scholarly journals A Needle in the Fetal Brain: The Rare Role of Transabdominal Cephalocentesis in Fetal Hydrocephalus

Cureus ◽  
2021 ◽  
Author(s):  
P Swetha ◽  
Shobha Dhananjaya ◽  
Amogh Ananda Rao ◽  
Ashutosh Suresh ◽  
Chiranth Nadig
Keyword(s):  
Fetal Brain ◽  
Fetal Hydrocephalus

The role of placental growth factor in regulating fetal brain vascular development

2014 ◽  
Author(s):  
Matthew T Ratsep ◽  
Bruno Zavan ◽  
Nicki Peterson ◽  
Leandra Tolusso ◽  
Vanessa Kay ◽  
...  
Keyword(s):  
Growth Factor ◽  
Vascular Development ◽  
Fetal Brain ◽  
Placental Growth Factor

scholarly journals Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes

2021 ◽  
Author(s):  
Rachel L. Leon ◽  
Imran N. Mir ◽  
Christina L. Herrera ◽  
Kavita Sharma ◽  
Catherine Y. Spong ◽  
...  
Keyword(s):  
Brain Development ◽  
Congenital Heart ◽  
Fetal Brain ◽  
In Utero ◽  
Structure And Function ◽  
Brain Growth ◽  
Neurodevelopmental Outcomes ◽  
Fetal Brain Development ◽  
And Function

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

The Importance of Iron To Support Optimum Cognitive Development

2021 ◽  
Vol 5 (1-1) ◽  
pp. 25-32
Author(s):  
Rini Sekartini
Keyword(s):  
Iron Deficiency ◽  
Iron Supplementation ◽  
Fetal Brain ◽  
Nutrient Deficiency ◽  
Deficiency Anemia ◽  
Neural Systems ◽  
Brain Anatomy ◽  
Micronutrient Status ◽  
The Central Nervous System

The fetal brain anatomy development starts during the last trimester of pregnancy and continue in early months of life. This critical process makes it vulnerable to insufficient nutrition, while brain growth continues into adulthood, micronutrient status can affect functioning beyond childhood. Iron is an important nutrient for the production and growth of cells in the immune and neural systems. Iron deficiency (ID) is the most common nutrient deficiency in the world, affecting about half of all pregnant women and their offspring. Iron deficiency anemia has long been believed to have an effect on the central nervous system. Iron deficiency in late trimester and in newborn leads to abnormal cognitive function and emotional control that may continue in adulthood. In summary, despite some evidence that iron supplementation enhances cognitive performance. Evidence of the role of iron in brain development and the effect of iron deficiency or iron supplementation on early development is uncertain.

scholarly journals The role of thickness inhomogeneities in hierarchical cortical folding

2020 ◽  
Author(s):  
Lucas da Costa Campos ◽  
Raphael Hornung ◽  
Gerhard Gompper ◽  
Jens Elgeti ◽  
Svenja Caspers
Keyword(s):  
Fetal Brain ◽  
Epileptic Seizures ◽  
Quantitative Model ◽  
Higher Order ◽  
Mammalian Brain ◽  
Cortical Folding ◽  
Differential Growth ◽  
The Brain ◽  
Short Life Expectancy

AbstractThe morphology of the mammalian brain cortex is highly folded. For long it has been known that specific patterns of folding are necessary for an optimally functioning brain. On the extremes, lissencephaly, a lack of folds in humans, and polymicrogyria, an overly folded brain, can lead to severe mental retardation, short life expectancy, epileptic seizures, and tetraplegia. The construction of a quantitative model on how and why these folds appear during the development of the brain is the first step in understanding the cause of these conditions. In recent years, there have been various attempts to understand and model the mechanisms of brain folding. Previous works have shown that mechanical instabilities play a crucial role in the formation of brain folds, and that the geometry of the fetal brain is one of the main factors in dictating the folding characteristics. However, modeling higher-order folding, one of the main characteristics of the highly gyrencephalic brain, has not been fully tackled. The effects of thickness inhomogeneity in the gyrogenesis of the mammalian brain are studied in silico. Finite-element simulations of rectangular slabs are performed. The slabs are divided into two distinct regions, where the outer layer mimics the gray matter, and the inner layer the underlying white matter. Differential growth is introduced by growing the top layer tangentially, while keeping the underlying layer untouched. The brain tissue is modeled as a neo-Hookean hyperelastic material. Simulations are performed with both, homogeneous and inhomogeneous cortical thickness. The homogeneous cortex is shown to fold into a single wavelength, as is common for bilayered materials, while the inhomogeneous cortex folds into more complex conformations. In the early stages of development of the inhomogeneous cortex, structures reminiscent of the deep sulci in the brain are obtained. As the cortex continues to develop, secondary undulations, which are shallower and more variable than the structures obtained in earlier gyrification stage emerge, reproducing well-known characteristics of higher-order folding in the mammalian, and particularly the human, brain.

scholarly journals Novel role of mortalin in attenuating HIV-1 Tat-mediated astrogliosis

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Priyanka ◽  
Renu Wadhwa ◽  
Rituparna Chaudhuri ◽  
Tapas Chandra Nag ◽  
Pankaj Seth
Keyword(s):  
Western Blotting ◽  
Neuronal Death ◽  
Neuronal Damage ◽  
Fetal Brain ◽  
Luciferase Assay ◽  
Expression Vectors ◽  
Neurocognitive Dysfunction ◽  
Hiv 1

Abstract Background In human immunodeficiency virus-1 (HIV-1) infection, activation of astrocytes induces imbalance in physiological functions due to perturbed astrocytic functions that unleashes toxicity on neurons. This leads to inflammatory response finally culminating into neurocognitive dysfunction. In neuroAIDS, HIV-1 protein, transactivator of transcription (Tat) is detected in the cerebrospinal fluid of infected patients. Mortalin, a multifunctional protein, has anti-inflammatory role following its activation in various stress conditions. Recent studies demonstrate downregulation of mortalin in neurodegenerative diseases. Here, we explored the mechanisms of mortalin in modulating HIV-1 Tat-mediated neuroinflammation. Methods Expression of mortalin in autopsy section in normal and diseased individuals were examined using immunohistochemistry. To decipher the role of mortalin in HIV-1 Tat-induced activation, human fetal brain-derived astrocytes were transiently transfected with Tat and mortalin using expression vectors. HIV-1 Tat-mediated damage was analyzed using RT-PCR and western blotting. Modulatory role of mortalin was examined by coexpressing it with Tat, followed by examination of mitochondrial morphodynamics using biochemical assay and confocal and electron microscopy. Extracellular ATP release was monitored using luciferase assay. Neuroinflammation in astrocytes was examined using flow cytometry, dye based study, immunocytochemistry, immunoprecipitation, and western blotting. Indirect neuronal damage was also analyzed. Results HIV-1 Tat downregulates the expression of mortalin in astrocytes, and this is corroborated with autopsy sections of HIV-1 patients. We found that overexpression of mortalin with Tat reduced inflammation and also rescued astrocytic-mediated neuronal death. Using bioinformatics, we discovered that binding of mortalin with Tat leads to Tat degradation and rescues the cell from neuroinflammation. Blocking of proteosomal pathway rescued the Tat degradation and revealed the ubiquitination of Tat. Conclusion Overall, our data demonstrated the protective role of mortalin in combating HIV-1 Tat-mediated damage. We also showed that mortalin could degrade Tat through direct binding with HIV-1 Tat. Overexpression of mortalin in the presence of Tat could significantly reduce cytotoxic effects of Tat in astrocytes. Indirect neuronal death was also found to be rescued. Our in vitro findings were validated as we found attenuated expression of mortalin in the autopsy sections of HIV-1 patients.

Thyroid hormone availability in the human fetal brain: novel entry pathways and role of radial glia

2019 ◽  
Vol 224 (6) ◽  
pp. 2103-2119 ◽  
Author(s):  
Daniela López-Espíndola ◽  
Ángel García-Aldea ◽  
Inés Gómez de la Riva ◽  
Ana Margarita Rodríguez-García ◽  
Domenico Salvatore ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Radial Glia ◽  
Fetal Brain ◽  
Human Fetal Brain

Role of mitochondrial permeability transition in fetal brain damage in rats

2004 ◽  
Vol 30 (4) ◽  
pp. 247-253 ◽  
Author(s):  
Akihito Nakai ◽  
Yukino Shibazaki ◽  
Yoshinari Taniuchi ◽  
Hidehiko Miyake ◽  
Atsuko Oya ◽  
...  
Keyword(s):  
Brain Damage ◽  
Mitochondrial Permeability Transition ◽  
Fetal Brain ◽  
Permeability Transition ◽  
Mitochondrial Permeability

Are We Ready to investigate Cognitive Function of Fetal Brain? The Role of Advanced Four-dimensional Sonography

2016 ◽  
Vol 10 (2) ◽  
pp. 116-124 ◽  
Author(s):  
Aida Salihagic Kadic ◽  
Lara Spalldi Barisic
Keyword(s):  
Cognitive Function ◽  
Cognitive Functions ◽  
Fetal Brain ◽  
Building Blocks ◽  
Time Lapse ◽  
Functional Development ◽  
4D Ultrasound ◽  
And Behavior

ABATRACT Human brain is fascinating organ in so many ways. Some of its cognitive functions, such as ability to learn, memorize, think, percept different sensations, such as pain, to have emotion, process audio-visual inputs, and to coordinate reaction and movements have been subjects of studies for many years. Yet, till recently, we could only make assumptions about prenatal activities, interactions and its construction of complex structures in the time frame of antenatal life. With the prenatal assessment (sonoembryology, neurosonoembryology, KANET test, etc.) by latest advanced HDlive, Silhouette and Flow 3D/4D imaging there is possibility to follow in continuity normal structural and functional development from the early beginnings of “life” and on the other hand consider what might be different (not necessarily abnormal) and deviate from normal development and behavior. On this way, we are able to supplement knowledge of fundamental building blocks of development of fetal cognitive functions, to pay more attention and follow up fetuses at higher risk and finally find some of the possible origins of cognitive dysfunctions which may manifest in childhood or later in life.82 With the introduction of different 3D/4D ultrasound modes we have ability to observe all of this in vivo while emerging, and make “time-lapse” of fetal neurodevelopment and behavior in correlation to its cognitive functional development How to cite this article Kurjak A, Spalldi Barisic L, Stanojevic M, Salihagic Kadic A, Porovic S. Are We Ready to investigate Cognitive Function of Fetal Brain? The Role of Advanced Fourdimensional Sonography. Donald School J Ultrasound Obstet Gynecol 2016;10(2):116-124.

Ethanol neurobehavioural teratogenesis and the role of L-glutamate in the fetal hippocampus

1995 ◽  
Vol 73 (9) ◽  
pp. 1209-1223 ◽  
Author(s):  
James D. Reynolds ◽  
James F. Brien
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Neuronal Development ◽  
Excitatory Amino Acid ◽  
Fetal Brain ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Fetal Alcohol ◽  
Current State ◽  
Developing Neurons

The purpose of this article is to review the current state of knowledge of ethanol neurobehavioural teratogenesis and its postulated mechanisms. The review comprises an examination of ethanol teratogenesis in the human, including the fetal alcohol syndrome, and in experimental animals. Several current proposed mechanisms of ethanol neurobehavioural teratogenesis are critically assessed, including the role of acetaldehyde as the proximate metabolite of ethanol; fetal hypoxia; placental dysfunction; fetal prostaglandin metabolism; and action of ethanol on developing neurons in the fetal brain, including the hippocampus, one of ethanol's main target sites. The effect of ethanol on the release of L-glutamate, an excitatory amino acid neurotransmitter, in the fetal hippocampus is described, and the role of L-glutamate in ethanol teratogenesis involving the hippocampus is discussed. A novel mechanism for abnormal neuronal development in the fetal hippocampus produced by prenatal ethanol exposure is presented, and future experiments to test this hypothesis are proposed.Key words: ethanol neurobehavioural teratogenesis, fetal alcohol syndrome, hippocampus, L-glutamate.

Sign in / Sign up

Export Citation Format

Share Document