Author
Tracey A. Johnston
Other affiliations: University of Manchester
Bio: Tracey A. Johnston is an academic researcher from St Mary's Hospital. The author has contributed to research in topics: Pregnancy & Population. The author has an hindex of 12, co-authored 24 publications receiving 386 citations. Previous affiliations of Tracey A. Johnston include University of Manchester.
Topics: Pregnancy, Population, Haematopoiesis, Risk assessment, Blood flow
Papers
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TL;DR: This Framework has been developed by a multidisciplinary working group in the light of evidence of improving outcomes for babies born before 27 completed weeks of gestation, and evolving national and international changes in the approach to their care.
Abstract: 1. This Framework has been developed by a multidisciplinary working group in the light
of evidence of improving outcomes for babies born before 27 completed weeks of
gestation, and evolving national and international changes in the approach to their
care. 2. Management of labour, birth and the immediate neonatal period should reflect
the wishes and values of the mother and her partner, informed and supported by
consultation and in partnership with obstetric and neonatal professionals. 3. Whenever possible, extreme preterm birth should be managed in a maternity facility
co-located with a designated neonatal intensive care unit. 4. Neonatal stabilisation may be considered for babies born from 22+0 weeks of
gestation following assessment of risk and multiprofessional discussion with parents.
It is not appropriate to attempt to resuscitate babies born before 22+0 weeks of
gestation.
5. Decision-making for babies born before 27 weeks of gestation should not be based
on gestational age alone, but on assessment of the baby’s prognosis taking into
account multiple factors. Decisions should be made with input from obstetric and
neonatal teams in the relevant referral centre if transfer is being contemplated. 6. Risk assessment should be performed with the aim of stratifying the risk of a poor
outcome into three groups: extremely high risk, high risk and moderate risk. 7. For fetuses/babies at extremely high risk, palliative (comfort focused) care would be
the usual management. 8. For fetuses/babies at high risk of poor outcome, the decision to provide either active
(survival focused) management or palliative care should be based primarily on the
wishes of the parents. 9. For fetuses/babies at moderate risk, active management should be planned. 10. If life-sustaining treatment for the baby is anticipated, pregnancy and delivery
should be managed with the aim of optimising the baby’s condition at birth and
subsequently. 11. Conversations with parents should be clearly documented and care taken to ensure
that the agreed management plan is communicated between professionals and staff
shifts. 12. Decisions and management should be regularly reviewed before and after birth in
conjunction with the parents; plans may be reconsidered if the risk for the fetus/baby
changes or if parental wishes change.
100 citations
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TL;DR: The ability of colour/pulsed Doppler ultrasound to detect failed physiologic change of the spiral arteries in pregnancies complicated by pre‐eclampsia is assessed.
72 citations
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TL;DR: Significant improvements in the management of labours which fail to progress are needed if normal vaginal delivery rates are to approach those seen inlabours which progress without the need for augmentation.
41 citations
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TL;DR: A more accentuated rate of telomere loss in leukocytes from pre term infants compared to human foetuses of comparable age followed longitudinally for 8–12 weeks in a longitudinal study points to a difference in HSC behaviour between foetal and early postnatal life which is independent of age but may be influenced by events at birth itself.
Abstract: Haemopoietic stem cells (HSC) undergo a process of self renewal to constantly maintain blood cell turnover. However, it has become apparent that adult HSC lose their self-renewal ability with age. Telomere shortening in peripheral blood leukocytes has been seen to occur with age and it has been associated with loss of HSC proliferative capacity and cellular ageing. In contrast foetal HSC are known to have greater proliferative capacity than post-natal stem cells. However it is unknown whether they undergo a similar process of telomere shortening. In this study we show a more accentuated rate of telomere loss in leukocytes from pre term infants compared to human foetuses of comparable age followed longitudinally for 8-12 weeks in a longitudinal study. Our results point to a difference in HSC behaviour between foetal and early postnatal life which is independent of age but may be influenced by events at birth itself.
33 citations
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TL;DR: It is found that hematopoietic stem/progenitor cell deficiency and telomere shortening occurs in individuals with DS in fetal life, and it is proposed that stem cell deficiency may be a primary predisposing event to DS leukemia development.
24 citations
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TL;DR: In this article, the authors focused on the management of VTE and thrombophilia as well as the use of antithrombotic agents during pregnancy. But they did not consider the risk of pregnancy complications.
1,098 citations
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TL;DR: Several features of the human placental bed are mirrored by processes in other species with haemochorial placentation, and studying such models may help to illuminate poorly understood aspects of human placenta and fetus.
1,011 citations
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TL;DR: Dilation has a surprisingly modest impact on total blood flow, and so it is suggested the placental pathology associated with deficient conversion is dominated by rheological consequences rather than chronic hypoxia.
938 citations
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TL;DR: The results indicate that endothelial function is impaired in women with previous preeclampsia and is not explained by established maternal risk factors but is reversed by antioxidant ascorbic acid administration.
Abstract: ContextPreeclampsia is believed to result from release of placental factors
that damage maternal vascular endothelium. However, because most studies have
been conducted during pregnancy, it has not been possible to separate maternal
from placental mechanisms underlying endothelial dysfunction in preeclampsia.ObjectiveTo determine whether endothelial function is impaired in nonpregnant
women with previous preeclampsia and whether endothelial dysfunction is mediated
by oxidative stress.Design and SettingCase-control study conducted at 3 hospital maternity units in London,
England, between July 1997 and June 2000.ParticipantsA total of 113 women with previous preeclampsia (n = 35 with recurrent
episodes; n = 78 with a single episode) and 48 women with previous uncomplicated
pregnancies, all of whom were at least 3 months (median, 3 years) postpartum.Main Outcome MeasuresBrachial artery flow-mediated (endothelium-dependent) and glyceryl trinitrate–induced
(endothelium-independent) dilatation were compared between previously preeclamptic
women and controls. To investigate oxidative stress, these measurements were
repeated after administration of ascorbic acid, 1 g intravenously, in 15 cases
and 15 controls.ResultsMean (SD) flow-mediated dilatation was lower in women with previous
preeclampsia compared with controls (recurrent group, 0.9% [4.1%]; single-episode
group, 2.7% [3.5%]; and control group, 4.7% [4.3%]; P<.001).
In contrast, glyceryl trinitrate–induced dilatation was similar in the
3 groups (recurrent, 19.5% [5.9%]; single-episode, 21.0% [8.0%]; and control,
21.0% [8.3%]; P = .65). Impaired flow-mediated dilatation
in previously preeclamptic women was not accounted for by recognized vascular
risk factors. Ascorbic acid administration increased flow-mediated dilatation
in previously preeclamptic women (baseline, 2.6% [3.3%]; after administration,
5.6% [3.0%]; P = .001) but not in controls (baseline,
6.2% [3.3%]; after administration, 6.7% [5.0%]; P
= .72).ConclusionsOur results indicate that endothelial function is impaired in women
with previous preeclampsia and is not explained by established maternal risk
factors but is reversed by antioxidant ascorbic acid administration.
495 citations
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TL;DR: The main-stay of therapy for preeclampsia re-mainsclinicalrecognition through pre-natal care and termination of treatment with delivery with delivery, which leads to recognition throughpre-natalcare andtermination of treatment as well as prophylactic seizure therapy.
Abstract: The main-stay of therapy for preeclampsia re-mainsclinicalrecognitionthroughpre-natalcareandterminationofthediseaseprocess with delivery. Maternal mor-tality has been reduced in the UnitedStates, but in countries where prena-tal care is not adequate, preeclampsia/eclampsia accounts for 40% to 80% ofmaternal deaths, an estimated 50000per year. Many of these deaths may bepreventablewithprenatalcareandevi-dence-based prophylactic seizuretherapy.Infants of women with preeclamp-sia have a 5-fold increase in mortalitycomparedwithinfantsofmotherswith-out the disorder. Much of the neona-tal mortality is attributable to iatro-genicprematurity.Approximately10%ofpreeclampsiaoccursbefore34weeks’gestational age, and indicated deliveryforpreeclampsiaisresponsiblefor15%of preterm US births.
433 citations