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R Yanagihara

Publications and source records attributed to R Yanagihara.

At least 109 records · Page 6Linked to original sources
PubMed1991

Amyloid beta-protein in cerebral amyloid angiopathy, senile plaques, and preamyloidotic lesions in subcortical arteriosclerotic encephalopathy (Binswanger disease).

Cerebral vascular amyloid deposits, senile plaques and neurofibrillary tangles have been found in subcortical arteriosclerotic encephalopathy (Binswanger disease). A mouse antiserum, prepared against a 43-amino acid synthetic peptide homologous to the amyloid beta-protein of Alzheimer disease (anti-SP43), revealed immunoreactive amyloid deposits in meningeal and intracortical blood vessels, senile plaques, intraneuronal amyloid and preamyloid in a neuropathologically confirmed case of Binswanger disease previously reported to have cerebral vascular amyloid deposits. These lesions contained sulfated glycosaminoglycans as determined by the Alcian blue/critical electrolyte concentration method. Similar findings were not observed in a case of Binswanger encephalopathy without cerebral amyloid deposits. Our study indicates that amyloidotic lesions in Binswanger encephalopathy with cerebral amyloid deposits contain amyloid beta-protein and sulfated glycosaminoglycans.

Amyloid beta-Peptides↗
PubMed1991

Characterization of a variant of human T-lymphotropic virus type I isolated from a healthy member of a remote, recently contacted group in Papua New Guinea.

We report the characterization of a variant of human T-lymphotropic virus type I (HTLV-I) isolated from an interleukin 2-dependent, CD8+ T-cell line derived from peripheral blood mononuclear cells of a healthy member of a remote, recently contacted hunter-horticulturalist group (Hagahai) in Madang province of Papua New Guinea. Antigenic characterization of this variant, designated PNG-1, by immunofluorescence, indicated no expression of gag-encoded proteins p19 and p24 (even after incubation with 5-bromo-2'-deoxyuridine), using monoclonal and polyclonal antibodies against HTLV-I gag gene products. Virus-specific proteins of 15, 19, 46, 53, and 61/68 kDa were demonstrated by Western blot analysis, using sera from patients with serologically and/or virologically confirmed HTLV-I myeloneuropathy, sera from HTLV-I-infected rabbits, and antibodies prepared against the C terminus of the major envelope glycoprotein gp46. Restriction endonuclease maps of PNG-1 proviral DNA differed from that of a prototype strain of HTLV-I (MT-2), but, as verified by polymerase chain reaction, PNG-1 was definitely HTLV-I, not HTLV-II. Nucleotide sequencing and further molecular genetic studies of this variant may provide insights into the origin and evolution of HTLV-I.

Cells, Cultured↗
PubMed1991

Detection of hantavirus RNA in tissues of experimentally infected mice using reverse transcriptase-directed polymerase chain reaction.

Detection of hantaviruses, the etiological agents of hemorrhagic fever with renal syndrome (HFRS), by virus isolation using experimental animals or cell culture is time-consuming. A more rapid but equally specific method is needed. We used a reverse transcriptase-directed polymerase chain reaction (RT-PCR) to detect hantavirus genomic sequences and compared its sensitivity with conventional virus isolation. RNA, extracted by the guanidinium isothiocyanate-cesium chloride method from hantavirus-infected Vero E6 cells and from tissues of infant mice inoculated intracerebrally with 100 LD50 of hantavirus, was initially reverse transcribed using avian myeloblastosis virus reverse transcriptase. The resulting complementary DNA (cDNA) was used as template to amplify the glycoprotein 2-encoding region of the hantavirus M segment. With this method, Vero E6 cell cultures infected with Hantaan virus strains 76-118 (prototype) and HV114 (an isolate from the urine of an HFRS patient in China) were positive, while control cultures were negative. Brain, lung, and heart tissues from hantavirus-infected mice were positive by RT-PCR at 5, 8, and 11 days after intracerebral inoculation. The specificity of the positive results was confirmed by restriction endonuclease digestion of the amplified fragments with AluI and HpaI. The sensitivity of the RT-PCR was equal to cell culture amplification but required less time. This method is being adapted for detection of hantavirus genomic sequences in clinical specimens and postmortem tissues from patients with HFRS.

Animals↗
PubMed1991

Mechanism of the damage to myelinated axons in experimental Creutzfeldt-Jakob disease in mice: an ultrastructural study.

We report the ultrastructural pathology of myelinated axons in mice infected experimentally with the Fujisaki strain of Creutzfeldt-Jakob disease (CJD). Initially the myelin sheath was separated into several concentric bands, and cellular processes penetrated between layers of myelin and lifted away the outermost lamella. Then a complicated labyrinth of the concentric cellular processes, clearly belonging to either astrocytes or macrophages, invested myelinated axons. In terminal stages axons completely denuded of myelin were seen in the center of concentric networks of cellular processes. Myelin remnants were seen within astrocytes and macrophages. We conclude that the mechanism(s) of damage to myelinated axons in CJD may be similar to that operating in immunologically mediated demyelinating disorders.

Animals↗
PubMed1991

Localization of amyloidogenic proteins and sulfated glycosaminoglycans in nontransmissible and transmissible cerebral amyloidoses.

We report the localization of amyloid beta-protein and sulfated glycosaminoglycans in senile plaques and vascular amyloid deposits in brain tissues from patients with Down's syndrome and Alzheimer's disease, and in neurofibrillary tangles of these diseases and those of Guamanian parkinsonism-dementia and amyotrophic lateral sclerosis. We also report the immunolocalization of scrapie amyloid in amyloid plaques containing glycosaminoglycans in kuru, Creutzfeldt-Jakob disease, and Gerstmann-Sträussler's syndrome. Thus, amyloidogenic proteins and sulfated glycosaminoglycans may be copolymerized in amyloid deposits in the nontransmissible and transmissible cerebral amyloidoses.

Adult↗
PubMed1991

N-butyl benzenesulfonamide: a neurotoxic plasticizer inducing a spastic myelopathy in rabbits.

N-Butyl benzenesulfonamide (NBBS), a plasticizer used commercially in the polymerization of polyamide compounds, is neurotoxic. Young adult New Zealand white rabbits, inoculated repeatedly with NBBS by the intracisternal or intraperitoneal routes, developed a dose-dependent motor dysfunction characterized by limb splaying, hyperreflexia, hypertonia, gait impairment, and abnormal righting reflexes. Histopathological changes consisted of intramedullary thickening of the ventral horn axons, random neuroaxonal spheroids confined to brain stem nuclei and spinal motor neurons, and swollen dendritic processes of spinal motor neurons. Immunoreactivity to a monoclonal antibody against microtubule-associated protein-2 (MAP-2) was markedly increased in the dendrites of spinal motor neurons following thrice weekly intraperitoneal inoculations of NBBS for 4 months, whereas after 12 monthly intracisternal inoculations, MAP-2 immunoreactivity was absent or strikingly reduced in the same neuronal populations. Ultrastructurally, postsynaptic zones contained vacuoles and multilamellar bodies. These findings raise questions about the safety of NBBS to humans.

Animals↗
PubMed1991

Topographic distribution of scrapie amyloid-immunoreactive plaques in chronic wasting disease in captive mule deer (Odocoileus hemionus hemionus).

Chronic wasting disease (CWD), a progressive neurological disorder of captive mule deer, black-tailed deer, hybrids of mule deer and white-tailed deer and Rocky Mountain elk, is characterized neuropathologically by widespread spongiform change of the neuropil, intracytoplasmic vacuolation in neuronal perikarya and astrocytic hypertrophy and hyperplasia. We report the topographic distribution of amyloid plaques reactive to antibodies prepared against scrapie amyloid in CWD-affected captive mule deer (Odocoileus hemionus hemionus). Scrapie amyloid-immunoreactive plaques were found in the cerebral gray and white matter, in deep subcortical nuclei, in isolation or in clusters in areas of vacuolation, and perivascularly, in subpial and subependymal regions. In the cerebellum, immunoreactive amyloid plaques were observed in the molecular, pyramidal and granular layers. Scrapie amyloid-immunoreactive deposits were also seen in neuronal perikarya. Furthermore, amyloid plaques in CWD-affected captive mule deer were alcianophilic at 0.3 M magnesium chloride indicating the presence of weakly to moderately sulfated glycosaminoglycans. Our data corroborate that CWD in captive mule deer belongs to the subacute virus spongiform encephalopathies.

Alcian Blue↗
PubMed1991

Comparison between strains of human T lymphotropic virus type I isolated from inhabitants of the Solomon Islands and Papua New Guinea.

Strains of human T lymphotropic virus type I (HTLV-I) isolated from T cell lines (SI-1, SI-3, and SI-5) from three individuals in separate regions of the Solomon Islands were compared with a variant (PNG-1) isolated from a healthy person in Papua New Guinea and a prototype strain from Japan (MT-2). The SI-1, SI-3, and SI-5 cell lines were predominantly CD8+. Expression of gag- and env-encoded virus-specific proteins was detected in SI-1, SI-3, and SI-5 and in MT-2 cells by immunofluorescence and Western immunoblot; gag proteins p19 and p24 were absent in PNG-1 cells. HTLV-1 gag and pol gene sequences were detected in DNA extracted from SI-1, SI-3, and SI-5 cells by polymerase chain reaction; env sequences were not found in SI-5 cells. Genomic Southern analysis of PstI digests of SI-1, SI-3, and SI-5 DNA exhibited the three moderate-sized fragments typical of prototype HTLV-I. By contrast, PstI digests of PNG-1 DNA yielded two larger fragments.

Adult↗
PubMed1991

Verification of HTLV-I infection in the Solomon Islands by virus isolation and gene amplification.

We report the detection of human T-lymphotropic virus type I (HTLV-I) genomic sequences by polymerase chain reaction in lymphocyte cultures of three unrelated native Solomon Islanders, including a patient with HTLV-I myeloneuropathy, residing in widely separated regions. In addition, we have isolated HTLV-I from T-cell lines derived from two of these individuals. Virus-specific proteins of 15, 19, 24, 46 and 53 kilodaltons were detected by immunofluorescence and Western immunoblot, using serum from a Colombian patient with HTLV-I myeloneuropathy, sera from HTLV-I-infected rabbits, and monoclonal and polyclonal antibodies against HTLV-I gag and env gene products. Amplification of HTLV-I gag, pol and env sequences by polymerase chain reaction confirmed that the viral isolates were HTLV-I, not HTLV-II. Our data clearly demonstrate that HTLV-I does exist in Melanesia. Although the Solomon Islands viral isolates resemble prototype strains of HTLV-I, we believe they represent variants of HTLV-I, particularly in the light of our recent isolation of an HTLV-I variant from Papua New Guinea. Nucleotide sequence analysis of these viral strains, now in progress, should clarify the molecular epidemiology and phylogeny of HTLV-I.

Adult↗
PubMed1991

Prevalence of human T-cell lymphotropic virus type I infection in Singapore: a preliminary report.

Human T-cell lymphotropic virus type I (HTLV-I) infection is endemic in southwestern Japan, the Caribbean basin, Colombia, Africa and in several isolated populations in Papua New Guinea, the Solomon Islands and Vanuatu. To determine the seroprevalence of HTLV-I infection in Singapore, we tested sera from 115 hospitalized patients with acute nephritis, 50 patients with suspected leptospirosis, 34 patients with non-A, non-B hepatitis, and from 28 healthy volunteers for IgG antibodies against HTLV-I using an enzyme-linked immunosorbent assay. Antibodies were detected in sera from 6 of the 199 patients and from 3 of the 28 healthy volunteers, but these positives could not be confirmed by Western immunoblotting. Our data are consistent with other reports of low seroprevalence of HTLV-I infection despite extensive Japanese contact in Korea, Taiwan, the People's Republic of China and Micronesia. Further studies on a larger sample size, however, are necessary to confirm the absence of any focus of infection in the Singapore population.

Adolescent↗
PubMed1991

Human T-lymphotropic virus type I infection in the Solomon Islands.

To ascertain the prevalence of human T-lymphotropic virus type I (HTLV-I) infection and the occurrence of diseases caused by HTLV-I in the Solomon Islands, we tested 1141 sera from 851 patients (317 females and 534 males), who were hospitalized at the Central Hospital in Honiara between February 1984 and November 1988, for antibodies to HTLV-I using an enzyme-linked immunosorbent assay (ELISA). Sera from 69 of 81 ELISA-positive patients and from 56 ELISA-negative patients were then tested by Western analysis. As verified by strict Western immunoblot criteria, the overall HTLV-I seroprevalence was 2.2% (19/851). Age- and gender-specific prevalence data indicated an age-related acquisition of infection with no sexual predominance. No diagnosis category was over-represented among the seropositive patients. HTLV-I-specific antibodies were found in serum and cerebrospinal fluid samples from one of six patients with spastic paraparesis. As in other Melanesian populations, the majority of ELISA-positive sera could not be confirmed by Western analysis. Reactivity to three or more gag-encoded proteins was found in 85% (45/53) of ELISA-positive, Western blot-indeterminate sera, and 30% (16/53) reacted to p19 and an env gene product but lacked reactivity to p24. Whether or not the high frequency of indeterminate HTLV-I Western immunoblots in the Solomon Islands is indicative of incomplete specific reactivity to HTLV-I or the existence of antigenically related retroviruses is being investigated.

Adolescent↗
PubMed1991

Experimental Creutzfeldt-Jakob disease: light microscopic, immunohistochemical and ultrastructural studies of the Fujisaki strain of Creutzfeldt-Jakob disease virus in NIH Swiss mice.

Ultrastructural findings in mice terminally affected with the Fujisaki strain of Creutzfeldt-Jakob disease virus are reported. Spongiform vacuolation, extensive myelin and axonal lesions and neuroaxonal dystrophy accompanied by abundant astrocytic gliosis comprise the pattern of the pathological changes at the ultrastructural level. Neuronal intranuclear inclusions and swelling of the astrocytic and dendritic processes were unspecific findings also observed in control animals.

Animals↗
PubMed1990

Appearance of tubulovesicular structures in experimental Creutzfeldt-Jakob disease and scrapie precedes the onset of clinical disease.

We have consistently observed tubulovesicular structures in brain tissues during the terminal stages of naturally occurring and experimentally induced spongiform encephalopathies, irrespective of the host species and virus strain. In NIH Swiss mice inoculated intracerebrally or intraocularly with the Fujisaki strain of Creutzfeldt-Jakob disease (CJD) virus, tubulovesicular structures, measuring 20-50 nm in diameter, were particularly prominent in dilated, pre- and postsynaptic neuronal processes, occasionally being mixed with synaptic vesicles. These structures appeared 13 weeks following intracerebral inoculation, 5 weeks before the onset of clinical signs, when spongiform changes were also detected. The number and density of tubulovesicular structures increased steadily during the course of clinical disease, and were particularly abundant in mice 47 to 51 weeks after intraocular inoculation. In hamsters infected with the 263 K strain of scrapie virus, these structures were initially detected 3 weeks following intracerebral inoculation and increased dramatically at 10 weeks postinoculation. The appearance of tubulovesicular structures before the onset of overt disease in mice inoculated with CJD virus by either the intracerebral or intraocular route, and before the appearance of other neuropathological changes in hamsters infected with scrapie virus, indicate that they represent either a part or aggregate of the infectious virus or a pathological product of the infection.

Animals↗