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  • 1
    Online Resource
    Online Resource
    Lidocaine Inhibits Tyrosine Kinase Activity of the Epidermal Growth Factor Receptor and Suppresses Proliferation of Corneal Epithelial Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Anesthesiology Vol. 100, No. 5 ( 2004-05-01), p. 1206-1210
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 5 ( 2004-05-01), p. 1206-1210
    Abstract: Although lidocaine is recognized as an excellent topical corneal analgesic, its toxic effect on corneal epithelial cells limits its use during corneal epithelial wound healing. Mechanism of the impairment of corneal reepithelialization with lidocaine, however, has not been evaluated. The authors' previous study revealed that lidocaine inhibits the activity of tyrosine kinase receptors through the interaction with specific amino acid sequences around autophosphorylation sites, including acidic, basic, and aromatic amino acids. Epidermal growth factor receptor (EGFR), a tyrosine kinase receptor with an important role in epithelial cell proliferation after corneal wounding, also possesses these amino acids sequences around autophosphorylation sites. The authors hypothesized that lidocaine would suppress tyrosine kinase activity of EGFR and would impair corneal epithelial cell proliferation. Methods To investigate the effect of lidocaine (4 microM-40 mM) on epidermal growth factor (EGF)-stimulated autophosphorylation of EGFR, the authors studied purified EGFR in microtubes. They cultured human corneal epithelial cells (HCECs) with EGF and lidocaine to investigate the effect of lidocaine on cell proliferation and on autophosphorylation of EGFR in HCECs. Results Lidocaine ( & gt; or =400 microM) significantly suppressed EGF-stimulated autophosphorylation of the purified EGFR. In the HCEC study, EGF alone stimulated cell proliferation and increased autophosphorylation of EGFR in HCECs. Lidocaine ( & gt; or = 400 microM) significantly suppressed both the proliferation of HCECs promoted by EGF and EGF-stimulated autophosphorylation of EGFR. Conclusion Lidocaine directly inhibits tyrosine kinase activity of EGFR and suppresses the corneal epithelial cell proliferation.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/00000542-200405000-00024
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 2016092-6
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  • 2
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    Online Resource
    Phosphodiesterase 3 Inhibition Reduces Platelet Activation and Monocyte Tissue Factor Expression in Knee Arthroplasty Patients
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Anesthesiology Vol. 111, No. 6 ( 2009-12-01), p. 1227-1237
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 111, No. 6 ( 2009-12-01), p. 1227-1237
    Abstract: Tissue damage during surgery activates platelets and provokes a prothrombic state. The current study attempted to determine the impact of phosphodiesterase 3 inhibitors on platelet activation, platelet-leukocyte aggregate formation, and monocyte tissue factor expression during and after total knee arthroplasty. Methods Thirty-four patients undergoing scheduled total knee arthroplasty were randomly assigned to receive either the phosphodiesterase 3 inhibitor milrinone or the same amount of saline perioperatively. The effects of milrinone on platelet and leukocyte function in vitro were then assessed in healthy volunteers. Results Perioperative infusion of milrinone significantly attenuated platelet activation; phosphorylation of intraplatelet p38 mitogen-activated protein kinase, extracellular signal-regulated kinase 1/2, and Akt; and platelet-leukocyte aggregation. Furthermore, perioperative tissue factor expression on monocytes and fibrin monomer complex production were reduced by milrinone infusion in patients undergoing total knee arthroplasty. In vitro studies using adenosine diphosphate- and collagen-stimulated blood samples from healthy volunteers confirmed the antiplatelet effects and reduced monocyte tissue factor expression by milrinone. These studies further showed that platelet aggregation and integrin alpha(IIb)beta(3) activation were modified by intraplatelet phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase/extracellular signal-regulated kinase pathways, and that P-selectin expression on platelets and platelet-leukocyte aggregation were modulated by intraplatelet p38 mitogen-activated protein kinase pathway. Conclusion Continuous milrinone infusion has the potential to reduce platelet activation and monocyte tissue factor expression during the perioperative period in total knee arthroplasty. These events may be mediated in part by the ability of milrinone to reduce activation of intraplatelet mitogen-activated protein kinases and phosphatidylinositol 3-kinase. The clinical impact of phosphodiesterase 3 inhibition on perioperative hemostasis remains to be elucidated.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/ALN.0b013e3181c155ce
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 2016092-6
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  • 3
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    Online Resource
    Sevoflurane Does Not Inhibit Human Platelet Aggregation Induced by Thrombin
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Anesthesiology Vol. 92, No. 1 ( 2000-01-01), p. 164-164
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 1 ( 2000-01-01), p. 164-164
    Abstract: Sevoflurane reportedly inhibits adenosine diphosphate-induced platelet aggregation by suppressing thromboxane A2 formation. The increase in intracellular calcium concentration that fosters platelet aggregation, however, is also induced by other cell signaling pathways, such as activation of the production of inositol 1,4,5-triphosphate by thrombin. The current study aimed to clarify the net influence of sevoflurane on thrombin-induced platelet aggregation. Methods Washed platelets were stimulated by thrombin after incubation with 0.5, 1.0, or 1.5 mM sevoflurane, halothane, or isoflurane. Aggregation curves were measured by an aggregometer. Intracellular calcium concentration was measured fluorometrically using fura-2. Calcium mobilization via plasma membrane calcium channels and the dense tubular system was assessed differentially. Intracellular inositol 1,4,5-triphosphate was measured by radioimmunoassay. Results Halothane significantly suppressed aggregation ratios at 5 min compared with those in controls (89 +/- 7%) to 71 +/- 10% (1.0 mM) and 60 +/- 11% (1.5 mM) and the increase in intracellular calcium concentration (controls, 821 +/- 95 nM vs. 440 +/- 124 nM [1.0 mM] or 410 +/- 74 nM [1.5 mM] ). Halothane also significantly inhibited release of calcium from the dense tubular system (controls, 220 +/- 48 nM vs. 142 +/- 31 nM [1.0 mM]). Neither sevoflurane nor isoflurane produced a net change in aggregation ratios, intracellular calcium concentration, or calcium mobilization. Halothane (1 mM) significantly suppressed inositol 1,4,5-triphosphate concentrations, whereas neither 1 mM isoflurane nor 1 mM sevoflurane had any effect. Conclusions Although sevoflurane has been reported to inhibit human platelet aggregation induced by weak agonists such as adenosine diphosphate, it does not inhibit human platelet aggregation induced by strong agonists such as thrombin.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/00000542-200001000-00028
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 2016092-6
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  • 4
    Online Resource
    Online Resource
    Profile of HIV Type 1 Infection and Genotypic Resistance Mutations to Antiretroviral Drugs in Treatment-Naive HIV Type 1-Infected Individuals in Hai Phong, Viet Nam
    Mary Ann Liebert Inc ; 2009
    In:  AIDS Research and Human Retroviruses Vol. 25, No. 2 ( 2009-02), p. 175-182
    Details
    In: AIDS Research and Human Retroviruses, Mary Ann Liebert Inc, Vol. 25, No. 2 ( 2009-02), p. 175-182
    Type of Medium: Online Resource
    ISSN: 0889-2229 , 1931-8405
    URL: Article
    DOI: 10.1089/aid.2008.0193
    RVK:
    XA 10000
    Language: English
    Publisher: Mary Ann Liebert Inc
    Publication Date: 2009
    detail.hit.zdb_id: 1475767-9
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