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Fetal Brain (fetal + brain)

Distribution by Scientific Domains

Life Sciences	50%
Medical Sciences	46%

Selected Abstracts

Hyperthermia in utero due to maternal influenza is an environmental risk factor for schizophrenia

CONGENITAL ANOMALIES, Issue 3 2007
Marshall J. Edwards
ABSTRACT A hypothesis is presented that the association between maternal influenza and other causes of fever during the second trimester of pregnancy and the subsequent development of schizophrenia in the child is due to the damage caused by hyperthermia to the developing amygdalohippocampal complex and associated structures in the fetal brain. Hyperthermia is a known cause of congenital defects of the central nervous system and other organs after sufficiently severe exposures during early organogenesis. The pathogenic mechanisms include death of actively dividing neuroblasts, disruption of cell migration and arborization and vascular damage. In experimental studies, hyperthermia during later stages of central nervous system development also caused damage to the developing brainstem that was associated with functional defects. This damage usually results in hypoplasia of the parts undergoing active development at the time of exposure. Recent studies have shown no evidence of direct invasion of the fetus by the influenza virus. Factors that might interact with hyperthermia include familial liability to schizophrenia, season of birth, maternal nutrition, severe stress and medications used to alleviate the symptoms of fevers. The time of the development of the fetal amygdalohippocampal complex and the changes found in its structure and associated areas of the brain are compatible with the known effects of hyperthermia. [source]

Cover Picture: Electrophoresis 3'2010

ELECTROPHORESIS, Issue 3 2010
Article first published online: 29 JAN 2010
Issue no. 3 is a regular issue with Emphasis on "Proteins and Proteomics". The first part has 8 articles on proteins and proteomics covering various topics, e.g. preparative divergent flow IEF, multichannel gel electrophoresis, capillary gel electrophoresis, nanoparticle-based CE of proteins, 2-DE in a radial gel format, depletion of high abundance proteins, and proteomic investigation of fetal brain and lentil seed. The remaining 10 articles are concerned with nucleic acids, gene expression, methodologies and application. Featured articles include: Preparative divergent flow IEF without carrier ampholytes for separation of complex biological samples ((10.1002/elps.200900484)) SDS-PAGE and two-dimensional maps in a radial gel format ((10.1002/elps.200900526)) Analysis of Effect of Electrolyte Types on Electrokinetic Energy Conversion in Nanoscale Capillaries ((10.1002/elps.200900409)) A simple method to determine the surface charge in microfluidic channels ((10.1002/elps.200900603)) [source]

Prenatal stress reduces postnatal neurogenesis in rats selectively bred for high, but not low, anxiety: possible key role of placental 11,-hydroxysteroid dehydrogenase type 2

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2009
P. J. Lucassen
Abstract Prenatal stress (PS) produces persistent abnormalities in anxiety-related behaviors, stress responsivity, susceptibility to psychopathology and hippocampal changes in adult offspring. The hippocampus shows a remarkable degree of structural plasticity, notably in response to stress and glucocorticoids. We hypothesized that PS would differentially affect hippocampal neurogenesis in rats selectively bred for genetic differences in anxiety-related behaviors and stress responsivity. Pregnant dams of high anxiety-related behavior (HAB) and low anxiety-related behavior (LAB) strains were stressed between days 5 and 20 of pregnancy. The survival of newly generated hippocampal cells was found to be significantly lower in 43-day-old HAB than in LAB male offspring of unstressed pregnancies. PS further reduced newly generated cell numbers only in HAB rats, and this was paralleled by a reduction in doublecortin-positive cell numbers, indicative of reduced neurogenesis. As maternal plasma corticosterone levels during PS were similar in both strains, we examined placental 11,-hydroxysteroid dehydrogenase type 2 (11,-HSD2), which catalyses rapid inactivation of maternal corticosterone to inert 11-dehydrocorticosterone and thus serves as a physiological ,barrier' to maternal glucocorticoids. PS significantly increased placental 11,-HSD2 activity in LAB, but not HAB, rats. We conclude that PS differentially affects the number of surviving newly generated cells and neurogenesis in HAB and LAB rats. The high sensitivity of hippocampal neurogenesis to PS in HAB rats is paralleled by a failure to increase placental 11,-HSD2 activity after stress rather than by different maternal corticosterone responses. Hence, stress-induced placental 11,-HSD2 expression may be critical in protecting the fetal brain from maternal stress-induced effects on adult neurogenesis. [source]

Distribution and functional characterization of human Nav1.3 splice variants

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2005
R. Thimmapaya
Abstract The focus of the present study is the molecular and functional characterization of four splice variants of the human Nav1.3 , subunit. These subtypes arise due to the use of alternative splice donor sites of exon 12, which encodes a region of the , subunit that resides in the intracellular loop between domains I and II. This region contains several important phosphorylation sites that modulate Na+ channel kinetics in related sodium channels, i.e. Nav1.2. While three of the four Nav1.3 isoforms, 12v1, 12v3 and 12v4 have been previously identified in human, 12v2 has only been reported in rat. Herein, we evaluate the distribution of these splice variants in human tissues and the functional characterization of each of these subtypes. We demonstrate by reverse transcriptase-polymerase chain reaction (RT-PCR) that each subtype is expressed in the spinal cord, thalamus, amygdala, cerebellum, adult and fetal whole brain and heart. To investigate the functional properties of these different splice variants, each , subunit isoform was cloned by RT-PCR from human fetal brain and expressed in Xenopus oocytes. Each isoform exhibited functional voltage-dependent Na+ channels with similar sensitivities to tetrodotoxin (TTX) and comparable current amplitudes. Subtle shifts in the V1/2 of activation and inactivation (2,3 mV) were observed among the four isoforms, although the functional significance of these differences remains unclear. This study has demonstrated that all four human splice variants of the Nav1.3 channel , subunit are widely expressed and generate functional TTX-sensitive Na+ channels that likely modulate cellular excitability. [source]

Strange Anatomy: Gertrude Stein and the Avant-Garde Embryo

HYPATIA, Issue 1 2006
Lynn M. Morgan
Today's personable, sanitized images of human embryos and fetuses require an audience that is literally and metaphorically distanced from dead specimens. Yet scientists must handle dead specimens to produce embryological knowledge, which only then can be transformed into beautiful photographs and talking fetuses. I begin with an account of Gertrude Stein's experience making a model of a fetal brain. Her tactile encounter is contrasted to the avant-garde artistic tradition that later came to dominate embryo imagery. This essay shows the embryo visualizations portrayed in a contemporary coffee-table book about gestational development to be a remarkable political achievement predicated, in part, on keeping hidden the unsavory details of anatomical technique that transform dead specimens into icons of life. [source]

Human tissue distribution of paraoxonases 1 and 2 mRNA

IUBMB LIFE, Issue 6 2010
Bharti Mackness
Abstract We have studied the distribution of mRNA for paraoxonases (PON) 1 and 2 in 24 human tissues using Gene Expression Panels. PON1 mRNA was restricted to adult kidney, liver, and colon as well as fetal liver, whereas PON2 mRNA was more widely distributed in adult human brain, heart, kidney, spleen, liver, colon, lung, small intestine, muscle, stomach, testis, placenta, salivary, thyroid and adrenal glands, pancreas, skin, and bone marrow, as well as fetal brain and liver. PON2 mRNA was not found in ovary, uterus, or plasma leukocytes using the panels. However, using real time PCR, we found PON2 mRNA expression in human plasma leukocytes. There were differences between the tissue distribution of mRNAs found in this study and the immunohistochemical localization of the PON1 and PON2 proteins reported previously. In particular, PON1 protein is much more widely distributed than its mRNA, possibly indicating the delivery of PON1 to various tissues by HDL. In addition, differences between PON2 mRNA and protein distributions could be due to missence mutations in the PON2 gene, causing nontranslation of mRNA to protein in some tissues. © 2010 IUBMB IUBMB Life, 62(6): 484,486, 2010 [source]

Ultrafast MRI of the fetus

JOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 1 2002
Christine M Glastonbury
SUMMARY During the last decade there has been increasing interest in MRI for the evaluation of ultrasound-detected fetal abnormalities. Motion artefacts previously precluded detailed imaging, but this is now possible using single-shot rapid acquisition sequences. These ultrafast techniques with subsecond images capture ,snap-shot' views of the fetus. By virtue of the infinitely long relaxation time (TR) these images are heavily T2-weighted so that fluid around and within the fetus delineates the anatomy. Currently, fetal MRI has shown to be most beneficial in the investigation of cerebral abnormalities suspected from sonography, and in the detection of subtle associated anomalies. It clearly has a role in the evaluation of complex somatic abnormalities, and is helpful in the evaluation of fetuses prior to surgery. We present a pictorial review of our experience with single-shot fast spin-echo (SSFSE) imaging, demonstrating normal anatomy of the fetal brain and body. In addition we present cerebral and somatic abnormalities to illustrate cases where we have found fetal MRI to be a useful adjunct to sonography. [source]

Human fetal cortical and striatal neural stem cells generate region-specific neurons in vitro and differentiate extensively to neurons after intrastriatal transplantation in neonatal rats

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2006
Therése Kallur
Abstract Human fetal brain is a potential source of neural stem cells (NSCs) for cell replacement therapy in neurodegenerative diseases. We explored whether NSCs isolated from cortex and striatum of human fetuses, aged 6,9 weeks post-conception, maintain their regional identity and differentiate into specific neuron types in culture and after intrastriatal transplantation in neonatal rats. We observed no differences between cortex- and striatum-derived NSCs expanded as neurospheres in proliferative capacity, growth rate, secondary sphere formation, and expression of neural markers. After 4 weeks of differentiation in vitro, cortical and striatal NSCs gave rise to similar numbers of GABAergic and VMAT2- and parvalbumin-containing neurons. However, whereas cortical NSCs produced higher number of glutamatergic and tyrosine hydroxylase- and calretinin-positive neurons, several-fold more neurons expressing the striatal projection neuron marker, DARPP-32, were observed in cultures of striatal NSCs. Human cortical and striatal NSCs survived and migrated equally well after transplantation. The two NSC types also generated similar numbers of mature NeuN-positive neurons, which were several-fold higher at 4 months as compared to at 1 month after grafting. At 4 months, the grafts contained cells with morphologic characteristics of neurons, astrocytes, and oligodendrocytes. Many of neurons were expressing parvalbumin. Our data show that NSCs derived from human fetal cortex and striatum exhibit region-specific differentiation in vitro, and survive, migrate, and form mature neurons to the same extent after intrastriatal transplantation in newborn rats. © 2006 Wiley-Liss, Inc. [source]

Transmembrane signaling through phospholipase C-, in the developing human prefrontal cortex

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2006
Iñigo Ruiz de Azúa
Abstract To investigate changes in muscarinic receptor-stimulated phospholipase C-, (PLC-,) activity during brain development, we examined the functional coupling of each of the three major protein components of the phosphoinositide system (M1, M3, and M5 muscarinic receptor subtypes; Gq/11 proteins; PLC-,1,4 isoforms) in membrane preparations from post-mortem human prefrontal cerebral cortex collected at several stages of prenatal and postnatal development. In human prenatal brain membranes, PLC was found to be present and could be activated by calcium, but the ability of guanosine-5,-o-3 thiotriphosphate (GTP,S) or carbachol (in the presence of GTP,S) to modulate prenatal PLC-, was significantly weaker than that associated with postnatal PLC-,. Western blot analysis revealed that the levels of G,q/11 did not change significantly during development. In contrast, dramatically higher levels of expression of PLC-,1,4 isoforms and of M1, M3, and M5 muscarinic receptors were detected in the child vs. the fetal brain, a finding that might underlie the observed increased activity of PLC. Thus, inositol phosphate production may be more efficiently regulated by altering the amount of effectors (PLC-,1,4) and receptors (M1,3,5 subtypes) than by altering the level of G,q/11 subunits. These results demonstrate that different PLC isoforms are expressed in the prefrontal cortex of the developing human brain in an age-specific manner, suggesting specific roles not only in synaptic transmission but also in the differentiation and maturation of neurons in the developing brain. © 2006 Wiley-Liss, Inc. [source]

Ascorbate-induced differentiation of embryonic cortical precursors into neurons and astrocytes

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2003
Ji-Yeon Lee
Abstract A specific role for ascorbate (AA) in brain development has been postulated based on a rise of AA levels in fetal brain (Kratzing et al., 1985). To evaluate the role of AA during CNS development, we analyzed the survival, proliferation, and differentiation of AA-treated CNS precursor cells isolated from rat embryonic cortex. Immunocytochemical analyses revealed that AA promoted the in vitro differentiation of CNS precursor cells into neurons and astrocytes in a cell density-dependent manner. Additionally, AA increased the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs) of postmitotic neurons in primary neuronal cultures. Differential expression analysis of genes specific to neuronal or glial differentiation revealed an AA-dependent increase in the expression of genes that could potentially compound the effects of AA on cell differentiation. These data suggest that AA may act in the developing brain to stimulate the generation of CNS neurons and glia, thereby assisting in the formation of neural circuits by promoting the acquisition of neuronal synaptic functions. © 2003 Wiley-Liss, Inc. [source]

Melatonin increases activities of glutathione peroxidase and superoxide dismutase in fetal rat brain

JOURNAL OF PINEAL RESEARCH, Issue 2 2000
Yuji Okatani
Melatonin is a powerful scavenger of oxygen free radicals. In humans, melatonin is rapidly transferred from the maternal to the fetal circulation. To investigate whether or not maternal melatonin administration can protect the fetal rat brain from radical-induced damage by increasing the activities of antioxidant enzymes, we administered melatonin to pregnant rats on day 20 of gestation. Melatonin (10 mg/kg) was injected intraperitoneally at daytime (14:00 hr) and, to remove the fetuses, a laparotomy was performed at 1, 2, or 3 hr after its administration. We measured the melatonin concentration in the maternal serum and in fetal brain homogenates and determined the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in fetal brain homogenates. Melatonin administration markedly increased melatonin concentrations in the maternal serum and fetal brain homogenates, with peak levels achieved 1 hr after melatonin administration (serum: 538.2±160.7 pM/mL; brain homogenates: 13.8±2.8 pM/mg protein). Between 1 and 3 hr after melatonin administration, GSH-Px activity in fetal brain homogenates increased significantly (P<0.01). Similarly, SOD activity increased significantly between 1 and 2 hr after melatonin administration (P<0.01). These results indicate that melatonin administration to the mother increases antioxidant enzyme activities in the fetal brain and may thereby provide indirect protection against free radical injury. Thus, melatonin may potentially be useful in the treatment of neurodegenerative conditions that may involve excessive free radical production, such as fetal hypoxia and preeclampsia. [source]

Maturation-Dependent Alcohol Resistance in the Developing Mouse: Cerebellar Neuronal Loss and Gene Expression During Alcohol-Vulnerable and -Resistant Periods

ALCOHOLISM, Issue 8 2008
Bahri Karaçay
Background:, Alcohol abuse during pregnancy injures the fetal brain. One of alcohol's most important neuroteratogenic effects is neuronal loss. Rat models have shown that the cerebellum becomes less vulnerable to alcohol-induced neuronal death as it matures. We determined if maturation-dependent alcohol resistance occurs in mice and compared patterns of gene expression during the alcohol resistant and sensitive periods. Methods:, Neonatal mice received alcohol daily over postnatal day (PD) 2 to 4 or PD8 to 10. Purkinje cells and granule cells were quantified on PD25. The temporal expression patterns of 4 neuro-developmental genes and 3 neuro-protective genes in the cerebellum were determined daily over PD0 to 15 to determine how gene expression changes as the cerebellum transitions from alcohol-vulnerable to alcohol-resistant. The effect of alcohol on expression of these genes was determined when the cerebellum is alcohol sensitive (PD4) and resistant (PD10). Results:, Purkinje and granule cells were vulnerable to alcohol-induced death at PD2 to 4, but not at PD8 to 10. Acquisition of maturation-dependent alcohol resistance coincided with changes in the expression of neurodevelopmental genes. The vulnerability of cerebellar neurons to alcohol toxicity declined in parallel with decreasing levels of Math1 and Cyclin D2, markers of immature granule cells. Likewise, the rising resistance to alcohol toxicity paralleled increasing levels of GABA ,-6 and Wnt-7a, markers of mature granule neurons. Expression of growth factors and genes with survival promoting function (IGF-1, BDNF, and cyclic AMP response element binding protein) did not rise as the cerebellum transitioned from alcohol-vulnerable to alcohol-resistant. All 3 were expressed at substantial levels during the vulnerable period and were not expressed at higher levels later. Acute alcohol exposure altered the expression of neurodevelopmental genes and growth factor genes when administered either during the alcohol vulnerable period or resistant period. However, the patterns in which gene expression changed varied among the genes and depended on timing of alcohol administration. Conclusions:, Mice have a temporal window of vulnerability in the first week of life, during which cerebellar neurons are more sensitive to alcohol toxicity than during the second week. Expression of genes governing neuronal maturation changes in synchrony with the acquisition of alcohol resistance. Growth factors do not rise as the cerebellum transitions from alcohol-vulnerable to alcohol-resistant. Thus, a process intrinsic to neuronal maturation, rather than rising levels of growth factors, likely underlies maturation-dependent alcohol resistance. [source]

Fatty Acid Ethyl Esters in Meconium: Are They Biomarkers of Fetal Alcohol Exposure and Effect?

ALCOHOLISM, Issue 7 2006
Enrique M. Ostrea Jr.
Background: Biomarkers of fetal exposure to alcohol are important to establish so that early detection and intervention can be made on these infants to prevent undesirable outcomes. The aim of this study was to analyze long-chain fatty acid ethyl esters (FAEEs) in meconium as potential biomarkers of fetal alcohol exposure and effect. Methods: Fatty acid ethyl esters were analyzed in the meconium of 124 singleton infants by positive chemical ionization gas chromatography/mass spectrometry (GC/MS) and correlated to maternal ethanol use. Results: A total of 124 mother/infant dyads were enrolled in the study: 31 were in the control group and 93 were in the alcohol-exposed group. The incidence (28% vs 9.7%, p=0.037) of ethyl linoleate detected in meconium was significantly higher in the alcohol-exposed groups than the control groups. Similarly, when the concentrations of ethyl linoleate in meconium were grouped (trichotomized), there was a significant linear by linear association between alcohol exposure and group concentrations of ethyl linoleate (p=0.013). Furthermore, only alcohol-exposed infants were found in the group with the highest ethyl linoleate concentration. The sensitivity of ethyl linoleate in detecting prenatal alcohol exposure was only 26.9%, and its specificity and positive predictive value were 96.8 and 96.2%, respectively. There was no significant correlation between the concentration of ethyl linoleate in meconium and absolute alcohol consumed (oz) per drinking day across pregnancy, although a trend toward a positive correlation is seen at lower amounts of alcohol consumed. Among the polyunsaturated, long-chain FAEEs, there was weak evidence that the incidence (21.5% vs 6.5%, p=0.057) and concentration (p=0.064) of ethyl arachidonate (AA) were significantly higher in the alcohol-exposed groups than the control groups. Ethyl linolenate and ethyl docosahexanoate (DHA) in meconium were found only in the alcohol group, although not at statistically significant levels. Highly significant correlations were found among the concentrations of ethyl linoleate, ethyl linolenate, ethyl AA, and ethyl DHA in meconium (correlations ranged between rs=0.203, p=0.024; and rs=0.594, p<0.001). Conclusion: We conclude that FAEEs in meconium, particularly ethyl linoleate and ethyl AA, are biomarkers of high specificity for prenatal exposure to alcohol in newborn infants. We also propose that ethyl AA and DHA could be potential biomarkers of fetal alcohol effects on the developing fetal brain and should be investigated further. [source]

Reproductive adaptations to a large-brained fetus open a vulnerability to anovulation similar to polycystic ovary syndrome

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 3 2003
Deborah K. Barnett
During the ovarian or menstrual cycle, prior to ovulation, many female primates exhibit a relatively prolonged follicular phase and terminate the postovulatory luteal phase with menstrual bleeding. The prolonged follicular phase is a trait that distinguishes primate from nonprimate species. It enables extended estrogen-induced proliferation and growth of the uterine endometrium prior to progesterone-induced maturation during the luteal phase to accommodate a potential pregnancy with a rapidly invading placenta. Progressive development of both an extended duration of estrogen-induced, preimplantation endometrial proliferation and a rapidly invading placenta across the Primate order may well have been necessary to accommodate differentiation and growth of an increasingly large fetal brain. Prolongation of the follicular phase in primates has also led to the isolation of the final stages of follicle selection (growth deviation of the dominant follicle from its contemporaries) solely within the follicular phase and thus outside the protection of luteal phase progesterone inhibition of pituitary luteinizing hormone (LH) secretion. Such primate reproductive characteristics put the latter stages of ovarian follicle selection at risk of exposure to excessive pituitary secretion of LH. Excessive secretion of LH during follicle selection could result not only in impaired follicle development, excessive ovarian androgen secretion, and ovulation failure, but also in excessive estrogenic stimulation of the uterine endometrium without intervening menstrual periods. Such reproductive abnormalities are all found in a single, prevalent infertility syndrome afflicting women in their reproductive years: polycystic ovary syndrome (PCOS). We propose that successful female reproductive adaptations to accommodate the growth demands of large-brained primate fetuses have facilitated a particular vulnerability of higher primates to hypergonadotropic disruption of ovulatory function, as found in PCOS. Am. J. Hum. Biol. 15:296,319, 2003. © 2003 Wiley-Liss. [source]

Mental retardation and prenatal methylmercury toxicity

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 3 2006
Leonardo Trasande MD
Abstract Background Methylmercury (MeHg) is a developmental neurotoxicant; exposure results principally from consumption of seafood contaminated by mercury (Hg). In this analysis, the burden of mental retardation (MR) associated with methylmercury exposure in the 2000 U.S. birth cohort is estimated, and the portion of this burden attributable to mercury (Hg) emissions from coal-fired power plants is identified. Methods The aggregate loss in cognition associated with MeHg exposure in the 2000 U.S. birth cohort was estimated using two previously published dose-response models that relate increases in cord blood Hg concentrations with decrements in IQ. MeHg exposure was assumed not to be correlated with native cognitive ability. Previously published estimates were used to estimate economic costs of MR caused by MeHg. Results Downward shifts in IQ resulting from prenatal exposure to MeHg of anthropogenic origin are associated with 1,566 excess cases of MR annually (range: 376,14,293). This represents 3.2% of MR cases in the US (range: 0.8%,29.2%). The MR costs associated with decreases in IQ in these children amount to $2.0 billion/year (range: $0.5,17.9 billion). Hg from American power plants accounts for 231 of the excess MR cases/year (range: 28,2,109), or 0.5% (range: 0.06%,4.3%) of all MR. These cases cost $289 million (range: $35 million,2.6 billion). Conclusions Toxic injury to the fetal brain caused by Hg emitted from coal-fired power plants exacts a significant human and economic toll on American children. Am. J. Ind. Med. 49:153,158, 2006. © 2006 Wiley-Liss, Inc. [source]

Prenatal diagnosis of cavum velum interpositum cysts: significance and outcome

PRENATAL DIAGNOSIS, Issue 10 2003
Vered H. Eisenberg
Abstract Objectives To describe a fetal cavum velum interpositum cyst (CVIC) and to review its clinical significance. Methods Description and follow-up of two cases with prenatal diagnosis of a midline cyst in the fetal brain, at the Chaim Sheba Medical Center. The cases were reviewed and followed-up by a multidisciplinary team that included sonographers, pediatric neurologists, pediatric neurosurgeons, radiologists, and clinical geneticists. Medline search of cases of cysts of the cavum velum interpositum as reported in the English literature. Results Two patients referred for consultation owing to midline cysts were diagnosed with isolated cysts of the cavum velum interpositum without other anomalies. Magnetic resonance imaging (MRI) of the fetal brain did not reveal any additional malformations in either case. Prenatal follow-up showed the cysts to be stable in one case and decreased in size in the other. Postnatal neurodevelopmental outcome to date is normal. (Range of follow-up: 6,24 months.) Eight cases reported in the literature as CVIC resulted in favorable prognosis in all without further intervention. However, one infant required ventriculoperitoneal shunting due to progressive hydrocephalus, but developed normally nonetheless. Conclusion Prenatal diagnosis of cysts of the cavum velum interpositum, which are isolated, single, stable in size, and not associated with other anomalies, is consistent with a favorable postnatal outcome. Copyright © 2003 John Wiley & Sons, Ltd. [source]

Prenatal diagnosis of the Dandy-Walker malformation and ventriculomegaly associated with partial trisomy 9p and distal 12p deletion

PRENATAL DIAGNOSIS, Issue 12 2002
Chih-Ping Chen
Abstract Objectives To present the prenatal diagnosis and perinatal findings of partial trisomy 9p and distal 12p deletion. Methods and results Amniocentesis was performed at 17 gestational weeks due to a balanced reciprocal translocation t(9;12)(p11.2;p13.3) in the mother. The father's karyotype was normal. The family had a 5-year-old daughter with a Dandy-Walker malformation and a trisomy 9p syndrome. Cytogenetic analysis of the cultured amniotic fluid cells revealed a 46,XY,der(12)t(9;12)(p11.2;p13.3)mat karyotype with partial monosomy 12p(12pter,p13.3) and partial trisomy 9p(9pter,p11.2). Sonographic examination of the fetal brain and skull showed bilateral ventriculomegaly, brachycephaly and a Dandy-Walker malformation with an enlarged cisterna magna and absence of the cerebellar vermis. The pregnancy was terminated subsequently. At autopsy, the proband manifested agenesis of the cerebellar vermis and a typical trisomy 9p phenotype. Conclusion Fetuses with partial trisomy 9p(9pter,p11.2) may present a Dandy-Walker malformation and ventriculomegaly on prenatal ultrasound in the second trimester. A dosage effect of genes located on 9pter,p11.2 may be associated with the abnormal development of the central nervous system in patients with partial or complete trisomy 9. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Tetrahydrobiopterin in the prevention of hypertonia in hypoxic fetal brain,

ANNALS OF NEUROLOGY, Issue 3 2009
Jeannette Vásquez-Vivar PhD
Objective Tetrahydrobiopterin (BH4) deficiency is a cause of dystonia at birth. We hypothesized that BH4 is a developmental factor determining vulnerability of the immature fetal brain to hypoxic-ischemic injury and subsequent motor deficits in newborns. Methods Pregnant rabbits were subjected to 40-minute uterine ischemia, and fetal brains were investigated for global and focal changes in BH4. Newborn kits were assessed by neurobehavioral tests following vehicle and sepiapterin (BH4 analog) treatment of dams. Results Naive fetal brains at 70% gestation (E22) were severely deficient for BH4 compared with maternal and other fetal tissues. BH4 concentration rapidly increased normally in the perinatal period, with the highest concentrations found in the thalamus compared with basal ganglia, frontal, occipital, hippocampus, and parietal cortex. Global sustained 40-minute hypoxia-ischemia depleted BH4 in E22 thalamus and to a lesser extent in basal ganglia, but not in the frontal, occipital, and parietal regions. Maternal supplementation prior to hypoxia-ischemia with sepiapterin increased BH4 in all brain regions and especially in the thalamus, but did not increase the intermediary metabolite, 7,8-BH2. Sepiapterin treatment also reduced incidence of severe motor deficits and perinatal death following E22 hypoxia-ischemia. Interpretation We conclude that early developmental BH4 deficiency plays a critical role in hypoxic-ischemic brain injury. Increasing brain BH4 via maternal supplementation may be an effective strategy in preventing motor deficits from antenatal hypoxia-ischemia. Ann Neurol 2009;66:323,331 [source]

Selective neuronal nitric oxide synthase inhibitors and the prevention of cerebral palsy,

ANNALS OF NEUROLOGY, Issue 2 2009
Haitao Ji PhD
Objective To design a new class of selective neuronal nitric oxide synthase (NOS) inhibitors, and demonstrate that administration in a rabbit model for cerebral palsy (CP) prevents hypoxia-ischemia,induced deaths and reduces the number of newborn kits exhibiting signs of CP. Methods We used a novel computer-based drug design method called fragment hopping to identify new chemical entities, synthesized them, and conducted in vitro enzyme inhibition studies with the three isozymes of NOS and in vivo experiments to monitor cardiovascular effects on pregnant rabbit dams, NOS activity, and NOx (NO and NO2) concentration in fetal brain, and assess neurobehavioral effects on kits born to saline- and compound treated dams. Results The computer-based design led to the development of powerful and highly selective compounds for inhibition of neuronal NOS over the other isozymes. After maternal administration in a rabbit model of CP, these compounds were found to distribute to fetal brain, to be nontoxic, without cardiovascular effects, inhibit fetal brain NOS activity in vivo, reduce NO concentration in fetal brain, and dramatically ameliorate deaths and number of newborn kits exhibiting signs of CP. Interpretation This approach may lead to new preventive strategies for CP. Ann Neurol 2008 [source]

Flavonoids and thyroid disease

BIOFACTORS, Issue 3-4 2003
Daan Van Der Heide
Abstract The most potent natural plant-derived compounds that can affect thyroid function, thyroid hormone secretion and availability to tissues is the group of flavonoids, i.e. plant pigments. They are present in our daily food, such as vegetables, fruits, grains, nuts, wine, and tea. Epidemiological studies suggest beneficial effects on health of flavonoids, which are commonly attributed to their activity as antioxidants. Experimental studies in vitro, however, showed inhibition of organification in thyroid cells and follicles by several flavonoids. Studies in vivo and vitro with synthetic and natural flavonoids showed displacement of T4 from transthyretin leading to disturbances in thyroid hormone availability in tissues. Radioactive labeled flavonoids appeared to be eliminated rapidly from the body mainly through excretion in the feces. In pregnant rats synthetic flavonoids cross the placenta and accumulate in the fetal compartment, including the fetal brain. Therefore, a high intake of flavonoids is contraindicated. In conclusion: flavonoids show strong interference with many aspects of thyroid hormone synthesis and availability. [source]

The prognostic value of ultrasound abnormalities and biological parameters in blood of fetuses infected with cytomegalovirus

BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 7 2008
G Benoist
Objective, To evaluate the prognostic value of ultrasound abnormalities and of selected biological parameters in blood of fetuses infected with cytomegalovirus (CMV). Design, Retrospective observational study. Setting, Two fetal medicine units in Paris, France. Population, All fetuses infected with CMV referred between 1998 and 2006. Methods, We retrospectively analysed data collected prospectively in 73 fetuses infected by CMV with a positive CMV polymerase chain reaction in amniotic fluid. Fetal blood sampling (FBS) was performed for evaluation of platelet count, plasma levels of aminotransferases and gamma-glutamyl transpeptidases (GGT), presence of viraemia and specific fetal immunoglobulin M. Targeted ultrasound examination was performed every fortnight. Ultrasound findings were categorised into normal examination and any ultrasound abnormality, which was further grouped as ultrasound abnormality of the fetal brain and noncerebral ultrasound abnormality. Main outcome measures, A combination of histological findings after termination of pregnancy and evidence of cytomegalic inclusion disease at birth when pregnancies were continued. Clinical symptoms at birth or histological lesions attributable to CMV were considered as poor outcome. Statistical analysis was conducted to determine the value of each parameter to predict outcome. Logistic regression was used to build up a multivariate model combining the relevant parameters. Results, In univariate analysis, only thrombocytopenia and the presence of any ultrasound abnormality were associated with a poor outcome (P < 10,4 for both abnormalities). In the multivariate analysis, both thrombocytopenia and the presence of ultrasound abnormalities remained significant independent predictors of a poor outcome. Based on univariate logistic regression, odds ratio for a poor outcome were 1.24, 7.2, 22.5 and 25.5 for each 10 000/mm3 decrease in platelet count, the presence of noncerebral, any ultrasound and cerebral ultrasound abnormalities, respectively. Conclusions, The prognosis of CMV-infected fetuses relies independently on both targeted ultrasound examination and fetal platelet count. FBS for platelet count may therefore justify FBS in infected fetuses even in the absence of ultrasound. features of brain involvement. [source]

Organs/Systems Potentially Involved In One Model Of Programmed Hypertension In Sheep

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2001
Miodrag Dodic
SUMMARY 1. When pregnant ewes and their fetuses are exposed to the synthetic glucocorticoid dexamethasone for 2 days early in pregnancy (days 26,28; term 145,150 days), female offspring have increased blood pressure relative to a control group. In one series, this was shown to be due to increased cardiac output, concomitant with a reset mean arterial pressure/heart rate reflex. The first group of such animals had, by the age of 7 years, left ventricular hypertrophy and reduced cardiac functional capacity. 2. The elevation in blood pressure is not maintained by any change in the peripheral renin,angiotensin system (RAS). 3. There is, however, preliminary evidence that some aspects of local RAS (particularly in the kidney and brain) could have participated in the ,programming' event. The levels of mRNA for angiotensin II receptors (AT1, AT2) and angiotensinogen are increased in the kidney of such dexamethasone-treated fetuses in late gestation (130 days), some 100 days after steroid treatment. Similar increases in AT1 mRNA in the medulla oblongata of the fetal brain and large increases of mRNA for angiotensinogen occur in the hypothalamus. 4. These findings, together with evidence from the literature, suggest that both the kidney and parts of the brain are affected by events that also ,program' high blood pressure in the offspring of animals in which the intra-uterine environment has been perturbed at some stage. [source]

The role of intrauterine bacteria in brain injury

ACTA PAEDIATRICA, Issue 2004
MHF Sullivan
Organisms appear to be present in human fetal membranes without any apparent impact on pregnancy maintenance or the fetal brain. A clear link between chorioamnionitis and fetal brain damage suggests that tissue responses at the feto-maternal interface may be the key determinant of whether preterm labour and brain damage occur. [source]

Temporal Vulnerability of Fetal Cerebellar Purkinje Cells to Chronic Binge Alcohol Exposure: Ovine Model

ALCOHOLISM, Issue 10 2007
Jayanth Ramadoss
Background: Human magnetic resonance imaging (MRI) and autopsy studies reveal abnormal cerebellar development in children who had been exposed to alcohol prenatally, independent of the exposure period. Animal studies conducted utilizing the rat model similarly demonstrate a broad period of vulnerability, albeit the third trimester-equivalent of human brain development is reported to be the most vulnerable period, and the first trimester-equivalent exposure produces cerebellar Purkinje cell loss only at high doses of alcohol. However, in the rat model, all 3 trimester-equivalents do not occur prenatally, requiring the assumption that intrauterine environment, placenta, maternal interactions, and parturition do not play an important role in mediating the damage. In this study, we utilized the ovine model, where all 3 trimester-equivalents occur in utero, to determine the critical window of vulnerability of fetal cerebellar Purkinje cells. Methods: Four groups of pregnant sheep were used: first trimester-equivalent pair-fed saline control group, first trimester-equivalent alcohol group (1.75 g/kg), third trimester-equivalent pair-fed saline control group, and third trimester-equivalent alcohol group (1.75 g/kg). The alcohol exposure regimen was designed to mimic a human binge pattern. Alcohol was administered intravenously on 3 consecutive days beginning on day 4 and day 109 of gestation in the first and third trimester-equivalent groups, respectively, and the alcohol treatment was followed by a 4-day inter-treatment interval when the animals were not exposed to alcohol. Such treatment episodes were replicated until gestational day 41 and 132 in the first and third trimester-equivalent groups, respectively. All fetal brains were harvested on day 133 and processed for stereological cerebellar Purkinje cell counting. Results: Significant deficits were found in the fetal cerebellar Purkinje cell number and density in the first and third trimester-equivalent alcohol exposed fetuses compared with those in the saline controls. However, there was no difference between the first and third trimester-equivalent alcohol administered groups. When comparing the present findings to those from a previous study where the duration of alcohol exposure was all 3 trimester-equivalents of gestation, we did not detect a difference in fetal cerebellar Purkinje cell number. Conclusions: We conclude that the fetal cerebellar Purkinje cells are sensitive to alcohol exposure at any time during gestation and that women who engage in binge drinking during the first trimester are at a high risk of giving birth to children with cerebellar damage even if drinking ceases after the first trimester. Our findings also support the hypothesis that only a certain population of Purkinje cells are vulnerable to alcohol-induced depletion irrespective of the timing or duration of alcohol exposure. [source]

Neuroanatomy of the Subadult and Fetal Brain of the Atlantic White-sided Dolphin (Lagenorhynchus acutus) from in Situ Magnetic Resonance Images

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 12 2007
Eric W. Montie
Abstract This article provides the first anatomically labeled, magnetic resonance imaging (MRI) -based atlas of the subadult and fetal Atlantic white-sided dolphin (Lagenorhynchus acutus) brain. It differs from previous MRI-based atlases of cetaceans in that it was created from images of fresh, postmortem brains in situ rather than extracted, formalin-fixed brains. The in situ images displayed the classic hallmarks of odontocete brains: fore-shortened orbital lobes and pronounced temporal width. Olfactory structures were absent and auditory regions (e.g., temporal lobes and inferior colliculi) were enlarged. In the subadult and fetal postmortem MRI scans, the hippocampus was identifiable, despite the relatively small size of this structure in cetaceans. The white matter tracts of the fetal hindbrain and cerebellum were pronounced, but in the telencephalon, the white matter tracts were much less distinct, consistent with less myelin. The white matter tracts of the auditory pathways in the fetal brains were myelinated, as shown by the T2 hypointensity signals for the inferior colliculus, cochlear nuclei, and trapezoid bodies. This finding is consistent with hearing and auditory processing regions maturing in utero in L. acutus, as has been observed for most mammals. In situ MRI scanning of fresh, postmortem specimens can be used not only to study the evolution and developmental patterns of cetacean brains but also to investigate the impacts of natural toxins (such as domoic acid), anthropogenic chemicals (such as polychlorinated biphenyls, polybrominated diphenyl ethers, and their hydroxylated metabolites), biological agents (parasites), and noise on the central nervous system of marine mammal species. Anat Rec, 2007. © 2007 Wiley-Liss, Inc. [source]