Yr Athro Ros John

Cyfarwyddwr Ymchwil, Athro

Ysgol y Biowyddorau

: JohnRM@caerdydd.ac.uk
: +44 29208 70145
: Adeilad Syr Martin Evans, Ystafell Cardiff School of Biosciences, The Sir Martin Evans Building, Museum Avenue, Cardiff, CF10 3AX, Rhodfa'r Amgueddfa, Caerdydd, CF10 3AX

: Sylwebydd y cyfryngau
: Ar gael fel goruchwyliwr ôl-raddedig

Trosolwg ymchwil

Mae fy ymchwil yn ceisio mynd i'r afael ag un o'r cwestiynau mwyaf heriol a sylfaenol bwysig ym maes iechyd pobl, sef sut i fanteisio i'r eithaf ar y siawns o feichiogrwydd iach a llwyddiannus. Mae gofal sy'n gysylltiedig â beichiogrwydd yn costio tua £5.8 biliwn y flwyddyn i'r GIG, ond dim ond 2.4% o'r holl gyllid ymchwil iechyd uniongyrchol, nad yw'n ddiwydiant sy'n cael ei wario ar ymchwil sy'n gysylltiedig â beichiogrwydd (adroddiad RAND, 2020). Mae hyn yn nodi mai ymchwil beichiogrwydd yw un o'r meysydd ymchwil sydd wedi'u tanariannu fwyaf yn y DU. Ac eto, dyma lle mae iechyd pobl yn dechrau a lle gallwn wneud y newidiadau mwyaf effeithiol i wella iechyd nid yn unig y fam ond hefyd ar gyfer cenedlaethau'r dyfodol. Mae fy ngrwpiau ymchwil yn defnyddio data carfan ddynol (The Grown in Wales Study) a systemau arbrofol i archwilio sut mae adfyd cynenedigol, yr amcangyfrifir ei fod yn effeithio ar fwy na hanner holl feichiogrwydd y DU, yn peryglu twf ffetws ac iechyd meddwl mamol, ac yn rhaglennu rhai o'r clefydau mwyaf cyffredin a threiddiol sy'n effeithio ar boblogaethau dynol.

Rolau

Cyfarwyddwr Ymchwil
Arweinydd Tîm Academaidd

Date
Type

2018

Garcia-Martin, I., Penketh, R., Janssen, A. B., Jones, R. E., Grimstead, J., Baird, D. and John, R. 2018. Meformin and insulin treatment prevent placental telomere attrition in boys exposed to maternal diabetes. PLoS ONE 13(12), article number: : e0208533. (10.1371/journal.pone.0208533)
Millership, S. J. et al. 2018. Neuronatin deletion causes postnatal growth restriction and adult obesity in 129S2/Sv mice. Molecular Metabolism 18, pp. 97-106. (10.1016/j.molmet.2018.09.001)
Tunster, S. J., Van de Pette, M., Creeth, H. D. J., Lefebvre, L. and John, R. M. 2018. Fetal growth restriction in a genetic model of sporadic Beckwith-Wiedemann syndrome. Disease Models and Mechanisms 11, article number: dmm035832. (10.1242/dmm.035832)
John, R. and Rougelle, C. 2018. Developmental epigenetics: phenotype and the flexible epigenome. Frontiers in Cell and Developmental Biology 6, article number: 130. (10.3389/fcell.2018.00130)
Tunster, S. J., Boque Sastre, R., McNamara, G., Hunter, S. M., Creeth, H. D. J. and John, R. M. 2018. Peg3 deficiency results in sexually dimorphic losses and gains in the normal repertoire of placental hormones. Frontiers in Cell and Developmental Biology 6, article number: 123. (10.3389/fcell.2018.00123)
Van de Pette, M., Tunster, S. J. and John, R. M. 2018. Loss of imprinting of Cdkn1c protects against age and diet-induced obesity. International Journal of Molecular Sciences 19(9), article number: 2734. (10.3390/ijms19092734)
Janssen, A. et al. 2018. Persistence of anxiety symptoms after elective caesarean delivery. Bjpsych Open 4(5), pp. 354-360. (10.1192/bjo.2018.48)
Millership, S. J. et al. 2018. Neuronatin regulates pancreatic β cell insulin content and secretion. Journal of Clinical Investigation 128(8), pp. 3369-3381. (10.1172/JCI120115)
Creeth, H. D. J. et al. 2018. Maternal care boosted by paternal imprinting in mammals. PLoS Biology 16(7), article number: e2006599. (10.1371/journal.pbio.2006599)
McNamara, G. I. et al. 2018. Dopaminergic and behavioral changes in a loss-of-imprinting model of Cdkn1c. Genes, Brain and Behavior 17(2), pp. 149-157. (10.1111/gbb.12422)
McNamara, G., John, R. and Isles, A. 2018. Territorial behaviour and social stability in the mouse require correct expression of imprinted Cdkn1c. Frontiers in Behavioral Neuroscience 12, article number: 28. (10.3389/fnbeh.2018.00028)
McNamara, G. I., Creeth, H. D. J., Harrison, D. J., Tansey, K. E., Andrews, R. M., Isles, A. R. and John, R. M. 2018. Loss of offspring Peg3 reduces neonatal ultrasonic vocalizations and increases maternal anxiety in wild-type mothers. Human Molecular Genetics 27(3), pp. 440-450. (10.1093/hmg/ddx412)

2017

Garcia Martin, I., Janssen, A., Jones, R., Grimstead, J. W., Penketh, R. J. A., Baird, D. M. and John, R. M. 2017. Telomere length heterogeneity in placenta revealed with high-resolution telomere length analysis. Placenta 59, pp. 61-68. (10.1016/j.placenta.2017.09.007)
John, R. M. 2017. Imprinted genes and the regulation of placental endocrine function: pregnancy and beyond. Placenta 56, pp. 86-90. (10.1016/j.placenta.2017.01.099)
Nomura, Y. et al. 2017. Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes. Archives of Gynecology and Obstetrics 295(6), pp. 1319-1329. (10.1007/s00404-017-4347-3)
Van de Pette, M. et al. 2017. Visualizing changes in Cdkn1c expression links early-Life adversity to imprint mis-regulation in adults. Cell Reports 18(5), pp. 1090-1099. (10.1016/j.celrep.2017.01.010)

2016

McNamara, G. I., Davis, B. A., Dwyer, D. M., John, R. M. and Isles, A. R. 2016. Behavioural abnormalities in a novel mouse model for Silver Russell Syndrome. Human Molecular Genetics 25(24), pp. 5407-5417. (10.1093/hmg/ddw357)
Janssen, A. et al. 2016. Maternal prenatal depression is associated with decreased placental expression of the imprinted gene PEG3. Psychological Medicine 46(14), pp. 2999-3011. (10.1017/S0033291716001598)
Tunster, S. J., McNamara, G., Creeth, H. and John, R. M. 2016. Increased dosage of the imprinted Ascl2 gene restrains two key endocrine lineages of the mouse Placenta. Developmental Biology 418(1), pp. 55-65. (10.1016/j.ydbio.2016.08.014)
Janssen, A. B., Kertes, D. A., McNamara, G., Braithwaite, E. C., Creeth, H., Glover, V. I. and John, R. M. 2016. A role for the placenta in programming maternal mood and childhood behavioural disorders. Journal of Neuroendocrinology 28(8) (10.1111/jne.12373)
Van De Pette, M. et al. 2016. Cdkn1c boosts the development of brown adipose tissue in a murine model of Silver Russell Syndrome. PLoS Genetics 12(3), article number: e1005916. (10.1371/journal.pgen.1005916)
Janssen, A. B., Tunster, S. J., Heazell, A. E. P. and John, R. M. 2016. Placental PHLDA2 expression is increased in cases of fetal growth restriction following reduced fetal movements. BMC Medical Genetics 17(1), article number: 17. (10.1186/s12881-016-0279-1)
Tunster, S. J., Creeth, H. and John, R. M. 2016. The imprinted Phlda2 gene modulates a major endocrine compartment of the placenta to regulate placental demands for maternal resources. Developmental Biology 409(1), pp. 251-260. (10.1016/j.ydbio.2015.10.015)

2015

Janssen, A. B. et al. 2015. Placental expression of imprinted genes varies with sampling site and mode of delivery. Placenta 36(8), pp. 790-795. (10.1016/j.placenta.2015.06.011)
Kitamura, A. et al. 2015. Epigenetic alterations in sperm associated with male infertility. Congenital Anomalies 55(3), pp. 133-144. (10.1111/cga.12113)

2014

Tunster, S. J., Van De Pette, M. and John, R. M. 2014. Isolating the role of elevated Phlda2 in asymmetric late fetal growth restriction in mice. Disease Models & Mechanisms 7(10), pp. 1185-1191. (10.1242/dmm.017079)
Jensen, A. B., Tunster, S. J. and John, R. M. 2014. The significance of elevated placental PHLDA2 in human growth restricted pregnancies. Placenta 35(8), pp. 528-532. (10.1016/j.placenta.2014.04.018)
Hiura, H. et al. 2014. A tripartite paternally methylated region within the Gpr1-Zdbf2 imprinted domain on mouse chromosome 1 identified by meDIP-on-chip [Correction]. Nucleic Acids Research 42(16), article number: 10869. (10.1093/nar/gku624)

2013

Tunster, S. J., Jensen, A. B. and John, R. M. 2013. Imprinted genes in mouse placental development and the regulation of fetal energy stores. Reproduction 145(5), pp. R117-R137. (10.1530/REP-12-0511)
John, R. M. 2013. Epigenetic regulation of placental endocrine lineages and complications of pregnancy. Biochemical Society Transactions 41(3), pp. 701-709. (10.1042/BST20130002)

2012

Reed, K. R., Tunster, S. J., Young, M., Carrico, A. S., John, R. M. and Clarke, A. R. 2012. Entopic overexpression of Ascl2 does not accelerate tumourigenesis in ApcMin mice. Gut 61(10), pp. 1435-1438. (10.1136/gutjnl-2011-300842)
Tunster, S. J., Van De Pette, M. and John, R. M. 2012. Impact of genetic background on placental glycogen storage in mice.. Placenta 33(2), pp. 124-127. (10.1016/j.placenta.2011.11.011)
Ackerman, W. E. I. et al. 2012. IFPA Meeting 2011 workshop report III: Placental immunology; epigenetic and microRNA-dependent gene regulation; comparative placentation; trophoblast differentiation; stem cells.. Placenta 33(Suppl), pp. S15-S22. (10.1016/j.placenta.2011.11.022)
Lewis, R. M. et al. 2012. Relationship between placental expression of the imprinted PHLDA2 gene, intrauterine skeletal growth and childhood bone mass. Bone 50(1), pp. 337-342. (10.1016/j.bone.2011.11.003)
John, R. M. and Hemberger, M. 2012. A placenta for life. Reproductive BioMedicine Online 25(1), pp. 5-11. (10.1016/j.rbmo.2012.03.018)
Clarke, A. J. et al. 2012. 'Sifting the significance from the data' - the impact of high-throughput genomic technologies on human genetics and health care. Human Genomics 6, article number: 11. (10.1186/1479-7364-6-11)
Hiura, H. et al. 2012. Characterization of DNA methylation errors in patients with imprinting disorders conceived by assisted reproduction technologies. Human Reproduction 27(8), pp. 2541-2548. (10.1093/humrep/des197)

2011

John, R. M. and Lefebvre, L. 2011. Developmental regulation of somatic imprints.. Differentiation 81(5), pp. 270-280. (10.1016/j.diff.2011.01.007)
Tunster, S. J., Van De Pette, M. and John, R. M. 2011. BACs as tools for the study of genomic imprinting. Journal of Biomedicine and Biotechnology 2011, article number: 283013. (10.1155/2011/283013)
Tunster, S. J., Van De Pette, M. and John, R. M. 2011. Fetal overgrowth in the Cdkn1c mouse model of Beckwith-Wiedemann syndrome. Disease Models & Mechanisms 4(6), pp. 814-821. (10.1242/dmm.007328)

2010

Wood, M. D., Hiura, H., Tunster, S. J., Arima, T., Shin, J., Higgins, M. and John, R. M. 2010. Autonomous silencing of the imprinted Cdkn1c gene in stem cells. Epigenetics 5(3), pp. 214-221. (10.4161/epi.5.3.11275)
Tunster, S. J., Tycko, B. and John, R. M. 2010. The imprinted Phlda2 gene regulates extraembryonic energy stores. Molecular and Cellular Biology 30(1), pp. 295-306. (10.1128/MCB.00662-09)
John, R. M. 2010. Engineering mouse models to investigate the function of imprinting. Briefings in Functional Genomics 9(4), pp. 294-303. (10.1093/bfgp/elq010)
Hiura, H. et al. 2010. A tripartite paternally methylated region within the Gpr1-Zdbf2 imprinted domain on mouse chromosome 1 identified by meDIP-on-chip. Nucleic Acids Research 38(15), pp. 4929-4945. (10.1093/nar/gkq200)

2009

Kobayashi, H. et al. 2009. DNA methylation errors at imprinted loci after assisted conception originate in the parental sperm. European Journal of Human Genetics 17(1582-1) (10.1038/ejhg.2009.68)

2008

Sowpati, D. et al. 2008. An intronic DNA sequence within the mouse Neuronatin gene exhibits biochemical characteristics of an ICR and acts as a transcriptional activator in Drosophila. Mechanisms of Development 125(11/12), pp. 963-973. (10.1016/j.mod.2008.08.002 |)

2007

Andrews, S. C., Wood, M. D., Tunster, S. J., Barton, S. C., Surani, M. A. and John, R. M. 2007. Cdkn1c (p57Kip2) is the major regulator of embryonic growth within its imprinted domain on mouse distal chromosome 7. BMC Developmental Biology 7, article number: 53. (10.1186/1471-213x-7-53)

2006

Azuara, V. et al. 2006. Chromatin signatures of pluripotent cell lines. Nature Cell Biology 8(5), pp. 532-538. (10.1038/ncb1403)
Arima, T. et al. 2006. The human HYMAI/PLAGL1 differentially methylated region acts as an imprint control region in mice. Genomics 88(5), pp. 650-658. (10.1016/j.ygeno.2006.07.005)

2005

Zvetkova, I. et al. 2005. Global hypomethylation of the genome in XX embryonic stem cells. Nature Genetics 37(11), pp. 1274-1279. (10.1038/ng1663)

2004

Baxter, J. et al. 2004. Histone hypomethylation is an indicator of epigenetic plasticity in quiescent lymphocytes. EMBO Journal 23(22), pp. 4462-4472. (10.1038/sj.emboj.7600414)
Salas, M. et al. 2004. Placental growth retardation due to loss of imprinting of Phlda2. Mechanisms of Development 121(10), pp. 1199-1210. (10.1016/j.mod.2004.05.017)

2002

John, R. M., Ainscough, J. and Barton, S. C. 2002. A transgenic approach to studying imprinted genes: modified BACs and PACs. In: Ward, A. ed. Genomic Imprinting., Vol. 181. Methods in Molecular Biology Humana Press, pp. 67-81., (10.1385/1-59259-211-2:67)
Ainscough, J., John, R. M. and Barton, S. C. 2002. Production of YAC transgenic mice by pronuclear injection. In: Ward, A. ed. Genomic Imprinting., Vol. 181. Methods in Molecular Biology Humana Press, pp. 55-65., (10.1385/1-59259-211-2:55)

2001

John, R. M., Ainscough, J., Aparicio, S. and Surani, M. 2001. Imprinted Expression of Neuronatin from Modified BAC Transgenes Reveals Regulation by Distinct and Distant Enhancers. Developmental Biology 236(2), pp. 387-399. (10.1006/dbio.2001.0327)
John, R. M., Ainscough, J., Barton, S. C. and Surani, M. A. 2001. Distant cis-elements regulate imprinted expression of the mouse p57Kip2 (Cdkn1c) gene: Implications for the human disorder, Beckwith–Wiedemann syndrome. Human Molecular Genetics Vol.10(15), pp. 1601-1609. (10.1093/hmg/10.15.1601)

2000

Ainscough, J., John, R. M., Barton, S. and Surani, M. A. 2000. A skeletal muscle-specific mouse Igf2 repressor lies 40 kb downstream of the gene. Development 127(18), pp. 3923-3930.
John, R. M. 2000. Genomic imprinting, mammalian evolution, and the mystery of egg-laying mammals. Cell 101(6), pp. 585-588.

Summary

The principal interest of my laboratory lies in understanding how epigenetic marks direct mammalian development with a particular focus on in utero processes, and how exposure during critically sensitive windows in development can alter outcomes for both mother and child.

Genomic Imprinting

Genomic imprinting is an epigenetic system, first initiated in the germ line, that directs the allele-specific expression of a small set of developmentally important genes (Figure 1). Imprinted genes function within a myriad of networks to regulate fetal growth, placental development, metabolism and behaviour. The aberrant expression of imprinted genes has been reported in relation to low birth weight, placental dysfunction, metabolic and psychiatric diseases. A goal of our research is to further understand the dosage-related function of imprinted genes in development and disease. We are also investigating factors and lifestyles which may influence the expression of imprinted genes early in life resulting in pregnancy complications, mood disorders and poorer behavioural outcomes for children both in the short term and across the life course.

The placenta

We have demonstrated that certain imprinted genes regulate the size of the endocrine compartment of the placenta and consequently modulate the production of placental hormones (Figure 2). During pregnancy placental hormones flood the maternal circulation to induce the physiological changes required for a successful pregnancy. Placental hormones ensure nutrient availability to ensure appropriate fetal growth. Placental hormones also prime the maternal brain in preparation for mothering the newborn infant. Funded by BBSRC, we are using unique experimental models based on the genetically modified expression of imprinted genes to experimentally show that imprinted genes influence fetal growth and maternal caregiving through the regulation of placental endocrine lineages (Figure 3).

Environmental programming

Imprinted genes are regulated by epigenetic marks that can respond to environmental factors. In addition to exploring the consequences of aberrant imprinted gene expression, funded by BBSRC we are investigating whether specific maternal diets or conditions can influence gene expression in the placenta causing placental endocrine dysfunction (Figure 4) and in the fetus directly influencing development, both of which may be linked to the poorer outcomes for children.

Lifelong health

It is well known that prenatal adversity is associated with poorer outcomes for children including behavioural difficulties and metabolic disorders. Funded by BBSRC and Wellcome Trust, we are exploring the consequences of placental endocrine dysfunction on offspring outcomes focusing on offspring behaviour (Figure 4).

Clinical engagement

The imprinted genes we are studying regulate placental development, fetal growth and maternal adaptations to pregnancy via the regulation of placental signalling. The aberrant expression of imprinted genes is common in a number of human disorders of pregnancy including low birth weight, gestational diabetes and preeclampsia. Our recent work suggests that aberrant imprinting may also have relevance to maternal mood disorders programmed by placental dysfunction. Funded by MRC, we initiated “The Grown in Wales” Study (Figure 5) to collect of data and biological samples including placenta from women delivering locally at University Hospital Wales to integrate the knowledge gained from our experimental models with studies on human samples. We are also assessing the development and behaviour of the children from this study in “The Grown in Wales Infant Study” funded by The Waterloo Foundation. Our work will promote the optimal interpretation of clinical data with a longer-term goal of improving diagnostic performance and the identification of possible therapeutic targets for treatment.

Clinical study

“The Grown in Wales Study: Developing and placentomic tool for characterising atypical pregnancies and predicting outcomes.”

REC reference number 15/WA/0004; IRAS project ID 166243; UKCRN ID 18894

Current grant support

Active grants as lead applicant

BBSRC (2017-21) Exposing the link between placental endocrine dysfunction and offspring behavioural outcomes.

TWF “Brain-derived neurotrophic factor (BDNF) in pregnancy: Are infant outcomes associated with BDNF levels in the maternal and foetal circulation” (2021; £21K)

Wellcome Trust Neuroscience DTG “Placental Peg3 expression and Social Communication Behaviour” (2018-2021)

BBSRC “Prenatal adversity and the intergenerational transmission of atypical maternal caregiving” (2021-24; FEC £705,275)

Active grants as co-applicant

BBSRC (2017-20) Lipid droplets in oocytes: shedding new light on why fats are good or bad for development.

Wellcome Trust Neuroscience DTG “A system level approach to identify and validate imprinted genes involved in parental care” (2019-2022)

External Collaborators

Amanda Fisher (MRC London Institute of Medical Sciences, Imperial College, London)

Takahiro Arima (Tokoyu University, Japan)

Jay Cross (Calgary University, Canada)

Meeting organization

Annual Mammalian Genes, Development and Disease meeting (funded by The Genetics Society)

(Rotates between Cardiff, Bath, Bristol and Exeter)

Affiliated staff

Postgraduate research students

As principle supervisor

Samantha Garay (MRC Biomed DTP PhD)

Hannah Tyson (Wellcome Trust Neuroscience DTP PhD)

As second supervisor

Matt Higgs (Wellcome Trust Neuroscience DTP PhD)

Cindy Ikie (BIOSI PhD)

Links

http://safemotherhoodweek.org/maternal-rights-a-professional-perspective/

BI2332 Concepts of Disease: Epigenetics and Underlying Principles

BI3351 Contemporary Topics in Disease: Mouse models of imprinting

BI3001 Biosciences Final Year Project.

BIT002 MRes Research Techniques in Bioscience: Research seminar

Mae Rosalind M John yn Athro Epigenetig Datblygiadol ac yn Gyfarwyddwr Ymchwil ar gyfer Ysgol y Biowyddorau ym Mhrifysgol Caerdydd. Derbyniodd ei PhD o Goleg Imperial, Prifysgol Llundain a hyfforddodd ym Mhrifysgol San Francisco California (UCSF) a Stanford, UDA, a Phrifysgol Caergrawnt. Mae ganddi hanes o >20 mlynedd yn epigeneteg datblygiad ffetws a brych gan ddefnyddio modelau anifeiliaid i astudio perthnasedd mewnbrintio genomig, a sut y gall ffactorau amgylcheddol gyfryngu canlyniadau ffenoteipig byr a gydol oes. Mae hi'n arbenigwr ar gynhyrchu llygod trawsgenig BAC (Phlda2, Cdkn1c ac Ascl2) a'r defnydd o fodelau colli swyddogaeth (Cdkn1c, Phlda2 a Peg3) i gael mewnwelediad ym mherthnasedd dos genynnau rheoledig. Mae ei grŵp wedi adrodd am ffenoteipiau sy'n effeithio ar dwf ffetws, datblygiad brychol, metaboledd, ymddygiad oedolion ac, yn fwyaf diweddar, ymddygiad mamau mewn ymateb i gamweithrediad endocrin brychol. Sefydlodd yr Athro John yr Astudiaeth Tyfu yng Nghymru a'r astudiaeth babanod Tyfu yng Nghymru i gyfieithu ei chanfyddiadau o fodelau arbrofol i bobl sy'n berthnasol i fabanod pwysau geni isel, anhwylderau hwyliau mamau ac anhwylderau niwroddatblygiadol mewn plant. Ariennir grŵp yr Athro John gan MRC, BBSRC, Wellcome, Sefydliad Waterloo a Llywodraeth Cymru. Mae'r Athro John yn gwasanaethu ar baneli MRC PSMB a UKRI FLF.

Aelodaethau proffesiynol

The Genetics Society;
British Society of Developmental Biology;
International Society for Developmental Origins of Health and Disease;
International Federation Placenta Associations;
European Placenta Group;
ESRC InteSTELA network;
GeCIPs (Genomics England Clinical Interpretation Partnerships) subdomain Imprinting Disorders: Epigenomics, Aetiology and Stratification, or IDEAS);

Pwyllgorau ac adolygu

Cymrodoriaethau Arweinydd y Dyfodol UKRI Rownd 7 2023 -
Bwrdd cynghori gwyddonol Rhwydwaith Geneteg Llygoden Cenedlaethol MRC, Cadeirydd (2023- )
Bwrdd Meddygaeth Poblogaeth a Systemau MRC 2021 -
Panel Chwilio Gwobrau Biolegol y Gymdeithas Frenhinol 2021 -
Cymdeithas Geneteg Aelod Pwyllgor Cyffredin 2021 -(Geneteg Celloedd a Datblygiadol)
Prif Olygydd Arbenigol ar gyfer Frontiers in Cell and Developmental Biology: Epigenetics Datblygiadol (2019-2023)
Panel Iechyd a Chyd-destun UKRI GCRF (2019-20)
Panel Cyfweld Cymrodoriaethau Arweinwyr y Dyfodol UKRI Rownd 2 (2019)
Panel Adolygu Arbenigol MRC ar gyfer Gwobrau Cydweithredol NRP y DU (2019).
Panel Adolygu Arbenigol BBSRC A (2011-2017)

I am interested in supervising PhD students in the areas of:

genomic imprinting
developmental epigenetics
fetal programming
mammalian placental biology
maternal behaviour/maternal mood disorders

Themâu ymchwil

Arbenigeddau

Epigeneteg
Bioleg datblygiadol ac atgenhedlu anifeiliaid
Agweddau seicogymdeithasol ar enedigaeth ac iechyd meddwl amenedigol
Ymddygiad Rhieni
Endocrinoleg

‘Iselder yn ystod beichiogrwydd yn newid ymddygiad babanod gwryw - heb i famau sylwi’

06 December 2019

Ymchwil newydd yn cynnig esboniad pam mae babanod sy’n cael eu geni yn ystod y gaeaf yn fwy tebygol o ddatblygu anhwylderau iechyd meddwl

01 August 2019

Deiet iachus yn ystod beichiogrwydd yn lleihau’r risg o gael babi bach yn sylweddol

10 April 2019