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  • 1
    Electronic Resource
    Electronic Resource
    Characterization of purification-associated reduction in IgE-dependent histamine release from rat peritoneal mast cells (1995)
    Springer
    Inflammation research 44 (1995), S. 541-547 
    Details
    ISSN: 1420-908X
    Keywords: Rat peritoneal mast cell ; Rat peritoneal non-mast cell ; IgE ; Histamine release ; Regulation of histamine release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Histamine release from purified rat peritoneal mast cells (PMC) was examined and compared to that from a non-purified preparation (PEC). Both PEC and PMC released similar amounts of histamine upon stimulation with compound 48/80, calcium ionophore A23187 and substance P. In contrast, IgE-dependent histamine release from PMC caused by antigen, anti-IgE and concanavalin A was very low compared to that of PEC. The reduced IgE-dependent histamine release from PMC, however, was recovered when PMC was reconstituted with non-mast cells (NMC) present in the peritoneal cavity. The effect was time-dependent and reached a plateau in 30 min. NMC from both sensitized and non-sensitized rats recovered the reduced histamine release from PMC dose-dependently. The potentiating effect of NMC was observed even in the presence of excess amount of phosphatidylserine. Supernatants of NMC and a mixture of PMC and NMC incubated for 1 hr at 37°C, however, failed to potentiate the histamine release. These results demonstrate that IgE-dependent histamine release from rat peritoneal mast cells is upregulated by other cells present in the peritoneal cavity, and that the mechanism involved is distinct from that of phosphatidylserine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01757359
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  • 2
    Electronic Resource
    Electronic Resource
    Induction of plasma hepatocyte growth factor in acute colitis of mice (1997)
    Springer
    Inflammation research 46 (1997), S. 166-167 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Hepatocyte growth factor — Acute colitis — Mouse model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective and Design: The study examined plasma levels of hepatocyte growth factor (HGF) in acute colitis models on mice.¶Materials: Acute colitis was induced in male FVB mice (about 25 g) by intrarectal administration of 200 〈mu〉l of 0.5% acetic acid.¶Methods: Plasma was taken at 0, 12, 24, 36, 48 and 72 h after acetic acid treatment. Plasma HGF was measured by an enzyme immunoassay in duplicate.¶Results: Plasma levels of HGF at 0, 12, 24, 36, 48 and 72 h after acetic acid administration were 0.31 ± 0.11 ng/ml (n = 4), 0.45 ± 0.04 ng/ml (n = 4), 0.46 ± 0.13 ng/ml (n = 4), 0.71 ± 0.22 ng/ml (n = 4), 0.82 ± 0.15 ng/ml (n = 4) and 0.44 ± 0.04 ng/ml (n = 4), respectively. Significant increases in plasma HGF levels were observed at 36 and 48 h after the treatment (p 〈 0.05, compared to at 0 h).¶Conclusions: Plasma HGF was induced by acute inflammation of colonic tissues. These findings suggest that HGF in blood may be one of the non-specific markers of inflammation in mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050161
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  • 3
    Electronic Resource
    Electronic Resource
    Pancreatic beta-cell secretory defect associated with mitochondrial point mutation of the tRNALEU(UUR) gene: a study in seven families with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) (1994)
    Springer
    Diabetologia 37 (1994), S. 818-825 
    Details
    ISSN: 1432-0428
    Keywords: C-peptide ; diabetes mellitus ; insulin secretion ; MELAS ; mitochondrial gene mutation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent evidence suggests possible linkage between diabetes mellitus and mitochondrial gene mutation. We surveyed mitochondrial tRNALEU(UUR) (3243) mutation in 7 mitochondrial encephalomyopathy, lactic acidosis and stroke-like episode (MELAS) families and identified 24 mutated subjects (7 MELAS probands and 17 non-MELAS relatives) as well as 11 non-mutant family members. An OGTT in the 24 mutant relatives revealed 14 diabetic subjects, 3 with impaired glucose tolerance and 7 with normal glucose tolerance and all non-mutant family members as having normal glucose tolerance. Insulinogenic index was significantly reduced in the mutant diabetic subjects and those with impaired and normal glucose tolerance in comparison with the normal control subjects and the non-mutant members. Urinary 24-h C-peptide immunoreactivity excretion was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance, compared with the control subjects and the non-mutant family members. Plasma C-peptide immunoreactivity 6 min after glucagon injection was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance compared with the control subjects and the non-mutant family members. Si, an index of insulin sensitivity of the four mutant subjects was within normal range. Islet cell antibodies were negative in sera of eight mutated diabetic subjects, 2 and 6 with impaired and normal glucose tolerance, respectively. Diabetic retinopathy and nephropathy were demonstrated in 7 (50%) and 12 (85.7%) of 14 mutant diabetic subjects, respectively. Neurosensory deafness was demonstrated in 12 (85.7%) of 14 mutated diabetic subjects, (66.7%) of 3 mutated impaired glucose tolerant subjects, but not detected in 6 mutated normal glucose tolerant subjects and 11 non-mutant family members. These findings suggest that the tRNALEU(UUR) mutation is associated with pancreatic beta-cell secretory defect of insulin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404339
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  • 4
    Electronic Resource
    Electronic Resource
    Pancreatic beta-cell secretory defect associated with mitochondrial point mutation of the tRNA L E U ( U U R ) gene: a study in seven families with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) (1994)
    Springer
    Diabetologia 37 (1994), S. 818-825 
    Details
    ISSN: 1432-0428
    Keywords: Key words C-peptide, diabetes mellitus, insulin secretion, MELAS, mitochondrial gene mutation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent evidence suggests possible linkage between diabetes mellitus and mitochondrial gene mutation. We surveyed mitochondrial tRNALEU(UUR) (3243) mutation in 7 mitochondrial encephalomyopathy, lactic acidosis and stroke-like episode (MELAS) families and identified 24 mutated subjects (7 MELAS probands and 17 non-MELAS relatives) as well as 11 non-mutant family members. An OGTT in the 24 mutant relatives revealed 14 diabetic subjects, 3 with impaired glucose tolerance and 7 with normal glucose tolerance and all non-mutant family members as having normal glucose tolerance. Insulinogenic index was significantly reduced in the mutant diabetic subjects and those with impaired and normal glucose tolerance in comparison with the normal control subjects and the non-mutant members. Urinary 24-h C-peptide immunoreactivity excretion was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance, compared with the control subjects and the non-mutant family members. Plasma C-peptide immunoreactivity 6 min after glucagon injection was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance compared with the control subjects and the non-mutant family members. Si, an index of insulin sensitivity of the four mutant subjects was within normal range. Islet cell antibodies were negative in sera of eight mutated diabetic subjects, 2 and 6 with impaired and normal glucose tolerance, respectively. Diabetic retinopathy and nephropathy were demonstrated in 7 (50 %) and 12 (85.7 %) of 14 mutant diabetic subjects, respectively. Neurosensory deafness was demonstrated in 12 (85.7 %) of 14 mutated diabetic subjects, (66.7 %) of 3 mutated impaired glucose tolerant subjects, but not detected in 6 mutated normal glucose tolerant subjects and 11 non-mutant family members. These findings suggest that the tRNALEU(UUR) mutation is associated with pancreatic beta-cell secretory defect of insulin. [Diabetologia (1994) 37: 818–825]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404339
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  • 5
    Electronic Resource
    Electronic Resource
    Clinico-pathological study on macular mutant mouse (1987)
    Springer
    Acta neuropathologica 72 (1987), S. 256-260 
    Details
    ISSN: 1432-0533
    Keywords: Macular mouse ; Menkes kinky hair disease ; Copper metabolism ; Mitochondrial abnormality ; Cerebrum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The macular mutant mouse was clinically and pathologically examined. The hemizygotes began to show white fur color and curly whiskers around postnatal day 3, then seizures and ataxia around day 8, while the normal littermates did not. The hemizygotes also increased weight gradually from birth to day 9, but then showed weight loss and died around day 15 with severe emaciation. These clinical features resembled those in Menkes kinky hair disease. There were no pathological changes in the cerebral cortex in the hemizygotes on day 7. On day 10, two to three clear vacuoles began to appear in a few neurons in the cerebrum. These neurons with vacuoles increased gradually in number and degenerative neurons were also observed by day 14. Ultrastructurally, they corresponded to giant abnormal mitochondria with an electron-lucent matrix and short peripherally located cristae. Other abnormal mitochondria, which were characterized by an electron-dense matrix with tubular or vesicular cristae, were also observed in the cerebral cortical neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691098
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  • 6
    Electronic Resource
    Electronic Resource
    Golgi study on brain of macular mutant mouse as a model of Menkes kinky hair disease (1987)
    Springer
    Acta neuropathologica 72 (1987), S. 349-354 
    Details
    ISSN: 1432-0533
    Keywords: Macular mutant mouse ; Menkes kinky hair disease ; Golgi study ; Purkinje cell ; Copper metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study was undertaken to elucidate, using the Golgi method, the neuropathological change in the brain of the macular mutant mouse, whose hemizygote (Ml/y) is considered to be a model of Menkes kinky hair disease (MKHD). The hemizygote mice gradually lost weight after 10 days of age and died with emaciation and seizure around day 15. The normal littermate (+/y) was well developed. In the cerebrum, the arborization of pyramidal neurons in the layer V of the Ml/y was the same as that in the +/y on day 10. However, development of arborization in the Ml/y was delayed in comparison with that in the +/y on days 12 and 14. Purkinje cells with several somal sprouts were observed in the cerebellum in both the Ml/y and +/y on day 7. The somal sprouts in the +/y had regressed gradually by day 12, while they were still in the anterior and middle lobes of the Ml/y on day 14. Additionally, the trunks of Ml/y stem dendrites became thicker and a cactus formation was recognized on the branching portion of the dendrites on day 14. Arborization of these abnormal Purkinje cells was distinctly poor compared with that in the +/y. These results suggest that the growth of the neurons is delayed in the Ml/y and simultaneously their cytoskeletal developments are disturbed, especially in the Purkinje cells. There is a close similarity in many respects to the neuropathological change in MKHD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687266
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  • 7
    Electronic Resource
    Electronic Resource
    Peculiar pattern of glial fibrillary acidic protein production in extracranial metastatic tumor cells of malignant astrocytoma (1987)
    Springer
    Acta neuropathologica 74 (1987), S. 89-91 
    Details
    ISSN: 1432-0533
    Keywords: Astrocytoma ; Extracranial metastasis ; Glial fibrillary acidic protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An 83-year-old woman suffered from malignant astrocytoma originating in the temporal lobe. Autopsy revealed its extracranial metastasis to the liver, lung and bone marrow. The tumor tissue at the primary site was composed of plump, process-forming cells and small cells with scanty cytoplasm, and showed dural invasion. In the metastatic areas, most of the tumor cells were small cells, although proliferation of the plump cells in contact with perivascular connective tissue was marked, particularly in the liver. These plump cells were positively stained with antiserum to glial fibrillary acidic protein (GFAP), showing that the collagenous tissue was able to induce increased production of GFAP by the glial tumor cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688344
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  • 8
    Electronic Resource
    Electronic Resource
    Neurofibrillary tangles in human upper cervical ganglia (1987)
    Springer
    Acta neuropathologica 75 (1987), S. 156-159 
    Details
    ISSN: 1432-0533
    Keywords: Neurofibrillary tangles ; Paired helical filaments ; Upper cervical ganglion ; Ubiquitin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neurofibrillary tangles (NFTs) are one of the main pathological hallmarks of Alzheimer's disease or senile dementia, and are seen in the cerebral cortex and some other nuclei in the central nervous system (CNS). No NFTs have been reported in the human peripheral nervous system, although NFTs were recognized in the dorsal root ganglion of the aged rodents. We report here the presence of NFTs in the upper cervical ganglia (UCGs), but not in the stellate nor in the celiac ganglia, of an elderly patient, who was not demented and had only minimal senile changes in the CNS. Immunohistochemically the antibodies to microtubule-associated protein 2, paired helical filaments and ubiquitin stained positively the NFTs in the UCGs. On electron microscopic examination a periodical twisted pattern of the filaments was identified; these findings suggest that the NFTs of the UCGs have just the same properties as those of the cerebral cortex. This is the first report of the demonstration of NFTs in the peripheral ganglia and might contribute to the study of mechanism of NFT production.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687076
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  • 9
    Electronic Resource
    Electronic Resource
    Electron microscopic study on brain of macular mutant mouse after copper therapy (1988)
    Springer
    Acta neuropathologica 76 (1988), S. 574-580 
    Details
    ISSN: 1432-0533
    Keywords: Macular mouse ; Menkes kinky hair disease ; Copper therapy ; Mitochondrial abnormalities
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The hemizygote of the macular mutant mice, which is clinically and neuropathologically considered to be a model of Menkes kinky hair disease (MKHD), were injected intraperitoneally four times with 10, 20, 20 and 30 μg of cupric chloride on days 4, 6, 8 and 10 after birth, respectively. Their cerebral and cerebellar cortices were chronologically examined by electron microscopy. In the cerebral cortes, only a few abnormal mitochondria with electron-lucent matrix and short peripherally located cristae were scattered in the neurons on day 14, and these had almost entirely vanished after day 21. In the cerebellar cortex, abnormal mitochondria were frequently found on day 14 in the dendrites of the Purkinje cells, whereas they were only occasionally observed in their cytoplasm. Those in the dendrites had decreased in number on day 30, and only a few of them were seen in the cerebellum after day 45. These results show that the copper therapy reduced ultrastructural abnormalities in the hemizygote of this mutant mouse.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689595
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  • 10
    Electronic Resource
    Electronic Resource
    Golgi study on macular mutant mouse after copper therapy (1988)
    Springer
    Acta neuropathologica 76 (1988), S. 606-612 
    Details
    ISSN: 1432-0533
    Keywords: Macular mouse ; Menkes kinky hair disease ; Copper therapy ; Golgi study ; Purkinje cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study was undertaken to elucidate the clinical and neuropathological effects of copper administration on the macular mutant mouse. Its hemizygote, which is considered to be a model of Menkes kinky hair disease (MKHD), was injected intraperitoneally four times with 10, 20, 20 and 30 μg of cupric chloride on days 4, 6, 8 and 10, respectively. The hemizygote's curly whiskers gradually straightened and the frequent tonic seizures and ataxia disappeared after the injections. The body weight also gradually increased. In the cerebral cortex, the dendritic arborization of the pyramidal neurons in both the normal littermate and the treated hemizygote developed with time and reached the maximum around day 60. In the treated hemizygote, however, the arborization of the dendrites was significantly poor in comparison with that in the normal littermate from day 20 to 90. In the cerebellum of the treated hemizygote, the abnormal Purkinje cells with the few somal sprouts, thick stem dendrite and/or poor arborization, which were seen in the non-treated hemizygote, were improved by day 30, while their focal dendritic swellings remained even on day 60. These results indicate that the copper therapy improves not only the clinical manifestations but also the neuropathological changes, especially in the cerebellum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689600
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