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Zeitschriftenartikel zum Thema "Fetal growth retardation":
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M N, Dharmavijaya, Kala K, Sujata Datti, Anupama Rani V, Kumar Kumar und Guruprasad G A. „Antepartum Fetal Surveillance in Intra Uterine Growth Retardation“. JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 03, Nr. 1 (15.03.2013): 27–31. http://dx.doi.org/10.58739/jcbs/v03i1.6.
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Kempley, S. „Doppler and fetal growth retardation.“ Archives of Disease in Childhood - Fetal and Neonatal Edition 70, Nr. 2 (01.03.1994): F160. http://dx.doi.org/10.1136/fn.70.2.f160-a.
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Soothill, R. W., R. A. Ajayi und K. N. Nicolaides. „Fetal biochemistry in growth retardation“. Early Human Development 29, Nr. 1-3 (Juni 1992): 91–97. http://dx.doi.org/10.1016/0378-3782(92)90062-l.
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Beattie, R. B., und M. J. Whittle. „Doppler and fetal growth retardation.“ Archives of Disease in Childhood 69, Nr. 3 Spec No (01.09.1993): 271–73. http://dx.doi.org/10.1136/adc.69.3_spec_no.271.
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Intrauterine growth retardation can result from a variety of environmental and genetic influences on fetal growth. The sequelae of intrauterine growth retardation resulting from impairment of nutrient flow include low birth weight with sparing of brain growth, polycythemia, and hypoglycemia resulting from decreased storage fuels and defective gluconeogenesis. Available data suggest that the vast majority of nutritionally growthretarded infants have normal postnatal development without significant difference in IQ or neurologic scores from normal infants. The outcome of infants in whom there is decreased growth potential relates to the condition underlying growth retardation and may, of course, result in later severe handicap. Infants with nutritional intrauterine growth retardation may exhibit decreased fetal size and sparing of brain growth as an adaptive stage in the presence of lower oxygen and substrate availability. Under such conditions, a smaller size may decrease substrate and oxygen needs and improve outcome. All infants with intrauterine growth retardation, however, require follow-up and careful developmental evaluation.
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Lazareva, V. K., R. S. Zamaleeva und N. A. Cherepanova. „Clinical significance of regulatory antibodies content evaluation in pregnant women with fetal growth retardation“. Kazan medical journal 95, Nr. 6 (15.12.2014): 836–40. http://dx.doi.org/10.17816/kmj1990.
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Aim. To identify the possibility of fetal growth retardation prediction at early stages of pregnancy by revealing changes in the content of some regulatory autoantibodies. Methods. A comprehensive examination of 388 pregnant women at risk of gestational complications was performed. After standardization of groups 185 pregnant women were selected for the analysis. Out of these, 80 patients with fetal growth retardation were included into the main group, 80 matched pairs were selected from the group of pregnant women at risk of fetal growth retardation (comparison group). The control group consisted of 25 healthy pregnant women with physiological pregnancy and childbirth. Patients with fetal growth retardation were divided into three subgroups. The first subgroup consisted of 40 pregnant women with grade I of fetal growth retardation, 24 pregnant women with grade II of fetal growth retardation formed the second subgroup, and 16 pregnant women with grade III of fetal growth retardation were included into the third subgroup. Along with the standard methods of examination the serum levels of regulatory class G antibodies binding with double-stranded deoxyribonucleic acid, β2-glycoprotein, total phospholipids, human chorionic gonadotropin, collagen, pregnancy-associated plasma protein-A, insulin, and the level of anti-neutrophil cytoplasmic antibodies, on the dates of 11-14 and 26-28 weeks of pregnancy. Results. The peculiarities of the regulatory autoantibodies content in pregnant women with fetal growth retardation and in women at risk of this condition were revealed. Pregnant women with grade I and II of fetal growth retardation had higher values of autoantibodies, whereas severe forms of fetal growth retardation were characterized by diverse changes of the examined regulatory autoantibodies with a predominance of low values. In case of pregnant women at risk of fetal growth retardation changes in the content of regulatory autoantibodies were diverse. Conclusion. The revealed changes in the content of regulatory autoantibodies can be used for prediction of fetal growth retardation in pregnant women.
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Kopteyeva, Ekaterina V., Elizaveta V. Shelayeva, Elena N. Alekseenkova, Stanislava V. Nagorneva, Roman V. Kapustin und Igor Yu Kogan. „Fetal growth restriction in diabetic pregnancy: a retrospective single-center study“. Journal of obstetrics and women's diseases 71, Nr. 6 (07.02.2023): 15–27. http://dx.doi.org/10.17816/jowd115018.
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BACKGROUND: The high risk of adverse maternal and perinatal complications in patients with fetal growth restriction and diabetes mellitus requires a detailed assessment of the major risk factors and outcomes.
AIM: The aim of this study was to determine the main risk factors for fetal growth retardation in pregnant women with pregestational and gestational diabetes mellitus, and to assess obstetric and perinatal outcomes in these patients.
MATERIALS AND METHODS: We conducted a retrospective single-center cohort study at the premises of the Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott, Saint Petersburg, Russia. The study included 103 patients with type 1 diabetes mellitus, type 2 diabetes mellitus, or gestational diabetes mellitus with fetal growth retardation who delivered a singleton neonate from January 2017 to December 2021. Based on the antenatal diagnosis, the patients were divided into the following comparison groups: group I early fetal growth retardation (n = 29), group II late fetal growth retardation (n = 27), group III small for gestational age (n = 47). Relative risk calculations were used to assess the contribution of risk factors and the risk of developing secondary outcomes.
RESULTS: Pregestational diabetes mellitus was the major risk factor for early fetal growth retardation development (relative risk 1.91; 95% confidence interval 1.043.50); especially type 1 diabetes mellitus (relative risk 1.64; 95% confidence interval 1.022.74) and more than 10 years of pregestational diabetes mellitus duration (relative risk 2.62; 95% confidence interval 1.126.17). Chronic hypertension increases the risk of early fetal growth retardation (relative risk 2.11; 95% confidence interval 2.213.68), while gestational hypertension was a significant risk factor for late fetal growth retardation development (relative risk 1.81; 95% confidence interval 1.013.70). Preeclampsia is associated with both early and late forms of fetal growth retardation. Maternal characteristics, such as age over 35 years, obesity, and in vitro fertilization pregnancy, increased the risk of early fetal growth retardation development. In turn, the presence of fetal growth retardation in patients with diabetes mellitus is associated with increased risk of cesarean section, prolonged stay of the newborn in the neonatal intensive care unit (5 days), low Apgar scores (7 at the 5th minute), and neonatal hypoglycemia. Early fetal growth retardation is a significant risk factor for preterm birth (relative risk 6.23; 95% confidence interval 2.8713.42) and fetal distress (relative risk 5.51; 95% confidence interval 2.2813.33).
CONCLUSIONS: Being associated with a highly increased risk of adverse obstetric and perinatal outcomes, early fetal growth retardation in diabetic pregnancy is related to pregestational diabetes mellitus, especially type 1 diabetes mellitus, with a long history, as well as with hypertension in pregnancy.
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Kravchenko, E. N., und L. V. Kuklina. „Risk factors for fetal growth retardation“. Problemy reproduktsii 28, Nr. 5 (2022): 72. http://dx.doi.org/10.17116/repro20222805172.
Dissertationen zum Thema "Fetal growth retardation":
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Lok, Fong. „Role of IGF-I in ovine fetal and placental growth and development /“. Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phl836.pdf.
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De, Blasio Miles Jonathon. „Placental restriction and endocrine control of postnatal growth“. Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phd2869.pdf.
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Turner, Anita Jillian Connelly. „Ultrasound measures of growth in the normal and the growth restricted fetal guinea pig“. Thesis, The University of Sydney, 1997. https://hdl.handle.net/2123/27664.
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The first chapter gives an overview of the literature available on the topic of IUGR. The second and third chapters involve the creation of normal ranges for ultrasound measures of growth and umbilical placental blood flow in the fetal guinea pig. The fourth chapter describes techniques used to cause growth parameters mentioned above, to describe the pattern of IUGR.
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Jain, Arjun. „Role of ET-1 in the induction of placental endoplasmic reticulum stress in pre-eclampsia and intrauterine growth restriction“. Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610243.
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Collins, Sally. „Development of placental ultrasound markers to screen for the term, small for gestational age (SGA) baby“. Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711642.
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Louey, Samantha 1977. „The effects of intrauterine growth restriction on postnatal growth, arterial pressure and the vasculature“. Monash University, Dept. of Physiology, 2003. http://arrow.monash.edu.au/hdl/1959.1/7939.
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Lam, Shih-en, und 林詩恩. „A pilot study on potential involvement of epigenetic regulations secondary to perturbed intrauterine environment“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41509018.
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Lam, Shih-en. „A pilot study on potential involvement of epigenetic regulations secondary to perturbed intrauterine environment“. Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41509018.
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Mahendran, Dhushyanthan. Transcellular transport in human placenta: Changes in fetal growth retardation and during gestation. Manchester: University of Manchester, 1993.
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Detmer, Ann. Intrauterine growth retardation: An experimental study of fetal growth, regional blood flow and hepatic lipid metabolism in the anaesthetized guinea pig. Uppsala: Sveriges Lantbruksuniversitet, 1992.
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Lin, Chin-Chu. „Fetal Growth Retardation“. In The High-Risk Fetus, 360–95. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9240-8_20.
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Nicolaides, K. H., D. L. Economides und G. Thorpe-Beeston. „Treatment of fetal growth retardation“. In Fetal Growth, 333–61. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1707-0_34.
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Campbell, S. „The detection of intrauterine growth retardation“. In Fetal Growth, 251–61. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1707-0_25.
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Chard, T., und R. J. S. Howell. „Detection of fetal growth retardation by biochemical tests“. In Fetal Growth, 263–72. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1707-0_26.
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Clapp, J. F., N. S. Peress, P. M. Catalano und L. I. Mann. „Fetal Heart Rate Patterns in Experimental Intrauterine Growth Retardation“. In Fetal Heart Rate Monitoring, 212–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70358-4_22.
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Rosso, Pedro, und Sofía P. Salas. „Mechanisms of Fetal Growth Retardation in the Underweight Mother“. In Advances in Experimental Medicine and Biology, 1–9. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-2575-6_1.
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Gluckman, P. D., J. E. Harding, M. H. Oliver, L. Liu, G. R. Ambler, M. Klempt und B. H. Breier. „Mechanisms of Intrauterine Growth Retardation: Role of Fetal and Maternal Hormones“. In Growth Hormone and Somatomedins during Lifespan, 147–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78217-6_14.
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Clapp, J. F. „Restricted Fetal Oxygen Supply: A Cause of Intrauterine Growth Retardation?“ In OXYGEN: Basis of the Regulation of Vital Functions in the Fetus, 217–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77469-0_29.
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Fitzhugh, Valerie A., und Debra S. Heller. „The Placenta in Noninfectious Causes of Fetal Intrauterine Growth Retardation: A Focus on Clinical Features and Placental Pathology“. In Handbook of Growth and Growth Monitoring in Health and Disease, 299–324. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1795-9_18.
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Konferenzberichte zum Thema "Fetal growth retardation":
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Nithya, J., und M. Madheswaran. „Detection of Intrauterine Growth Retardation Using Fetal Abdominal Circumference“. In 2009 International Conference on Computer Technology and Development. IEEE, 2009. http://dx.doi.org/10.1109/icctd.2009.213.
