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Biomedical subjects

C Itakura

Publications and source records attributed to C Itakura.

At least 37 records · Page 2Linked to original sources
PubMed1996

Peripheral neuropathy of dietary riboflavin deficiency in racing pigeons.

An occurrence of peripheral neuropathy in nine 14- to 55-day-old racing pigeons was documented. The predominant clinical signs were diarrhea, and leg and wing paralysis. Grossly, there was discoloration and swelling of all the peripheral nerve trunks. Microscopic lesions comprising swelling, fragmentation and demyelination of myelin sheaths, and proliferation of Schwann cells, were seen in the peripheral nerves of all birds examined. These changes were associated with moderate to severe swelling, fragmentation, atrophy and loss of axons. The peripheral nerve lesions in these cases were similar to those of dietary riboflavin deficiency in chickens. An analysis of the diet given to the pigeons indicated that the riboflavin concentration was only 0.9 mg/kg feed.

Animal Feed↗
PubMed1995

Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc gene.

Mutations in the APC (adenomatous polyposis coli) gene appear to be responsible for not only familial adenomatous polyposis but also many sporadic cases of gastrointestinal cancers. Using homologous recombination in mouse embryonic stem cells, we constructed mice that contained a mutant gene encoding a product truncated at a 716 (Apc delta 716). Mendelian transmission of the gene caused most homozygous mice to die in utero before day 8 of gestation. The heterozygotes developed multiple polyps throughout the intestinal tract, mostly in the small intestine. The earliest polyps arose multifocally during the third week after birth, and new polyps continued to appear thereafter. Surprisingly, every nascent polyp consisted of a microadenoma covered with a layer of the normal villous epithelium. These microadenomas originated from single crypts by forming abnormal outpockets into the inner (lacteal) side of the neighboring villi. We carefully dissected such microadenomas from nascent polyps by peeling off the normal epithelium and determined their genotype by PCR: all microadenomas had already lost the wild-type Apc allele, whereas the mutant allele remained unchanged. These results indicate that loss of heterozygosity followed by formation of intravillous microadenomas is responsible for polyposis in Apc delta 716 intestinal mucosa. It is therefore unlikely that the truncated product interacts directly with the wild-type protein and causes the microadenomas by a dominant negative mechanism.

Adenoma↗
PubMed1995

Ultrastructural and histochemical studies of the epiphyseal plate in normal chicks.

BACKGROUND: Chondrocytes in the epiphyseal plate undergo a series of well-defined stages, each stage containing a morphologically homogeneous cell population. However, biochemical studies show that there are some functionally heterogeneous cell types in the calcifying zone of the chick epiphyseal plate. METHODS: We studied the sequence of chondrocytic maturation in the normal chick epiphyseal plate ultrastructurally and histochemically. Chondrocytes in the calcifying zone were of three distinct types, the appearance of each cell type being closely related to the stage of matrix calcification. RESULTS: Clear cells were observed in the upper calcifying region, stellate cells appeared in the middle calcifying region, and hypertrophic clear cells appeared in the lower calcifying region. Rough endoplasmic reticulum (RER) and lysosome-rich cells were found, these being limited to the outermost layers of the calcifying zone and containing ACPase-positive products. Osteoclasts were attached to the matrix near the RER and lysosome-rich cells in the poorly calcified regions. CONCLUSION: We hypothesized that each cell type played a different role in the initiation, progression, and maintenance of cartilage calcification. RER and lysosome-rich cells may be responsible for the resorption of uncalcified cartilage matrix, this resulting in induction of the osteoclastic resorption of the calcified matrix. In addition, the fate of the chondrocytes was twofold: hypertrophic clear cells died, while the RER and lysosome-rich cells survived, suggesting that these cells were transformed into osteogenic cells.

Acid Phosphatase↗
PubMed1995

Acrylamide-induced peripheral neuropathy in normal and neurofilament-deficient Japanese quails.

Morphological effects of acrylamide (AC) on the peripheral nerves in normal and neurofilament (NF)-deficient (Quv) Japanese quails were investigated. AC (100 mg/kg) was injected intraperitoneally every other day. After the birds manifested neurological signs, they were necropsied (after 10 approximately 21 AC injections) and the sciatic and tibial nerves were examined. In both normal and Quv qualis, AC produced axonopathy with a distal-proximal progression. In AC-intoxicated normal quails, the nerve fiber pathology was characterized by typical Wallerian-like degeneration, consisting of axonal degeneration, myelin breakdown, macrophage migration. Schwann cell proliferation and regeneration of nerve fibers. Ultrastructurally, AC-induced NF accumulation was detected in the axon of myelinated nerve fibers. In AC-intoxicated Quv qualis, axonal degeneration with accumulation of membranous organelles occurred; however, sequential events of Wallerian-like degeneration were not as prominent as in AC-intoxicated normal qualis. These results demonstrated that NF-deficient Quv quails are sensitive to neurotoxic effects of AC. On the other hand, the different pathology of AC-intoxicated normal and Quv qualis indicates the presence or absence of NFs influences the appearance and extent of AC axonopathy.

Acrylamide↗
PubMed1995

Smaller axon and unaltered numbers of microtubules per axon in relation to number of myelin lamellae of myelinated fibers in the mutant quail deficient in neurofilaments.

To characterize the morphological features of the myelinated fibers in the mutant quails deficient in neurofilaments (NF), caused by a nonsense mutation in the NF-L gene, the morphological parameters of the axon and myelin sheath, and their relationships in the peroneal nerve were evaluated. In the mutant, the axonal area was smaller than in the control (P > 0.01), reflecting the lack of large diameter axons. There was no significant difference in the mean number of myelin lamellae and of their spacings between controls and mutants. Therefore, it was decided to analyze the alteration of axonal parameters in relation to the number of myelin lamellae. In the regression analysis, the number of microtubules (MT) per square micrometer of the axonal area was greater in the mutant than in the control (P < 0.05); however, the number of MT per axon was similar in controls and mutants with the same given number of myelin lamellae. The number of MT+NF per axon was smaller in the mutant than in the control only for myelinated fibers with more than 25 myelin lamellae (P > 0.05). These findings indicate that there was a less significant effect of NF deficiency on the smaller than on the larger myelinated fibers. There was no compensatory increase in the numbers of MT per axon of the myelinated fibers in the mutant as found previously in the unmyelinated fibers of the mutant.

Animals↗
PubMed1995

Ultrastructural studies of the epiphyseal plate of chicks fed a vitamin D-deficient and low-calcium diet.

The epiphyseal plates of rachitic chicks fed a vitamin D-deficient and low-calcium diet were examined ultrastructurally at 4, 7, 14, 18 and 21 days old. On and after 14 days, changes were observed. Chondrocytes in resting, proliferating and maturing zones commonly showed a reduction in cell organelles, suggestive of a decrease in synthetic activity of matrix components. In addition, the resting zone cells had numerous intracytoplasmic microfilaments. Mitotic figures were present but not increased in number in the proliferating zone. Autolysosome-like dense bodies in the chondrocytes and clusters of degenerative and necrotic chondrocytes were observed in the proliferating and maturing zones. In the calcifying zone of the rachitic epiphyseal plate, initial calcification was observed characterized by the deposition of apatite crystals in matrix vesicles and the formation of spherical crystal clusters. The crystal clusters were separated from each other by collagen fibrils on which only small amounts of apatite crystals had been deposited. In this zone, hypertrophic chondrocytes responsible for the initial calcification were seen, but not the stellate chondrocytes responsible for the progression of matrix calcification after its initiation. These findings suggest that accumulation of the proliferating and maturing zone cells as a characteristic lesion of the epiphyseal plate in rachitic chicks is caused by a disturbance of cell maturation. Such disturbance in the calcifying zone may explain the progression of the defect in matrix calcification.

Animals↗
PubMed1995

Inherited muscular disorder in mutant Japanese quail (Coturnix coturnix japonica): relationship between the development of muscle lesions and age.

The progression of the pathological changes that occur in the skeletal muscle was examined in 19 Japanese quail of the LWC strain, affected with an autosomal dominant inherited muscular disorder producing electrical myotonia. The muscle samples were obtained every 10 days from 20 to 70 days of age. Muscle samples from 18 age-matched commercial quail were used as normal controls. Characteristic histological lesions found in the skeletal muscles included sarcoplasmic masses, ringed fibres, internal migration of nuclei and fibre size variation. These lesions, which mainly occurred in the proximal muscles, appeared first in the pectoral region and later in the muscles of the thoracic and pelvic limbs. The most predominant lesion observed at all ages consisted of sarcoplasmic masses. The presence of histological changes did not affect muscle fibre typing by two staining methods, for myosin ATPase at pH 4.5, and by NADH-TR stain. The histological changes were observed in type 2A and less commonly in 2B fibres, but not in type 1. The pectoralis thoracicus muscle, in which lesions were particularly common, showed abnormally large type 2B muscle fibres at 20 days of age. These fibres began to decrease in size at 30 days of age, and at 70 days had become strikingly atrophic, their diameter being only about half that observed at 20 days. The atrophic type 2B muscle fibres were eventually replaced by lipocytes. Chronological staging of the histopathological changes in muscle was impossible since no inter-relationship was observed between the age of the quail, the severity of clinical signs and the extent of muscle lesions. This variability in the severity and age of onset may have been due to the variable expression or incomplete penetrance of the defective gene. Because the disorder is hereditary and progressive in nature, it can be classified as a type of progressive muscular dystrophy.

Aging↗
PubMed1995

Spontaneous diabetes mellitus associated with persistent bovine viral diarrhea (BVD) virus infection in young cattle.

Histologic and immunohistochemical studies were carried out on four young cattle with diabetes mellitus associated with persistent bovine viral diarrhea (BVD) virus infection. Clinical findings included persistent hyperglycemia, decreased glucose tolerance, glycosuria, polydipsia, and severe emaciation. Macroscopically, multiple erosions and ulcers in the mucosa of upper and lower alimentary tracts and swollen lymph nodes were commonly observed. Erosions and ulcers in the mucosa of tongue, esophagus, and forestomach were represented histologically by necrosis of squamous epithelium with neutrophilic infiltration. In the small and large intestines, villous atrophy and suppurative cryptitis were often observed, along with diffuse infiltration of lymphocytes and macrophages and fibroplasia in the lamina propria. In the pancreas of all cattle, there was a reduction in the number of islet cells, and most of the residual islet cells had hydropic degeneration and a decreased number of secretory granules. Immunohistochemical examination confirmed that these cells were severely degranulated beta-cells. In addition, many islets containing necrotic islet cells were observed. These islet cells had increased eosinophilia and shrinkage of cytoplasm, as well as pyknotic nuclei. Inflammation of the islets with mild infiltration of lymphocytes was observed in all pancreatic lobes. In addition, bovine IgG-immunoreactive cells were identified immunohistochemically in the affected pancreatic islets. The BVD virus antigen was not identified in the cytoplasm of the islet cells by immunohistochemical study, although it was identified in the epithelial cells of the small intestine. The histologic and immunohistochemical studies demonstrated that the pancreatic lesions in these animals were similar to those caused by acute insulin-dependent diabetes mellitus (IDDM) in human beings.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

A new inherited muscular disorder in Japanese quails (Coturnix coturnix japonica).

Thirteen adult mutant (LWC strain) Japanese quails (Coturnix coturnix japonica), between the ages of 8 and 60 weeks were examined for a progressive muscular disorder. The disorder, inherited as an autosomal dominant trait, was clinically apparent as early as 28 days of age; it was characterized by generalized myotonia, muscle stiffness, and muscle weakness. Affected birds were identified by their inability to lift their wings vertically upward and by their inability to right themselves when placed on their dorsum. Electromyographic studies in two mutant quails showed high-frequency repetitive discharges comparable to those of myotonic runs. These discharges persisted after nerve resection. The distinctive histopathologic changes in the various muscles examined were ring fibers, sarcoplasmic masses, and internal migration of sarcolemmal nuclei. A slight decrease in the size of type IIB muscle fibers and a slight increase in the size of type IIA fibers were observed in the M. pectoralis thoracicus of affected quails. In older affected birds, inter- and intrafascicular fatty infiltration with replacement of type IIB fibers by fat cells was seen in the pectoral muscles. Single fiber necrosis, nonspecific lymphorrages, and variations in the muscle fiber size and shape were also noted. The typical muscle lesions and multisystem involvement, which was manifested by testicular degeneration and atrophy in the male LWC specimens and bilateral lenticular cataracts in 6 of 13 affected mutant quails, suggest resemblance of this new inherited muscular disorder to myotonic dystrophy in man.

Animals↗
PubMed1995

Brain lesions in chickens experimentally infected with a neuroadapted strain of mesogenic Newcastle disease virus.

Neuroadapted Newcastle disease virus (Q10) was selected by tenth serial passage, in the chicken brain of a mesogenic strain (Q0) originally isolated from quails. Specific pathogen-free birds were inoculated intranasally with one of these viruses. At daily intervals for 7 days and then at 10, 14, and 21 days post-inoculation (PI), two birds from each group were killed and samples of the brain were collected for histopathological and virological examination. Q10 caused severe nonsuppurative encephalitis with nervous signs and high mortality. Lesions characterized by neuronal degeneration and necrosis, perivascular lymphocytic infiltration, and focal or diffuse astrogliosis occurred mainly in the parahippocampal cortex, hippocampus, hyperstriatum, neostriatum, subleptomeningeal and periventricular regions of the cerebrum. Spongy changes with neuronal degeneration and axonal spheroids were also observed in the brain stem of a few cases. The amount of virus in the brain reached a peak on day 4 PI and virus could not be recovered from the brain after 6 days PI. In contrast, Q0 caused nonfatal asymptomatic disease and virus could not be isolated from the brain, sections of which showed only minimal inflammatory changes. This difference in the lesions of the brain might be related to neurovirulence and, neuroadaptation by serial passage may occur by increased efficiency of viral replication in neurons.

Animals↗
PubMed1995

Suspected nutritional myopathy in two captive Bennett's wallabies (Macropus rufogriseus).

Between January and April, 1992, two captive Bennett's wallabies (Macropus rufogriseus) from a wildlife park in Iwamizawa City, Hokkaido, Japan, were diagnosed as having nutritional myopathy. One wallaby, four-year-old adult male, had mild fresh lesions, confined to the skeletal muscles, with poor cell reaction. The other wallaby, 8-month-old female joey, had marked and extensive lesions with cellular reactions and regenerative muscle fibers in the locomotor muscles. Involvement of other striated muscles such as those of the tongue, diaphragm and heart was mild with minimal cellular reaction. Age susceptibility may account for the difference in the extent of severity of the lesions between these two animals.

Aging↗
PubMed1994

Greater number of microtubules per axon of unmyelinated fibers of mutant quails deficient in neurofilaments: possible compensation for the absence of neurofilaments.

Morphometric evaluations were performed on the peroneal nerve from mutant quails deficient in neurofilaments (NF) to elucidate the effect of an absence of NF on unmyelinated axons. The diameter frequency distribution of unmyelinated axons was similar between controls and mutants. The mean transverse axonal area, axonal circumference and circularity index of the unmyelinated axons were also similar in controls and mutants. However, the number of microtubules (MT) per axon was greater (P < 0.01) in the mutants than in the controls. The regression analysis relating the number of MT per axon to the diameter of unmyelinated axons indicated a greater number of MT in the mutants than in the controls (P < 0.05-0.01). A significantly greater number of MT per axon in the mutants may suggest a compensatory increase of MT in the absence of NF. This may conserve the size and transverse circular profile of the unmyelinated axons which are probably maintained by both MT and NF in the controls. The number of MT may be increased at the expense of the soluble fraction of tubulin.

Animals↗
PubMed1994

Malignant mesothelioma with metastases and mast cell leukaemia in a cat.

Abdominal malignant mesothelioma was found in a 17-year-old, spayed female Japanese domestic cat with mast cell leukaemia. The mesothelioma was mainly located at the periphery of the pancreas, spleen and stomach, and showed metastases to the lung, an anterior mediastinal lymph node and lymph ducts in the tracheal mucosa. Micro-circulatory defects caused by the mast cell leukaemia may have been partly responsible for the distant metastases.

Abdominal Neoplasms↗
PubMed1994

Necrotizing meningoencephalitis in pug dogs in Japan.

This report records necrotizing meningoencephalitis in three pug dogs. It is the first record of the disease in Japan. There were three characteristic histopathological findings, namely (1) a non-suppurative inflammatory cell infiltration of the cerebral hemispheres, including both gray and white matter, (2) meningeal and perivascular infiltrates of mononuclear cells, with a strong tendency to invade the underlying or surrounding brain parenchyma, and (3) selective cerebral cortical necrosis, often occurring without a concurrent inflammatory reaction. The three cases, which were diagnosed as pug dog encephalitis, resembled those previously reported in the United States of America, Switzerland and Italy. All affected animals were females with clinical histories of pregnancy or phantom pregnancy 2 weeks or less before the onset of the clinical signs.

Animals↗
PubMed1994

Acrylamide-induced neurotoxicity in the central nervous system of Japanese quails. Comparative studies of normal and neurofilament-deficient quails.

Acrylamide (AC) neurotoxicity in the central nervous system (CNS) in normal and neurofilament (NF)-deficient mutant (Quv) Japanese quails was investigated. Acrylamide (100 mg/kg) was injected intraperitoneally every other day. After the birds manifested neurological signs, they were necropsied (after 10-30 AC injections) and examined morphologically. All of the AC-intoxicated normal quails showed distal, retrograde nerve fiber degeneration associated with neurofilamentous axonal swellings in the spinal nerve tracts. There were axonal swellings without degenerative changes in other parts of the CNS. In Quv quails, distal nerve fiber degeneration was not observed in the spinal nerve tracts, although AC-induced membranous organelle accumulations were found in preterminal and terminal nerve fibers. Cytological remodeling similar to the axon reaction was seen mainly in dorsal root ganglia of AC-intoxicated normal and Quv quails. In addition, perikaryal response indicating impaired metabolic activity was observed in Quv quails. The present study showed that Quv quails are sensitive to neurotoxic effects of AC. It is suggested that AC-induced neurotoxicity is not initiated exclusively through its action on NF.

Acrylamide↗
PubMed1994

Potential for transmission of avian influenza viruses to pigs.

Pandemic strains of influenza A virus arise by genetic reassortment between avian and human viruses. Pigs have been suggested to generate such reassortants as intermediate hosts. In order for pigs to serve as 'mixing vessels' in genetic reassortment events, they must be susceptible to both human and avian influenza viruses. The ability of avian influenza viruses to replicate in pigs, however, has not been examined comprehensively. In this study, we assessed the growth potential of 42 strains of influenza virus in pigs. Of these, 38 were avian strains, including 27 with non-human-type haemagglutinins (HA; H4 to H13). At least one strain of each HA subtype replicated in the respiratory tract of pigs for 5 to 7 days to a level equivalent to that of swine and human viruses. These results indicate that avian influenza viruses with or without non-human-type HAs can be transmitted to pigs, thus raising the possibility of introduction of their genes into humans. Sera from pigs infected with avian viruses showed high titres of antibodies in ELISA and neutralization tests, but did not inhibit haemagglutination of homologous viruses, cautioning against the use of haemagglutination-inhibition tests to identify pigs infected with avian influenza viruses. Co-infection of pigs with a swine virus and with an avian virus unable to replicate in this animal generated reassortant viruses, whose polymerase and HA genes were entirely of avian origin, that could be passaged in pigs. This finding indicates that even avian viruses that do not replicate in pigs can contribute genes in the generation of reassortants.

Animals↗
PubMed1994

Experimental Borrelia garinii infection of Japanese quail.

Japanese quail inoculated subcutaneously with Borrelia garinii responded to infection. B. garinii was reisolated mainly from skin and randomly from several organs between 7 and 56 days postinoculation. Skin lesions were occasionally observed in association with spirochete recovery. All birds were positive for antibody at 53 to 56 days postinoculation. These results suggest that the Japanese quail is a model for experimental infection with B. garinii and that birds are reservoirs for Lyme disease spirochetes.

Animals↗