• Title/Summary/Keyword: early brain development

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Review of Magnetocardiography Technology based on SQUIDs (SQUID를 이용한 심자도 기술의 개발동향)

  • Lee, Y.H.;Kwon, H.;Kim, J.M.;Kim, K.;Yu, K.K.;Park, Y.K.
    • Progress in Superconductivity
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    • v.13 no.3
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    • pp.139-145
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    • 2012
  • Electric activity of cardiac muscles generates magnetic fields. Magnetocardiography (or MCG) technology, measuring these magnetic signals, can provide useful information for the diagnosis of heart diseases. It is already about 40 years ago that the first measurement of MCG signals was done by D. Cohen using SQUID (superconducting quantum interference device) sensor inside a magnetically shielded room. In the early period of MCG history, bulky point-contact RF-SQUID was used as the magnetic sensor. Thanks to the development of Nb-based Josephson junction technology in mid 1980s and new design of tightly-coupled DC-SQUID, low-noise SQUID sensors could be developed in late 1980s. In around 1990, several groups developed multi-channel MCG systems and started clinical study. However, it is quite recent years that the true usefulness of MCG was verified in clinical practice, for example, in the diagnosis of coronary artery disease. For the practical MCG system, technical elements of MCG system should be optimized in terms of performance, fabrication cost and operation cost. In this review, development history, technical issue, and future development direction of MCG technology are described.

Olfactory neuropathology in Alzheimer's disease: a sign of ongoing neurodegeneration

  • Son, Gowoon;Jahanshahi, Ali;Yoo, Seung-Jun;Boonstra, Jackson T.;Hopkins, David A.;Steinbusch, Harry W.M.;Moon, Cheil
    • BMB Reports
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    • v.54 no.6
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    • pp.295-304
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    • 2021
  • Olfactory neuropathology is a cause of olfactory loss in Alzheimer's disease (AD). Olfactory dysfunction is also associated with memory and cognitive dysfunction and is an incidental finding of AD dementia. Here we review neuropathological research on the olfactory system in AD, considering both structural and functional evidence. Experimental and clinical findings identify olfactory dysfunction as an early indicator of AD. In keeping with this, amyloid-β production and neuroinflammation are related to underlying causes of impaired olfaction. Notably, physiological features of the spatial map in the olfactory system suggest the evidence of ongoing neurodegeneration. Our aim in this review is to examine olfactory pathology findings essential to identifying mechanisms of olfactory dysfunction in the development of AD in hopes of supporting investigations leading towards revealing potential diagnostic methods and causes of early pathogenesis in the olfactory system.

In Vivo Expression of the PTB-deleted Odin Mutant Results in Hydrocephalus

  • Park, Sunjung;Lee, Haeryung;Park, Soochul
    • Molecules and Cells
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    • v.38 no.5
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    • pp.426-431
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    • 2015
  • Odin has been implicated in the downstream signaling pathway of receptor tyrosine kinases, such as the epidermal growth factor and Eph receptors. However, the physiologically relevant function of Odin needs to be further determined. In this study, we used Odin heterozygous mice to analyze the Odin expression pattern; the targeted allele contained a ${\beta}$-geo gene trap vector inserted into the 14t intron of the Odin gene. Interestingly, we found that Odin was exclusively expressed in ependymal cells along the brain ventricles. In particular, Odin was highly expressed in the subcommissural organ, a small ependymal glandular tissue. However, we did not observe any morphological abnormalities in the brain ventricles or ependymal cells of Odin null-mutant mice. We also generated BAC transgenic mice that expressed the PTB-deleted Odin (dPTB) after a floxed GFP-STOP cassette was excised by tissue-specific Cre expression. Strikingly, Odin-dPTB expression played a causative role in the development of the hydrocephalic phenotype, primarily in the midbrain. In addition, Odin-dPTB expression disrupted proper development of the subcommissural organ and interfered with ependymal cell maturation in the cerebral aqueduct. Taken together, our findings strongly suggest that Odin plays a role in the differentiation of ependymal cells during early postnatal brain development.

Human Capacity Issues Along the STEM Pipeline

  • Melkers, Julia
    • STI Policy Review
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    • v.1 no.2
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    • pp.1-18
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    • 2010
  • The development and maintenance of human capacity in economies is critical to long term competitiveness, but also for the overall health and environment of regions. Yet, human science and technology-based capacity is multidimensional and has interrelated characteristics which present certain policy challenges. This paper addresses a range of issues specific to a discussion on human capacity in S&T. First, the paper emphasizes the importance of acknowledging the complexity of human capacity issues and how they evolve along the STEM (science, technology, engineering, and mathematics) pipeline. The pipeline is an often used reference to describe the training and development in STEM disciplines, from early childhood education, to more advanced training, and finally to professional collaboration and interaction and serves as a useful organizing framework for the discussion of capacity along the career evolution process. Second, the paper offers an organizing framework for discussion of policy mechanisms that have been developed to address issues and gaps that occur along this STEM pipeline. Specifically, it contrasts the traditional mechanisms of building human capacity in STEM areas with newer "gap filling" and integrated approached to addressed human capacity disparities and priorities. Third, the paper addresses core challenges in human capacity in STEM, including the education and training, participation of women and underrepresented groups, brain drain/brain circulation issues, and the globalization of science. The paper concludes with a discussion of policy implication for the development of human capacity.

Synergistic Action Modes of Arabinan Degradation by Exo- and Endo-Arabinosyl Hydrolases

  • Park, Jung-Mi;Jang, Myoung-Uoon;Oh, Gyo Won;Lee, Eun-Hee;Kang, Jung-Hyun;Song, Yeong-Bok;Han, Nam Soo;Kim, Tae-Jip
    • Journal of Microbiology and Biotechnology
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    • v.25 no.2
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    • pp.227-233
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    • 2015
  • Two recombinant arabinosyl hydrolases, α-L-arabinofuranosidase from Geobacillus sp. KCTC 3012 (GAFase) and endo-(1,5)-α-L-arabinanase from Bacillus licheniformis DSM13 (BlABNase), were overexpressed in Escherichia coli, and their synergistic modes of action against sugar beet (branched) arabinan were investigated. Whereas GAFase hydrolyzed 35.9% of L-arabinose residues from sugar beet (branched) arabinan, endo-action of BlABNase released only 0.5% of L-arabinose owing to its extremely low accessibility towards branched arabinan. Interestingly, the simultaneous treatment of GAFase and BlABNase could liberate approximately 91.2% of L-arabinose from arabinan, which was significantly higher than any single exo-enzyme treatment (35.9%) or even stepwise exo- after endo-enzyme treatment (75.5%). Based on their unique modes of action, both exo- and endo-arabinosyl hydrolases can work in concert to catalyze the hydrolysis of arabinan to L-arabinose. At the early stage in arabinan degradation, exo-acting GAFase could remove the terminal arabinose branches to generate debranched arabinan, which could be successively hydrolyzed into arabinooligosaccharides via the endo-action of BlABNase. At the final stage, the simultaneous actions of exo- and endo-hydrolases could synergistically accelerate the L-arabinose production with high conversion yield.

The Effects of the Expression of GATA Binding Protein 6 on Heart and Brain Development (심장과 뇌 발달에서 GATA6 유전자 발현 감소가 미치는 영향)

  • Seo, Jungwon
    • Journal of Life Science
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    • v.25 no.11
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    • pp.1230-1234
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    • 2015
  • GATA binding protein 6 (GATA6) is a transcription factor that is expressed in the early blastocyst stage and controls the expression of important genes in the differentiation and development of the heart, pancreas, and intestine. This study confirmed the role of GATA6 in cell differentiation and organ development using mouse embryonic stem cells and zebrafish, respectively. First, the mouse embryonic stem cells were differentiated into pacemaker cardiomyocytes. An RT-PCR analysis revealed that the expression of the GATA6 gene was greatly increased from day 4 of differentiation. The expression of GATA6 was upregulated prior to increased expression of NK2 homeobox 5 (Nkx2.5) and myocyte enhancer factor 2C (MEF2C), which are critical transcription factors involved in regulating heart formation. To examine the role of GATA6 in development, GATA6 morpholino was microinjected into zebrafish embryos. Knockdown of GATA6 expression significantly decreased the heart size and heart rate in the zebrafish compared to a control. In addition, the brains were degenerated in the GATA6 morpholino-injected zebrafish. Acridine orange staining showed that knockdown of GATA6 expression increased apoptotic cells in the brain. Interestingly, knockdown of GATA6 expression decreased apoptotic cells in the early bud stage. This study points to the importance of the GATA6 gene in heart and brain development.

Selective and Random Patterning of Programmed Cell Death in Zebrafish Embryonic Development

  • Hwang, Chang-Nam;Kim, Joon;Lee, Sang-Ho
    • Proceedings of the Korean Society of Embryo Transfer Conference
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    • 2002.11a
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    • pp.118-118
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    • 2002
  • Programmed cell death (PCD) is thought as a well-controlled process by which unwanted cells are selectively eliminated. During the last decade many researches have elucidated molecules and their interactions involved in cell death by using largely in vitro induction of cell death or survival signals in a more defined manner, While these critical information and novel findings provide us with clearer understanding of mechanisms underlying cell death, it does by no means explain how PCD occurs and which cells or tissues are affected during normal embryonic development in vivo. In this study, we used zebrafish to examine whether the PCD is occurring selectively or randomly in developing embryos by whole mount in situ TUNEL analysis with specific markers for neural cells. The result revealed that the degree and distribution of TUNEL staining varied considerably throughout gastrulation stage, and there was also a number of TUNEL-negative embryos. Most of TUNEL-positive cells were scattered randomly throughout the blastoderm. During the gastrulation stage about 75 % of the embryos analyzed exhibited more than 5 TUNEL-positive cells. As the dorsal epiblast begins to thicken rather abruptly near the end of gastrulation, TUNEL-positive cells were mainly located along the dorsal side. Although there were some variations in TUNEL staining during segmentation and pharyngeal stages, TUNEL staining continued to be localized to the central nervous system, and was also detected in the sensory organs, trigeminal ganglions, and the primary sensory neurons. High levels of the cell death in developing brain between 20-somite and prim-6 stages are thought to play a role in the morphogenesis and organization of the brain. At prim-16 stage, cell death is considerably reduced in the brain region. Dying cells are mainly localized to the prospective brain region where ectodermal cells are about to initiate neurogenesis. As development progressed, high levels and more reproducible patterns of cell death were observed in the developing nervous system. Intensive TUNEL staining was restricted to the trigeminal ganglions, the primary sensory neurons, and sensory organs, such as olfactory pits and otic vesicles. Thus, PCD patterning in zebrafish embryos occurs randomly at early stages and becomes restricted to certain region of the embryos. The spatio-temporal pattern of PCD during the early embryonic development in zebrafish will provide basic information for further studies to elucidate genes involved in. regulation of PCD largely unknown in vivo during vertebrate embryogenesis.

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Retinoic Acid Induces Abnormal Palate During Embryogenesis in Rat

  • Shin, Jeong-Oh;Park, Hyoung-Woo;Bok, Jin-Woong;Kim, Myoung-Hee
    • Biomedical Science Letters
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    • v.16 no.1
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    • pp.1-9
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    • 2010
  • In order to understand the effects of all-trans-RA on palate development, RA was injected into the abdominal cavity of pregnant mice and then the embryos were taken in the following days and analyzed morphologically as well as molecular biologically. When RA was administered at the stage of E11 or E15, the overall craniofacial development was retarded. The length from jaw to eye was shortened, compared to that of normal group. When the E11 embryos were exposed to RA, cleft lip was also found along with the cleft palate. In vitro palate culture experiment also revealed that RA caused cleft palate. When RT-PCR was performed, early stage administration of RA at E11 inhibited the upregulation of Hoxa7 expression at E15 through E17. Whereas in control group, high level of Hoxa7 expression was detected in the palate of E15 to E17. In the case of Bax, the expression was decreased from E16, while remaining constant in control group. When TUNEL analysis was performed following the RA treatment at E15, TUNEL positive cells were detected in the mesenchymal cells as well as epithelial cells of palatal shelves of E16 and in E17 embryos. Whereas in normal control, TUNEL positive cells were observed mostly at the epithelium around the nasal cavity and oral cavity where rugae is made. These results altogether indicate that exposure to RA during palate development causes facial deformity including cleft palate and cleft lip by modulating the expression of homeotic genes such as Hoxa7 as well as an apoptosis-related gene, Bax, and thus malregulating the apoptosis.

Synthetic Maternal Stress Hormone Can Modulate the Expression of Hox Genes

  • Yu, Sook-Jin;Lee, Ji-Yeon;Kim, Sang-Hoon;Deocaris, Custer C.;Kim, Myoung-Hee
    • Biomedical Science Letters
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    • v.15 no.3
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    • pp.249-255
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    • 2009
  • All living things have been developed efficient strategies to cope with external and internal environmental changes via a process termed 'homeostasis'. However, chronic prenatal maternal stress may significantly contributes to pregnancy complications by disturbing hypothalamic-pituitary-adrenal (HPA) axis and the automatic nervous system (ANS), and results in unfavorable development of the fetus. Dysregulation of these two major stress response systems lead to the increased secretion of the glucocorticoids (GCs) which are known to be essential for normal development and the maturation of the central nervous system. As Hox genes are master key regulators of the embryonic morphogenesis and cell differentiation, we aimed to determine the effects of dexamethasone, a potent synthetic glucocorticoid, on gene expression in mesenchymal stem cell C3H10T1/2. Analysis of 39 Hox genes based on reverse transcription PCR (RT-PCR) method revealed that the expression patterns of Hox genes were overall upregulated by long dexametasone treatment. These results indicate that maternal stress may have a deleterious effect on early developing embryo through the stress hormone, glucocorticoid.

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Formation of Sensory Pigment Cells Requires Fibroblast Growth Factor Signaling during Ascidian Embryonic Development

  • Kim, Gil-Jung
    • Animal cells and systems
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    • v.7 no.3
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    • pp.221-225
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    • 2003
  • The tadpole larva of the ascidian Halocynthia roretzi has two sensory pigment cells in its brain vesicle. To elucidate the temporal requirement for FGF signaling in formation of the pigment cells, embryos were treated with an FGF receptor 1 inhibitor, SU5402, or an MEK inhibitor, U0126 during various embryonic stages. In the present study, it is shown that the embryos treated with SU5402 from the 16-cell stage to the early gastrula stage do not form pigment cells, whereas those treated after the early gastrula stage form pigment cells. In pigment cell formation, embryos suddenly exhibited the sensitivity to SU5402 only for 1 h at the neural plate stage(-4 h after the beginning of gastrulation). When U0126 treatment was carried out at various stages between the 8-cell and late neurula stages, the embryos scarcely formed pigment cells. Pigment cell formation occurred when the embryos were placed in U0126 at early tail bud stage. These results indicate that FGF signaling is involved in pigment cell formation at two separate processes during ascidian embryogenesis, whereas more prolonged period is required for MEK signaling.