Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    DNA single-strand breaks are increased in muscle diseases with rimmed vacuoles (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 390-394 
    Details
    ISSN: 1432-0533
    Keywords: Key words Rimmed vacuole ; In situ nick translation ; DNA single-strand breaks ; DNA double-strand breaks
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Some pathological similarities between Alzheimer’s disease and muscle diseases with rimmed vacuoles (RV) have been pointed out. For example, several pathological hallmark proteins have been reported to be immunopositive in the lesions of both diseases. Since apoptotic processes or primary DNA damage are suggested to play a role in the pathomechanism of Alzheimer’s disease, we examined DNA double-strand breaks (DSB) and single-strand breaks (SSB) in the muscle biopsy specimens of several diseases, including muscle diseases with RV. Although no DSB-positive myonuclei were detected in any muscles examined, the number of SSB-positive myonuclei markedly increased in the muscles from cases with polymyositis and muscle diseases with RV. In polymyositis, SSB-positive myonuclei were observed in regenerating fibers and muscle fibers in the vicinity of inflammatory infiltrates, suggesting that the increase of SSB is due to muscle fiber regeneration following necrosis and inflammation. In muscle diseases with RV, however, SSB-positive myonuclei were observed in small angulated fibers and in morphologically normal fibers, regardless of necrosis, regeneration or inflammation. These findings suggest that muscle diseases with RV may share a common pathological process involving DNA damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010000192
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Spinal cord multiple sclerosis lesions in Japanese patients: Schwann cell remyelination occurs in areas that lack glial fibrillary acidic protein (GFAP) (1985)
    Springer
    Acta neuropathologica 65 (1985), S. 217-223 
    Details
    ISSN: 1432-0533
    Keywords: Multiple sclerosis ; Schwann cell ; Remyelination ; Glial fibrillary acidic protein ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To extend earlier observations on Schwann cell remyelination in multiple sclerosis (MS) lesions (Itoyama et al. 1983) we immunostained spinal cord sections from eight Japanese MS patients with antiserum to Po glycoprotein, a major constituent of peripheral nervous system (PNS) myelin, myelin basic protein (MBP), and glial fibrillary acidic protein (GFAP). Spinal cord sections from six of the eight Japanese MS patients contained large clusters of peripheral myelin sheaths with anti-Po immunoreactivity. In lesions found in four of the six patients, thousands of Po-stained PNS myelin sheaths were present. Necrosis was prominent in these lesions which included more than half of the spinal cord's transverse area. The number and density of regenerating myelin sheaths of peripheral origin were much greater than we observed in MS spinal cord lesions of white people (Itoyama et al. 1983). Anti-GFAP immunoreactivity was present in most brain and spinal cord lesions. However, the areas in lesions that contained large groups of PNS myelin sheaths lacked anti-GFAP immunoreactivity. Our data suggest that spinal MS lesions that are large, severely demyelinated, and partially necrotic may contain factors that inhibit fibrous astrogliosis. These factors, other substances in the large lesions and/or the lack of astrocytic scarring could then promote Schwann cell invasion, multiplication, and remyelination of surviving axons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687001
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Age-related changes of sodium-dependentd-[3H]aspartate and [3H]FK506 binding in rat brain (1997)
    Springer
    Journal of neural transmission 104 (1997), S. 259-267 
    Details
    ISSN: 1435-1463
    Keywords: Aging ; excitatory amino acid transport sites ; FK506 ; immunophilin ; receptor autoradiography ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated age-related changes in excitatory amino acid transport sites and FK506 binding protein (FKBP) in 3-week-, and 6-, 12-, 18- and 24-month-old Fischer 344 rat brains using receptor autoradiography. Sodium-dependentd-[3H]aspartate and [3H]FK506 were used to label excitatory amino acid transport sites and immunophilin (FKBP), respectively. In immature rats (3-week-old), sodium-dependentd-[3H]aspartate binding was lower in the frontal cortex, parietal cortex, striatum, nucleus accumbens, whole hippocampus, thalamus and cerebellum as compared to adult animals (6-month-old), whereas [3H]FK506 binding was significantly lower only in the hippocampus, thalamus and cerebellum. [3H]FK506 binding exhibited no significant change in the brain regions examined during aging. However, sodium-dependentd-[3H]aspartate binding showed a conspicuous reduction in the substantia nigra in 18-month-old rats. Thereafter, a significant reduction in sodium-dependentd-[3H]aspartate binding was found in the thalamus, substantia nigra and cerebellum in 24-month-old rats. Other regions also showed about 10–25% reduction in sodium-dependentd-[3H]aspartate binding. The results indicate that excitatory amino acid transport sites are more susceptible to aging process than immunophilin. Further, our findings demonstrate the conspicuous differences in the developmental pattern between excitatory amino acid transport sites and immunophilin in immature rat brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01273186
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Sequential changes of cholinergic and dopaminergic receptors in brains after 6-hydroxydopamine lesions of the medial forebrain bundle in rats (2000)
    Springer
    Journal of neural transmission 107 (2000), S. 873-884 
    Details
    ISSN: 1435-1463
    Keywords: Keywords: Cholinergic receptors ; high-affinity choline uptake sites ; dopamine D2 receptors ; receptor autoradiography ; 6-hydroxydopamine ; nigrostriatal pathway ; rat.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. We studied sequential changes in muscarinic cholinergic receptors, high-affinity choline uptake sites and dopamine D2 receptors in the brain after 6-hydroxydopamine lesions of the medial forebrain bundle in rats. The animals were unilaterally lesioned in the medial forebrain bundle and the brains were analyzed at 1, 2, 4 and 8 weeks postlesion. [3H]Quinuclidinylbenzilate (QNB), [3H]hemicholinum-3 (HC-3) and [3H]raclopride were used to label muscarinic cholinergic receptors, high-affinity choline uptake sites and dopamine D2 receptors, respectively. The degeneration of nigrostriatal pathway produced a transient decrease in [3H]QNB binding in the parietal cortex of both ipislateral and contralateral sides at 2 and 8 weeks postlesion. [3H] QNB binding also showed a mild but insignificant decrease in the ipsilateral striatum throughout the postlesion periods. No significant change was observed in the substantia nigra (SN) of both ipsilateral and contralateral sides throughout the postlesion periods. In contrast, [3H]HC-3 binding showed no significant change in the parietal cortex of both ipsilateral and contralateral sides during the postlesion. However, [3H]HC-3 binding was upregulated in the ipsilateral dorsolateral striatum throughout the postlesion periods. The ventromedial striatum also showed a significant increase in [3H]HC-3 binding at 1 week and 2 weeks postlesion. On the other hand, no significant change in [3H]raclopride binding was found in the parietal cortex of both ipsilateral and contralateral sides during the postlesion. [3H]Raclopride binding showed a conspicuous increase in the ipsilateral striatum (35–52% of the sham-operated values in the lateral part and 39–54% in the medial part) throughout the postlesion periods. In the contralateral side, a mild increase in [3H]raclopride binding was also found in the striatum (10–15% of the sham-operated values in the lateral part and 22% in the medial part) after lesioning. However, a significant decline in [3H]raclopride binding was observed in the ipsilateral SN and ventral tegmental area during the postlesion. The present study indicates that 6-hydroxydopamine injection of medial forebrain bundle in rats can cause functional changes in high-affinity choline uptake site in the striatum, as compared with muscarinic cholinergic receptors. Furthermore, our studies demonstrate an upregulation in dopamine D2 receptors in the striatum and a decrease in the receptors in the SN and ventral tegmental area after the 6-hydroxydopamine injection. Thus, these findings provide further support for neurodegeneration of the nigrostriatal pathway that occurs in Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007020070039
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Effects of chronic treatment with a cyclic AMP-selective phosphodiesterase inhibitor, rolipram, on excitatory amino acid neurotransmission systems in young and aged rat brains (1997)
    Springer
    Journal of neural transmission 104 (1997), S. 269-280 
    Details
    ISSN: 1435-1463
    Keywords: Rolipram ; aging ; excitatory amino acids ; autoradiography ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rolipram selectively inhibits cyclic AMP-specific phosphodiesterase, and leads to an increase in cyclic AMP levels in the brain. In this study, we investigated the effects of chronic rolipram treatment on excitatory and inhibitory amino acid neurotransmission systems in young and aged Wistar rat brains. We used in vitro autoradiography with [3H]MK-801, [3H]glycine, D-[3H]aspartate, and [3H]muscimol to label N-methyl-D-aspartate (NMDA) receptors, glycine modulatory sites, glutamate transport sites, and γ-aminobutyric acid-A (GABA) receptors, respectively. Rolipram (0.01 or 0.1 mg/kg, per os) or its vehicle (distilled water) was administered once a day for 4 weeks. The highest binding of [3H]MK-801, [3H]glycine, and d-[3H]aspartate was seen in the hippocampus in vehicle-treated rats. No significant differences in these binding activities were seen between young and aged rat brains. [3H]Muscimol binding was the highest in the cerebellum, and decreased in many brain regions in aged rats. The chronic rolipram treatment resulted in (1) an increase in [3H]MK-801 binding in the dentate gyrus in both young and aged rats, (2) remarkable reductions in D-[3H]aspartate binding in many regions of both young and aged rats, and (3) no or minimal changes in [3H]glycine and [3H]muscimol binding. These results suggest that the chronic rolipram treatment modifies the excitatory amino acid neurotransmission system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01273187
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Amplification of JC virus regulatory DNA sequences from cerebrospinal fluid: diagnostic value for progressive multifocal leukoencephalopathy (1998)
    Springer
    Archives of virology 143 (1998), S. 249-262 
    Details
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary.  Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease in the central nervous system caused by a ubiquitous human polyomavirus designated as JC virus (JCV). PML affects individuals with decreased immune competence and is now one of the common opportunistic infections in patients with AIDS. JCV DNAs in the brain of PML patients contain various PML-type regulatory regions that were generated from the archetypal regulatory region during persistence. Recently, many studies have suggested that detection of JCV DNA from the cerebrospinal fluid (CSF) may offer a tool for diagnosing PML. However, in all of these studies, coding sequences within the T antigen or capsid protein gene have been targeted for amplification. To amplify the JCV regulatory region, we established a nested PCR that could efficiently amplify the regulatory region from most JCV subtypes prevalent in the world. Using this PCR, we amplified JCV regulatory regions from the CSF samples from 4 patients strongly suspected of PML, whereas amplification was negative from 80 CSF samples from patients without PML. Sequencing of the amplified fragments revealed that they had unique deletions and/or duplications. Furthermore, in 3 PML patients, we analyzed the structures of regulatory regions derived from the brain as well as CSF. In each of these cases, the major regulatory sequence of both origins were identical. This finding indicates that JCV DNA in brain lesions is excreted in the CSF. Since the structures of PML-type JCV regulatory regions are unique to individual patients, the current PCR, if the amplified fragments are sequenced, can eliminate false positives that may arise from contaminations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007050050284
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Familial myopathy with scapulohumeral distribution, rigid spine, cardiopathy and mitochondrial abnormality (1989)
    Springer
    Journal of neurology 236 (1989), S. 52-54 
    Details
    ISSN: 1432-1459
    Keywords: Autosomal dominant inheritance ; Rigid spine syndrome ; Emery-Dreifuss muscular dystrophy ; Mitochondrial myopathy ; Scapulohumeral muscular atrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A 37-year-old woman with scapulohumeral muscular atrophy, rigid spine and cardiopathy is reported. Muscle weakness, advanced atrioventricular block and contractures at the neck, elbows and ankles had occurred during her childhood. An autosomal dominant mode of inheritance was suggested because her mother, sister and brother had the same disorder. Pleomorphic mitochondria had accumulated in the subsarcolemmal space of the skeletal muscle. There was no evident enzyme defect in the mitochondrial electron transport system. Although the clinical features had some similarity with those of Emergy-Dreifuss muscular dystrophy or rigid spine syndrome, the pattern of inheritance and the muscle pathology differed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00314219
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Stress Protein Inductions After Brain Ischemia (1998)
    Springer
    Cellular and molecular neurobiology 18 (1998), S. 709-719 
    Details
    ISSN: 1573-6830
    Keywords: HSP72 ; HSC73 ; HSP60 ; cytochrome c oxidase ; ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1. Hippocampal CA1 neurons are the most vulnerable to transient cerebral ischemia. However, the mechanism has not been fully understood. 2. The mRNAs for 72-kd (HSP72) and 73-kd (HSC73) heat shock proteins (HSPs), which are located mainly in the cytoplasm, were greatly induced together in CA1 cells, with a peak at 1–2 days in gerbils. However, immunoreactive HSP72 protein was only minimally expressed in CA1 neurons. 3. The mRNA for mitochondrial HSP60 began to increase at 3 hr in CA1 cells and was sustained until 1 day. 4. The level of mRNA for cytochrome c oxidase subunit I (COX-I) progressively decreased in CA1 neurons after a transient ischemia and completely disappeared at 7 days. The activity of cytochrome c oxidase (COX) protein also showed an early decrease in CA1 cells and was followed by a reduction in the level of COX-I DNA after 2 days. 5. These results suggest that HSP gene inductions were inhibited at the translational level but that mitochondrial DNA expression was disturbed at the transcriptional level. A disturbance of mitochondrial DNA expression could cause progressive failure of energy production of CA1 cells that eventually results in neuronal cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020694205003
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Post-Ischemic Alterations in [3H]FK506 Binding in the Gerbil and Rat Brains (1998)
    Springer
    Metabolic brain disease 13 (1998), S. 9-19 
    Details
    ISSN: 1573-7365
    Keywords: FK506 ; immunophilin ; global ischemia, focal ischemia, receptor autoradiography, gerbil, rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated post-ischemic changes in FK506 binding protein (FKBP) in the brain after transient global ischemia in gerbils or transient focal ischemia in rats. [3H]FK506 was used to label FKBP as a immunophilin. In transient global ischemia, [3H]FK506 binding showed a transient reduction in the frontal cortex only 1 h after recirculation. In the striatum, the dorsolateral part exhibited a significant increase in [3H]FK506 binding 5, 24 and 48 h after ischemia. However, the ventromedial part showed a transient elevation in [3H]FK506 binding 24 h after ischemia. Thereafter, the ventromedial part showed no conspicuous change in [3H]FK506 binding up to 7 days after ischemia. The dorsolateral part also showed no significant change in [3H]FK506 binding 7 days after ischemia. In the hippocampus and thalamus, [3H]FK506 binding was unchanged in the stratum radiatum of the hippocampal CA1 sector, hippocampal CA3 sector, dentate gyrus and thalamus up to 7 days after ischemia. However, the stratum oriens of the hippocampal CA1 sector showed a significant reduction in [3H]FK506 binding 48 h and 7 days after ischemia. A histological study showed that transient cerebral ischemia caused a severe damage in the striatum and hippocampal CA1 sector. In a model of transient focal ischemia, a marked increase in [3H]FK506 binding was also found in the striatum and cerebral cortex where severe infarctions were observed. These results demonstrate that post-ischemic change in [3H]FK506 binding between the striatum and hippocampus may be produced by different mechanisms. Furthermore, our findings suggest that immunophilins may play some role in the pathogenesis of ischemic diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020622827351
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Protective Effect of Riluzole on MPTP-Induced Depletion of Dopamine and Its Metabolite Content in Mice (2000)
    Springer
    Metabolic brain disease 15 (2000), S. 193-201 
    Details
    ISSN: 1573-7365
    Keywords: MPTP ; riluzole ; pargyline ; MK-801 ; dopamine ; mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The neuroprotective effects of riluzole (2-amino-6-trifluoromethoxy benzothiazole), a Na+ channel blocker with antiglutamatergic activity, MK-801, a blocker of N-methyl-D-aspartate (NMDA) receptors and monoamine oxidase (MAO) inhibitor pargyline were compared in the model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced depletion of dopamine and its metabolite 3, 4-dihydroxyphenylacetic acid (DOPAC) levels in mice. The mice received four intraperitoneal injections of MPTP (10 mg/kg) at 1-hr intervals and then the brains were analyzed at 1, 3 and 7 days after the treatments. Dopamine and DOPAC levels were significantly decreased in the striatum from 1 day after MPTP treatments. A severe depletion in dopamine and DOPAC levels was found in the striatum 3 and 7 days after MPTP treatments. Riluzole dose-dependently antagonized the MPTP-induced decrease in dopamine and DOPAC levels in the striatum. Pargyline also protected against MPTP-induced decrease in dopamine levels in the striatum. However, this drug showed no significant change in the striatal DOPAC levels. On the other hand, MK-801 failed to protect against MPTP-induced decrease in dopamine levels in the striatum. However, MK-801 reversed the MPTP-induced decrease in DOPAC levels. These results suggest that riluzole can protect against MPTP-induced striatal dopamine and DOPAC depletion in mice. This protective effect may be caused by inactivation of voltage-dependent Na+ channels by riluzole. Furthermore, the present study suggests that the activation of NMDA receptors does not mainly contribute to MPTP-induced neurodegeneration, whereas MAO, especially MAO type B(MAO-B) plays a crucial role in MPTP-induced degeneration of the nigrostriatal dopaminergic neuronal pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1011111708901
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...