Biomedical subjects
Publications and source records attributed to J Sotelo.
Glial fibrillary acidic protein has been widely used in neurobiology and neuropathology as a specific marker for normal and abnormal astrocytes. Here, we report the immunostaining of 107 brain tumors and controls using an antiserum against glial fibrillary acidic protein. Selection of astroglia-derived tumors was easy and of high accuracy. Pattern of staining and usefulness of the method are described.
A case of glial tissue in a polypoid structure of the uterine cervix is presented; the presence of glial fibrillary acidic protein was demonstrated by immunoperoxidase, confirming the astrocytic nature of the tissue. The main hypotheses to explain this unusual finding are discussed.
Thirty-five patients with active neurocysticercosis were treated with praziquantel and followed for 1 year after therapy. CT and CSF analysis showed that 91% of patients with parenchymal cysts improved, and 47% of patients with chronic arachnoiditis had remission. A single treatment with praziquantel for 2 weeks, administered in a daily dose of 50 mg/kg of body weight, was highly effective in parenchymal cysticercosis but less effective in meningeal cysticercosis. The benefits were sustained for at least 1 year.
Cysticercosis of the central nervous system, because of the combination of inflammatory response, topography of lesions, degree of parasitic infestation, and sequelae of previous infestations produces a most variable clinical picture. The symptomatology may range from a discrete neurological disturbance to the most dramatic brain disorder. Severity of the disease, prognosis, and medical or surgical decision for treatment largely depend on the individual amalgam of the above-referred factors. An improved classification of neurocysticercosis (NCC) that delineates active from inactive forms of the disease will eventually be important in the research of immunodiagnosis and in therapeutic trials. In this report, a classification is presented that separates active from nonactive forms of NCC and is based on our experience with 735 patients studied. Characteristics of each form of NCC, frequency of principal signs and symptoms, and findings in cerebrospinal fluid analysis are discussed.
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Twenty-six patients with cysticercosis of the brain parenchyma were treated with the antihelmintic agent praziquantel (50 mg per kilogram of body weight daily for 15 days). During treatment a strong inflammatory reaction occurred, as evidenced by increased protein and cells in the cerebrospinal fluid. This finding correlated with headache, exacerbation of neurologic symptoms, and edema and inflammation around cystic lesions. After three months of treatment all patients had improved clinically, and 13 (50 per cent) were asymptomatic. The total number of cysts on CT scans had decreased from 152 at the beginning of treatment to 51, and the mean diameter of cysts was reduced by 72 per cent. CT scans showed improvement in 25 of the 26 patients, with total remission of all cysts in nine. Seventeen control patients followed with CT studies for a mean of 9 +/- 2 months had no spontaneous remission of lesions, and in many cases the scans showed worsening during the observation period. Our results indicate that praziquantel is effective in cysticercosis of the brain parenchyma.
Sequential electron microscopic studies of cultures of neurons derived from dissociated fetal mouse brain on the eleventh day of gestation revealed the formation of well-developed synapses during the second and third weeks of growth in vitro. Synaptic junctions were associated with synaptic vesicles nd dense synaptic membranes. Dense-core vesicles were also observed frequently in presynaptic terminals.
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The fourth ventricle is frequently affected in patients with cysticercosis of the central nervous system, due either to a large cyst occluding the cavity or to granular ependymitis (ventriculitis) as a consequence of diffuse inflammation within the intraventricular and subarachnoid spaces. In some cases, the differential diagnosis between these two forms of neurocysticercosis is difficult to make, even after special radiological procedures. It is important to establish the correct diagnosis, since a surgical approach is beneficial only when the fourth ventricle is obstructed by a large cyst. In this paper, the clinical differences between fourth ventricle cysts and ventriculitis are presented in 16 patients with neurocysticercosis who were subjected to surgical exploration of the posterior fossa. Patients with a large cyst occluding the fourth ventricle had a short evolution of signs and symptoms, Bruns' syndrome, and discrete or no inflammatory reaction in the cerebrospinal fluid (CSF). Patients with ventriculitis generally had a longer duration of signs and symptoms, Parinaud's syndrome, a consistently positive complement fixation test to cysticerci, and more cells and proteins in the CSF. The clinical picture and ancillary studies can give the precise diagnosis in most patients before surgical exploration is performed.
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A rapid and technically simple method for demonstrating anti-neurofilament antibodies using longitudinal sections of rat spinal cord as substratum and indirect immunofluorescent technique is reported. The results compare well with those obtained by the technically more difficult and time-consuming methods using as substratum central neurons cultivated in vitro. A total of 195 serum specimens from different neurological disorders and healthy subjects were studied. Immunofluorescent autoantibodies to neurofilaments were found in specimens of serum from patients with Creutzfeldt-Jakob disease (CJD), kuru, amyotrophic lateral sclerosis, parkinsonism dementia (Guam), Alzheimer's disease, and multiple sclerosis but in higher frequency in CJD and kuru than in the other disease or in healthy control subjects.
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Heterogeneic autoantibodies against axonal neurofilament proteins of mature mouse neurons grown in vitro were detected by the indirect immunofluorescence technique in 12.7% (9 of 71) of the sera from nonhuman primates infected with kuru, in 14.5% (17 of 117) and 4% (1 of 25), respectively, of the sera from nonhuman primates and laboratory rodents infected with Creutzfeldt-Jakob disease, and in 35% (7 of 20) of the sera from sheep naturally infected with scrapie. Autoantibody titers ranged from 1:16 to 1:512 in Creutzfeldt-Jakob disease-infected animals, 1:32 to 1:512 in kuru-infected animals, and 1:64 to 1:1,024 in sheep with natural scrapie. The sera from 11 monkeys and 17 hamsters infected with scrapie and from 19 chimpanzees inoculated with brain tissues from humans with other neurological diseases did not contain autoantibodies. Of the 41 chimpanzees with Creutzfeldt-Jakob disease, 6 had autoantibodies against neurofilament proteins before experimental inoculation, whereas 6 others developed autoantibodies after inoculation, 4 developed autoantibodies during the asymptomatic phase, and 2 developed autoantibodies during the terminal clinical phase. Of the 48 chimpanzees with kuru, 2 had autoantibodies before inoculation, 6 developed autoantibodies after inoculation, 3 developed autoantibodies during the asymptomatic phase, and 3 developed autoantibodies during the terminal clinical phase. Among the normal nonhuman primate controls, 4.6% (9 of 195) had autoantibodies. In contrast, no autoantibodies were detected in 49 control rodents and 13 control sheep. The increased incidence of autoantibodies against neurofilament proteins in animals with kuru, Creutzfeldt-Jakob disease, and scrapie constitutes the first evidence of an immunological reaction in this group of atypical infections caused by unconventional viruses and suggests that neurofilaments may be involved in pathogenesis.
The serums of some patients with subacute spongiform encephalopathies contain an autoantibody in higher titer against a normal fibrillar protein within the axon of mature central neurons in culture. The morphological features of this neurofilament, as demonstrated by immunofluorescence and immunoperoxidase staining, and the partial characterization of the antibody are described. The detection of this hetero-specific autoantibody is the first evidence of an immune reaction in the spongiform encephalopathies.
Human smooth muscle autoantibody (SMA) of defined anti-actin specificity was tested by the indirect immunoperoxidase staining method on frozen sections of tissues and on cultured rat lung fibroblasts. The serum stained tissue sections and cultured fibroblasts in a pattern identical with that obtained by indirect immunofluorescence. Ultrastructural studies carried out on the immunoperoxidase stained cells showed that the long parallel filaments spanning the long axis of cultured fibroblasts seen by light microscopy correspond with the thick bundles of microfilaments.
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We report a simplified method for culturing fetal central nervous system cells predominantly inducing neurons that grow, differentiate, and live in vitro for as long as 10 weeks. These central nervous system cells form a confluent cell culture in which about 80% of the cells are fully differentiated neurons producing interconnecting axons and dendrite processes and live upon a sparse underlying population of fibrillary and protoplasmic astrocytes, oligodendrocytes, and fibroblasts. Morphological and cytochemical characteristics of these cell types, based on immunofluorescent cell specific markers and silver staining of neurons, are presented.
Specific anti-actin and anti-myosin antibodies were shown to react in single and double immunofluorescence sandwich tests with identical sites in non-muscle cells in frozen sections of tissues and in cultured cells. In tissues, both antibodies reacted with liver cell membranes, parts of renal glomeruli, brush borders and peritubular fibrils of renal tubules, brain synaptic junctions, and membranes of lymphoid cells in thymic medulla, lymph nodes and spleen. Both antibodies reacted strongly with long parallel cytoplasmic fibrils in cultured fibroblasts, and with disrupted fibrils in cytochalasin-B treated cells. In neuroblastoma cells both antibodies gave prominent staining of growth cones and microspikes. The observation that the distribution of myosin parallels that of actin in non-muscle cells argues strongly in favour of a functional interaction between the two molecules in the generation of contractile activity in non-muscle cells.