigs – a breakthrough that would alleviate the worldwide shortage of kidneys for transplant operations.
Scientists grown entire kidneys in laboratory mice using human stem cells in a development that raises the prospect of growing full-sized human organs in pigs – a breakthrough that would alleviate the worldwide shortage of kidneys for transplant operations.
An Israeli team led by Professor Yair Reisner of the Weizmann Institute of Science in Rehovot grew miniature human kidneys inside the body cavities of mice in which human kidney stem cells had been transplanted. The kidneys were fully functional and produced urine.
The scientists were also able to produce pig kidneys with the same technique although in both cases the kidneys were the size of the normal mouse organ. The scientists hope now to attempt to grow human kidneys inside pigs to produce organs of a comparable size to those for human transplants.
Alternatively, they might be able to grow functioning pig kidneys inside human patients using pig foetal tissue, although this would require more careful ethical consideration because of the possibility of transferring pig viruses to people.
The study, published in the journal Nature Medicine, pinpointed the ideal time during embryonic development in which the stem cells had the best chance of forming well-functioning kidneys with minimal risk of immune rejection.
Their findings suggest that tissue seven to eight weeks old in humans and four-week-old pig tissue offers the best opportunity for transplantation. If taken earlier, the tissue could include non-kidney structures such as bone, cartilage and muscle. If taken later, then the risk of rejection by the immune system is substantial.
The work is part of a series of studies on growing entire organs using stem cells. In 1998, Marc Hammerman of Washington University in St Louis announced he had managed to grow miniature rat kidneys inside the body cavities of mice.
Professor Reisner's team also studied how the human immune system might respond to a kidney grown from human stem cells inside an animal. The scientists injected human lymphocytes – the "killer cells" of the immune system – into mice that lacked an immune system of their own.
"The findings were encouraging: as long as the kidney precursors were transplanted within the right time range, the lymphocytes did not attack the new pig or human kidneys – despite the fact that lymphocytes and kidney precursors originated from different donors," a spokesman for the Weizmann Institute said.
This suggests that such organs may not be rejected so readily if they were ever used in transplant medicine.
The team said the research was in a pre-clinical study stage, but that if all went well, a treatment could follow within a few years.
In SeptemberAmerican researchers said they had managed to grow teeth in rats, which suggested the existence of dental stem cells, and there was no reason why the technique used in rodents would not work in humans.
The shortage of kidneys for transplants is getting worse each year, according to the UK Transplant Authority. There are about 1,600 kidney transplants each year, with more than 5,000 people on the waiting list at any one time.
How Morphine Can Be Given More Effectively Without Having To Increase Dosages
ScienceDaily (Apr. 28, 2009) — Researchers at the Hebrew University of Jerusalem have found a way to maintain the pain-killing qualities of morphine over an extended period of time, thus providing a solution for the problem of having to administer increasing dosages of the drug in order to retain its effectiveness.
One of the limitations in long-term use of morphine for pain relief is the rapid development of tolerance. The effectiveness of morphine declines quickly, and one must increase the dosage in order to preserve effective pain relief. However, the increased dosage also increases negative side effects.
The Hebrew University researchers, Prof. Yehuda Shavit and his graduate student Gilly Wolf of the Psychology Department, found that administration of morphine causes a substance called interleukin-1 to be released.
Under normal circumstances, interleukin-1 plays an important role in survival. In case of tissue damage, nerve injury, or inflammatory reaction, inteleukin-1 is released and sets off a process which increases the sensitivity to pain in the injured area. This pain serves as a warning signal, telling the body that there is a problem that should be attended to. In case of chronic pain, morphine is still the drug of choice for pain relief.
However, since prolonged administration of morphine raises the level of interleukin-1, thereby enhancing pain sensitivity, the effectiveness of morphine as a pain killer is steadily reduced, requiring greater dosages with accompanying negative side effects.
The Hebrew University researchers were able to show in animal experiments that administering morphine together with another drug that blocks the activity of interleukin-1 provides more effective pain relief over the long term without having to increase the dosage.
Shavit, who is the Leon and Clara Sznajderman Professor of Psychology at the Hebrew University and whose specialty is psychoneuroimmunology, expressed hope that this research will make it possible for clinicians to make use of morphine, together with substances that block interluekin-1, in order to bring about better pain relief with lower dosages and with minimized side effects. The research will be presented at a conference on pain research on May 3 on the Mount Scopus campus of the university. The conference is open to journalists and to people in the field.
One of the limitations in long-term use of morphine for pain relief is the rapid development of tolerance. The effectiveness of morphine declines quickly, and one must increase the dosage in order to preserve effective pain relief. However, the increased dosage also increases negative side effects.
The Hebrew University researchers, Prof. Yehuda Shavit and his graduate student Gilly Wolf of the Psychology Department, found that administration of morphine causes a substance called interleukin-1 to be released.
Under normal circumstances, interleukin-1 plays an important role in survival. In case of tissue damage, nerve injury, or inflammatory reaction, inteleukin-1 is released and sets off a process which increases the sensitivity to pain in the injured area. This pain serves as a warning signal, telling the body that there is a problem that should be attended to. In case of chronic pain, morphine is still the drug of choice for pain relief.
However, since prolonged administration of morphine raises the level of interleukin-1, thereby enhancing pain sensitivity, the effectiveness of morphine as a pain killer is steadily reduced, requiring greater dosages with accompanying negative side effects.
The Hebrew University researchers were able to show in animal experiments that administering morphine together with another drug that blocks the activity of interleukin-1 provides more effective pain relief over the long term without having to increase the dosage.
Shavit, who is the Leon and Clara Sznajderman Professor of Psychology at the Hebrew University and whose specialty is psychoneuroimmunology, expressed hope that this research will make it possible for clinicians to make use of morphine, together with substances that block interluekin-1, in order to bring about better pain relief with lower dosages and with minimized side effects. The research will be presented at a conference on pain research on May 3 on the Mount Scopus campus of the university. The conference is open to journalists and to people in the field.
Thursday, March 5, 2009
Cal Closer to Building "Organs from Scratch"
Cal Closer to Building "Organs from Scratch"
By JOHN BOITNOTT
Updated 6:32 AM PST, Thu, Mar 5, 2009
Related Topics:Carolyn Bertozzi | Zev Gartner | Biology | Genetics | Life Sciences | Science and Technology | Sciences
Scientists say they expect that eventually, clusters of cells could be built on clusters to make artificial organs that someday may be implanted into humans.
Synthetic biologists are getting closer to creating man-made organs made out of genetically engineered cells.
Two Cal chemists announced Tuesday they have assembled different types of genetically engineered cells into synthetic microtissues that can perform functions such as secreting and responding to hormones.
They said that means more complex biological capabilities, like the kinds done by a liver or a heart or a kidney, are not out of the question at some point soon.
"While the synthetic tissues today comprise only a handful of cells, they could eventually be scaled up to make artificial organs," the university media office said in a statement. "Those could help scientists understand the interactions among cells in the body and might some day substitute for human organs."
"People used to think of the cell as the fundamental unit. But the truth is that there are collections of cells that can do things that no individual cell could ever be programmed to do. We are trying to achieve the properties of organs now, though not yet organisms," "This is like another level of hierarchical complexity for synthetic biology," said coauthor Carolyn Bertozzi, UC Berkeley professor of chemistry and of molecular and cell biology. She is also the director of the Molecular Foundry at Lawrence Berkeley National Laboratory.
"As synthetic biologists cram more and more genes into microbes to make genetically engineered organisms produce ever more complex drugs and chemicals, two University of California chemists have gone a step further," the university media office said.
"We are really taking this into the third dimension now, which for me is particularly exciting," said first author Zev J. Gartner, a former UC Berkeley post-doctoral fellow. "We are not simply linking cells together, we are linking them together in 3-D arrangements, which introduces a whole new level of cellular behavior which you would never see in 2-D environments."
The Hope: Build Organs "From Scratch"
Gartner and Bertozzi report on their assembly of three-dimensional microtissues this week in the online early edition of the journal Proceedings of the National Academy of Sciences.
One type of cell that needs other cells to make it work properly is the stem cell, Bertozzi said
Theoretically, using Gartner and Bertozzi's chemical technique, it should be possible to assemble stem cells with their helper cells into a functioning tissue that would make stem cells easier to study outside the body.
"In principal, we might be able to build a stem cell niche from scratch using our techniques, and then study those very well defined structures in controlled environments," Bertozzi said.
Bertozzi said that most of the body's organs are a collection of many cell types that need to be in actual physical contact to operate properly.
The pancreas, for example, is a collection of specialized cells, including insulin-secreting beta cells, that "sense glucose from the environment and respond by producing insulin. A complex feedback regulatory loop goes into all of this, and you need more than one cell type to achieve such regulation."
"If you really want to understand the way these cells behave in an organism, especially a human, you would like to recapitulate that environment as closely as possible in vitro," Gartner said. "We are trying to do that, with the aim that the rules we learn may help us control them better."
How They Did It…
Gartner and Bertozzi assembled three types of cultured cells into onion-like layers by using two established technologies: DNA hybridization and Staudinger chemistry.
DNA hybridization is like a "programmable glue," she said, that can stick cells together because of the highly precise nature of binding between complementary DNA strands: One strand of the DNA helix binds only to its complementary strand and nothing else. By putting a short DNA strand on the surface of one cell and its complementary strand on another cell, the researchers assure that the two lock together exclusively.
To get these specific DNA strands onto the cells, they used chemical reactions that do not interfere with cellular chemistry but nevertheless stick desired chemicals onto the cell surface.
The technique for adding unusual but benign chemicals to cells was developed by Bertozzi more than a decade ago based on a chemical reaction called the Staudinger ligation.
After proving that they could assemble cells into microtissues, Gartner and Bertozzi constructed a minute gland - analogous to a lymph node, for example - such that one cell type secreted interleukin-3 and thereby kept a second cell type alive.
"What we did is build a little miniaturized, stripped-down system that operates on the same principle and looks like a miniaturized lymph node, an arrangement where two cells communicate with each another and one requires a signal from the other," she said. "The critical thing is that the two cells have to have a cell junction. If you just mix the cells randomly without connection, the system doesn't have the same properties."
She expects that eventually, clusters could be built on clusters to make artificial organs that someday may be implanted into humans.
"Our method allows the assembly of multicellular structures from the bottom up. In other words, we can control the neighbors of each individual cell in a mixed population," she said. "By this method, it may be possible to assemble tissues with more sophisticated properties."
One aspect of the technique is that DNA hybridization seems to be temporary, like a suture. Eventually, the cells may substitute their own cell-cell adhesion molecules for the DNA, creating a well-knit and seemingly normal, biological system.
The research was funded by the U.S. Department of Energy as well as the Howard Hughes Medical Institute.
Find this article at:
http://www.nbcbayarea.com/news/local/Cal-Chemists-Get-Closer-to-Building-Organs-from-Scratch.html
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By JOHN BOITNOTT
Updated 6:32 AM PST, Thu, Mar 5, 2009
Related Topics:Carolyn Bertozzi | Zev Gartner | Biology | Genetics | Life Sciences | Science and Technology | Sciences
Scientists say they expect that eventually, clusters of cells could be built on clusters to make artificial organs that someday may be implanted into humans.
Synthetic biologists are getting closer to creating man-made organs made out of genetically engineered cells.
Two Cal chemists announced Tuesday they have assembled different types of genetically engineered cells into synthetic microtissues that can perform functions such as secreting and responding to hormones.
They said that means more complex biological capabilities, like the kinds done by a liver or a heart or a kidney, are not out of the question at some point soon.
"While the synthetic tissues today comprise only a handful of cells, they could eventually be scaled up to make artificial organs," the university media office said in a statement. "Those could help scientists understand the interactions among cells in the body and might some day substitute for human organs."
"People used to think of the cell as the fundamental unit. But the truth is that there are collections of cells that can do things that no individual cell could ever be programmed to do. We are trying to achieve the properties of organs now, though not yet organisms," "This is like another level of hierarchical complexity for synthetic biology," said coauthor Carolyn Bertozzi, UC Berkeley professor of chemistry and of molecular and cell biology. She is also the director of the Molecular Foundry at Lawrence Berkeley National Laboratory.
"As synthetic biologists cram more and more genes into microbes to make genetically engineered organisms produce ever more complex drugs and chemicals, two University of California chemists have gone a step further," the university media office said.
"We are really taking this into the third dimension now, which for me is particularly exciting," said first author Zev J. Gartner, a former UC Berkeley post-doctoral fellow. "We are not simply linking cells together, we are linking them together in 3-D arrangements, which introduces a whole new level of cellular behavior which you would never see in 2-D environments."
The Hope: Build Organs "From Scratch"
Gartner and Bertozzi report on their assembly of three-dimensional microtissues this week in the online early edition of the journal Proceedings of the National Academy of Sciences.
One type of cell that needs other cells to make it work properly is the stem cell, Bertozzi said
Theoretically, using Gartner and Bertozzi's chemical technique, it should be possible to assemble stem cells with their helper cells into a functioning tissue that would make stem cells easier to study outside the body.
"In principal, we might be able to build a stem cell niche from scratch using our techniques, and then study those very well defined structures in controlled environments," Bertozzi said.
Bertozzi said that most of the body's organs are a collection of many cell types that need to be in actual physical contact to operate properly.
The pancreas, for example, is a collection of specialized cells, including insulin-secreting beta cells, that "sense glucose from the environment and respond by producing insulin. A complex feedback regulatory loop goes into all of this, and you need more than one cell type to achieve such regulation."
"If you really want to understand the way these cells behave in an organism, especially a human, you would like to recapitulate that environment as closely as possible in vitro," Gartner said. "We are trying to do that, with the aim that the rules we learn may help us control them better."
How They Did It…
Gartner and Bertozzi assembled three types of cultured cells into onion-like layers by using two established technologies: DNA hybridization and Staudinger chemistry.
DNA hybridization is like a "programmable glue," she said, that can stick cells together because of the highly precise nature of binding between complementary DNA strands: One strand of the DNA helix binds only to its complementary strand and nothing else. By putting a short DNA strand on the surface of one cell and its complementary strand on another cell, the researchers assure that the two lock together exclusively.
To get these specific DNA strands onto the cells, they used chemical reactions that do not interfere with cellular chemistry but nevertheless stick desired chemicals onto the cell surface.
The technique for adding unusual but benign chemicals to cells was developed by Bertozzi more than a decade ago based on a chemical reaction called the Staudinger ligation.
After proving that they could assemble cells into microtissues, Gartner and Bertozzi constructed a minute gland - analogous to a lymph node, for example - such that one cell type secreted interleukin-3 and thereby kept a second cell type alive.
"What we did is build a little miniaturized, stripped-down system that operates on the same principle and looks like a miniaturized lymph node, an arrangement where two cells communicate with each another and one requires a signal from the other," she said. "The critical thing is that the two cells have to have a cell junction. If you just mix the cells randomly without connection, the system doesn't have the same properties."
She expects that eventually, clusters could be built on clusters to make artificial organs that someday may be implanted into humans.
"Our method allows the assembly of multicellular structures from the bottom up. In other words, we can control the neighbors of each individual cell in a mixed population," she said. "By this method, it may be possible to assemble tissues with more sophisticated properties."
One aspect of the technique is that DNA hybridization seems to be temporary, like a suture. Eventually, the cells may substitute their own cell-cell adhesion molecules for the DNA, creating a well-knit and seemingly normal, biological system.
The research was funded by the U.S. Department of Energy as well as the Howard Hughes Medical Institute.
Find this article at:
http://www.nbcbayarea.com/news/local/Cal-Chemists-Get-Closer-to-Building-Organs-from-Scratch.html
SAVE THIS | EMAIL THIS | Close
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© NBC Universal, Inc. | All Rights Reserved.
Thursday, February 12, 2009
The tale of the teenage toddlers
The tale of the teenage toddlers
By STAFF REPORTERS
Published: 10 Feb 2009
THIS brother and sister might look like cute primary school children but they are actually grown-up TEENAGERS aged 18 and 16.
Shockingly Azad Singh and his sister Laxmi Yadav have not grown at all since they were five or six and still look like little kids.
See incredible pics of the teen tots below:
Neither of the pair, who live in Haryana, India, have been through puberty due to a rare hormone disorder.
Azad is just 3ft tall but is studying for A-Levels in English and Maths with the help of a tutor, and Laxmi, who is 3ft 3ins, is at high school taking the equivalent of her GCSEs.
Mates ... Azad with his school chums
Barcroft Media
The pair face being trapped in children's bodies for their rest of their lives as treatment in the form of hormone injections would normally be given before the age of 16 or 17.
A simple, one-year, course of hormones costing just £18 per day could have allowed them to grow in height and develop sexually.
But the teens parents have always been too poor to fund the injections.
The pair now live in the constant care of mum Manju Bala, dad Bahadur Singh, a casual labourer, and sister Suman Yadav, 12, who is normal height.
Azad, who wants to train as an engineer, said: “I’m taking my exams in April. I’m doing a lot of revision and hard work.
Drive ... tiny Azad takes the wheel
Barcroft Media
“When I go out, such as to walk to my tutor’s house, my mum has to come with me.
“People think I’m still a kid and need looking after.”
He added: “If Laxmi or I go out alone, people stare and gather round us. Some unkind people even shout names at us in the street. So we normally have our parents or sister Suman with us.
“I cannot hang out with boys my age, because they say I cannot keep up with them. But I have two friends at school who spend time with me, and don’t mind that I’m small.”
Laxmi added: “When we were younger our parents had to change our school because the other kids laughed at us because of our size.”
Devoted mum Manju said: “I’m very protective of my children. If I do not accompany Azad when he goes out, people throw things at him on his bike, and might harm him.”
She explained: “When Azad and Laxmi were very young, they were the same size as other children. We didn’t realise anything was wrong until Azad was about five and we noticed he stopped growing.
“When Laxmi also reached five, she’d stopped growing too. We took them to the doctor but he had no idea what was wrong with them.
“Over the years we’ve been referred to many hospitals, but they all wanted payment for any treatment.
“We went to hospitals in Kalavati, Gangaram, but everywhere they were asking for huge money for the treatment. We were not able to afford it, so we had to leave.”
She added: “Once we looked into selling our house to get 15,000 rupees (2,910 pounds) for treatment. But the doctors at Gangaram Hospital could not guarantee us that the injections would work by this stage as Azad and Laxmi were older, so we decided no to go ahead.”
Finally, last year, the family were offered a lifeline by the All India Institute of Medical Sciences in Dehli, who looked into providing free treatment for the brother and sister.
But when the Azad and Laxmi arrived at the hospital, crowds of patients, visitors, and even people from the street went into to the ward to stare at them.
“We could not face all those people,” said Laxmi. “It was too frightening for Azad and me. We felt we would rather stay as we were than go through that.
“We decided we did not want the treatment, as doctors said there was only about a 40 to 50 per cent chance it would work.”
By STAFF REPORTERS
Published: 10 Feb 2009
THIS brother and sister might look like cute primary school children but they are actually grown-up TEENAGERS aged 18 and 16.
Shockingly Azad Singh and his sister Laxmi Yadav have not grown at all since they were five or six and still look like little kids.
See incredible pics of the teen tots below:
Neither of the pair, who live in Haryana, India, have been through puberty due to a rare hormone disorder.
Azad is just 3ft tall but is studying for A-Levels in English and Maths with the help of a tutor, and Laxmi, who is 3ft 3ins, is at high school taking the equivalent of her GCSEs.
Mates ... Azad with his school chums
Barcroft Media
The pair face being trapped in children's bodies for their rest of their lives as treatment in the form of hormone injections would normally be given before the age of 16 or 17.
A simple, one-year, course of hormones costing just £18 per day could have allowed them to grow in height and develop sexually.
But the teens parents have always been too poor to fund the injections.
The pair now live in the constant care of mum Manju Bala, dad Bahadur Singh, a casual labourer, and sister Suman Yadav, 12, who is normal height.
Azad, who wants to train as an engineer, said: “I’m taking my exams in April. I’m doing a lot of revision and hard work.
Drive ... tiny Azad takes the wheel
Barcroft Media
“When I go out, such as to walk to my tutor’s house, my mum has to come with me.
“People think I’m still a kid and need looking after.”
He added: “If Laxmi or I go out alone, people stare and gather round us. Some unkind people even shout names at us in the street. So we normally have our parents or sister Suman with us.
“I cannot hang out with boys my age, because they say I cannot keep up with them. But I have two friends at school who spend time with me, and don’t mind that I’m small.”
Laxmi added: “When we were younger our parents had to change our school because the other kids laughed at us because of our size.”
Devoted mum Manju said: “I’m very protective of my children. If I do not accompany Azad when he goes out, people throw things at him on his bike, and might harm him.”
She explained: “When Azad and Laxmi were very young, they were the same size as other children. We didn’t realise anything was wrong until Azad was about five and we noticed he stopped growing.
“When Laxmi also reached five, she’d stopped growing too. We took them to the doctor but he had no idea what was wrong with them.
“Over the years we’ve been referred to many hospitals, but they all wanted payment for any treatment.
“We went to hospitals in Kalavati, Gangaram, but everywhere they were asking for huge money for the treatment. We were not able to afford it, so we had to leave.”
She added: “Once we looked into selling our house to get 15,000 rupees (2,910 pounds) for treatment. But the doctors at Gangaram Hospital could not guarantee us that the injections would work by this stage as Azad and Laxmi were older, so we decided no to go ahead.”
Finally, last year, the family were offered a lifeline by the All India Institute of Medical Sciences in Dehli, who looked into providing free treatment for the brother and sister.
But when the Azad and Laxmi arrived at the hospital, crowds of patients, visitors, and even people from the street went into to the ward to stare at them.
“We could not face all those people,” said Laxmi. “It was too frightening for Azad and me. We felt we would rather stay as we were than go through that.
“We decided we did not want the treatment, as doctors said there was only about a 40 to 50 per cent chance it would work.”
Stem Cell Heart Trials in UK
Trials for revolutionary stem cell surgery in UK 'within a year'
Heart disease patients in Britain could soon take part in a revolutionary stem cell surgery trial that could change the nature of heart surgery andHeart disease patients in Britain could soon take part in a revolutionary stem cell surgery trial that could change the nature of heart surgery and ultimately end the need for transplants.
By Caroline Gammell
Last Updated: 4:31PM GMT 09 Feb 2009
Heart disease affects more than a million people in the UK and kills around 120,000 people a year Photo: GETTY
It is believed that British patents could take the pioneering treatment, in which a patient's own cells are extracted and grown in a laboratory, in as little as a year.
Scientists have worked out a technique where human bone marrow cells are turned into human heart stem cells and then injected into the heart.
Laboratory grown heart stem cells were initially extensively tested on animals and trials on humans in Europe are due to start later this month.
Dr Jonathan Hill, a consultant cardiologist at London's King's College Hospital, is hoping to perform trials on British patients next year in conjunction with King's College London University.
"I have seen the results of the trials and they are very encouraging," he said. "We are negotiating to carry out human trials in the UK."
Professor Sian Harding, of Imperial College London, said being able to convert bone marrow stem cells into heart stem cell was a "big leap forward" in finding an "effective" treatment for heart failure.
"Placing heart stem cells into the heart to repair has a very good chance of working because the stem cells are the patient's own there are no problems with rejection," she said.
Prof Harding is working on turning embryo stem cells into heart stem cells but said her research was "still years away" from being used in patients.
Dr Duncan Dymond, a consultant cardiologist at London's Bart's Hospital, added: "Turning human stem cells into human heart cells is very exciting news.
"People with bad heart failure often lead a wretched life confined to home and unable to get out and about. If you are lucky you might get a heart transplant but many simply die before their time."
Last month, a method of cloning specialist versions of heart stem cells - known as "progenitor" cells - found in small quantities in human hearts received an international innovation award.
Last year, the Daily Telegraph disclosed how two heart attack patients in Britain had stem cells taken from bone marrow injected into their hearts in a bid to repair damaged tissue.
The most recent process was developed at the Mayo Clinic research centre in Minnesota.
As part of the planned human trials, 40 millilitres of bone marrow will be taken from a volunteer's hips.
The bone marrow is then grown in a laboratory into human heart stem cells using a special 'growth factor' protein.
The growth factor delivers a chemical signal to the stem cells to turn them from bone marrow cells into heart cells.
These cells are then infused into the patient's heart via a catheter in the groin and an improvement in a patient's condition is expected within a couple of weeks.
The development was disclosed during a major stem cell conference in New York and has been submitted to a leading medical journal.
Dr Christian Homsy of Cardio3 Biosciences - the company which is developing human heart stem cells - said: "Human heart stem cells repaired damaged areas of mice hearts in our trials. And we are convinced that we can do the same in humans.
"It is a very straightforward procedure and we would expect to see a patient's health to change quite rapidly over a period of several weeks to a couple of months. In the mouse trials it was quite quick but in humans we don't know yet."
Heart disease affects more than a million people in the UK and kills around 120,000 people a year.
Heart disease patients in Britain could soon take part in a revolutionary stem cell surgery trial that could change the nature of heart surgery andHeart disease patients in Britain could soon take part in a revolutionary stem cell surgery trial that could change the nature of heart surgery and ultimately end the need for transplants.
By Caroline Gammell
Last Updated: 4:31PM GMT 09 Feb 2009
Heart disease affects more than a million people in the UK and kills around 120,000 people a year Photo: GETTY
It is believed that British patents could take the pioneering treatment, in which a patient's own cells are extracted and grown in a laboratory, in as little as a year.
Scientists have worked out a technique where human bone marrow cells are turned into human heart stem cells and then injected into the heart.
Laboratory grown heart stem cells were initially extensively tested on animals and trials on humans in Europe are due to start later this month.
Dr Jonathan Hill, a consultant cardiologist at London's King's College Hospital, is hoping to perform trials on British patients next year in conjunction with King's College London University.
"I have seen the results of the trials and they are very encouraging," he said. "We are negotiating to carry out human trials in the UK."
Professor Sian Harding, of Imperial College London, said being able to convert bone marrow stem cells into heart stem cell was a "big leap forward" in finding an "effective" treatment for heart failure.
"Placing heart stem cells into the heart to repair has a very good chance of working because the stem cells are the patient's own there are no problems with rejection," she said.
Prof Harding is working on turning embryo stem cells into heart stem cells but said her research was "still years away" from being used in patients.
Dr Duncan Dymond, a consultant cardiologist at London's Bart's Hospital, added: "Turning human stem cells into human heart cells is very exciting news.
"People with bad heart failure often lead a wretched life confined to home and unable to get out and about. If you are lucky you might get a heart transplant but many simply die before their time."
Last month, a method of cloning specialist versions of heart stem cells - known as "progenitor" cells - found in small quantities in human hearts received an international innovation award.
Last year, the Daily Telegraph disclosed how two heart attack patients in Britain had stem cells taken from bone marrow injected into their hearts in a bid to repair damaged tissue.
The most recent process was developed at the Mayo Clinic research centre in Minnesota.
As part of the planned human trials, 40 millilitres of bone marrow will be taken from a volunteer's hips.
The bone marrow is then grown in a laboratory into human heart stem cells using a special 'growth factor' protein.
The growth factor delivers a chemical signal to the stem cells to turn them from bone marrow cells into heart cells.
These cells are then infused into the patient's heart via a catheter in the groin and an improvement in a patient's condition is expected within a couple of weeks.
The development was disclosed during a major stem cell conference in New York and has been submitted to a leading medical journal.
Dr Christian Homsy of Cardio3 Biosciences - the company which is developing human heart stem cells - said: "Human heart stem cells repaired damaged areas of mice hearts in our trials. And we are convinced that we can do the same in humans.
"It is a very straightforward procedure and we would expect to see a patient's health to change quite rapidly over a period of several weeks to a couple of months. In the mouse trials it was quite quick but in humans we don't know yet."
Heart disease affects more than a million people in the UK and kills around 120,000 people a year.
Tuesday, January 6, 2009
Folic acid 'increases memory'
Folic acid 'increases memory'
By Nic Fleming, Medical Correspondent
Last Updated: 2:18AM GMT 19 Jan 2007
Folic acid supplements can significantly improve the memory and brain power of older people, according to a study to be published today.
Researchers found that men and post-menopausal women aged between 50 and 70 who took daily doses had the mental abilities of those almost five years their junior.
The supplements also helped maintain speed of information processing, reactions involving movement and overall brain power. These abilities decline with age, and their loss has been linked to a higher risk of dementia.
Folate, the natural form of synthetic folic acid, is found in broccoli, Brussels sprouts, peas, chickpeas, yeast extract, brown rice and fruit including oranges and bananas.
The research, published in the Lancet medical journal, was led by Dr Jane Durga, from the University of Wageningen in the Netherlands.
Dr Durga said: "Folic acid improves performance in tests that measure information processing speed and memory - domains known to decline with age.
"Trials similar to our own should now be repeated to provide greater insight into the clinical relevance of folic acid to people with mild cognitive impairment and dementia."
Folic acid supplements were also found to reduce levels of homocysteine, a blood chemical linked both to heart disease and dementia.
Age Concern has warned that increased consumption could have the side effect of masking deficiencies in the vitamin B12 - found in meat, eggs and dairy products - which could actually cause neurological damage.
"Further research is needed to reach a definitive answer on the benefits, or not, of folic acid," said the charity's director-general Gordon Lishman.
By Nic Fleming, Medical Correspondent
Last Updated: 2:18AM GMT 19 Jan 2007
Folic acid supplements can significantly improve the memory and brain power of older people, according to a study to be published today.
Researchers found that men and post-menopausal women aged between 50 and 70 who took daily doses had the mental abilities of those almost five years their junior.
The supplements also helped maintain speed of information processing, reactions involving movement and overall brain power. These abilities decline with age, and their loss has been linked to a higher risk of dementia.
Folate, the natural form of synthetic folic acid, is found in broccoli, Brussels sprouts, peas, chickpeas, yeast extract, brown rice and fruit including oranges and bananas.
The research, published in the Lancet medical journal, was led by Dr Jane Durga, from the University of Wageningen in the Netherlands.
Dr Durga said: "Folic acid improves performance in tests that measure information processing speed and memory - domains known to decline with age.
"Trials similar to our own should now be repeated to provide greater insight into the clinical relevance of folic acid to people with mild cognitive impairment and dementia."
Folic acid supplements were also found to reduce levels of homocysteine, a blood chemical linked both to heart disease and dementia.
Age Concern has warned that increased consumption could have the side effect of masking deficiencies in the vitamin B12 - found in meat, eggs and dairy products - which could actually cause neurological damage.
"Further research is needed to reach a definitive answer on the benefits, or not, of folic acid," said the charity's director-general Gordon Lishman.
Diabetes dulls the brain claim scientists
1/6/09 12:19 PM
Diabetes dulls the brain claim scientists - Telegraph
http://www.telegraph.co.uk/health/healthnews/4126051/Diabetes-dulls-the-brain-claim-scientists.html
Diabetes dulls the brain claim scientists
People with diabetes suffer a mental slowdown early in the disease, according to a new study.
By Richard Alleyne, Science Correspondent
Last Updated: 3:57PM GMT 05 Jan 2009
Researchers found that healthy adults performed significantly better in planning, paying attention and speed of thought
than those suffering from diabetes.
But the differences were not significant in terms of memory, verbal fluency or reaction time.
As Britain's diabetic population continues to rise sharply, the findings mean that millions of people could be in danger of
mental slow down.
The team from the University of Alberta in Canada tracked 41 people with type 2 diabetes - also known as adult-onset
diabetes - and 424 without to make the finding.
The study, published in the journal Neuropsychology, found that the mental deterioration was no better in younger adults
with diabetes than in an older group, suggesting that the damage is done early in the disease and remains stable
thereafter.
Professor Roger Dixon, the report's co-author, said that people with serious cases of type 2 diabetes should be screened
for these cognitive effects to make sure they get the right medication and advice on diet or mental training.
"There could be some ways to compensate for these declines, at least early and with proper management," he said.
Obesity is one of the principal causes of type 2 diabetes, and has contributed to a rapid rise in the numbers of people with
the condition.
About a quarter of English adults are obese, and one official forecast suggests nine out of ten adults will be overweight or
obese by 2050.
Diabetes is linked to heart disease, stroke, amputations, kidney failure and blindness, and about one in 10 deaths is linked
to the disease. This is forecast to rise to one in eight next year.
Diabetes dulls the brain claim scientists - Telegraph
http://www.telegraph.co.uk/health/healthnews/4126051/Diabetes-dulls-the-brain-claim-scientists.html
Diabetes dulls the brain claim scientists
People with diabetes suffer a mental slowdown early in the disease, according to a new study.
By Richard Alleyne, Science Correspondent
Last Updated: 3:57PM GMT 05 Jan 2009
Researchers found that healthy adults performed significantly better in planning, paying attention and speed of thought
than those suffering from diabetes.
But the differences were not significant in terms of memory, verbal fluency or reaction time.
As Britain's diabetic population continues to rise sharply, the findings mean that millions of people could be in danger of
mental slow down.
The team from the University of Alberta in Canada tracked 41 people with type 2 diabetes - also known as adult-onset
diabetes - and 424 without to make the finding.
The study, published in the journal Neuropsychology, found that the mental deterioration was no better in younger adults
with diabetes than in an older group, suggesting that the damage is done early in the disease and remains stable
thereafter.
Professor Roger Dixon, the report's co-author, said that people with serious cases of type 2 diabetes should be screened
for these cognitive effects to make sure they get the right medication and advice on diet or mental training.
"There could be some ways to compensate for these declines, at least early and with proper management," he said.
Obesity is one of the principal causes of type 2 diabetes, and has contributed to a rapid rise in the numbers of people with
the condition.
About a quarter of English adults are obese, and one official forecast suggests nine out of ten adults will be overweight or
obese by 2050.
Diabetes is linked to heart disease, stroke, amputations, kidney failure and blindness, and about one in 10 deaths is linked
to the disease. This is forecast to rise to one in eight next year.
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