Relevant bibliographies by topics / Intrauterine growth restriction (IUGR)

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Academic literature on the topic 'Intrauterine growth restriction (IUGR)'

Author: Grafiati
Published: 4 June 2021
Last updated: 27 April 2022

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Journal articles on the topic "Intrauterine growth restriction (IUGR)"

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Gulczyńska, Ewa, Ewa Peterson, Tomasz Radzik, and Ludmiła Żylińska. "BIOMARKERS OF INTRAUTERINE GROWTH RESTRICTION." Wiadomości Lekarskie 72, no. 3 (2019): 436–41. http://dx.doi.org/10.36740/wlek201903122.

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Intrauterine growth restriction (IUGR) is a serious clinical problem affecting about 10% of all pregnancies, and even up to 15% of all monochorionic twin pregnancies. This disorder is accompanied by strongly increased perinatal mortality. IUGR has multiple causes including maternal, fetal, placental, and environmental factors. Importantly, IUGR is associated with a number of negative effects exerted just after the birth, as well as during the later years of life. Despite multiple clinical trials conducted for many years, there is no reliable algorithm to diagnose the disease at an early stage, and lack of efficient therapy increases the risk of abnormal fetus development. In this short review, we present recent progress on potential IUGR biomarkers that could be determined during pregnancy and in the umbilical blood after delivery to provide more accurate diagnosis, prophylaxis and efficient treatment.
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Boutsikou, Theodora, George Mastorakos, Marialena Kyriakakou, Alexandra Margeli, Demetrios Hassiakos, Ioannis Papassotiriou, Christina Kanaka-Gantenbein, and Ariadne Malamitsi-Puchner. "Circulating Levels of Inflammatory Markers in Intrauterine Growth Restriction." Mediators of Inflammation 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/790605.

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We aimed to investigate possible alterations in circulating levels of the perinatal stress markers high sensitivity (hs)-CRP, PAI-1, and S100B—probably reflecting brain and adipose tissue inflammation—in intrauterine growth-restricted-(IUGR) and appropriate-for-gestational-age-(AGA) pregnancies, given that these groups differ in fat mass and metabolic mechanisms involving aseptic inflammation. Serum hs-CRP, PAI-1, and S100B levels were measured in 40 mothers, and their 20 AGA and 20 IUGR full-term fetuses and neonates on postnatal days 1 and 4. hs-CRP, PAI-1, and S100B levels did not differ at all time points between AGA and IUGR groups. We conclude that the lack of difference in hs-CRP, PAI-1 and S100B levels, between IUGR and AGA fetuses/neonates—despite the lower birth weight, reflecting reduced fat mass in the former—might indicate more intense adipose tissue and nervous system inflammation in IUGRs. However, implication of other inflammation-related mechanisms, common in the IUGR state (e.g. preeclampsia), cannot be excluded.
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Hăşmăşanu, Monica, Sorana Bolboacă, Tudor Drugan, Melinda Matyas, and Gabriela Zaharie. "Parental factors associated with intrauterine growth restriction." Srpski arhiv za celokupno lekarstvo 143, no. 11-12 (2015): 701–6. http://dx.doi.org/10.2298/sarh1512701h.

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Introduction. Linear growth failure is caused by multiple factors including parental factors. Objective. The aim of this study was to evaluate parental risk factors for intrauterine growth restriction (IUGR) on a population of Romanian newborn infants in a tertiary level maternity facility for a period of 2.5 years. Methods. A retrospective matched case-control study was conducted in the Emergency County Hospital of Cluj-Napoca, a university hospital in North-Western Romania. The sample was selected from 4,790 infants admitted to the Neonatal Ward at 1st Gynecology Clinic between January 2012 and June 2014. Results. The age of mothers was significantly lower in the IUGR group compared to controls (p=0.041). A significantly higher percentage of mothers had hypertension in the IUGR group compared to those in the control group (p<0.05). No other significant differences were identified with regard to the investigated characteristics of mothers between IUGR infants compared to controls (p>0.13). The age of fathers of infants with IUGR proved significantly lower compared to controls (p=0.0278). The analysis of infants? comorbidities revealed no significant difference between groups for respiratory distress, hyperbilirubinemia, hypocalcaemia, and heart failure (p>0.27). Intracranial hemorrhage, necrotizing enterocolitis and hypoglycemia were significantly higher in the IUGR group compared to controls. The logistic regression identified hypertension as a significant risk factor for IUGR (OR=2.4, 95% CI [1.3-4.5]). Conclusion. Although the age of the mothers and fathers proved significantly lower in the IUGR group compared to controls, only hypertension in the mothers proved significant risk factors for IUGR.
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Petca, Aida, Mihaela Boț, Mona Elena Zvâncă, and Alina Veduţa. "Fetal growth restriction – recent developments." Ginecologia.ro 20 (2), no. 1 (May 20, 2018): 26–29. http://dx.doi.org/10.26416/gine.20.2.2018.1710.

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Important progress has recently been made in the under­standing, diagnosis and treatment of intrauterine fetal growth restriction (IUGR). In 2016, a consensus on the definition of IUGR was reached. Early IUGR (IUGR before 32 weeks of gestation) is a relatively rare but severe con­di­tion. The diagnosis of early IUGR is straightforward, but the therapeutic results are negatively influenced by severe prematurity. The prevalence of late IUGR (IUGR after 32 weeks of gestation) is not clearly known. The therapeutic results are good in the diagnosed cases of late IUGR, but the diagnosis of the condition in the general pregnant population is difficult.
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Verma, Pankaj, and Hema Chaudhary. "Understanding intrauterine growth restriction (IUGR): a review." Journal of Biomedical Sciences 2, no. 4 (August 9, 2016): 31–37. http://dx.doi.org/10.3126/jbs.v2i4.15426.

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Intrauterine Growth Restriction (IUGR) is defined as the inability of a fetus to gain the normal growth potential due to maternal-placental-fetal factors. These factors mainly involve metabolic disorders, infections, substance abuse and exposure to harmful substances. Incidence of IUGR is higher in developing countries. Proper diagnosis at suitable time is necessary for proper treatment and management. Although, the mechanism is not clear but oxidative stress, immunological factors, aryl hydrocarbon receptor and adduct formation are some pathways which are involved in IUGR. The aftermaths of IUGR involves post-birth complications, perinatal mortality and morbidity. Therefore, management and treatment involves use of both pharmacological (Tocolytics, Corticosteroids, antibiotics) and non-pharmacological methods (bed rest, cerclage). This review highlights the possible risk factors, mechanisms, other biochemical pathways involved, as well as pharmacological and non-pharmacological management of IUGR.Journal of Biomedical Sciences. 2015;2(4):31-37
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Khajuria, Ruchi, and Megha Sharma. "Histopathology of placenta in intrauterine growth restriction (IUGR)." International Journal of Research in Medical Sciences 7, no. 3 (February 27, 2019): 889. http://dx.doi.org/10.18203/2320-6012.ijrms20190943.

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Background: Birth of healthy term baby depends on normal placenta. IUGR is a condition associated with placental insufficiency. There is a close relationship between IUGR and placental qualitative changes. The aim of the present study was to evaluate the morphological and histological changes in placentas of IUGR fetuses and in placentas of normal uncomplicated pregnancies and to determine the relationship that exists between morphological change and frequency of IUGR.Methods: In a cross sectional study conducted in the department of Pathology, GMC Jammu, a total of 60 placenta were received, 30 placenta of IUGR fetus (group 1-case) and 30 placenta of uncomplicated pregnancy with normal single fetus (group 2-control). Exclusion criteria: Twin pregnancy, gestational hypertension, diabetes, congenital anomaly, antepartum hemorrhage and systemic disorder.Results: Placental weights in IUGR group were significantly lower than control group. Average placental weight in IUGR group was 425 gms while in the control group (normal placenta) it was 550 gms. Infarction, intervillous thrombosis, chorionic villitis, hemorrhagic endovasculitis, placental intravascular thrombi, perivillous fibrin deposition, fibrinoid necrosis and villous edema were found to be more common in IUGR group (Group 1-case group) than Normal (Group 2- control group).Conclusions: This study highlightened that significant pathological differences were found between the placentas of IUGR fetus and normal fetus. The gross and microscopic measurement of a placenta is a good way to get proper information about IUGR and helps in management of the pregnancy.
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Sharma, Deepak, Sweta Shastri, and Pradeep Sharma. "Intrauterine Growth Restriction: Antenatal and Postnatal Aspects." Clinical Medicine Insights: Pediatrics 10 (January 2016): CMPed.S40070. http://dx.doi.org/10.4137/cmped.s40070.

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Intrauterine growth restriction (IUGR), a condition that occurs due to various reasons, is an important cause of fetal and neonatal morbidity and mortality. It has been defined as a rate of fetal growth that is less than normal in light of the growth potential of that specific infant. Usually, IUGR and small for gestational age (SGA) are used interchangeably in literature, even though there exist minute differences between them. SGA has been defined as having birth weight less than two standard deviations below the mean or less than the 10th percentile of a population-specific birth weight for specific gestational age. These infants have many acute neonatal problems that include perinatal asphyxia, hypothermia, hypoglycemia, and polycythemia. The likely long-term complications that are prone to develop when IUGR infants grow up includes growth retardation, major and subtle neurodevelopmental handicaps, and developmental origin of health and disease. In this review, we have covered various antenatal and postnatal aspects of IUGR.
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Devaskar, Sherin U., and Alison Chu. "Intrauterine Growth Restriction: Hungry for an Answer." Physiology 31, no. 2 (March 2016): 131–46. http://dx.doi.org/10.1152/physiol.00033.2015.

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Intrauterine growth restriction (IUGR) has been defined in several ways, but in general describes a condition in which the fetus exhibits poor growth in utero. This complication of pregnancy poses a significant public health burden as well as increased morbidity and mortality for the offspring. In human IUGR, alteration in fetal glucose and insulin homeostasis occurs in an effort to conserve energy and survive at the expense of fetal growth in an environment of inadequate nutrient provision. Several animal models of IUGR have been utilized to study the effects of IUGR on fetal glucose handling, as well as the postnatal reprogramming of energy metabolite handling, which may be unmasked in adulthood as a maladaptive propensity for cardiometabolic disease. This developmental programming may be mediated in part by epigenetic modification of essential regulators of glucose homeostasis. Several pharmacological therapies and nonpharmacological lifestyle modifications have shown early promise in mitigating the risk for or severity of adult metabolic phenotypes but still require further study of unanticipated and/or untoward side effects.
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Verschuren, M. T. C., J. S. Morton, A. Abdalvand, Y. Mansour, C. F. Rueda-Clausen, C. A. Compston, V. Luyckx, and S. T. Davidge. "The effect of hypoxia-induced intrauterine growth restriction on renal artery function." Journal of Developmental Origins of Health and Disease 3, no. 5 (April 25, 2012): 333–41. http://dx.doi.org/10.1017/s2040174412000268.

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The risk of developing cardiovascular diseases is known to begin before birth and the impact of the intrauterine environment on subsequent adult health is currently being investigated from many quarters. Following our studies demonstrating the impact of hypoxiain uteroand consequent intrauterine growth restriction (IUGR) on the rat cardiovascular system, we hypothesized that changes extend throughout the vasculature and alter function of the renal artery. In addition, we hypothesized that hypoxia induces renal senescence as a potential mediator of altered vascular function. We demonstrated that IUGR females had decreased responses to the adrenergic agonist phenylephrine (PE; pEC506.50 ± 0.05 controlv. 6.17 ± 0.09 IUGR,P< 0.05) and the endothelium-dependent vasodilator methylcholine (MCh;Emax89.8 ± 7.0% controlv. 41.0 ± 6.5% IUGR,P< 0.001). In IUGR females, this was characterised by increased basal nitric oxide (NO) modulation of vasoconstriction (PE pEC506.17 ± 0.09 IUGRv. 6.42 ± 0.08 in the presence of the NO synthase inhibitorN-nitro-l-arginine methyl ester hydrochloride (l-NAME;P< 0.01) but decreased activated NO modulation (no change in MCh responses in the presence ofl-NAME), respectively. In contrast, IUGR males had no changes in PE or MCh responses but demonstrated increased basal NO (PE pEC506.29 ± 0.06 IUGRv. 6.42 ± 0.12 plusl-NAME,P< 0.01) and activated NO (Emax37.8 ± 9.4% controlv. −0.8 ± 13.0% plusl-NAME,P< 0.05) modulation. No significant changes were found in gross kidney morphology, proteinuria or markers of cellular senescence in either sex. In summary, renal vascular function was altered by hypoxiain uteroin a sex-dependent manner but was unlikely to be mediated by premature renal senescence.
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Majewska, Marta, Aleksandra Lipka, Lukasz Paukszto, Jan Jastrzebski, Karol Szeszko, Marek Gowkielewicz, Ewa Lepiarczyk, Marcin Jozwik, and Mariusz Majewski. "Placenta Transcriptome Profiling in Intrauterine Growth Restriction (IUGR)." International Journal of Molecular Sciences 20, no. 6 (March 26, 2019): 1510. http://dx.doi.org/10.3390/ijms20061510.

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Intrauterine growth restriction (IUGR) is a serious pathological complication associated with compromised fetal development during pregnancy. The aim of the study was to broaden knowledge about the transcriptomic complexity of the human placenta by identifying genes potentially involved in IUGR pathophysiology. RNA-Seq data were used to profile protein-coding genes, detect alternative splicing events (AS), single nucleotide variant (SNV) calling, and RNA editing sites prediction in IUGR-affected placental transcriptome. The applied methodology enabled detection of 37,501 transcriptionally active regions and the selection of 28 differentially-expressed genes (DEGs), among them 10 were upregulated and 18 downregulated in IUGR-affected placentas. Functional enrichment annotation indicated that most of the DEGs were implicated in the processes of inflammation and immune disorders related to IUGR and preeclampsia. Additionally, we revealed that some genes (S100A13, GPR126, CTRP1, and TFPI) involved in the alternation of splicing events were mainly implicated in angiogenic-related processes. Significant SNVs were overlapped with 6533 transcripts and assigned to 2386 coding sequence (CDS), 1528 introns, 345 5’ untranslated region (UTR), 1260 3’UTR, 918 non-coding RNA (ncRNA), and 10 intergenic regions. Within CDS regions, 543 missense substitutions with functional effects were recognized. Two known mutations (rs4575, synonymous; rs3817, on the downstream region) were detected within the range of AS and DEG candidates: PA28β and PINLYP, respectively. Novel genes that are dysregulated in IUGR were detected in the current research. Investigating genes underlying the IUGR is crucial for identification of mechanisms regulating placental development during a complicated pregnancy.
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Dissertations / Theses on the topic "Intrauterine growth restriction (IUGR)"

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Hrabálková, Lenka. "The importance of poly(A)-binding protein 4 (PABP4) in healthy pregnancy." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/22923.

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Healthy pregnancy requires a tightly regulated materno-fetal dialogue for processes such as embryo implantation, endometrial decidualisation (in the mouse), placentation and maternal adaptation to occur. Disruption of placental development as well as maternal adaptation can lead to fetal intrauterine growth restriction (IUGR) which increases the risk of late miscarriage/stillbirth (e.g. 53% of preterm stillbirth and 26% of term stillbirth are found to be IUGR). Furthermore, IUGR is a risk factor for neurodevelopmental conditions in childhood and for a spectrum of related adult health disorders such as cardiovascular disease and type II diabetes, often termed metabolic syndrome. Despite these pregnancy disorders being common (e.g. 1 in 200 pregnancies results in stillbirth in the UK) the molecular lesion(s) underlying their pathophysiology are poorly understood and in particular those with placental and/or maternal aetiologies most frequently remain unexplained. Here we investigate the hypothesis that poly(A)-binding protein 4 (PABP4) is required for healthy pregnancy in mice. PABP4 is an RNA-binding protein and a member of the PABP family which are central regulators of mRNA translation and stability. Using all four permutations of wild-type and knock-out crosses, we find that maternal PABP4-deficiency results in a reduced litter size and IUGR. The number of implantations at e8.5 were not reduced in Pabp4-/- females, implying that the reduced litter size was not a consequence of decreased ovulation, fertilisation or implantation frequency. Further longitudinal analysis (at e13.5, e15.5 and e18.5) reveals that fetal death primarily occurred between e18.5 and birth, suggesting these mice may provide a unique opportunity to inform on the maternal causes of stillbirth. The onset of IUGR, which was found to be symmetrical in nature, was established by e15.5 preceding the majority of fetal death. During pregnancy, a materno-fetal dialogue directs and responds to changes in gene expression to give rise to the placenta and adapt the maternal physiology. Defects in these processes may result in reduced growth and/or fetal death and were examined in Pabp4-/- mice to shed light on the mechanistic basis of these related phenotypes. Fetal to placental (F:P) weight ratio, whose changes can be indicative of placental insufficiency or placental adaptation in an attempt to aid fetal growth, was found to be increased in Pabp4-/- dams at e15.5 and e18.5 due to the presence of IUGR fetuses with placentas of normal weight. Consistent with this observation, placental volume was unchanged at e18.5. Total placental weight and volume alone fails to discriminate potential differences in the individual placental zones which include the labyrinth zone, where materno-fetal gas and nutrient exchange occur; the junctional zone, which has endocrine functions including those that promote maternal adaptation; and the decidua basalis, derived from the maternal endometrium and is the site of trophoblast invasion and maternal vascular remodelling in early pregnancy. Therefore, volumetric analysis of these zones and the maternal blood spaces, which transcend the decidua basalis and junctional zone, was undertaken. This showed no change in the maternal blood spaces or the labyrinth, the latter being the zone whose size is most frequently altered in IUGR. Critically however, the size of the maternally-derived decidua basalis was increased with a concurrent decrease in the size of the junctional zone. These morphological changes may play a causative role either through directly affecting placental function and/or by the reduced junctional zone failing to promote appropriate maternal adaptation. Alternatively, they may reflect compensatory adaptations to a primary defect elsewhere in the mother. Complementing these morphological studies, functional studies were undertaken: remodelling of maternal vasculature and the resistance index of vessels delivering blood to the fetus were assessed; as was delivery of nutrients to the fetus (measured by fetal glucose); and systemic maternal adaptations (maternal hormonal profile, circulating glucose levels and organ weights). Uterine, umbilical and decidual spiral arteries were examined, but displayed no apparent differences suggestive of normal blood supply to the fetus. However fetal blood glucose was reduced suggesting a reduced delivery of nutrients important for fetal growth. This was not due to lower circulating maternal blood glucose levels, and mRNA levels of the placental glucose transporters Glut-1 and Glut-3 were not reduced but upregulated, suggestive of an attempt to compensate for reduced fetal glucose. Furthermore, upregulation of at least one system A amino acid transporter mRNA, Snat-2, was observed. The maternal physiological state of PABP4-deficient dams showed deviations in some organ weights (e.g. spleen weight is reduced at e13.5 and e15.5) and the levels of some circulating hormones (e.g. estradiol is deceased whereas progesterone is increased at e18.5). However, future work will be required to determine which, if any, of these changes are primary defects rather than downstream consequences and to identify which mis-regulated mRNAs/pathways within in the materno-fetal dialogue underlie the phenotype. Taken together, my results suggest that the regulation of mRNA translation/stability by PABP4 is critical to achieving the correct pattern of gene expression within the materno-fetal dialogue to enable appropriate placentation and maternal adaptation. Furthermore, my results suggest that Pabp4-/- mice provide a unique opportunity to further understand the maternal causes of a spectrum of related pregnancy complications including IUGR, late miscarriage and stillbirth.
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Huber, Hillary. "Aggressive Behavioral Phenotype in Intrauterine Growth Restricted (IUGR) Baboons Exposed to Moderate Nutrient Restriction Early in Development." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/824.

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The thrifty phenotype hypothesis proposes reduced nutrition alters the trajectory of development of metabolic regulatory systems to produce a phenotype better fitted to an environment of decreased later-life nutrient availability. Because organisms have physiological mechanisms for coping with poor nutrition, they may have sociobehavioral mechanisms as well. Aggressive behavior, especially in the context of feeding competition, may be advantageous in such environments. There could be an association between aggression and intrauterine growth restriction (IUGR), which can result from low maternal food intake during pregnancy. The main hypotheses of this study are [1] IUGR offspring demonstrate higher rates of aggressive behavior and [2] IUGR offspring attain higher ranks. Behavioral observations were conducted on 22 juvenile baboons (Papio sp., ages 3-5 yrs) living in groups. Male IUGR (n = 4) and female IUGR (n = 5) were offspring of mothers fed 70% the same feed eaten by control (CTR) mothers in pregnancy and lactation. CTR males (n = 8) and CTR females (n = 5) were offspring of mothers fed ad libitum. Some authorities recommend this moderate level of dietary restriction for health and longevity. Offspring have not experienced dietary restriction since weaning. IUGR, compared to CTR, showed significantly increased rates of aggressive behavior, especially threat displays. Differences were more dramatic in males than in females. IUGR baboons performed the affiliative display behaviors lipsmack and chatter at elevated rates too, perhaps to counteract the effects of increased aggressive displays. IUGR females exhibited increased rates of stereotypical chewing behavior, while IUGR males exhibited decreased rates of play behavior, possibly indicating elevated anxiety levels. There was only limited support for condition-based differences in rank. Elevated rates of aggression in IUGR baboons may reflect an aggressive behavioral phenotype that enhances fitness by improving access to resources. Alternatively, they could be a non-adaptive result of neurodevelopment with a potentially negative impact on fitness. Unraveling the dynamic relationship between experiences and development is essential for understanding how phenotypes are formed. This will improve the ability of mothers to assess benefits of different nutritional strategies, leading to healthier individuals not just during growth and development, but throughout life.
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Bahr, Brigham L. "Different Expression of Placental Pyruvate Kinase M2 in Normal, Preeclamptic, and Intrauterine Growth Restriction Pregnancies." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/3901.

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This thesis will be organized into two chapters discussing the placental expression of two proteins, pyruvate kinase M2 (PKM2) and heat shock protein 27 (HSP 27), in human placentas. Understanding the mechanisms of placental metabolism in healthy and diseased placentas helps us understand how placenta disorders occur and how we can treat these disorders. The goal is to investigate these proteins to gain an understanding of their roles in placental disorders and help decrease maternal and fetal mortality rates. Chapter one covers the background of pyruvate kinase M2 (PKM2) in cancer and embryonic tissues, and the expression of PKM2 in the human placenta. Cancer PKM2 has been studied extensively, but little is know about the role of placental PKM2. Expression of PKM2 is confirmed in normal human placenta samples and described in preeclamptic and intrauterine growth restriction (IUGR) affected human placentas. Proteins associated with elevated PKM2 in cancer are also associated with elevated PKM2 in human placentas. Comparing normal and diseased placenta samples helps understand the similarities between cancer PKM2 and placental PKM2. Understanding the mechanisms of placental metabolism and PKM2 expression in the human placenta will clarify how the placenta is affected by preeclampsia and IUGR and the role placental PKM2 plays in each of these diseases. Chapter two will cover a paper that I wrote on the expression of phosphorylated heat shock protein 27 (HSP27) in the human placenta. Heat shock proteins are involved in the stress response and help inhibit apoptosis. The object of the study was to look for correlations between p-HSP27 and apoptosis in human and ovine placenta samples. P-HSP27 was quantified in human placenta samples and in placenta sampled collected from ovine models. Pregnant control and hyperthermic sheep models were used to quantify expression of p-HSP27 across gestation. This study showed similarities between human IUGR and our ovine IUGR model, suggesting a link between decreased p-HSP27 and increased apoptosis in IUGR.
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Yunusova, Roza. "Effects of Maternal Nutrition, Intrauterine Growth Restriction (IUGR), and Estrogen (E2) Supplementation on Placental and Fetal Intestinal Growth and Development in Sheep." Thesis, North Dakota State University, 2012. https://hdl.handle.net/10365/26539.

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The placenta and fetal intestines are two key nutrient transport organs that sustain and nurture growing fetus. Insufficient placental development and consequently inadequate fetal nutrient supply can lead to IUGR resulting in low birth weight offspring. Our experimental objectives were to investigate the effects of elevated maternal nutrition, IUGR, and E2 supplementation during mid-gestation (in an attempt to rescue IUGR offspring) on placental and fetal intestinal cell proliferation, angiogenic gene expression, and vascularity. Limited responsiveness in placental development and vascularization to E2 supplementation was observed, likely due to inappropriate timing or dose of E2. However, maternal E2 supplementation increased fetal small intestinal length and GUCY1b3 mRNA expression, suggesting that E2 supplementation has positive effects on IUGR fetal intestinal growth. In conclusion, understanding molecular mechanisms associated with IUGR and possible effects of E2 supplementation in rescuing IUGR may lead to enhanced human health and livestock production efficiency.
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Iglesias, Platas Isabel. "Intrauterine Growth Restriction (IUGR) and imprinted gene expression in the placenta: Role of PLAGL1 and analysis of the 6q24.2 Region." Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/109049.

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BACKGROUND: Fetal growth is a complex process which depends on nutrient and oxygen availability and transport from the mother to the fetus across the placenta. This involves hormones and growth factors as well as maternal and fetal genes. The failure of the fetus to reach his or her full potential for growth is called Intrauterine Growth Restriction (IUGR) and implies risks for adverse short‐ and long‐ term outcomes. Imprinted genes are a specific subset of genes that display, in mammals and flowering plants, monoallelic expression depending on the parental origin of the allele. The regulation of imprinted expression depends on epigenetic mechanisms, a subset of heritable marks that have the ability to regulate DNA functions without altering its sequence. Imprinted genes tend to cluster in the genome due to coordinated regulation through Imprinting Control Centers, usually in the form of Differentially Methylated Regions between the paternally and maternally inherited alleles. Studies in both animals and humans as well as imprinting syndromes have uncovered a role for this group of genes in prenatal growth. Two imprinted genes (PLAGL1 and HYMAI) have been described in the 6q24 locus. Genetic and epigenetic defects in this region relate to the Transient Neonatal Diabetes Mellitus 1 phenotype, including severe growth restriction. We aimed to study the involvement of this region in non‐syndromic IUGR. PARTICIPANTS AND METHODS: One hundred placental samples from a cohort of healthy term singletons, fetal tissues from fifty‐four first trimester terminations and one hundred placental samples from healthy and complicated pregnancies of different gestational ages were used to analyze the role of the 6q24 region in normal fetal growth and IUGR, respectively. Relevant clinical data was obtained after informed consent. The methylation status of the 6q24 CpG islands was studied by array technology and bisulfite sequencing in normal term placenta and in first trimester fetal tissues. Methylation levels in the PLAGL1 DMR in healthy and IUGR placentas were compared by pyrosequencing. Allelic origin of expression was assessed by heterozygous DNA/cDNA SNP analysis. Levels of expression of imprinted transcripts were analyzed by qRT‐PCR. RESULTS: PLAGL1 P1, HYMAI and two newly described PLAGL1 isoforms (P3 and P4) were the only transcripts subjected to genomic imprinting in the investigated 6q24 region. Correspondingly, the CpG island associated to the P1 promoter was the only differentially methylated region. There was no correlation between PLAGL1 expression in the placenta and fetal size in uneventful pregnancies. In placentas from IUGR gestations, expression of HYMAI was significantly higher than in those from normally grown fetuses. Levels of expression of PLAGL1 were lower in IUGR and correlated positively and significantly with the presence of IUGR in placentas from girls, but not boys. These changes in expression were not mediated by Loss of Imprinting or abnormalities in the levels of methylation of the promoter‐associated DMR, but possibly by a change in regulatory posttranscriptional mechanisms, as suggested by the loss of correlation of PLAGL1 P1 and HYMAI expression in IUGR. CONCLUSIONS: Imprinted expression in the 6q24 region is limited to the PLAGL1/HYMAI locus, maybe due to demarcation of this region by CTCF boundaries. Intrauterine Growth Restriction is associated to abnormalities in expression of PLAGL1 and HYMAI in the placenta, which are not due to LOI or methylation changes.
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Fayyad, Abdalla Mustafa. "The role of soluble FMS-like tyrosine kinase (sFLT1) and FAS associated proteins in pregnancies complicated by preeclampsia and intrauterine growth restriction (IUGR)." Thesis, Queen Mary, University of London, 2005. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1750.

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Current thinking suggests that preeclampsia is associated with activation of the maternal vascular endothelium in response to factors released from the placenta due to placental hypoxia. Failure of physiological modification of spiral arteries due to impaired trophoblast invasion results in a several-fold increase in the risk of developing pre-eclampsia and/or (IUGR). The defect behind impaired trophoblast invasion is not fully explained and the aetiological factor(s) linked with the development of pre-eclampsia, compared to normotensive IUGR, is not known. In this thesis, I examined placental and serum levels of fms-like tyrosine kinase I (sFltl) and placental growth factor (PIGF), as mediators of angiogenesis, and Fas and FasL, as mediators of apoptosis, in three groups; preeclampsia, normotensive IUGR and controls who had abnormal mid-trimester uterine artery Doppler. Uterine artery Doppler flows were examined in 553 women at 24 weeks. 97 of them had abnormal uterine artery Doppler flow and were enrolled in this study. 86 women were followed up; among them eight women developed preeclampsia and seven developed normotensive IUGR. Umbilical artery Doppler examination 24 hours before delivery in both groups, showed significantly lowered resistance indices in the preeclampsia compared to the normotensive IUGR group. I examined placental and serum levels of fms-like tyrosine kinase I (FIt I) and Placental Growth Factor (PIGF) in three groups. Soluble FItI acts as an antagonist for both Vascular Endothelial Growth Factor (VEGF) and PIGF. Placental FIt 1 and serum sFlt 1 were higher and serum PIGF was lower in the preeclampsia group compared to the other two groups. This could be responsible for the systemic manifestations of preeclampsia. This dysregulation in serum sFltl and PIGF was found as early as 24 weeks in pregnancies with abnormal uterine artery Doppler examination. The normotensive IUGR group had significantly elevated serum sFlU compared to controls. This could be due to an element of placental hypoxia in the IUGR group. To investigate the in-vivo effect of sFltl on impaired placental angiogenesis and trophoblast invasion, I examined the correlations between uterine artery Doppler resistance indices and serum sFIU and PIGF at 24 weeks. Significant correlations were found between these markers and uterine artery Doppler pulsatility index (pn and resistance index (Rn on both the placental and non-placental sides at 24 weeks. Fas and Fas ligand (FasL) are membrane proteins that mediate cellular apoptosis, and recently were related to cellular growth and migration. Using western blotting and immunohistochemistry, placental expression of Fas (western blotting) and (FasL) (immunohistochemistry) was assessed in the three study groups. No differences in placental Fas or Fas ligand were found between the groups. In addition, serum levels of Fas and FasL were measured at 24 weeks and within 24 hours of delivery in the same groups. Serum Fas was not different between the three study groups at 24 weeks and within 24 hours of delivery. Serum FasL was below the kit's detection threshold in the samples studied. In conclusion, placental FlU and its soluble form sFltl seem to play an important role in the pathophysiology of preeclampsia. In addition, sFltl correlated positively with the severity of impaired trophoblast invasion and could playa central role in blocking placental angiogenesis in these pregnancies. This needs further evaluation. Fas and FasL do not seem to have a role In impaired placentation and development of preeclampsia and IUGR.
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Diderholm, Barbro. "Perinatal Energy Substrate Metabolism : Glucose Production and Lipolysis in Pregnant Women and Newborn Infants with Particular Reference to Intrauterine Growth Restriction (IUGR)." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4842.

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Kimball, Rebecca Lutz. "The Role of Hypoxia on Pyruvate Kinase M2, mammalian Target of Rapamycin, Mitochondrial Function, and Cell Invasion in the Trophoblast." BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/5723.

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This thesis will be organized into two chapters discussing the role of hypoxia in the human placenta. The goal of this thesis is to characterize pyruvate kinase M2, mammalian target of rapamycin, mitochondrial function, and cell invasion in hypoxic conditions in the trophoblast. Understanding the mechanisms of placental metabolism can lead to further treatments for placental diseases. Chapter one covers the background of intrauterine growth restriction, hypoxia, placental metabolism, and pyruvate kinase M2 (PKM2). Little is currently understood about the role of the mitochondria in placental diseases. Expression of PKM2, trophoblast cell invasion, and mitochondrial function is shown to be inhibited by hypoxia. PKM2 inhibition decreases trophoblast cell invasion and nuclear expression of PKM2, but increases mitochondrial function. Studying how hypoxia affects the placenta during placental diseases can help clarify the mechanisms by which these diseases occur. Chapter two further characterizes the background of intrauterine growth restriction and hypoxia. It also covers the background of mammalian target of rapamycin. The objective of this chapter was to assess activated mTOR in the trophoblast in hypoxia. Decreased placental and fetal weights, as well as trophoblast cell invasion were observed in hypoxia. A decrease in the activation of mTOR was also found in the hypoxic placenta. This study could provide insight into the physiological relevance of the pathways and could be targeted to help alleviate placental diseases.
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Hennig, Maria. "The role of the mTOR pathway and amino acid availability for pre- and postnatal cardiac development, growth and function." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17287.

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Die Entwicklung eines Embryos und Fetus beeinflusst die Anfälligkeit für kardiovaskuläre Erkrankungen im weiteren Verlauf des Lebens entscheidend. Zugrundeliegende Mechanismen sind jedoch weitestgehend unbekannt. Unter Zuhilfenahme eines neuen Mausmodells für intrauterine kardiale Wachstumsretardierung zielt die vorliegende Dissertation auf die Identifikation adaptiver Wachstumsmechanismen ab, welche die Anpassung der Organgröße und die Aufrechterhaltung einer normalen Herzfunktion ermöglichen. Vielzählige Gene des Aminosäure (AS)-Metabolismus und der Proteinhomeostase zeigten eine vermehrte Expression in neugeborenen Mausherzen nach gestörter Embryonalentwicklung. Es wurde angenommen, dass sowohl die AS-Verfügbarkeit als auch die Aktivität der mechanistic target of rapamycin (mTOR) Signalkaskade entscheidend für eine normale Herzentwicklung und postnatales kompensatorisches Wachstum sind. Der mTOR Komplex 1 (mTORC1) wurde in prä- und perinatalen Mäusen mittels Rapamycin-Behandlung trächtiger Weibchen inhibiert. Die Auswirkungen einer prä- und postnatalen AS-Restriktion wurden anhand einer Niedrigproteindiät untersucht. Rapamycin-behandelte Neugeborene zeichneten sich durch vermindertes Gesamtwachstum sowie Entwicklungsverzögerung aus. Dabei war die kardiale Entwicklung besonders betroffen. Kardiale Proliferationsraten waren nicht verändert, die verminderte Herzgröße wurde jedoch auf eine verringerte Kardiomyozytengröße sowie eine erhöhte Apoptoserate zurückgeführt. Die intrauterine AS-Restriktion wurde überraschend gut von den Mausherzen toleriert. Zusammenfassend konnte gezeigt werden, dass die mTOR Signalkaskade essentiell für eine normale Herzentwicklung sowie kompensatorisches kardiales Wachstum ist. Darüber hinaus stellt die pränatale Rapamycin-Behandlung möglicherweise ein neues Modell der intrauterinen Wachstumsretardierung dar, welches Untersuchungen von Programmierungs-Mechanismen vor allem während der fötalen und perinatalen Herzentwicklung ermöglicht.
Intrauterine development influences the susceptibility to cardiovascular disease in adulthood, although the underlying molecular mechanisms are vastly unknown. Utilizing a new mouse model of impaired heart development, this thesis aims at identifying pre- and postnatal adaptive growth mechanisms to restore organ size and allow normal cardiac function. Unbiased functional annotation of genes differentially expressed in neonatal hearts after impaired intrauterine development revealed numerous gene clusters involved in amino acid (AA) metabolism and protein homeostasis. It was hypothesized that both AA availability and mechanistic target of rapamycin (mTOR) pathway activation are crucial for normal heart development and compensatory cardiac growth. mTOR complex 1 (mTORC1) was inhibited in fetal and neonatal mice by rapamycin treatment of pregnant dams. The effects of pre- and postnatal AA restriction were studied by feeding dams a low protein diet (LPD) throughout pregnancy and keeping the offspring on LPD postnatally. Rapamycin treated neonates were characterized by overall growth restriction and developmental delay, where cardiac development was especially affected (reduction of heart size, weight and heart weight to body weight ratio, severe thinning and noncompaction of the ventricular myocardium as well as immature myocardial morphology). While proliferation rates were unaffected, the reduced neonatal heart size was attributed to decreased cardiomyocyte size and increased apoptosis. Strikingly, the murine heart appeared to be surprisingly resistant to intrauterine AA restriction. In conclusion, the data revealed mTOR being essential for normal as well as compensatory cardiac development and growth. Moreover, prenatal rapamycin treatment might represent a new model of intrauterine growth restriction, which potentially allows the investigation of developmental programming mechanisms within the heart particularly in the fetal and neonatal phase of development.
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Zhu, Haibo. "Muscle Growth and Development in Intrauterine Growth Restricted Pigs." Diss., Virginia Tech, 2015. http://hdl.handle.net/10919/72883.

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Intrauterine growth restriction causes impaired growth and development of mammalian fetus, and leads to long-term negative effect on postnatal growth. Among domestic animals, pigs exhibit the most severe naturally occurring IUGR and reduced postnatal muscle growth. The objectives of this research project were to: 1) determine muscle stem cell characteristics in IUGR pigs; 2) determine how intrauterine growth restriction alters protein deposition in skeletal muscle; 3) investigate whether branched-chain amino acids (BCAA) are able to enhance protein synthesis in intrauterine growth restricted (IUGR) pig muscle. Newborn piglets were considered normal body weight (NBWT) or IUGR when birth weight was within ± 0.5 SD and -2 SD of litter average respectively. Muscle satellite cell numbers, believed to be the major nuclei source for postnatal muscle growth, were lower in newborn IUGR pigs which could result in reduced muscle hypertrophy potential. In addition, cultures derived from IUGR muscle satellite cells had a lower fusion percentage. Fewer satellite cells and impaired differentiation ability may contributor to impaired muscle growth in these pigs. Protein synthesis rate was significantly lower in IUGR pig hindquarter in the first hour after feeding, but BCAA supplementation had no effect on protein synthesis in IUGR pigs. Further, eukaryotic translation initiation factor 4E (eIF4E) expression is down regulated in IUGR pig muscle. These results suggest that impaired translation initiation may provide a plausible explanation for the lower protein synthesis rates observed in IUGR pigs. Overall, reduced muscle stem cell number and changes in their activity, as well as impaired translation initiation may be important explanations for compromised postnatal muscle growth in intrauterine growth restricted pigs.
Ph. D.
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Books on the topic "Intrauterine growth restriction (IUGR)"

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Kingdom, John, and Philip Baker, eds. Intrauterine Growth Restriction. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0735-4.

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Stanhope, Richard. Intrauterine growth retardation (IUGR) including Russell Silver Syndrome: A guide for paretns and patients. London: Child Growth Foundation, 1997.

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Jeffress, Andrea Toulson. Prenatal ultrasound biometry combined with umbilical and middle cerebral artery doppler velocimetry for the detection of intrauterine growth restriction. [New Haven, Conn: s.n.], 1996.

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(Editor), John Kingdom, Philip Baker (Editor), and M. Whittle (Preface), eds. Intrauterine Growth Restriction: Aetiology and Management. Springer, 2000.

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Kingdom, John, Philip Baker, and M. Whittle. Intrauterine Growth Restriction: Aetiology and Management. Springer, 2011.

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Winterhager, Elke, Ivo Bendix, and Suzanne Lee Miller, eds. Causes and Consequences of Intrauterine Growth Restriction. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-768-3.

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Medforth, Janet, Linda Ball, Angela Walker, Sue Battersby, and Sarah Stables. Pregnancy complications. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754787.003.0012.

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The chapter is concerned with recognition and the most recent guidance on the management of commonly seen pregnancy complications. These include early pregnancy bleeding, antepartum haemorrhage, hyperemesis, obstetric cholestasis, multiple pregnancy, breech presentation, intrauterine growth restriction, thromboembolic disorders, and the principles of thromboprophylaxis. Each section describes the condition and factors that may lead to its development. Signs and symptoms are described, along with contraindications and aspects of treatment. Special considerations in the antenatal management plans are included.
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Olson-Chen, Courtney. Neurologic Infections in Pregnancy. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0011.

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Despite advances in prevention, diagnosis, and treatment, infectious diseases continue to be a major cause of maternal, fetal, and neonatal morbidity and mortality. Immunologic changes in pregnancy can increase both susceptibility to certain infections and the severity of infection. Infectious diseases in pregnancy contribute to the development of congenital fetal syndromes in addition to adverse outcomes including preterm birth, stillbirth, and intrauterine growth restriction. While infections of the maternal central nervous system, or CNS, are rare during pregnancy, the potential impact can be critical.1 This chapter will cover both the types of infections within the CNS and the potential organisms that cause these infections. The chapter will also provide general management recommendations for pregnancy in order to both prevent and maintain awareness about CNS infections.
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Fox, Grenville, Nicholas Hoque, and Timothy Watts. Antenatal care, obstetrics, and fetal medicine. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198703952.003.0001.

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This chapter contains details of methods used for screening and diagnosis of fetal anomalies using antenatal blood tests, ultrasound scanning, chorionic villous sampling, amniocentesis, and fetal blood sampling. There are sections on pre-existing maternal diseases presenting risks to the fetus including maternal diabetes, systemic lupus erythematosus, thrombocytopenia, and neuromuscular disease, as well as those specific to pregnancy—pre-eclampsia, HELLP syndrome, and eclampsia. Intrauterine growth restriction and monitoring is covered in detail. The increased fetal risks of multiple birth due to twin-to-twin transfusion syndrome and other pregnancy complications are described, with detail on oligohydramnios, polyhydramnios, antepartum haemorrhage, preterm prelabour rupture of membranes, cord prolapse, preterm labour, and breech presentation. Intrapartum fetal assessment using electronic fetal monitoring and fetal blood sampling to diagnose fetal distress is covered to enable health professionals involved in care of the newborn to understand events which may have resulted in a baby born in poor condition.
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Jacquemyn, Yves, and Anneke Kwee. Antenatal and intrapartum fetal evaluation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0006.

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Antenatal and intrapartum fetal monitoring aim to identify the beginning of the process of fetal hypoxia before irreversible fetal damage has taken place. Fetal movement counting by the mother has not been reported to be of any benefit. The biophysical profile score, incorporating ultrasound and fetal heart rate monitoring, has not been proven to reduce perinatal mortality in randomized trials. Doppler ultrasound allows the exploration of the perfusion of different fetal organ systems and provides data on possible hypoxia and fetal anaemia. Maternal uterine artery Doppler can be used to select women with a high risk for intrauterine growth restriction and pre-eclampsia but does not directly provide information on fetal status. Umbilical artery Doppler has been shown to reduce perinatal mortality significantly in high-risk pregnancies (but not in low-risk women). Adding middle cerebral artery Doppler to umbilical artery Doppler does not increase accuracy for detecting adverse perinatal outcome. Ductus venosus Doppler demonstrates moderate value in diagnosing fetal compromise; it is not known whether its use adds any value to umbilical artery Doppler alone. Cardiotocography (CTG) reflects the interaction between the fetal brain and peripheral cardiovascular system. Prelabour routine use of CTG in low-risk pregnancies has not been proven to improve outcome; computerized CTG significantly reduces perinatal mortality in high-risk pregnancies. Monitoring the fetus during labour with intermittent auscultation has not been compared to no monitoring at all; when compared with CTG no difference in perinatal mortality or cerebral palsy has been noted. CTG does lower neonatal seizures and is accompanied by a statistically non-significant rise in caesarean delivery. Fetal blood sampling to detect fetal pH and base deficit lowers caesarean delivery rate and neonatal convulsions when used in adjunct to CTG. Determination of fetal scalp lactate has not been shown to have an effect on neonatal outcome or on the rate of instrumental deliveries but is less often hampered by technical failure than fetal scalp pH. Analysis of the ST segment of the fetal ECG (STAN®) in combination with CTG during labour results in fewer vaginal operative deliveries, less need for neonatal intensive care, and less use of fetal blood sampling during labour, without a change in fetal metabolic acidosis when compared to CTG alone.
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Book chapters on the topic "Intrauterine growth restriction (IUGR)"

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Wolstenholme, John, and Chris Wright. "Genes, Chromosomes and IUGR." In Intrauterine Growth Restriction, 7–27. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0735-4_2.

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Kingdom, John, and Graeme Smith. "Diagnosis and Management of IUGR." In Intrauterine Growth Restriction, 257–73. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0735-4_13.

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Walker, James J., Graeme Smith, and Gustaaf A. Dekker. "Prevention and Treatment of IUGR." In Intrauterine Growth Restriction, 307–18. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0735-4_16.

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Kohnen, Gaby, and John Kingdom. "Villous Development and the Pathogenesis of IUGR." In Intrauterine Growth Restriction, 131–45. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0735-4_7.

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Blair, Eve. "Paediatric Implications of IUGR with Special Reference to Cerebral Palsy." In Intrauterine Growth Restriction, 351–66. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0735-4_19.

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Sel, Görker. "Fetal Growth Restriction, Intrauterine Growth Restriction (IUGR)." In Practical Guide to Oral Exams in Obstetrics and Gynecology, 87–90. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-29669-8_14.

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Serchi, Tommaso, Jenny Renaut, Lucien Hoffmann, Arno C. Gutleb, Jane Robinson, and Neil Evans. "Intrauterine treated lambs as a model for the study of Intrauterine Growth Restriction (IUGR) and consequent metabolic disorders." In Farm animal proteomics 2013, 230–33. Wageningen: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-776-9_58.

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Lyons, Paul. "Intrauterine Growth Restriction." In Obstetrics in Family Medicine, 45–53. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20077-4_6.

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Lyons, Paul, and Nathan McLaughlin. "Intrauterine Growth Restriction." In Obstetrics in Family Medicine, 53–62. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39888-0_7.

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Kovacs, Gab, and Paula Briggs. "Intrauterine Growth Restriction." In Lectures in Obstetrics, Gynaecology and Women’s Health, 131–32. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14863-2_28.

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Conference papers on the topic "Intrauterine growth restriction (IUGR)"

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Dodson, Reuben Blair, Paul J. Rozance, Kendall S. Hunter, and Virginia L. Ferguson. "Increased Stiffness of the Abdominal Aorta With Intrauterine Growth Restriction in the Near-Term Fetal Sheep." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80634.

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Fetal intrauterine growth restriction (IUGR) results in increased placental resistance to blood flow, fetal hypertension and increased pulsatility [1]. These hemodynamic changes have been shown to lead to vascular remodeling in adolescents and adults [2, 3] but have received little study of its effect during this critical period of vascular formation. Epidemiological studies link IUGR to cardiovascular disease in adulthood [4], but the reason for this is not clearly understood. Here, we examine a large elastic artery for developmental alterations under hypertensive conditions. We hypothesize that fetal hypertension induces abdominal aorta (AA) stiffening in the fetal ovine model of IUGR and that the increased systemic artery stiffness is due to altered extracellular matrix (ECM) composition and structural changes.
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Dodson, Reuben Blair, Paul J. Rozance, Esther Reina-Romo, Virginia L. Ferguson, and Kendall S. Hunter. "Hyperelastic Model of Collagen Fiber Orientation in the Fetal Growth Restricted Carotid Artery." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80256.

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Intrauterine growth restriction (IUGR) is a common complication that is associated with hypertension in the developing fetal sheep [1]. Hypertension reduces arterial compliance, introducing health problems such as increased overall hydraulic impedance and cardiac workload [2, 3]. Both organ resistance and vascular compliance are critical factors in the progression of cardiovascular diseases (CVD) [3–5] with IUGR infants showing high incidence of CVD as adults [6]. Changes in circulation and the associated intrinsic hemodynamic forces during critical gestation influence the formation of the vessels, creating stiffer, less compliant arteries. While IUGR vessels are significantly stiffer than controls, the structural remodeling in response to hypertension is not biochemically quantitative and is believed to be due to fiber alignment [7].
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Cunha, Isabela de Oliveira, Alfredo de Almeida Cunha, Fernando Maia Peixoto Filho, and Paulo Roberto Nassar de Carvalho. "Predição de crescimento intrauterino restrito no rastreio combinado de primeiro trimestre." In 44° Congresso da SGORJ - XXIII Trocando Ideias. Zeppelini Editorial e Comunicação, 2020. http://dx.doi.org/10.5327/jbg-0368-1416-2020130250.

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Introdução: O conceito de restrição do crescimento fetal tardio (CFT) foi introduzido para descrever fetos com insuficiência placentária que não é grave o suficiente para resultar em CFT com fluxo arterial umbilical anormal, mas é grave o suficiente para associar-se com alto risco perinatal ou complicações de longo prazo. Entretanto, há necessidade de retroceder a investigação para o primeiro trimestre, na esperança de possível intervenção. Objetivo: Realizar revisão bibliográfica do tema. Material e Métodos: As palavras-chave CIUR (crescimento intrauterino restrito) e IUGR (intrauterine growth restriction) foram identificadas na Biblioteca Virtual em Saúde (BVS). O termo CIUR também foi pesquisado na Literatura Latino-americana e do Caribe em Ciências da Saúde (LILACS), nos últimos dez anos. Com o auxílio do Endnote, foram realizadas pesquisas no PubMed usando a palavra-chave (MeSH term) intrauterine growth restriction (IUGR), no período 2011‒2020. Os artigos foram baixados e foi montada uma pasta com eles em formato pdf. Posteriormente, foram importados pelo Endnote. Resultados: Na LILACS, nos últimos 10 anos, foram recuperados 20 artigos com texto completo. No PubMed, no período 2011‒2020 (até agosto), foram identificadas 5.551 referências sob o título “intrauterine growth restriction”. Utilizando como filtro a expressão “first trimester”, restaram 370 referências, e após um segundo filtro (“screening”), 308 referências. Destas, conseguimos os textos completos em .pdf de 101, que foram utilizados para a presente revisão. Modelos foram identificados incluindo dados clínicos maternos (método de contracepção, tabagismo, altura materna), métodos de imagem (Doppler da artéria uterina, avaliando o índice de pulsatilidade — PI) e avaliação bioquímica (fator de crescimento placentário — PlGF, gonadotrofina coriônica — βhCG, pregnancy-associated plasma protein-A — PAPP-A, soluble fms-like tytosine kinase — sFlt-1 e disintegrin and metalloprotease — ADAM 12). Conclusão: Neste estudo, foram utilizados diferentes modelos com associação dos fatores mencionados anteriormente. Ainda não se identificou o modelo ideal, necessitando de novos estudos.
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Liu, Pengbo, Max Mongelli, and Adrian Mondry. "Verification of a model for the detection of intrauterine growth restriction (IUGR) by receiver operating characteristics (ROC)." In Biomedical Optics 2004, edited by Gerald E. Cohn, Warren S. Grundfest, David A. Benaron, and Tuan Vo-Dinh. SPIE, 2004. http://dx.doi.org/10.1117/12.530989.

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Ortigosa, Nuria, Merida Rodriguez-Lopez, Raquel Bailón, Alvaro Sepulveda-Martinez, Eduard Gratacós, Fatima Crispi, and Pablo Laguna. "Intrauterine Growth Restriction Induced ECG Morphological Differences Measured in Adulthood." In 2018 Computing in Cardiology Conference. Computing in Cardiology, 2018. http://dx.doi.org/10.22489/cinc.2018.302.

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Batalle, Dafnis, Elisenda Eixarch, Emma Munoz-Moreno, Francesc Figueras, Ivan Amat-Roldan, and Eduard Gratacos. "Altered structural brain network topology in infants with intrauterine growth restriction." In 2012 IEEE 9th International Symposium on Biomedical Imaging (ISBI 2012). IEEE, 2012. http://dx.doi.org/10.1109/isbi.2012.6235608.

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Swartz, Daniel D., James A. Russell, Catalina Bazacliu, Melissa Carmen, Bobby Mathew, Rita M. Ryan, and Satyan Lakshminrusimha. "Intrauterine Growth Restriction Abolishes Airway Hyperresponsiveness To Methacholine in Female Rats." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4996.

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Bucur-Grosu, L&acaron;cr&acaron;mioara, Andreea Avasiloaiei, Cristina Dimitriu, Mihaela Moscalu, and Maria Stamatin. "OC-81 Umbilical cord ghrelin levels in newborns with intrauterine growth restriction." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.81.

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Wosiak, Agnieszka, Kinga Glinka, Agata Zamecznik, and Katarzyna Niewiadomska-Jarosik. "Imputing Missing Values for Improved Statistical Inference Applied to Intrauterine Growth Restriction Problem." In 2018 Federated Conference on Computer Science and Information Systems. IEEE, 2018. http://dx.doi.org/10.15439/2018f196.

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Wosiak, Agnieszka, Agata Zamecznik, and Katarzyna Niewiadomska-Jarosik. "Supervised and Unsupervised Machine Learning for Improved Identification of Intrauterine Growth Restriction Types." In 2016 Federated Conference on Computer Science and Information Systems. IEEE, 2016. http://dx.doi.org/10.15439/2016f515.

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Reports on the topic "Intrauterine growth restriction (IUGR)"

1

Pirnareva, Elena. Monitoring of Fetuses with Intrauterine Growth Restriction: a Longitudinal Study. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, April 2018. http://dx.doi.org/10.7546/crabs.2018.03.17.

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