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Parenteral ivermectin in Strongyloides hyperinfection

A Tamaoka, A Shimohata, Akihide Mochizuki

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Abstract

embedded sections (5 m) from different brain regions were stained with haematoxylin-eosin, Kluver-Barrera, and the modified Bielschowsky silver method for histology. All cases of Alzheimer’s disease met standard pathological criteria for definite Alzheimer’s disease. 3 Many neurofibrillary tangles appeared diffusely from a medial part of the temporal lobe to the association cortices of frontal and parietal lobes. In the middle frontal cortex the density was at most 12 counts in one case, and usually one to two counts per microscopic (200) field in the others. There was mild neuronal cell loss with astrocytosis. Frozen sections (40 m) taken from the middle frontal gyrus were immunostained with mouse monoclonal end-specific antibodies against free C-termini of A40 (BA27) and A42 (BC05), 2 and with monoclonal antibodies against C-termini and N-termini of -amyloid precursor protein (clone 2.F2.19B4 and 22C11, respectively, Boehringer Mannheim, Mannheim, Germany), by the avidin-biotin-peroxidase procedure. Amyloid plaques stained with the modified Bielschowsky silver method were seen in the cerebral cortex of the brains of patients with Alzheimer’s disease but not in the normal control brains. The core type of amyloid plaque was immunostained with BA27, whereas both core and diffuse types were positive for BC05. In addition, A42 immunoreactivity was strongly positive in the cytoplasm and the cell processes of some cells only in the brains of patients with Alzheimer’s disease (figure). These A42-positive cells were seen mainly in the second to fourth layers of the cortex and had small and round cytoplasm in comparison with the pyramidal neurons seen in the third and fifth layers of the cortex. Some of the A42-positive cells were located inside and some adjacent to

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embedded sections (5 m) from different brain regions were stained with haematoxylin-eosin, Kluver-Barrera, and the modified Bielschowsky silver method for histology. All cases of Alzheimer’s disease met standard pathological criteria for definite Alzheimer’s disease. 3 Many neurofibrillary tangles appeared diffusely from a medial part of the temporal lobe to the association cortices of frontal and parietal lobes. In the middle frontal cortex the density was at most 12 counts in one case, and usually one to two counts per microscopic (200) field in the others. There was mild neuronal cell loss with astrocytosis. Frozen sections (40 m) taken from the middle frontal gyrus were immunostained with mouse monoclonal end-specific antibodies against free C-termini of A40 (BA27) and A42 (BC05), 2 and with monoclonal antibodies against C-termini and N-termini of -amyloid precursor protein (clone 2.F2.19B4 and 22C11, respectively, Boehringer Mannheim, Mannheim, Germany), by the avidin-biotin-peroxidase procedure. Amyloid plaques stained with the modified Bielschowsky silver method were seen in the cerebral cortex of the brains of patients with Alzheimer’s disease but not in the normal control brains. The core type of amyloid plaque was immunostained with BA27, whereas both core and diffuse types were positive for BC05. In addition, A42 immunoreactivity was strongly positive in the cytoplasm and the cell processes of some cells only in the brains of patients with Alzheimer’s disease (figure). These A42-positive cells were seen mainly in the second to fourth layers of the cortex and had small and round cytoplasm in comparison with the pyramidal neurons seen in the third and fifth layers of the cortex. Some of the A42-positive cells were located inside and some adjacent to

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Available abstract

embedded sections (5 m) from different brain regions were stained with haematoxylin-eosin, Kluver-Barrera, and the modified Bielschowsky silver method for histology. All cases of Alzheimer’s disease met standard pathological criteria for definite Alzheimer’s disease. 3 Many neurofibrillary tangles appeared diffusely from a medial part of the temporal lobe to the association cortices of frontal and parietal lobes. In the middle frontal cortex the density was at most 12 counts in one case, and usually one to two counts per microscopic (200) field in the others. There was mild neuronal cell loss with astrocytosis. Frozen sections (40 m) taken from the middle frontal gyrus were immunostained with mouse monoclonal end-specific antibodies against free C-termini of A40 (BA27) and A42 (BC05), 2 and with monoclonal antibodies against C-termini and N-termini of -amyloid precursor protein (clone 2.F2.19B4 and 22C11, respectively, Boehringer Mannheim, Mannheim, Germany), by the avidin-biotin-peroxidase procedure. Amyloid plaques stained with the modified Bielschowsky silver method were seen in the cerebral cortex of the brains of patients with Alzheimer’s disease but not in the normal control brains. The core type of amyloid plaque was immunostained with BA27, whereas both core and diffuse types were positive for BC05. In addition, A42 immunoreactivity was strongly positive in the cytoplasm and the cell processes of some cells only in the brains of patients with Alzheimer’s disease (figure). These A42-positive cells were seen mainly in the second to fourth layers of the cortex and had small and round cytoplasm in comparison with the pyramidal neurons seen in the third and fifth layers of the cortex. Some of the A42-positive cells were located inside and some adjacent to

Key concepts: Pathology, Senile plaques, Neuropil, Cortex (anatomy), Amyloid (mycology), Neurofibrillary tangle, Cerebral cortex, Alzheimer's disease

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