Breakthrough could help prevent premature birth

A premature baby
A premature baby
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SCIENTISTS from Sheffield University have made an important medical discovery which could pave the way for new treatments to prevent premature births.

The research, led by Dr Neil Chapman from the university’s medical school, found key genes which stop labour occurring too early are ‘switched off’ by inflammation in the womb at the time labour starts.

The study focused on an experimental class of medicines which have been shown to stop the womb contracting in laboratory tests using tissue samples from pregnant women.

But when the research team analysed a chemical released during womb inflammation, they found it caused contractions to start again, even when the drugs - called histone deacetylase inhibitors - had stopped contractions.

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

He added: “Premature birth remains the biggest cause of infant death, primarily because we still do not know enough about the biochemistry and physiology of how the uterus goes into labour in normal term pregnancies.

“Our work demonstrates that while this experimental drug can stop the womb contracting, it cannot stop the inflammation associated with normal labour from switching off the genes which ensure the uterus does not start to contract too early.

“This means this class of drug may not be a suitable medication to give a pregnant woman when her labour starts prematurely because it cannot override the inflammation already present.”

Premature birth affects roughly one in 10 deliveries in the UK, and complications arising from pre-term birth are a leading cause of deaths among newborn babies.