BSE infection in bovine PrP transgenic mice leads to hyperphosphorylation of tau-protein.

We observed the changes in the central nervous system (CNS) of transgenic mice expressing bovine prion protein (Bo-PrP) as a contribution to our knowledge of the pathogenesis of bovine spongiform encephalopathy (BSE). The main result was the detection of hyperphosphorylated tau. This protein was detected for the first time, using immunohistochemical techniques, in the neurons and glial cells of mice experimentally infected with BSE. The results highlighted the involvement of tau protein in the pathogenesis of BSE and the close link between hyperphosphorylated tau deposits and prion protein. Ultrastructural examination revealed a novel arrangement of intraneuronal tau deposits not hitherto reported

BSE infection in bovine PrP transgenic mice leads to hyperphosphorylation of tau-protein.

We observed the changes in the central nervous system (CNS) of transgenic mice expressing bovine prion protein (Bo-PrP) as a contribution to our knowledge of the pathogenesis of bovine spongiform encephalopathy (BSE). The main result was the detection of hyperphosphorylated tau. This protein was detected for the first time, using immunohistochemical techniques, in the neurons and glial cells of mice experimentally infected with BSE. The results highlighted the involvement of tau protein in the pathogenesis of BSE and the close link between hyperphosphorylated tau deposits and prion protein. Ultrastructural examination revealed a novel arrangement of intraneuronal tau deposits not hitherto reported

TCE abatement with a plasma-catalytic combined system using MnO2 as catalyst

A

Neuropathologic study of experimental classical swine fever.

The aim of this study was to report on the lesions occurring in the central nervous system (CNS) during experimental classical swine fever (CSF) to clarify the spatial and chronologic distribution of the lesions and virus antigen in the CNS. To learn more about the pathogenetic mechanisms of the lesions during CSF in the CNS and to investigate the role of the virus in these mechanisms, cellular infiltrates and infected cells have been characterized. Twenty-eight pigs were inoculated with the virulent CSF virus isolate Alfort 187 and slaughtered from 2 to 15 postinoculation days; 4 animals of similar background served as a control group. Immunohistochemistry, electron microscopy, and the transferase-mediated deoxyuridine triphosphate nick-end labeling method were used to detect viral antigens and apoptosis. The results showed the presence of nonpurulent meningoencephalitis, occasional microhemorrhages, and apoptosis of the lymphocytes forming the perivascular and interstitital infiltrate in swine with CSF. Macrophages appeared to display little involvement in CNS lesions. The infected cells observed at the early stage of disease were lymphocytes and microglial cells in the rostral portion of the telencephalon, with infection of these cells in other areas in the next stages. The relationship between these lesions and the presence of viral antigen varied according to the type of lesion: hemorrhages were not associated with the presence of antigen in endothelial cells, but infiltrate-cell apoptosis was temporally and spacially associated to viral infection. However, the link between viral infection and the presence of cell infiltrate was far from clear

Neuropathologic study of experimental classical swine fever.

The aim of this study was to report on the lesions occurring in the central nervous system (CNS) during experimental classical swine fever (CSF) to clarify the spatial and chronologic distribution of the lesions and virus antigen in the CNS. To learn more about the pathogenetic mechanisms of the lesions during CSF in the CNS and to investigate the role of the virus in these mechanisms, cellular infiltrates and infected cells have been characterized. Twenty-eight pigs were inoculated with the virulent CSF virus isolate Alfort 187 and slaughtered from 2 to 15 postinoculation days; 4 animals of similar background served as a control group. Immunohistochemistry, electron microscopy, and the transferase-mediated deoxyuridine triphosphate nick-end labeling method were used to detect viral antigens and apoptosis. The results showed the presence of nonpurulent meningoencephalitis, occasional microhemorrhages, and apoptosis of the lymphocytes forming the perivascular and interstitital infiltrate in swine with CSF. Macrophages appeared to display little involvement in CNS lesions. The infected cells observed at the early stage of disease were lymphocytes and microglial cells in the rostral portion of the telencephalon, with infection of these cells in other areas in the next stages. The relationship between these lesions and the presence of viral antigen varied according to the type of lesion: hemorrhages were not associated with the presence of antigen in endothelial cells, but infiltrate-cell apoptosis was temporally and spacially associated to viral infection. However, the link between viral infection and the presence of cell infiltrate was far from clear

Evaluation of phenylene-bridged periodic mesoporous organosilica as a stationary phase for solid phase extraction

A