Dr Neil Chapman, B.Sc.(Hons.), Ph.D., P.G.Cert.H.E., S.F.H.E.A.
Senior University Teacher
Academic Unit of Reproductive & Developmental Medicine
Department of Oncology and Metabolism
Level 4, The Jessop Wing
Tree Root Walk
Telephone 0114 215 9671
I joined the University of Sheffield as a Group Leader and Non-Clinical Lecturer in Reproductive Medicine in July 2005. Previous research positions included:
- July 2005-December 2017
Lecturer in Reproductive Medicine, Academic Unit of Reproductive and Developmental Medicine, University of Sheffield
- October 2003 - June 2005
Post-Doctoral Research Associate, School of Surgical and Reproductive Sciences, University of Newcastle-upon-Tyne. Research: Transcriptional regulation in the myometrium and cervix by the Nuclear Factor kappaB (NF-kappaB) and novel membrane-bound steroid receptors
- June 1997 - September 2003
Post-Doctoral Research Associate, School of Life Sciences, Division of Gene Expression and Regulation, Wellcome Trust Biocentre, University of Dundee. Research: Transcriptional regulation by NF-kappaB; determining how NF-kappaB regulates mammalian gene expression in conjunction with other proteins (Egr-1, WT-1, CBP/p300 and c-Myc) with an emphasis on tumourigenesis
- September 1994 - May 1997
May 1997 Ph.D. student, University of Sheffield. Research: Expression and characterisation of the ZP3 protein; to develop purification strategies to isolate recombinant copies of ZP3 and then characterise their effects on human spermatozoa
Premature Birth …
Globally, being born too early affects roughly 15 million pregnancies per year. Of these about 1 million babies will die because they were born too early and suffered complications of that. The majority of these deaths are in those babies that are born extremely prematurely: before 28-30 weeks gestation. To put this number into context, here in Sheffield the Jessop Maternity Wing manages in the region of 7,000 deliveries per year. To reach the annual global death toll attributable to premature birth there would need to be no live births in the Jessop for approximately the next 140 years.
See how staff and local people help to raise the profile of premature birth research at the Big Knit event as part of the University of Sheffield’s Life Festival https://www.youtube.com/watch?v=RyvogMqXoQc
We also know that those babies that do survive prematurity also have an increased risk of major long-term health problems. It is principally because of these observations that these babies have a disproportionate effect on health-care budgets worldwide; a recent U.K. estimate of the total cost of preterm birth to the public sector over the first 18 year of life was £2.95 billion. Therefore, being born too early is a very much a problem for life. For those readers wanting further details of this, please visit the EPICURE website (www.epicure.ac.uk/).
So why does premature birth happen? The simple answer is that despite intensive research efforts, together with a major shortage of research funding into this problem, we still don’t know enough about the fundamental biological principles that control how the womb works during pregnancy and labour. As such, it is of little surprise that doctors have few truly effective medicines to stop labour when it has started too early. Those drugs that are available are relatively ineffective and can be associated with unwanted side-effects for both the unborn baby and mother.
My research work uses muscle cells from the womb (called myocytes). We get these samples by asking women to donate a piece of their womb lining when they have an elective Caesarean section. From this piece of womb muscle we can then grow the individual muscle cells and study how they work.
Within the womb muscle cells are structures called the nuclei. It is within each nucleus that the blueprint of the womb muscle cell (the DNA or genome) is stored and used to control when the womb starts to contract. The genome or DNA can be thought of as a library of instruction books. Each book represents an individual gene, with each gene being used to make a specific building block - a protein - in the cell. Importantly, however, these books are not written with words: only four letters are used – A, T, C, and G – and different arrangements of these letters are what gives rise to all the different proteins in your body as well telling cells what proteins to make and when to make them.
In humans, the biology by which the womb changes from a relaxed state which cannot contract regularly, to an organ which undergoes the regular contractions seen in labour is not known. At present, our current knowledge about the human birth process suggests that normal human labour is a highly-regulated inflammatory process similar to that which occurs when the body is injured or ill.
My work has shown that the inflammation seen in the womb at term modifies how the blueprint of the womb muscle cells (the DNA or genome) works to regulate when the womb contracts with inflammation seemingly able to promote labour (see this BBC News story: www.bbc.co.uk/news/health-21628912). Consequently, my research focuses on learning how the womb reads its genome book when such inflammatory chemicals are present. I am also interested in finding out which parts of the book (i.e. which genes) the womb cells use before labour starts, when there is very little inflammation around, because understanding this change may allow us to understand how the womb muscle cells start contracting too early in some women who then go into labour prematurely.
- Press et al. (2017). Measurements of rates of cooling of a manikin insulated with different mountain rescue casualty bags. Extrem Physiol Med 6:1 DOI 10.1186/s13728-017-0055-7
- Cookson V.J. and Chapman N.R. (2010) NF-kappaB function in the human myometrium during pregnancy and parturition. Histol Histopathol 25, 945-956
- SBAs for the Part 1 MRCOG. Andrew Sizer and Neil Chapman. RCOG Press, London 2012. ISBN: 978-1-906985-58-5
- Webster et al., (2013) Regulation of GTP-binding Protein (Galphas) Expression in Human Myometrial Cells: A Role for Tumour Necrosis Factor in Modulating Galphas Promoter Acetylation by Transcriptional Complexes. J Biol Chem 288: 6704-6716
- www.bbc.co.uk/news/health-21628912 - BBC news report highlighting the findings published in Webster et al. (2013)
- Waite et al., (2014) The Effect of Trichostatin-A and Tumour Necrosis Factor on Expression of Splice Variants of the MaxiK and L-Type Channels in Human Myometrium. Front Physiol 5:261
- Cookson et al. (2015) Binding Loci of RelA-containing Nuclear Factor-kappaB (NF-kappaB) Dimers in Promoter Regions of PHM1-31 Myometrial Smooth Muscle Cells. Mol Hum Reprod 21:864-883
- Chapman and Press. Immediate Care Skills for Your Elective: Two simple frameworks to help you wherever you are. Student BMJ 2016;24:i2049 DOI: 10.1136/sbmj.i2049 http://student.bmj.com/student/view-article.html?id=sbmj.i2049
- Academic Lead - Phase 3A SSC Programme (Medicine)
- Academic Lead - Phase 3B Electives (Medicine)
- Academic Lead – Incoming International Electives Programme (Medicine)
- Admissions Tutor - Incoming Medical Electives Programme (https://www.sheffield.ac.uk/medicine/electives)
- Admissions Tutor - M.Sc. Reproductive and Developmental Medicine (http://www.sheffield.ac.uk/humanmetabolism/units/rdm/msc)
- Deputy Module Leader – Physiology Module of the M.Sc. Human Nutrition (https://www.sheffield.ac.uk/postgraduate/taught/courses/medicine/biomedical/human-nutrition-mmedsci-diploma)
- Invited speaker - Part 1 MRCOG Revision Course at the Royal College of Obstetricians and Gynaecologists, London.
- Member - The MRC-Arthritis Research UK Centre for Integrated Research into Musculoskeletal Ageing (CIMA) (www.sheffield.ac.uk/humanmetabolism/mresmusculoskeletalageing/cima)
For a full list of publications please visit myPublications