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  1. Article: Role of bilirubin oxidation products in the pathophysiology of DIND following SAH.

    Pyne-Geithman, Gail J / Nair, Sunil G / Stamper, Danielle N Caudell / Clark, Joseph F

    Acta neurochirurgica. Supplement

    2013  Volume 115, Page(s) 267–273

    Abstract: Despite intensive research efforts, by our own team and many others, the molecules responsible for acute neurological damage following subarachnoid hemorrhage (SAH) and contributing to delayed ischemic neurological deficit (DIND) have not yet been ... ...

    Abstract Despite intensive research efforts, by our own team and many others, the molecules responsible for acute neurological damage following subarachnoid hemorrhage (SAH) and contributing to delayed ischemic neurological deficit (DIND) have not yet been elucidated. While there are a number of candidate mechanisms, including nitric oxide (NO) scavenging, endothelin-1, protein kinase C (PKC) activation, and rho kinase activation, to name but a few, that have been investigated using animal models and human trials, we are, it seems, no closer to discovering the true nature of this complex and enigmatic pathology. Efforts in our laboratory have focused on the chemical milieu present in hemorrhagic cerebrospinal fluid (CSF) following SAH and the interaction of the environment with the molecules generated by SAH and subsequent events, including NO scavenging, immune response, and clot breakdown. We have identified and characterized a group of molecules formed by the oxidative degradation of bilirubin (a clot breakdown product) and known as BOXes (bilirubin oxidation products). We present a synopsis of the characterization of BOXes as found in human SAH patients' CSF and the multiple signaling pathways by which BOXes act. In summary, BOXes are likely to play an essential role in the etiology of acute brain injury following SAH, as well as DIND.
    MeSH term(s) Animals ; Bilirubin/cerebrospinal fluid ; Brain Injuries/etiology ; Brain Ischemia/cerebrospinal fluid ; Brain Ischemia/complications ; Brain Ischemia/etiology ; Endothelin-1/cerebrospinal fluid ; Humans ; Models, Biological ; Muscle, Smooth, Vascular/metabolism ; Nitric Oxide/cerebrospinal fluid ; Oxidation-Reduction ; Protein Kinase C/cerebrospinal fluid ; Signal Transduction/physiology ; Subarachnoid Hemorrhage/cerebrospinal fluid ; Subarachnoid Hemorrhage/complications ; rho-Associated Kinases/cerebrospinal fluid
    Chemical Substances Endothelin-1 ; Nitric Oxide (31C4KY9ESH) ; rho-Associated Kinases (EC 2.7.11.1) ; Protein Kinase C (EC 2.7.11.13) ; Bilirubin (RFM9X3LJ49)
    Language English
    Publishing date 2013
    Publishing country Austria
    Document type Journal Article ; Review
    ISSN 0065-1419
    ISSN 0065-1419
    DOI 10.1007/978-3-7091-1192-5_47
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: PKC and Rho in vascular smooth muscle: activation by BOXes and SAH CSF.

    Pyne-Geithman, Gail J / Nair, Sunil G / Caudell, Danielle N / Clark, Joseph F

    Frontiers in bioscience : a journal and virtual library

    2008  Volume 13, Page(s) 1526–1534

    Abstract: Cerebral vasospasm (CV) remains a significant cause of delayed neurological deficit and ischemic damage after subarachnoid hemorrhage (SAH), despite intensive research effort. The current lack of an effective therapeutic approach is somewhat due to our ... ...

    Abstract Cerebral vasospasm (CV) remains a significant cause of delayed neurological deficit and ischemic damage after subarachnoid hemorrhage (SAH), despite intensive research effort. The current lack of an effective therapeutic approach is somewhat due to our lack of understanding regarding the mechanism by which this pathological constriction develops. Recent evidence implicates bilirubin oxidation products (BOXes) in the etiology of CV after SAH: BOXes are found in cerebrospinal fluid from SAH patients with symptomatic or angiographically visible vasospasm (CSFV) but not in CSF from SAH patients with no vasospasm (CSFC). We have previously published research suggesting that the etiology of CV comprises two components: a physiological stimulation to constrict and a pathological failure to relax. Both these components are elicited by CSFV, but not CSFC, and BOXes synthesized in the laboratory potentiate physiological constriction in arterial smooth muscle in vitro, and elicit contraction in pial arteries in vivo. In this paper, we will present our results concerning the action of BOXes on arterial smooth muscle constriction, compared with CSFV. We will also present evidence implicating temporal changes in PKC isoforms and Rho expression in both BOXes- and CSFV-elicited smooth muscle responses.
    MeSH term(s) Animals ; Bilirubin/metabolism ; Cerebral Arteries/pathology ; Hemorrhage ; Models, Biological ; Muscle, Smooth, Vascular/metabolism ; Oxygen/metabolism ; Protein Kinase C/metabolism ; Subarachnoid Hemorrhage/pathology ; Swine ; Time Factors ; Vasospasm, Intracranial/pathology ; rho-Associated Kinases/metabolism
    Chemical Substances rho-Associated Kinases (EC 2.7.11.1) ; Protein Kinase C (EC 2.7.11.13) ; Bilirubin (RFM9X3LJ49) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2008-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2141320-4
    ISSN 1093-9946
    ISSN 1093-9946
    DOI 10.2741/2778
    Database MEDical Literature Analysis and Retrieval System OnLINE

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