Shinya Yasumoto - Academia.edu (original) (raw)

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Papers by Shinya Yasumoto

Fish Pathology

Clinostomids are common parasites worldwide. Snails are the first intermediate host, fishes are t... more Clinostomids are common parasites worldwide. Snails are the first intermediate host, fishes are the second intermediate host, and herons are the final host of these trematodes (Bullard and Overstreet, 2008). In Japan, several fish species serve as a second intermediate host of Clinostomum complanatum, including goldfish Carassius auratus, common carp Cyprinus carpio, l o a c h M i s g u r n u s a n g u i l l i c a u d a t u s , a n d a y u Plecoglossus altivelis (Aohagi et al., 1992; Aohagi et al., 1995). In fish, the cercariae of these parasites develop int o me t ac er c a ri a e w i t h i n a c y s t. Ge ner al ly, Clinostomum does not cause great harm to infected fish except in cases of heavy infection (

Bioscience, Biotechnology, and Biochemistry, 2015

Tropomyosins are defined as risk factors for shrimp allergy. However, their concentration in diff... more Tropomyosins are defined as risk factors for shrimp allergy. However, their concentration in different preparations has not been clarified. We quantified the tropomyosin concentration in shrimp meat, which was cooked using several methods or was stored under various conditions. The results demonstrated that shrimp meat from various preparations and storage conditions maintained tropomyosin concentrations that were sufficient to cause food allergies.

Journal of fish diseases, Jan 13, 2014

Fish Pathology, 2008

-Penaeid acute viremia (PAV) or white spot disease (WSD) causes mass mortality in cultured penaei... more -Penaeid acute viremia (PAV) or white spot disease (WSD) causes mass mortality in cultured penaeid shrimp. Despite many histopathological studies, the principal lesion in the diseased shrimp remained unclear. Here we reevaluated the histopathology and ultrastructure of moribund kuruma prawn Penaeus japonicus artificially infected with penaeid rod-shaped DNA virus (PRDV) as a pathogen of PAV. We showed that PRDV infected cardiac satellite cells, primary myocardial cells and myocardial cells of the heart, where the nuclei of these cells displayed virus propagation that resulted in severe myocardial necrosis. Myocardial necrosis was suggested to be a primary cause of the viremia of PAV.

Acta Neuropathologica, 1998

Human spinocerebellar degeneration is one of the intractable diseases. We studied the detailed ne... more Human spinocerebellar degeneration is one of the intractable diseases. We studied the detailed neuropathology of cats with hereditary cerebellar degeneration obtained from the experimental breeding. The findings included almost total loss of Purkinje cells with an increase in Bergmann's glia in the cerebellar hemisphere, preservation of some Purkinje cells in the vermis and moderate neuronal depletion of the olive nucleus. Cerebellar and pontine nuclei were normal. The cerebrum and spinal cord as well as the peripheral nervous system appeared normal. Electron microscopic examination revealed swelling of the distal dendrites of Purkinje cells in the less-affected nodule of the vermis, and clusters of presynaptic boutons without any synaptic contact in the severely affected folia where Purkinje cell bodies and dendrites disappeared. Prolonged existence of presynapses in the molecular and Purkinje cell layers was confirmed by positive immunoreactivity to anti-synaptophysin. Quantitative analysis using electron microscopy demonstrated an apparent increase in the density and mean size of presynapses in the molecular layer of the severely affected folia. These findings indicate that degeneration of Purkinje cells started at the most distal part of the dendrite in this animal model of cerebellar degeneration, and that presynapses, axon terminals of the granular cells and basket cells can exist for a long time even after complete degeneration of the Purkinje cells. Further investigation of this novel animal model may promote a better understanding of pathogenesis of human hereditary cerebellar degeneration.