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Biomedical subjects

J S Wolinsky

Publications and source records attributed to J S Wolinsky.

143 records · Page 8Linked to original sources
PubMed1976

The neuropathology of progressive rubella panencephalitis of late onset.

The clinicopathological changes in a case of progressive rubella panencephalitis of late onset have been presented. The prominent pathological findings in the brain included diffuse destruction of white matter with perivascular inflammatory cells and gliosis, moderate neuronal loss, numerous amorphous vascular deposits in the white matter and severe generalized cerebellar atrophy. These changes are compared and contrasted with those found in congenital rubella and other latent viral illnesses.

Adult↗
PubMed1976

Persistence of neuroadapted mumps virus in brains of newborn hamsters after intraperitoneal inoculation.

Neuroadapted mumps virus produces systemic infection in newborn hamsters after intraperitoneal inoculation. Virus is disseminated via a low-level viremia and appears to enter the central nervous system by passage through the choroid plexus. At such sites, choroidal and ependymal epithelial cells are productively infected and become a source for further viral spread throughout the brain parenchyma. The development of neutralizing and hemagglutination-inhibiting antibodies in serum correlates with the clearance of virus from most systemic sites. However, peristence of virus in both brain and kidney is demonstrated late in this infection.

Animals↗
PubMed1976

Experimental panencephalitis induced in suckling mice by parainfluenza type 1 (6/94) virus. I. Clinical and pathological features.

Intracerebral inoculation of two strains of suckling mice with 6/94 virus, a parainfluenza type 1 virus originally isolated from two patients with multiple sclerosis, produced clinical disease 1-2 weeks after inoculation. Of 528 animals inoculated, 33% died (26% of the ICR strain and 76% of the BALB/c strain) usually between two or three weeks after injection. Animals that recovered appeared to develop normally. Pathological changes were of two types. Initially, there was a necrotizing panencephalitis with virus-specific intracytoplasmic inclusions in choroid and ependymal epithelial cells and neurons. The second major lesion appeared about 6 weeks post inoculation and consisted of a noninflammatory spongiform degeneration of white matter that primarily involved the cerebral hemispheres; a diffuse vacuolar encephalapathy primarily affecting the brain stem; and a persistent minimal inflammation.

Animals↗
PubMed1976

Experimental panencephalitis induced in suckling mice, by parainfluenza type 1 (6/94) virus, II. Virologic studies.

6/94 virus, a parainfluenza type 1 isolate from multiple sclerosis brain tissue, produced a chronic panencephalitis when inoculated intracerebrally into suckling ICR mice. Immunofluorescent staining revealed 6/94 viral antigen in ependyma, meninges, choroid plexus, and perivascular parenchymal sites from day 3 to 128 days after infection. Hemadsorption-neutralizing antibody was first detected between 20-25 days after infection and remained at high titers for 7 months. Using embryonated chicken eggs, virus was recovered from mouse brains for only 8 days, but could be recovered from brains grown in vitro as explants for 37 days after infection. In cell lines established from explanted brain tissue, immunofluorescence was the most sensitive indicator of virus presence, although infectious virus was not produced. Fusion of these mouse brain cells with human (W138) indicator cells was the most effective means of rescuing 6/94 virus.

Animals↗
PubMed1976

Experimental panencephalitis induced in suckling mice by parainfluenza I (6/94) virus. III. Ultrastructural studies.

Intracerebral inoculation of newborn mice with Parainfluenza I (6/94) virus produces a chronic panencephalitis. Electron microscopic studies were carried out over 125 days of the infection. Productive infection of choroidal and ependymal epithelial cells was seen from postinoculation days 2nd to the 8th. Fusion of adjacent choroid and ependymal cells resulted in giant cell formation. Completed virions were seen adsorbed to circulating macrophages and these cells replicated intracytoplasmic nucleocapsids. Neuronal infection was evident on the 3rd postinoculation day, was widespread by the 6th day postinoculation and persisted to the 35th day postinoculation. Nucleocapsid alignment and budding from neuronal plasma membranes was never seen. An initially intense mononuclear cell infiltrate subsided by the 35th day but residual inflammation persisted throughout the study. Late in the course of the infection, vacuolation of the neuropil and a periventricular and deep cerebral spongiform change was seen which could not be directly associated with local viral replication. These ultrastructural findings are correlated with prior light microscopic, virological and immunofluorescent studies of the infection and compared to other experimental models of myxovirus central nervous system infections.

Animals↗
PubMed1976

Ultrastructure of mumps virus replication in organotypic cultures of hamster choroid plexus.

Organotypic cultures of newborn hamster choroid plexus were inoculated with equal titre doses of newly isolated or hamster adapted strains of mumps virus. The ultrastructure of virus replication in choroid epithelial cells of the cultures was compared. No qualitative differences were observed; however, the adapted strain produced significantly greater numbers of virions and earlier destruction of the cultures. These findings are consistent with previous in vivo observations of the ultrastructure of the replication of these strains in the newborn hamster central nervous system. This in vitro study leads further support to the hypothesis that differences in the in vivo biological effects of the virus strains are primarily the result of virus-cell rather than virus-host interactions.

Animals↗
PubMed1975

Progressive rubella panencephalitis. Late onset after congenital rubella.

In children with congenital rubella infection the deficits remain stable; neurologic deterioration after the first few years of life is not believed to occur. We have encountered three patients with a definite or presumptive diagnosis of congenital rubella, in whom a progressive neurologic illness developed that began in the second decade and was characterized by spasticity, ataxia, intellectual deterioration, and seizures. High antibody titers to rubella virus in serum and spinal fluid were present in two, and all had increased cerebrospinal-fluid protein and gamma globulin. Extensive attempts to recover a virus from brain and body fluids were unsuccessful. The brains of two patients showed a widespread, progressive, subacute panencephalitis mainly affecting white matter. These data suggest that rubella virus may be a cause of progressive panencephalitis.

Adolescent↗
PubMed1975

Acquired toxoplasmosis. A neglected cause of treatable nervous system disease.

The neurological manifestations of six cases of acquired central nervous system toxoplasmosis are compared with the 39 well-documented cases from the literature. Half of the patients had underlying systemic diseases (18 malignant neoplasms, two renal transplants, three collagen vascular diseases) treated with intensive immunosuppressive therapy. The remainder had primary toxoplasmosis. Three major neurological patterns were seen: (1) diffuse encephalopathy with or without seizures, (2) meningoencephalitis, and (3) singular or multiple progressive mass lesions. Routine neurological diagnostic studies were not helpful. The Sabin-Feldman dye test or IgM indirect fluorescent antibody test or both were effective in confirming the diagnosis. Twenty-seven patients died without a clinical diagnosis of toxoplasmosis. The diagnosis was made terminally in four additional patients. Thirteen of fourteen patients who received a full course of sulfadiazine or pyrimethamine or both did well. Toxoplasmosis should be considered in the immunosuppressed patient who appears with neurological involvement.

Adult↗
PubMed1975

In vivo studies of parainfluenza I (6/94) virus: mononuclear cell interactions.

Adsorption to and penetration of migratory mononuclear cells in vivo by Para-influenza I (6/94) virus were documented by electron microscopy during the acute phase of an experimental meningoencephalitis in ICR mice. Phagocytosis of virions was the apparent and predominant mode of viral entry into these cells. Penetration by fusion was also seen. Nucleocapsids were replicated by the mononuclear cells which became a potential reservoir for the further spread of virus.

Adsorption↗
PubMedDate not supplied

Proton MR spectroscopy of gadolinium-enhanced multiple sclerosis plaques.

Magnetic resonance (MR) imaging and proton MR spectroscopy were performed in 14 patients with clinically definite multiple sclerosis (MS). Prominent resonances in the 0.5-2.0-ppm region were seen in the spectra of six of nine gadopentetate dimeglumine-enhanced plaques in seven patients. These resonances were presumed to originate in lipids and other myelin breakdown products. Similar resonances were detected in only seven of 21 unenhancing plaques. The more frequent presence of such signals in the gadolinium-enhanced regions indicates that myelin breakdown is often associated with the inflammation that occurs in early stages of MS plaque evolution. It remains uncertain, however, whether active inflammation as indicated by gadolinium enhancement is a necessary precursor of myelin breakdown as detected at MR spectroscopy. Quantitative spectral analysis did not indicate statistically significant differences in N-acetyl aspartate and choline levels relative to creatine plus phosphocreatine between healthy volunteers and MS patients.

Adult↗
PubMedDate not supplied

Short TE hydrogen-1 spectroscopic MR imaging of normal human brain: reproducibility studies.

Studies have been performed to evaluate the reproducibility of longitudinal acquisitions with short TE spectroscopic magnetic resonance (MR) imaging of human brain. In healthy volunteers, the ratios of N-acetyl-aspartate (NAA) and choline (Cho) with respect to total creatine (Cr) (creatine and phosphocreatine) have been examined in terms of voxel-to-voxel, acquisition-to-acquisition, and subject-to-subject variation. Overall coefficients of variation for NAA/Cr ratios and Cho/Cr ratios were 18% and 16%, respectively. The interacquisition variation was not statistically significant (P = .05) for either ratio. In terms of F ratios, the dominant source of variation in the NAA/Cr ratio was intersubject variability, whereas for the Cho/Cr ratio the dominant source of variation was intervoxel variability. Consequences of spectroscopic processing with spatial apodization and postacquisition water suppression and resolution enhancement were also examined. Such reproducibility studies are crucial if longitudinal spectroscopic evaluations are to be performed in a clinical setting to follow the natural course of disease states or the effects of therapy.

Adult↗
PubMedDate not supplied

A model of the structural organization of rubella virions.

Rubella virus contains three major structural polypeptides designated E1, E2, and C with molecular weights of 62,000, 47,000-54,000 (a complex), and 38,000, respectively, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reduced conditions. Limited-digest peptide maps confirm that each of these polypeptides is distinct and the E2 is a series of three closely related glycopolypeptides. Both E1 and E2 are glycosylated and covalently incorporate [3H]palmitic acid. Enzymatic digestion of intact virus with trypsin completely degrades both E1 and E2, while the C polypeptide remains intact. E1 has an isoelectric point of pH 6.5. E2 exhibits at least 15 different isoelectric species, which focus over the pH range of 5.0-8.6, and C has two distinct isoelectric species of pH 8.8 and pH 9.5. Under unreduced conditions, E1 exists as a disulfide-bonded dimer (E1-E1) with a molecular weight of 105,000; a disulfide-bounded heterodimer (E1-E2) with a molecular weight of 95,000; and in monomeric form (E1). E2 is found predominantly in heterodimeric form (E1-E2), and C is found only in dimeric form when unreduced. Functional-inhibition studies with selected monoclonal antibodies show at least three distinct antigenic domains on E1 that include sites involved in hemagglutination and lysis of red blood cells.

Antibodies, Monoclonal↗
PubMedDate not supplied

Accuracy and reproducibility in volumetric analysis of multiple sclerosis lesions.

The accuracy and reproducibility of dual-contrast segmentation based on nonparametric feature map analysis have been investigated in a multicomponent gelatin phantom. The root mean square errors in volume ranged from 0.02 cm3 for small volumes to 3.8 cm3 for larger volumes, with a mean error of 0.97 cm3. Average inter- and intraobserver coefficients of variation were found to be < 7% for all compartments. To evaluate the reproducibility of segmentation of clinical image data, volumes of total brain, CSF, and multiple sclerosis (MS) lesions were obtained from five image sets of MS patients. Inter- and intraobserver coefficients of variations were computed for the patient data and were found to be < 5% for brain, 17% for CSF, and 20% for MS lesions. Such variations were found to be reduced by appropriate preprocessing of the images.

Adult↗