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R Yanagihara

Publications and source records attributed to R Yanagihara.

At least 127 records · Page 7Linked to original sources
PubMed1990

Spread of Creutzfeldt-Jakob disease virus along visual pathways after intraocular inoculation.

We studied the targeting of spongiform lesions within the visual pathways after intraocular injection with the Fujisaki strain of Creutzfeldt-Jakob disease (CJD) virus. The first lesions were observed 18 weeks postinoculation in the most superficial layer of the superior colliculus and in the lateral geniculate body contralateral to the side of the inoculation. Asymmetrical lesions in the superior colliculus were found also in mice sacrificed at 19, 22, and 27 weeks postinoculation. These results demonstrate that CJD virus spreads within the CNS via central axons of the visual pathways following intraocular inoculation.

Animals↗
PubMed1990

Experimental infection of human vascular endothelial cells by pathogenic and nonpathogenic hantaviruses.

To investigate whether the hantaviruses replicate in endothelial cells, we inoculated human umbilical vein endothelial cells with several pathogenic and nonpathogenic strains of hantavirus. Intracytoplasmic, virus-specific granular fluorescence was detected initially at three days postinoculation and nearly 100% of cells contained viral antigen at 10 days. Cytopathic effect or inclusion bodies were not observed. The in vitro demonstration of the susceptibility of endothelial cells to hantaviruses corroborates in vivo findings, and suggests that endothelial cells may serve as target cells in hemorrhagic fever with renal syndrome.

Animals↗
PubMed1990

Reevaluation of the ultrastructural pathology of experimental Creutzfeldt-Jakob disease. Serial studies of the Fujisaki strain of Creutzfeldt-Jakob disease virus in mice.

We describe the serial ultrastructural pathology of experimental Creutzfeldt-Jakob disease (CJD) in mice. Spongiform vacuoles, widespread myelin and axonal pathology, accompanied by abundant macrophagic reaction and neuroaxonal dystrophy, were consistently found in mice infected with CJD virus. By contrast, intranuclear vacuolation and swelling of astrocytic and neuronal processes were nonspecific changes that also occurred in control animals. We conclude that CJD-related neuropathological phenomena do not accumulate gradually through the incubation period but develop relatively abruptly and in complete form.

Animals↗
PubMed1990

Human T lymphotropic virus type I infection in Papua New Guinea: high prevalence among the Hagahai confirmed by western analysis.

A serologic survey for human T lymphotropic virus type I (HTLV-I) infection was conducted on nearly half of the entire 260-member Hagahai population, a hunter-horticulturist group occupying the northern banks of the Yuat River Gorge in Madang Province of Papua New Guinea. For comparison, sera from two neighboring groups, the Pinai and Haruai, were tested. As determined by enzyme-linked immunosorbent assay (ELISA) and verified by Western immunoblot, IgG antibodies against HTLV-I were detected in 17 of 120 Hagahai, giving an HTLV-I seroprevalence of 14%, which is as high as that found in HTLV-I-endemic regions such as southwestern Japan and the Caribbean basin. Infection tended to cluster in family groups and was more common with increasing age. The majority of ELISA-positive (45/61) Hagahai sera were indeterminate, with 62% (28/45) exhibiting reactivity to three or more gag-encoded proteins. The clinical significance of the high frequency of indeterminate HTLV-I Western immunoblots is unknown, but it is not unlike that encountered in other Melanesian populations. Whether this reflects incomplete specific reactivity to HTLV-I or the existence of HTLV-I-related retroviruses in Papua New Guinea is being investigated.

Age Factors↗
PubMed1989

Bone mass in Guamanian patients with amyotrophic lateral sclerosis and parkinsonism-dementia.

Bone mass, as assessed by measurements of total subperiosteal diameter and medullary width of the second metacarpal bone on hand-wrist radiographs, was evaluated for 31 Guamanian patients (15 males, 16 females) with amyotrophic lateral sclerosis (ALS), 67 patients (39 males, 28 females) with parkinsonism-dementia (PD), and 66 (34 males, 32 females) nonaffected Guamanian controls. Comparisons between the two disease groups and between each disease group and the nonaffected controls were made taking into account the sex, age, and disability status of each participant. At all ages, ALS patients of both sexes had significantly lower percent cortical areas (PCA) than did nonaffected controls. The ALS males also had significantly lower PCA than PD males, although no significant differences were observed between female ALS and PD patients. The PD patients of either sex had a lower PCA when compared to controls, but the differences were not statistically significant. The observed differences in PCA were due solely to increased medullary width, suggesting that the diminished cortical bone thickness resulted from greater bone resorption rather than differential bone growth. Longitudinal studies support the cross-sectional findings of accelerated bone loss among ALS patients. It is not possible to determine from the present data whether the observed differences in PCA of the second metacarpal of the ALS patients are due to atrophy of the first interosseous muscle, to a generalized resorption process inherently associated with the development and progression of ALS, or to factors not accounted for by the present analysis.

Adult↗
PubMed1989

Immunocytochemical characterization of neurofibrillary tangles in amyotrophic lateral sclerosis and parkinsonism-dementia of Guam.

Cryostat-cut sections of formalin-fixed and unfixed hippocampus from 23 Guamanian Chamorros with clinically and neuropathologically verified amyotrophic lateral sclerosis (ALS) (8 cases) and parkinsonism-dementia (PD) (15 cases) and from 12 neurologically normal Guamanians (5 with and 7 without neurofibrillary degeneration) were evaluated by the immunoperoxidase technique, using monoclonal antibodies against phosphorylated neurofilament, human fetal microtubule-associated protein tau, and paired helical filaments. On immunostaining, all three antibodies showed intracellular tangles in the hippocampal neurons of patients with ALS, patients with PD, and in neurologically normal Guamanians with neurofibrillary pathology, but the correlation of immunostaining between these antibodies was not absolute. Extracellular or ghost tangles were immunostained only with the antibody against paired helical filaments. Our immunocytochemical data indicate that the antigenic composition of neurofibrillary tangles in Guamanian ALS and PD is similar to that of Alzheimer's disease, suggesting a common pathogenetic pathway for neurofibrillary tangle formation in these neurodegenerative disorders.

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

Low-calcium, high-aluminum diet-induced motor neuron pathology in cynomolgus monkeys.

Long-term epidemiological studies indicate that environmental factors play a causative role in high-incidence amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia (PD) in the western Pacific. An increased risk for disease is acquired in youth and remains for life. The low concentrations of calcium and magnesium and high levels of aluminum in the soil and drinking water, along with the relative isolation of these populations, constitute an unusual environmental feature common to all three high-incidence foci. Studies of mineral deposition in brain tissue of Guamanian ALS and PD patients, as well as of neurologically normal Guamanians with neurofibrillary degeneration, demonstrate accumulations of calcium, aluminum and silicon in neurofibrillary tangle-bearing neurons. In an attempt to duplicate the low calcium and high aluminum and manganese in soil and drinking water in these foci, we maintained juvenile cynomolgus monkeys for 41 to 46 months on a low-calcium diet with or without supplemental aluminum and manganese. Experimental animals exhibited mild calcium and aluminum deposition and degenerative changes, compatible with those of early ALS and PD, in motor neurons of the spinal cord, brain stem, substantia nigra and cerebrum. Neuropathological findings included chromatolysis, aberrant perikaryal accumulation of phosphorylated neurofilament, neurofibrillary tangles, axonal spheroids, and basophilic and hyaline-like inclusions consisting of abnormal cytoskeletal elements by electron microscopy. The magnitude and extent of these lesions far exceeded those found in normal aged monkeys.

Aluminum↗
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

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

Seroprevalence of antibodies to HTLV-I in patients with chronic neurological disorders other than tropical spastic paraparesis.

Human T-lymphotropic virus type I (HTLV-I), the etiological agent of adult T-cell leukemia/lymphoma, also appears to be the cause of tropical spastic paraparesis, a chronic myelopathy reported in several different regions of the world. The prevalence of antibodies to HTLV-I in patients with chronic neurodegenerative disorders other than tropical spastic paraparesis and in patients with some muscle inflammatory disorders has been investigated. IgG antibodies to HTLV-I were measured in the sera and/or cerebrospinal fluid from 82 Guamanian patients with amyotrophic lateral sclerosis and parkinsonism-dementia, 164 Guamanian normal controls, 10 patients with kuru from the Eastern Highlands of Papua New Guinea, 4 patients with Viliuisk encephalomyelitis from the Iakut region of eastern Siberia, 45 Italian patients with multiple sclerosis, and 56 patients with polymyositis (49 from the United States and 7 from Jamaica). As determined by enzyme-linked immunosorbent assay, Western immunoblot, and gelatin particle agglutination techniques, serological evidence of HTLV-I infection was found in 1 patient with amyotrophic lateral sclerosis and 1 control subject from Guam, and in 1 patient from the United States and all 7 Jamaican patients with polymyositis. Except for the high seropositivity rate among the group of Jamaican patients with polymyositis, our data indicate that HTLV-I is an unlikely causative agent in the spectrum of the neurological diseases examined. The seropositivity of the 7 Jamaican patients with polymyositis requires further study.

Adult↗
PubMed1988

Histochemical and X-ray microanalytical localization of aluminum in amyotrophic lateral sclerosis and parkinsonism-dementia of Guam.

Histochemical staining for aluminum, using Solochrome azurine or Morin, provided a rapid, simple and reliable means of identifying areas and structures of the brain of interest for closer scrutiny by X-ray microanalysis in patients with amyotrophic lateral sclerosis and parkinsonism-dementia of Guam. Neuronal perikarya, dendritic processes, and the walls of some cerebral vessels were aluminum positive by Solochrome azurine staining. In some cases, the deposition of aluminum was rather diffuse, particularly in the white matter. Fluorescent localization of aluminum using Morin was equally sensitive and specific, but provided less morphological detail than Solochrome azurine. Confirmation of histochemical detection of aluminum was achieved by examining adjacent tissue sections using wavelength-dispersive spectrometry coupled to a computer-controlled electron beam X-ray microprobe. Although the minimum detectable limits for aluminum by these histochemical procedures are unknown, the lower detection limit of our X-ray microanalytical technique is 10-100 ppm dry weight. Solochrome and Morin staining, as verified by X-ray microanalysis, afford a useful and reliable means of surveying multiple anatomical regions for aluminum deposition in naturally occurring and experimentally induced neurodegenerative disorders.

Adolescent↗
PubMed1988

Experimental hantavirus infection in nonhuman primates.

Mild, transient proteinuria and azotemia were produced in three cynomolgus monkeys (Macaca fascicularis) and a chimpanzee (Pan troglodytes) following intravenous inoculation with Prospect Hill virus, a hantavirus isolated from meadow voles in the United States. This is the first demonstration of an acute nephropathy in nonhuman primates with the viruses causing hemorrhagic fever with renal syndrome.

Animals↗
PubMed1988

Serological evidence of hantavirus infection in laboratory rats and personnel.

Laboratory-acquired haemorrhagic fever with renal syndrome (HFRS) has been reported in many countries. A serological survey of laboratory white rats and of laboratory personnel for antibodies to hantaviruses was conducted in Singapore. Forty-four per cent (143/329) of rats were seropositive by the indirect immunofluorescent antibody test but none had hantaviral antigens in lung tissues. Two of 74 laboratory personnel were seropositive but neither had a history of clinical illness. The high seropositivity rate among laboratory rats led to their replacement with Hantaan virus-free strains. To eliminate the hazard of laboratory-acquired HFRS, regular serological screening of laboratory rats and replacement of infected animals with seronegative stocks should be implemented. High risk techniques with laboratory rats, which are likely to generate aerosols, should be performed in biological safety cabinets. Serological surveillance of laboratory personnel and reporting of suspected HFRS cases are useful in the early detection of hantavirus infection.

Animals↗