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  • 1
    Electronic Resource
    Electronic Resource
    Complement neoantigen and vitronectin are components of plaques in amyloid AL neuropathy (1992)
    Springer
    Neurological sciences 13 (1992), S. 493-499 
    Details
    ISSN: 1590-3478
    Keywords: Peripheral neuropathy ; amyloidosis ; complement ; vitronectin ; immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario Sono stati studiati tre pazienti con neuropatia sensitivo-motoria e autonomica ad esordio tardivo e decorso cronico in corso di discrasia plasmacellulare con proteinuria di Bence Jones. L'esame della biopsia di nervo surale mostrava perdita diffusa di fibre mieliniche ed amieliniche; erano inoltre presenti depositi endoneurali, prevalentemente perivascolari, di materiale amorfo con le caratteristiche fisico-chimiche ed ultrastrutturali dell'amiloide. Lo studio immunoistochimico ha dimostrato la presenza di catene leggere dello stesso tipo di quelle circolanti, frazioni della via classica del complemento, neoantigene del complemento e vitronectina a livello dei noduli di amiloide. La co-localizzazione del neoantigene del complemento e della vitronectina suggerisce che tale complesso sia di origine circolante. L'elucidazione dell'esatta composizione chimica delle varie componenti dell'amiloide può portare ad una migliore comprensione della patogenesi delle varie forme.
    Notes: Abstract We studied three patients with late onset, chronic sensorimotor and autonomic neuropathy in course of plasma cell dyscrasia with Bence Jones proteinuria. Histopathological findings of nerve biopsies consisted in diffuse loss of myelinated and unmyelinated fibers associated with perivascular deposits of amorphous material with physico-chemical and ultrastructural features of amyloid. By immunohistochemistry, light chains of the same type as Bence Jones protein, components of the classic and lytic pathways of the complement and vitronectin were detected at the level of amyloid nodules. The colocalization of complement neoantigen and vitronectin suggests that this complex derives from the circulation. The elucidation of the chemical composition of amyloid might shed some light in the pathogenesis of these disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02230870
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Increased serum levels of ICAM-1, ELAM-1 and TNF-α in inflammatory disorders of the peripheral nervous system (1994)
    Springer
    Neurological sciences 15 (1994), S. 267-271 
    Details
    ISSN: 1590-3478
    Keywords: Guillain-Barré syndrome ; chronic inflammatory demyelinating polyradiculopathy ; cryoglobulinemic neuropathy ; ICAM-1 ; ELAM-1 ; TNF-α
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario L'infiltrazione leucocitaria nelle aree di infiammazione viene mediata dalle molecole di adesione ICAM-1 (intercellular adhesion molecule-1) ed ELAM-1 (E-selectin). In corso di disordini infiammatori del SNC vi è un marcato incremento sierico di ICAM-1. In questo studio abbiamo dosato i livelli sierici di ICAM-1, ELAM-1 e TNF-α (tumor necrosis factor-α) in pazienti con neuropatia crioglobulinemica (CGN) e poliradicolonevrite acuta (AIDP) e cronica (CIDP). Dosaggi immunoenzimatici hanno evidenziato un incremento di sICAM-1 in alcuni pazienti con tali patologie; inoltre in 2 pazienti con AIDP ed in 1 paziente con CGN sono stati rilevati elevati titoli di ELAM-1 e TNF-α. I nostri dati ampliano le osservazioni precedenti riguardo ai disordini infiammatori del SNP, dimostrando che ELAM-1, insieme a ICAM-1, può essere un utile marker di attivazione endoteliale e che entrambi possono servire come indicatori di meccanismi patogenetici specifici.
    Notes: Abstract Endothelial intercellular adhesion molecule-1 (ICAM-1) and glycoprotein E-selectin (ELAM-1) allow the homing of leukocytes to inflammation sites. A circulating form of ICAM-1 markedly increases in inflammatory CNS disorders. In the present study, the serum levels of ICAM-1, ELAM-1 and tumor necrosis factor-α (TNF-α) were measured in patients with acute (AIDP) and chronic (CIDP) inflammatory demyelinating polyneuropathies and cryoglobulinemic neuropathy (CGN). Immunoenzymometric assays revealed increased sICAM-1 levels in some of these patients; furthermore, high titres of ELAM-1 and TNF-α were detected in two patients with AIDP and one patient with CGN. Our data extend previous observations on inflammatory PNS disorders by showing that, in addition to ICAM-1, ELAM-1 also represents a useful marker of endothelial activation and that, taken together, the two molecules may serve as an indicator of specific pathogenetic mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02339236
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    AZT-induced mitochondrial myopathy (1992)
    Springer
    Neurological sciences 13 (1992), S. 723-728 
    Details
    ISSN: 1590-3478
    Keywords: AIDS ; AZT ; mitochondrial myopathy ; cytochrome c oxidase ; succinate cytochrome c reductase ; type 2 fiber atrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario Sono state esaminate le biipsie muscolari di 11 pazienti affetti da AIDS in trattamento con Zidovudina. Si è riscontrato una caratteristica associazione di anormalità strutturali delle fibre e di disfunzione mitocondriale. Un deficit focale di citocromo c ossidasi (COX) era presente nelle sezioni muscolari di nove pazienti, otto dei quali avevano subito un trattamento di lunga durata, mentre uno era stato trattato solo per un mese. La microscopia elettronica mostrava modificazioni della struttura, del numero e volume dei mitocrondri. Le indagini biochimiche hanno evidenziato un deficit parziale di COX e di succinato citocromo c reduttasi (SCR) di quattro pazienti, mentre in un paziente riduzione di attività della sola SCR. I nostri dati confermano che la terapia con AZT può causare una miopatia tossica con disfunzione dei mitocondri.
    Notes: Abstract Histochemical, electron microscopy and biochemical studies were performed on muscle biopsy specimens from 11 AIDS patients treated with zidovudine. A peculiar association of structural abnormalities and mitochondrial dysfunction was found. Focal cytochrome c oxidase (COX) deficiency was evident in muscle sections from 9 patients, 8 of whom had received long-term treatment while one had been treated for 1 month only. Electron microscopy showed changes in number, size and structure of mitochondria. Biochemical studies proved partial COX and succinate cytochrome c reductase (SCR) deficiency in 4 patients; one patient had only reduced SCR activity. Our data confirm that AZT therapy can cause toxic myopathy with mitochondrial dysfunction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02229156
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Demyelinating polyradiculoneuritis following Coxiella burnetii infection (Q fever) (1991)
    Springer
    Neurological sciences 12 (1991), S. 415-417 
    Details
    ISSN: 1590-3478
    Keywords: Coxiella burnetii ; Q fever ; demyelination ; polyradiculoneuritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario Le complicanze neurologiche in corso di infezione da Coxiella burnetii (febbre Q) sono rare, sebbene siano state frequentemente segnalate cefalea, parestesie e deficit focali transitori. Viene riportato il caso diun paziente con una poliradicolonervite demielinizzante ricorrente quale conseguenza di un 'infezione polmonare e cardiaca causata dalla C. burnetii.
    Notes: Abstract Neurological complications of Coxiella burnetii infection (Q fever) are rare, although the occurrence of headache, paresthesias, and transient focal deficits has been reported. We report the case of a patient with a relapsing demyelinating polyradiculoneuritis as an aftermath of C. burnetii endocarditis and pneumonia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02335782
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    Paper (German National Licenses)
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