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Intrauterine Growth Retardation

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81. IGF1R variants in patients with growth impairment: Four novel variants and genotype-phenotype correlations. Full Text available with Trip Pro

IGF1R variants in patients with growth impairment: Four novel variants and genotype-phenotype correlations. IGF1R gene mutations have been associated with varying degrees of intrauterine and postnatal growth retardation, as well as microcephaly. Both autosomal-dominant and autosomal-recessive inheritance patterns have been reported. This study aimed to analyze the IGF1R gene in children with growth impairment using whole-exome sequencing (WES) and assess the clinical features with the autosomal (...) gene, which expanded the known mutation spectrum. Through a comparison among patients with reported IGF1R pathogenic variations, this study determined that an autosomal-recessive inheritance model of the IGF1R gene may result in a more severe phenotype with developmental and speech delays, as well as mental retardation.

2018 Journal of Clinical Endocrinology and Metabolism

82. Indicators of Growth, Nutritional Status and Comorbide Disorders of Newborns With Down Syndrome

to 2015) were included. The data were obtained from the medical histories of mothers, infants and the delivery protocol. The objective was to access predictive values of the auxological parameters and indexes for risk of comorbid malformations in newborns with Down syndrome (DS) Conclusion Higher CI were found in hyportrophic (SGA) newborns with DS and indicated their intrauterine growth restriction with brain sparing and increased further risk of severe psychomotor retardation. The SGA newborns have (...) lower parameters and indexes of nutritive status and significantly differed from eutrophic and hypertrophic newborns. These SGA newborns with DS have increased developmental risks and that requires further diagnostic attention. Condition or disease Down Syndrome,Auxological Indexes, Auxological Parametars, Intrauterine Growth Restriction Detailed Description: Use of anthropometric charts developed specifically for children with DS have a better expression of real growth restriction (small

2018 Clinical Trials

83. Growth and Asymmetric diMethylArginine

): University Hospital, Lille Study Details Study Description Go to Brief Summary: Principal objective : Validation of a handy biochemical parameter, plasma concentration of Asymmetric DimethylArginine (ADMA), based on a recognize biochemical parameter, the dilation of the brachial artery, at ultrasound examination, after the deflation of a cushion to evaluate artery dysfunction (vascular suffering) in growth diseases, growth hormone deficiency (GHD) and intrauterine growth retardation (IUGR) Secondary (...) Perspective: Prospective Official Title: Validation of the Dosage of Asymmetric Dimethylarginine (ADMA) Plasma in the Assessment of Endothelial Dysfunction During Growth Hormone Deficiency and Intrauterine Growth Retardation Study Start Date : June 2014 Estimated Primary Completion Date : December 2020 Estimated Study Completion Date : December 2020 Resource links provided by the National Library of Medicine related topics: related topics: resources: Groups and Cohorts Go to Group/Cohort Intervention

2018 Clinical Trials

84. Loss of function of PCDH12 underlies recessive microcephaly mimicking intrauterine infection. Full Text available with Trip Pro

brain foci, microcephaly, and intrauterine growth retardation. Postnatally, patients had progressive severe microcephaly, neonatal seizures, and virtually no developmental milestones. Brain imaging revealed dysplastic elongated masses in the midbrain-hypothalamus-optic tract area. Whole exome sequencing of one affected child revealed only PCDH12 c.2515C>T, p.R839X, to be homozygous in the proband and to cosegregate with the condition in her family. The allele frequency of PCDH12 p.R839X is <0.00001 (...) Loss of function of PCDH12 underlies recessive microcephaly mimicking intrauterine infection. To identify the genetic basis of a recessive syndrome characterized by prenatal hyperechogenic brain foci, congenital microcephaly, hypothalamic midbrain dysplasia, epilepsy, and profound global developmental disability.Identification of the responsible gene by whole exome sequencing and homozygosity mapping.Ten patients from 4 consanguineous Palestinian families manifested in utero with hyperechogenic

2016 Neurology

85. Prenatal caffeine exposure-induced adrenal developmental abnormality in male offspring rats and its possible intrauterine programming mechanisms Full Text available with Trip Pro

unknown. In the present study, a rat model of intrauterine growth retardation (IUGR) was established by PCE, male fetuses and adult offspring were sacrificed at postnatal day (PD) 1, PD7, PD35, PD100 and PD168, respectively. Results showed that the PCE fetal weight decreased and the IUGR rate increased, while the serum corticosterone (CORT) level increased but the insulin-like growth factor 1 (IGF1) level decreased. Fetal adrenal exhibited an enhanced GC-activation system (11β-hydroxysteroid (...) Prenatal caffeine exposure-induced adrenal developmental abnormality in male offspring rats and its possible intrauterine programming mechanisms Glucocorticoid (GC) is a major factor for fetal tissue maturation and fate decision after birth. We previously demonstrated that prenatal caffeine exposure (PCE) suppressed fetal adrenal steroidogenesis and resulted in adrenal dysplasia. However, whether these changes play a role until adulthood and its intrauterine programming mechanisms remain

2016 Toxicology research

86. The Influence of Down-regulation of Suppressor of Cellular Signaling Proteins by RNAi on Glucose Transport of Intrauterine Growth Retardation Rats. Full Text available with Trip Pro

The Influence of Down-regulation of Suppressor of Cellular Signaling Proteins by RNAi on Glucose Transport of Intrauterine Growth Retardation Rats. Intrauterine growth retardation (IUGR) has been linked to metabolic syndrome including insulin resistance, and overexpression of suppressors of cytokine signaling (SOCSs) proteins is thought to be associated with increased whole-body insulin sensitivity. The insulin-resistant IUGR rat model was established by maternal food restriction (about 30

2011 Pediatric Research

87. Exendin-4 increases histone acetylase activity and reverses epigenetic modifications that silence Pdx1 in the intrauterine growth retarded rat. Full Text available with Trip Pro

Exendin-4 increases histone acetylase activity and reverses epigenetic modifications that silence Pdx1 in the intrauterine growth retarded rat. The abnormal intrauterine milieu of intrauterine growth retardation (IUGR) permanently alters gene expression and function of pancreatic beta cells leading to the development of diabetes in adulthood. Expression of the pancreatic homeobox transcription factor Pdx1 is permanently reduced in IUGR islets suggesting an epigenetic mechanism. Exendin-4 (Ex-4

2011 Diabetologia

88. Maternal health-related quality of life after induction of labor or expectant monitoring in pregnancy complicated by intrauterine growth retardation beyond 36 weeks. Full Text available with Trip Pro

Maternal health-related quality of life after induction of labor or expectant monitoring in pregnancy complicated by intrauterine growth retardation beyond 36 weeks. Pregnancies complicated by intrauterine growth retardation (IUGR) beyond 36 weeks of gestation are at increased risk of neonatal morbidity and mortality. Optimal treatment in IUGR at term is highly debated. Results from the multicenter DIGITAT (Disproportionate Intrauterine Growth Intervention Trial At Term) trial show

2011 Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation Controlled trial quality: uncertain

89. Investigating the Structured Use of Ultrasound Scanning for Fetal Growth

/ reference ranges for ultrasound values. Condition or disease Stillbirth Fetal Death Fetal Growth Retardation Small for Gestational Age Fetal Growth Restriction Perinatal Death Intrauterine Growth Restriction Detailed Description: There is no requirement for patient participation in this study. All data collected and analysed is routinely collected clinical data. Study Design Go to Layout table for study information Study Type : Observational Estimated Enrollment : 56000 participants Observational Model (...) : September 7, 2018 Last Update Posted: September 7, 2018 Last Verified: September 2018 Layout table for additional information Studies a U.S. FDA-regulated Drug Product: No Studies a U.S. FDA-regulated Device Product: No Additional relevant MeSH terms: Layout table for MeSH terms Death Fetal Growth Retardation Stillbirth Fetal Death Perinatal Death Pathologic Processes Fetal Diseases Pregnancy Complications Growth Disorders

2017 Clinical Trials

90. Effect of Maternal Obesity on Fetal Growth and Expression of Placental Fatty Acid Transporters Full Text available with Trip Pro

levels of CD36, FATP-1, and FATP-4 in DIO dams were decreased significantly (p<0.05).Maternal obesity induced by a HF diet led to intrauterine growth retardation and down-regulated the expression of placental fatty acid transporters. (...) Effect of Maternal Obesity on Fetal Growth and Expression of Placental Fatty Acid Transporters To explore the effects of maternal high-fat (HF) diet-induced obesity on fetal growth and the expression of placental nutrient transporters.Maternal obesity was established in rats by 8 weeks of pre-pregnancy fed HF diet, while rats in the control group were fed normal (CON) diet. Diet-induced obesity (DIO) rats and diet-induced obesity-resistant (DIR) rats were selected according to body weight gain

2017 Journal of clinical research in pediatric endocrinology

91. De novo chromosome 7q36.1q36.2 triplication in a child with developmental delay, growth failure, distinctive facial features, and multiple congenital anomalies: a case report. Full Text available with Trip Pro

De novo chromosome 7q36.1q36.2 triplication in a child with developmental delay, growth failure, distinctive facial features, and multiple congenital anomalies: a case report. Studying human genome using chromosomal microarrays has significantly improved the accuracy and yield of diagnosing genomic disorders. Chromosome 7q36 deletions and duplications are rare genomic disorders that have been reported in a limited number of children with developmental delay, growth retardation, and congenital (...) malformation. Altered dosage of SHH and HLXB9, both located in 7q36.3, is believed to play roles in the phenotypes associated with these rearrangements. In this report we describe a child with 7q36.1q36.2 triplication that is proximal to the 7q36.3 region. In addition to the clinical description, we discuss the genes located in the triplicated region.We report a 22 month old male child with a de novo 1.35 Mb triplication at 7q36.1q36.2. His prenatal course was complicated by oligohydramnios, intrauterine

2017 BMC Medical Genetics

92. Plasmodium falciparum infection early in pregnancy has profound consequences for foetal growth. Full Text available with Trip Pro

in pregnancy. Compared with uninfected controls, women with early Plasmodium falciparum exposure had retarded intrauterine growth between gestational ages of 212 and 253 days (difference between means, 107 g [95% confidence interval {CI}, 26-188]; P = .0099) and a shorter pregnancy duration (difference between means, 6.6 days [95% CI, 1.0-112.5]; P = .0087). The birth weight (difference between means, 221 g [95% CI, 6-436]; P = .044) and the placental weight (difference between means, 84 g [95% CI, 18-150 (...) Plasmodium falciparum infection early in pregnancy has profound consequences for foetal growth. Malaria during pregnancy constitutes a large health problem in areas of endemicity. The World Health Organization recommends that interventions are initiated at the first antenatal visit, and these improve pregnancy outcomes. This study evaluated fetal growth by ultrasonography and birth outcomes in women who were infected prior to the first antenatal visit (gestational age, <120 days) and not later

2017 Journal of Infectious Diseases

93. Octreotide therapy and restricted fetal growth: pregnancy in familial hyperinsulinemic hypoglycemia Full Text available with Trip Pro

restriction. During pregnancy, management of blood glucose levels in familial hyperinsulinemic hypoglycemia thus forms a medical dilemma. We report on pregnancy outcomes in a woman with symptomatic familial hyperinsulinemic hypoglycemia, type 3. During the patient's first pregnancy with a viable fetus octreotide treatment was instituted in gestational age 23 weeks to prevent severe hypoglycemic incidences. Fetal growth velocity declined, and at 37 weeks of gestation, intrauterine growth retardation (...) Octreotide therapy and restricted fetal growth: pregnancy in familial hyperinsulinemic hypoglycemia Hypoglycemia during pregnancy can have serious health implications for both mother and fetus. Although not generally recommended in pregnancy, synthetic somatostatin analogues are used for the management of blood glucose levels in expectant hyperinsulinemic mothers. Recent reports suggest that octreotide treatment in pregnancy, as well as hypoglycemia in itself, may pose a risk of fetal growth

2017 Endocrinology, diabetes & metabolism case reports

94. Air pollution and in utero programming of poor fetal growth Full Text available with Trip Pro

Development Fetal Growth Retardation etiology Humans Maternal Exposure adverse effects Pregnancy Smoking adverse effects AHRR DNA methylation PM2.5 air pollution aryl hydrocarbon receptor repressor cigarette smoke fetal growth fetal programming intrauterine growth restriction tobacco 2017 2 25 6 0 2017 2 25 6 0 2018 9 27 6 0 ppublish 28234022 10.2217/epi-2017-0008 PMC5985501 JAMA. 2002 Mar 6;287(9):1132-41 11879110 Obstet Gynecol. 2002 Mar;99(3):490-6 11864679 BMC Genomics. 2014 Feb 22;15:151 24559495 Am (...) Air pollution and in utero programming of poor fetal growth 28234022 2018 09 26 2018 11 13 1750-192X 9 3 2017 03 Epigenomics Epigenomics Air pollution and in utero programming of poor fetal growth. 213-216 10.2217/epi-2017-0008 Burris Heather H HH Department of Neonatology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. Departments of Pediatrics & Obstetrics, Gynecology & Reproductive Biology, Harvard Medical School, Boston, MA 02215, USA. Department of Environmental Health

2017 Epigenomics

95. Growth hormone reverses dyslipidemia in adult offspring after maternal undernutrition Full Text available with Trip Pro

Growth hormone reverses dyslipidemia in adult offspring after maternal undernutrition The abnormal intrauterine milieu of fetal growth retardation could lead to dyslipidemia in adulthood. Studies have shown that growth hormone (GH) therapy in small for gestational age (SGA) children would be beneficial for metabolic parameters. Here we investigated whether GH treatment introduced at adolescent period in SGA could reverse dyslipidemia during later life. SGA rat model was established by using

2017 Scientific reports

96. Timing of Delivery in Fetal Growth Restriction of Uncomplicated Women

in Fetal Growth Restriction of Uncomplicated Women (GROW) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. of clinical studies and talk to your health care provider before participating. Read our for details. ClinicalTrials.gov Identifier: NCT03046355 Recruitment Status : Recruiting First Posted : February 8, 2017 Last Update Posted : July 17, 2017 See (...) Procedure: Labor induction at 37.0 to 37.6 weeks of gestation Procedure: Expectant monitoring until delivery Not Applicable Study Design Go to Layout table for study information Study Type : Interventional (Clinical Trial) Estimated Enrollment : 320 participants Allocation: Randomized Intervention Model: Parallel Assignment Masking: None (Open Label) Primary Purpose: Treatment Official Title: Timing of Delivery in Fetal Growth Restriction of Uncomplicated Women: A Randomized Controlled Trial (GROW Trial

2017 Clinical Trials

97. Sildenafil Versus Low Molecular Weight Heparin in Fetal Growth Restriction Treatment

: One hundred pregnant women with documented intrauterine growth restriction due to placental insufficiency at 28-35 weeks of gestation will be distributed into two groups: Group S: 50 women will receive Sildenafil citrate 25 mg tab 3 times daily. Group H: 50 women will receive single dose of LMWH subcutaneous daily. Both groups will undergo strict fetal surveillance in the form of: Umbilical artery Doppler (UAD) is the primary surveillance tool in the FGR fetus: middle cerebral artery (MCA) Doppler (...) ClinicalTrials.gov Identifier: Other Study ID Numbers: Ain shams university maternity First Posted: July 26, 2017 Last Update Posted: July 26, 2017 Last Verified: July 2017 Individual Participant Data (IPD) Sharing Statement: Plan to Share IPD: Undecided Layout table for additional information Studies a U.S. FDA-regulated Drug Product: No Studies a U.S. FDA-regulated Device Product: No Additional relevant MeSH terms: Layout table for MeSH terms Fetal Growth Retardation Fetal Diseases Pregnancy Complications

2017 Clinical Trials

98. Optimal Growth of Preterm Infants With Growth Restriction

- University of Munich University Hospital Tuebingen University of Erlangen-Nürnberg Medical School University of Milan Poznan University of Medical Sciences Lund University Information provided by (Responsible Party): Nadja Haiden,MD, Medical University of Vienna Study Details Study Description Go to Brief Summary: In this prospective randomized controlled multi center trial the investigators stratify "Very Low Birthweight " (VLBW)-infants with growth retardation in small for gestational age (SGA (...) ) or intrauterine growth restricted (IUGR) - infants and aim to investigate the impact of a nutritional management with enhanced nutrients from discharge up to the 52nd week of postconceptional age on growth, body composition, metabolic programming, metabolomics, microbiome and long term neurodevelopmental outcome. In this study, the investigators will evaluate the difference in metabolic profiles of SGA and IUGR preterm infants. The investigators will further longitudinally assess, how different nutritional

2016 Clinical Trials

99. Growth Delay Onset Determination

Determination Growth Delay Onset Determination Aka: Growth Delay Onset Determination From Related Chapters II. Causes: Intrauterine Growth Retardation tic or chromosomal abnormality Transplacental infectious disease ( ) Toxins Nicotine Medications III. Causes: Birth Prolonged Panhypopituitarism IV. Causes: Childhood See Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Growth Delay Onset Determination." Click on the image (or right click (...) Growth Delay Onset Determination Growth Delay Onset Determination Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Growth Delay Onset

2018 FP Notebook

100. Mental Retardation (Diagnosis)

among children with seizure disorders, microcephaly, macrocephaly, history of intrauterine or postnatal growth retardation, prematurity, and congenital anomalies Evaluation of patients for ID can include the following examinations: Head circumference: Microcephaly correlates highly with cognitive deficits; macrocephaly may indicate hydrocephalus, is associated with some inborn errors of metabolism, and may be seen early on in some children later diagnosed with autism [ , ] Height: Short stature may (...) Mental Retardation (Diagnosis) Intellectual Disability: Practice Essentials, Background, Pathophysiology Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTE4MDcwOS1vdmVydmlldw== processing > Intellectual Disability

2014 eMedicine.com

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