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  • 1
    Electronic Resource
    Electronic Resource
    Morphology of cerebral plaque-like lesions in hereditary cerebral hemorrhage with amyloidosis (Dutch) (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 674-679 
    Details
    ISSN: 1432-0533
    Keywords: Hereditary cerebral hemorrhage with amyloidosis ; Dutch type ; Amyloid β/A4 protein ; Diffuse plaques ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the presence and morphology of plaque-like lesions in the frontal cortex of six patients, aged 40 to 76 years, with hereditary cerebral hemorrhage with amyloidosis — Dutch type (HCHWA-D), using β/A4 immuno-, silver, Congo red and thioflavin S staining. Two types of β/A4 immunoreactive and Congo red-negative plaques were detected. The first type was composed of argyrophilic fibrous material in periodic acid-methenamine silver (PAM) and modified Bielschowsky staining and lacked silver-stained degenerating neurites. Therefore, this type of plaque has the same staining properties as the diffuse plaque described in Alzheimer's disease, Down's syndrome and nondemented elderly. The second type of plaque, occurring only in the three oldest patients and numerically increasing with age, consisted of a spherical non-argyrophilic area of granular texture with a rim of PAM-positive material. The PAM-positive fibrous material of both types of plaques was mingled with coarser and compact, irregular-shaped argyrophilic structures in the oldest patient. The described plaques did not show bright fluorescence with thioflavin S staining. These results indicate, that the morphology of plaques, encountered in HCHWA-D, is diverse and changes with age.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227745
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  • 2
    Electronic Resource
    Electronic Resource
    Neuropathy accompanying IgMλ monoclonal gammopathy (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 255-261 
    Details
    ISSN: 1432-0533
    Keywords: IgM monoclonal gammopathy ; Neuropathy ; Myelin-associated glycoprotein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A set of observations made on a patient with IgMλ monoclonal gammopathy and neuropathy implicate humoral immunity in the pathogenesis of the neuropathy. A sural nerve biopsy from the patient showed a characteristic increase in the width of the intraperiod lines. Deposits of μ-heavy chains and λ-light chains were found in myelin sheaths of the nerve biopsy. Immunohistochemically, it was demonstrated that μ-heavy chains and λ-light chains from the patient's serum bound to myelin sheaths of normal peripheral nerves and to a lesser extent to myelin sheaths in the central nervous system (CNS). By immunoblots it was demonstrated that μ-heavy chains and λ-light chains from the patient's serum bound to myelin associated glycoprotein but to no other antigens from the peripheral and central nervous systems. γ and α heavy chains and ϰ light chains from the patient's serum were also shown to bind to myelin-associated glycoprotein but not as distinctly as the μ and λ chains. It is postulated that the monoclonal gammopathy may have arisen on the background of polyclonal autoimmune attack directed against myelin-assoiated glycoprotein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691490
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  • 3
    Electronic Resource
    Electronic Resource
    Zur Klinik und Prognose der Nierenmanifestationen bei Lupus erythematodes (1970)
    Springer
    Journal of molecular medicine 48 (1970), S. 711-723 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Clinical, serological and biopsy findings in 37 patients with systemic lupus erythematosus and lupus nephropathy are reported. Lupus nephropathy has to be suspected clinically if persistent proteinuria, abnormal sediment findings or symptoms of impaired renal function are observed during the course of SLE. Lupus nephropathy may be the only manifestation of SLE. In these cases serological investigations can help to detect the real nature of the underlying disease. In clinical practice renal biopsy has become a valuable tool in establishing the diagnosis of lupus nephropathy. Therapy with glucosteroids may slow down the progressive course of lupus nephritis and prevent or postpone renal failure in certain cases. Results of treatment are documented by renal histology. It is still uncertain however to deduct prognosis from histologic patterns.
    Notes: Zusammenfassung An eine Beteiligung der Nieren am Krankheitsgeschehen wird man beim Lupus erythematodes disseminatus denken, wenn im Rahmen eines akuten Krankheitsschubs eine persistierende Proteinurie, abnorme Sedimentbefunde (Hämaturie, Leukocyturie, Cylindrurie) und eine eingeschränkte Nierenfunktion auftreten. In der Remissionsphase des Erythematodes kann die Lupusnephritis die einzige Organmanifestation sein. Ist in diesem Stadium die Grunderkrankung nicht bekannt, so kann die klinische Serologie zur richtigen Diagnose führen. Eine wertvolle Ergänzung klinisch diagnostischer Verfahren stellt die Nierenbiopsie dar, mit deren Hilfe man Veränderungen im Bereich des Glomerulums (Nekrosen, celluläre Reaktionen, Hämatoxylinbodies, Fibrinoideinlagerungen an die Basalmembran, hyaline Thromben), des Interstitiums (Ödem, celluläre Infiltration) und selten der Nierengefäße (Arteriitis) nachweisen kann. Durch die Einführung von Glucocorticosteroidpräparaten zur Behandlung der Lupusnephritis gelingt es in den meisten Fällen, die drohende Niereninsuffizienz zeitlich hinauszuschieben und einen Teil der klinischen Befunde wenigstens vorübergehend zu bessern. Eine Prognosestellung hinsichtlich Verlaufstendenz und Überlebenschance ist anhand der derzeitig verfügbaren klinischen und bioptischen Kriterien nur mit großen Vorbehalten möglich. Aus klinischer Sicht werden nephrotische Verlaufsformen quoad vitam schlecht beurteilt. Von echten nephrotischen Verläufen zu trennen sind nephroseähnliche Syndrome, die im Rahmen der akuten Phase des Erythematodes auftreten können, unter einer optimalen Behandlung aber vielfach dauerhaft rückbildungsfähig sind.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01497128
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  • 4
    Electronic Resource
    Electronic Resource
    Severe pulmonary vascular occlusive disease following bone marrow transplantation in Omenn syndrome (1991)
    Springer
    European journal of pediatrics 150 (1991), S. 242-245 
    Details
    ISSN: 1432-1076
    Keywords: Omenn syndrome ; Hypereosinophilia ; Endomyocardial disease ; Bone marrow transplantation ; Pulmonary vascular obstruction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 5-month-old infant presented with severe combined immunodeficiency disease, reticuloendotheliosis, and hypereosinophilia (Omenn syndrome) resulting in recurrent infections and endomyocardial disease. Bone marrow transplantation from an HLA-identical donor after chemotherapeutic conditioning led to both immunological and clinical recovery. Bone marrow transplantation, however, was followed by severe pulmonary occlusive disease. The patient gradually recovered while on increased inspiratory oxygen and the calcium channel blocker nifedipine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01955521
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  • 5
    Electronic Resource
    Electronic Resource
    Congenital microcephaly, infantile spasms, psychomotor retardation, and nephrotic syndrome in two sibs (1987)
    Springer
    European journal of pediatrics 146 (1987), S. 532-536 
    Details
    ISSN: 1432-1076
    Keywords: Infantile spasms ; Microcephaly ; Nephrotic syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two boys are described with congenital microcephaly, infantile spasms, psychomotor retardation and an early-onset nephrotic syndrome. The autopsy findings of one patient are described in detail. Polymicrogyria was the most prominent feature and the kidneys showed focal segmental glomerulosclerosis. These findings have been described as a clinical entity, the leading symptoms being congenital microcephaly, early-onset nephrotic syndrome and mental retardation, accompanied by various other clinical symptoms. A review of the literature suggests an autosomal recessive mode of inheritance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00441612
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  • 6
    Electronic Resource
    Electronic Resource
    Relevance of vesico-ureteric reflux in development of lipid a antibodies in recurrent urinary tract infections in children — a preliminary study (1987)
    Springer
    European journal of pediatrics 146 (1987), S. 51-55 
    Details
    ISSN: 1432-1076
    Keywords: Vesico-ureteric reflux ; Lipid A antibodies ; Urinary tract infection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The serum titres of IgG and IgM antibodies to lipid A were measured in 24 children with chronic pyelonephritis (PN), 55 with recurrent lower urinary tract infections (LUTI), 13 with gram-negative sepsis (S), and in 50 control children using an enzyme-linked immunosorbent assay (ELISA). Children ranged in age from 1 month-17 years. Patients with PN were differentiated by the presence or absence of an acute infectious episode and/or vesico-ureteric reflux (VUR). During an acute episode in PN and LUTI, IgG titres were significantly higher than in controls, but only PN patients with an acute infectious episode also had significantly elevated IgM titres. Overall, children with LUTI showed a significantly lower frequency of detectable IgG lipid A antibodies (27%) than in PN (63%). In PN children with VUR not accompanied by an infectious episode, lipid A antibody was found at relatively low titres, while an episode not accompanied by VUR displayed significantly elevated IgG titres, and an episode accompanied by VUR showed elevation of both IgG and IgM anti-lipid A antibody titres.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00647284
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  • 7
    Electronic Resource
    Electronic Resource
    A European multicenter randomized controlled trial of single dose surfactant therapy for idiopathic respiratory distress syndrome (1990)
    Springer
    European journal of pediatrics 149 (1990), S. 416-423 
    Details
    ISSN: 1432-1076
    Keywords: Surfactant ; Idiopathic respiratory distress syndrome ; Clinical trial ; Randomization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We performed a multicenter prospective randomized controlled trial to determine the efficacy and safety of the surfactant preparation, Survanta (Abbott Laboratories, Chicago, USA), for 750–1750 g infants with idiopathic respiratory distress syndrome, (IRDS) receiving assisted ventilation with 40% or more oxygen. One hundred and six eligible infants from the eight participating centers were randomly assigned between March 1986 and June 1987 to receive either surfactant (100 mg phospholipid/kg, 4 ml/kg) or air (4 ml/kg) administered into the trachea within 8 h of brith (median time of treatment 6.2 h, range 3.2–9.1 h). The study was stopped before enrollment was completed at the request of the United States Food and Drug Administration when significant differences were observed in incidence of periventricular-intraventricular hemorrhage (PIH), between the surfactant treated and control infants. Surfactant treated infants had larger average increases in the arterial-alveolar oxygen ratio, (a/A ratio) (P〈0.0001), and larger average decreases in FiO2 (P〈0.0001) and mean airway pressure, (MAP) (P〈0.017) than controls over the 48 h following treatment. The magnitude of the differences between the surfactant and control groups were 0.19 (SE=0.03) for a/A ratio, −0.28 (SE=0.04) for FiO2 and −1.7 cm H2O (SE=0.70) for MAP. The clinical status on days 7 and 28 after treatment was classified using four predefined ordered categories: (1) no respiratory support; (2) supplemental O2 with or without continuous positive airway pressure (CPAP); (3) intermittent mandatory ventilation; and (4) death. There were no statistically significant differences in the status categories on days 7 or 28 between surfactant and control infants. There were no significant differences between the groups with respect to the incidence of patent ductus arteriosus, bronchopulmonary dysplasia, necrotizing entero-colitis, air leaks or death. There was a statistically significant difference between treated and control infants in the frequency and severity of periventricular-intraventricular hemorrhage (PIH) (Cochran-Mantel-Haenszelχ 2adj=6.36,P=0.01). Hemorrhages occurred in 59.6% of surfactant treated infants and 26.9% of controls. Severe hemorrhages (grades 3 or 4) occurred in 38.5% of surfactant treated infants and 15.4% of controls (χ 2adj=4.01,P=0.045). We conclude that the intratracheal administration of Survanta prior to 8 h of age to infants with IRDS receiving assisted ventilation with 40% or more oxygen results in a reduction in the severity of respiratory distress during the 48 h after therapy. Because of the difference in incidence of PIH between surfactant and control infants in this study, we recommend that future clinical trials of surfactant include more frequent prospective serial ultrasound evaluations for diagnosis of hemorrhage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02009663
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  • 8
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of tiapride in patients with tardive dyskinesia and Huntington's disease (1986)
    Springer
    European journal of clinical pharmacology 31 (1986), S. 191-194 
    Details
    ISSN: 1432-1041
    Keywords: tiapride ; Huntington's disease ; pharmacokinetics ; tardive dyskinesia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The pharmacokinetics of tiapride were determined at steady-state in 5 patients with tardive dyskinesia and 2 patients with Huntington's disease given tiapride 100 mg t.i.d. for 7 days. The maximum serum concentration of tiapride of 1.47±0.35 µg/ml was reached after 1.4±0.67 h. The half-life time of elimination was 229±41 min. About 50% of the dose of tiapride was excreted unchanged by the kidney. Neither protein binding nor glucuronide, sulphate or acetyl conjugation was observed. Renal clearance in the patients appeared to be lower but the other pharmacokinetic parameters did not differ from previous findings in healthy young volunteers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00606657
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  • 9
    Electronic Resource
    Electronic Resource
    No correlation between aggregates of Cu/Zn superoxide dismutase and cell death in familial amyotrophic lateral sclerosis (2002)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 82 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aggregates of Cu/Zn superoxide dismutase (SOD) have been demonstrated in familial amyotrophic lateral sclerosis (FALS) and other neurodegenerative diseases; however, their role in disease pathogenesis is unclear. In this study, we investigated the presence of SOD aggregates in nerve growth factor (NGF)-differentiated PC12 cells and cell viability following: (i) transduction with replication-deficient recombinant adenoviruses (AdVs) expressing wild-type SOD (SODWT) or mutant SOD (SODMT, V148G or A4V); (ii) transfection of yellow fluorescent protein-tagged SODWT (SODWT-YFP) or SODMT (SODA4V-YFP, SODV148G-YFP). SOD aggregates were more prominent in cells following transduction of AdSODMT than AdSODWT and following treatment with H2O2, suggesting that mutant SOD leads to oxidation of cellular components. In addition, cells expressing SODMT-YFP yielded SOD aggregates that were significantly larger and more frequent than SOD aggregates in cells expressing SODWT-YFP. Proteasome inhibitors, but not cathepsin B inhibitors, increased aggregate formation but did not increase cell death. In addition, treatments that increased cell viability did not significantly decrease SOD aggregates. Taken together, our data demonstrate that there is no association between SOD aggregates and cell death in FALS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2002.01056.x
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  • 10
    Electronic Resource
    Electronic Resource
    Ca2+ and Reactive Oxygen Species in Staurosporine-Induced Neuronal Apoptosis (1997)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 68 (1997), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Staurosporine (0.03–0.5 µM) induced a dose-dependent, apoptotic degeneration in cultured rat hippocampal neurons that was sensitive to 24-h pretreatments with the protein synthesis inhibitor cycloheximide (1 µM) or the cell cycle inhibitor mimosine (100 µM). To investigate the role of Ca2+ and reactive oxygen species in staurosporine-induced neuronal apoptosis, we overexpressed calbindin D28K, a Ca2+ binding protein, and Cu/Zn superoxide dismutase, an antioxidative enzyme, in the hippocampal neurons using adenovirus-mediated gene transfer. Infection of the cultures with the recombinant adenoviruses (100 multiplicity of infection) resulted in a stable expression of the respective proteins assessed 48 h later. Overexpression of both calbindin D28K and Cu/Zn superoxide dismutase significantly reduced staurosporine neurotoxicity compared with control cultures infected with a β-galactosidase overexpressing adenovirus. Staurosporine-induced neuronal apoptosis was also significantly reduced when the culture medium was supplemented with 10 or 30 mM K+, suggesting that Ca2+ influx via voltage-sensitive Ca2+ channels reduces this apoptotic cell death. In contrast, neither the glutamate receptor agonist NMDA (1–10 µM) nor the NMDA receptor antagonist dizocilpine (MK-801; 1 µM) was able to reduce staurosporine neurotoxicity. Cultures treated with the antioxidants U-74500A (1–10 µM) and N-acetylcysteine (100 µM) also demonstrated reduced staurosporine neurotoxicity. These results suggest a fundamental role for both Ca2+ and reactive oxygen species in staurosporine-induced neuronal apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1997.68041679.x
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