Search PubMed⌕ Search

Biomedical subjects

D H Gilden

Publications and source records attributed to D H Gilden.

At least 127 records · Page 7Linked to original sources
PubMed1978

Herpes simplex virus latency in patients with multiple sclerosis, lymphoma and normal humans.

Herpes simplex virus (HSV) was isolated from the trigeminal ganglia (TG) of 12 cadavers (10 traumatic deaths, one lymphoma and one multiple sclerosis). The cadaver with multiple sclerosis showed large bilateral trigeminal nerve root entry zone areas of demyelination. It is hypothesized that HSV is capable of migrating to the trigeminal nerve root entry zone and initiating demyelinating disease.

Adolescent↗
PubMed1977

Isolation of Herpes simplex virus from human trigeminal ganglia, including ganglia from one patient with multiple sclerosis.

Herpes-simplex virus (H.S.V.) was isolated from 18 of 39 trigeminal ganglia (T.G.) obtained within 12 h of death. The virus was isolated from ten persons who had died of trauma, from one case of lymphoma, and from one case of multiple sclerosis. In the cadaver with histologically confirmed multiple sclerosis, large bilateral areas of demyelination were present near the points of entry of the nerve root, and the possibility that H.S.V. migration to the root entry zone caused demyelination cannot be excluded.

Adolescent↗
PubMed1977

Experimental infection of human leukocytes with parainfluenza 1 (6/94) virus.

Parainfluenza 1 (6/94) virus replicated in both unstimulated and phytohemagglutinin (PHA)-stimulated human peripheral blood leukocytes (PBL). After exposure of PBL to 6/94 virus at a multiplicity of infection of 1, the presence of viral antigen was demonstrated by immunofluorescence in the cytoplasm of less than 1% of unstimulated PBL and 1 to 5% of macrophages. Small amounts (less than 50 mean egg infective doses per ml in most instances) of cell-free virus were present in 18 of 30 (60%) cell cultures tested from 3 to 8 days postinfection. Cell-free virus peaked 6 days postinfection. Virus replication was enhanced in PHA-stimulated cells. Approximately 1 to 10% of PHA-stimulated PBL contained viral antigen as evidenced by immunofluorescence, and cell-free virus was present in 19 of 25 (76%) of the cell cultures tested from 3 to 8 days postinfection. Paramyxovirus nucleocapsids and tubular aggregates were seen in the cytoplasm of approximately 5% of PHA-stimulated PBL and were visualized only in lymphocytes. No other unusual intracytoplasmic or intranuclear structures were seen.

Capsid↗
PubMed1977

Evolution of cerebral abscess: correlation of clinical features with computed tomography. A case report.

Computed tomography demonstrated the evolution of a cerebral abscess. Intravenous contrast material was essential for visualization of the abscess capsule. Computed tomography was more specific than technetium 99 brain scanning and cerebral angiography, and is the only diagnostic tool so far capable of differentiating acute focal encephalitis (cerebritis) from a well-developed abscess.

Adult↗
PubMed1976

Human brain in tissue culture. Part. 5. Identification of glial cells by immunofluorescence.

Glial fibrillary acidic (GFA) protein was demonstrated by immunofluorescence in both primary and long-term cultures of adult human brain cells explanted from normal, neoplastic and non-neoplastic CNS diseases, and in mouse brain cells subcultivated in vitro. GFA protein was present in the cytoplasm of at least 4 distinct cell types and persisted throughout the finite lifetime of brain cell cultures.

Brain↗
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↗
PubMed1975

Human brain in tissue culture. I. Acquisition, initial processing, and establishment of brain cell cultures.

This paper details the in vitro techniques used to establish cells in culture from the brains of 40 patients, most of whom had chronic neurologic disease. The clinical and pathologic features of these patients are given. The success in establihsing cell lines was dependent upon the origin of tissue (biopsy vs. autopsy), the site of removal from the brain, and various environmental and technical manipulations in vitro.

Adolescent↗
PubMed1975

Human brain in tissue culture. II. Studies of long-term cultures.

This paper describes the techniques used to maintain and reconstitute from storage adult human brain cells in culture. Growth characteristics, cell morphology, lifespan, and karyotypic analysis of cell lines derived from patients with multiple sclerosis (MS), non-MS neurologic diseases, and normal brains are compared.

Aging↗
PubMed1975

Human brain in tissue culture. III. PML-SV40-induced transformation of brain cells and establishment of permanent lines.

Cells from explants and monolayer subcultures of adult human brain obtained from biopsies or autopsies of ten multiple sclerosis (MS) cases, one case each of Jakob-Creutzfeld (JC) and amyotrophic lateral sclerosis (ALS) and three cases with no central nervous system (CNS) involvement were transformed with PML-SV40 virus. Transformation was effected to establish permanent lines of these particular adult brain cells so that sufficient quantities would be available for other research projects. The procedure previously used to transform human fibroblasts (Koprowski et al., '62) was successfully applied to human brain cells. The success of transformation was dependent on the growth condition of the cultures at the time of infection. Events occurring after viral infection and during the pre-transformation and the post-transformation phases are described.

Amyotrophic Lateral Sclerosis↗
PubMed1975

Human brain in tissue culture. IV. Morphological characteristics.

The morphology of cells from normal and diseased brains and PML-SV40 transformed brain cells grown on glass cover slips in cultures is described. Seven types of cells are identifiable, four of which are probably of mesenchymal origin whereas the remaining three are neurologlial. A classification on the basis of the morphologic features is presented.

Amyotrophic Lateral Sclerosis↗
PubMed1975

Hydrocephalus produced by the 6/94 virus; A parainfluenza type 1 isolate from multiple sclerosis brain tissue.

The 6/94 virus, parainfluenza type 1 isolate from multiple sclerosis brain tissue, produced hydrocephalus in newborn Syrian hamsters. All animals developed clinical disease and died within a week. Ependymal cells lining the aqueduct of Sylvius became necrotic and fused, resulting in obstructive hydrocephalus. The 6/94 virus antigen was seen in ependyma and meninges. Paramyxovirus nucleocapsids were seen within cytoplasm of ependymal cells. Virus was recovered from hamster brains for only two days. Infectious virus could be recovered from brains grown in vitro as explants for 21 days. No evidence of rising hemagglutination-inhibiting antibody was noted for up to one month after infection. Intraperitoneal or subcutaneous injection of 6/94 virus did not produce hydrocephalus. HA2 virus and the temperature sensitive mutant of HA2 virus failed to produce hydrocephalus, while Sendai virus caused lesions similar to those of 6/94 virus.

Animals↗
PubMed1975

Acute SSPE.

Two patients had acute fulminanting encephalitis and the typical pathological changes of subacute slcerosing panencephalitis (SSPE). It is suggested that SSPE should be considered in the differential diagnosis of acute viral encephalitis.

Adolescent↗
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↗
PubMed1975

The effect of neonatal thymectomy on Tamiami virus-induced central nervous system disease.

Tamiami virus, a member of the arenavirus group, produces an acute CNS disease in suckling mice manifested primarily by cerebellar ataxia, paralysis, convulsions, and death. Animals that survive are left with an asymptomatic cerebellar heterotopia. Neonatal thymectomy prevents both acute CNS disease and the resultant cerebellar heterotopia despite equivalent titers of virus and concentrations of viral antigen in the brains of both thymectomized and nonthymectomized infected mice. Inflammatory CNS disease and cerebellar germinal cell necrosis do not develop in thymectomized mice examined more than three months after infection. Viremia and complement-fixing antibody occur in both groups of mice with slightly higher antibody titers in nonthymectomized mice. Tamiami virus-induced cerebellar heterotopia appears to be immunologically-mediated, but the immunopathologic cerebellar lesion differs from the frank necrosis of the brain produced by both Tacaribe and LCM virus in newborn mice.

Animals↗