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  • 1
    Electronic Resource
    Electronic Resource
    Quantitative investigations on the human entorhinal area: left-right asymmetry and age-related changes (1994)
    Springer
    Anatomy and embryology 190 (1994), S. 181-194 
    Details
    ISSN: 1432-0568
    Keywords: Human entorhinal area ; Ageing ; Lateralitity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The total nerve cell numbers in the right and in the left human entorhinal areas have been calculated by volume estimations with the Cavalieri principle and by cell density determinations with the optical disector. Thick gallocyanin-stained serial frozen sections through the parahippocampal gyrus of 22 human subjects (10 female, 12 male) ranging from 18 to 86 years were analysed. The laminar composition of gallocyanin (Nissl)-stained sections could easily be compared with Braak's (1972, 1980) pigmentoarchitectonic study, and Braak's nomenclature of the entorhinal laminas was adopted. Cellsparse laminae dissecantes can more clearly be distinguished in Nissl than in aldehydefuchsin preparations. These cell-poor dissecantes, lamina dissecans externa (dis-ext), lamina dissecans 1 (dis-1) and lamina dissecans 2 (dis-2), were excluded from nerve cell number determinations. An exact delineation of the entorhinal area is indispensable for any kind of quantitative investigation. We have defined the entorhinal area by the presence of pre-alpha cell clusters and the deeper layers of lamina principalis externa (pre-beta and gamma) separated from lamina principalis interna (pri) by lamina dissecans 1 (dis-1). The human entorhinal area is quantitatively characterized by a left-sided (asymmetric) higher pre-alpha cell number and an age-related nerve cell loss in pre as well as pri layers. At variance with other CNS cortical and subcortical structures, the neuronal number of the entorhinal area appears to decrease continuously from the earliest stages analysed, although a secular trend has to be considered. The asymmetry in pre-alpha cell number is discussed in the context of higher human mental capabilities, especially language.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00193414
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  • 2
    Electronic Resource
    Electronic Resource
    Time to remission with budesonide in collagenous colitis (2005)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 21 (2005), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2005.02500.x
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  • 3
    Electronic Resource
    Electronic Resource
    Long-term follow-up of collagenous colitis after induction of clinical remission with budesonide (2005)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 22 (2005), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  Budesonide (Entocort) is effective for the treatment of collagenous colitis.Aim:  To assess the long-term outcome of patients after induction of clinical remission by budesonide treatment.Methods:  Fifty-one patients with chronic diarrhoea and histologically proven collagenous colitis were enrolled in randomized, placebo-controlled crossover trial using budesonide 9 mg daily for 6 weeks. Patients in clinical remission after either initial or crossover budesonide treatment were followed using standardized questionaires. Clinical relapse was defined as five or more loose stools/day for at least 4 consecutive days.Results:  A total of 33 patients achieved clinical remission (85% per-protocol). During a median follow-up of 16 months, clinical relapse occurred in 20 patients (61%), after a median time of 2 weeks (range: 1–104, mean: 10 weeks). Patient age 〈60 years was identified as a significant risk factor for clinical relapse (OR = 7.4, P = 0.048). Budesonide was used for treatment of clinical relapse in 80% of patients achieving clinical response in all of them.Conclusions:  Budesonide is effective in the treatment of collagenous colitis. Clinical relapses may occur in a considerable number of patients, particularly in those 〈60 years. Treatment of clinical relapse with budesonide appears to be an effective option.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2005.02688.x
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  • 4
    Electronic Resource
    Electronic Resource
    Nerve cell loss in the thalamic centromedian-parafascicular complex in patients with Huntington's disease (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 161-168 
    Details
    ISSN: 1432-0533
    Keywords: Key words Huntington's disease ; Human brain ; Thalamus ; Nuclei centromedianus-parafascicularis ; Neurone number
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The centromedian-parafascicular complex represents a nodal point in the neuronal loop comprising striatum – globulus pallidus – thalamus – striatum. Striatal neurone degeneration is a hallmark in Huntington's disease and we were interested in estimating total neurone and glial number in this thalamic nuclear complex. Serial 500-μm-thick gallocyanin-stained frontal sections of the left hemisphere from six cases of Huntington's disease patients (three females, three males) and six age- and sex-matched controls were investigated applying Cavalieri's principle and the optical disector. Mean neurone number in the controls was 646,952 ± 129,668 cells versus 291,763 ± 60,122 in Huntington's disease patients (Mann-Whitney U-test, P 〈 0.001). Total glial cell number (astrocytes, oligodendrocytes, microglia, and unclassifiable glial profiles) was higher in controls with 9,544,191 ± 3,028,944 versus 6,961,989 ± 2,241,543 in Huntington's disease patients (Mann-Whitney U-test, P 〈 0.021). Considerable increase of fibrous astroglia within the centromedian-parafascicular complex could be observed after Gallyas' impregnation. Most probably this cell type enhanced the numerical ratio between glial number and neurone number (glial index: Huntington's disease patients = 24.4 ± 8.1; controls = 15.0 ± 5.2; Mann-Whitney U-test, P 〈 0.013). The neurone number in the centromedian-parafascicular complex correlated negatively, although statistically not significantly, with the striatal neurone number. This lack of correlation between an 80% neuronal loss in the striatum and a 55% neurone loss in the centromedian-parafascicular complex points to viable neuronal circuits connecting the centromedian-parafascicular complex with cortical and subcortical regions that are less affected in Huntington's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050408
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    Paper (German National Licenses)
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