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Biomedical subjects

B H Choi

Publications and source records attributed to B H Choi.

At least 73 records · Page 4Linked to original sources
PubMed1992

Density and distribution of excitatory amino acid receptors in the developing human fetal brain: a quantitative autoradiographic study.

The binding of [alpha-3H]amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) to quisqualate receptors, [3H]kainate (KA) to KA receptors, and L-[3H]glutamate to N-methyl-D-aspartate (NMDA) receptors was determined by quantitative autoradiography in brains obtained from twelve aborted human fetuses ranging from 16.5 to 26 weeks of gestational age. Among the three receptor subtypes, specific binding to AMPA was the highest, followed by NMDA and KA, respectively, in all age groups. Receptor binding was already apparent by 16.5 weeks in the hippocampus, thalamus, and subthalamic nucleus, rose sharply by 20-21.5 weeks, and subsequently declined to their lowest levels by 24-26 weeks. Anatomically distinct binding patterns for each of the three major excitatory amino acid (EAA) receptor subtypes were well established by 20-21.5 weeks. Within the hippocampus, AMPA was localized primarily in the stratum pyramidale, NMDA in the stratum radiatum, and KA in the molecular layer of the dentate gyrus and in the stratum lucidum of the CA3 region. The cerebral cortex showed dense labeling of AMPA in the outer layers, whereas KA binding was more prominent within the inner layers. The putamen and globus pallidus also showed relatively dense receptor binding in all age groups. The sharp rise in receptor density at 20-21.5 weeks of age suggests involvement of EAA pathways in developmental plasticity, including reorganization of neuronal processes or synapses, during this period of development. Developmental changes in the density and distribution of EAA receptors, as shown in this study, may also provide insight into shifts in the localization of age-dependent selective vulnerability within the developing human fetal brain.

Autoradiography↗
PubMed1992

The ventriculus terminalis and filum terminale of the human spinal cord.

Serial sections of the conus medullaris and the filum terminale of 23 randomly selected human spinal cords were studied by light and electron microscopy, and following immunoperoxidase staining for glial fibrillary acidic protein (GFAP), vimentin, neuron-specific enolase (NSE), amyloid beta protein, and S-100 protein. The intradural portion of the filum contains bundles of GFAP-positive glial fibers, scattered silver- and NSE-positive neurons, segments of peripheral nerve, blood vessels, fibrous connective tissue, and fat. Glial cell clusters varying from five to 100 cell layers thick at times constitute the bulk of the filum. The periependymal glial cells possess moderate amounts of eosinophilic cytoplasm and relatively uniform round to ovoid nuclei containing evenly distributed chromatin. They are distributed diffusely with no specific pattern of organization, although some of them showed a tendency to form acinar structures. A minority of the glial cells showed GFAP immunoreactivity, and some were immunoreactive for vimentin. Electron microscopy demonstrated the presence of periependymal cells showing cilia, microvilli, and the formation of intercellular junctional complexes, as well as cells containing bundles of glial filaments within the cytoplasm. Degenerated NSE-positive neurons and degenerated neurites resembling neuritic plaques were also demonstrated. However, immunoperoxidase staining for amyloid beta protein was negative in these structures. Thus, the filum terminale is endowed with an abundance of glial cells and neurons and is not simply a fibrovascular tag. Periependymal glial cells in the filum terminale should not be mistaken for neoplasm. The presence of neuropil with profuse astroglial and neuronal components within the filum terminale suggests a possible functional role for these structures.

Adolescent↗
PubMed1991

Effects of methylmercury on neuroepithelial germinal cells in the developing telencephalic vesicles of mice.

Methylmercury (MeHg) poisoning (20 mg/kg body weight) in embryonic mice resulted in significant reductions of mitotic indices in the neuroepithelial germinal cells of the telencephalon at the ventricular surface 4 to 12 h following intoxication. After 24 h, no significant difference in the mitotic indices was observed as compared to controls. However, after 48 h there was an increase in mitotic indices of MeHg group as compared to controls. Analysis of the mitotic figures revealed features suggestive of early-phase mitotic arrest in MeHg-exposed animals. Radioautographic studies suggest a disturbance in the interkinetic nuclear migration of proliferating ventricular cells in the MeHg group. Acute degenerative changes in scattered ventricular cells characterized by edema and spongy changes of cytoplasm associated with dissolution of ribosomes, clearing of the cytoplasmic matrix and loss of organelles including microtubules were observed by electron microscopy. Loss of microtubules was also evident within mitotic figures in MeHg-poisoned animals. It is suggested that reduction and arrest of mitotic activity and disturbances in the interkinetic nuclear migration of neuroepithelial germinal cells are related to cytotoxic effects of MeHg on ventricular cells, including effects on microtubules. These findings suggest in that MeHg severely affects proliferating neuroepithelial germinal cells during the acute phases of MeHg poisoning, and that these changes may eventually affect the architectonic makeup of the cortical plate as the brain matures.

Animals↗
PubMed1991

Repair and reconstruction of the cortical plate following closed cryogenic injury to the neonatal rat cerebrum.

A cryogenic lesion was induced in the parietal cortex of neonatal rats at postnatal day 2, and the chronological sequence of cellular events during repair and reconstruction of the cortical plate examined. Serial sections of cerebra obtained at varying intervals ranging from 1 to 60 days postinjury were studied by light and electron microscopy and by immunocytochemistry for fibronectin, laminin, type IV collagen, vimentin and glial fibrillary acidic protein. In addition, localization of heavily labeled neurons (generated on embryonic day 20) in the cerebral cortical plate was examined by [3H]thymidine radioautography. Repair of a well-defined coagulative lesion was accomplished with little or no mesenchymal cell proliferation in either the necrotic zone or the leptomeninges. Eventually, fusion of the adjacent cortical plates took place with the formation of a microsulcus. Migration of neurons continued to take place along the outer margins of the lesion, and postmigratory neurons accumulated within the upper cortical layers. Around the microsulcus, heavily labeled neurons aligned themselves with layers II-III of the adjacent normal cortical plate. Irregular clusters of neurons closely abutting the leptomeningeal surface were frequently noted when repair took place without an intervening molecular layer and/or a well-defined pial-glial barrier. Supplementing intrinsic information inherent in migrating neurons, local environmental signals provided by the radial glia, glia limitans, basal lamina and pial-glial barrier appear to influence the polarity and final positioning of postmigratory neurons within the cortical plate. The necrotic zone within the deeper layers of the cortex eventually healed with a cell-sparse gliotic layer. The end result was a histological pattern that, in many respects, resembled that of human micropolygyria.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Sucking efficiency of early orthopaedic plate and teats in infants with cleft lip and palate.

Intraoral negative pressure during bottle feeding with two kinds of teats (a regular Nuk and a cleft Nuk) was measured in 7 infants with cleft lip and palate, 8 infants with cleft palate, 2 infants with cleft lip, 4 infants with operated cleft lip and palate and 7 normal infants. Infants with cleft lip and palate or cleft palate were unable to generate negative pressure before cleft lip and palate closure. The presence or absence of an early orthopaedic plate did not make any difference. In infants with unoperated cleft lip and with operated cleft lip and palate, peak negative pressure during feeding differed little from that of normal infants.

Bottle Feeding↗
PubMed1990

Absence of isochromosome 12p in a pineal region malignant germ cell tumor.

We report the first cytogenetic investigation of a rare pineal region mixed germ cell tumor. The mean modal number was 78. Multiple numerical and structural abnormalities were noted. Chromosomes 21 and 1q were consistently overrepresented, and chromosome 13 was underrepresented. A translocation involving chromosome 11 occurred in all metaphases examined. The Y chromosome was lost, and three copies of the X chromosome were present. No isochromosome 12p was identified, but four copies of chromosome 12 were present.

Adolescent↗
PubMed1990

Increased expression of the embryonic form of a developmentally regulated mRNA in Alzheimer's disease.

There is increasing evidence that an aberrant sprouting response may contribute to some of the neuronal alterations observed in Alzheimer's disease (AD). In this study, we demonstrate that in the rat CNS, sprouting results in the reinduction of the embryonic form of the mRNA for alpha-tubulin. The fetal form of alpha-tubulin mRNA was also elevated in the hippocampus obtained from five AD patients, as compared to five elderly controls. These results suggest that the reexpression of embryonic forms of cytoskeletal proteins, in association with an aberrant sprouting response, may contribute to the neuropathological alterations in AD.

Adult↗
PubMed1990

The behavior of the extracellular matrix and the basal lamina during the repair of cryogenic injury in the adult rat cerebral cortex.

A well-defined coagulative lesion was produced in the fronto-parietal cortex of adult rats by application of a cold probe, and the chronological sequence of events during the healing process, particularly the relationship between astroglial processes and the newly forming basal lamina (BL) and the behavior of the extracellular matrix (ECM) was examined immunocytochemically and ultrastructurally. By electron microscopy, new BL synthesis was first noted 7 days following injury, and a continuous and well-defined BL was present from 14 days onward. These findings correlated well with the pattern of immunoreactivity for laminin and for type IV collagen. Both laminin and type IV collagen appeared both to be produced primarily by mesenchymal cells within and around the wound as well as those of the blood vessels, and to become an integral part of the new BL. Although there was no immunocytochemical evidence to indicate secretion of laminin, type IV collagen or fibronectin by astrocytes, a well-defined BL appeared to form only in tight apposition with astroglial processes over the pial surface. This suggests that the BL is formed by subpial astrocytes in close interaction with ECM components at the pial surface. Fibronectin appears to contribute significantly to the formation of the BL by providing a suitable substratum for the coordinated cellular interaction necessary for successful regeneration of the BL.

Animals↗
PubMed1990

Altered distribution of excitatory amino acid receptors in temporal lobe epilepsy.

In temporal lobe epilepsy, excitatory amino acid receptors in the hippocampus and temporal lobe may contribute to both increased excitability and vulnerability to excitotoxic damage. We used receptor autoradiography to examine the density of N-methyl-D-aspartate (NMDA) and kainic acid (KA) receptors in the hippocampus and parahippocampal gyrus obtained from five patients who had undergone anterior temporal lobectomy for the treatment of intractable seizures and from six control individuals, in which the hippocampus was obtained postmortem. Within the hippocampal formation, loss of [3H]KA and NMDA-sensitive L-[3H]glutamate binding was apparent in the sclerotic regions CA3, hilus, and CA1. In the subiculum and molecular layer of the denate gyrus, binding densities were maintained or even increased in some of the epileptic patients. A two-fold increase in L-[3H]glutamate binding, along with an increase in [3H]KA binding, was observed in the parahippocampal gyrus obtained from the epileptic patients. The results suggest that the vulnerability of the hippocampus in temporal lobe epilepsy may result, at least in part, from the presence of aberrant excitatory circuits in the parahippocampal gyrus.

Adult↗
PubMed1990

Molecular analysis of a myxoid chondrosarcoma with rearrangements of chromosomes 10 and 22.

Myxoid chondrosarcoma is a rare tumor of adulthood. An associated nonrandom reciprocal translocation between chromosome 9 and 22 was previously reported in this tumor. We performed cytogenetic and molecular genetic analysis of a myxoid chondrosarcoma derived from the sphenoid bone. Using restriction fragment length polymorphism (RFLP) analysis, we demonstrated rearrangement and a possible allele loss close to the chromosome 22 breakpoint. In addition, structural rearrangement in the chromosome 10q21.1 region and an allele loss in the chromosome 10q21-q23 region were also detected. In tumor DNA an additional hybridization fragment was detected by pAS-1 probe, which recognizes multiple pseudogenes of argininosuccinate synthetase dispersed in various chromosomes. We were unable to detect chromosomal abnormalities with two additional chromosome 9q probes. This study suggests that multiple gene rearrangements occurred in the myxoid chondrosarcoma and the significance of this is discussed.

Adult↗
PubMed1990

Excitotoxic amino acid receptors in human complex partial epilepsy.

It has long been recognized that mesial temporal sclerosis is the most common pathologic finding in temporal lobes removed for the treatment of medically refractory complex partial epilepsy. The regions of the hippocampus most vulnerable contain the highest densities of excitatory amino acid receptors in the brain. We used receptor autoradiography to determine the density of N-methyl-D-aspartate (NMDA) and kainic acid (KA) receptors from 5 patients undergoing such surgery and compared the findings with 6 specimens obtained at postmortem. A 2-fold increase in the density of NMDA receptors and an increased density of KA receptors was found in entorhinal cortex in epileptic specimens. Loss of NMDA and KA receptor density was apparent in the sclerotic regions CA3 and CA1, but not in other areas of the hippocampus or dentate gyrus. These findings suggest that damage in the hippocampus may result, at least in part, from the presence of aberrant excitatory circuits in the entorhinal cortex.

Autoradiography↗
PubMed1990

Protease nexin-1. Localization in the human brain suggests a protective role against extravasated serine proteases.

Protease nexin-1 (PN-1) is a potent thrombin inhibitor that is identical to the glia-derived neurite-promoting factor or glia-derived nexin. Here we report immunocytochemical studies of adult human cerebral cortex that revealed the presence of strong immunoreactivity for PN-1 in capillaries and in the smooth muscle cells of arteries and arterioles. Expression of PN-1 was also abundant in astroglial processes in the parenchyma and in perivascular astroglial endfeet of human cerebral cortex. In situ hybridization with an 35S-labeled RNA antisense probe for PN-1 resulted in significant labeling of astrocytes and blood vessels. Because thrombin is known to cause retraction of neurites and modification of astrocytic morphology at low concentrations, PN-1 around blood vessels may play a major protective role against extravasation of thrombin and possibly other serine protease into the human brain.

Alzheimer Disease↗
PubMed1989

Protease nexin-II, a potent antichymotrypsin, shows identity to amyloid beta-protein precursor.

Protease nexin-II (PN-II) is a protease inhibitor that forms SDS-resistant inhibitory complexes with the epidermal growth factor (EGF)-binding protein, the gamma-subunit of nerve growth factor, and trypsin. The properties of PN-II indicate that it has a role in the regulation of certain proteases in the extracellular environment. Here we describe more of the amino-acid sequence of PN-II and its identity to the deduced sequence of the amyloid beta-protein precursor (APP). Amyloid beta-protein is present in neuritic plaques and cerebrovascular deposits in individuals with Alzheimer's disease and Down's syndrome. A monoclonal antibody against PN-II (designated mAbP2-1) recognized PN-II in immunoblots of serum-free culture medium from human glioblastoma cells and neuroblastoma cells, as well as in homogenates of normal and Alzheimer's disease brains. In addition, mAbP2-1 stained neuritic plaques in Alzheimer's disease brain. PN-II was a potent inhibitor of chymotrypsin with an inhibition constant Ki of 6 x 10(-10)M. Together, these data demonstrate that PN-II and APP are probably the same protein. The regulation of extracellular proteolysis by PN-II and the deposition of at least parts of the molecule in senile plaques is consistent with previous reports that implicate altered proteolysis in the pathogenesis of Alzheimer's disease.

Alzheimer Disease↗
PubMed1989

Hemodynamic and electrophysiological effects of mercury in intact anesthetized rabbits and in isolated perfused hearts.

Using intact anesthetized rabbits and isolated perfused hearts, the hemodynamic and electrophysiological effects of mercury (Hg) were examined in order to assess the role of cardiovascular dysfunction in Hg intoxication. The most consistent and prominent cardiovascular effect was a significant reduction in blood pressure. This cardiodepressive action was probably brought about by the primary action of Hg on the heart rather than by altered sympathetic activity, as evidenced by normal renal nerve activity at times when the hemodynamic actions of Hg were clearly manifest. Although the principal target organ for the toxic actions of inorganic Hg is the kidney, chronic exposure to both inorganic and organic Hg frequently results in signs and symptoms of CNS dysfunction. The profound hemodynamic effects of Hg that we have observed emphasize the potential importance of Hg cardiotoxicity and indicate the need to differentiate between the primary and the secondary effects of Hg intoxication on CNS tissues for evaluation of the toxic effects of Hg compounds.

Animals↗
PubMed1989

Massive craniospinal collagen deposition after persistent postoperative intraventricular bleeding.

A 39-year-old man developed persistent bleeding into the ventricular system after having undergone needle biopsy of what was presumed to be a left frontal neoplasm. He subsequently developed obstructive hydrocephalus that required shunting and died in a semivegetative state some 5 1/2 months later. At autopsy, although no neoplasm was identified at the operative site, there was massive collagen deposition within the ventricular system that extended into the spinal subarachnoid compartment. Although we have been able to find only three cases in the literature with detailed descriptions of similar pathological findings, we believe that our observations emphasize the potential for a complication of intraventricular and subarachnoid hemorrhage that is not widely recognized.

Adult↗
PubMed1988

Prenatal gliogenesis in the developing cerebrum of the mouse.

A correlative light microscopic, ultrastructural, and immunocytochemical study was made of the brains of C57BL/6J mice obtained between embryonic day (E-) 11 to postnatal day (P-) 3. The deployment of radially oriented glial cells within the neopallium was already apparent by E-12, at which time the expanded endfeet of processes abutting the basement membrane at the pial surface showed ultrastructural evidence of glial differentiation. Scattered, horizontally arranged glial cells were also observed within the marginal zone prior to the arrival of the cortical plate neurons. Indirect immunofluorescence for glial fibrillary acidic protein (GFAP) was detected at the outer margins of the neopallium at E-12, antedating the expression of GFAP in radially organized fibers. Radial fibers traversing the full thickness of the neopallium became strongly immunoreactive for GFAP only at and after day E-16. These findings provide evidence of early gliogenesis in the developing mouse forebrain and indicate that GFAP is as readily demonstrable in mouse astrocytes and radial glial fibers as it is in those of man and subhuman primates.

Animals↗
PubMed1988

Developmental events during the early stages of cerebral cortical neurogenesis in man. A correlative light, electron microscopic, immunohistochemical and Golgi study.

The telencephalic vesicles of early human embryos and fetuses ranging from 6-18 weeks of ovulation age were subjected to correlative light and electron microscopic, immunocytochemical and Golgi analysis. The cellular events that take place during the early stages of cortical neurogenesis are characterized by the early maturation of layer I. The deployment of radial glia, the formation of the glia limitans, the establishment of the pial-glial barrier, and the migration and maturation of Cajal-Retzius cells within the marginal zone (MZ) all take place by 6-7 weeks. Neurons destined to populate the cortical plate (CP) arrive within the MZ by 7-8 weeks of age and appear to divide the MZ into two layers. Progressive compaction of CP neurons and widening of the intermediate zone characterize the next stage. It is suggested that the early establishment of the pial-glial barrier and the early maturation of the layer I are critical to the subsequent growth and development of the CP.

Cerebral Cortex↗