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Biomedical subjects

C J Gibbs

Publications and source records attributed to C J Gibbs.

At least 109 records · Page 6Linked to original sources
PubMed1989

Neuronal degeneration and neurofilament accumulation in the trigeminal ganglia in Creutzfeldt-Jakob disease.

We report the pathological and immunohistochemical changes in the first-order neurons in the trigeminal ganglia in Creutzfeldt-Jakob disease (CJD). Degenerative changes consisted of cytoplasmic vacuolation and fenestration, abundant satellite cells, neurofilament accumulation in neurons, and axonal dystrophy with spheroid formation and torpedolike structures arising from the neuronal cytoplasm. Dystrophic axons, axonal spheroids, and some ganglion cells were labeled with monoclonal antibodies to a phosphorylated epitope of neurofilaments (200 kDa). Polyclonal antibodies to purified scrapie-associated fibril/prion protein (molecular weight 27-30 kDa) extracted from scrapie-infected hamster brains, as well as polyclonal and monoclonal antibodies to a synthetic 15-amino acid polypeptide of the 27- to 30-kDa protein, demonstrated variable immunoreactivity with degenerating neurons in the CJD cases, but not in the controls. Furthermore, some of the satellite cells and dystrophic axons were stained by the antibodies to the synthetic peptide. These data indicate that the first-order neurons of the trigeminal ganglia may form a route by which the CJD agent may travel from the brain to the periphery or vice versa. As in other chronic neurodegenerative diseases, disturbances of neuroaxonal transport seem to occur in CJD.

Adult↗
PubMed1989

White matter ultrastructural pathology of experimental Creutzfeldt-Jakob disease in mice.

Creutzfeldt-Jakob disease (CJD), previously regarded as a neurodegenerative disorder strictly of the gray matter, occasionally occurs as a panencephalopathic form which is characterized by severe white matter damage. An ultrastructural study of the white matter pathology in mice experimentally infected with the Fujisaki strain of CJD virus revealed: (1) vacuoles within myelin sheaths, formed by splitting either at the major dense or intraperiod lines, or within axons; (2) macrophages filled with numerous myelin figures, lipid droplets and paracrystalline inclusions; (3) astrocytes actively digesting myelin debris; (4) unusual wrapping of several axons by a common myelin sheath; (5) vesicular degeneration of myelin sheaths; (6) close contact between numerous coated pits and outer myelin lamellae; and (7) proliferation of inner mesaxons. Our data indicate that the damage to myelinated axons in the panencephalopathic type of CJD is accomplished primarily by active degradation of myelin by macrophages and astrocytes and by formation of intra-axonal and intra-myelin vacuoles. The myelin vacuolation is most consistent with that produced by leukolysins released from activated macrophages and astrocytes.

Animals↗
PubMed1989

Scrapie as a model for neuroaxonal dystrophy: ultrastructural studies.

Neuritic degeneration is a prominent ultrastructural feature of scrapie in hamsters. To investigate the morphogenesis of neuritic degeneration, we examined brain tissues from hamsters infected with the 263K strain of scrapie virus and from age-matched controls at varying intervals following intracerebral inoculation. Dystrophic neurites--defined as dendrites, axonal preterminals, and myelinated axons containing mitochondria and pleomorphic, electron-dense inclusion bodies--were found as early as 2 weeks postinoculation. Their numbers increased with the incubation period, and their highest density was observed at the terminal stage of disease. Occasionally, small clusters of these structures formed neuritic plaques. Such dystrophic neurites were only rarely seen in brains of uninfected hamsters. Experimental scrapie thus provides an animal model for human neuroaxonal dystrophies. In addition, since this model allows predictable formation of brain amyloid, it may serve as a model for the study of neuronal aging and Alzheimer's disease.

Animals↗
PubMed1989

Serial ultrastructural studies of scrapie in hamsters.

We report sequential studies of the ultrastructural neuropathology of the subcortical grey matter of hamsters infected with the 263K strain of scrapie virus. Vacuolation in this model develops relatively late in the incubation period, while tubulovesicular structures appear early. Furthermore, neuroaxonal dystrophy, accumulations of branching tubules, and neuronal change consisting of intracytoplasmic "whorls" of proliferating membranes constitute prominent features of scrapie-related neurodegeneration.

Animals↗
PubMed1989

A prospective study of asthma during pregnancy and the puerperium.

Thirty-one asthmatic women recruited in an ante-natal clinic were followed during pregnancy and for six weeks of the puerperium. Subjectively 22 (69%) women considered their asthma to have improved, two were worse and in seven (22%) there was no change. Analysis of peak flow rate, symptoms score and bronchodilator use showed that in ten pregnancies there was improvement in the third trimester and that in 11 there was deterioration in the puerperium. The results suggest that in patients with mild or moderate asthma an improvement is likely to occur during pregnancy, particularly in the last trimester, but that in over one-third there may be a post-natal deterioration. Review of the literature suggests that severe asthmatics are at greater risk of deterioration, particularly late in pregnancy.

Adult↗
PubMed1989

Comparison of a human T-cell lymphotropic virus type I strain from cerebrospinal fluid of a Jamaican patient with tropical spastic paraparesis with a prototype human T-cell lymphotropic virus type I.

The isolation and characterization of a human T-cell lymphotropic retrovirus related to human T-cell lymphotropic virus type I (HTLV-I) from cerebrospinal fluid of a Jamaican patient with tropical spastic paraparesis is described. The virus isolate is a typical type C retrovirus as seen by electron microscopy and is related to prototype HTLV-I isolated from patients with adult T-cell leukemia but is not identical to this prototype HTLV-I as seen by restriction enzyme mapping.

Aged↗
PubMed1989

Isolation and characterization of HTLV-I from symptomatic family members with tropical spastic paraparesis (HTLV-I encephalomyeloneuropathy).

Human T lymphotropic virus type I (HTLV-I) was isolated from peripheral blood- and cerebrospinal fluid-derived mononuclear cells of a 13-y-old boy and from the peripheral blood lymphocytes of both his parents. All three had IgG antibodies to HTLV-I and varying degrees of the clinical features of tropical spastic paraparesis (TSP). The son also had IgM antibodies specific for HTLV-I in his serum. Isolations were successfully made from peripheral blood lymphocytes and cerebrospinal fluid lymphocytes stimulated with interleukin-2 or cocultivated with umbilical cord blood mononuclear cells. Established cell lines contained HTLV-I antigen by immunfluorescence and cell-associated virus by electron microscopy; cells became transformed in vitro as determined by their continuous growth in the absence of exogenous interleukin-2. This boy is the youngest TSP patient known to be reported, and the isolation of HTLV-I from all three family members suggests the causative role of this virus in TSP.

Adult↗
PubMed1989

Epidemic hemorrhagic fever with renal syndrome in Yugoslavia, 1986.

An epidemic of hemorrhagic fever with renal syndrome (HFRS) occurred in Yugoslavia May-November 1986; all Republics and Provinces were involved. Serum samples were received from 260 of 276 persons with symptoms clinically compatible with a diagnosis of HFRS. Presumptive infection with a hantavirus was determined serologically for 161 of these. Many patients with serious clinical pictures, including severe renal insufficiency and shock, were hospitalized; 11 died. Indirect fluorescent antibody tests with antigens of 4 hantaviruses (Hantaan, Fojnica, Puumala, and the Vranica strain of Puumala virus) showed that greater than 1 serotype was circulating during this epidemic. Hantavirus antigens were detected in the lungs of 86 of 302 (28.5%) wild-caught small mammals.

Disease Outbreaks↗
PubMed1989

Hemorrhagic fever with renal syndrome in Yugoslavia: antigenic characterization of hantaviruses isolated from Apodemus flavicollis and Clethrionomys glareolus.

Hantavirus antigens were detected in lung tissues of 8/113 Apodemus flavicollis and 2/17 Clethrionomys glareolus captured in 1984 in Fojnica, a region of Yugoslavia endemic for hemorrhagic fever with renal syndrome; hantavirus antigens were not detected in lung tissues from 126 other mammals collected in Fojnica. Three hantaviruses, 2 from A. flavicollis and 1 from C. glareolus, were isolated directly in Vero E6 cells and were partially characterized. The isolates from A. flavicollis, designated Fojnica virus, were antigenically similar but not identical to Hantaan virus strain 76-118, whereas the isolate from C. glareolus was antigenically indistinguishable from Puumala virus, strain Hällnäs B1. These data are consistent with previous studies that indicate the existence of at least 2 hantavirus serotypes in Yugoslavia.

Animals↗
PubMed1988

Intracerebral inoculation of experimental animals with brain tissue from patients with schizophrenia. Failure to observe consistent or specific behavioral and neuropathological effects.

To test the possibility that some cases of schizophrenia result from infection with a transmissible slow viral agent, 57 experimental animals (six chimpanzees, 12 Old World monkeys, 17 New World monkeys, and 22 guinea pigs) were inoculated intracerebrally with brain tissue from ten patients and followed up for six years. Behavioral comparisons with control animals revealed no consistent behavioral differences. Histological, immunohistochemical, and morphometric examination of brains of animals that died revealed no specific neuropathological abnormalities. These findings do not support a role for a virus-induced slow infection in the pathogenesis of schizophrenia but must be weighed against methodological limitations in animal susceptibility, disease communicability, and assay sensitivity.

Adult↗
PubMed1988

The role of HTLV-I in tropical spastic paraparesis in Jamaica.

We report clinical and laboratory investigations of 47 native-born Jamaican patients with endemic tropical spastic paraparesis and of 1 patient with tropical ataxic neuropathy. Mean age at onset was 40 years, with a female-male preponderance (2.7:1). Neurological features of endemic tropical spastic paraparesis are predominantly those of a spastic paraparesis with variable degrees of proprioceptive and/or superficial sensory impairment. Using enzyme-linked immunoabsorbent assay (ELISA), IgG antibodies to human T-lymphotropic virus type I (HTLV-I) were present in 82% of sera and 77% of cerebrospinal fluids. On Western blot analysis, IgG antibodies detected the p19 and p24 gag-encoded core proteins in both serum and cerebrospinal fluid. Titers were tenfold higher by ELISA in serum than in cerebrospinal fluid, and some oligoclonal bands present in fluid were not seen in serum. Serum-cerebrospinal fluid albumin ratios were normal, and IgG indexes indicated intrathecal IgG synthesis. Histopathological changes showed a chronic inflammatory reaction with mononuclear cell infiltration, perivascular cuffing, and demyelination that was predominant in the lateral columns. In 1 patient, a retrovirus morphologically similar to HTLV-I on electron microscopy was isolated from spinal fluid. Our investigations show that endemic tropical spastic paraparesis in Jamaica is a retrovirus-associated myelopathy and that HTLV-I or an antigenically similar retrovirus is the causal agent.

Adolescent↗
PubMed1988

Spastic paraparesis and HTLV-I infection in Peru.

Three of 6 patients with spastic paraparesis in Lima, Peru, were found to have antibodies to human T-lymphotropic virus type I (HTLV-I). Blood and cerebrospinal fluid antibodies were confirmed by Western blot analysis. Multilobulated lymphocytes in blood and cerebrospinal fluid of the index case stained with monoclonal antibodies for T-helper cells and for T10, an activation marker. Blood mononuclear cells from patients with HTLV-I-associated myelopathy showed spontaneous proliferation in culture, evidence of interleukin-2 receptors, and decreased natural killer cell activity.

Adult↗
PubMed1988

Epidemiology of tropical spastic paraparesis in Columbia and associated HTLV-I infection.

The clinical syndrome earlier designated as paraparesia espástica del Pacífico is an isolated form of tropical spastic paraparesis (TSP) that was reported in 1981 in the southern Pacific lowlands of Columbia in and near Tumaco. The clinical features are similar to those of TSP reported in Jamaica, Martinique, the Seychelles, and the Ivory Coast of Africa and resemble also those clinical features of the human T-lymphotropic virus type I (HTLV-I)-associated myelopathy described in southern Japan. Since HTLV-I infection is closely associated with TSP, we conducted a case-control study to evaluate the role of HTLV-I-associated risk factors among patients from the endemic focus in Tumaco, Colombia, and the seroprevalence rates of this virus in other geographical areas of the Pacific Colombian lowlands with and without TSP. From our seroprevalence study of antibodies to HTLV-I among TSP index patients, matched controls, household contacts (first- and second-degree relatives), and healthy controls from these areas, we found a strong association between HTLV-I and TSP. Also, there is a high seroprevalence of HTLV-I among sexual partners of patients and to a lesser extent among their offspring and other relatives some of whom had an early mean acquisition of antibodies to HTLV-I. Heterosexual promiscuity and other close interpersonal contact may play an important role in the transmission of TSP in the Pacific lowlands of Colombia.

Adolescent↗
PubMed1988

HTLV-I-like viral particles in spinal cord cells in Jamaican tropical spastic paraparesis.

Viral-like particles morphologically identical to human T-lymphotropic virus type I or II, but distinct from human T-lymphotropic virus type III, have been seen by electron microscopy in spinal cord tissue from a Jamaican tropical spastic paraparesis patient who was known to be positive for human T-lymphotropic virus I antibody before death. This is the first electron microscopy report on a patient from an endemic tropical spastic paraparesis region.

Adult↗