DNA differences which appear to affect the risk of giving birth early have been found by US scientists.

The US National Institutes of Health study found the variants in both babies and mothers, a US conference was told.

It is thought they may play a role in controlling immune responses which could theoretically trigger labour if they become too powerful.

Premature birth – which accounts for 7% of UK births – is one of the biggest threats to a baby’s future health.

The causes of premature birth are poorly understood, although infections and other medical complications are blamed in some cases.

The study looked at 700 DNA variants in 190 genes in women who delivered early, and those who carried their baby to term.

The cord blood of the babies was also tested for these variations.

They narrowed the search down to a handful of gene variations found more often in the women who gave birth prematurely, and their babies.

In particular, babies who carried the gene for the “Interleukin 6 receptor” were more likely to be born early.

This was a good candidate gene because Interleukin 6 is produced by cells in response to infection and is involved in inflammation.

High levels of Interleukin 6 in the amniotic fluid and foetal blood have been linked to the onset of premature labour.

Baby threat

Dr Roberto Romero, who led the study, said: “Our hypothesis is that the mother and/or the foetus signal the onset of preterm labour when the environment inside the uterus is unfavourable and threatens the survival of the maternal-foetal pair.

“When there is an infection in the uterus, the onset of premature labour appears to have survival value – it would allow the mother to rid herself of infected tissue and preserve her ability to have future pregnancies.”

The chief executive of charity Bliss, Andy Cole, welcomed the study results.

“In England alone, 54,000 babies are born prematurely each year, a third of these for no known reason,” he said.

“The development of a reliable test for identifying these mothers is vital in ensuring our most vulnerable babies have the best possible outcomes.”

Scientists have shown how a family of “limpet-like” proteins play a crucial role in repairing the DNA damage which can lead to cancer.

They hope the finding could pave the way for a new type of drug which could help kill cancer cells, and promote production of healthy replacements.

The proteins seem to have a remarkable ability to zero in on damaged areas.

The breakthrough, uncovered independently by two teams, appears in the journal Nature.

The family of Small Ubiquitin-like Modifier (SUMO) proteins track down sites in the body where DNA damage has occurred.

They attach themselves to normal proteins, and guide them in to fix the genetic faults.

Using this method, the proteins are even able to repair double strand DNA breaks – the most severe type of DNA damage.

When their work is done, the proteins detach themselves and move on.

Breast cancer gene

One of the study teams was able to follow this process of repair taking place on the BRCA1 gene, which, if damaged, is associated with a very high risk of breast cancer.

SUMO was shown to attach to the damaged gene, and switch it back on – helping prevent breast cancer forming.

Researcher Dr Jo Morris, from King’s College London, said: “This new insight is the first step towards developing drugs which may protect normal cells from the side effects of chemotherapy, or improve the effectiveness of current breast cancer treatments.”

Dr Lesley Walker, of Cancer Research UK, which part-funded the study, said: “DNA damage, particularly double strand DNA breaks, are a fundamental cause of cancer and we know that people who have mutations in the BRCA1 gene have a higher risk of developing some kinds of cancer.

“Discovering that these limpet-like proteins play such an important role in repair may provide new opportunities to stop cancer from growing.”

But she added: “This is an extremely complex and intricate biological process so it may be many years before we can use this knowledge to safely intervene and help treat cancer patients.”

People blessed with youthful faces are more likely to live to a ripe old age than those who look more than their years, work shows.

Danish scientists say appearance alone can predict survival, after they studied 387 pairs of twins.

The researchers asked nurses, trainee teachers and peers to guess the age of the twins from mug shots.

Those rated younger-looking tended to outlive their older-looking sibling, the British Medical Journal reports.

Survival advantage

The researchers also found a plausible biological explanation for their results.

Key pieces of DNA called telomeres, which indicate the ability of cells to replicate, are also linked to how young a person looks.

A telomere of shorter length is thought to signify faster ageing and has been linked with a number of diseases.

In the study, the people who looked younger had longer telomeres.

All of the twins were in their 70s, 80s or 90s when they were photographed.

Over a seven-year follow-up the researchers, led by Professor Kaare Christensen of the University of Southern Denmark, found that the bigger the difference in perceived age within a pair, the more likely it was that the older-looking twin died first.

The age, sex and professional background of the assessors made no difference to any of the results.

Professor Christensen said it might be that people who have had a tougher life are more likely to die early – and their life is reflected in their face.

The researchers told the BMJ: “Perceived age, which is widely used by clinicians as a general indication of a patient’s health, is a robust biomarker of ageing that predicts survival among those aged over 70.”

Professor Tim Spector, a UK expert who has been doing his own twin research, said: “We are also finding this in our study.

“It’s probably a combination of genes plus environment over a lifetime that are important.”

He said the findings also show that people are good at assessing how well someone is and that doctors should eyeball their patients.

“If a patient looks older than their years then perhaps they should be more concerned,” he said.

Scientists have discovered what they believe is a genetic cause of severe obesity in children.

The team concluded that the loss of a key segment of DNA can be to blame.

It said the findings might improve diagnosis of severe obesity – which on occasion has been wrongly attributed to abusive overfeeding.

The study, of 300 children with severe obesity by the University of Cambridge and the Wellcome Trust Sanger Institute, appears in Nature.

Some of the children in the study had been formally placed on the social services ‘at risk’ register on the assumption that their parents were deliberately overfeeding them. They have now been removed from the register.

Obesity is increasing throughout the world and is recognised as a major global public health concern.

Although much of the problem is due to lifestyle factors such as an unhealthy diet, and lack of exercise, some cases are thought to be down to genetics.

The latest study examined each child’s entire genome, looking for deletions or duplications of DNA, known as copy number variants (CNVs).

Experts increasingly believe these CNVs play an important role in genetic disease.

Genome scan

By comparing the DNA profile of obese children with others of a normal weight they found certain parts of the genome were missing in the obese group.

In particular they zeroed in on a missing part of chromosome 16 which seemed to have a strong link to severe obesity.

Researcher Dr Sadaf Farooqi said: “Our results suggest that one particular gene on chromosome 16 called SH2B1 plays a key role in regulating weight and also in handling blood sugar levels.

“People with deletions involving this gene had a strong drive to eat and gained weight very easily.

“It adds to the growing weight of evidence that a wide range of genetic variants can produce a strong drive to eat.

“We hope that this will alter attitudes and practices amongst those with professional responsibility for the health and well-being of children.”

Dr Matt Hurles, who also worked on the study, said: “This is the first evidence that copy number variants have been linked to a metabolic condition such as obesity.

“They are already known to cause other disorders such as autism and learning difficulties.”

Dr Ian Campbell, medical director of the charity Weight Concern, stressed most children did not have significant genetic factors that predisposed them to obesity, and that lifestyle, diet and exercise remained important.

But he added that the causes of obesity – and the potential solutions – were complex.

He said: “The fact that several of the study children have been taken out of social care and returned to their parents as a result is disturbing in itself and must surely put an end to the claims by some that childhood obesity is a simple case of parental abuse.

“It clearly isn’t. These families need our support.”

Tiny metal particles have been shown to cause changes to DNA across a cellular barrier – without having to cross it.

The nanometre and micrometre scale particles resulted in an increase of damage to DNA across the barrier via a never-before-seen cell signal process.

Reporting in Nature Nanotechnology, the researchers say the mechanism could be both a risk and an opportunity.

They say the preliminary result is relevant as more medical therapies rely on small-scale particles.

For instance, nanoparticle-based approaches are being considered for use to improve MRI images or direct the delivery of cancer drugs.

However, they concede their model system is far simpler than the human body, where the effects will be harder to unpick.

As yet, the researchers are not even certain of the mechanism by which the signalling molecules cause damage to DNA.

Communication skills

The team studied the effects of particles made from cobalt and chromium, either 30 billionths of a metre or four millionths of a metre across.

These metals are used in implants such as artificial hips or knees.

They grew a thin, artificial membrane from human cells and placed the particles on the membrane. Beneath it, they placed fibroblast cells, which in the body help to form connective tissue.

Although the team showed that the particles had not crossed the membrane, the fibroblast cells beneath were shown to have about 10 times as many damage sites in their DNA than the case in which no particles were used.

Gevdeep Bhabra, lead author on the research from the Bristol Implant Research Centre, explained that cells in close contact are known to exhibit cell-to-cell communication through structures known as gap junctions and hemichannels.

“We used a variety of chemicals to block this cell-to-cell signalling and found that in the presence of these blockers, the damage we were seeing was completely prevented,” he said.

The team stressed that the concentrations of the particles were thousands of times higher than would be found in the human body, for instance from wear and tear on implants.

As a result, there is no reason to believe that implants pose a risk via the signalling mechanism.

However, its discovery suggests that there is much work to be done to establish if the mechanism that appears to be responsible for the DNA damage is limited to those materials, or can occur in the presence of other materials of a similar size.

That issue is of particular importance as more therapeutic and imaging approaches begin to make use of nano-scale materials.

Ashley Blom, head of orthopaedic surgery at the University of Bristol, explained that although the signalling could pose a future risk, once understood it could be put to good therapeutic use.

“If the barriers in the human body do work in this way, the first exciting thing is: can we deliver novel therapies across barriers without having to cross them?

“For example, if you have a condition that affects the brain, maybe we could treat you with something that doesn’t cross the blood-brain barrier, that does not come in contact with the brain.”

A new study conducted at Oregon State University finds that even minor zinc deficiencies can cause DNA damage.

“Zinc deficiencies have been somewhat under the radar because we just don’t know that much about mechanisms that control its absorption, role or even how to test for it in people with any accuracy,” said Emily Ho, a researcher at OSU.

Adequate zinc intake is essential for fighting off infectious disease, boosting immune function, repairing DNA damage and fighting cancer.
Zinc is naturally found in proteins like beef and poultry, and in even higher levels in shellfish like oysters. It’s available in plants but poorly absorbed from them, raising additional concerns for vegetarians.

Inadequate zinc intake is so prevalent in the elderly that Ho suggests they consider nutritional supplements to ensure adequate levels.