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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 106 (1995), S. 493-498 
    ISSN: 1432-1106
    Keywords: Somatosensory cortex ; Hand movement ; Sensorimotor integration ; Cerebral blood flow ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hemispheric dominance for motor control in the human brain is still unclear. Here we propose asymmetric sensorimotor integration during human hand movements. We investigated the dexterity of hand movements and related sensory functions in four right-handed patients with cerebrovascular lesions in the postcentral gyrus. To clarify the distributions of cortical damage, semiquantitative analysis of regional cerebral blood flow (rCBF) was performed using single photon emission computed tomography (SPECT), and a three-dimensional surface display was generated from SPECT. Scores on motor and sensory tasks and rCBF values in the patients were compared with those in control subjects. All patients presented with asymmetric clumsiness of complex finger movements, in association with impairments of combined sensations such as stereognosis. These findings were indicative of a disorder of sensory information processing necessary to guide the movements. Two patients with left hemispheric damage showed bilateral clumsy hands, predominating on the right side, while the other two patients with right hemispheric damage showed only a left clumsy hand. In agreement with asymmetric clumsiness, measurement of rCBF along with a three-dimensional surface display revealed cortical hypoperfused areas, mainly in the perirolandic cortices, comprising the primary motor and somatosensory cortices. Perirolandic cortical hypoperfusion was bilateral in the two patients with bilateral clumsy hands, but only on the right side in the other two patients with left clumsy hands. These results suggest a dominant role of the left somatosensory cortex in sensorimotor integration for complex finger movements of humans.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 17 (1983), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A B-cell subset with Fc receptors for IgA (Bα cells) has been observed in human peripheral blood. To investigate aberrations of B cells in a diseased state, the percentages of Bα cells were enumerated in peripheral blood from patients with IgA nephropathy, which is characterized by preponderant deposition of IgA-dominant immune complexes in the glomerular mesangial area. The present study showed a significant increase in Bα cells in peripheral blood from patients with IgA nephropathy but not in those with chronic proliferative glomerulo-nephritis without mesangial IgA deposition. Most FcαR-bearing cells were observed in surface IgA bearing lymphocytes. No linear correlation was observed between the levels of serum IgA and the percentages of Bα cells. The addition of aggregated IgA to cultures did not induce FcαR-bearing B cells in vitro. It is postulated that Bα cells might have some pathogenetic role in the development of IgA nephropathy and that some antigenic stimuli might play a role in the increase of peripheral blood Bα cells in patients with IgA nephropathy.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 4 (1998), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2307
    Keywords: Masugi nephritis ; Glomerular damage ; Podocytes ; Focal segmental glomerulosclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We analysed the sequence of structural changes leading to focal segmental glomerulosclerosis (FSGS) in chronic Masugi nephritis. The protocol resulted in an immediate onset of the disease and the development of segmental sclerosis in a considerable proportion of glomeruli within 28 days of serum injection. Throughout the study, the degree of structural damage was significantly correlated with protein excretion. Even 1 day after injection of the serum, the whole spectrum of early lesions was encountered involving all three cell types. Endothelial detachments, mesangiolysis and podocyte foot process effacement were most prominent. There was focal persistence of capillary microthrombosis but, generally, mesangial and endothelial injuries recovered. The development of podocyte lesions was different: on one hand recovery was seen leading to the re-establishment of an interdigitating foot process pattern, and on the other persistent podocyte detachments from peripheral capillaries allowed the attachment of parietal epithelial cells to “naked” portions of the glomerular basement membrane (GBM), and thus to the formation of a tuft adhesion to Bowman's capsule. Progressive podocyte degeneration at the flanks of an adhesion permitted expansion of the adhesion by encroachment of parietal cells onto the tuft along the denuded GBM. Inside an adhesion, capillaries and mesangial areas either collapse or become obstructed by hyalinosis or thrombosis. Resident cells disappear progressively from inside an adhesion; macrophages may invade. Segmental sclerosis in this model consists of collapsed tuft structures adhering broadly to the cortical interstitium. Proliferation of mesangial cells did not contribute to this development. Recovery of endothelial and mesangial lesions was associated with cell proliferation in early stages of the disease; podocyte proliferation was not encountered at any stage. We conclude that the inability to replace an outmatched podocyte crucially underlies the development of sclerosis. Severe podocyte damage cannot be repaired but leads to tuft adhesions to Bowman's capsule followed by progressive collapse of tuft structures inside an adhesion, resulting in segmental glomerulosclerosis.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1920
    Keywords: Cerebral blood flow ; Three-dimensional display ; Parkinson's disease ; Dementia ; Single-Photon emission computed tomography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We reconstructed three-dimensional (3D) surface images from single-photon emission computed tomography (SPECT) data using N-isopropyl-p[123I]-iodoamphetamine (123I-IMP) in 27 patients with Parkinson's disease and 11 normal control subjects. The 3D reconstruction was performed using distance-shaded methods at threshold levels with an interval of 5% from 45–80%. Any area of decreased perfusion at each threshold level was visualised as a defect area by the algorithm. In nondemented patients with Parkinson's disease, perfusion defects were frequently found in the parietal cortex at a threshold value of 65%. In demented patients, perfusion defects were frequently seen at thresholds of 45–65%, and were more marked in the temporal and parietal cortex bilaterally. This suggests that dementia in Parkinson's disease is related to a reduction of perfusion in the temporoparietal cortex.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0584
    Keywords: Key words Multicentric Castleman's disease ; Amyloidosis ; Pure red-cell aplasia ; Immunosuppressive therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A 50-year-old man was admitted suffering from severe anemia and renal dysfunction. He had been admitted for the first time at the age of 49, and was diagnosed with multicentric Castleman's disease (MCD) and secondary amyloidosis. At that time, marked erythroid hypoplasia was demonstrated by both aspiration and biopsy of bone marrow. A diagnosis of pure red-cell aplasia (PRCA) was made. Immunosuppressive agents improved his symptoms and laboratory data. We report here a very rare case of PRCA following MCD and amyloidosis, and with reference to the literature, we discuss the relation between MCD and related diseases.
    Type of Medium: Electronic Resource
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