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Biomedical subjects

B H Choi

Publications and source records attributed to B H Choi.

At least 91 records · Page 5Linked to original sources
PubMed1988

Abnormal neuronal distribution within the cerebral cortex after prenatal methylmercury intoxication.

C57BL/6J mice were poisoned with methylmercury during pregnancy, and the location of heavily labeled neurons generated at embryonic day 16 was determined by tritiated thymidine autoradiography of the cerebral cortex of offspring at postnatal day 10. Camera lucida plotting of the distribution of radioactively labeled cortical neurons revealed statistically significant differences between control and methylmercury-treated groups. While control animals showed regular and tight packing of labeled neurons within the upper part of the cortical layer II, in methylmercury-treated animals such neurons were irregularly distributed throughout cortical layers II and III. Short-term intermittent and long-term low-dosage regimens of intoxication produced similar results. These findings support the hypothesis that prenatal methylmercury poisoning results in abnormal neuronal migration and anomalous cortical cytoarchitectonic patterning within the developing brain and provide a possible morphological basis for some of the neurobehavioral abnormalities that may be observed in association with sublethal prenatal intoxication in humans.

Animals↗
PubMed1988

Hydrocephalus following prenatal methylmercury poisoning.

Prenatal methylmercury poisoning of C57BL/6J mice was followed by the development of communicating hydrocephalus in 15% to 25% of surviving offspring. Although examination of the serially sectioned cerebral aqueduct in hydrocephalic animals revealed the presence of stenosis, complete occlusion of the lumen was not observed. The ependymal epithelium of the cerebral aqueduct was preserved, and there was no evidence of periaqueductal inflammation or reactive gliosis. Edema and vacuolar change were, however, observed subependymally. The cerebral white matter, which bore the brunt of the degenerative changes seen in hydrocephalic brains, showed edema, spongy degeneration, gross cystic change and loss of parenchyma. In addition, ependymal cells and choroid plexus epithelial cells in Hg-treated animals contained large amounts of mercury within their cytoplasm, and it is possible that this may have contributed to the development of hydrocephalus by causing disturbances of CSF homeostasis. We believe that the appearance of aqueductal stenosis in Hg-intoxicated animals represents the result rather than the cause of the hydrocephalus.

Animals↗
PubMed1988

Non-traumatic ischaemic myelopathy: a review of 25 cases.

The causes of ischaemic myelopathy are described in 25 patients. Nine developed following surgical manipulation or traumatic laceration of the aorta, 1 following intercostal artery ligation, 3 following aortic aneurysm dissection, 2 following myocardial infarction and/or cardiac arrest, 7 in the absence of any specifically identifiable predisposing factors, and 3 in association with decompression sickness. The degree of clinical recovery was greater among those with incomplete spastic (as opposed to complete flaccid) paralysis and among those in whom sensory loss below the level of injury was incomplete. Despite the diversity of mechanisms that may lead to the development of spinal cord ischaemia, structural damage seems in most instances to affect either grey matter or white matter predominantly. Some of the possible reasons for these preferential sites of damage are discussed.

Aorta↗
PubMed1988

Myelopathy after the intrathecal administration of hypertonic saline.

The neuropathological effects of intrathecally administered hypertonic saline have not been described previously. We report a patient who, within a day of receiving 20 ml of hypertonic (7.5%) saline intrathecally, developed flaccid paraplegia and complete sensory loss below the umbilicus. Subsequently, there was some transitory return of motor and coarse sensory function. The patient died 16 months after the injection. At autopsy, there was peripherally accentuated loss of myelinated fibers within the spinal cord from T12 downward, as well as dense collagenous thickening of the dorsal leptomeninges from T9 to T11. The findings in this case, coupled with observations made by others, serve to emphasize the need for extreme caution whenever planning any form of intrathecal therapy.

Humans↗
PubMed1987

Cortical dysplasia associated with massive ectopia of neurons and glial cells within the subarachnoid space.

A detailed neuropathological study of the brain of a 31-day-old premature newborn infant revealed the presence of massive ectopia of neurons and glial cells within the subarachnoid space. The extrusion of neural tissue into the subarachnoid space appeared to have taken place through multiple pial-glial bridges. The laminar cortical pattern was also severely disturbed at these sites. Narrow strips of normal and dysplastic cortex alternated in direct relationship to the presence or absence of the pial-glial gaps. Migration of postmitotic neurons and the final positioning of postmigratory neurons appear to take place within highly specified and restricted pathways entrained in a radial direction. Our findings suggest that the pial-glial barrier plays an important role in the control of neuronal migration, and that its disruption may lead to the development of neuronal and glial cell ectopias in the subarachnoid space. The crucial role played by radial glia, the glia limitans and the basal lamina during cortical neurogenesis is emphasized.

Cerebral Cortex↗
PubMed1986

Disturbances in neuronal migration and laminar cortical organization associated with multicystic encephalopathy in the Pena-Shokeir syndrome.

The Pena-Shokeir syndrome is characterized by intrauterine growth retardation, camptodactyly, multiple ankyloses, facial anomalies and pulmonary hypoplasia. The condition is thought to be inherited in an autosomal recessive fashion. A detailed neuropathological analysis of the brain of a stillborn full-term male infant who exhibited the gross features of the Pena-Shokeir syndrome revealed diffuse bilateral cerebral polymicrogyria associated with multicystic encephalopathy. Abnormal brain development, which was characterized by disturbances in neuronal migration and laminar cortical organization, was clearly associated with changes of an encephaloclastic nature, namely reactive gliosis and infiltration by macrophages. These findings suggest strongly that the Pena-Shokeir syndrome may also result from teratogenic factors such as intrauterine ischemic and/or hypoxic insults to the developing brain.

Abnormalities, Multiple↗
PubMed1986

Expression of glial fibrillary acidic protein by neoplastic cells of müllerian origin.

Immunocytochemical studies of malignant mixed Müllerian tumors revealed the presence of neoplastic cells showing strong immunoreactivity for glial fibrillary acidic protein, a protein specific for astrocytes, in 9 of 13 cases. Undifferentiated malignant tumor cells of endometrial stromal sarcoma and astrocytes in glioma of the uterus also demonstrate GFAP immunoreactivity. GFAP immunostaining in these neoplastic cells is highly specific and shows no cross-reactivity with cytokeratin, actin, myoglobin, epithelial membrane antigen or factor VIII. It is postulated that the GFAP immunostaining within neoplastic cells of Müllerian origin may be a reflection of the phenotypic diversity of intermediate filament proteins that can be expressed by malignant neoplastic cells, that the polypeptides of GFAP may be heterogeneous, that there may be an ontogenic relationship between the cells of Müllerian origin and neuroectodermal cells, or that this may represent neometaplasia of Müllerian cells.

Female↗
PubMed1986

Surface charge alterations in mouse fetal astrocytes due to methyl mercury: an ultrastructural study with cationized ferritin.

A brief exposure of low dose methylmercuric chloride to monolayer cultures of mouse fetal astrocytes caused a marked shift in the distribution of anionic groups on the surface membrane as evidenced by irregular disruption of cationized ferritin. It is suggested that one of the earliest changes following methyl mercury exposure in embryonic astrocytes includes alterations in the surface charge which may in turn trigger cascading toxic actions of methyl mercury in the developing brain.

Animals↗
PubMed1986

Changes in the molecular structure of mouse fetal astrocyte nucleosomes produced in vitro by methylmercuric chloride.

The fluorescent probe N-(3-pyrene)maleimide, which specifically labels the cysteine residues of histone H3 within the nucleosome, was used to monitor changes in the nucleosomal structure of mouse fetal astrocytes exposed to varying concentrations of methylmercuric chloride. Methylmercuric chloride treatment (10 microM) for 6 hr produced a significant decrease in the degree of fluorescence of the probe. The decrease was much smaller following a 4-hr incubation period. These results correlate with recent observations showing that significant changes in the thymidine labeling index occur following 4-6 hr of exposure to methylmercury (MeHg). It is hypothesized that MeHg enters the cells during the growth phase and attaches to the protein moiety of the nucleosome in or near the cysteine groups of histone H3, thus diminishing the binding capacity of the fluorescent probe. Addition of a detergent (sodium dodecyl sulfate) resulted in only a small increase in the degree of fluorescence of the treated nucleosomes as compared to controls, showing that the interaction of MeHg with the nuclear proteins was not dissociated by detergent. In view of the strong interaction between DNA and the histone dimer H3-H4 and the potential importance of the latter in gene regulation, these results suggest an additional means by which MeHg may exert its toxic effects.

Animals↗
PubMed1986

Glial fibrillary acidic protein in radial glia of early human fetal cerebrum: a light and electron microscopic immunoperoxidase study.

In order to assess the nature of glial fibrillary acidic protein (GFAP) immunoreactivity in the radial glia of early human fetal cerebrum, full thickness blocks from the midconvexity of the frontoparietal region of the cerebrum of 25 human fetuses ranging from ten to 20 weeks of ovulation age were studied by light and electron microscopic (EM) immunoperoxidase methods. The presence of GFAP within radial glia was demonstrated in vibratome sections, in de-eponized 1 micron sections and in paraffin-embedded sections both at light and EM levels in suitably fixed human fetal cerebral tissue. The results indicate that the pattern of GFAP immunoreactivity observed in "routinely" processed autopsy brains, in which fixation is suboptimal, must be interpreted with care.

Brain↗
PubMed1986

Myelin-forming oligodendrocytes of developing mouse spinal cord: immunocytochemical and ultrastructural studies.

The development and differentiation of oligodendrocytes (OC) in developing mouse spinal cord (MSC) were investigated by correlative analysis of light and electron microscopy (EM), and immunoperoxidase studies for glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP). The sequential development of glial cells within the subpial region of the MSC bears a striking resemblance to the developing human fetal spinal cord. A rise in the level of mitotic activity among subpial astrocytes just prior to the onset of myelination was followed by the appearance of OC within the same region. The finding of "transitional" cells with the cytological and ultrastructural features of both astrocytes and OC and the finding of GFAP within the immature OC strongly support the hypothesis that OC in the developing central nervous system may arise from astroglial precursors. These observations also suggest that the MSC may be a suitable model for the study of OC differentiation and myelinogenesis in man.

Animals↗
PubMed1985

Prolonged survival after severe traumatic injury limited to the brainstem.

It has been suggested that primary traumatic lesions of the brainstem do not occur in the absence of widespread injury to other parts of the brain. We describe a patient who suffered a severe head injury that left him with paralysis of three extremities and weakness in the fourth. Intellectual function was entirely preserved. Neuropathological examination 39 years after the injury disclosed the presence of a cavitary lesion within the basis pontis. There was no pathological evidence of traumatic injury to any other part of the central nervous system.

Brain↗
PubMed1985

Expression of glial fibrillary acidic protein by immature oligodendroglia and its implications.

Correlative immunocytochemical and electron-microscopic studies of the subpial region of the human fetal spinal cord between 12-18 weeks of ovulation age revealed immature oligodendroglial cells showing immunoreactive GFAP within both the cytoplasm and its processes. By 17-18 weeks, however, GFAP immunoreactivity is no longer evident within such cells. The expression of GFAP by immature oligodendroglial cells in the developing human fetal spinal cord prior to the formation of compact myelin sheaths supports the hypothesis that oligodendrocytes, along with astrocytes, are ultimately derived from radial glial cells.

Cytoplasm↗