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  • 1
    Electronic Resource
    Electronic Resource
    Brain iron homeostasis
    Amsterdam : Elsevier
    Journal of Inorganic Biochemistry 47 (1992), S. 257-265 
    Details
    ISSN: 0162-0134
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0162-0134(92)84071-T
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  • 2
    Electronic Resource
    Electronic Resource
    Brain iron homeostasis
    Amsterdam : Elsevier
    Journal of Inorganic Biochemistry 47 (1992), S. 257-265 
    Details
    ISSN: 0162-0134
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0162-0134(92)84071-T
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Erstmanifestation eines Abbaudefekts überlangkettiger Fettsäuren (VLCADD) mit letalem Ausgang (1998)
    Springer
    Monatsschrift Kinderheilkunde 146 (1998), S. 484-486 
    Details
    ISSN: 1433-0474
    Keywords: Schlüsselwörter Acyl-CoA-Dehydrogenase-Defekt überlangkettiger Fettsäuren ; Dikarbonazidurie ; Hypertrophische Kardiomyopathie ; Key words Very-long-chain acyl-CoA dehydrogenase deficiency ; Dicarboxylic aciduria ; Hypertrophic cardiomyopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Very-long-chain acyl-CoA dehydrogenase deficiency (VLCADD) is a rare disorder of the mitochondrial β-oxidation pathway. A female infant at 2,5 months of age presented with coma, cardiorespiratory arrest, hypoketotic hypoglycemia, hepatomegaly and hypertrophic cardiomyopathy. Urinary dicarboxylic acid profile suggested VLCADD. This diagnosis was confirmed by reduced enzyme activity in fibroblasts (20% of controls). After a few days the infant died of peritonitis caused by a penetrating ulcer of the duodenum. Discussion: A higher incidence of upper gastrointestinal ulcera is reported in patients with medium-chain acyl-CoA dehydrogenase deficiency (MCADD). VLCADD is characterized by early onset and high mortality due to cardiac disease. Gastrointestinal complications may contribute to or be directly responsible for death.
    Notes: Zusammenfassung Der Acyl-CoA-Dehydrogenasedefekt überlangkettiger Fettsäuren (very-long-chain acyl-CoA dehydrogenase deficiency, VLCADD) ist eine seltene Störung der mitochondrialen β-Oxidation. Wir berichten über einen weiblichen Säugling, bei dem im Alter von 2,5 Monaten im Rahmen eines Infekts Koma, Herz- und Atemstillstand, hypoketotische Hypoglykämie, Hepatomegalie und hypertrophe Kardiomyopathie auftraten. Ein charakteristisches Dikarbonsäurenmuster im Urin führte zu der Verdachtsdiagnose eines VLCADD, der durch den Nachweis einer auf 20% der Norm herabgesetzten Enzymaktivität in kultivierten Fibroblasten bestätigt wurde. Das Kind verstarb nach wenigen Tagen an einer Peritonitis infolge eines perforierten Ulcus duodeni. Diskussion: Ein gehäuftes Auftreten penetrierender Ulzera des oberen Magen-Darm-Trakts wurde bereits im Zusammenhang mit dem Abbaudefekt mittelkettiger Fettsäuren (medium-chain acyl-CoA dehydrogenase deficiency, MCADD) beschrieben. VLCADD ist charakterisiert durch frühe Erstmanifestation und eine hohe Mortalität, die v.a. auf die Kardiomyopathie zurückgeführt wird, zu der aber auch gastrointestinale Komplikationen beitragen können.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001120050290
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  • 4
    Electronic Resource
    Electronic Resource
    Changes in glial cell markers in recent and old demyelinated lesions in central pontine myelinolysis (1990)
    Springer
    Acta neuropathologica 80 (1990), S. 46-58 
    Details
    ISSN: 1432-0533
    Keywords: Central pontine myelinolysis ; Demyelination ; Astrocytes ; Cell adhesion molecules ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An immunohistochemical study was performed to compare glial reactions in recent and old lesions of central pontine myelinolysis (CPM). Regions of demyelination and destruction of oligodendrocytes, showed reduced immunoreactivity of myelin basic protein (MBP), myelin-associated glycoprotein (MAG), transferrin, and carbonic anhydrase C (CA C). In addition, labeling of glial fibrillary acidic protein (GFAP) and S-100 protein revealed distinct dystrophic alterations of the astroglia. Remarkably, immunolabeling of GFAP was drastically reduced in astrocytic cytoplasm within freshly demyelinated lesions. Immunostaining of vimentin revealed a differential intracytoplasmic decoration of hypertrophic and dystrophic astrocytes in recent and old CPM lesions. Immunolabeling of desmin failed to stain glial cells. Monoclonal antibodies against HNK-1 exhibited greatly increased immunoreactivity both of persisting oligodendrocytes and of reactive fibrillary astrocytes in old CPM foci. In freshly demyelinated lesions, enhanced immunoreactivity of the X-hapten (3-fucosyl-N-acetyllactosamine) was prominent in astroglia and oligodendrocytes. Simultaneously, reactive astrocytes revealed intracytoplasmic labeling of laminin. Quantitation of GFAP+ astroglia in fresh CPM and control cases revealed an increase in the number of astrocytes within the demyelinated foci and in the surrounding nondemyelinated pontine tissue of CPM cases. The occurrence of astroglial alterations in the demyelinated foci of CPM could be interpreted as “astroglial dystrophy” which may represent a pathogenic factor in CPM. Furthermore, it is possible that changes of the glial microenvironment may influence the astroglia to revert transiently back to an immature phenotype as indicated by the enhanced expression of the X-hapten and HNK-1, and the de novo synthesis of vimentin and laminin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294221
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  • 5
    Electronic Resource
    Electronic Resource
    Changed expression of 9-O-acetyl GD3 (CDw60) in benign and atypical proliferative lesions and carcinomas of the human breast (1998)
    Springer
    Histochemistry and cell biology 110 (1998), S. 217-229 
    Details
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  Expression of gangliosides is affected in various ways by malignant cell transformation. In the present study, we investigated the expression of CDw60, a constituent of O-acetylated disialogangliosides, in benign and atypical proliferative breast diseases, and preinvasive and invasive carcinomas by immunohistochemistry and thin-layer chromatography (TLC). In normal ducts, antibodies to CDw60 (mAb M-T21) reacted to membranes of the Golgi apparatus in the juxtaluminal cell compartment. A similar polarized distribution of Golgi cisterns in epithelial cells was observed in several benign lesions, i.e., fibroadenomas, intraductal papillomas, and gynecomastia. In contrast, blunt duct adenosis and duct hyperplasia exhibited an abnormal cytosolic and cell surface staining, whereas atypical duct hyperplasia showed randomly dispersed immunoreactive Golgi cisterns, indicating loss of epithelial polarity. In mammary carcinomas and in two breast carcinoma cell lines (MCF-7 and EFM-19) the neoplastic cells contained CDw60-immunolabelled Golgi complexes, which were distributed in a disorderly fashion throughout the cytoplasm, thus reflecting a loss of epithelial polarity. Additionally, only well differentiated ductal carcinomas in situ or invasive ductal carcinomas disclosed a strong cell surface labelling, which was absent in lower differentiated carcinomas of the same types. In all carcinomas, the intensity of CDw60 immunostaining decreased with progressing loss of differentiation (grade of dedifferentiation), as demonstrated by staining intensity in paraffin sections and by evaluation of the relative amounts of extracted 9-O-acetyl GD3 by TLC. Our results indicate that abnormal CDw60 expression is already detectable in benign proliferative breast lesions with different risk rates to develop into malignant lesions. Downregulation of CDw60 expression in poorly differentiated invasive carcinomas may be the consequence of loss of cell functions usually associated with poor prognosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004180050284
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  • 6
    Electronic Resource
    Electronic Resource
    Microenvironmental changes during axonal regrowth in the optic nerve of the myelin deficient rat. Immunocytochemical and ultrastructural observations (1993)
    Springer
    Journal of neurocytology 22 (1993), S. 461-479 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lesion-induced regenerative sprouting of CNS axons is accompanied by reactions of the supporting glia and vascular and connective tissue which may influence the extent of regeneration. In a previous report, it was shown that after crush injury, the amyelinated optic nerve of the myelin deficient (md) mutant rat contains greater numbers of regrowing axons proximal to the site of crush than that of normally myelinated littermates. The present study was designed to compare the response of the microenvironment, i.e. glial cells and vascular and connective tissue, in md and normally myelinated optic nerves 2, 4 and 6 days after crush injury. In unoperated normal optic nerves monoclonal antibodies to the HNK-1 carbohydrate labelled astrocytic processes at the ultrastructural level whereas in unoperated md mutants HNK-1 staining was restricted to axonal surfaces. Immunoreactivity with monoclonal antibodies to stage-specific embryonic antigen-1 (SSEA-1) was confined to astrocytic surfaces in both md and wildtype animals. After axotomy of md optic nerves regrowing axons were more numerous in the proximal site of the crush and extended further into the lesion than in wildtype animals. In both md and wildtype rats regrowing axons were HNK-1-positive. In md rats strong reaction with antibodies to laminin and fibronectin was only seen in 6-day-old lesions of md rats whereas immunoreactivity was less distinct in operated littermate controls. Immunolabelling was obviously associated with blood vessels, since crush lesions in both md and wildtype rats were Schwann cell-free as assessed by electron microscopy and immunocytochemistry. In both operated md and normal littermates crush lesions contained degenerating astrocytes as well as reactive astrocytes in which the intermediate filaments of the perikarya failed to stain immunocytochemically for GFAP, vimentin, desmin, and a common determinant of intermediate filaments. In contrast, reactive astrocytes in the lesion site of normally myelinated rats expressed the SSEA-1 antigen intracytoplasmically whereas in md mutants astrocytes were completely SSEA-1-negative. Infiltration of crush lesions by macrophages was less extensive in md rats than in normal littermates. However the overall content of macrophages in the peritoneal cavity was also reduced. The present study demonstrates that (1) md optic nerves lack HNK-1-reactive astrocytes; (2) in the axotomized wildtype optic nerve impaired axonal regrowth may be associated with distinct immuno-phenotypes of the supporting glial cells, i.e. SSEA-1-positive astrocytes; (3) laminin and fibronectin seem not to be essential for improved axonal regrowth in md rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01181566
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