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26 results

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  • Chapter 25 - Screening and Intervention for Fetal Growth Restriction
  • from Fetal Growth and Well-being
  • Edited by Mark D. Kilby, University of Birmingham, Anthony Johnson, Dick Oepkes
  • Book: Fetal Therapy
  • Published online: 21 October 2019
  • Print publication: 02 January 2020, pp 279-286
  • View extract

    Summary

    Fetal growth restriction (FGR) can be defined as the failure of the fetus to meet its genetically predetermined growth potential [1] and is associated with significant fetal and perinatal morbidity and mortality. In addition, there is evidence to suggest a longer-term impact of FGR on childhood neurodevelopmental outcomes [2] and cardiovascular and metabolic diseases that manifest in adulthood [3]. However, predicting FGR is not straightforward and methods for screening and diagnosis are imprecise. In the UK and USA, ultrasound scans in the second half of pregnancy are not performed routinely but targeted at women considered to be at risk for FGR, where high risk is identified by maternal characteristics (including anthropometry and pre-existing disease), the development of complications, or clinical suspicion based on being ‘small for dates’ on physical examination. For practical purposes, FGR may be suspected if biometric measurements are below a given threshold of the distribution in the population, typically <10th, 5th or 3rd centile for gestational age, or if there is a reduction in growth velocity (‘crossing centiles’) from previous scans [4]. The difficulty with using biometry alone is that it does not differentiate between the growth-restricted fetus affected by placental insufficiency, and the healthy, constitutionally small fetus. Therefore, additional measures may be employed to diagnose placental dysfunction, such as Doppler studies of the fetal and uteroplacental circulation, and analysis of maternal serum biomarkers. At present, the only treatment available for FGR is to expedite delivery, but at preterm gestations this can also can cause harm. However, new genomics-based research could help us better understand the etiology of growth restriction and identify more accurate diagnostic biomarkers or potential therapeutic targets. This chapter will focus on current practice in screening for and intervention in FGR and will also consider new developments and the future of the field.

  • 15 - Clinical biomarkers of placental development
  • Edited by Graham J. Burton, David J. P. Barker, Ashley Moffett, Kent Thornburg
  • Book: The Placenta and Human Developmental Programming
  • Published online: 04 February 2011
  • Print publication: 16 December 2010, pp 188-200
  • View extract

    Summary

    This chapter summarizes some of the most important aspects of current knowledge in relation to clinical assessment of placentation. Ultrasound allows the assessment of some physical characteristics of the placenta, such as thickness and, more recently using 3D methods, volume. Uterine artery Doppler flow velocimetry can be used to assess the resistance to blood flow in the uterine circulation. First-trimester maternal serum levels of pregnancy-associated plasma protein A (PAPP-A) have been widely studied in the assessment of Down's syndrome risk. Clinical manifestations of serious complications of pregnancy, such as growth restriction, pre-eclampsia and stillbirth are preceded by abnormalities in clinical biomarkers of placentation. Several large-scale prospective cohort studies are in progress which aims to improve on currently available methods for clinical detection of impaired placentation. Multiple lines of evidence indicate an important role for abnormal placentation in the pathophysiology of many of the most important complications of pregnancy.
  • Chapter 22 - Periconceptual and early pregnancy approach
  • from Section 8: - Translation to obstetrics
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book: Placental Bed Disorders
  • Published online: 06 July 2010
  • Print publication: 03 June 2010, pp 243-255
  • View abstract

    Summary

    At the time of the discovery of the physiological changes of spiral arteries in the pregnant uterus, Brosens and colleagues suggested that these changes result from the destructive action of the invading trophoblasts on the vascular smooth muscle and the elastic membrane. This chapter reiterates the main findings regarding the successive spiral artery remodeling steps. It seems appropriate to relate the time-course of the vascular remodeling process to the new insights in uteroplacental flow changes during this pregnancy period. In preeclampsia, trophoblast-associated remodeling is restricted to decidual spiral arteries throughout the placental bed. Spiral artery conversion is obviously important for safeguarding an adequate maternal blood supply to the placenta. Deep trophoblast invasion and spiral artery remodeling of the inner 'junctional zone' myometrium is a feature of normal human pregnancy, while in preeclampsia and maybe in other pregnancy complications this process may be seriously impaired.
  • Genetic utility of broadly defined bipolar schizoaffective disorder as a diagnostic concept
  • M. L. Hamshere, E. K. Green, I. R. Jones, L. Jones, V. Moskvina, G. Kirov, D. Grozeva, I. Nikolov, D. Vukcevic, S. Caesar, K. Gordon-Smith, C. Fraser, E. Russell, G. Breen, D. St Clair, D. A. Collier, A. H. Young, I. N. Ferrier, A. Farmer, P. McGuffin, P. A. Holmans, M. J. Owen, M. C. O'Donovan, N. Craddock, Wellcome Trust Case Control Consortium
  • Journal: The British Journal of Psychiatry / Volume 195 / Issue 1 / July 2009
  • Published online by Cambridge University Press: 02 January 2018, pp. 23-29
  • Print publication: July 2009
    • Article
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  • View abstract
    Background

    Psychiatric phenotypes are currently defined according to sets of descriptive criteria. Although many of these phenotypes are heritable, it would be useful to know whether any of the various diagnostic categories in current use identify cases that are particularly helpful for biological–genetic research.

    Aims

    To use genome-wide genetic association data to explore the relative genetic utility of seven different descriptive operational diagnostic categories relevant to bipolar illness within a large UK case–control bipolar disorder sample.

    Method

    We analysed our previously published Wellcome Trust Case Control Consortium (WTCCC) bipolar disorder genome-wide association data-set, comprising 1868 individuals with bipolar disorder and 2938 controls genotyped for 276 122 single nucleotide polymorphisms (SNPs) that met stringent criteria for genotype quality. For each SNP we performed a test of association (bipolar disorder group v. control group) and used the number of associated independent SNPs statistically significant at P<0.00001 as a metric for the overall genetic signal in the sample. We next compared this metric with that obtained using each of seven diagnostic subsets of the group with bipolar disorder: Research Diagnostic Criteria (RDC): bipolar I disorder; manic disorder; bipolar II disorder; schizoaffective disorder, bipolar type; DSM–IV: bipolar I disorder; bipolar II disorder; schizoaffective disorder, bipolar type.

    Results

    The RDC schizoaffective disorder, bipolar type (v. controls) stood out from the other diagnostic subsets as having a significant excess of independent association signals (P<0.003) compared with that expected in samples of the same size selected randomly from the total bipolar disorder group data-set. The strongest association in this subset of participants with bipolar disorder was at rs4818065 (P = 2.42 × 10–7). Biological systems implicated included gamma amniobutyric acid (GABA)A receptors. Genes having at least one associated polymorphism at P<10–4 included B3GALTS, A2BP1, GABRB1, AUTS2, BSN, PTPRG, GIRK2 and CDH12.

    Conclusions

    Our findings show that individuals with broadly defined bipolar schizoaffective features have either a particularly strong genetic contribution or that, as a group, are genetically more homogeneous than the other phenotypes tested. The results point to the importance of using diagnostic approaches that recognise this group of individuals. Our approach can be applied to similar data-sets for other psychiatric and non-psychiatric phenotypes.

  • 16 - Long-term implications of pre-eclampsia for maternal health
  • from Part I - Basic science
  • Edited by Fiona Lyall, University of Glasgow, Michael Belfort, University of Utah
  • Book: Pre-eclampsia
  • Published online: 03 September 2009
  • Print publication: 10 May 2007, pp 232-240
  • View extract

    Summary

    Introduction

    The immediate clinical consequences and associations of pre-eclampsia are the subject of intense study and are reviewed in depth throughout this volume. It is natural for any woman who experiences a hypertensive disorder in pregnancy to enquire what implications this has, if any, for her future health. While the long-term outcome of women who experience pre-eclampsia has been the subject of research, there are still major uncertainties regarding this area due to the inherent problems of long-term longitudinal clinical studies. The aim of this chapter is to summarize the recent evidence regarding the implications of pre-eclampsia occurring during pregnancy for a woman's health in later life. Moreover, methodological issues related to addressing this research question will also be reviewed both to assist interpretation of the existing literature and to provide guidance for how future studies might be conducted.

    Methodological issues in determining long-term associations with pre-eclampsia

    Study design

    Epidemiological studies generally aim to quantify the association between developing a given disease and some characteristic in a population. The characteristic can take many forms, such as a blood test, environmental exposure or socio-economic factor. The first step in any study is to determine whether the outcome and exposure are associated to a degree which is greater than expected by chance. Any analysis assumes that a sufficient number of individuals were studied to allow detection of an association, were any to exist. Having demonstrated an association, the next step is to determine whether the association is likely to be causal.

  • Screening cool-season legume cover crops for pecan orchards
  • Michael W. Smith, Raymond D. Eikenbary, Don C. Arnold, B. Scott Landgraf, Glenn G. Taylor, Gordon E. Barlow, Becky L. Carroll, Becky S. Cheary, Natasha R. Rice, Robert Knight
  • Journal: American Journal of Alternative Agriculture / Volume 9 / Issue 3 / September 1994
  • Published online by Cambridge University Press: 30 October 2009, pp. 127-134
  • Print publication: September 1994
  • View abstract

    We evaluated selected cool-season annual and perennial legumes as potential ground covers to supply nitrogen and to increase beneficial arthropod populations in a pecan orchard. Densities of aphids (Homoptera: Aphididae), lady beetles (Coleoptera: Coccinellidae), damsel bug (Hemiptera: Nabidae), green lacewings (Neuroptera: Chrysopidae), brown lacewings (Neuroptera: Hemerobiidae), hover flies (Diptera: Syrphidae), spined soldier bug and other stink bugs (Hemiptera: Pentatomidae), and spiders (Araneida) were monitored at 7–14 day intervals during the growing season for three years. Aboveground biomass production and nitrogen content of the legumes was measured for two years. Aphids peaked during early spring each year, with the highest density usually on ‘Dixie’ crimson clover and ‘Kenland’ red clover. Density of lady beetles was positively correlated with that of aphids, but spider densities were not. Other arthropods usually were not abundant. Nitrogen in the tops of the annual legumes ranged from 20 kg/ha to 89 kg/ha when assessed after a single harvest at anthesis; for the perennial legumes it was from 108 kg/ha to 179 kg/ha following two harvests in June and September. We chose two annual legumes (‘Dixie’ crimson clover and hairy vetch) and two perennial legumes (‘Louisiana S-1’ white clover and ‘Kenland’ red clover) for further evaluation.

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