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  • 1
    Electronic Resource
    Electronic Resource
    SPECT, CT and MRI in a Turkish family with huntington's disease (1993)
    Springer
    Neuroradiology 35 (1993), S. 525-528 
    Details
    ISSN: 1432-1920
    Keywords: Huntington's disease ; Computed tomography ; Magnetic resonance imaging ; Single photon emission computed tomography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A Turkish family with Huntington's disease documented on CT, MRI and SPECT is reported. Whereas in clinically definite cases CT and MRI are of limited value and SPECT does not add anything of value, in one asymptomatic subject SPECT showed moderate caudate nucleus hypoperfusion, underlining the hypothesis that SPECT may have a role in predicting Huntington's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00588713
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  • 2
    Electronic Resource
    Electronic Resource
    High spin level structure of 63 143 Eu80 (1992)
    Springer
    The European physical journal 343 (1992), S. 367-368 
    Details
    ISSN: 1434-601X
    Keywords: 23.20.Lv ; 25.70.Gh ; 27.60.+j
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract The level scheme of 143 Eu has been extended to I=75/2 in an experiment with the NORDBALL Compton-suppressed Ge detector array and the 110 Pd(37 Cl, 4n) reaction. Most of the scheme shows irregular structure of multiparticle excitations. A strongly populated straight cascade of more than 10 stretched E2 transitions suggests the onset of collectivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01291538
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  • 3
    Electronic Resource
    Electronic Resource
    Differential effects of sympathetic activity on AV junctional automaticity and AV conduction (1986)
    Springer
    Basic research in cardiology 81 (1986), S. 497-507 
    Details
    ISSN: 1435-1803
    Keywords: AV junctional automaticity ; retrograde VA conduction ; antegrade AV conduction ; sympathetic deficit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rapid ventricular response during episodes of supraventricular tachycardia are often followed, on abrupt cessation of the tachycardia, by prolonged pauses terminated by a sluggish and sometimes erratic escape of a supraventricular pacemaker. Such chronotropic-dromotropic paradoxes are readily reproduced in the animal laboratory following elimination of the sinus node and bilateral decentralization of the stellate ganglia and vagi. This study examined whether left stellate stimulation (0.5, 1, 2, 4, 8 and 16 Hz) or lack thereof differentially affected AV junctional automaticity and AV conduction. In the absence of any sympathetic neural activity (maximal sympathetic deficit), the AV junctional rate averaged a mere 22±2 percent of its peak performance, whereas under the same conditions, anterograde AV conduction averaged 73±5 percent and retrograde VA conduction 56 ±13 percent of their respective peak performances. On comparing the response curve (normalized responses) for AV junctional automaticity with that obtained for anterograde AV conduction the differences were significant at all frequencies between 0 and 4 Hz. Retrograde VA conduction (as assessed by the fastest ventricular pacing rate still conducted 1∶1 to the atria) was always significantly less than anterograde AV conduction (as assessed by the fastest atrial pacing still conducted 1∶1 to the ventricles). These results indicate that AV junctional automaticity is considerably more affected by sympathetic deficit than are either anterograde or retrograde AV conduction. In other words, AV junctional automaticity is far more dependent upon sympathetic input than AV conduction. While sympathetic influence is critical to the escape and maintenance of AV junctional automaticity both anterograde and retrograde AV conduction are remarkably resilient even under conditions of severe sympathetic deficit.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907756
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  • 4
    Electronic Resource
    Electronic Resource
    Parkinsonism, pyramidal signs, polyneuropathy, and cognitive decline after long-term occupational solvent exposure (1999)
    Springer
    Journal of neurology 246 (1999), S. 198-206 
    Details
    ISSN: 1432-1459
    Keywords: Key words Parkinsonism ; Solvents ; Neurotoxicity ; Occupational disease ; Chronic toxic encephalopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is well known that exposure to manganese, solvents, or carbon monoxide in an occupational setting may lead to central nervous system damage and parkinsonism. The most important solvents in this respect are methanol, toluene, carbon disulfide, and n-hexane. We describe three patients who had been exposed to various solvents for more than 20 years (25, 34, and 46 years). They presented with parkinsonism, pyramidal signs, mild cognitive decline, and unresponsiveness to levodopa. Two patients had a predominantly axonal and sensory polyneuropathy of the lower legs with fasciculations in one of them. Parkinsonian features were progressive, even after the patients had stopped work. We present clinical data, neuropsychological findings, and results of brain computed tomography or magnetic resonance imaging, electroneuromyography, evoked potentials, single photon emission computed tomography, and positron-emission tomography. There is growing evidence that various organic solvents give rise to a parkinsonism syndrome with pyramidal features in susceptible individuals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004150050334
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  • 5
    Electronic Resource
    Electronic Resource
    Post-excitatory depression in thoracic sympathetic efferent neural traffic during a cardiogenic hypertensive chemoreflex (1982)
    Springer
    Basic research in cardiology 77 (1982), S. 423-430 
    Details
    ISSN: 1435-1803
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Serotonin bewirkt bei Injektion in den linken Vorhof von Hunden einen hypertensiven Chemoreflex. Um das Muster der nervalen Übermittlung zu klären, wurden bei 8 narkotisierten Hunden mit offenem Thorax Ableitungen von thorakalen sympathischen (efferenten) Nerven vorgenommen. Serotonin (200 μg) verursacht massive sympathische Entladungen während der Hypertension und Bradykardie, die für den Chemoreflex charakteristisch sind. Nach der initialen sympathischen Entladung kam es regelmäßig zu einer postexzitatorischen Depression auf ein Niveau, das eindeutig unter Kontrollbedingungen lag. Diese postexzitatorische Depression begann im Mittel 11 s nach der Serotoninjektion und durchschnittlich 6,6 s nach der neuralen Spitzenentladung. Sie dauerte im Mittel 140 s und erreichte initial maximale Werte mit allmählichem Rückgang. Komplette Blockierung der hypertensiven Reaktion durch kombinierte Verabreichung von Phentolamin. Propranolol und Nitroglycerin konnte die nervalen Vorgänge nicht beseitigen einschließlich der postexzitatorischen Depression (mit Ausnahme eines Hundes). Wir schließen daraus, daß die postexzitatorische Depression thorakaler sympathischer Efferenzen nicht ausschließlich durch die sekundäre Beteiligung eines Barorezeptormechanismus vermittelt werden kann. Sie gehört wahrscheinlich zum Wesen des kardiogenen hypertensiven Chemoreflexes.
    Notes: Summary Serotonin injected in the left atrium activates a cardiogenic hypertensive chemoreflex in dogs. To elucidate patterns of the neural traffic, records were obtained from thoracic sympathetic efferent nerves (either the anterior ansa of the left stellate ganglion or the T4 input to the left stellate) in 8 anesthetized dogs with chests open. Serotonin (200 μg, left atrium) caused a massive sympathetic discharge during the hypertension and bradycardia characteristic of the chemoreflex. Following the initial sympathetic discharge, there was a consistent post-excitatory depression of neural traffic, to a level significantly less than control discharge (two-tailed p≤.05). This post-excitatory depression began 11±5.4 (S.D.) seconds after injection of serotonin and 6.6±5.3 seconds after the peak neural discharge. It lasted 140±94 seconds, being maximal initially with gradual recovery. Complete block of the hypertension by the combined administration of phentolamine, propranolol, and nitroglycerin failed to abolish the efferent neural events, including postexcitatory depression, in all but one dog. We conclude that post-excitatory depression in thoracic sympathetic efferent neural traffic cannot be mediated exclusively through the secondary engagement of a baroreceptor mechanism and that it most likely is an integral part of the cardiogenic hypertensive chemoreflex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02005342
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