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Background: Down syndrome (trisomy 21) is a well-known cause of mental retardation. It can be diagnosed in early pregnancy. Scientists have made great strides in outlining the pathophysiologic mechanisms of mental retardation in Down syndrome. Much less has been published on human therapy. To cur knowledge, these are the first published cases of fetal therapy for Down syndrome. Methodology: Reports of three cases. In all cases, treatment was both biochemical (e.g. nutritional) and educational. In all cases, treatment was both befcre and after birth. Results: All children lacked the characteristic faces usually seen in the children with Down syndrome. This suggests a treatment effect before birth. All children had better than expected development. Discussion: Enhancement of development is preposed as a new therapeutic principle. Developing neurons exchange neurotrophic factors during development when they give or receive stimulation from other neurons. Neurons which receive neurotrophic stimulation survive, and those, which do not, are lost to apoptosis. The developmental therapeutic principle seeks to optimize brain development. Biochemical inputs (neurotransmitters, drugs, hormones, nutrients) and functional stimulation are integrated to optimize the growth and survival of neurons individually; other cells; subcellular organelles; and the brain as a whole. Treatment may be before and after birth, both biochemical and functional. These principles may be applied to Down syndrome, other conditions, and normal fetuses or children. Previously published: Baggot PJ and Baggot RM (2014). Fetal Therapy for Down Syndrome: Report of three cases and review of the literature. J Am Phys Surg 19(l):20-24. [ABSTRACT FROM AUTHOR]

Objective According to the classification system used, 15–60% of stillbirths remain unexplained, despite undergoing recommended autopsy examination, with variable attribution of fetal growth restriction (FGR) as a cause of death. Distinguishing small-for-gestational age (SGA) from pathological FGR is a challenge at postmortem examination. This study uses data from a large, well-characterized series of intrauterine death autopsies to investigate the effects of secondary changes such as fetal maceration, intrauterine retention and postmortem interval on body weight. Methods Autopsy findings from intrauterine death investigations (2005–2013 inclusive, from Great Ormond Street Hospital and St George’s Hospital, London) were collated into a research database. Growth charts published by the World Health Organization were used to determine normal expected weight centiles for fetuses born ≥24 weeks’ gestation, and the effects of intrauterine retention (maceration) and postmortem interval were calculated. Results There were 1064 intrauterine deaths, including 533 stillbirths ≥24 weeks’ gestation with a recorded birth weight. Of these, 192 (36%) had an unadjusted birth weight below the 10th centile and were defined as SGA. The majority (86%) of stillborn SGA fetuses demonstrated some degree of maceration, indicating a significant period of intrauterine retention after death. A significantly greater proportion of macerated fetuses were present in the SGA population compared with the non-SGA population (P=0.01). There was a significant relationship between increasing intrauterine retention interval and both more severe maceration and reduction in birth weight (P<0.0001 for both), with an average artifactual reduction in birth weight of around −0.8 SD of expected weight. There was an average 12% reduction in fetal weight between delivery and autopsy and, as postmortem interval increased, fetal weight loss increased (P=0.0001). Conclusion Based on birth weight alone, 36% of stillbirths are classified as SGA. However, fetuses lose weight in utero with increasing intrauterine retention and continue to lose weight between delivery and autopsy, resulting in erroneous overestimation of FGR. [ABSTRACT FROM AUTHOR]

Intrauterine growth restriction ( IUGR) is interconnected with developmental programming of lifelong pathophysiology. IUGR is seen in human multifetal pregnancies, with stepwise rises in fetal numbers interfering with placental nutrient delivery. It remains unknown whether fetal blood analyses would reflect fetal nutrition, liver, and excretory function in the last trimester of human or ovine IUGR. In an ovine model, we hypothesized that fetal plasma biochemical values would reflect progressive placental, fetal liver, and fetal kidney dysfunction as the number of fetuses per gestation rose. To determine fetal plasma biochemical values in singleton, twin, triplet, and quadruplet/quintuplet ovine gestation, we investigated morphometric measures and comprehensive metabolic panels with nutritional measures, liver enzymes, and placental and fetal kidney excretory measures at gestational day ( GD) 130 (90% gestation). As anticipated, placental dysfunction was supported by a stepwise fall in fetal weight, fetal plasma glucose, and triglyceride levels as fetal number per ewe rose. Fetal glucose and triglycerides were directly related to fetal weight. Plasma creatinine, reflecting fetal renal excretory function, and plasma cholesterol, reflecting placental excretory function, were inversely correlated with fetal weight. Progressive biochemical disturbances and growth restriction accompanied the rise in fetal number. Understanding the compensatory and adaptive responses of growth-restricted fetuses at the biochemical level may help explain how metabolic pathways in growth restriction can be predetermined at birth. This physiological understanding is important for clinical care and generating interventional strategies to prevent altered developmental programming in multifetal gestation. [ABSTRACT FROM AUTHOR]

Ultrasound prenatal examination enables one to assess the facial skeleton and the neck from the first weeks of gestation. Cervicofacial tumors detected via prenatal ultrasound are very rarely reported fetal pathologies. They include cystic hygromas, teratomas, epulides, vascular tumors, and thyroid tumors. The tumor category, its location and vascularization pattern allow one to accurately establish a diagnosis which is usually confirmed by clinical examination of the neonate or a pathological examination (surgical specimen, biopsy, autopsy). The prenatal ultrasound diagnosis of cervicofacial tumor in the fetus allows planning of pregnancy management and fetal therapy, preparation of the delivery, and perinatal as well as neonatal treatment. [ABSTRACT FROM AUTHOR]

Background: Preeclampsia, traditionally characterized by high blood pressure and proteinuria, is a common pregnancy complication, which affects 2-8% of all pregnancies. Although children born to women with preeclampsia have a higher risk of hypertension in later life, the mechanism of this increased risk is unknown. DNA methylation is an epigenetic modification that has been studied as a mediator of cellular memory of adverse exposures in utero. Since each cell type in the body has a unique DNA profile, cell subtype composition is a major confounding factor in studies of tissues with heterogeneous cell types. The best way to avoid this confounding effect is by using purified cell types. However, using purified cell types in large cohort translational studies is difficult. The amnion, the inner layer of the fetal membranes of the placenta, is derived from the epiblast and consists of two cell types, which are easy to isolate from the delivered placenta. In this study, we demonstrate the value of using amnion samples for DNA methylation studies, revealing distinctive patterns between fetuses exposed to proteinuria or hypertension and fetuses from normal pregnancies. Results: We performed a genome-wide DNA methylation analysis, HpaII tiny fragment Enrichment by Ligation-mediated PCR (HELP)-tagging, on 62 amnion samples from the placentas of uncomplicated, normal pregnancies and from those with complications of preeclampsia or hypertension. Using a regression model approach, we found 123, 85, and 99 loci with high-confidence hypertension-associated, proteinuria-associated, and hypertension- and proteinuria-associated DNA methylation changes, respectively. A gene ontology analysis showed DNA methylation changes to be selecting genes with different biological processes in exposure status. We also found that these differentially methylated regions overlap loci previously reported as differentially methylated regions in preeclampsia. Conclusions: Our findings support prior observations that preeclampsia is associated with changes of DNA methylation near genes that have previously been found to be dysregulated in preeclampsia. We propose that amniotic membranes represent a valuable surrogate fetal tissue on which to perform epigenome-wide association studies of adverse intrauterine conditions. [ABSTRACT FROM AUTHOR]

Key points The fetus responds to decreases in arterial partial pressure of oxygen by redirecting the blood flow mainly to the brain and the heart, at a cost to other peripheral organs like the kidneys., Renal hypoxia and ischaemia stimulate inflammatory and apoptotic responses., Ketamine, an NMDA receptor antagonist, is able to reduce renal immune and inflammatory gene expressions stimulated by hypoxia., Ketamine may have therapeutic potential for protection against ischaemic renal damage in fetuses subjected to acute hypoxia., Abstract Acute fetal hypoxia is a form of fetal stress that stimulates renal vasoconstriction and ischaemia as a consequence of the physiological redistribution of combined ventricular output. Because of the potential ischaemia-reperfusion injury to the kidney, we hypothesized that it would respond to hypoxia with an increase in the expression of inflammatory genes, and that ketamine (an N-methyl- d-aspartate receptor antagonist) would reduce or block this response. Hypoxia was induced for 30 min in chronically catheterized fetal sheep (125 ± 3 days), with or without ketamine (3 mg kg−1) administered intravenously to the fetus 10 min prior to hypoxia. Gene expression in fetal kidney cortex collected 24 h after the onset of hypoxia was analysed using ovine Agilent 15.5k array and validated with qPCR and immunohistochemistry in four groups of ewes: normoxic control, normoxia + ketamine, hypoxic control and hypoxia + ketamine ( n = 3-4 per group). Significant differences in gene expression between groups were determined with t-statistics using the limma package for R ( P ≤ 0.05). Enriched biological processes for the 427 upregulated genes were immune and inflammatory responses and for the 946 downregulated genes were metabolic processes. Ketamine countered the effects of hypoxia on upregulated immune/inflammatory responses as well as the downregulated metabolic responses. We conclude that our transcriptomics modelling predicts that hypoxia activates inflammatory pathways and reduces metabolism in the fetal kidney cortex, and ketamine blocks or ameliorates this response. The results suggest that ketamine may have therapeutic potential for protection from ischaemic renal damage. [ABSTRACT FROM AUTHOR]

Fetal exposure to five parabens was investigated due to their endocrine-disrupting potential and possible impact on fetal development. Body burdens occurring from real-world exposures were determined typically as total concentrations after conjugate hydrolysis in 181 maternal urine and 38 umbilical cord blood plasma samples from a multiethnic cohort of 185 predominantly-black, pregnant women recruited in Brooklyn, New York between 2007/9. For 33 participants, both sample types (maternal urine and cord blood) were available. Methyl- (MePB), ethyl- (EtPB), propyl- (PrPB), butyl- (BuPB), and benzylparaben (BePB) were detected in 100, 73.5, 100, 66.3 and 0.0% of the urine samples at median concentrations of 279, 1.44, 75.3, 0.39, and < 0.02 μg/L, respectively. Median concentrations of MePB and PrPB were, respectively 4.4- and 8.7-fold higher compared to those reported previously for the general U.S. population (NHANES, 2005/6). Listed in the order above, the five parabens were detected in 97.4, 94.7, 47.4, 47.4, and 44.7% of cord blood plasma samples at median total concentrations of 25.0, 0.36, < 0.27, < 0.09, and < 0.10 μg/L, respectively. Free MePB, EtPB, and PrPB were detected in a subset of cord blood plasma samples at, respectively, 3.9, 71.7, and 6.4% of their total concentrations, whereas free BuPB and BePB were not detected. Literature data and those reported here show the urban community studied here to rank highest in the world for MePB and PrPB exposure in pregnant women, whereas it ranks among the lowest for EtPB and BuPB. This study is the first to report the occurrence of parabens in human umbilical cord blood. Maternal exposure to parabens is widespread, and substantial differences were found to exist between communities and countries both in the spectrum and degree of paraben exposures. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective To compare left myocardial performance index ( MPI) values and reproducibility using different settings and ultrasound equipment in order to standardize optimal machine settings. Methods Left MPI was prospectively evaluated by one observer performing conventional Doppler in 62 fetuses (28-36 weeks of gestational age) using different settings (changing sweep speed, gain and wall motion filter ( WMF)) and two different ultrasound devices (Siemens Antares, Siemens; Voluson 730 Expert, GE Medical Systems). Intraclass coefficients of agreement ( ICCs) were calculated using Bland-Altman analysis. Results Using baseline settings on the Siemens, mean ( SD) MPI was 0.44 (0.05) with an ICC of 0.81. Decreasing the sweep speed resulted in decreasing average MPI values (0.43) and decreasing ICC (0.61). Lowering gain also influenced average MPI values (0.46) and ICC (0.76). Raising gain resulted in similar MPI values (0.45) with better ICC (0.90) compared with baseline settings. Raising wall motion filter ( WMF) provided the best ICC (0.94) compared with the other settings. Changing the ultrasound equipment resulted in an ICC of 0.64. The optimal settings to achieve the highest reproducibility in measurement of MPI were sweep speed 8, gain 60 dB and WMF 281 Hz for Siemens Antares and sweep speed 5, gain −10 dB and WMF 210 Hz for Voluson 730 Expert. Conclusion Changing ultrasound settings or equipment may affect the calculation and repeatability of measurement of MPI values. Strict standardization of methods decreases the variability of this parameter for fetal cardiac function assessment. Copyright © 2014 ISUOG. Published by John Wiley & Sons Ltd. [ABSTRACT FROM AUTHOR]

Pregnancy presents an immunological conundrum because two genetically different individuals coexist. The maternal lymphocytes at the uterine maternal-fetal interface that can recognize mismatched placental cells are T cells and abundant distinctive uterine NK (uNK) cells. Multiple mechanisms exist that avoid damaging T cell responses to the fetus, whereas activation of uNK cells is probably physiological. Indeed, genetic epidemiological data suggest that the variability of NK cell receptors and their MHC ligands define pregnancy success; however, exactly how uNK cells function in normal and pathological pregnancy is still unclear, and any therapies aimed at suppressing NK cells must be viewed with caution. Allorecognition of fetal placental cells by uNK cells is emerging as the key maternalfetal immune mechanism that regulates placentation. [ABSTRACT FROM AUTHOR]

Adult β-cell dysfunction, a hallmark of type 2 diabetes, can be programmed by adverse fetal environment. We have shown that fetal glucocorticoids (GCs) participate in this programming through inhibition of β-cell development. Here we have investigated the molecular mechanisms underlying this regulation. We showed that GCs stimulate the expression of peroxisome proliferator--activated receptor-γ coactivator-1α (PGC-1α), a coregulator of the GCs receptor (GR), and that the overexpression of PGC-1α represses genes important for β-cell development and function. More precisely, PGC-1α inhibited the expression of the key β-cell transcription factor pancreatic duodenal homeobox 1 (Pdx1). This repression required the GR and was mediated through binding of a GR/PGC-1α complex to the Pdx1 promoter. To explore PGC-1α function, we generated mice with inducible β-cell PGC-1α overexpression. Mice overexpressing PGC-1α exhibited at adult age impaired glucose tolerance associated with reduced insulin secretion, decreased β-cell mass, and β-cell hypotrophy. Interestingly, PGC-1α expression in fetal life only was sufficient to impair adult β-cell function whereas β-cell PGC-1α overexpression from adult age had no consequence on β-cell function. Altogether, our results demonstrate that the GR and PGC-1α participate in the fetal programming of adult β-cell function through inhibition of Pdx1 expression. [ABSTRACT FROM AUTHOR]

El artículo presenta información sobre tres drogas auxiliares en la obstetricia. Se incluyen los detalles del origen, la fisiopatogenia y los efectos de las drogas Flaxedil, Nisentil y Largactil, además de la historia de las drogas e información sobre la efectividad y la investigación referida a las drogas.

The article analyzes aspects of the ultrasound evaluation of the malformations in the human fetal venous system. It states that an abnormal development in the system can be based from any of its embryonic systems including umbilical and cardinal systems. It presents several abnormalities in the system which include heterotaxy syndromes and primary failure to create critical anastomoses. It concludes that fetal system anomalies can be diagnosed by recognition of their sonographic appearance.

This article summarizes the essentials of studies on the craniofacial skeleton performed over 17 years. It presents data from research into foetal pathology resulting in new views on craniofacial patterning and/or fields for further discussion. [ABSTRACT FROM PUBLISHER]

Background: Malnutrition in fetal life and during suckling have in some animal studies resulted in adaptive changes related to the fat and glucose metabolism, which in the long term might predispose the offspring for metabolic disorders such as obesity later in life. The objective was to study the effect of fetal life malnutrition in male mink on the gene expression of leptin and adiponectin in different adipose tissue sites. Results: Thirty-two male mink, strict carnivore species, exposed to low (FL) or adequate (FA) protein provision the last 16.3 ± 1.8 days of fetal life and randomly assigned to a low (LP) or adequate (AP) protein diet from 7 to 9.5 weeks of age were used. Adipose tissues (subcutaneous, perirenal and mesenteric) were analyzed using qPCR. Fetal life or postweaning protein provision did not affect the relative abundances of leptin and adiponectin mRNAs in adipose tissue at 9.5 weeks of age. Relative abundances of leptin and adiponectin mRNAs were different between adipose tissue sites and were significantly higher in subcutaneous than in perirenal and mesenteric tissues. Conclusion: Fetal life protein malnutrition in male mink, did not result in adaptive changes in the gene expression of leptin and adiponectin mRNAs in adipose tissue at 9.5 weeks of age as found in rodents. However, both leptin and adiponectin mRNAs were significantly differently expressed between tissue sites. [ABSTRACT FROM AUTHOR]

Embryo implantation consists of a series of events promoting the invasion of the endometrium and then the uterine arterial system by the extra-embryonic trophoblast. In order for this semi-heterologous implantation to succeed, the endometrium has to first undergo a number of structural and biochemical changes (decidualization). The decidua's various constituents subsequently play a role in the embryonic implantation. The third step is the transformation of the uterine vascular system and the growth of the placenta, which will provide the foetoplacental unit with nutrients. Several physiopathological aspects will be discussed: 1) the implantation window, regulated by maternal and embryonic hormonal secretions and thus influenced by any defects in the latter: dysharmonic luteal phase, 21-hydroxylase block, abnormal integrin expression, 2) the successive trophoblast invasions of uterine vessels which, when defective, lead to early embryo loss or late-onset vascular pathologies, as preeclampsia, 3) the pregnancy's immunological equilibrium, with a spontaneously tolerated semi-allogeneic implant, 4) the impact of pro-coagulant factors (thrombophilia) on the pregnancy's progression, 5) the environment of the uterus, ranging from hydrosalpinx to uterine contractions. In summary, the least anatomical or physiological perturbation can interfere with human embryonic implantation - a very particular phenomenon and a true biological paradox. [ABSTRACT FROM AUTHOR]

We exploit time reversibility analysis, checking the invariance of statistical features of a series after time reversal, to detect temporal asymmetries of short-term heart period variability series. Reversibility indexes were extracted from 22 healthy fetuses between 16th to 40th wk of gestation and from 17 healthy humans (aged 21 to 54, median = 28) during graded head-up tilt with table inclination angles randomly selected inside the set (15, 30, 45, 60, 75, 90}. Irreversibility analysis showed that nonlinear dynamics observed in short-term heart period variability are mostly due to asymmetric patterns characterized by bradycardic runs shorter than tachycardic ones. These temporal asymmetries were I) more likely over short temporal scales than over longer, dominant ones; 2) more frequent during the late period of pregnancy (from 25th to 40th week of gestation); 3) significantly present in healthy humans at rest in supine position; 4) more numerous during 75 and 90° head-up tilt. Results suggest that asymmetric patterns observable in short-term heart period variability might be the result of a fully developed autonomic regulation and that an important shift of the sympathovagal balance toward sympathetic predominance (and vagal withdrawal) can increase their presence. [ABSTRACT FROM AUTHOR]

Objectives To corn pare magnetic resonance imaging (MRI) and fetopathological findings in the evaluation of non-cystic fetal posterior fossa anomalies and to describe associated abnormalities. Methods This was a prospective study from 2000 to 2005 of fetuses identified on ultrasound as having sonographic suspicion of posterior fossa malformation. All underwent a thorough MRI examination of the fetal brain, after which we classified each fetus as presenting one of the following pathologies: vermian hypoplasia or agenesis, cerebellar and/or brain stem hypoplasia, destructive or dysplastic lesions. All of the pregnancies were then terminated, after which the whole fetus underwent fetopathological examination. We compared the findings from MRI and fetopathological examinations and recorded the associated cerebral and extracerebral abnormalities. Results Twenty-five fetuses were included. MRI was performed at a mean gestational age of 31 weeks, and fetopathological examination at 33 weeks. In 12 cases we observed vermian hypoplasia, six had partial vermian agenesis, 11 had cerebellar hemisphere hypoplasia, seven had brain stem hypoplasia, four had destructive lesions and six had dysplastic lesions. The two techniques were similar in their performance with respect to the detection of vermian agenesis, brain stem hypoplasia and destructive lesions. There were four false-positive results of MRI for vermian hypoplasia and a poor agreement regarding cerebellar hemisphere hypoplasia. No dysplastic lesions were diagnosed by MRI. None of the posterior fossa malformations was isolated and many cerebral and extracerebral abnormalities were found. Conclusion A systematic analysis of the posterior fossa in fetal MRI makes it possible to diagnose accurately most posterior fossa malformations. These malformations never occurred in isolation in our study. [ABSTRACT FROM AUTHOR]

Sections from all spinal cord levels from 20 human fetuses, age range 7.5–17 gestational weeks (GW) were immunostained for non-phosphorylated neurofilaments (to reveal motoneurones, spinocerebellar neurones and other large neurones), the calcium-binding protein parvalbumin (large proprioreceptive afferents), growth-associated protein 43 kDa (growing axons), glial fibrillary acidic protein (radial glia), synaptophysin (synaptic terminals) the cell–cell recognition molecule ephrin A4 (EphA4) and the ETS transcription factor Er81 (subclasses of motoneurone and proprioreceptive neurone). Muscle afferents crossed the dorsal horn by 7.5 GW and innervated motoneurones by 9 GW. An alignment of glial fibres guided them from dorsal columns to ventral horn, at right angles to the radial glia. They continued to provide a dense innervation of motoneurone pools up to 17 GW. By 13 GW motoneurones were segregated into distinct columns, all of which expressed EphA4 although only certain lateral groups expressed Er81. However, Er81 expression was more widespread amongst dorsal root ganglion neurones. From 9 GW Clarke's column neurones were identified and by 14 GW were heavily innervated by parvalbumin-positive afferents whilst their efferent axons could be traced to the lateral funiculus. This investigation contributes towards a timetable for the functional development of human motor control and makes comparisons with well-studied rodent models. [ABSTRACT FROM AUTHOR]

Antepartum fetal monitoring based on the classical cardiotocography (CTG) is a noninvasive and simple tool for checking fetal status. Its introduction in the clinical routine limited the occurrence of fetal problems leading to a reduction of the precocious child mortality. Nevertheless, very poor indications on fetal pathologies can be inferred from the even automatic CTG analysis methods, which are actually employed. The feeling is that fetal heart rate (FHR) signals and uterine contractions carry much more information on fetal state than is usually extracted by classical analysis methods. In particular, FHR signal contains indications about the neural development of the fetus. However, the methods actually adopted for judging a CTG trace as "abnormal" give weak predictive indications about fetal dangers. We propose a new methodological approach for the CTG monitoring, based on a multiparametric FHR analysis, which includes spectral parameters from autoregressive models and nonlinear algorithms (approximate entropy). This preliminary study considers 14 normal fetuses, eight cases of gestational (maternal) diabetes, and 13 intrauterine growth retarded fetuses. A comparison with the traditional time domain analysis is also included. This paper shows that the proposed new parameters are able to separate normal from pathological fetuses. Results constitute the first step for realizing a new clinical classification system for the early diagnosis of most common fetal pathologies. [ABSTRACT FROM AUTHOR]

ABSTRACTBackgroundDoppler studies of the ductus venosus are increasingly being integrated in the assessment of fetal well-being. Establishing the precise morphology and structure of the ductus venosus would provide a better understanding of Doppler findings during fetal adaptation. There is conflicting evidence from previous studies about the structure of the ductus venosus, especially with regard to the presence of a sphincter at the ductus venosus inlet. The aim of this study was to examine the morphology and histological structure of the ductus venosus wall and surrounding tissues at 13–17 weeks’ gestation. DesignThis was a prospective study on 28 fetuses obtained from medical termination of pregnancies between 13 and 17 weeks’ gestation. Scanning electron microscopy and histological and immunohistochemical studies were carried out on ductus venosus sections obtained from different spatial planes. ResultsThe inlet of the ductus venosus contained a shelf which was rich in elastin, but devoid of any evidence of a smooth muscle sphincter. The isthmus of the ductus venosus above the inlet was narrowed, giving the lumen of the vessel an hourglass appearance. The endothelial surface of the ductus venosus, above the level of the inlet, showed longitudinal corrugations along its entire length. Longitudinally arranged elastin fibers were also seen along the length of the ductus venosus. A single layer of longitudinally arranged smooth muscle cells was present along the entire length of the ductus venosus, with occasional individual nerve cells visible in this layer. ConclusionsThe presence of an elastin-rich shelf and a narrow ductus venosus inlet orifice may act to accelerate flow from the portal sinus into a high-velocity system in the ductus venosus. The abundant elastin fibers in the adventitia of the ductus venosus may help antegrade wave propagation by elastic recoil. This study clearly demonstrates the lack of an anatomical smooth muscle... [ABSTRACT FROM AUTHOR]

Abstract Fetus in fetu is an unusual digression from the normal twinning process which often presents as a mass in neonates. Approximately 80 reports have been documented in the literature to date. The increasing use of routine obstetric ultrasound has identified more cases during the antenatal period. This allows more time for both the neonatology team and the parents to develop a coordinated treatment plan for the anticipated child. We report a case of a fetus in fetu which was first seen as a complex cystic mass during antenatal ultrasound at 21 weeks and was confirmed by subsequent imaging and surgical treatment shortly after birth. [ABSTRACT FROM AUTHOR]

Abstract Background Cardiac anomalies may be associated with abnormal coronary vascular connections. We report the prenatal diagnosis of ventriculocoronary fistula in three fetuses with associated cardiac anomalies. Materials and Methods Fetal echocardiography was performed in three patients referred for suspected cardiac anomaly. Two-dimensional fetal echocardiography was complemented by color Doppler flow imaging and spectral Doppler in all cases. Results A ventriculocoronary fistula was diagnosed in three patients referred at 22, 23 and 32 weeks. The first patient had hypoplastic left heart associated with transposition of the great arteries and pulmonary atresia with an intact interventricular septum. The coronary fistula arose from the transposed aorta to the left ventricle. In two patients ventriculocoronary fistula was found in association with pulmonary atresia and an intact interventricular septum. In all cases there was bidirectional flow within the fistula (diastolic blood flow towards the ventricle with reversal during ventricular systole). The pregnancy with hypoplastic left heart with transposition, and one of those with pulmonary atresia resulted in neonatal death and stillbirth, respectively. In the third instance the ventriculocoronary fistula was verified by postpartum cardiac angiography. The infant initially received a Blalock–Taussig shunt, subsequently replaced by a bidirectional Glenn shunt, and was doing well at the time of writing. Conclusion A ventriculocoronary fistula can be identified prenatally by color and spectral Doppler. This anomaly should be sought in fetuses with outflow tract obstructive cardiac lesions and an intact interventricular septum. Prenatal diagnosis allows early angiography postnatally. Delineation of coronary vascular regions may therefore facilitate preoperative planning. [ABSTRACT FROM AUTHOR]

Focuses on the incidence of nuchal translucency (NT) with normal karyotype in the first trimester of pregnancy. Details on the names associated with diseases in the fetal nuchal area; Examination of NT screening; Assessment of nuchal edema during the pregnancy period.

Presents information on a study which examined six sheep fetuses to determine the effects of neuropeptide Y in fetal swallowing. Materials and methods; Results; Discussion.

Examines whether protein synthesis and breakdown are diminished during decreased fetal oxygen availability. Analysis of the factors that affect fetal growth; Comparison of leucine kinetics from different fetal lambs; Role of fetal oxygen availability in the balancing of protein synthesis level and proteolysis.

The author reflects the significance of abnormal umbilical cord coiling index and diverse adverse of pregnancy outcome. The author explained that the calculation of the umbilical coiling index (UCI) is the general accepted method of assessing the degree of the umbilical cord coiling. In addition, the apparent discrepancy is a reflection of the fact that the umbilical vessels are distended with fetal blood antenatally.

The article discusses some of the issues concerning obstetrical medication and its implication for the infant outcome. Drugs are historically intended to produce a desired effect on pregnant women. However, it is expected with the understanding of fetal physiology and biochemistry, that the drugs are also given because of their effects on the fetus. Maternally, the administered drugs influence the fetus in various ways including the effects of thalidomide on the development of fetal malformations and the effects of drugs that interfere with organogenesis.

The author discusses embryonic heart failure. The author states that less is known about embryonic heart failure, particularly its pathophysiology, and studies were focused more on methodological aspects. Meanwhile, the author presents a study from the Phoon laboratory, which examines the embryonic heart function of mice, in the absence of bone morphogenetic protein (BMP) recepter type 1A in the neural crest cells, using structure-function analysis.

The article features Spanish-born orthopedic surgeon Ignacio Ponseti and his Ponseti method of treatment for congenital clubfoot and comments on Vonda J. Wright and Brett C. Perricelli's study of the tendency of older athletes to slow down in their athletic performances. Ponseti published results of his clinical studies and on his research on pediatric orthopedics. The Ponseti method consists of sequential manipulation and serial casting based on Ponseti's detailed studies of the fetal pathoanatomy of congenital clubfoot.

The article comments on a hypothesized pathophysiological process which attempts to prove that antenatal events can have profound influences on the subsequent development of mood disorders. It refers to the foetal origins hypothesis which states that the foetus's exposure to an adverse environment in utero leads to permanent scheduling of tissue function and subsequent increased risk of developing adult cardiovascular and metabolic diseases.