Daily Aspirin Cuts Many Cancer Risks

http://www.foxnews.com/health/2010/12/07/study-daily-aspirin-cuts-cancer-risks/#ixzz17RlnbXiH

Published December 07, 2010 | Reuters


Taking low doses of aspirin can reduce the risk of many kinds of cancer, scientists said on Tuesday, and the evidence is strong enough to suggest people over 40 should take it daily as protection.
The findings will fuel an already intense debate about the merits of taking aspirin, which increases the risk of bleeding in the stomach to around one patient in every thousand per year.

In a study of eight trials involving 25,570 patients, researchers found that cancer deaths among those who took aspirin in doses as low as 75 milligrams a day were 21 percent lower during the studies and 34 percent lower after five years.
Aspirin protected people against gastrointestinal cancers the most, the study found, with rates of death from these cancers around 54 percent lower after five years among those who took aspirin compared to those who did not.

Peter Rothwell of Britain's Oxford University said that while taking aspirin carries a small risk of stomach bleeding, that risk was beginning to be "drowned out" by its benefits in reducing the risk of cancer and the risk of heart attacks.
"Previous guidelines have rightly cautioned that in healthy middle-aged people the small risk of bleeding on aspirin partly offsets the benefit from prevention of strokes and heart attacks, but the reductions in deaths due to several common cancers will now alter this balance for many people," he said.

His suggestion was that healthy people could start taking a small 75 mg dose of aspirin every day from the age of about 40 or 45 and continue doing so until they reached around 70 to 75, when the risk of the aspirin causing stomach bleeding rises.
"REMARKABLE DRUG"

Aspirin, originally developed by Bayer, is a cheap over-the-counter drug used for pain and to reduce fever.
Previous studies have found taking aspirin can cut the risk of developing colon or bowel cancer and suggested it does so by blocking the enzyme cyclooxygenase2 which promotes inflammation and cell division and is found in high levels in tumors.

Alastair Watson, professor of translational medicine at the University of East Anglia, said the study was an important step in scientists' understanding of how to prevent cancer.
"It is further proof that aspirin is, by a long way, the most amazing drug in the world," he said.

In Rothwell's study, published in The Lancet, researchers found the 20-year risk of death was reduced by about 10 percent for prostate cancer, 30 percent for lung cancer, 40 percent for colorectal or bowel cancer and 60 percent for esophageal cancer in those taking aspirin.

Reductions in pancreas, stomach and brain cancers were difficult to quantify because of smaller numbers of deaths.
The researchers added, however, that treatment with aspirin during the trials lasted for only for between four and eight years on average, so the effects on risk of deaths due to cancer may underestimate possible results of longer-term treatment.

Peter Elwood, an expert on aspirin from Cardiff University's medical school who was not involved in this study, described aspirin as "a remarkable drug". "This risk of a bleed is so small compared to the benefits," he told reporters. "Yes, okay, it's a tragedy if a person is rushed into hospital and given a transfusion (because of a stomach bleed) but in relation to the things we are preventing, that is trivial."

Mercury poisoning makes male birds homosexual

01 December 2010 by Michael Marshall


Low levels of mercury in the diet of male white ibises cause the birds to mate with each other rather than with females. As a result many of the females can't breed, and fewer chicks are produced.

It's the first time a pollutant has been found to change an animal's sexual preference. Many chemicals can "feminise" males or reduce fertility, but males affected in these ways still prefer females.

Mercury is extremely toxic, particularly in the form of methylmercury, which reduces breeding in wild birds by disrupting their parenting behaviours. To find out if it also affected mating, Peter Frederick of the University of Florida in Gainesville and Nilmini Jayasena of the University of Peradeniya, Sri Lanka, captured 160 young white ibises from south Florida. They gave them food laced with methylmercury and monitored them closely.

The birds were split into four groups. One group ate food with 0.3 parts per million methylmercury, which most US states would regard as too high for human consumption. A second group got 0.1 ppm, and the third 0.05 ppm, a low dose that wild birds would be exposed to frequently. The fourth group received none.

Poisoned

All three dosed groups had significantly more homosexual males than the control group. Male-male pairs courted, built nests together and paired off for several weeks. Higher doses increased the effect, with 55 per cent of males in the 0.3 ppm group affected. Male-male matings were responsible for 81 per cent of unproductive nests in the dosed groups.

Meanwhile the heterosexual pairs courted less and were bad at parenting – patterns of behaviour that were both already known to be caused by methylmercury poisoning. The combined effects of male-male pairing and poor performance by male-female pairs could be severe. "In the worst-case scenario, the production of young would fall by 50 per cent," says Frederick.

Looking for effects on courtship and mating is novel, says Tony Scheuhammer of Environment Canada's National Wildlife Research Center in Ottawa, Ontario. "People normally study pairs that have already mated to see how good they are at parenting," he says.

Other birds would probably be similarly affected, though both Frederick and Scheuhammer say it's far from clear whether other animal groups would be. In particular, there's no evidence for increased homosexuality in humans resulting from mercury poisoning, despite several long-term studies. "If the effect was as strong in humans as in the ibises, they'd have found it," Frederick says.

Journal reference: Proceedings of the Royal Society B, DOI: 10.1098/rspb.2010.2189

Spray-On Stem Cells Speed Healing Process For Burn Victims

http://www.care2.com/causes/health-policy/blog/spray-on-stem-cells-accelerate-healing-for-burn-victims/




An experimental stem cell treatment is helping to speed up the healing process for burn victims, according to researchers at the University of Utah.

We've all heard of spray-on tans, and (ahem) clothing, but now the same principle of instant-application is being used to provide a speedy recovery process for those that are suffering from serious burns.

In clinical trials, surgeons Amit Patel and Amalia Cochran are testing "a concentrate of [the patient's own] platelets and progenitor cells with calcium and thrombin to create a Jello-like substance accelerates the healing process".

Popular Science reports that "in tests, the spray has proven effective in the treatment of small burns and seems to improve the likelihood that a skin graft will take, which could carry positive implications for the application of this technology to other types of transplants."


A similar treatment, called ReCell, is already being used in Australia, Europe and China and made headlines when it was used to treat of victims of a 2002 bombing in Bali.

So far, the spray-on treatment is only being used on patients with small burns, but the researchers hope that someday they maybe able to scale up the process to treat those who sustain burns on large areas of their body, like military personnel or people that have been caught in a house fire.

Harvard scientists reverse the aging process in mice – now for humans

http://www.guardian.co.uk/science/2010/nov/28/scientists-reverse-ageing-mice-humans

Harvard scientists reverse the ageing process in mice – now for humans
Harvard scientists were surprised that they saw a dramatic reversal, not just a slowing down, of the ageing in mice. Now they believe they might be able to regenerate human organs


Ian Sample, science correspondent
guardian.co.uk, Sunday 28 November 2010 18.01 GMT


In mice, reactivating the enzyme telomerase led to the repair of damaged tissues and reversed the signs of ageing. Photograph: Robert F. Bukaty/AP
Scientists claim to be a step closer to reversing the ageing process after rejuvenating worn out organs in elderly mice. The experimental treatment developed by researchers at Harvard Medical School turned weak and feeble old mice into healthy animals by regenerating their aged bodies.

The surprise recovery of the animals has raised hopes among scientists that it may be possible to achieve a similar feat in humans – or at least to slow down the ageing process.

An anti-ageing therapy could have a dramatic impact on public health by reducing the burden of age-related health problems, such as dementia, stroke and heart disease, and prolonging the quality of life for an increasingly aged population.

"What we saw in these animals was not a slowing down or stabilisation of the ageing process. We saw a dramatic reversal – and that was unexpected," said Ronald DePinho, who led the study, which was published in the journal Nature.

"This could lead to strategies that enhance the regenerative potential of organs as individuals age and so increase their quality of life. Whether it serves to increase longevity is a question we are not yet in a position to answer."

The ageing process is poorly understood, but scientists know it is caused by many factors. Highly reactive particles called free radicals are made naturally in the body and cause damage to cells, while smoking, ultraviolet light and other environmental factors contribute to ageing.

The Harvard group focused on a process called telomere shortening. Most cells in the body contain 23 pairs of chromosomes, which carry our DNA. At the ends of each chromosome is a protective cap called a telomere. Each time a cell divides, the telomeres are snipped shorter, until eventually they stop working and the cell dies or goes into a suspended state called "senescence". The process is behind much of the wear and tear associated with ageing.

At Harvard, they bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter. Without the enzyme, the mice aged prematurely and suffered ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. But when DePinho gave the mice injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of ageing.

"These were severely aged animals, but after a month of treatment they showed a substantial restoration, including the growth of new neurons in their brains," said DePinho.

Repeating the trick in humans will be more difficult. Mice make telomerase throughout their lives, but the enzyme is switched off in adult humans, an evolutionary compromise that stops cells growing out of control and turning into cancer. Raising levels of telomerase in people might slow the ageing process, but it makes the risk of cancer soar.

DePinho said the treatment might be safe in humans if it were given periodically and only to younger people who do not have tiny clumps of cancer cells already living, unnoticed, in their bodies.

David Kipling, who studies ageing at Cardiff University, said: "The goal for human tissue 'rejuvenation' would be to remove senescent cells, or else compensate for the deleterious effects they have on tissues and organs. Although this is a fascinating study, it must be remembered that mice are not little men, particularly with regard to their telomeres, and it remains unclear whether a similar telomerase reactivation in adult humans would lead to the removal of senescent cells."

Lynne Cox, a biochemist at Oxford University, said the study was "extremely important" and "provides proof of principle that short-term treatment to restore telomerase in adults already showing age-related tissue degeneration can rejuvenate aged tissues and restore physiological function."

DePinho said none of Harvard's mice developed cancer after the treatment. The team is now investigating whether it extends the lifespan of mice or enables them to live healthier lives into old age.

Tom Kirkwood, director of the Institute for Ageing and Health at Newcastle University, said: "The key question is what might this mean for human therapies against age-related diseases? While there is some evidence that telomere erosion contributes to age-associated human pathology, it is surely not the only, or even dominant, cause, as it appears to be in mice engineered to lack telomerase. Furthermore, there is the ever-present anxiety that telomerase reactivation is a hallmark of most human cancers."

Merck cholesterol drug extremely effective in study

http://www.reuters.com/article/idUSN1719543320101117

Wed, Nov 17 2010
* Raises good HDL cholesterol 138 pct
* Cuts bad LDL cholesterol 40 pct in patients on statins
* No safety or torcetrapib-like problems observed
* 30,000-patient outcomes study to begin in 2011 Q2
By Bill Berkrot and Ransdell Pierson
NEW YORK/CHICAGO, Nov 17 (Reuters) - An experimental Merck & Co (MRK.N: Quote, Profile, Research, Stock Buzz) heart drug, from a class of medicine with a troubled past, appeared to be safe and had a "jaw dropping" effect on both good and bad cholesterol levels, according to data from a clinical trial.
Merck's anacetrapib increased good HDL levels by a stunning 138 percent after 24 weeks of treatment, and lowered levels of bad LDL cholesterol by 40 percent in patients already taking LDL-lowering statins, researchers said.
"The lipid effects are jaw dropping in both directions," said Dr. Christopher Cannon, the study's lead investigator from Brigham and Women's Hospital in Boston. He presented the data at the American Heart Association scientific meeting in Chicago on Wednesday.
Researchers found no anacetrapib safety issues during the 18-month study, and patients receiving the drug had fewer serious heart problems than those given a placebo.
Even if development of the medicine continues without a hitch, it will likely be at least five years before Merck can begin selling the drug.
Anacetrapib belongs to a class of drugs called CETP inhibitors that produced one of the most spectacular clinical failures in pharmaceutical history. A pivotal study of Pfizer Inc's (PFE.N: Quote, Profile, Research, Stock Buzz) highly touted torcetrapib was stopped in late 2006 after higher death rates were found among those taking the drug, pulling the plug on an $800 million Phase III program.
Based on the data from the anacetrapib trial, called Define, "we are 94 percent confident that anacetrapib doesn't have the clinical (side) effects of torcetrapib," Cannon said.
The HDL increase seen with anacetrapib "is double what torcetrapib does; it's four times what niacin can do if you can push niacin to its full 2 gram dose; and 10 times the effect seen with statins," Cannon said, comparing anacetrapib with other therapies.
It is believed that HDL has a heart protective effect, possibly by carrying LDL away from the arteries.
Anacetrapib also cut by 36 percent levels of LP(a), which is believed to be an independent cardiovascular risk factor.
The 1,623-patient, 18-month Define trial was designed to show anacetrapib does not have the unintended effects on blood chemistry and blood pressure found in detailed analyses of what went wrong with the Pfizer drug.
"It's been found that torcetrapib unfortunately as a molecule somehow lands itself in the adrenal gland and then pumps out aldosterone, other hormones, and has all these effects," Cannon explained.
Compared with the placebo group, patients receiving anacetrapib in the study showed no difference in electrolytes, aldosterone or blood pressure, and no other safety concerns were seen with the drug, he said.
"This trial was set up so that we would have some more reassurance that the drug was safe before doing a gigantic trial. And that's what we found, that it looks safe so far," Cannon said.
In the wake of torcetrapib, Merck has long known that to gain approval for anacetrapib, it will have to conduct a large so-called outcomes trial to prove its drug cuts heart attacks and death rather than just impacts cholesterol levels.
Plans for such a study were announced on Wednesday. It will include some 30,000 patients at high risk of heart attack or other serious heart problems, and take about four years to complete. Enrollment is expected to begin in the second quarter of 2011, researchers said.
Patients in the 18-month Define study all had coronary disease or were at high risk for heart disease, and were already taking a statin, such as Lipitor, to lower their LDL levels. They received either 100 milligrams of anacetrapib or a placebo once a day on top of their statin.
At the start of the study, patients on average had a baseline HDL of 40 and LDL of 81. Those on anacetrapib on average saw HDL leap to 101 and LDL drop to 45. HDL levels of placebo patients rose only to 46, while LDL fell to 77.
Patients whose LDL dropped below 25 were taken off the drug as a precaution, which was part of the study's design. "We didn't see any problems, but this gets the LDL down as low as its ever been in any study," Cannon said.
Researchers observed a trend toward lower rates of cardiovascular death, heart attack, stroke and hospitalization for unstable angina. The need for angioplasty or bypass surgery over 18 months was significantly lower on anacetrapib -- eight patients versus 28 on placebo.
While the dramatic impact on HDL is clear, it remains to be determined if raising it through the CETP inhibitor mechanism can save lives and hospitalizations.
Roche (ROG.VX: Quote, Profile, Research, Stock Buzz) and Japan Tobacco (2914.T: Quote, Profile, Research, Stock Buzz) are also forging ahead with development of a CETP inhibitor, called dalcetrapib.
"There is very real uncertainty as to what anacetrapib will do on clinical outcomes," said Rory Collins, co-director of the clinical trial service unit at the University of Oxford, who will lead the outcomes study program.
"It is incredibly exciting. It could be really the next big thing in cardiovascular disease," Collins said. (Reporting by Bill Berkrot and Randell Pierson; editing by John Wallace)

Researchers Grow a Liver in a Lab Setting

Researchers have created a buzz in the organ transplant world by growing a liver in a lab setting. However, this liver may function just like any other liver but it is miniature, a test to see if the technology was possible. The group used stem cells to create the liver which is said to be genetically identical to that of a human liver.
The idea that human organs can be grown in labs has been the stuff of science fiction novels for years. However, it has become a reality these days. Still, the researchers have said that it will be years before the technology and science are advanced far enough to create full size organs.
When the advancements are complete it will revolutionize the transplant world. Patients will no longer have to wait years for a new organ when one can be specifically grown for them in a lab setting.
One issue is the fact that these organs are designed by using stem cell research. This gives them a specific DNA structure that must be unique to the patient. Stem cell research has only recently restarted in the US after President Obama lifted a ban imposed by former President Bush.
Organ transplants are a hot commodity in this world today. Black markets buy and sell organs through underground medical facilities, often causing fatalities when the patients develop infections from unsterile conditions.
With the advancement of lab grown organs research may be able to save the lives of millions every year.

Short URL: http://thenewsportalonline.com/?p=3946

Brain Connections Break Down as We Age, Study Suggests

http://www.sciencedaily.com/releases/2010/08/100818151822.htm


The circled portion of the older adult' brain on the left indicates the cross-talk between the two hemispheres that is not apparent in the younger brain on the right. Click above image for higher resolution. (Credit: Rachael Seidler)
ScienceDaily (Aug. 19, 2010) — It's unavoidable: breakdowns in brain connections slow down our physical response times as we age, a new study suggests.

This slower reactivity is associated with an age-related breakdown in the corpus callosum, a part of the brain that acts as a dam during one-sided motor activities to prevent unwanted connectivity, or cross-talk, between the two halves of the brain, said Rachael Seidler, associate professor in the University of Michigan School of Kinesiology and Department of Psychology, and lead study author.

At other times the corpus callosum acts at a bridge and cross-talk is helpful, such as in certain cognitive functions or two-sided motor skills.

The U-M study is the first known to show that this cross-talk happens even while older adults are at rest, said Seidler, who also has appointments in the Institute of Gerontology and the Neuroscience Graduate Program. This resting cross-talk suggests that it is not helpful or compensatory for the two halves of the brain to communicate during one-sided motor movements because the opposite side of the brain controls the part of the body that is moving. So, when both sides of the brain talk simultaneously while one side of the body tries to move, confusion and slower responses result, Seidler said.

Previous studies have shown that cross-talk in the brain during certain motor tasks increases with age but it wasn't clear if that cross-talk helped or hindered brain function, said Seidler.

"Cross-talk is not a function of task difficulty, because we see these changes in the brain when people are not moving," Seidler said.

In some diseases where the corpus callosum is very deteriorated, such as in people with multiple sclerosis, you can see "mirror movements" during one sided-motor tasks, where both sides move in concert because there is so much communication between the two hemispheres of the brain, Seidler said. These mirror movements also happen normally in very young children before the corpus callosum is fully developed.

In the study, researchers gave joysticks to adults between the ages of 65 and 75 and measured and compared their response times against a group approximately 20-25 years old.

Researchers then used a functional MRI to image the blood-oxygen levels in different parts of the brain, a measurement of brain activity.

"The more they recruited the other side of the brain, the slower they responded," Seidler said.

However there is hope, and just because we inevitably age doesn't mean it's our fate to react more slowly. Seidler's group is working on developing and piloting motor training studies that might rebuild or maintain the corpus callosum to limit overflow between hemispheres, she said.

A previous study done by another group showed that doing aerobic training for three months helped to rebuild the corpus callosum, she said, which suggests that physical activity can help to counteract the effects of the age-related degeneration.

Seidler's group also has a study in review that uses the same brain imaging techniques to examine disease related brain changes in Parkinson's patients.

The study appeared in the journal Frontiers in Systems Neuroscience.

Newts' ability to regenerate tissue replicated in mouse cells

Found at: http://www.physorg.com/news200224844.html

August 5, 2010
Tissue regeneration a la salamanders and newts seems like it should be the stuff of science fiction. But it happens routinely. Why can't we mammals just re-grow a limb or churn out a few new heart muscle cells as needed? New research suggests there might be a very good reason: Restricting our cells' ability to pop in and out of the cell cycle at will -- a prerequisite for the cell division necessary to make new tissue -- reduces the chances that they'll run amok and form potentially deadly cancers.


Now scientists at the Stanford University School of Medicine have taken a big step toward being able to confer this regenerative capacity on mammalian muscle cells; they accomplished this feat in experiments with laboratory mice in which they blocked the expression of just two tumor-suppressing proteins. The finding may move us closer to future regenerative therapies in humans — surprisingly, by sending us shimmying back down the evolutionary tree.

"Newts regenerate tissues very effectively," said Helen Blau, PhD, the Donald E. and Delia B. Baxter Professor and a member of Stanford's Institute for Stem Cell Biology and Regenerative Medicine. "In contrast, mammals are pathetic. We can regenerate our livers, and that's about it. Until now it's been a mystery as to how they do it."

Blau is the senior author of the research, which will be published in Cell Stem Cell on Aug. 6. Kostandin Pajcini, PhD, a former graduate student, and Jason Pomerantz, MD, a former postdoctoral scholar in Blau's laboratory, are primarily responsible for the work and are first author and co-senior author, respectively.

Although there's been a lot of discussion about using adult or embryonic stem cells to repair or revitalize tissues throughout the body, in this case the researchers weren't studying stem cells. Instead they were investigating whether myocytes, run-of-the mill muscle cells that normally don't divide, can be induced to re-enter the cell cycle and begin proliferating. This is important because most specialized, or differentiated, cells in mammals are locked into a steady state that does not allow cell division. And without cell division, it is not possible to get regeneration.

In contrast, the cells of some types of amphibians are able to replace lost or damaged tissue by entering the cell cycle to give rise to more muscle cells. While doing so, the cells maintain their muscle identity, which prevents them from straying from the beaten path and becoming other, less useful cell types.


Pomerantz and Blau wondered if it could be possible to coax mammalian cells to follow a similar path. To do so, though, they needed to pinpoint what was different between mammalian and salamander cells when it comes to cell cycle control. One aspect involves a class of proteins called tumor suppressors that block inappropriate cell division.
Previous research had shown that a tumor suppressor called retinoblastoma, or Rb, plays an important role in preventing many types of specialized mammalian cells, including those found in muscle, from dividing willy-nilly. But the effect of blocking the expression of Rb in mammalian cells has been inconsistent: In some cases it has allowed the cells to hop back into the cell cycle; in others, it hasn't.

The researchers employed some evolutionary detective work to figure out that another tumor suppressor called ARF might be involved. Like Rb, ARF works to throw the brakes on the cell cycle in response to internal signals. An examination of the evolutionary tree provided a key clue. They saw that ARF first arose in chickens. It is found in other birds and mammals, but not in animals like salamanders nestled on the lower branches. Tellingly, it's also missing in cell lines that begin cycling when Rb is lost, and it is expressed at lower-than-normal levels in mammalian livers — the only organ that we humans can regenerate.

Based on previous investigators' work with newts, Blau said it "seemed to us that they don't have the same limitations on growth. We hypothesized that maybe, during evolution, humans gained a tumor suppressor not present in lower animals at the expense of regeneration."

Sure enough, Pajcini and Pomerantz found that blocking the expression of both Rb and ARF allowed individual myocytes isolated from mouse muscle to dedifferentiate and begin dividing. When they put the cells back into the mice, they were able to merge with existing muscle fibers — as long as Rb expression was restored. Without Rb the transplanted cells proliferated excessively and disrupted the structure of the original muscle.

"These myocytes have reached the point of no return," said Blau. "They can't just start dividing again. But here we show that temporarily blocking the expression of just two proteins can restore an ancient ability to contribute to mammalian muscle."
The key word here is "temporarily." As is clear from the mouse experiments, blocking the expression of tumor suppressors in mammalian cells can be a tricky gambit. Permanently removing these proteins can lead to uncontrolled cell division. But, a temporary and well-controlled loss — as the researchers devised here — could be a useful therapeutic tool.

The research required some sophisticated technology to separate individual myocytes from one another for study. To do so, Pajcini traveled to Munich to learn how to optimize a technique normally used on cryopreserved and fixed tissue sections — "laser micro-dissection catapulting" — for use with living cells. But the effort paid off when he was able to prove conclusively that once the expression of the two proteins was blocked, individual live cells were, in fact, dividing in culture.

Next, the researchers would like to see if the technique works in other cell types, like those of the pancreas or the heart, and whether they can induce it to happen in tissue at sites of injury. If so, it may be possible to trigger temporary cell proliferation as a means of therapy for a variety of ailments.
Provided by Stanford University Medical Center

'Grow-your-own' organs hope after scientists produce liver in lab from stem cells

http://www.dailymail.co.uk/health/article-1286266/Scientists-grow-laboratory-liver-giving-hope-millions-diseased-organs.html##ixzz0u3oK7EdV


Scientists have grown a liver in a laboratory, offering fresh hope to hundreds of thousands of patients with diseased and damaged organs.

It raises the prospect of those in need of transplants one day being offered livers that are ‘made to order’.

The first pieces of lab-grown livers could be used in hospitals within just five years, the researchers said.


Patches of artificial tissue could be used to repair livers damaged by injury, disease, alcohol abuse and paracetamol overdose.

Other possibilities include sections of artificial livers to keep those needing transplants alive – in much the same way as a dialysis machine is used to treat kidney failure.

At least one million of Britons live with liver disease and it claims more than 16,000 lives a year – more than diabetes and traffic accidents combined. Up to 600 transplants are carried out a year.

The latest experiments, which were carried out on animal livers, are still in the early stages but could one day lead to an alternative supply of organs.

The process began with a donor liver being ‘washed’ in detergent, stripping it of its cells, leaving only a collagen and blood vessel ‘scaffold’ in which the new liver cells could grow.

The U.S. scientists then injected it with up to 200 million healthy liver cells, in four shots, each ten minutes apart.

The cells spread across the scaffold, and, provided with an artificial blood supply, the liver survived in a petri dish for up to ten days, the journal Nature Medicine reports.

Tests showed that, just like a real liver, it was capable of breaking up toxins.

The researchers, from Massachusetts General Hospital, Boston, also transplanted the liver into a rat, for several hours.

Lead researcher Dr Korkut Uygun said: ‘As far as we know, a transplantable liver graft has never been constructed in a laboratory setting before.

‘Even though this is very exciting and promising, it is a proof-of-concept study only. Much more work will be required to make long-term functional liver grafts that can actually be transplanted into humans.

‘We haven’t been able to go beyond several hours in rats, but it’s a great start.’

Hurdles to overcome include creating a liver with all the types of cells needed for full function, including specialised cells that destroy bacteria and other invaders.

A spokesman for the British Liver Trust said: 'We find these insights very interesting, particularly the concept of making sub-standard livers suitable for transplantation. The results from this study holds promise however it is a long way from helping liver patients.

'We desperately need to increase the supply of donor organs and see new treatments for advanced liver disease. Everyone has a role to play by joining the organ donor register and talking to their families about their wishes.'

Scientists Theorize Why Black Athletes Run Fastest

Twenty-eight of the last 38 world record holders in the men's 100-meter dash have been black athletes, and researchers at two universities think they know why.

A new study by researchers at Howard University, a historically black school in Washington D.C., and Duke University in North Carolina suggests why black athletes may outperform athletes of other races in running events. Physical differences in the length of the limbs and the structure of the body mean the center of gravity tends to be higher in the bodies of black people, the researchers say.

Since 1968, the world record holders in the men's 100-meter dash have been black athletes. And since 1912, when the International Association of Athletics Federations started keeping track of the record holders in that event, only 10 non-black athletes out of 38 individuals have held the title.

"There is a whole body of evidence showing that there are distinct differences in body types among blacks and whites," said researcher Edward Jones, who researches adolescent obesity, nutrition and body composition at Howard University. "These are real patterns being described here. Whether the fastest sprinters are Jamaican, African or Canadian, most of them can be traced back generally to Western Africa."

Why center of gravity matters

Although there are also cultural factors at work, it all comes down to body makeup, Jones said.

"Blacks tend to have longer limbs with smaller circumferences, meaning that their centers of gravity are higher compared to whites of the same height," said Adrian Bejan, Jones' co-author, an engineering professor at Duke University. "Asians and whites tend to have longer torsos, so their centers of gravity are lower."

"These differences are small, and we don't really see them when we look at someone," Bejan told Life's Little Mysteries. "We are only rarely struck by how long someone's legs are."

But these small differences certainly matter in races lasting less than 10 seconds, Bejan said.

The height of a person's center of gravity affects how fast his feet are moving when they hit the ground, Bejan said. Each step a runner takes is like falling except the athlete breaks the fall with his foot. So the feet of a person with a higher center of gravity will hit the ground faster than someone with a lower center of gravity.

Torsos and legs

In the study, the scientists gathered data available from the militaries of 17 nations. Militaries measure their recruits for uniform fittings and are a reliable source of data, Bejan said. To approximate torso length, the scientists compared the average height of the military men with their sitting height - the distance from a chair to the top of the head.

Results showed the average sitting height of blacks was about 1.5 inches (3 cm) shorter than that of whites who were the same height. This means that, among blacks and whites of the same height, the legs of blacks were longer (think of a high-waisted person), while the torsos of whites were longer.

This physical difference gives a black athlete an advantage, even against an athlete of another race is who is taller and has a higher center of gravity, said Bejan. From a physics perspective, Bejan said, the legs do the work of running and the torso of the body is just extra weight that the legs must carry, so the race goes to the runners with longer legs and shorter torsos.

By contrast, whites tend to have the advantage in swimming, where a longer torso allows for faster speeds.

"Swimming actually generates a wave. The sport is the art of surfacing on that wave. When the wave is bigger - because the torso is longer - they go faster," Bejan said.

The study was published online this week in the International Journal of Design and Nature and Ecodynamics.

Oncologists cool on prostate test

Hormone-infused nasal spray found to help people with autism

By Rob Stein
Washington Post Staff Writer
Tuesday, February 16, 2010; A02

A nasal spray containing a hormone that is known to make women more maternal and men less shy apparently can help those with autism make eye contact and interact better with others, according to a provocative study released Monday.

The study, involving 13 adults with either a high-functioning form of autism or Asperger syndrome, a mild form of the disorder, found that when the subjects inhaled the hormone oxytocin, they scored significantly better on a test that involved recognizing faces and performed much better in a game that involved tossing a ball with others.

Although more research is needed to confirm and explore the findings, the results are the latest in a growing body of evidence indicating that the hormone could lead to ways to help people with the often devastating brain disorder function better.

"This is the first study that looked at whether oxytocin has an effect on social behavior, which is a major deficit in autism," said Angela Sirigu, who directs the National Center for Scientific Research in France and led the study, published online by the Proceedings of the National Academy of Sciences. "It looks like it could be very helpful."

Researchers who were not involved in the study praised the work, saying the findings were promising and could lead to the first effective treatment for the central problems affecting people with autism.

"I think it's going to be a very exciting finding for a lot of people," said Alex Martin, chief of cognitive neuropsychology at the National Institute of Mental Health.

Because oxytocin does not last long in the body and produces its effects for a relatively brief period, some experts said the findings were more likely to encourage drug companies to develop alternative substances that had the same benefits.

"This paper suggests that's worth doing," said Thomas R. Insel, director of the institute. "It adds another brick in the wall that suggests there may be an opportunity to develop treatment for one of the core symptoms of autism. That's been the brass ring."

But Sirigu was among those who said the finding should encourage more research on the potential benefits of oxytocin itself, especially for children. Administering the hormone soon after a child's autism is diagnosed might help him or her develop more normally, she said.

"It's possible it can become a cure, if it's given early when the problems are detected in the little kids," Sirigu said. "We can change the way these patients interact with people from childhood."

Because previous research has indicated that some people with autism might have abnormally low levels of oxytocin, conducting tests to identify those people and administering them the hormone might help as well, said Karen Parker, an assistant professor of psychiatry at Stanford University School of Medicine.

"If you can find someone who appears to have deficits in oxytocin biology, giving them what you might argue would be replacement oxytocin may be helpful," Parker said.

Autism is a baffling disorder that can cause a variety of symptoms, including speech and learning problems and profound, disabling difficulties understanding emotions and social cues when interacting with people. The number of children found to have autism has been increasing for reasons that remain mysterious.

Oxytocin is produced naturally in the bodies of humans and animals. It plays a key role in social interaction, promoting maternal behavior and monogamy in animals. The hormone also heightens social sensitivity, social awareness, generosity and trust in people.

Previous U.S. studies found that people with autism who received the hormone intravenously were less likely to engage in repetitive behavior that is another hallmark of autism and were more likely to be able to identify emotions in voices. Another study being published in the journal Biological Psychiatry found that 16 autistic males in Australia ages 12 to 19 who received the hormone through a nasal spray were better able to recognize other people's facial expressions.

"All the data seem to suggest that manipulating the oxytocin system has a powerful effect on the core symptoms of autism," said Eric Hollander, director of the compulsive, impulsive and autism spectrum disorders program at the Montefiore Medical Center in New York.

While cautioning that more research is needed on children and additional patients to make sure oxytocin is safe and effective, advocates for families with children with autism welcomed the findings. Oxytocin has been in use for several years as an "alternative" therapy for autism.

"Many families are using it with success and reporting improvement," said Wendy Fournier, president of the National Autism Association. "Getting double-blind clinical studies like this one published helps to bring credibility to parental reports."

"We need to be mindful of the fact that the majority of human studies of oxytocin have been conducted using adults, including this study, and only one paper has included individuals between the ages of 12 and 18. We have to be careful about the safety and efficacy of oxytocin on pediatric populations," said Clara Lajonchere, vice president of clinical programs for Autism Speaks.

Research points to link between low vitamin D, mortality

A new study shows that people with higher levels of the vitamin D were less likely to die from a a variety of causes - including cardiovascular disease, the No. 1 killer of Canadians - following an eight-year study.

BY CANWEST NEWS SERVICEJUNE 23, 2008


In the latest run of good news for vitamin D comes a new study showing that people with higher levels of the “sunshine” vitamin were less likely to die from any cause - including cardiovascular disease, the No. 1 killer of Canadians - after eight years of tracking.

The finding held even when researchers took coronary artery disease, exercise and other factors into account.

Low vitamin D levels “can be considered a strong risk indicator for all-cause mortality in women and in men,” researchers report Tuesday in the journal Archives of Internal Medicine.

By the time the paper had been accepted for publication, the team had dug deeper and found low vitamin D status “had other significant negative effects in terms of incidence of cancer, stroke, sudden cardiac death and death of heart failure,” lead author Dr. Harald Dobnig, of the Medical University of Graz in Austria, said in an e-mail.

It’s still not “ultimate proof” of the harmful effects of too little vitamin D, he says. “But the evidence is just becoming overwhelming at this point.”

Researchers can’t rule out that sicker patients had lower vitamin D levels and, therefore, were already at an increased risk of dying to begin with.

But, “this was not a bedridden, immobile or very sick population that we studied,” Dobnig says. People with an acute illness other than cardiac disease were excluded from the study.

“Low levels of vitamin D may carry a potential health risk,” Dobnig says. “Physicians should be aware of the widespread problem of low vitamin D status.”

He says those at high risk for vitamin D deficiency - including the elderly, nursing home residents and people who work night shifts or spend a lot of time indoors - should take 800 international units of vitamin D3 daily. “Whether we can go to higher (or even much higher) doses is unclear at the moment.”

About 50 to 60 per cent of older adults in North America are low in vitamin D, and it also seems to be a widespread problem in children as well.

In the past year, studies have linked low vitamin D to an increased risk of cancers, notably breast, colon and endometrial cancers, as well as multiple sclerosis - a disease more common in northern countries. And, in back-to-back studies this month, researchers reported that men with too little vitamin D appear to be at increased risk of heart attacks, while colon cancer patients with abundant vitamin D were less likely to die during followup.

The new study is based on 3,258 consecutive patients scheduled for an angiogram - an X-ray to check for abnormalities in the arteries — at a medical centre in Germany between 1997 and 2000.

Before and after the test, their blood was measured for vitamin D3, and a compound called 25-hydroxyvitamin D, considered the best indicator of a person’s vitamin D status.

After an average followup of nearly eight years, 737 people (about 23 per cent) had died, including 463 who died of cardiovascular causes.

People who had 25-hydroxyvitamin D levels in the lower half of the vitamin D range were up to twice as likely to die during the followup period compared with those in the highest. Similar results were found in people with the lowest levels of vitamin D3.

Overall, two-thirds of the patients had coronary artery disease. But whether or not they had signs of congestive heart failure or artery disease, low levels of vitamin D were “always significantly associated” with a higher risk of death, Dobnig says.

People with low vitamin D had signs of inflammation and oxygen-related damage to cells, “which all points towards a higher vascular risk profile,” Dobnig says.

“This is the first study showing a significant association between serum (blood) vitamin D levels and risk of all-cause and cardiovascular mortality,” he says.

But it’s just that - an association, cautions Dr. Beth Abramson, a cardiologist at St. Michael’s Hospital in Toronto and spokeswoman for the Heart and Stroke Foundation.

People with higher vitamin D levels tended to be healthier and more fit. Rather than focus on a “trendy risk factor,” Abramson says Canadians should be aware of traditional risk factors for heart disease, such as high blood pressure, high cholesterol, smoking, diabetes and a family history of the disease.

Roughly 80 to 90 per cent of 25-hydroxyvitamin D is derived from exposure to sunlight, the rest from foods, such as fatty fish and eggs, Dobnig says. But in Canada, our bodies can’t make the vitamin under weak fall and winter sunlight, and experts say more research is needed about the amount of sunlight exposure needed to achieve the optimum vitamin D levels.

As well, sun exposure increases skin cancer risk. “Don’t sit and bake. There’s no evidence that’s helping you in the long run,” Abramson says.

Tengion Pipeline as of December 2009

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