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Biomedical subjects

E S Cho

Publications and source records attributed to E S Cho.

At least 19 recordsLinked to original sources
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↗
PubMed1988

Comparison of simian immunodeficiency virus and human immunodeficiency virus encephalitides in the immature host.

The simian immunodeficiency virus (SIV) is closely related to the human immunodeficiency virus (HIV) in genomic organization and morphology. More important, SIV and HIV are both primate lentiviruses that cause transmissible immunodeficiency and encephalitis, with an apparently increased virulence in the immature host. The neuropathological features in common between SIV encephalitis in juvenile macaque monkeys and HIV encephalitis in children include the invasion of brain with virus-laden macrophages, the formation of multinucleated (syncytial) giant cells, and white matter lesions and subtle white matter astrocytosis. Important differences include giant cell leptomeningitis and evidence of necrosis and karyorrhexis in brain macrophage infiltrates in SIV-infected monkeys. These changes probably represent a more acute inflammatory process. The importance of future studies to define pathogenetic features of SIV encephalitis, using molecularly characterized isolates with varying neurovirulence and host range, are emphasized.

Acquired Immunodeficiency Syndrome↗
PubMed1987

HIV antigen in the brains of patients with the AIDS dementia complex.

Human immunodeficiency virus infection was identified immunohistochemically in the brains of 8 patients with acquired immune deficiency syndrome dementia complex. Using a monoclonal antibody against a structural viral protein (p25), infection was detected in white matter and basal ganglia in a distribution paralleling that of the major neuropathological abnormalities. Viral antigen was identified principally in perivascular and parenchymal macrophages and in multinucleated cells of macrophage origin that were identified morphologically and by immunocytochemical staining for acid phosphatase isozyme. In 4 of the 8 patients, viral antigen was also detected in acid-phosphatase-negative, process-bearing neuroglial cells; in 2 patients, antigen was detected in basal ganglion cells that were morphologically consistent with neurons and in alkaline-phosphatase-positive cells with elongated nuclei that were most likely of endothelial origin.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Cerebral infarction from non-bacterial thrombotic endocarditis. Clinical and pathological study including the effects of anticoagulation.

The clinical and pathologic findings in 42 autopsy proved cases of cerebral infarction from cancer-associated non-bacterial thrombotic endocarditis were reviewed. Carcinoma of the lung was the most common malignancy. Most patients had disseminated cancer, but in six patients, the condition was stable or in remission, and six patients had localized cancer; two patients were not known to have cancer until neurologic symptoms developed. Neurologic symptoms were focal, suggesting stroke in 18; diffuse, suggesting metabolic encephalopathy in nine; and mixed in five. Neurologic signs were often the only evidence of thromboembolism. The definitive diagnostic test was cerebral angiography showing multiple arterial occlusions. Anticoagulation with heparin appeared to help some patients and did not promote brain hemorrhage. Early diagnosis and vigorous treatment of non-bacterial endocarditis may prevent severe neurologic disability.

Adenocarcinoma↗
PubMed1987

Plasma and urine diketopiperazine concentrations in normal adults ingesting large quantities of aspartame.

In aqueous solution, aspartame can cyclicize to form its corresponding diketopiperazine (3-carboxymethyl-6-benzyl-2,5-diketopiperazine; DKP) and methanol. We measured plasma and urinary concentrations of DKP in samples obtained from six normal adult subjects ingesting 2.2 mg DKP/kg body weight. The DKP was administered as part of a dose of 200 mg aspartame/kg body weight. DKP concentrations in plasma were below the detection limit (less than 1 microgram/ml) of the high-pressure liquid chromatographic method at each time interval after ingestion at which they were measured. Mean (+/- SD) total urinary DKP excreted during the first 24-hr period after dosing was 6.68 +/- 1.30 mg (4.83 +/- 0.23% of the ingested DKP dose). Approximately 44% of the total DKP excreted was excreted in the first 4 hr after dosing.

Adult↗
PubMed1987

Cytomegalovirus encephalitis in patients with acquired immunodeficiency syndrome: an autopsy study of 30 cases and a review of the literature.

The pathology of cytomegalovirus (CMV) encephalitis was studied at autopsy in thirty patients with acquired immunodeficiency syndrome. Lesions could be segregated into five major categories: microglial nodules, isolated inclusion-bearing cells, focal parenchymal necrosis, necrotizing ventriculo-encephalitis, and necrotizing radiculo-myelitis. Microglial nodules and CMV inclusions were present in all brains. Microglial nodules were found with variable frequency and had greatest density in subcortical grey matter. Only a small percentage (average, 6.5 per cent) contained CMV inclusion-bearing cells. Isolated inclusion-bearing cells unaccompanied by microglial nodules or inflammatory infiltrates were seen in half the patients. CMV inclusions were identified in capillary endothelia, astrocytes, and neurons. Focal CMV necrosis, ventriculo-encephalitis, and radiculo-myelitis were less frequent. The presence of CMV inclusions in capillary endothelia suggests a vascular portal of entry for the virus into the central nervous system. The diffuse ependymal and/or subpial distribution of CMV in several patients suggests additional dissemination via the cerebrospinal fluid. Isolated inclusion-bearing cells may reflect the relative nonpermissiveness of surrounding central nervous system parenchyma for CMV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Ultrastructural morphology and intracellular production of human immunodeficiency virus (HIV) in brain.

This is a comparative ultrastructural study of human immunodeficiency virus (HIV) particles in infected H9 lymphocyte cultures and in the brain of a six-year-old boy with acquired immunodeficiency syndrome (AIDS) encephalopathy. Viral particles in the cultures and the brain were of various sizes and shapes; particles ranged from 70 to over 160 nm in diameter, with a variable position of dense nucleoids and less dense core shells. In the brain, viral particles were located free in the cytoplasm of both multinucleated giant cells and mononuclear macrophage-like cells. There was intracellular budding of HIV particles from unidentified membranes, yielding intracellular immature or recently budded particles, with crescentic densities. By contrast, HIV particles in the infected H9 lymphocytes were not free in the cytoplasm but were instead located either extracellularly or in intracellular vacuoles. A small percentage of cells in the cultures were surrounded by immature particles only. Production (replication) of HIV occurred within infected macrophage-like cells in the brain of the child.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Protective effect of steroids in electrolyte-induced demyelination.

Electrolyte-induced demyelination (EID), an experimental model for central pontine myelinolysis was produced in rats by inducing hyponatremia followed by hypernatremia. There was a marked reduction in the number and size of lesions developing in animals that were bled repeatedly by tail transection during induction of the disease. Subsequently a similar protective effect was produced in animals by injecting a single dose of dexamethasone, one hour before the induction of hypernatremia. These findings suggest that steroids may be useful in preventing central pontine myelinolysis from developing in high risk patients requiring urgent correction of hyponatremia.

Animals↗
PubMed1986

Cerebral toxoplasmosis complicating the acquired immune deficiency syndrome: clinical and neuropathological findings in 27 patients.

We reviewed the clinical, neuroradiological, and serological findings in 27 patients with cerebral toxoplasmosis complicating the acquired immune deficiency syndrome, 19 of whom were also analyzed neuropathologically. The clinical manifestations of this disorder varied, ranging from headache and fever to coma. However, the characteristic presentation included focal neurological symptoms and signs, usually of subacute onset. In addition, two-thirds of the patients exhibited more generalized cerebral dysfunction with confusion and lethargy. The computed tomographic (CT) scan most commonly revealed ring contrast enhancement, which appeared to correlate best with the histological presence of vascular proliferation and inflammation surrounding the abscesses. However, in 5 patients the CT scan revealed either homogeneous enhancement or no enhancement, and in 3 patients the scans were negative. In general, CT scans underrepresented the number of lesions eventually documented pathologically. Double-dose contrast administration and preliminary experience with magnetic resonance imaging suggested that these techniques were superior to standard CT scanning in detecting Toxoplasma lesions. All patients were seropositive for IgG antibody against Toxoplasma gondii in blood, both before the onset of illness and at the time of presentation, although titers in some patients were as low as 1:8 and most patients did not exhibit rising titers. Prompt therapy resulted in rapid clinical improvement, documented by CT scan, associated with the development of an organizing tissue response in the host and elimination of free organisms. Response to treatment was sufficiently rapid in most patients to allow a trial of therapy as the favored approach to diagnosis.

Acquired Immunodeficiency Syndrome↗
PubMed1986

The AIDS dementia complex: II. Neuropathology.

In order to define the histopathological substrate of the dementia that frequently complicates the acquired immune deficiency syndrome (AIDS), we analyzed the neuropathological findings in 70 autopsied adult AIDS patients, 46 of whom had suffered clinically overt dementia. Less than 10% of the brains were histologically normal. Abnormalities were found predominantly in the white matter and in subcortical structures, with relative sparing of the cortex. Their frequency and severity generally correlated well with the degree and duration of clinical dementia. Most commonly noted was diffuse pallor in the white matter, which in the pathologically milder cases was accompanied by scanty perivascular infiltrates of lymphocytes and brown-pigmented macrophages, and in the most advanced cases by clusters of foamy macrophages and multinucleated cells associated with multifocal rarefaction of the white matter. However, in nearly one third of the demented cases the histopathological findings were remarkably bland in relation to the severity of clinical dysfunction. In addition, similar mild changes were noted in over one half of the nondemented patients, consistent with subclinical involvement. Vacuolar myelopathy was found in 23 patients and was generally more common and severe in patients with advanced brain pathology. Evidence of cytomegalovirus (CMV) infection was noted in nearly one quarter of the brains and was associated with a relative abundance of microglial nodules, but correlated neither with the major subcortical neuropathology nor with the clinical dementia, indicating that CMV infection likely represented a second, superimposed process. This study establishes the AIDS dementia complex as a distinct clinical and pathological entity and, together with accumulating virological evidence, suggests that it is caused by direct LAV/HTLV-III brain infection.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Pathologic features of AIDS encephalopathy in children: evidence for LAV/HTLV-III infection of brain.

The neuropathologic findings in 11 children with a new CNS disorder that occurs in children with the acquired immunodeficiency syndrome (AIDS) and is postulated to be due to LAV/HTLV-III, the virus that causes AIDS, are reported. The children, who ranged in age from 4 months to 11 years, died of AIDS complicated by progressive encephalopathy. Ten of the children either had positive serum antibody for LAV/HTLV-III or had received blood products from donors later found to be antibody-positive. Examination of the brains of these children at autopsy revealed a unique constellation of findings, including varying degrees of diminished brain weight in all cases, inflammatory cell infiltrates in nine brains, multinucleated cells in eight, three of which also contained multinucleated giant cells, vascular calcification in ten, vascular and perivascular inflammation in five, and white matter changes in nine. Inflammatory and vascular lesions were most prominent in basal ganglia and pons. LAV/HTLV-III retroviral particles, associated with multinucleated giant cells, were observed in two brains on electron microscopic examination. These two and one additional brain had evidence of the LAV/HTLV-III genome by hybridization studies. Only one brain had a recognizable opportunistic infection.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Neuropathology of acquired immunodeficiency syndrome (AIDS): an autopsy review.

In the brains and spinal cords of 153 adult patients dying with acquired immunodeficiency syndrome (AIDS) at New York and Memorial Hospitals a subacute encephalitis with multinucleated cells was present in 28% of all patients. This encephalitis was characterized by multinucleated cells primarily located in the white matter and associated with myelin pallor and sparse infiltrates of rod cells, macrophages, gemistocytic astrocytes and lymphocytes. The incidence per 12 month period ranged from 0 to 43% and significantly increased between 1983-84 (14%) and 1984-85 (43%). Recent virologic and pathologic studies suggest that this encephalitis may be caused by direct LAV/HTLV-III infection of the central nervous system (CNS). Cytomegalovirus encephalomyelitis and toxoplasmosis were the most common opportunistic infections (26% and 10%, respectively). Progressive multifocal leukoencephalopathy, herpes simplex ventriculitis, varicella-zoster leukoencephalitis and fungal infections were infrequent (less than 3% each). A nonspecific encephalitis with microglial nodules and with mild white matter changes occurred in 17%, vacuolar myelopathy in 29% and CNS lymphoma in 6%. Less than 20% of patients had either normal brains or terminal metabolic encephalopathies. This survey shows that neuropathologic complications of AIDS are frequent. Infections are the most common complication and are caused by probable LAV/HTLV-III infection, or by opportunistic organisms.

Acquired Immunodeficiency Syndrome↗
PubMed1986

AIDS encephalopathy.

It is now recognized that AIDS is frequently complicated by a progressive encephalopathy characterized by dementia and motor dysfunction. This article reviews the early and late clinical features of this disorder and examines current evidence that it is due to direct brain infection by the retrovirus that causes AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Vacuolar myelopathy pathologically resembling subacute combined degeneration in patients with the acquired immunodeficiency syndrome.

Twenty of 89 consecutive patients with the acquired immunodeficiency syndrome (AIDS) in whom autopsies were performed over a 3 1/2-year period had a vacuolar myelopathy that was most severe in the lateral and posterior columns of the thoracic cord. Light and electron microscopy showed that vacuoles were surrounded by a thin myelin sheath and appeared to arise from swelling within myelin sheaths. Signs and symptoms referable to the spinal-cord lesions, including paraparesis, often accompanied by spasticity or ataxia (or both), were present in all five patients with marked pathological changes, in five of seven patients with moderate changes, and in two of eight patients with mild changes. Fourteen patients were demented. The clinical presentation was sufficiently distinctive to provide a guide for antemortem diagnosis. Possible causes of the vacuolar changes include uncharacterized viral infection or a metabolic derangement related to selective nutritional deficiency.

Acquired Immunodeficiency Syndrome↗