• 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.

• 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 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.

• Journal of Yeungnam Medical Science
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• v.28 no.2
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• pp.105-115
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• 2011

Mercury is a toxic, persistent pollutant that bioaccumulates and biomagnifies through food webs. People are exposed to methyhnercruy mainly through their diet, especially through the consumption of freshwater and marine fish and of other animals that consume fish (e.g., marine mammals). All humans are exposed to low levels of mercury. Dietary patterns can increase exposure to a fish-eating population where the fish and seafood are contaminated with mercury. The primary toxicity targets of mercury and mercury compounds are the nervous system, kidneys, and cardiovascular system. It is generally accepted that developing organ systems are most sensitive to the toxic effects of mercury. The fetal-brain mercury levels appear to be significantly higher than the maternal-blood mercury levels, and the developing central nervous system of the fetus is currently regarded as the main system of concern as it demonstrates the greatest sensitivity. The subpopulation that may be at greater risk for mercury toxicity are those exposed to higher levels of methylmercury due to carnivorous fish, including sharks.

• 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

• Asian-Australasian Journal of Animal Sciences
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• v.24 no.8
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• pp.1053-1059
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• 2011

The objective of this study was to assess the teratogenic and embryotoxic effects of clomiphene citrate in mice. The pregnant mice were administered a single dose of clomiphene citrate at different concentrations i.e 1.0, 2.0, 4.0 and 6.0 ${\mu}g/g$ BW on day 8 of gestation. Fetuses recovered on day 18 of gestation were analyzed on morphological, morphometric and histological basis. Morphological observations showed defects like open eyelids, anophthalmia, fore and hindlimb micromelia, meromelia, amelia, sacral hygroma, hydrocephaly, hemorrhagic spots, kyphosis and clubbed feet. Morphometric analysis indicated a significant (p<0.001) reduction in fetal body weight, crown rump length, head circumference, eye circumference, forelimb and hindlimb lengths and tail size against controls. The histological observations showed brain defects like hydrocephaly, enlarged ventricles and undifferentiated neuroglial cells in cerebellum. Cleft palate, underdeveloped pharynx and atrophy of jaw muscles were the common anatomical defects of pharyngeal region. It is concluded that the concentrations of clomiphene citrate used during the present study proved teratogenic in mice fetuses.

• 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.99-99
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• 2001

• 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

• 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.