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  • 1
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Tetrahedron 35 (1979), S. 1607-1613 
    ISSN: 0040-4020
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 233 (1983), S. 1-8 
    ISSN: 1433-8491
    Keywords: Disulfiram intoxication ; Toxic encephalopathy ; Peripheral neuropathy ; Neurofilamentous axonopathy ; Disulfiram-Intoxikation ; toxische Encephalopathie ; Polyneuropathie ; neurofilamentöse Axonopathie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Unter Dauertherapie mit Disulfiram können toxische Encephalopathien und Neuropathien auftreten. Ein 37jähriger Alkoholabhängiger unternahm einen Suizidversuch mit 22,5 g Disulfiram. Während der ersten 6 Tage nach Einnahme der Überdosis war er stuporös und hatte eine ausgeprägte cerebelläre Ataxie und Dysarthrie. Danach wurde er komatös. Nach Abklingen des Komas bestand eine Polyneuropathie mit Diplegia faciei und schwerer, schlaffer Tetraparese. Elektromyographisch fand sich eine ausgeprägte Denervationstätigkeit im Bereich der mimischen Muskulatur und der distalen Muskelgruppen an Armen und Beinen bei normaler Nervenleitgeschwindigkeit. Die Suralisbiopsie ergab eine vorwiegend axonale Degeneration. Darüber hinaus war eine neurofilamentöse Axonopathie nachweisbar. Die Paresen bildeten sich innerhalb von zwei Jahren zurück.
    Notes: Summary Disulfiram is known to produce toxic encephalopathy and peripheral neuropathy. The case of a 37-year-old alcoholic who attempted to commit suicide by taking 22.5 g disulfiram is described. During the first 6 days after the intoxication he was stuporous and had cerebellar ataxia and dysarthric speech. Then he became comatous, and as he recovered from coma, he showed peripheral neuropathy including diplegia faciei and severe tetraparesis. Denervation potentials were detected in both facial muscles and distal muscles of the upper and lower limbs, while conduction velocity was normal. Axonal degeneration was verified by sural nerve biopsy. In addition neurofilamentous axonopathy was documented. The recovery from his paresis lasted 2 years.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1459
    Keywords: Brain tumors, supratentorial ; Brain edema ; Cerebrospinal fluid pressure ; Dexamethasone treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Mit der kontinuierlichen lumbalen Liquordruckmessung wurde bei 10 Patienten mit supratentoriellen Hirntumoren und klinischen Zeichen intrakranieller Drucksteigerung über 24 Std die Wirkung hoher Dosen Dexamethason (80 mg) auf den Liquordruck (CSFP) untersucht. Während es bei der Kontrollgruppe (unbehandelte Patienten) im Laufe der Registrierung zu einem weiteren leichten CSFP-Anstieg bei unverändertem Druckmuster kam, wurde bei 7 der behandelten Patienten innerhalb 6 Std nach initialer intravenöser Dexamethasongabe eine deutliche CSFP-Senkung beobachtet. Bei 4 der behandelten Patienten wurde zum Ende der Registrierung eine eindeutige, bei 5 eine nur mäßige CSFP-Senkung gemessen. 1 Patient wies einen leichten Druckanstieg auf. Bei allen behandelten Patienten nahmen die Plateauwellen innerhalb der ersten Stunden an Höhe, Häufigkeit und Dauer ab, Druckniveauschwankungen und Liquordruckamplituden verringerten sich.
    Notes: Summary The effect of large doses of dexamethasone (80 mg) on the cerebrospinal fluid pressure (CSFP) was investigated with continuous lumbar CSFP measurement over 24h in 10 patients with supratentorial cerebral tumors and clinical signs of elevated intracranial pressure. There was a further slight rise in CSFP with an unchanged pressure pattern in the course of observation of the untreated control group. A marked lowering of CSFP was observed within 6h after initial intravenous administration of dexamethasone to seven of the treated patients. In four of the treated patients an unequivocal and in five only a moderate CSFP lowering was measured at the end of the registration. One patient had a slight rise in pressure. The plateau waves of all the patients treated decreased in height, frequency and duration within the first hours, while fluctuations in pressure level and CSFP amplitude were reduced.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1459
    Keywords: Lactic acidosis ; Mitochondrial myopathy ; Mitochondrial encephalopathy ; Stroke-like episodes ; Myoclonus epilepsy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute episodes of focal neurological dysfunction are a well-recognized complication of the mitochondrial encephalomyopathies. Because of rapid remission, biochemical tests and other diagnostic procedures are mostly performed after the acute phase. We report the case of a patient suffering from mitochondrial disease manifesting primarily with seizures, progressive deafness and dementia, who experienced multiple stroke-like episodes. Other members of the family with evidence of mitochondrial dysfunction are presented briefly. EEG and biochemical findings in the acute stage are correlated with clinical symptoms, showing characteristics distinct from the chronic illness. The possible involvement of dietary factors in the provocation of stroke-like episodes is discussed and regulation of glucose intake suggested as a strategy in the prevention of stroke-like episodes.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Archives of gynecology and obstetrics 216 (1974), S. 205-218 
    ISSN: 1432-0711
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Glomeruläre Kbrinniederschläge, das Hauptmerkmal der generalisierten Shwartzman-Reaktion, kann bei Kaninchen und Ratten durch eine kontinuierliche intravenöse Infusion von Endotoxinen ausgelöst werden. Im Vergleich zu virginellen Kaninchen führte die Infusion von Endotoxin beim trächtigen Tier in einer kürzeren Zeit und quantitativ vermehrt zu Fibrinniederschlägen in der Niere. Dies weist erneut auf die stärkere Empfindlichkeit von trächtigen Tieren gegenüber Gerinnungsvorgängen hin. Die Infusion von Endotoxoid mit geringer pyrogener Aktivität resultierte nicht in glomerulären Fibrinniederschlägen, obwohl ein Abfall der Thrombozyten entstand. Die Ergebnisse deuten darauf hin, daß Endotoxoid eine ähnliche cytotoxische Aktivität auf Plättchen wie das Endotoxin ausübt, jedoch der Teil des Moleküls, der glomeruläre Fibrinniederschläge hervorruft, durch die biochemische Alteration verloren ging.
    Notes: Summary Glomerular fibrin deposition, the hallmark of the Generalized Shwartzman Reaction, can be produced by a continuous infusion of a sublethal dose of endotoxin in rabbits and rats. The infusion of the active endotoxin into pregnant rabbits produced disseminated intravascular coagulation in a shorter time and quantitatively more pronounced than in the non-pregnant animal. Although the higher susceptibility of pregnant animals to endotoxin is well established, the infusion of an endotoxoid with little pyrogenic activity did not result in glomerular fibrin deposition, but a decrease in platelet number was noted. These data indicate that the endotoxoid has the cytotoxic activity of the original endotoxin molecule but the part of the molecule which induces fibrin deposition in the microcirculation is missing after the biochemical alteration.
    Type of Medium: Electronic Resource
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