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  • 1
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  • 2
    Keywords: PHASE-III ; PHASE ; GLIOBLASTOMA ; enzastaurin ; NOV ; INFORMATION ; VOLUME
    Abstract: MA-35
    Type of Publication: Meeting abstract published
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  • 3
    Keywords: enzastaurin ; PHASE ; PHASE-III ; GLIOBLASTOMA ; VOLUME ; INFORMATION ; ASSOCIATION
    Abstract: O22
    Type of Publication: Meeting abstract published
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  • 4
    ISSN: 0278-6915
    Keywords: [abr] SAR = structure activity relationship ; [abr] TER = transcutaneous electrical resistance
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Propranolol ; blood-clucose ; Free-fatty acids ; Plasma-Insulin ; glucose-tolerance ; exercise
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Trois types d'expérience ont été effectués chez des sujets normaux afin de déterminer l'effet de doses thérapeutiques orales de propranolol sur 1. la glycémie, l'insuline et les acides gras libres (FFA) du plasma au cours du jeûne prolongé et de l'exercice, 2. la tolérance au glucose intraveineux et l'augmentation du taux d'insuline après glucose intraveineux, et 3. la tolérance au glucose intraveineux pendant l'exercice. Le propranolol ne provoquait qu'un léger abaissement de la glycémie chez les sujets normaux, même après 24 h de jeûne. Ceci était plus décelable au cours de l'exercice. Le propranolol n'exerçait aucun effet significatif sur les taux d'insuline à jeun, la tolérance au glucose au repos ou en cours d'exercice, ou sur la réponse des taux d'insuline plasmatique au glucose intraveineux. On a observé un abaissement des taux de FFA plaematiques chez tous les sujets après absorption de propranolol, particulièrement au cours ou après un exercice. Les mécanismes possibles d'hypoglycémie dans les cas décrits dans la littérature sont discutés. Les auteurs concluent que l'hypoglycémie n'est pas un problème majeur dans la thérapeutique par le propranolol.
    Abstract: Zusammenfassung Bei Normalpersonen wurden die Effekte von oral verabreichten Dosen von Propanolol in 3 verschiedenen Versuchsanordnungen überprüft: 1. auf Blutzucker, Plasmainsulin und freie Fettsäuren (FFS) während längerer Fastenperioden und unter körperlicher Belastung, 2. auf die Glucosetoleranz und den Anstieg der Seruminsulinspiegel nach i.v. Glucosezufuhr, 3. auf die i.v. Glucosetoleranz bei Muskelarbeit. Propranolol senkte den Blutzucker bei Normalpersonen auch nach 24-stündigem Fasten nur geringfügig. Dies war besonders auffällig unter körperlicher Belastung. Es ließen sich keine signifikanten Propanolol-Effekte auf die Nüchterninsulinspiegel, auf die Glucosetoleranz in Ruhe und bei Musekelarbeit und auf den Anstieg der Plasmainsulinspiegel nach i.v. Glucosegabe nachweisen. Bei allen Probanden führte Propanolol zu einer Senkung der Plasma FFS-Spiegel, vor allem während und nach Muskelarbeit. Mechanismen, die die in der Literatur beschriebenen Beobachtungen von Hypoglykämien nach Propanolol ausgelöst haben könnten, werden diskutiert. Es wird gefolgert, daß Hypoglykämien bei der Propanolol-Therapie kein größeres Problem darstellen.
    Notes: Summary Three types of experiment were carried out in normal subjects to determine the effect of therapeutic doses of oral Propranolol on 1. the blood sugar, plasma insulin and free fatty acids (FFA) during prolonged fasting and exercise, 2. intravenous glucose tolerance and the rise in insulin level after intravenous glucose, and 3. the intravenous glucose tolerance on exercise. Propranolol caused only slight lowering of the blood sugar in normals, even after 24 h fasting. This was most noticeable during exercise. There was no significant effect of Propranolol on fasting insulin levels, on glucose tolerance at rest or exercise, or on the response of plasma insulin levels to intravenous glucose. Lowering of plasma FFA levels was found in all subjects when taking Propranolol particularly during and after exercise. Possible mechanisms of hypoglycaemia in those cases reported in the literature are discussed. It is concluded that hypoglycaemia is not a major problem in Propranolol therapy.
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  • 6
    ISSN: 1432-0738
    Keywords: Key words Methyl iodide ; Olfactory toxicity ; Glutathione ; Cytochromes P450 ; Glutathione S-transferases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to investigate the role of metabolic activation in the olfactory toxicity of methyl iodide (MeI). Adult male rats were exposed via nose-only inhalation to 100ppm MeI for 0–6h, and non-protein sulphydryl (NP-SH) concentrations determined in selected tissues. Depletion of NP-SH occurred in all tissues, but was most marked and rapid in the respiratory epithelium of the nasal cavity and the kidney. Olfactory, lung and liver NP-SH levels were affected to a lesser extent, and those of the brain declined by only 20–30% over the whole time course. In order to modulate glutathione (GSH) status, animals were pre-treated with (1) phorone plus l-buthionine sulphoximine (BSO), which depleted NP-SH levels in all the tissues examined, or (2) the isopropyl ester of GSH (IP-GSH), which was shown to replenish NP-SH concentrations in all tissues except the liver of animals previously administered phorone. When animals were pre-treated with phorone plus BSO and then exposed to 100ppm MeI for 2h, there was a potentiation of the toxicity of MeI as judged by the clinical observations on the animals. In contrast, treatment with IP-GSH prior to and during exposure to MeI for 4h afforded a marked protection to the olfactory epithelium. In order to inhibit cytochromes P450, animals were pre-treated with cobalt protoporphyrin IX. This decreased hepatic cytochrome P450 concentrations by 〉90%, but when animals were then exposed to 100ppm MeI for 4h there was no effect on the severity of the olfactory lesion. These results indicate that conjugation of MeI with GSH is a detoxification rather than an activation pathway. Also, there is no major role for cytochrome P450-dependent oxidation in the development of the olfactory lesion.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Aeromonas hydrophila secretes protein toxins via the type II pathway, involving the products of at least two operons, exeAB (gspAB) and exeC-N (gspC-N). In the studies reported here, aerolysin secretion was restored to C5.84, an exeA::Tn5–751 mutant, by overexpression of exeD alone in trans. Expression studies indicated that these results did not reflect a role of ExeAB in the regulation of the exeC-N operon. Instead, immunoblot analysis showed that ExeD did not multimerize in C5.84, and fractionation of the membranes showed that the monomeric ExeD remained in the inner membrane. Expression of ExeAB, but not either protein alone, from a plasmid in C5.84 resulted in increases in the amount of multimeric ExeD, which correlated with increases in aerolysin secretion. Pulse-chase analysis also sug-gested that the induction of ExeAB allowed multimerization of previously accumulated monomer ExeD. In C5.84 cells overproducing ExeD, it multimerized even in the absence of ExeAB and, although most remained in the inner membrane, an amount similar to that in wild-type outer membranes fractionated with the outer membrane of the overproducing cells. These results indicate that the secretion defect of exeAB mutants is a result of an inability to assemble the ExeD secretin in the outer membrane. The localization and multimerization of overproduced ExeD in these mutants further suggests that the ExeAB complex plays either a direct or indirect role in the transport of ExeD into the outer membrane.
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  • 8
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    The @journal of organic chemistry 27 (1962), S. 3321-3323 
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: From previous work, it appears that glutamate can activate the hypothalamic-pituitary-adrenocortical (HPA) axis by an interaction at either ionotopic or metabotropic (G-protein coupled) receptors. For example, (1S,3R)-1-aminocyclopentane-1,3-dicarboxylate (ACPD), a metabotropic glutamate (mGlu) receptor agonist, has been shown to increase the levels of serum corticosterone in rats. The present study was undertaken to further characterize which of the mGlu receptors are substantially involved in control of the HPA axis. The group I mGlu receptor agonists, 3,5-dihydroxyphenylglycine (DHPG), 1S,3R-ACPD, and 2-chloro-5-hydroxyphenylglycine (CHPG) but not the inactive isomer 1R,3S-ACPD were found to dose-dependently increase serum corticosterone 1 h after intracerebroventricular (i.c.v.) injection in male rats. The relative potency, DHPG (EC50 = 520 nmol) 〉 1S,3R-ACPD (1.4 µmol) = CHPG (2.7 µmol) ≫ 1R,3S-ACPD (≫ 3 µmol) is consistent with activation of group I (mGlu1/5) receptors. The effects of DHPG were long lasting with substantial elevations in corticosterone remaining for at least 3 h. In a similar manner, the group III mGlu receptor agonists, L-AP4 (4-phosphono-2-aminobutyric acid) and L-SOP (serine-O-phosphate), were found to increase serum corticosterone levels at 1 h. In contrast, the mGlu group II selective agonists LY354740 (10 mg/kg, i.p.) and subtype-selective doses of the group II antagonist LY341495 (1 mg/kg, i.p.) did not significantly elevate serum corticosterone. Given the group I agonists results, it was surprising to find that group I selective and mGlu1 selective antagonists given alone also increased serum corticosterone. As with the agonists, the rise in serum corticosterone with LY393675 (an mGlu1/5 antagonist, EC50 = 20 nmol, i.c.v.) and LY367385 (an mGlu1 antagonist, 325 nmol, i.c.v.) were dose-dependent and consistent with their relative affinity for the group I mGlu receptors. The selective mGlu5 antagonist MPEP [2-methyl-6-(phenylethylnyl)pyridine] increased serum cortocosterone but only at high doses (〉 30 mg/kg, i.p.). A model involving the high glutamatergic tone on GABAergic interneurons in the paraventricular nucleus of the hypothalamus is discussed as a possible explanation for these results.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Anaesthesia 40 (1985), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A case is presented in which there was a need for a ‘wake-up test’. A technique is described, employing alfentanil and vecuronium given by infusion, and the problems of anaesthetic management are discussed.
    Type of Medium: Electronic Resource
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