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Biomedical subjects

E S Cho

Publications and source records attributed to E S Cho.

At least 37 records · Page 2Linked to original sources
PubMed1998

Localization of atrial natriuretic peptide receptors in the rat tongue and hard palate.

Atrial natriuretic peptide (ANP) receptors were characterized in rat oral mucosa using quantitative in vitro autoradiography and activation of particulate guanylyl cyclase (GC) by natriuretic peptides. Competition-binding analysis performed by quantitative in vitro autoradiography demonstrated specific [125I]rANP(1-28) binding sites in the tongue and hard palate. The precise location of this binding was revealed on the basal and parabasal cells of the epithelia by microautoradiography. The dissociation constant (Kd) and maximal binding capacity (Bmax) of these sites were 3.34+/-1.35 nM and 2.71+/-2.21 fmol/mm2 on the epithelium of the tongue, and 4.09+/-1.52 nM and 3.45+/-3.01 fmol/mm2 on the epithelium of the hard palate, respectively. Receptor subtypes were characterized by competition with des [Gln18, Ser19, Gly20, Leu21, Gly22] ANP(4-23) (C-ANP), a specific ligand for the clearance receptor (NPR-C). These binding sites were displaced by C-ANP with inhibition constant (Ki) of 8.96+/-3.18 nM and Bmax of 2.89+/-2.45 fmol/mm2 on the epithelium of the tongue, and Ki of 9.12+/-2.71 nM and Bmax of 3.08+/-2.94 fmol/mm2 on the epithelium of the hard palate, respectively. Production of cyclic GMP by particulate GC in the epithelial membranes of the tongue and hard palate was stimulated by rANP(1-28), porcine brain natriuretic peptide (BNP)(1-26), and C-type natriuretic peptide (CNP)(1-22) in a dose-dependent manner. These results indicate that ANP-binding sites in the epithelium of the tongue and hard palate are mainly clearance receptors (NPR-C) but biological receptors (NPR-A and/or NPR-B) with GC activity are also present, and suggest that ANP may have a role in the proliferation of the oral epithelial cells, especially in the tongue and hard palate.

Analysis of Variance↗
PubMed1998

HIV-associated brain pathology: a comparative international study.

Little is known about the frequency and variation of HIV-associated brain pathology in different geographical centres. To assess whether there is an association between the frequency of disease and demographic factors we examined the neuropathological findings in four European and two American cities. The cities included London, Edinburgh, Paris, Budapest, Baltimore and Newark. Information was collected on a total of 1144 cases. HIV encephalitis was the most common observation in all the centres. although its frequency varied between them (P < 0.01). Furthermore, there were significant differences (P < 0.001) between the various categories of exposure and the frequency of HIV encephalitis in Edinburgh and other centres. The occurrence of toxoplasmosis, progressive multifocal leukoencephalolpathy (PML) and cryptococcal infection also differed between the various centres (P < 0.01). None of the findings was attributable to age, sex, or ethnic origin, but the introduction of anti-retroviral treatment, such as Zidovudine, may have been important. Overall, this study highlights geographical variability and the potential importance for group of exposure and anti-retroviral medication as factors affecting the development of various HIV-associated brain lesions.

AIDS Dementia Complex↗
PubMed1998

Neuropathologic applications of immunohistochemical fiber typing in the non-neoplastic muscle biopsy.

The determination of fiber types is routinely accomplished in skeletal muscle biopsy specimens by enzymatic histochemical analysis, which detects adenosine triphosphatase (ATPase) activity on cryostat sections. This study assesses postmortem antigen degradation, the effects of fixation and processing, and the neuropathologic applications of MY-32, a monoclonal antibody to fast twitch skeletal myosin. Formalin-fixed, paraffin-embedded sections of skeletal muscle biopsy specimens obtained from the quadriceps femoris were immunoreacted with this antibody. Cryostat sections of the same muscle biopsy specimens were examined after brief fixation in either acetone or formalin. Parallel cryostat sections of frozen muscle were also assessed with ATPase preparations at pH 9.4 and 4.3. To evaluate the effect of postmortem interval and autolysis on antigen degradation, skeletal muscle samples obtained at 12 hours postmortem were immunoreacted after 12, 24, or 36 additional hours. These specimens were examined as immunoreacted cryostat sections and compared with parallel sections reacted for ATPase at pH 9.4 and 4.3. Representative sections from each time point were also fixed in formalin, routinely processed, paraffin embedded, and immunoreacted. Selected muscle biopsy specimens with a range of neuropathologic diagnoses, including fiber type grouping, Type II atrophy, and congenital fiber type disproportion, were also assessed for immunoreactivity. Our results indicate that the MY-32 monoclonal antibody specifically reacts with Type II (fast twitch) fibers. Immunoreactivity is most intense in cryostat sections immersion fixed in acetone, but moderately intense, specific immunoreactivity can be clearly identified in formalin-fixed (frozen or paraffin-embedded) tissue obtained even 48 hours after death. Application of this nonenzymatic method for fiber type determinations in the neuropathologic evaluation of skeletal muscle biopsies is presented.

Adenosine Triphosphatases↗
PubMed1997

Neurosarcoid infiltration of the ventricular catheter causing shunt failure: a case report.

BACKGROUND: Neurosarcoid is known to develop in 5% of patients with sarcoidosis. A frequent manifestation of this condition is hydrocephalus, which will often require treatment with a ventricular shunt. METHODS: Presented here is the case of a patient whose initial manifestation of neurosarcoidosis was hydrocephalus, and who then represented with multiple shunt failures. RESULTS: On two revisions, the proximal catheter, after removal, was found to be occluded with noncaseating granulomatous material that had infiltrated the shunt lumen. CONCLUSIONS: Although shunts may become occluded by inspissated proteinaceous or cellular debris, the occlusion of a shunt catheter by the ingrowth of the noncaseating granulomatous material of neurosarcoid has not been described before. This patient's course, the histopathologic findings, and neurosarcoidosis in general are discussed here.

Adult↗
PubMed1996

Embryonic expression of glial cell-line derived neurotrophic factor (GDNF) suggests multiple developmental roles in neural differentiation and epithelial-mesenchymal interactions.

We describe the cloning of the mouse glial cell line-derived neurotrophic factor (GDNF) gene and its expression during embryogenesis. GDNF is a distant member of the superfamily of TGF-beta related genes that was originally identified on the basis of its striking neurotrophic activity. GDNF is expressed in a highly dynamic pattern in the anterior neuroectoderm during early stages of neurogenesis between E7.5 and E10.5. Beginning at E10.5 GDNF is also expressed in several organs that develop through inductive epithelial-mesenchymal interactions. In those organs, GDNF expression is strictly confined to mesenchymal tissues and is not found in epithelia. Our results suggest multiple roles for GDNF during early stages of neuronal development and in epithelial-mesenchymal interactions.

Amino Acid Sequence↗
PubMed1995

Central nervous system tuberculosis: medical management and surgical indications.

BACKGROUND: An increase in the incidence of tuberculosis in industrialized nations has prompted a need for earlier diagnosis, treatment, and isolation of disease. An associated rise in the number of patients with central nervous system tuberculosis (CNS TB) has forced neurosurgical services to reevaluate the indications for operative intervention. METHODS: Seventeen cases of CNS TB were found in a retrospective review of all cases managed on the neurosurgical service between 1989 and 1994. These cases included eight with tuberculous meningitis, seven cases of supratentorial tuberculomas, and two cases of infratentorial tuberculomas. RESULTS: Major permanent neurologic morbidity was seen in one case (6%). Five patients (29.4%) died of complications associated with their primary disease. Eleven patients (64.6%) had excellent outcomes. All patients in the latter group completed an 18-month course of antituberculous therapy. Cerebrospinal fluid shunts were necessary in three cases and emergent craniotomy was performed in three cases. Only four cases had human immunodeficiency virus (HIV) coinfection. CONCLUSION: The neurosurgeon's role in the management of CNS TB has once again become more evident. In the present series it is unclear as to whether this is due to multiple drug-resistant strains of Mycobacterium tuberculosis or HIV coinfection. It is clear, however, that vigilance over patient compliance and serial neurologic evaluation will determine the need for operative intervention.

Adult↗
PubMed1994

Electrolyte-induced demyelination in rats. 1. Role of the blood-brain barrier and edema.

The blood-brain barrier (BBB) was studied in rats with electrolyte-induced demyelination (EID), an experimental model for central pontine myelinolysis. Intravenously injected peroxidase was extravasated at 3 h post hypertonic saline injection (PHS) into regions frequently involved in EID. Increased pinocytotic activity and focal interendothelial gaps were seen at 3 h PHS and less frequently at 48 h PHS. Measurement of total cerebral water content revealed an increase during the hyponatremic phase. This was followed by a marked increase at 3 h PHS with continued increment at 48 h PHS. Intracellular edema with accumulation of fluid within neurites and astrocytic processes was noted during the hyponatremic phase, whereas extracellular edema developed after hypertonic saline injection. The implications of disrupted BBB and its role in the pathogenesis of EID are discussed.

Animals↗
PubMed1994

Electrolyte-induced demyelination in rats. 2. Ultrastructural evolution.

This study presents the electron microscopic evolution of lesions in electrolyte-induced demyelination (EID) in rats, a lesion which bears striking histological and clinical similarity to central pontine myelinolysis. The earliest change was observed during the hyponatremic phase and consisted of minimal intracellular edema present throughout the brain. Following the injection of hypertonic saline, additional changes were observed which were restricted to sites previously reported to be frequently involved in EID. Early dilatation of the inner tongue of oligodendrocyte cytoplasm in myelinated nerve fibers was observed at 3 h post hypertonic saline injection (PHS). This was followed, at 48 h PHS, by the appearance of degenerative changes consistent with dying oligodendrocytes. Well-delineated, vacuolar and spongy lesions, seen by light microscopy, were present by 48 h PHS at the same sites as above. Electron microscopically, this appearance was found to be due to striking intramyelinic edema. By 96 h PHS, macrophages containing myelin and other cellular debris were frequently present at these sites. Concomitantly, myelin sheaths underwent vesicular disruption and disintegration. This sequence of events suggests a lesion of the oligodendrocyte-myelin complex, secondary to initial blood-brain barrier damage and edema.

Animals↗
PubMed1993

Multiple sclerosis: remyelination of nascent lesions.

The relationship between plaque pathology and disease duration was examined in 15 patients with multiple sclerosis who died early in the course of their illness. Myelin-stained sections revealed that most plaques examined in patients who died during the first month of their illness showed evidence of ongoing myelin destruction accompanied by a loss of oligodendrocytes. Plaques containing large numbers of oligodendrocytes were not observed in these patients, but were relatively common in patients who died more than 1 month after clinical onset. Remyelination affecting more than 10% of the plaque area was observed in 3 of 82 plaques in 5 patients who died within 10 weeks of clinical onset, in 38 of 105 plaques in 5 patients who died 3 to 10 months after clinical onset, and in 19 of 92 plaques in 5 patients who died 18 months or longer after clinical onset. The study provides new evidence that both oligodendrocytes and myelin are destroyed in new lesions, that this activity ceases completely in many lesions within a few weeks, and that remyelination frequently ensues following repopulation of the plaque by oligodendrocytes. The findings suggest that new lesions normally remyelinate unless interrupted by recurrent activity and that remyelinated shadow plaques are the outcome of a single previous episode of focal demyelination.

Adolescent↗
PubMed1993

Multiple sclerosis. Pathology of recurrent lesions.

Recent autopsy studies suggest that remyelinated shadow plaques located in otherwise intact white matter are the outcome of a previous single episode of acute demyelination. In the present study, of 98 remyelinated plaques examined in 15 patients with multiple sclerosis who died between 27 days and 5 years after clinical onset, 15 showed evidence of a superimposed new demyelinating lesion. Inspection of old shadow plaques in a separate series of patients with subacute and long-standing multiple sclerosis revealed that such lesions sometimes exhibit punched-out areas of demyelination and gliosis similar in size and shape to fresh lesions located within or overlapping remyelinated shadow plaques. The findings support magnetic resonance imaging evidence that local recurrence may be as important or more important than progressive edge activity in determining plaque growth and the conversion of nascent lesions into classical demyelinated plaques. The findings also support experimental evidence that recurrent demyelination of the same area of white matter may be one of the factors underlying failed remyelination in multiple sclerosis.

Adult↗
PubMed1991

Herpes zoster myelitis.

We studied the clinical (10 patients) and pathological (9 patients) findings in 13 patients with herpes zoster myelitis, all of whom had systemic illnesses associated with immunosuppression. The median interval between the onset of the herpes zoster rash and myelopathic symptoms was 12 days, and the subsequent median interval to maximal deficit was 10.5 days. Presenting neurological symptoms were characteristically ipsilateral to the rash, with motor dysfunction predominating, followed by a spinothalamic and, less often, posterior column sensory deficit. Pathological involvement was most severe in the dorsal root entry zone and posterior horn of the spinal cord segment corresponding to the involved dermatome. There was variable spread both horizontally and vertically in the spinal cord. Direct varicella-zoster virus (VZV) infection of neuroectodermal cells, particularly oligodendrocytes, was demonstrated by immunostaining viral antigens (8 cases), and by the presence of Cowdry type A intranuclear inclusions (7 cases) and often was associated with focal demyelination (6 cases). In 4 patients a VZV vasculitis was associated with leptomeningitis and haemorrhagic necrosis (spinal cord in 1; brainstem or cerebellum in 3). The protracted evolution in many cases and the pathologically documented direct viral infection of the spinal cord provide a rational basis for the use of antiviral therapy in preventing or attenuating the evolving myelopathy.

Adult↗
PubMed1991

Propargylglycine infusion effects on tissue glutathione levels, plasma amino acid concentrations and tissue morphology in parenterally-fed growing rats.

Amino acid solutions currently used for total parenteral nutrition (TPN) contain little cysteine or cystine. Some premature human infants have low liver activities of gamma-cystathionase and presumably require preformed cysteine or cystine. Growing animals tend to have higher liver gamma-cystathionase activity, which makes them unsuitable as models to study effects of CSH precursors. Because propargylglycine (PPG) inhibits gamma-cystathionase specifically, rats infused with PPG as part of a TPN regimen were evaluated as a potential model. Two groups of rats (120-160 g) were infused for 15 d with TPN regimens, one without and one with PPG (40 mumols/d). A third group received the TPN-control regimen, with methionine added at toxic levels. Propargylglycine treatment significantly decreased plasma cystine and taurine concentrations and significantly increased plasma cystathionine concentration without affecting methionine concentration. Propargylglycine treatment significantly decreased brain, muscle, liver, intestine and stomach glutathione concentration without affecting erythrocyte or heart glutathione concentrations. Electron microscopic examination showed no abnormalities in heart and kidney of PPG-treated rats. Hepatocyte glycogen was lower in TPN-fed controls than in orally fed rats and was further reduced in TPN-PPG-fed animals. Growing rats infused with low doses of PPG show promise as an animal model to study a number of important issues concerning human sulfur amino acid metabolism.

Alkynes↗
PubMed1990

Interaction of astrocytes and newly formed oligodendrocytes in resolving multiple sclerosis lesions.

Cells resembling oligodendrocytes are sometimes seen within reactive astrocytes in fresh lesions in multiple sclerosis. Using immunostained paraffin and epoxy sections of fresh plaques obtained at autopsy from a series of cases of short clinical duration, it was found that small cells with round nuclei are commonly observed within reactive astrocytes in some hypercellular plaques and that these cells are phenotypically undifferentiated oligodendrocytes, i.e., nonmyelinating cells expressing intensely the oligodendrocyte determinants 2',3'-cyclic nucleotide 3'-phosphohydrolase and the carbohydrate epitope present on the family of cell adhesion molecules recognized by monoclonal antibody HNK-1. They also stain positively for IgG. This unusual astrocyte-oligodendrocyte interaction, which appears to be restricted to nonmyelinating oligodendrocytes in lesions of several weeks' to several months' duration, has not been described during normal oligodendrocyte differentiation or in experimental central remyelinating lesions. It bears some resemblance, however, to a pattern of slow oligodendrocyte destruction seen previously in organotypic perinatal central nervous tissue cultures exposed to multiple sclerosis serum. It is concluded that the evolution of some multiple sclerosis lesions early in the course of the disease is associated with abnormal binding and/or destruction of newly generated oligodendrocytes by reactive astrocytes. These observations raise new questions concerning mechanisms underlying failed remyelination in multiple sclerosis, including the novel possibility of an immune response directed against a developmentally restricted oligodendrocyte antigen.

2',3'-Cyclic Nucleotide 3'-Phosphodiesterase↗
PubMed1989

Neuropathology of HIV infection: adults versus children.

The lower incidence of complicating opportunistic and reactivated latent infections in the CNS of children with HIV infection has resulted in a "cleaner" system, allowing better appreciation of the lesions associated with primary HIV brain infection. The most striking differences that we have seen in the CNS of children, when compared to adults with regard to primary HIV infection, have been the following: More florid inflammation and more frequent MGC in the children; more frequent localization of MGC in the cerebral cortex in children; more basophilic mineralization in the children; more perivascular brown pigment in the adults; and more obvious white matter changes in the adults. It has been noted that the median survival time for children under one year of age with AIDS is significantly less than that for older children (6.5 months vs. 19.7 months). Thus the tempo of HIV infection would seem to be more rapid in children, particularly young children. Our own neuropathological observations would support the hypothesis of a more fulminant CNS disease in children, in keeping with the well-known phenomenon of increased virulence of viral infections in the immature central nervous system.

Adult↗