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Biomedical subjects

N Yuasa

Publications and source records attributed to N Yuasa.

62 records · Page 4Linked to original sources

Induction of hydropericardium in one-day-old specific-pathogen-free chicks by adenoviruses from inclusion body hepatitis.

The pathogenicities of inclusion body hepatitis (IBH) and hydropericardium syndrome (HPS) strains of adenovirus for specific-pathogen-free (SPF) chicks were compared. One-day-old SPF chicks inoculated intramuscularly with the DPI-2 (serotype 2), S-PL1 (serotype 2), TR630 (serotype 8), and Saga97 (serotype 8) strains from IBH and with the LVP-1 strain (serotype 4) from HPS exhibited the mortality, liver enlargement, and hydropericardium characteristic of gross change found in HPS. The chicks inoculated with the IBH and HPS strains exhibited similar histologic and immunohistochemical changes. Neither mortality nor pathologic changes occurred in 3-wk-old SPF chicks inoculated with IBH strains, although HPS strain induced HPS lesions in them. This study indicates that IBH strains of adenovirus can also reproduce HPS lesions and mortality in 1-day-old SPF chicks and that IBH and HPS strains may have similar pathogenicities except for their different virulence for older chickens.

Adenoviridae↗

Lesions of bone and bone marrow in myeloid leukosis occurring naturally in adult broiler breeders.

Lesions of bone and bone marrow in myeloid leukosis (ML) occurring naturally in adult broiler breeders were investigated pathologically. During gross examination, nodules and protrusions were commonly observed on the surface of the sternum, ribs, vertebrae, and synsacrum. The bone marrow of all the bones of the body was pale in color. Histologically, granulated myelocytes proliferated in the bone marrow of various bones and in the periosteum of the sternum, ribs, vertebrae, and synsacrum. The first proliferation of tumor cells occurred in the bone marrow of epiphysis. The myelocytes invaded through haversian and Volkmann's canals from the bone marrow to periosteal areas. Hematopoiesis was suppressed by marked proliferation of tumor cells in the bone marrow of the whole bone. Atrophy was also seen in the bones, including medullary bones of the chickens suffering from ML. Proliferation of myelocytes was seen in the bone marrow and periosteum of ossified cartilaginous rings of the trachea and larynx. Marked proliferation of myelocytes was seen in the dura mater of spinal cords, and it subsequently depressed the spinal cords. Bone formation with cartilage was seen in the periosteum of the sternum having marked proliferation of myelocytes in the bone marrow and periosteum. Ultrastructurally, tumor cells showed large nuclei and cytoplasm with large round electron-dense lysosomes. The virus particles were rarely detected in the cytoplasm of tumor cells. The polymerase chain reaction test of tumor samples showed positive for subgroup J avian leukosis virus. This study indicates that the myelocytes can invade through the compact bones to the periosteum in the sternum, ribs, vertebrae, synsarcum, and ossified cartilage of trachea and larynx having thinner compact bones. In addition, the periosteal osteogenesis with cartilage in the sternum may be reactive change against the bone atrophy because of the marked proliferation of myelocytes.

Animals↗

Mucosal dysplasia in the bile duct after choledochoduodenostomy: a case report.

A 60-year-old woman who had undergone cholecystectomy, choledocholithotomy and choledochoduodenostomy 21 years previously for cholecystolithiasis and choledocholithiasis, presented with nausea and vomiting. With a preoperative diagnosis of recurrent common bile duct stones, the extrahepatic bile duct was excised and choledochojejunostomy was performed. Histologic examination of the resected specimen disclosed chronic cholangitis, papillary epithelial hyperplasia, and mild dysplasia. Choledochoduodenostomy predisposes to reflux of duodenal contents, resulting in chronic mechanical and chemical irritation likely to induce histopathologic alterations in the bile duct mucosa. Since bile duct dysplasia induced by chronic inflammation may be a precursor of cancer, indication for choledochoduodenostomy should be specific and limited, and careful long-term follow-up is mandatory.

Bile Ducts↗

Gizzard erosion in broiler chicks by group I avian adenovirus.

Incidences of mortality without any clinical signs occurred in growing chicks in a broiler flock. Five 17-day-old dead broilers with gizzard erosions were investigated pathologically. Macroscopically, the gizzards were found to be dilated with bloody fluids. The koilin layer of the gizzards showed multifocal black patches (erosions). Histologically, there was necrosis of the koilin layer, degeneration and depletion of the gizzard glandular epithelium with intranuclear inclusion bodies, and hyperplasia of the macrophages in the lamina propria. An immunohistochemical analysis revealed intranuclear inclusion bodies in the degenerating gizzard glandular epithelial cells that stained positively for group I avian adenovirus antigen. Ultrastructurally, numerous viral particles (an average of 72 nm in diameter, from 63 to 88 nm) were in the intranuclear inclusions of glandular epithelium. This study suggests that the gizzard erosions may have been caused by group I avian adenovirus. In addition, the degeneration and depletion of gizzard glands secreting koilin substances, by adenovirus, may induce a reduction of koilin substances, which may then cause gizzard erosion (focal loss of the koilin layer).

Adenoviridae Infections↗

Sarcoid granuloma-like lesions in the lungs of broiler chicks.

Sarcoid granuloma-like lesions were observed in the lungs of two broiler chicks showing depressed growth. Multinucleated giant cells in the lesions often contained foreign bodies comprising amorphous and laminated material. These were morphologically similar to Schaumann bodies found in human sarcoidosis. This is the first report of sarcoid granuloma-like lesions and Schaumann body-like material in chickens.

Anemia↗

Percutaneous transhepatic balloon dilation for papillary stenosis.

In this study, a case of primary common bile duct stone due to papillary stenosis is reported. The patient was a 68-year-old man with complaints of epigastric pain and fever who had undergone gastrectomy at age 55 and cholecystectomy with choledocholithotomy at age 62. Laboratory data revealed elevation of the transaminases acid biliary enzymes. Both abdominal ultrasonography and CT scan revealed dilatation of the common bile duct with stones. Since endoscopic retrograde cholangiopancreatography could not visualize the bile duct, percutaneous transhepatic biliary drainage was carried out. After lithotripsy by percutaneous transhepatic cholangioscopy a diagnosis of papillary stenosis was made following percutaneous transhepatic manometry of the sphincter of Oddi, and balloon dilatation through the PTBD fistula was successfully performed. In this case report, emphasis is placed on the diagnosis and treatment of papillary stenosis.

Aged↗

Multiple hepatic cysts along the intrahepatic bile duct--case report.

A case of multiple hepatic cysts of the periductal gland located along the left intrahepatic bile duct is described. Ultrasonography and computed tomography disclosed many cystic lesions along the left portal vein in the left lateral segment of the liver. Percutaneous transhepatic cholangiography showed many compressed lesions. The resected specimen revealed multiple cysts of 2-7mm in diameter along the intrahepatic bile duct. Microscopically, cysts within the large Glisson's capsule were intermixed with lobuli of the periductal glands, thus suggesting periductal gland origin. Histopathological features of these cysts were similar to those of "multiple hilar cysts" reported by Nakanuma, but lack of portal hypertension and underlying chronic liver disease is the significant characteristics in this case which is different from "multiple hilar cysts".

Aged↗

Histology, immunohistochemistry, and ultrastructure of hydropericardium syndrome in adult broiler breeders and broiler chicks.

Ten 250-day-old broiler breeders, seven 16-day-old broiler chicks, and three 25-day-old broiler chicks suffering from hydropericardium syndrome (HPS) in Japan were examined histologically, immunohistochemically, and ultrastructurally. Clinically, the chickens died suddenly without apparent signs. The mortality rates were 6.4%, 20.2%, and 26.1%, respectively. The common characteristic histologic lesion was necrosis of hepatocytes, accompanied by intranuclear inclusions of hepatocytes and hemorrhages. In the spleen, there were activation of macrophages in splenic sinus and ellipsoids and erythrophagocytosis in the splenic sinus. The interlobular interstitium of the lung showed marked edema. The air and blood capillary areas of parabronchi included many macrophages with yellow pigments. With immunoperoxidase staining, intranuclear inclusion bodies within degenerating hepatocytes stained positively for group I adenovirus antigen. Ultrastructurally, numerous viral particles (65-70 nm in diameter) were demonstrated in the intranuclear inclusions of hepatocytes. Group I adenovirus (serotype 4) was isolated from liver samples of adult broiler breeders and broiler chicks with HPS. This study suggests that HPS may be caused by group I adenovirus.

Animals↗