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Godfried M Roomans – One of the best experts on this subject based on the ideXlab platform.

  • Methods for X‐ray microanalysis of epidermis: the effect of local anaesthesia
    Journal of Microscopy, 1997
    Co-Authors: A. Grängsjö, Magnus Lindberg, Godfried M Roomans
    Abstract:

    The effect of local anaesthesia on the elemental content of cells in human epidermis was studied by electron probe X-ray micrmicroanalysis. Local anaesthesia with lidocaine was given by intracutaneous injection within 1 min prior to taking a skin biopsy. Biopsies taken without local anaesthesia were used as controls. Lidocaine with or without Adrenaline caused a significant increase in the concentrations of Na and Cl, and a decrease in the concentration of K in the cells of the stratum basale and the stratum spinosum, compared with the control samples. The presence of adrenalin in the anaesthetic did not change the effect of lidocaine. The effects of local anaesthesia have to be considered in planning and interpretation of clinical applications of X-ray micrmicroanalysis.

  • Methods for X-ray microanalysis of epidermis: the effect of local anaesthesia.
    Journal of Microscopy, 1997
    Co-Authors: A. Grängsjö, Magnus Lindberg, Godfried M Roomans
    Abstract:

    The effect of local anaesthesia on the elemental content of cells in human epidermis was studied by electron probe X-ray micrmicroanalysis. Local anaesthesia with lidocaine was given by intracutaneous injection within 1 min prior to taking a skin biopsy. Biopsies taken without local anaesthesia were used as controls. Lidocaine with or without Adrenaline caused a significant increase in the concentrations of Na and Cl, and a decrease in the concentration of K in the cells of the stratum basale and the stratum spinosum, compared with the control samples. The presence of adrenalin in the anaesthetic did not change the effect of lidocaine. The effects of local anaesthesia have to be considered in planning and interpretation of clinical applications of X-ray micrmicroanalysis.

A. Grängsjö – One of the best experts on this subject based on the ideXlab platform.

  • Methods for X‐ray microanalysis of epidermis: the effect of local anaesthesia
    Journal of Microscopy, 1997
    Co-Authors: A. Grängsjö, Magnus Lindberg, Godfried M Roomans
    Abstract:

    The effect of local anaesthesia on the elemental content of cells in human epidermis was studied by electron probe X-ray microanalysis. Local anaesthesia with lidocaine was given by intracutaneous injection within 1 min prior to taking a skin biopsy. Biopsies taken without local anaesthesia were used as controls. Lidocaine with or without Adrenaline caused a significant increase in the concentrations of Na and Cl, and a decrease in the concentration of K in the cells of the stratum basale and the stratum spinosum, compared with the control samples. The presence of adrenalin in the anaesthetic did not change the effect of lidocaine. The effects of local anaesthesia have to be considered in planning and interpretation of clinical applications of X-ray microanalysis.

  • Methods for X-ray microanalysis of epidermis: the effect of local anaesthesia.
    Journal of Microscopy, 1997
    Co-Authors: A. Grängsjö, Magnus Lindberg, Godfried M Roomans
    Abstract:

    The effect of local anaesthesia on the elemental content of cells in human epidermis was studied by electron probe X-ray microanalysis. Local anaesthesia with lidocaine was given by intracutaneous injection within 1 min prior to taking a skin biopsy. Biopsies taken without local anaesthesia were used as controls. Lidocaine with or without Adrenaline caused a significant increase in the concentrations of Na and Cl, and a decrease in the concentration of K in the cells of the stratum basale and the stratum spinosum, compared with the control samples. The presence of adrenalin in the anaesthetic did not change the effect of lidocaine. The effects of local anaesthesia have to be considered in planning and interpretation of clinical applications of X-ray microanalysis.

Enrique Cadenas – One of the best experts on this subject based on the ideXlab platform.

  • OXIDATION OF Adrenaline BY FERRYLMYOGLOBIN
    Free radical biology & medicine, 1998
    Co-Authors: Cecilia R Giulivi, Enrique Cadenas
    Abstract:

    Abstract The oxidation of Adrenaline by ferrylmyoglobin, the product formed by the oxidation of myoglobin with H 2 O 2 , was examined by absorption, fluorescence, and EPR spectroscopy in terms of the formation of intermediate free radicals and stable molecular products and the binding of Adrenaline oxidation products to the apoprotein. The reaction of Adrenaline with ferrylmyoglobin resulted in reduction of the hemoprotein to metmyoglobin and consumption of Adrenaline. Quantification of metmyoglobin formed per Adrenaline yielded a ratio of 1.66. The reaction was found first order on Adrenaline concentration and second order on ferrylmyoglobin concentration. This, together with the above ratio, suggested a mechanism by which two oxoferryl moieties (ferrylmyoglobin) were reduced by Adrenaline yielding metmyoglobin and the o -semiquinone state of Adrenaline. The decay of the o -semiquinone to adrenochrome was confirmed by an increase in absorbance at 485 nm. The product was nonfluorescent; alkalinization of the reaction mixture resulted in a strong fluorescence at 540 nm ascribed to 3,5,6-trihydroxyindol or adrenolutin. Hence, adrenochrome and its alkali-catalyzed product, adrenolutin, are the major molecular products formed during the oxidation of Adrenaline by ferrylmyoglobin. Semiquinones formed during the Adrenaline/ferrylmyoglobin interaction were detected by EPR, spin stabilizing these species with Mg 2+ . The six-line EPR spectrum observed (a N = 4.5 G, a N (CH 3 ) = 5.1, and a 2H = 0.91; g = 2.0040) may be assigned to the semiquinone forms of adrenochrome and/or adrenolutin or a composite of these species. The intensity of the EPR signal increased with time and its subsequent decay followed a second-order kinetics as inferred by the proportionality of the square of the EPR line intensity with H 2 O 2 concentration. Heme destruction and lysine loss, inherent in the reaction of metmyoglobin with H 2 O 2 , were prevented 80 and 34% by Adrenaline, respectively. The low protection exerted by Adrenaline against lysine loss was possibly due to the formation of Schiff bases between the ϵ-NH 2 group of lysine and the o -quinone oxidation product(s) of Adrenaline. The yield of Schiff base formation was 20–25%. The autoxidation of Adrenaline at physiological pH is extremely slow or nonexistent. These data provide a rationale for the primary oxidoxidation of Adrenaline by the pseudoperoxidatic activity of ferrylmyoglobin and suggest implications of the free radicals thereby formed for the oxidative damage in reperfusion injury.

S G Bown – One of the best experts on this subject based on the ideXlab platform.

  • Endoscopic treatment for bleeding peptic ulcers: randomised comparison of Adrenaline injection and Adrenaline injection + Nd:YAG laser photocoagulation.
    Gut, 1991
    Co-Authors: L A Loizou, S G Bown
    Abstract:

    Forty two patients with haemorrhage from peptic ulcers with visible vessels were enrolled in a randomised study comparing endoscopic haemostasis with Adrenaline (1:10,000) injections (Adrenaline group) and Adrenaline injection + neodymium yttrium-aluminium-garnet (Nd:YAG) laser photocoagulation (Adrenaline + laser group). The two groups (21 patients each) were well matched for factors affecting outcome. Surgery was performed for continued haemorrhage uncontrolled by endoscopic treatment or rebleeding after two endoscopic treatments. Haemostasis after one treatment was similar in the two groups: Adrenaline 16/21 (76%), Adrenaline + laser 18/21 (86%). Haemostasis after two treatments was numerically (0.05 less than p less than 0.10) greater in the Adrenaline + laser group: 21/21 (100%) v 18/21 (86%). Three patients (14%) in the Adrenaline group underwent uneventful emergency surgery. There were no deaths or procedure related complications in either group. Most bleeds from peptic ulcers with visible vessels can be controlled endoscopically without the need for surgery. Both treatments in this study proved highly efficacious in securing haemostasis. Adrenaline injection treatment seems to be the treatment of choice in view of its simplicity, low cost, and availability. Additional Nd:YAG laser treatment may provide a marginal improvement in efficacy, although a much larger trial would be required to prove this.

Jørgen Jensen – One of the best experts on this subject based on the ideXlab platform.

  • Adrenaline potentiates insulin stimulated pkb activation via camp and epac implications for cross talk between insulin and Adrenaline
    Cellular Signalling, 2005
    Co-Authors: Erlend O. Brennesvik, Chariklia Ktori, Jérôme Ruzzin, Einar Jebens, Peter R. Shepherd, Jørgen Jensen
    Abstract:

    Adrenaline and insulin are two of the most important hormones regulating a number of physiological processes in skeletal muscle. Insulin‘s effects are generally requiring PKB and Adrenaline effects cAMP and PICA. Recent evidence indicates cAMP can regulate PKB in some cell types via Epac (Exchange protein directly activated by cAMP). This suggests possible crossover between insulin and Adrenaline signalling in muscle. Here we find that Adrenaline alone did not influence PKB activation, but Adrenaline dramatically potentiated insulin-stimulated phosphorylation of PKB (both Ser 4 7 3 and Thr 3 0 8 ) and of PKBa and PKBp enzyme activities. These effects were inhibited by wortmannin but Adrenaline did not increase insulin-stimulated p85a PI 3-kinase activity. Adrenaline effects occurred via β-adrenergic receptors and accumulation of cAMP. Interestingly, the Epac specific cAMP analogue 8-(4-chlorophenylthio)-2′-O-methyl-cAMP potentiated insulin-stimulated PKB phosphorylation in a similar manner as Adrenaline did without activating glycogen phosphorylase. Inhibition of PKA by H89 decreased Adrenaline-stimulated glycogen phosphorylase activation but increased PKB activation, which further supports that Adrenaline increases insulin-stimulated PKB phosphorylation via Epac. Further, while Adrenaline and the Epac activator alone did not promote p70 S 6 K Thr 3 8 9 phosphorylation, they potentiated insulin effects. In conclusion, Adrenaline potentiates insulin-stimulated activation of PKB and p70 S 6 K via cAMP and Epac in skeletal muscle. Furthermore, the fact that Adrenaline alone did not activate PKB or p70 S 6 K suggests that a hormone can be a potent regulator of signalling despite no effects being seen when co-activators are lacking.

  • Adrenaline potentiates insulin-stimulated PKB activation via cAMP and Epac: implications for cross talk between insulin and Adrenaline.
    Cellular signalling, 2005
    Co-Authors: Erlend O. Brennesvik, Chariklia Ktori, Jérôme Ruzzin, Einar Jebens, Peter R. Shepherd, Jørgen Jensen
    Abstract:

    Adrenaline and insulin are two of the most important hormones regulating a number of physiological processes in skeletal muscle. Insulin‘s effects are generally requiring PKB and Adrenaline effects cAMP and PKA. Recent evidence indicates cAMP can regulate PKB in some cell types via Epac (Exchange protein directly activated by cAMP). This suggests possible crossover between insulin and Adrenaline signalling in muscle. Here we find that Adrenaline alone did not influence PKB activation, but Adrenaline dramatically potentiated insulin-stimulated phosphorylation of PKB (both Ser473 and Thr308) and of PKBalpha and PKBbeta enzyme activities. These effects were inhibited by wortmannin but Adrenaline did not increase insulin-stimulated p85alpha PI 3-kinase activity. Adrenaline effects occurred via beta-adrenergic receptors and accumulation of cAMP. Interestingly, the Epac specific cAMP analogue 8-(4-chlorophenylthio)-2′-O-methyl-cAMP potentiated insulin-stimulated PKB phosphorylation in a similar manner as Adrenaline did without activating glycogen phosphorylase. Inhibition of PKA by H89 decreased Adrenaline-stimulated glycogen phosphorylase activation but increased PKB activation, which further supports that Adrenaline increases insulin-stimulated PKB phosphorylation via Epac. Further, while Adrenaline and the Epac activator alone did not promote p70(S6K) Thr389 phosphorylation, they potentiated insulin effects. In conclusion, Adrenaline potentiates insulin-stimulated activation of PKB and p70(S6K) via cAMP and Epac in skeletal muscle. Furthermore, the fact that Adrenaline alone did not activate PKB or p70(S6K) suggests that a hormone can be a potent regulator of signalling despite no effects being seen when co-activators are lacking.