scholarly journals Prenatal yolk corticosterone exposure promotes skeletal growth and induces oxidative imbalance in yellow-legged gull embryos

2021 ◽  
Author(s):  
Andrea Romano ◽  
Cristina Daniela Possenti ◽  
Manuela Caprioli ◽  
Beatrice De Felice ◽  
Diego Rubolini ◽  
...  
Keyword(s):  
Oxidative Status ◽  
Skeletal Growth ◽  
Postnatal Life ◽  
Liver Mass ◽  
Skeletal Size ◽  
Laying Sequence ◽  
Organ Specific ◽  
Larus Michahellis ◽  
Carry Over ◽  
The Brain

Maternally-derived hormones induce variation in offspring phenotype, with consequences that can carry-over into post-natal life and even into adulthood. In birds, maternal egg corticosterone (CORT) is known to exert contrasting effects on offspring morphology, physiology and behaviour after hatching. However, information on the effects of CORT exposure on pre-hatching embryonic development is limited. We experimentally increased yolk CORT levels in yellow-legged gull (Larus michahellis) eggs, and assessed the effects on embryo pre-hatching development and oxidative status of brain and liver. CORT-supplemented embryos reached a larger skeletal size and liver mass compared to controls. Embryos from CORT-injected last-laid eggs showed decreased activity of the hepatic antioxidant enzymes superoxide dismutase and catalase, while intermediate-laid eggs showed an increased levels of lipid peroxidation. However, elevated yolk CORT did not affect oxidative stress endpoints in the brain. Our results indicate that elevated yolk CORT levels affect prenatal embryo development by promoting skeletal growth, and induce laying sequence- and organ-specific oxidative imbalance, with potential adverse consequences during postnatal life especially for late-hatched offspring.

scholarly journals Tackling Dysfunction of Mitochondrial Bioenergetics in the Brain

2021 ◽  
Vol 22 (15) ◽  
pp. 8325
Author(s):  
Paola Zanfardino ◽  
Stefano Doccini ◽  
Filippo M. Santorelli ◽  
Vittoria Petruzzella
Keyword(s):  
Human Brain ◽  
Basic Function ◽  
Mitochondrial Proteome ◽  
Novel Proteins ◽  
Mitochondrial Functions ◽  
Organ Specific ◽  
Oxphos System ◽  
Mitochondrial Defects ◽  
Energy Dependent ◽  
The Brain

Oxidative phosphorylation (OxPhos) is the basic function of mitochondria, although the landscape of mitochondrial functions is continuously growing to include more aspects of cellular homeostasis. Thanks to the application of -omics technologies to the study of the OxPhos system, novel features emerge from the cataloging of novel proteins as mitochondrial thus adding details to the mitochondrial proteome and defining novel metabolic cellular interrelations, especially in the human brain. We focussed on the diversity of bioenergetics demand and different aspects of mitochondrial structure, functions, and dysfunction in the brain. Definition such as ‘mitoexome’, ‘mitoproteome’ and ‘mitointeractome’ have entered the field of ‘mitochondrial medicine’. In this context, we reviewed several genetic defects that hamper the last step of aerobic metabolism, mostly involving the nervous tissue as one of the most prominent energy-dependent tissues and, as consequence, as a primary target of mitochondrial dysfunction. The dual genetic origin of the OxPhos complexes is one of the reasons for the complexity of the genotype-phenotype correlation when facing human diseases associated with mitochondrial defects. Such complexity clinically manifests with extremely heterogeneous symptoms, ranging from organ-specific to multisystemic dysfunction with different clinical courses. Finally, we briefly discuss the future directions of the multi-omics study of human brain disorders.

Expression of vascular permeability factor/vascular endothelial growth factor in normal rat tissues

1993 ◽  
Vol 264 (4) ◽  
pp. C995-C1002 ◽  
Author(s):  
W. T. Monacci ◽  
M. J. Merrill ◽  
E. H. Oldfield
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
In Situ Hybridization ◽  
Rat Tissues ◽  
Vascular Endothelial ◽  
Vascular Permeability Factor ◽  
Organ Specific ◽  
Normal Rat ◽  
Endothelial Growth Factor ◽  
The Brain

Vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF) is a approximately 43-kDa secreted protein that has been shown in bioassays to induce endothelial proliferation, angiogenesis, and capillary hyperpermeability. VPF has been suggested to play an important role in the physiology of normal vasculature. To further elucidate the natural functions of VPF in vivo, the expression of VPF in normal tissues was examined using Northern blot analysis and in situ hybridization histochemistry. VPF mRNA is expressed in the brain, kidney, liver, lung, and spleen of the healthy adult rat. On Northern blots, the relative abundance of VPF mRNA observed in these tissues was highest in the lung and lowest in the spleen. As determined by in situ hybridization, the patterns of VPF expression are organ specific. Hybridization of an antisense VPF probe was concentrated in the cerebellar granule cell layer of the brain and in the glomeruli and tubules of the kidney. In the liver and lung, intense hybridization was observed homogeneously throughout both tissues, demonstrating that VPF mRNA is present in virtually every hepatocyte and pulmonary alveolar cell. Hybridization to the spleen was weaker and more diffuse. The widespread expression and organ-specific distribution of VPF mRNA in normal rat tissues supports the suggestion of an extensive role for this factor in the physiology of normal vasculature.

scholarly journals Porencephaly and intraparenchymal hyperacute infarct due to bilateral anterior cerebral artery embolism in adult: A rare case

2021 ◽  
Vol 12 (6) ◽  
pp. 118-121
Author(s):  
Ricky Suryamin ◽  
Subagia Santosa Sudjono
Keyword(s):  
Neurological Disease ◽  
Physical Disability ◽  
Rare Case ◽  
Anterior Cerebral Artery ◽  
Postnatal Life ◽  
Artery Embolism ◽  
Disease Case ◽  
The Brain ◽  
Loss Of Strength ◽  
Space Occupying Lesion

Porencephaly is a very unique rare neurological disease identified by the presence of single or multiple cerebrospinal fluid (CSF) cyst inside the brain matter. This is an intra-cranial cyst that rarely occurs in adults. The diagnosis depends on a well-defined CSF fluid space-occupying lesion (SOL) that communicates with the ventricles on a CT scan or MRI of the brain. Cerebral damage during labor or as unknown trauma during infancy can present with porencephaly much later in life. This might be the aftermath of trauma, ischemic, infection or bleeding in the postnatal life. These cysts may be mild enough to show any symptoms or severe enough to cause mental and physical disability. Here we present a case of a 76-year-old female attended in the emergency department with loss of strength in her right arm, four days ago. Porencephaly in adult is a rare neurological disease case. In this case, porencephaly caused by stroke ischemic 4 years ago due to anterior carotid artery embolism.

scholarly journals An Extensive Genetic Program Occurring during Postnatal Growth in Multiple Tissues

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1791-1800 ◽  
Author(s):  
Gabriela P. Finkielstain ◽  
Patricia Forcinito ◽  
Julian C. K. Lui ◽  
Kevin M. Barnes ◽  
Rose Marino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Pattern ◽  
Somatic Growth ◽  
Postnatal Growth ◽  
Genetic Program ◽  
Male Rats ◽  
Postnatal Life ◽  
Multiple Organs ◽  
Organ Specific ◽  
Parenchymal Cells

Mammalian somatic growth is rapid in early postnatal life but then slows and eventually ceases in multiple tissues. We hypothesized that there exists a postnatal gene expression program that is common to multiple tissues and is responsible for this coordinate growth deceleration. Consistent with this hypothesis, microarray analysis identified more than 1600 genes that were regulated with age (1 vs. 4 wk) coordinately in kidney, lung, and heart of male mice, including many genes that regulate proliferation. As examples, we focused on three growth-promoting genes, Igf2, Mest, and Peg3, that were markedly down-regulated with age. In situ hybridization revealed that expression occurred in organ-specific parenchymal cells and suggested that the decreasing expression with age was due primarily to decreased expression per cell rather than a decreased number of expressing cells. The declining expression of these genes was slowed during hypothyroidism and growth inhibition (induced by propylthiouracil at 0–5 wk of age) in male rats, suggesting that the normal decline in expression is driven by growth rather than by age per se. We conclude that there exists an extensive genetic program occurring during postnatal life. Many of the involved genes are regulated coordinately in multiple organs, including many genes that regulate cell proliferation. At least some of these are themselves apparently regulated by growth, suggesting that, in the embryo, a gene expression pattern is established that allows for rapid somatic growth of multiple tissues, but then, during postnatal life, this growth leads to negative-feedback changes in gene expression that in turn slow and eventually halt somatic growth, thus imposing a fundamental limit on adult body size.

scholarly journals Effects of Lycopene, Indole-3-Carbinol, and Luteolin on Nitric Oxide Production and iNOS Expression are Organ-Specific in Rats

2010 ◽  
Vol 61 (3) ◽  
pp. 275-285 ◽  
Author(s):  
Evita Rostoka ◽  
Sergejs Isajevs ◽  
Larisa Baumane ◽  
Aija Line ◽  
Karina Silina ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Cortex ◽  
Natural Compounds ◽  
Inos Expression ◽  
No Production ◽  
Nitric Oxide Production ◽  
Inos Gene ◽  
Organ Specific ◽  
The Brain ◽  
Inos Gene Expression

Effects of Lycopene, Indole-3-Carbinol, and Luteolin on Nitric Oxide Production and iNOS Expression are Organ-Specific in RatsNatural compounds are known to modify NO content in tissues; however, the biological activity of polyphenol-rich food often does not correspond to the effects of individual polyphenols on NO synthase activity. The aim of this study was to see how natural compounds luteolin, indole-3-carbinol, and lycopene modify NO production in rat tissues and change the expression of the iNOS gene and protein. Indole-3-carbinol produced multiple effects on the NO level; it significantly decreased NO concentration in blood, lungs, and skeletal muscles and increased it in the liver. Indole-3-carbinol enhanced lipopolyssaccharide (LPS)-induced NO production in all rat organs. It decreased iNOS gene expression in the brain cortex of animals that did not receive LPS and up-regulated it in the LPS-treated animals. Lycopene increased the iNOS gene transcription rate in the brain cortex of LPS-treated animals. Luteolin did not modify NO production in any organ of LPS-untreated rats, nor did it affect gene expression in the liver. In the brain it slightly decreased iNOS gene expression. Luteolin decreased NO production in the blood of LPS-treated animals and the number of iNOS-positive cells in these animals. Our results suggest that changes in tissue NO levels caused by natural compounds cannot be predicted from their effect on NOS expression or activity obtained in model systems. This stresses the importance of direct measurements of NO and NOS expression in animal tissues.

scholarly journals The N-myc proto-oncogene and IGF-II growth factor mRNAs are expressed by distinct cells in human fetal kidney and brain.

1989 ◽  
Vol 108 (3) ◽  
pp. 1093-1104 ◽  
Author(s):  
H Hirvonen ◽  
M Sandberg ◽  
H Kalimo ◽  
V Hukkanen ◽  
E Vuorio ◽  
...  
Keyword(s):  
Growth Factor ◽  
Wilms Tumor ◽  
Expression Patterns ◽  
Regional Distribution ◽  
Cell Types ◽  
Cortical Plate ◽  
Northern Hybridization ◽  
Postnatal Life ◽  
Fetal Kidney ◽  
The Brain

We studied the expression of the N-myc proto-oncogene and the insulin-like growth factor-II (IGF-II) gene in human fetuses of 16-19 gestational wk. Both genes have specific roles in the growth and differentiation of embryonic tissues, such as the kidney and neural tissue. Since continued expression of N-myc and IGF-II mRNAs is also a characteristic feature of Wilms' tumor, a childhood neoplasm of probable fetal kidney origin, we were particularly interested in the possibility that their expression might be linked or coordinately regulated in the developing kidney. Expression of N-myc mRNA was observed in the brain and in the kidney by Northern hybridization analysis. In in situ hybridization of the kidney, N-myc autoradiographic grains were primarily located over epithelially differentiating mesenchyme while most of the mesenchymal stromal cells showed only a background signal with the N-myc probe. N-myc mRNA was detectable throughout the developing brain with a slight accentuation in the intermediate zone cells in between the subependymal and cortical layers. Thus, even postmitotic neuroepithelial cells of the fetal cerebrum expressed N-myc mRNA. In Northern hybridization, IGF-II mRNA signal was abundant in the kidney but much weaker, though definite, in the brain. The regional distribution of IGF-II mRNA in the kidney was largely complementary to that of N-myc. IGF-II autoradiographic grains were located predominantly over the stromal and blastemal cells with a relative lack of hybridization over the epithelial structures. In the brain, IGF-II mRNA was about two- to threefold more abundant in the subependymal and intermediate layers than in the cortical plate and ependymal zone, respectively. The fetal expression patterns of the N-myc and IGF-II mRNAs are reflected by the types of tumors known to express the corresponding genes during postnatal life such as Wilms' tumor. However, the apparent coexpression of the IGF-II and N-myc genes in immature kidneys occurs largely in distinct cell types.

scholarly journals Study of fetal and postnatal morphological development of the brain sulci

2013 ◽  
Vol 11 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Koshiro Nishikuni ◽  
Guilherme Carvalhal Ribas
Keyword(s):  
Morphological Changes ◽  
Fetal Brain ◽  
Postnatal Period ◽  
Postnatal Life ◽  
Morphological Development ◽  
Fetal Life ◽  
Brain Hemispheres ◽  
Collateral Sulcus ◽  
Fetal Brain Development ◽  
The Brain

Object The surface of the developing fetal brain undergoes significant morphological changes during fetal growth. The purpose of this study was to evaluate the morphological development of the brain sulci from the fetal to the early postnatal period. Methods Two hundred fourteen brain hemispheres from 107 human brain specimens were examined to evaluate the timing of sulcal formation, from its appearance to its complete development. These brains were obtained from cadavers ranging in age from 12 weeks of gestation to 8 months of postnatal life. Results The order of appearance of the cerebral sulci, and the number and percentages of specimens found in this study were as follows: longitudinal cerebral fissure at 12 weeks (10/10, 100%); callosal sulcus at 12 weeks (10/10, 100%); hippocampal sulcus at 15 weeks (7/10, 70%); lateral sulcus at 17 weeks (20/22, 90.9%); circular insular sulcus at 17 weeks (18/22, 81.8%); olfactory sulcus at 17 weeks (18/22, 81.8%); calcarine sulcus at 17 weeks (14/22, 63.6%); parietooccipital sulcus at 17 weeks (11/22, 50%); cingulate sulcus at 19 weeks (16/20, 80%); central sulcus at 21 weeks (22/38, 57.9%); orbital sulcus at 22 weeks (9/16, 56.2%); lunate sulcus at 24 ± 2 weeks (12/16, 75%); collateral sulcus at 24 ± 2 weeks (8/16, 50%); superior frontal sulcus at 25 ± 2 weeks (5/6, 83.3%); rhinal sulcus at 25 ± 2 weeks (3/6, 50%); precentral sulcus at 26 ± 3 weeks (2/4, 50%); postcentral sulcus at 26 ± 3 weeks (2/4, 50%); superior temporal sulcus at 26 ± 3 weeks (2/4, 50%); central insular sulcus at 29 ± 2 weeks (4/4, 100%); intraparietal sulcus at 29 ± 2 weeks (2/4, 50%); paraolfactory sulcus at 29 ± 2 weeks (2/4, 50%); inferior frontal sulcus at 30 ± 3 weeks (2/4, 50%); transverse occipital sulcus at 30 ± 3 weeks (2/4, 50%); occipitotemporal sulcus at 30 ± 3 weeks (2/4, 50%); marginal branch of the cingulate sulcus at 30 ± 3 weeks (2/4, 50%); paracentral sulcus at 30 ± 3 weeks (2/4, 50%); subparietal sulcus at 30 ± 3 weeks (2/4, 50%); inferior temporal sulcus at 31 ± 3 weeks (3/6, 50%); transverse temporal sulcus at 33 ± 3 weeks (6/8, 75%); and secondary sulcus at 38 ± 3 weeks (2/4, 50%). Conclusions The brain is subjected to considerable morphological changes throughout gestation. During fetal brain development the cortex begins to fold in, thereby increasing the cortical surface. All primary sulci are formed during fetal life. The appearance of each sulcus follows a characteristic timing pattern, which may be used as one of the reliable guides pertinent to gestational age and normal fetal development.

scholarly journals Canadian Association of Neurosciences Review: Postnatal Development of the Mammalian Neocortex: Role of Activity Revisited

2006 ◽  
Vol 33 (2) ◽  
pp. 158-169 ◽  
Author(s):  
Zhong-wei Zhang
Keyword(s):  
Spontaneous Activity ◽  
Brain Function ◽  
Postnatal Life ◽  
Synaptic Connections ◽  
Synaptic Remodeling ◽  
Canadian Association ◽  
Selective Elimination ◽  
Neuronal Connections ◽  
The Brain

ABSTRACT:The mammalian neocortex is the largest structure in the brain, and plays a key role in brain function. A critical period for the development of the neocortex is the early postnatal life, when the majority of synapses are formed and when much of synaptic remodeling takes place. Early studies suggest that initial synaptic connections lack precision, and this rudimentary wiring pattern is refined by experience-related activity through selective elimination and consolidation. This view has been challenged by recent studies revealing the presence of a relatively precise pattern of connections before the onset of sensory experience. The recent data support a model in which specificity of neuronal connections is largely determined by genetic factors. Spontaneous activity is required for the formation of neural circuits, but whether it plays an instructive role is still controversial. Neurotransmitters including acetylcholine, serotonin, and γ-Aminobutyric acid (GABA) may have key roles in the regulation of spontaneous activity, and in the maturation of synapses in the developing brain.

scholarly journals DR5 Knockout Mice Are Compromised in Radiation-Induced Apoptosis

2005 ◽  
Vol 25 (5) ◽  
pp. 2000-2013 ◽  
Author(s):  
Niklas Finnberg ◽  
Joshua J. Gruber ◽  
Peiwen Fei ◽  
Dorothea Rudolph ◽  
Anka Bric ◽  
...  
Keyword(s):  
Cell Death ◽  
Null Mouse ◽  
Organ Specific ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
The Brain ◽  
Necrosis Factor

ABSTRACT DR5 (also called TRAIL receptor 2 and KILLER) is an apoptosis-inducing membrane receptor for tumor necrosis factor-related apoptosis-inducing ligand (also called TRAIL and Apo2 ligand). DR5 is a transcriptional target of p53, and its overexpression induces cell death in vitro. However, the in vivo biology of DR5 has remained largely unexplored. To better understand the role of DR5 in development and in adult tissues, we have created a knockout mouse lacking DR5. This mouse is viable and develops normally with the exception of having an enlarged thymus. We show that DR5 is not expressed in developing embryos but is present in the decidua and chorion early in development. DR5-null mouse embryo fibroblasts expressing E1A are resistant to treatment with TRAIL, suggesting that DR5 may be the primary proapoptotic receptor for TRAIL in the mouse. When exposed to ionizing radiation, DR5-null tissues exhibit reduced amounts of apoptosis compared to wild-type thymus, spleen, Peyer's patches, and the white matter of the brain. In the ileum, colon, and stomach, DR5 deficiency was associated with a subtle phenotype of radiation-induced cell death. These results indicate that DR5 has a limited role during embryogenesis and early stages of development but plays an organ-specific role in the response to DNA-damaging stimuli.

Sign in / Sign up

Export Citation Format

Share Document