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  1. Article ; Online: An anti-inflammatory role for tranexamic acid in cardiac surgery?

    Robertshaw, Heidi J

    Critical care (London, England)

    2008  Volume 12, Issue 1, Page(s) 105

    Abstract: Pro- and anti-inflammatory cytokines are elevated after cardiac surgery. The control of the release of these major paracrine proteins is becoming clearer and they have been shown to be involved in the activation of the coagulation/fibrinolysis pathway, ... ...

    Abstract Pro- and anti-inflammatory cytokines are elevated after cardiac surgery. The control of the release of these major paracrine proteins is becoming clearer and they have been shown to be involved in the activation of the coagulation/fibrinolysis pathway, among other cascades. The association of a predominance of pro-inflammatory cytokines with morbidity in some patients, particularly following cardiac surgery, is well described but still incompletely understood. Clinical studies elucidating how clinicians may influence this cytokine release directly will improve our knowledge of the processes involved and could ultimately show benefit in better outcomes for patients.
    MeSH term(s) Antifibrinolytic Agents/therapeutic use ; Cardiac Surgical Procedures ; Cytokines/drug effects ; Cytokines/metabolism ; Cytokines/physiology ; Humans ; Inflammation Mediators/therapeutic use ; Postoperative Complications/metabolism ; Postoperative Complications/prevention & control ; Tranexamic Acid/therapeutic use
    Chemical Substances Antifibrinolytic Agents ; Cytokines ; Inflammation Mediators ; Tranexamic Acid (6T84R30KC1)
    Language English
    Publishing date 2008-01-16
    Publishing country England
    Document type Comment ; Editorial
    ZDB-ID 2041406-7
    ISSN 1466-609X ; 1364-8535
    ISSN (online) 1466-609X
    ISSN 1364-8535
    DOI 10.1186/cc6210
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5517: Show issues Location:
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  2. Article: Interleukin-10 regulates TNF-alpha-converting enzyme (TACE/ADAM-17) involving a TIMP-3 dependent and independent mechanism.

    Brennan, Fionula M / Green, Patricia / Amjadi, Parisa / Robertshaw, Heidi J / Alvarez-Iglesias, Montserrat / Takata, Masao

    European journal of immunology

    2008  Volume 38, Issue 4, Page(s) 1106–1117

    Abstract: IL-10 is a potent anti-inflammatory molecule, which regulates TNF-alpha at multiple levels. We investigated whether IL-10 also modulated the activity of the TNF-alpha-converting enzyme (TACE). Using an ex vivo fluorogenic assay we observed that LPS ... ...

    Abstract IL-10 is a potent anti-inflammatory molecule, which regulates TNF-alpha at multiple levels. We investigated whether IL-10 also modulated the activity of the TNF-alpha-converting enzyme (TACE). Using an ex vivo fluorogenic assay we observed that LPS rapidly induced TACE activity in monocytes coinciding with release of soluble TNF-alpha. In the presence of IL-10, TNF-alpha production and activation of surface TACE was significantly inhibited. Paradoxically, both LPS with or without IL-10 led to accumulation of surface TACE (albeit catalytically inactive) over a 24 h period. We investigated whether this was mediated through induction of endogenous tissue inhibitor metalloproteinase-3 (TIMP-3). We found that the inhibition of TACE activity at 2 h by IL-10 was not TIMP-3 dependent but that the late accumulation of surface TACE was prevented with TIMP-3 antibodies. Furthermore, induction of endogenous TIMP-3 was observed by western blotting in both LPS- and in LPS with IL-10-treated monocytes from 6 to 8 h of culture. These results indicate that IL-10 further regulates TNF-alpha by modulating TACE activation at early time points and by contributing to the induction of TIMP-3, the natural inhibitor of active TACE, at later time points. These observations add to our understanding of inflammation and the importance of homeostatic regulators of these events.
    MeSH term(s) ADAM Proteins/metabolism ; ADAM17 Protein ; Antibodies/immunology ; Catalysis ; Cell Membrane/drug effects ; Cell Membrane/enzymology ; Cells, Cultured ; Humans ; Interleukin-10/pharmacology ; Lipopolysaccharides/pharmacology ; Microscopy, Confocal ; Monocytes/drug effects ; Monocytes/immunology ; Monocytes/metabolism ; Solubility ; Tissue Inhibitor of Metalloproteinase-3/immunology ; Tissue Inhibitor of Metalloproteinase-3/metabolism ; Tumor Necrosis Factor-alpha/biosynthesis ; Up-Regulation
    Chemical Substances Antibodies ; Lipopolysaccharides ; Tissue Inhibitor of Metalloproteinase-3 ; Tumor Necrosis Factor-alpha ; Interleukin-10 (130068-27-8) ; ADAM Proteins (EC 3.4.24.-) ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86)
    Language English
    Publishing date 2008-04
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.200737821
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 489: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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    Zs.MG 85: Show issues

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  3. Article: Strategies for managing the diabetic patient.

    Robertshaw, Heidi J / McAnulty, Gregory R / Hall, George H

    Best practice & research. Clinical anaesthesiology

    2004  Volume 18, Issue 4, Page(s) 631–643

    Abstract: Diabetes mellitus is now classified as either 'type 1' (failure of endogenous insulin production) or 'type 2' ('insulin resistance') and can be diagnosed if fasting blood glucose is >6.1 mmol/l (110mg/dl) on two separate occasions or there is unequivocal ...

    Abstract Diabetes mellitus is now classified as either 'type 1' (failure of endogenous insulin production) or 'type 2' ('insulin resistance') and can be diagnosed if fasting blood glucose is >6.1 mmol/l (110mg/dl) on two separate occasions or there is unequivocal hyperglycaemia with acute metabolic decompensation or obvious symptoms. The prevalence of the disease is rising and may be as great as 12-14% in western populations aged over 40 years. Diabetes is complicated by micro- and macrovascular consequences of chronically elevated blood glucose concentrations, and diabetic patients are over-represented in hospital populations, particularly among patients requiring surgical interventions. It is associated with increased perioperative mortality and morbidity. Evidence is now accumulating that intensive glycaemic monitoring and the administration of insulin infusions to achieve tight glycaemic control are associated with an improvement of both perioperative mortality and morbidity.
    MeSH term(s) Adult ; Anesthesia, Conduction ; Anesthesia, General ; Blood Glucose ; Child ; Diabetes Mellitus/blood ; Diabetes Mellitus/classification ; Diabetes Mellitus/drug therapy ; Humans ; Hypoglycemic Agents/administration & dosage ; Hypoglycemic Agents/therapeutic use ; Insulin/administration & dosage ; Insulin/therapeutic use ; Intraoperative Care/methods
    Chemical Substances Blood Glucose ; Hypoglycemic Agents ; Insulin
    Language English
    Publishing date 2004-09-25
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1499424-0
    ISSN 1521-6896
    ISSN 1521-6896
    DOI 10.1016/j.bpa.2004.05.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Se 1117: Show issues Location:
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  4. Article: Interleukin-10 regulates TNF-α-converting enzyme (TACE/ADAM-17) involving a TIMP-3 dependent and independent mechanism

    Brennan, Fionula M / Green, Patricia / Amjadi, Parisa / Robertshaw, Heidi J / Alvarez-Iglesias, Montserrat / Takata, Masao

    European journal of immunology. 2008 Apr., v. 38, no. 4

    2008  

    Abstract: IL-10 is a potent anti-inflammatory molecule, which regulates TNF-α at multiple levels. We investigated whether IL-10 also modulated the activity of the TNF-α-converting enzyme (TACE). Using an ex vivo fluorogenic assay we observed that LPS rapidly ... ...

    Abstract IL-10 is a potent anti-inflammatory molecule, which regulates TNF-α at multiple levels. We investigated whether IL-10 also modulated the activity of the TNF-α-converting enzyme (TACE). Using an ex vivo fluorogenic assay we observed that LPS rapidly induced TACE activity in monocytes coinciding with release of soluble TNF-α. In the presence of IL-10, TNF-α production and activation of surface TACE was significantly inhibited. Paradoxically, both LPS with or without IL-10 led to accumulation of surface TACE (albeit catalytically inactive) over a 24 h period. We investigated whether this was mediated through induction of endogenous tissue inhibitor metalloproteinase-3 (TIMP-3). We found that the inhibition of TACE activity at 2 h by IL-10 was not TIMP-3 dependent but that the late accumulation of surface TACE was prevented with TIMP-3 antibodies. Furthermore, induction of endogenous TIMP-3 was observed by western blotting in both LPS- and in LPS with IL-10-treated monocytes from 6 to 8 h of culture. These results indicate that IL-10 further regulates TNF-α by modulating TACE activation at early time points and by contributing to the induction of TIMP-3, the natural inhibitor of active TACE, at later time points. These observations add to our understanding of inflammation and the importance of homeostatic regulators of these events.
    Language English
    Dates of publication 2008-04
    Size p. 1106-1117.
    Publishing place Wiley-VCH Verlag
    Document type Article
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.200737821
    Database NAL-Catalogue (AGRICOLA)

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    Z 2005/701: Show issues

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  5. Article: Identification and characterization of 4-[[4-(2-butynyloxy)phenyl]sulfonyl]-N-hydroxy-2,2-dimethyl-(3S)thiomorpholinecarboxamide (TMI-1), a novel dual tumor necrosis factor-alpha-converting enzyme/matrix metalloprotease inhibitor for the treatment of rheumatoid arthritis.

    Zhang, Yuhua / Xu, Jun / Levin, Jeremy / Hegen, Martin / Li, Guangde / Robertshaw, Heidi / Brennan, Fionula / Cummons, Terri / Clarke, Dave / Vansell, Nichole / Nickerson-Nutter, Cheryl / Barone, Dauphine / Mohler, Ken / Black, Roy / Skotnicki, Jerry / Gibbons, Jay / Feldmann, Marc / Frost, Philip / Larsen, Glenn /
    Lin, Lih-Ling

    The Journal of pharmacology and experimental therapeutics

    2004  Volume 309, Issue 1, Page(s) 348–355

    Abstract: Tumor necrosis factor (TNF)-alpha is a well validated therapeutic target for the treatment of rheumatoid arthritis. TNF-alpha is initially synthesized as a 26-kDa membrane-bound form (pro-TNF) that is cleaved by a Zn-metalloprotease named TNF-alpha- ... ...

    Abstract Tumor necrosis factor (TNF)-alpha is a well validated therapeutic target for the treatment of rheumatoid arthritis. TNF-alpha is initially synthesized as a 26-kDa membrane-bound form (pro-TNF) that is cleaved by a Zn-metalloprotease named TNF-alpha-converting enzyme (TACE) to generate the 17-kDa, soluble, mature TNF-alpha. TACE inhibitors that prevent the secretion of soluble TNF-alpha may be effective in treating rheumatoid arthritis (RA) patients. Using a structure-based design approach, we have identified a novel dual TACE/matrix metalloprotease (MMP) inhibitor 4-[[4-(2-butynyloxy)phenyl]sulfonyl]-N-hydroxy-2,2-dimethyl-(3S)thiomorpholinecarboxamide (TMI-1). This molecule inhibits TACE and several MMPs with nanomolar IC(50) values in vitro. In cell-based assays such as monocyte cell lines, human primary monocytes, and human whole blood, it inhibits lipopolysaccharide (LPS)-induced TNF-alpha secretion at submicromolar concentrations, whereas there is no effect on the TNF-alpha mRNA level as judged by RNase protection assay. The inhibition of LPS-induced TNF-alpha secretion is selective because TMI-1 has no effect on the secretion of other proinflammatory cytokines such as interleukin (IL)-1beta, IL-6, and IL-8. Importantly, TMI-1 potently inhibits TNF-alpha secretion by human synovium tissue explants of RA patients. In vivo, TMI-1 is highly effective in reducing clinical severity scores in mouse prophylactic collagen-induced arthritis (CIA) at 5, 10, and 20 mg/kg p.o. b.i.d. and therapeutic CIA model at 100 mg/kg p.o. b.i.d. In summary, TMI-1, a dual TACE/MMP inhibitor, represents a unique class of orally bioavailable small molecule TNF inhibitors that may be effective and beneficial for treating RA.
    MeSH term(s) ADAM Proteins ; ADAM17 Protein ; Animals ; Arthritis, Rheumatoid/drug therapy ; Cells, Cultured ; Disease Models, Animal ; Drug Interactions ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Female ; Humans ; Lipopolysaccharides/pharmacology ; Matrix Metalloproteinase Inhibitors ; Matrix Metalloproteinases/metabolism ; Metalloendopeptidases/antagonists & inhibitors ; Metalloendopeptidases/metabolism ; Mice ; Mice, Inbred DBA ; Morpholines/pharmacology ; Morpholines/therapeutic use ; RNA, Messenger/drug effects ; RNA, Messenger/metabolism ; Synovial Membrane/drug effects ; Synovial Membrane/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/secretion
    Chemical Substances Enzyme Inhibitors ; Lipopolysaccharides ; Matrix Metalloproteinase Inhibitors ; Morpholines ; RNA, Messenger ; Tumor Necrosis Factor-alpha ; apratastat (C6BZ5263BJ) ; ADAM Proteins (EC 3.4.24.-) ; Matrix Metalloproteinases (EC 3.4.24.-) ; Metalloendopeptidases (EC 3.4.24.-) ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86) ; Adam17 protein, mouse (EC 3.4.24.86)
    Language English
    Publishing date 2004-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3106-9
    ISSN 1521-0103 ; 0022-3565
    ISSN (online) 1521-0103
    ISSN 0022-3565
    DOI 10.1124/jpet.103.059675
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uf I Zs.40: Show issues Location:
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