Day: 11/07/2013

Fountain of youth? Scientists discover why wounds heal quicker for young people

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Fountain of youth? Scientists discover why wounds heal quicker for young people .

The mystery of why wounds heal more quickly in the young compared to the elderly may soon be solved following the discovery of two of the genes involved in tissue regeneration.

Scientists believe that the findings will help to develop new drugs and treatments for faster wound-healing as well as shedding light on the ageing process itself, and what could amount to a genetic “fountain of youth”.

Two teams of researchers found separate genes that accelerate tissue regeneration in laboratory mice. Both genes, which are also present in the human genome, are more active in young mice compared to older mice.

The scientists believe that the genes, called Lin28a and IMP1, are designed to be especially active during the foetal stages of development and are gradually turned off as an animal ages – which could explain why wounds take longer to heal in the elderly and how ageing occurs.

One of the teams, led by George Daley of the Boston Children’s Hospital and Harvard Medical School, activated the Lin28a gene in adult mice and found that shaved fur on their backs grew back much faster than in ordinary adult mice where the gene had not be artificially boosted.

“It sounds like science fiction, but Lin28a could be part of a healing cocktail that gives adults the superior tissue repair seen in juvenile animals,” said Dr Daley, whose study is published in the journal Cell.

Asked what the implications are for human health, Dr Daley said: “My strongest conclusion is that Lin28a, or drug manipulations that mimic the metabolic effects of Lin28a, enhances wound healing and tissue repair, and thus in the future might translate into improved healing of wounds after surgery or trauma in patients.”

The study revealed that the Lin28a gene is responsible for a protein that binds to the key molecules of RNA involved in the metabolism of energy within the mitochondria, the “power packs” of the cells. The result is that when the gene is active, the cells are better and more efficient at repairing themselves – the activated genes also accelerated the repair of injuries.

Tissue regeneration is important in early foetal development and when damaged tissues need to be healed. A gradual loss of tissue regeneration and repair is one of the hallmarks of ageing so anything that could improve it could lead to anti-ageing treatments

“We were surprised that what was previously believed to be a mundane cellular ‘housekeeping’ function would be so important for tissue repair,” said Shyh-Chang Ng of Harvard Medical School, the lead author of the Cell study.

“One of our experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing, suggesting that it could be possible to use drugs to promote tissue repair in humans.”

The second gene, IMP1, also produces a protein that binds to the RNA molecules, but this time it promotes the self-renewal of key stem cells during foetal development, and also during tissue repair in later life, said Hao Zhu of the University of Texas in Dallas.

“This finding opens up an exciting possibility that metabolism could be modulated to improve tissue repair, whereby metabolic drugs could be employed to promote regeneration,” Dr Zhu said.

Scientists believe that the findings will help to develop new drugs and treatments for faster wound-healing as well as shedding light on the ageing process itself, and what could amount to a genetic “fountain of youth”.

Two teams of researchers found separate genes that accelerate tissue regeneration in laboratory mice. Both genes, which are also present in the human genome, are more active in young mice compared to older mice.

The scientists believe that the genes, called Lin28a and IMP1, are designed to be especially active during the foetal stages of development and are gradually turned off as an animal ages – which could explain why wounds take longer to heal in the elderly and how ageing occurs.

One of the teams, led by George Daley of the Boston Children’s Hospital and Harvard Medical School, activated the Lin28a gene in adult mice and found that shaved fur on their backs grew back much faster than in ordinary adult mice where the gene had not be artificially boosted.

“It sounds like science fiction, but Lin28a could be part of a healing cocktail that gives adults the superior tissue repair seen in juvenile animals,” said Dr Daley, whose study is published in the journal Cell.

Asked what the implications are for human health, Dr Daley said: “My strongest conclusion is that Lin28a, or drug manipulations that mimic the metabolic effects of Lin28a, enhances wound healing and tissue repair, and thus in the future might translate into improved healing of wounds after surgery or trauma in patients.”

The study revealed that the Lin28a gene is responsible for a protein that binds to the key molecules of RNA involved in the metabolism of energy within the mitochondria, the “power packs” of the cells. The result is that when the gene is active, the cells are better and more efficient at repairing themselves – the activated genes also accelerated the repair of injuries.

Tissue regeneration is important in early foetal development and when damaged tissues need to be healed. A gradual loss of tissue regeneration and repair is one of the hallmarks of ageing so anything that could improve it could lead to anti-ageing treatments

“We were surprised that what was previously believed to be a mundane cellular ‘housekeeping’ function would be so important for tissue repair,” said Shyh-Chang Ng of Harvard Medical School, the lead author of the Cell study.

“One of our experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing, suggesting that it could be possible to use drugs to promote tissue repair in humans.”

The second gene, IMP1, also produces a protein that binds to the RNA molecules, but this time it promotes the self-renewal of key stem cells during foetal development, and also during tissue repair in later life, said Hao Zhu of the University of Texas in Dallas.

“This finding opens up an exciting possibility that metabolism could be modulated to improve tissue repair, whereby metabolic drugs could be employed to promote regeneration,” Dr Zhu said.

Scientists believe that the findings will help to develop new drugs and treatments for faster wound-healing as well as shedding light on the ageing process itself, and what could amount to a genetic “fountain of youth”.

Two teams of researchers found separate genes that accelerate tissue regeneration in laboratory mice. Both genes, which are also present in the human genome, are more active in young mice compared to older mice.

The scientists believe that the genes, called Lin28a and IMP1, are designed to be especially active during the foetal stages of development and are gradually turned off as an animal ages – which could explain why wounds take longer to heal in the elderly and how ageing occurs.

One of the teams, led by George Daley of the Boston Children’s Hospital and Harvard Medical School, activated the Lin28a gene in adult mice and found that shaved fur on their backs grew back much faster than in ordinary adult mice where the gene had not be artificially boosted.

“It sounds like science fiction, but Lin28a could be part of a healing cocktail that gives adults the superior tissue repair seen in juvenile animals,” said Dr Daley, whose study is published in the journal Cell.

Asked what the implications are for human health, Dr Daley said: “My strongest conclusion is that Lin28a, or drug manipulations that mimic the metabolic effects of Lin28a, enhances wound healing and tissue repair, and thus in the future might translate into improved healing of wounds after surgery or trauma in patients.”

The study revealed that the Lin28a gene is responsible for a protein that binds to the key molecules of RNA involved in the metabolism of energy within the mitochondria, the “power packs” of the cells. The result is that when the gene is active, the cells are better and more efficient at repairing themselves – the activated genes also accelerated the repair of injuries.

Tissue regeneration is important in early foetal development and when damaged tissues need to be healed. A gradual loss of tissue regeneration and repair is one of the hallmarks of ageing so anything that could improve it could lead to anti-ageing treatments

“We were surprised that what was previously believed to be a mundane cellular ‘housekeeping’ function would be so important for tissue repair,” said Shyh-Chang Ng of Harvard Medical School, the lead author of the Cell study.

“One of our experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing, suggesting that it could be possible to use drugs to promote tissue repair in humans.”

The second gene, IMP1, also produces a protein that binds to the RNA molecules, but this time it promotes the self-renewal of key stem cells during foetal development, and also during tissue repair in later life, said Hao Zhu of the University of Texas in Dallas.

“This finding opens up an exciting possibility that metabolism could be modulated to improve tissue repair, whereby metabolic drugs could be employed to promote regeneration,” Dr Zhu said.

Massive DNA volunteer hunt begins

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DNA

Scientists are looking for 100,000 volunteers prepared to have their DNA sequenced and published online for anyone to look at.

The UK Personal Genome Project could provide a massive free tool for scientists to further understanding of disease and human genetics.

Participants will get an analysis of their DNA, but so will the rest of the world, and anonymity is not guaranteed.

They are warned there could be unknown consequences for them and relatives.

Unlocking the secrets of DNA could transform the understanding of disease.

“Start Quote

There is potentially huge public benefit, but there is the potential for it to rebound, but how that rebounds on the person, families and those yet to be born is very difficult to know”

Dr Peter Mills Nuffield Council on Bioethics

A deeper understanding of Alzheimer’s disease is emerging by looking for differences in the DNA of people with and without the disease.

Prof George Church, who runs the US version of the project, said analysing 100,000 genomes could lead to advances in common diseases such as diabetes.

He said: “We’re finding more and more of these common diseases are a collection of rare diseases.

“Cancer used to be a disease, then it broke up into lots of different diseases by tissue, then lots of sub-categories based on the genes that are impacted, so now it’s thousands of diseases.”

Participants will have to pass tests to prove they fully understand the risks of making their genetic identities freely available for the world to use before taking part.

There will be immediate risks and those that emerge as genetic technology advances including:

  • finding out about a genetic disease
  • a partner being put off by a higher risk of Alzheimer’s or other illnesses
  • targeted advertising or insurance premiums based on genomes
  • cloning without permission
  • copies of DNA being used to implicate people in a crime

Family factor

Dr Peter Mills, who is investigating the ethical issues around biological and health data with the Nuffield Council on Bioethics, told the BBC: “The difference with genetic data is you’re not just committing yourself to something you might not fully envisage, but you’re also implicating biological relatives.

“Start Quote

Human Genetics Alert would strongly advise people not to give their genetic information to a project which will share it with the world”

Dr David King Human Genetics Alert

“There is potentially huge public benefit, but there is the potential for it to rebound, but how that rebounds on the person, families and those yet to be born is very difficult to know.”

Cian Murphy, a 24-year-old PhD student at University College London, wants to take part. He said: “Very few people live their whole lives not affected by some genetic illness, your sample could be the difference between a cure being discovered or not.”

As part of the study, participants will find out intimate details about their genome, such as the presence of any high-risk breast-cancer genes.

They will be given a list of doctors they can go to if they need further medical advice.

While people will not have their name published, studies have shown it is possible to work out someone’s identity from genetic databases and other public records.

Dr David King, from the group Human Genetics Alert, said: “Human Genetics Alert would strongly advise people not to give their genetic information to a project which will share it with the world.

“Once your data is online, you will never be able to recall it. The project’s informed-consent procedures are not valid, because they do not tell you all of the risks. That is not informed consent.”

He warned the data could be used for any purpose including those people objected to ethically and said there was “no reason” for it to be public.

More genomes

Meanwhile, the government’s Genomics England project is trying to sequence 100,000 NHS patient’s DNA, which is private and carries a threat of legal action if patients are identified.

Sir John Chisholm, executive chairman of Genomics England, said: “We would want anyone consenting to their DNA being used for sequencing to have a clear understanding of what they are contributing to, and to do so on a voluntary basis which we understand will be the case with Personal Genome Project.

“Anyone who takes part in any initiative that involves giving a DNA sample for sequencing should be as clear at the time of giving their consent as they can be of how that sample will be used, and who will have access to it, and what future purposes it can be put to.”

‘King of gore’ dinosaur discovered

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A new super-predator dinosaur that roamed the Earth 80 million years ago has been discovered in southern Utah.

It was closely related to its slightly larger relative, Tyrannosaurus rex, but lived earlier, making it the largest living land predator of its time.

Growing to about 30ft (9m) long, the predator has been named Lythronax argestes which means “king of gore”.

The research, published in the journal Plos One, highlights once more that the age of discovery is far from over.

The team also hopes this new find will help uncover what the climate was like towards the end of the age of dinosaurs.

“It’s always exciting to find new species but what’s really significant is what these species tell us about their ancient world,” said Randall Irmis, co-author of the study at the Natural History Museum of Utah, US.

“This was a very different place 80 million years ago. It was a very lush, wet, tropical environment and there were no polar ice caps at the time.”

Tyrannosaurid dinosaurs

Artist's impression of the new tyrannosaur Lythronax announced by paleontologists
  • Lythronax belongs to a group of carnivorous dinosaurs called Tyrannosaurids, the same group as the T. rex
  • They are the greatest carnivores – though not the largest – to have walked the Earth
  • Lived in the Late Cretaceous Period, between 95-70 million years ago
  • The new find lived on a strip of land called Laramidia in western North America
  • This same area was home to a range of species such as the the horned and duck billed dinosaurs
  • Recently an unusual new species of horned dinosaur with a big nose was also discovered in the area

Short snout

First discovered in 2009, the partial skeleton included a number of bones from the skull and some from the rest of the body. The fossils were then excavated and studied in the lab.

The new discovery was closely related to T. rex and shows that similar features evolved 10 million years earlier than previously thought.

Lythronax had a short and narrow snout and forward slanting eyes. Like its evolutionary relative, it had a head full of sharp teeth and was a ferocious predator, the largest of its ecosystem.

The team also uncovered the most complete fossils of another named species of Tyrannosaur – Teratophoneus curriei. It was previously only known from a few skull bones but the team now have more than 70% of its skeleton.

“There’s a whole diversity of different branches of the Tyrannosaur family tree that are waiting to be found out there,” Dr Irmis told BBC News.

It was previously unclear why there were so many different Tyrannosaurid species present in a similar area, as the animals were able to move around freely. The palaeontologists believe this was due to a changing of sea level.

“We think that when the sea level was high it was isolating areas in western North America that caused different species to evolve in isolation and that’s why we’re finding so many different species,” added Dr Irmis.

He explained that the creature had been named the “King of Gore” because of its super-predator status. The second part of its name “argestes” comes from Greek poet Homer’s naming of a south-westerly wind.

Lythronax fossil
Lythronax had binocular vision which made it a ferocious hunter

“Tyrannosaurids were the really large predators in their ecosystem. It’s fairly certain based on what we can see on their skull, teeth and body size they probably ate whatever they could fit in their mouths,” added Dr Irmis.

Apex predator

Another research member of the team, Joseph Sertich of the Denver Museum of Nature and Science, US, explained that the back of its skull was very wide which gave it good hunting eyes.

“One of the things that makes T. rex different from other dinosaurs is that it is able to look forward, it has binocular vision. Lythronax had that feature as well, its field of view could overlap which probably made it a better hunter,” Dr Sertich told BBC News.

“It was the apex predator of it’s time. It was the oldest advanced Tyrannosaur of its group, which is quite surprising.

“This is the tip of the iceberg. It’s amazing what we’re finding in southern Utah right now. You can walk over some of the hills and find fossils littering the sides of the slopes,” he added.

Mike Benton at the University of Bristol, UK, who was not involved with the study, said the new find was important for understanding patterns of evolution of the Tyrannosaurids.

“Previously, Tyrannosauri origins were uncertain, whether in Asia or North America, and the new find tends to suggest a mainly North American evolution for the group.”

Reconstructed skull and skeleton
The specimen discovered was 24ft long but was not a fully grown adult – estimated to be 30ft long

US moves to ban trans fats in foods

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US food safety officials have taken steps to ban the use of trans fats, saying they are a threat to health.

Trans fats, also known as partially hydrogenated oils, are no longer “generally recognised as safe“, said the Food and Drug Administration (FDA).

The regulator said a ban could prevent 7,000 deaths and 20,000 heart attacks in the US each year.

The FDA is opening a 60-day consultation period on the plan, which would gradually phase out trans fats.

“While consumption of potentially harmful artificial trans fat has declined over the last two decades in the United States, current intake remains a significant public health concern,” FDA Commissioner Margaret Hamburg said in a statement.

“The FDA’s action today is an important step toward protecting more Americans from the potential dangers of trans fat.”

‘Industrially produced ingredient’

If the agency’s plan is successful, the heart-clogging oils would be considered food additives and could not be used in food unless officially approved.

The ruling does not affect foods with naturally occurring trans fats, which are present in small amounts in certain meat and dairy products.

Foods containing trans fat

Trans fat label
  • Some processed baked goods such as cakes, cookies, pies
  • Microwave popcorn, frozen pizza, some fast food
  • Margarine and other spreads, coffee creamer
  • Refrigerator dough products such as cinnamon rolls

Source: US Food and Drug Administration

Artificial trans fats are used both in processed food and in restaurants as a way to improve the shelf life or flavour of foods. The fats are created when hydrogen is added to vegetable oil, making it a solid.

Nutritionists have long criticised their use, saying they contribute to heart disease more than saturated fat.

Some companies have already phased out trans fats, prompted by new nutritional labels introduced in 2006 requiring it to be listed on food packaging.

New York City and some other local governments have also banned it.

But trans fats persist primarily in processed foods – including some microwave popcorns and frozen pizzas – and in restaurants that use the oils for frying.

According to the FDA, trans fat intake among Americans declined from 4.6g per day in 2003 to around 1g per day in 2012.

Generic picture of overweight man

The American Heart Association said the FDA’s proposal was a step forward in the battle against heart disease.

“We commend the FDA for responding to the numerous concerns and evidence submitted over the years about the dangers of this industrially produced ingredient,” said its chief executive, Nancy Brown.

Outgoing New York Mayor Michael Bloomberg, who led the charge to ban trans fats in that city, said the FDA plan “deserves great credit”.

“The groundbreaking public health policies we have adopted here in New York City have become a model for the nation for one reason: they’ve worked,” he said.