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Biomedical subjects

C Itakura

Publications and source records attributed to C Itakura.

At least 55 records · Page 3Linked to original sources
PubMed1994

The monoamine content of the brain in the neurofilament-deficient quail, (the Quiver quail).

Changes in neurotransmission are known to take place in a variety of conditions, such as Parkinson's disease. A neurofilament-deficient mutant of the Japanese quail, named the Quiver quail, exhibits generalized quivering as a clinical sign. The content of monoamines (noradrenaline (NA), dopamine and 5-hydroxytryptamine) and the uptake and release of L-[3H]NA were measured in brain of this bird. In Quiver, the NA content in neostriatum and thalamus, and the 5-hydroxytryptamine content in neostriatum, paleostriatum and thalamus were significantly increased, in comparison with the normal quail. The dopamine content and L-[3H]NA uptake and release in the Quiver mutant were similar to those in normal quail.

Animals↗
PubMed1994

Pneumocystis carinii pneumonia in a thoroughbred foal.

Typical Pneumocystis carinii pneumonia was found in a male thoroughbred foal (46 days old) suffering from diarrhea and hypogammaglobulinemia after birth. The characteristics of the organisms were demonstrated by Grocott methenamine silver staining, and scanning and transmission electron microscopy. The present focal had no histological lesions suggesting immunodeficiency. However, he could not get adequate colostrum from his dam, because she died of hemorrhagic shock due to immuno-mediated thrombocytopenia at delivery. This condition was considered to have predisposed the foal to the pneumonia.

Animals↗
PubMed1994

Acquisition of pathogenicity of a Newcastle disease virus isolated from a Japanese quail by intracerebral passage in chickens.

Newcastle disease virus (NDV) was isolated from a Japanese quail (Cotornix cotornix japonica). The effect of intracerebral and intranasal passages of the NDV in chickens on the pathogenicity was studied. Pathogenicity of the viruses of different passage levels was compared with that of the original isolate by the mean death time with the minimum lethal dose in chicken embryos, intracerebral pathogenicity index in day-old chicks, intravenous pathogenicity index with 6-week-old chickens and the mortality rates of chickens and quails inoculated intravenously or intranasally. The original isolate from the quail did not kill chickens but only embryos and some one-day-old chicks, exhibiting a mesogenic character. Pathogenicity of the virus of the 10th intranasal passage was not different from that of the original isolate. The viruses passaged intracerebrally, on the other hand, killed chickens of all ages by either route of inoculation, showing a velogenic property. Virus recovery from the blood and the brain was positive only in the chickens infected with brain-passaged viruses by any route of inoculation. Virus titers in the tissues of chickens infected with the brain-passaged viruses were higher than those with the original isolate and the virus of the 10th intranasal passage. These results indicate that the enhanced pathogenicity of the mesogenic NDV isolate from the quail for chickens was induced by acquiring the properties of neurotropism and pantropism through intracerebral passage in chickens.

Animals↗
PubMed1993

beta,beta'-Iminodipropionitrile toxicity in normal and congenitally neurofilament-deficient Japanese quails.

Morphological effects of a neurotoxin, beta,beta'-iminodipropionitrile (IDPN) were analyzed in normal and congenitally neurofilament (NF)-deficient Japanese quails. These quails (6 weeks old) were injected intraperitoneally with IDPN (0.2 g/kg body weight) three times every 3 days. They were necropsied at 10 to 12 days after the first injection. In normal quails, axonal swellings were observed histologically in the ventral motoneurons, ventral root, commissura grisea and spinal ganglion in the cervical and synsacral spinal cord. Electron microscopically, the changes consisted of increased NFs, with scattered mitochondria, smooth endoplasmic reticulum and microtubules. The myelin sheaths of the involved nerves were thinner than those of the normal axons. These lesions were similar to those induced by IDPN intoxication in mammalian experimental animals. In NF-deficient quails injected with IDPN, no axonal changes were detected. These findings suggested that IDPN selectively attacked the NFs.

Animals↗
PubMed1993

Smaller number of large myelinated fibers and focal myelin thickening in mutant quails deficient in neurofilaments.

The peripheral nervous system of a mutant of a Japanese quail deficient in neurofilaments (mutant) and of a normal Japanese quail (control) was morphometrically evaluated to characterize the morphological findings, especially those of the myelinated fibers of the mutant. In the proximal peroneal nerves, the frequency of the teased myelinated fibers showing the focal myelin thickening was higher in mutant than in control (P < 0.001) without obvious ongoing axonal degeneration and segmental demyelination. The total numbers of the myelinated fibers in the proximal and distal peroneal nerve, and in the tibial nerve branch to gastrocnemius muscle (pars medialis) were similar between control and mutant, although the number of the large myelinated fibers was less (P < 0.01) and the number of the small myelinated fibers was greater (P < 0.01) in mutant compared with control. The median diameters of neuronal cell bodies of the sacral dorsal root ganglia were similar in control and mutant. The percentages of light, dark and unclassified cells evaluated based on the histologic cytoplasmic features were also similar in control and mutant. Therefore, morphometric alterations were more pronounced in the peripheral myelinated nerve fibers compared with those in the cell bodies of the spinal dorsal root ganglia. We concluded that a smaller number of large myelinated fibers with a greater number of small myelinated fibers and the presence of focal myelin thickening are the main morphologic findings in this mutant, probably due to the arrest of radial growth or maturation of the axons of the myelinated fibers in the absence of ongoing myelinated fiber degeneration.

Animals↗
PubMed1993

Pathomorphologic findings of lead poisoning in white-fronted geese (Anser albifrons).

Nineteen lead-poisoned white-fronted geese (Anser albifrons), including nine immature birds, were examined pathologically. Subacute lead poisoning due to ingestion of spent lead shots was diagnosed pathologically and confirmed by demonstrating high lead concentration in the liver. The liver lead concentration ranged from 6.9 to 67.7 mg/kg wet weight. The most suggestive gross lesions were mottled bile-stained liver in eight geese and proventricular impaction and/or the presence of lead pellets in the gizzard. Histologic lesions of the liver consisted of Kupffer cell hemosiderosis, large bile plugs in dilated canaliculi, bile pigmentation in hepatocytes, and bile extravasation and associated hepatic necrosis. Seven geese of the remaining 11 birds also had hepatic necrosis in the liver, the greenish discoloration of which was obscure macroscopically. The liver discoloration was considered a jaundice due to both rapid overproduction of bile from increased breakdown of erythrocytes and intrahepatic impaired excretion of bile. The severity of lesions was not correlated to the liver lead concentrations. All examined geese had hemosiderosis of mononuclear phagocytic system cells in the spleen and hypoplasia or edema of the bone marrow with increased numbers of polychromatic erythroblasts. These prominent changes probably resulted from excess breakdown of erythrocytes, hypercholia followed by intrahepatic cholestasis, and disrupted erythropoiesis in bone marrow caused by lead.

Animals↗
PubMed1993

Direct ABC immunohistochemistry to Encephalitozoon cuniculi.

Among the sera from 9 rabbits spontaneously infected with Encephalitozoon cuniculi, a serum which revealed a high titer for E. cuniculi by indirect protein A-gold (IPAG) immunohistochemistry and reacted with the outer layer of the shell of E. cuniculi spores on immunoelectron microscopical examination, was biotinylated. The biotinylated rabbit anti-E. cuniculi IgG reacted immunohistochemically with E. cuniculi, but not with other protozoa tested, namely Neospora caninum, Toxoplasma gondii and sarcocystis. The direct avidin-biotin-peroxidase complex (ABC) immunohistochemistry using biotinylated rabbit anti-E. cuniculi IgG in this study is a useful tool for the diagnosis and study of encephalitozoonosis.

Animals↗
PubMed1993

Dual infection with canine distemper virus and infectious canine hepatitis virus (canine adenovirus type 1) in a dog.

A 72-day-old, female, Golden Retriever dog showed anorexia, coughing, nasal discharge, diarrhea and hematochezia, and died on the 15th clinical day. Pathological examination revealed dual infection with canine distemper virus (CDV) and canine adenovirus (CAV). CAV inclusion bodies occurred only in the liver, and biliary and respiratory system, whereas CDV inclusions were demonstrated in the visceral organs systematically. The CAV inclusions were associated with multifocal hepatocellular necrosis and edematous swelling of the wall of the gall bladder, suggesting infectious canine hepatitis virus (canine adenovirus type 1) infection.

Adenoviridae Infections↗
PubMed1993

A survey of lead poisoning in wild waterfowl in Japan.

Ingested shotgun pellets were found in 13 of 56 hunter-killed wild waterfowl between October and December 1991 from two hunting grounds in Japan. Four of 33 other waterfowl found dead in lightly hunted areas between January 1991 and March 1992 were diagnosed as having lead poisoning. We propose that lead poisoning maybe a threat to waterfowl in Japan.

Animals↗
PubMed1993

Nutritional secondary hyperparathyroidism occurring in a strain of German shepherd puppies.

Five German shepherd puppies, aged between 66 and 174 days (4 of which had the same parents) had ananastasia with deformation of limbs. Histopathologically, all the puppies showed moderate to marked fibrous osteodystrophy with parathyroid gland activation. These puppies were fed a diet consisting of 80% steamed rice and 20% raw meat. It was implied that though the diet contained the required level of calcium, it contained more than the required level of phosphorus. From the results, the present cases were diagnosed as nutritional secondary hyperparathyroidism caused by a diet containing too much phosphorus. Based on the clinical aspects concerning the development of this condition a familial factor was suggested.

Animal Nutritional Physiological Phenomena↗
PubMed1992

Detection of rabbit haemorrhagic disease virus particles in the rabbit liver tissues.

Liver tissues from rabbits experimentally infected with rabbit haemorrhagic disease virus (RHDV) were studied electron microscopically. The earliest change in hepatocytes of the rabbits infected with RHDV was hydropic degeneration. Rough endoplasmic reticulum was dilated with a mild increase in polysomes and cytoplasmic cisternae in degenerated hepatocytes. Characteristic cytopathological changes of necrotic hepatocytes included shrinkage of the cell body, formation of cytoplasmic vesicles, vacuoles or cisternae and karyolysis. A large number of viral particles resembling a calicivirus in size and morphology was demonstrated in the cytoplasm of many necrotic hepatocytes. The particles had accumulated mainly in the membrane-bound cisternae or scattered around the membrane-bound vacuoles of the necrotic hepatocytes. Western blot analysis demonstrated that RHDV antigen was present in the infected hepatocytes. RHDV particles were also detected by immunoelectron microscopy. Replicating patterns of RHDV particles and subsequent cytopathology resembled those in other calicivirus infections.

Animals↗
PubMed1992

Detection of rabbit haemorrhagic disease virus antigen in tissues by immunohistochemistry.

Formalin fixed liver, spleen, kidney, heart, lung, duodenum and appendix tissues from nine rabbits, experimentally infected with rabbit haemorrhagic disease virus (RHDV), were investigated for evidence of RHDV antigen by the direct avidin-biotin peroxidase complex immunohistochemical method. In all the rabbits examined, RHDV antigen was detected in degenerative and necrotic hepatocytes of the liver tissues. The area involved coincided with histopathological lesions on serial liver sections. The RHDV antigen was expressed in the cytoplasm of the hepatocytes, suggesting that RHDV replicated in these cells. RHDV antigen was also detected in the spleen. The results of immunohistochemistry were supported by the demonstration of RHDV protein by Western blot analysis and of RHDV particles by protein A-gold immunoelectron microscopy in the liver homogenate from all the rabbits that were examined.

Animals↗
PubMed1992

Langerhans' cells in equine cutaneous papillomas and normal skin.

Langerhans' cells (LC) were investigated immunohistochemically and electron microscopically in normal equine epidermis and 133 equine cutaneous papillomas experimentally induced in five 2-year-old Thoroughbred horses. Class II major histocompatibility complex antigen-positive dendritic LC were found in the normal epidermis and ultrastructurally had the characteristic Birbeck's granules. In the developing phase of the papillomas, LC were significantly decreased in number and size, indicative of a hypofunctional state. In the regressing phase of the papillomas, LC were markedly increased in number, especially at the epidermis-dermis junction. LC with long dendrites were rich in cytoplasm with well-developed cytoplasmic organelles, including Golgi apparatus, lysosomes, Birbeck's granules, and multivesicular bodies. These LC were hyperfunctional. An infiltration of many T lymphocytes was also observed at the epidermis-dermis junction.

Animals↗
PubMed1992

A pathologic and bacteriologic study on otitis media in swine.

A pathologic and bacteriologic study on otitis media in swine was performed on 237 swine, ranging in age from 1 day to 1 year. These 237 swine from eight selected farms were slaughtered due to unfavorable prognosis associated with clinical signs of illness. One hundred sixty-three (68.8%) of the 237 swine were found to be affected with otitis, though only a few swine showed clinical signs characteristic of the disease. One hundred fifty-one (63.7%), 53 (22.4%), and 39 (16.5%) had lesions in the middle, external, and internal ear, respectively. Of the 151 cases with otitis media, bilateral and unilateral infection accounted for 114 (75.5%) and 37 (24.5%), respectively. Only 5/53 swine with otitis externa and 6/39 swine with otitis interna failed to show otitis media. All swine with infection in the tympanic cavity had inflammatory lesions in the auditory tube. Examination of the swine grouped by age revealed that, regardless of age, incidence of otitis media was 50-70%. In swine younger than 1 month old, otitis media tended to center on the auditory tube, where a mild infiltration of neutrophils into the mucous membrane was frequent. Thereafter, otitis media increased in degree and extent with age. Forty (26.5%) of the 151 swine affected with otitis media were accompanied by a substantial amount of inflammatory exudate in the tympanic cavity and bulla. Purulent exudate was found in 20/40 (50%) swine. Severe otitis media prevailed in swine between 1 and 4 months of age, showing inspissation of a suppurative exudate in the tympanic cavity and lysis of the underlying osseous wall of the tympanic bulla with subsequent fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Actinomyces↗
PubMed1992

Topographic relationship between senile plaques and cerebrovascular amyloidosis in the brain of aged dogs.

The distributions of senile plaques (SP) and cerebrovascular amyloidosis (CA) were studied by employing thioflavin S and modified Bielschowsky stains, and beta-protein immunohistochemistry on serial sections of the brains of aged dogs older than 10 years. Mature and perivascular plaques, both of which contained compact amyloid deposits, always showed a close topographic relationship to CA. In contrast, the majority of diffuse plaques showed no topographic relationship to CA. Cell bodies of neurons and/or glia were almost always involved in the diffuse plaques. In addition, beta-protein immunohistochemistry demonstrated amyloid deposits on the periphery of occasional neurons. These findings suggest that different mechanisms may be involved in the development of the different subtypes of SP in the brains of aged dogs.

Aging↗
PubMed1992

An immunohistochemical and ultrastructural study on age-related astrocytic gliosis in the central nervous system of dogs.

The pattern of astrocytic gliosis (AG) was examined in 2-month-old to 18-year-old dogs using glial fibrillary acidic protein (GFAP) immunohistochemistry and electron microscopy. Coronal sections from various levels of the central nervous system (CNS) were stained with hematoxylin & eosin, Luxol Fast Blue, Nissl, and Bodian in addition to GFAP. A consistent pattern of age-related AG was observed in the dogs. The white matter, cortico-medullary junction, and subcortical nuclei in the cerebrum, central nuclei in the cerebellum, various nuclei in the brain stem, and grey matter of the spinal cord showed even and intense GFAP staining. AG was also prominent in the cerebral and cerebellar cortices and thalamus. Moderate AG was observed in the hippocampus and white matter of the cerebellum and spinal cord. Electron microscopy demonstrated increased number of profiles of degenerative neural components in the vicinity of hypertrophic astrocytes in the cerebral cortex of the aged dogs. Moderate to severe AG was consistently shown in the CNS of the aged dogs. In contrast, young normal dogs showed minimum amounts of GFAP-positive astrocytes in the CNS. These findings suggest that the observed AG in the CNS of the dogs is a morphological expression of aging.

Aging↗
PubMed1992

Endocrine cell populations in the pancreas of diabetic WBN/Kob rats.

Numerical changes of insulin-, glucagon- and somatostatin-positive cells in the pancreas of WBN/Kob male rats with spontaneously occurring diabetes were examined. The rats examined were divided into three different age groups: Groups I (12 weeks old) and II (33 weeks old) were clinically prediabetic and group III (60-90 weeks old) was diabetic. Serum glucose value was in the normal range in groups I and II, while it was much higher in group III. B and A cells were markedly decreased in number in groups II and III. In group II, the ratio of B to A cells was normally preserved, though the total endocrine cell number was markedly decreased as compared with that in group I. In group III, the percentage of B cells was decreased significantly. The normal ratio in group II seemed to keep serum glucose within the normal level. In addition to the total endocrine cell reduction, an altered ratio of B and A cells was considered to cause the diabetic condition.

Animals↗