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  • 1
    Electronic Resource
    Electronic Resource
    Effects of the calcium ionophore A23187 on airway responsiveness to histamine and substance P in guinea pigs (1997)
    Springer
    Inflammation research 46 (1997), S. 108-113 
    Details
    ISSN: 1420-908X
    Keywords: Key words: A23187 — Histamine — Neutral endopeptidase — Nitric oxide — Substance P
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: We evaluated the mechanism of the airway hyperresponsiveness (AHR) induced by a calcium ionophore in guinea pigs. ¶Materials and Methods: Airway responsiveness to intravenous histamine (HS) and substance P (SP) was measured 24 h after a 1-h exposure to aerosolized A23187 (0.03 or 0.1 mg/ml) or its vehicle (10% DMSO). Changes were assessed by calculating – logPC350HS and – logPC350SP. Neutral endopeptidase (NEP) activity in the airway tissues, as well as the nitrite (NO2 −) levels and the cell population in bronchoalveolar lavage fluid (BALF) was determined after measurement of pulmonary function. Changes in SP-induced vascular permeability 24 h after exposure to A23187 were measured by the Evans Blue dye extravasation technique. ¶Results: Exposure to A23187 caused a significant AHR to SP, along with a significant increase in the number of neutrophils and epithelial cells in the BALF. While there was no significant change in NEP activity in the airway tissues, the levels of nitrite in the BALF were significantly decreased in A23187-exposed animals. Significant correlations were found between the number of epithelial cells in the BALF and – logPC350SP (r = 0.477, p 〈 0.05) and between nitrite levels in the BALF and – logPC350SP (r = −0.491, p 〈 0.05). A23187 exposure did not significantly change the SP-induced airway microvascular leakage. ¶Conclusions: These data suggest that A23187 exposure induced AHR to SP possibly by reducing NO levels in the airway tissues. This may be due to damaged airway epithelium and/or NO breakdown by activated inflammatory cells in the airways of these guinea pigs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050125
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  • 2
    Electronic Resource
    Electronic Resource
    An autopsy case of acute porphyria with a decrease of both uroporphyrinogen I synthetase and ferrochelatase activities (1984)
    Springer
    Acta neuropathologica 64 (1984), S. 6-11 
    Details
    ISSN: 1432-0533
    Keywords: Acute porphyria ; Porphyric neuropathy ; Axonal degeneration ; Uroporhyrinogen I synthetase ; Ferrochelatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An autopsy case of a 37-year-old woman with acute porphyria is reported. The patient began to complain of severe menstrual pains, and later developed serious peripheral neuropathy and various autonomic nervous symptoms. The autopsy revealed a marked loss and degeneration of axons and myelin sheaths in the peripheral nervous system (PNS), and prominent central chromatolysis of the spinal anterior horn cells. The predominant process of the peripheral neuropathy appeared to be axonal degeneration. Biochemical analysis showed a marked increase of delta-aminolevulinic acid (ALA), porphobilinogen, uroporphyrin, and coproporphyrin in the urine, and an increase of coproporphyrin and protoporphyrin in the stools and blood. In the analysis of the enzymatic activities of the liver and bone narrow, the activity of ALA synthetase (ALA-S) was markedly increased, and the activities of both uroporphyrinogen I synthetase (URO-S) and ferrochelatase were decreased. It was characteristic in this case that the enzymatic abnormalities found in both acute intermittent porphyria (AIP) and variegate porphyria (VP) coexisted. Biochemical analysis of the sciatic nerve showed an increase of ALA-S activity and a decrease of both URO-S and ALA dehydrase activities. This was the first report that indicated the presence of abnormal activities of the heme biosynthetic enzymes in the peripheral nerves of porphyric patients. The possibility was discussed that these enzymatic abnormalities of the heme biosynthesis in the peripheral nerve itself might be strongly related to the pathogenesis of the porphyric neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00695599
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  • 3
    Electronic Resource
    Electronic Resource
    Chronic manganese poisoning: A neuropathological study with determination of manganese distribution in the brain (1986)
    Springer
    Acta neuropathologica 70 (1986), S. 273-278 
    Details
    ISSN: 1432-0533
    Keywords: Chronic manganese poisoning ; Pallidal lesion ; Distribution of manganese
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An autopsy case of a 52-year-old man suffering from chronic manganese poisoning (CMP) is reported with determination of the manganese distribution in the brain. The patient had been working in a manganese ore crushing plant since 1965. In 1967 he began to complain of difficulties in walking and diminished libido. Later, he developed various neuro-psychiatric symptoms including euphoria, emotional incontinence, masked face, monotonous speech, “cock-walk”, increased muscle tone, weakness of upper and lower extremities, tremor of the eye lids, and exaggeration of knee jerks. The major neuro-pathological change was degeneration of the basal ganglia, in which the pallidum was severely affected. The pallidum discolsed a loss and degeneration of nerve cells, which was especially marked in the medial segment, a prominent decrease of myelinated fibers, and moderate astrocytic proliferation. The substantia nigra was intact. Distribution of manganese in the brain of the present case of CMP was determined using flameless atomic absorption spectrometry and compared with control cases and also a case of Parkinson's disease (PD). There was no significant difference between the control cases and the case of PD in average concentration of manganese and its ditribution in the brain. The present case of CMP showed no elevation in average concentration of manganese in the brain. However, there were some changes in its distribution. Thus, the continuance of neurological disorders in CMP is not linked to an elevated manganese concentration itself in the brain. CMP appears to be different from PD in neuropathology and manganese behavior in brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00686083
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  • 4
    Electronic Resource
    Electronic Resource
    Nervous tissue injury induced by immune complexes (1982)
    Springer
    Acta neuropathologica 56 (1982), S. 279-284 
    Details
    ISSN: 1432-0533
    Keywords: Ferritin ; Galactocerebroside ; Immune complexes ; Proliferative changes in choroid plexus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Studies on acute and chronic serum sickness in mice were carried out to clarify the effects of immune complexes on the brain. These complexes were prepared with either anti-ferritin or anti-galactocerebroside rabbit antibodies and were injected i.m. into C57/BL mice. They were shown to be deposited in the choroid plexus, subependymal regions and meninges, and were accompanied by proliferative and destructive changes. The probable allergic mechanisms involved in the pathogenesis of these lesions are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691259
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  • 5
    Electronic Resource
    Electronic Resource
    Cortical cerebellar degeneration with testicular neoplasm (1985)
    Springer
    Acta neuropathologica 66 (1985), S. 170-172 
    Details
    ISSN: 1432-0533
    Keywords: Cortical cerebellar degeneration ; Testicular neoplasm ; Paraneoplastic syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cortical cerebellar degeneration was found in a 28-year-old man with testicular neoplasm. The patient, who had undergone a left orchidectomy for the testicular tumor, developed progressive cerebellar symptoms with mental changes 7 months later. The autopsy revealed the spread of a malignant germ cell tumor of the testis, and cortical cerebellar degeneration in the central nervous system (CNS) which was characterized by almost complete loss of Purkinje cells and degeneration of the both dentate nuclei and superior cerebellar peduncles. The present case is the first of cortical cerebellar degeneration combined with testicular neoplasms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688695
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  • 6
    Electronic Resource
    Electronic Resource
    Immunolocalization of cathepsins B, H and L in skeletal muscle of X-linked muscular dystrophy (mdx) mouse (1988)
    Springer
    Acta neuropathologica 75 (1988), S. 217-225 
    Details
    ISSN: 1432-0533
    Keywords: mdx mouse ; Cathepsin L ; Macrophages ; Muscle structural proteins ; Proteolysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The amounts of non-collagen proteins (muscle structural proteins) and the activity of creatine kinase were significantly decreased in muscles of 28-day-old mdx mice. The activities of lysosomal thiol proteases such as cathepsins B and L were increased in muscles of mdx mice at as early as 10 days of age. Endogenous thiol proteinase inhibitor and various lysosomal hydrolases also showed increased activities. The localization of cathepsins B, H and L, and endogenous thiol proteinase inhibitor was investigated using the respective specific antibodies. While only invading macrophages were stained strongly with anticathepsin B and H, and anti-thiol proteinase inhibitor antibodies, cathepsin L was localized in muscle cells as well as in invading macrophages. Cathepsin L in muscle cells itself may initially degrade muscle structural proteins, before lysosomal thiol proteases, mainly derived from macrophages, degrade them in skeletal muscles of mdx mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690529
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  • 7
    Electronic Resource
    Electronic Resource
    Systemic amyloid deposition in old age and dementia of Alzheimer type: the relationship of brain amyloid to other amyloid (1988)
    Springer
    Acta neuropathologica 77 (1988), S. 136-141 
    Details
    ISSN: 1432-0533
    Keywords: Amyloid deposition ; Amyloid protein ; Ageing ; Dementia of Alzheimer type
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated amyloid deposition in the brain and other organs in 105 consecutive autopsy cases, aged 59 to 101 years. They consisted of two groups; 15 patients with dementia of Alzheimer type (DAT) and 90 patients without DAT. Amyloid deposition was found in 93% of all cases. The incidence of amyloid deposition increased with age. The number of organs affected with amyloid deposition in each case also increased with age. The incidence of amyloid deposition in each organ was as follows; 88% in pituitary gland, 66% in brain [amyloid of senile plaque (SP) (61%) and/or cerebral amyloid angiopathy (CAA) (56%)], 33% in pancreas, 3% in heart, and less in others. In immunohistochemical studies using the antisera to the various kinds of amyloid or related proteins, amyloid β protein was demonstrated in brain amyloids including SP and CAA, but not in others. Cardiac amyloid was positive for prealbumin. Pituitary amyloid and CAA were positive for amyloid P-component. The incidence of brain amyloids in DAT were significantly higher than that in non-DAT. There was no significant difference in the incidence of pituitary and pancreatic amyloid between DAT and non-DAT. In the non-DAT patients, there were significant positive correlations in amyloid deposition between the brain and pituitary gland and between the brain and pancreas. Acceleration of amyloid deposition would be a process confined to the brain in the patients with DAT. The pathogenesis of the accelerated deposition of brain amyloids is discussed from the point of view of amyloidosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687423
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  • 8
    Electronic Resource
    Electronic Resource
    Selective loss of nigral neurons in Alzheimer's disease: a morphometric study (1992)
    Springer
    Acta neuropathologica 83 (1992), S. 271-276 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Substantia nigra ; Pigmented neurons ; Neurofibrillary tangles ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Loss of neurons from the substantia nigra (SN), which is sometimes observed in Alzheimer's disease (AD), was quantitatively analyzed in 10 cases of presenile AD and 19 age-matched controls. On sections from the upper and lower portions of the SN, the pigmented zone (zona compacta) and the nonpigmented zone (zona reticulata) were delineated, and these zones were partitioned into quarters: medial, mid-medial, mid-lateral and lateral. This approach clarified topographical preference of neuronal depletion in the SN of AD; namely (1) pigmented neurons were more severely affected than non-pigmented neurons, (2) neuronal depletion was more marked in the lower SN (−38%, P〈0.001), where the pigmented neurons in the medial quarter were most severely affected (−51%, P〈0.001), (3) in the upper SN (neuronal loss: −21%, P 〈0.01), the pigmented neurons in the mid-medial quarter were most severely affected (−43%, P〈0.01). These findings suggest that some groups of nigral neurons are primarily involved in presenile AD. Gallyas staining after bleaching of melanin pigments uncovered a large number of neurofibrillary tangles (NFTs) mainly in the pigmented zone, especially in the medial quarter. A large number of NFTs, scarse senile plaques, and substantial depletion of neurons form an unique combination of Alzheimer pathology in the SN not well recognized so far.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296789
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  • 9
    Electronic Resource
    Electronic Resource
    Presence of endothelin-1-like immunoreactivity in human cerebrospinal fluid
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 166 (1990), S. 1274-1278 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0006-291X(90)91003-B
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  • 10
    Electronic Resource
    Electronic Resource
    Detection of tryptase−, chymase+ cells in human CD34+ bone marrow progenitors (2004)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 34 (2004), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Mast cells (MCs) arise from haematopoietic stem cells. We have recently reported that CD34+ progenitors derived from human bone marrow (BM) develop into tryptase+, chymase+ MCs when cultured in the presence of recombinant human stem cell factor (rhSCF) and recombinant human IL-6 (rhIL-6). In an experiment for the expression of chymase during differentiation, chymase+ cells were detected in human BM, but tryptase+ cells were not found.Objective The purpose of this study was to show the appearance of chymase+ cells in CD34+ cells with an origin different from MC differentiation.Methods CD34+ cells from human BM were sorted with anti-CD117 monoclonal antibody (mAb), and cytospins of CD34+, CD34+CD117+, or CD34+CD117− were prepared. These cells were cultured with rhSCF+rhIL-6 for 12 weeks. Some of the cells were subjected to either histological stain with Wright–Giemsa or immunocytochemistry with anti-chymase mAb. Real-time RT-PCR was also performed to compare the transcriptional level of chymase from each cell preparation.Results Chymase was expressed in CD34+ cells as well as human MCs by immunocytochemistry. Substantial CD34+CD117− cells, but not CD34+CD117+ cells, were stained immunocytochemically with anti-chymase mAb. For 1 week culture with rhSCF+rhIL-6, no cells expressed chymase in any preparation. Real-time RT-PCR revealed positivity for chymase mRNA in CD34+ cells, but it reduced at 1 week of culture, and increased as cells developed into MCs. Chymase mRNA in CD34+CD117+ cells was negligible compared with that in CD34+CD117−. Tryptase mRNA was below the detectable level in CD34+ cells, and increased along with MC differentiation. After 12 weeks of culture, CD34+CD117+ developed predominantly into MCs, whereas CD34+CD117− developed into monocytes/macrophages.Conclusion Our findings suggested that chymase is present not only in MCs but also in CD34+CD117− BM progenitors, but that its origin is different from the MC lineage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2004.02105.x
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