• Toxicological Research
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• v.17
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• pp.11-16
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• 2001

The development of the central nervous system is a continuous process during the embryonic and fetal periods. For a better understanding of congenital anomalies of central nervous system, three major events of normal development, i.e., neurulation (3 to 4 weeks), brain vesicle formation (4 to 7 weeks) and mantle formation (over 8 weeks) should be kept in mind. The first category of anomalies is neural tube defect. Neural tube defects encompass all the anomalies arise in completion of neurulation. The second category of central nervous system anomalies is disorders of brain vesicle formation. This is anomaly that applies for "the face predicts the brain". Holoprosencephaly covers a spectrum of anomalies of intracranial and midfacial development which result from incomplete development and septation of midline structures within the forebrain or prosencephalon. The last category of central nervous system malformation is disorders involving the process of mantle formation. In the human, neurons are generated in two bursts, the first from 8 to 10 weeks and next from 12 to 14 weeks. By 16 weeks, most of the neurons have been generated and have started their migration into the cortex. Mechanism of migration disorders are multifactorial. Abnormal migration into the cortex, abnormal neurons, faulty neural growth within the cortex, unstable pial-glial border, degeneration of neurons, neural death by exogenous factors are some of the proposed mechanism. Agyria-pachygyria are characterized by a four-layerd cortex. Polymicrogyria is gyri that are too numerous and too small, and is morphologically heterogeneous. Cortical dysplasia is characterized by the presence Q[ abnormal neurons and glia arranged abnormally in focal areas of the cerebral cortex. Neuroglial malformative lesions associated with medically intractable epilepsy are hamartia or hamartoma, focal cortical dysplasia and microdysgenesis.ysgenesis.

• Proceedings of the Zoological Society Korea Conference
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• 2001.10a
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• pp.116.1-116
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• 2001

No Abstract, See Full Text

• Proceedings of the Korean Society of Life Science Conference
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• 2001.09a
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• pp.99-99
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• 2001

• Applied Microscopy
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• v.23 no.1
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• pp.109-124
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• 1993

The prenatal development of thoracic spinal cord was studied by electron microscope in human embryos and fetuses ranging from 9mm to 260mm crown-rump length (5-30 weeks of gestational age). Ependymal cells in all fetal ages had conspicuous junctional complexes close to the lumen of the central canal into which microvilli and cilia projected. The ependymal cells contained numerous longitudinally arranged mitochondria, flattened cisternae of endoplasmic reticulum and Golgi complex. At 20 mm embryo, the floor and roof plates were composed of ependymoglial cells and undifferentiated neuroepithelial cells. The neuroepithelia of the sacral spinal cord were delineated from central medullary cord. By 100 mm fetus few undifferentiated neuroepithelial cells remained in the floor and roof plates. At 150 mm fetus, the whole central canal was formed by ciliated columnar epithelial cells containing cilia with basal bodies. The microvilli became tangled and club-shaped and formed a matted surface. The canal was filled with areas of dark and pale amorphous materials bounded by membrane-like structure. These two types of material were found throughout the whole central canal from 100 mm fetus onwards. By 260 mm fetus, microfibrils were first observed in the ependymal cells. In conclusion, it seems that early development and differentiation of central canal ependyma are simlar to that in other part of the brain ventricular system although ependymoglial cells are more prominent.

• Proceedings of the Zoological Society Korea Conference
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• 2000.10a
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• pp.116.3-117
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• 2000

No Abstract, See Full Text

• Proceedings of the Korean Society of Life Science Conference
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• 2001.09a
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• pp.104-104
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• 2001

• Journal of Korean Neurosurgical Society
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• v.30 no.sup2
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• pp.189-196
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• 2001

Objective : We tested the hypothesis that photodynamic therapy(PDT) with Photofrin inhibits tumor invasion of U87 human glioma cells using several in vitro assay to measure tumor invasiveness. The effects of PDT on cell growth, directional migration and cell invasion were investigated. Material and Method : Tumor cells were treated with Photofrin at various doses and at a fixed optical(632nm) dose of $100mJ/cm^2$. Cytotoxicity was tested using the MTT method. Invasion assays including the matrigelartificial basement membrane barrier migration and spheroid confrontation with confocal microscopic analysis were used to study the relationship between PDT and invasiveness. Result : U87 cells showed a dose dependent cytotoxic response to increasing Photofrin dose. Data from the matrigel artificial basement membrane assay indicate that PDT inhibits the U87 cell migration dose dependently. Low doses of subcytotoxic PDT treatment, such as 2.5ug/ml Photofrin dose, also appeared to significantly inhibit migration of U87 cells(p<0.05). In co-cultures between U87 cell spheroids and brain aggregates, progressive invasion with destruction of the brain aggregate occurs. The extent of tumor cell infiltration and proportion or intact brain aggregate remaining after 24h differs in Photofrin PDT treated versus Photofrin only control, with changes suggestive of a dose-response effect. Conclusion : our data indicate that PDT with Photofrin significantly inhibits the invasiveness of U87 cells, and this inhibition is dose dependent.

• BMB Reports
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• v.31 no.6
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• pp.578-584
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• 1998

In a previous paper (Kim et al., 1996a), the immediate 5' -flanking region and coding region of the human UDP-N -acetylglucosamine:-D-mannoside-1,4-Nacetylglucosaminyltransferase III (N-acetylglucosaminyitransferase- III; GnT-III) gene was reported, isolated and analyzed. Herein, we report on amplification of a new 5' -noncoding region of the GnT-III mRNA by single-strand ligation to single-stranded cDNA-PCR (5' -RACE PCR) using poly(A)+ RNA isolated from human fetal liver cells. A cDNA clone was obtained with 5' sequences (96 bp) that diverged seven nucleotides upstream from the ATG (+1) start codon. A concensus splice junction sequence, TCTCCCGCAG, was found immediately 5' to the position where the sequences of the cDNA diverged. The result suggested the presence of an intron in the 5' -noncoding region and that the cDNA was an incompletely reversetranscribed cDNA product derived from an mRNA containing a new noncoding exon. When mRNA expression of GnT-III in various human tissues and cancer cell lines was examined, Northern blot analysis indicated high expression levels of GnT-III in human fetal kidney and brain tissues, as well as for a number of leukemia and lymphoma cancer cell lines. Promoter activities of the 5' -flanking regions of exon 1 and the new noncoding region were measured in a human hepatoma cell line, HepG2, by luciferase assays. The 5'-flanking region of exon 1 was the most active, whilst that of exon 2 was inactive.

• Proceedings of the KSAR Conference
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• 2003.06a
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• pp.18-18
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• 2003

In human, sudden infant death syndrome(SIDS) is synonyms for the sudden, unexpected and unexplained death of an infant. The incidence of SIDS has been estimated to be from 1 to 3%. Cloning has a relatively high rate of late abortion and early postnatal death, particularly when somatic cells are used as donors of nuclei and rates as high as 40 to 70% have been reported. However, the mechanisms for SIDS in cloned animals are not known yet. To date, few reports provide detailed information regarding phenotypic abnormality of cloned pigs. In this study, most of the cloned piglets were alive at term and readily recovered respiration. However, approximately 82% of male cloned piglets (81/22) died within a week after birth. Significant findings from histological examinations showed that 42% of somatic cloned male piglets died earlier than somatic cloned female piglets, most probably due to severe congestion of lung and liver or neutrophilic inflammation in brain, which indicates that unexpected phenotypes can appear as a result of somatic cell cloning. No anatomical defects in cloned female piglets were detected, but three of the piglets had died by diarrhea due to bacterial infection within 15 days after birth. Although most of male cloned piglets can be born normal in terms of gross anatomy, they develop phenotypic anomalies that include leydig cell hypoplasia and growth retardation post-delivery under adverse fetal environment and depigmentation of hair- and skin-color form puberty onset. This may provide a mechanism for development of multiple organ system failure in some cloned piglets. Th birth weights of male cloned pig in comparison with those of female cloned piglets are significantly reduced(0.8 vs 1.4kg) and showed longer gestational day(120 vs 114). In conclusion, brain meningitis and hepatopneumonic congestion are a major risk factor for SIDS and such pregnancy in cloned animals requires close and intensive antenatal monitoring.

• Korean Journal of Environmental Biology
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• v.29 no.4
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• pp.241-250
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• 2011

The safety of human exposure to an ever-increasing number and diversity of electromagnetic field (EMF) sources both at work and at home has clearly become a public health issue. To date many $in$ $vivo$ and $in$ $vitro$ studies revealed that EMF exposure can alter cellular metabolism, endocrine function, immune activity, reproductive function, and fetal development in animal system. The major parameters found to be altered in cells or individuals following EMF exposure include an increase of free radicals, DNA damage, cancer risk, developmental defect, and reproductive dysfunctions. Epidemiological studies reported EMF can increase life-threatening illnesses such as leukemia, brain cancer, amyotrophic lateral sclerosis, clinical depression, suicide, and Alzheimer's disease has been identified. These effects of EMF exposure differ according to duration of exposure, frequency of waves, and strength (energy) of EMF. In the present review, we briefly introduced the physical properties of EMF and summarized the effect of EMF on human and wildlife animals according to types of EMF, duration of exposure at cellular and organism levels.