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  • 1
    Electronic Resource
    Electronic Resource
    Chronic progressive sensory ataxic neuropathy: clinicopathological features of idiopathic and Sjögren's syndrome-associated cases (1993)
    Springer
    Journal of neurology 240 (1993), S. 1-7 
    Details
    ISSN: 1432-1459
    Keywords: Chronic ataxic neuropathy ; Sjögren's syndrome ; Cellular infiltration ; Ganglioneuritis ; Idiopathic chronic ataxic neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Eleven patients with chronic progressive sensory ataxic neuropathy were examined clinicopathologically. Three cases were associated with primary Sjögren's syndrome (SS-SAN) and the others were considered to be idiopathic (ISAN). The major clinical symptom in both was loss of proprioceptive and kinesthetic sensation with some impairment of superficial sensation, with multifocal and asymmetrical distribution and progression. The truncal and trigeminal nerves were frequently involved. The motor system was substantially preserved. These somatic sensory and motor symptoms did not differ between ISAN and SS-SAN, but autonomic nervous system signs were more frequent in SS-SAN. Polyclonal elevations of serum IgG and/or IgA were seen in 8 patients. One autopsied case with ISAN combined with previous reports suggested that systemic T-and B-cell infiltration into the nervous tissues, as well as a wide variety of the visceral organs, may be a common finding in ISAN and SS-SAN, and could participate in the cause of this neuropathy and polyclonal hypergammaglobulinaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00838437
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Somatic Mosaicism of the Expanded CAG Trinucleotide Repeat in mRNAs for the Responsible Gene of Machado-Joseph Disease (MJD), Dentatorubral-Pallidoluysian Atrophy (DRPLA), and Spinal and Bulbar Muscular Atrophy (SBMA) (1998)
    Springer
    Neurochemical research 23 (1998), S. 25-32 
    Details
    ISSN: 1573-6903
    Keywords: Machado-Joseph disease (MJD) ; dentatorubral-pallidoluysian atrophy (DRPLA) ; X-linked spinal and bulbar muscular atrophy (SBMA) ; trinucleotide repeat ; mRNA ; somatic mosaicism ; gene expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The CAG trinucleotide repeats in mRNAs for the responsible genes of Machado-Joseph disease (MJD), dentatorubral-pallidoluysian atrophy (DRPLA), and X-linked spinal and bulbal muscular atrophy (SBMA) were examined in various neural and nonneural tissues of affected individuals. The tissue-specific variation of expanded CAG repeat alleles were apparent for mRNAs of all three genes. The expanded CAG repeats of the mRNA were shorter in the cerebellum than in other regions of the central nervous system in DRPLA and MJD, but not in SBMA, and were longer in the liver and colon in MJD. Transcripts of the responsible genes with expanded CAG repeats were detected in all tissues studied, and the tissue-specific variation in the CAG repeat size of the mRNA did not correlate with the tissue-specific severity of pathological involvement in these diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1022441101801
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Expression of GDNF and GDNFR-α mRNAs in Muscles of Patients with Motor Neuron Diseases (1999)
    Springer
    Neurochemical research 24 (1999), S. 785-790 
    Details
    ISSN: 1573-6903
    Keywords: GDNF, GDNFR-α ; mRNA ; motor neuron disease ; muscle, in situ hybridization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mRNA expression levels of GDNF, GDNFR-α and RET were examined in the muscles of amyotrophic lateral screlosis (ALS) and X-linked spinal and bulbar muscular atrophy (SBMA). GDNF mRNA levels were significantly elevated to variable extent in the diseased muscles compared to control muscles, although they were not specific to the type of the diseases. The diseased muscles also have a different expression pattern of GDNF mRNA isoforms from controls. GDNF mRNA expression, however, tended to reduce in advanced muscle pathology. On the other hand, GDNFR-α mRNA levels were not changed significantly on expression levels in the diseased muscles. In situ hybridization study revealed that GDNF and GDNFR-α mRNAs were localized in subsarcolemmal space of muscle cells. RET mRNA was not detected in control nor diseased muscles. These results suggest that the elevated muscle GDNF acts as a trophic signal for motor neurons of motor neuron diseases, implying a possible therapeutic implication of GDNF to this type of diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020739831778
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    Paper (German National Licenses)
    Fulltext
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