Scientists gain new clues over premature births

SCIENTISTS from Yorkshire have made a breakthrough which could pave the way for developing new treatments to prevent premature births.

Experts from Sheffield University have discovered a key gene in the womb, which stops labour occurring early, is switched off by inflammation in the uterus at the time labour begins.

They say the advance could lead to the development of new treatments to premature deliveries.

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In the UK, premature birth affects roughly one in 10 deliveries and complications from pre-term birth are a leading cause of death in newborn babies.

Babies surviving premature birth are at an increased risk of developing long-term problems including cerebral palsy, breathing difficulties, deafness and blindness.

The process behind how women go into labour is still poorly understood but it is vital it happens when the baby is ready to be born and can survive. There are few reliable drugs that can be used to stop labour if it starts too early.

The ground-breaking research, led by Neil Chapman from Sheffield’s medical school in collaboration with experts from the city hospitals and Newcastle and Nottingham universities, focuses on how inflammation in the uterus affects experimental drugs, which aim to delay labour when it starts prematurely.

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In laboratory studies using tissue samples from pregnant women, the drugs stopped the womb contracting. But if inflammation in the womb occurred, muscle contraction began again even if the drug had successfully stopped it.

Dr Chapman said: “Our research is a major step forward in unlocking the mysteries behind the processes of normal labour. We have shown that the inflammation of the uterus switches off the genes which stops labour occurring too early.

“Understanding how to prevent this inflammation or how to stop it blocking those key genes needed to stop contraction of the womb would lead to new treatments to prevent premature births.”

The research was funded by the Medical Research Council and Jessop Wing Ellen Webster Legacy.